Deepak Chopra & Seva.Love Announce "ChopraVerse: House of Enlightenment," the Metaverse for Wellbeing in Collaboration with Utopia – PR…

LOS ANGELES, Sept. 21, 2022 /PRNewswire/ -- Deepak Chopra and SEVA.LOVE, a first-of-its-kind platform that is empowering a culture of wellbeing in the metaverse, today announced "ChopraVerse," the metaverse for wellbeing in collaboration with Utopia. Utopia is a Web3 ecosystem brought together by Alejandro Saez, Maria Bravo, Eva Longoria, and Javier Garcia. The ChopraVerse initiative is part of Seva.Love's ongoing mission to create a more conscious Web3 community for a peaceful, just, sustainable, healthier and joyful world. The House of Enlightenment, designed by Vera Iconica Architecture, is Deepak Chopra's personal home in the metaverse that was initially designed for the physical world incorporating eastern wisdom design principles and the latest in wellness architecture.

The Metaverse today is mostly about gaming. The ChopraVerse is about creating a world which enhances our wellbeing. A world that will be photorealistic and inhabited by human avatars and AI beings. A world where no one will feel alone one that offers infinite experiences and possibilities. As part of the initial launch, The ChopraVerse will make the "Deepak Chopra - House of Enlightenment" available for everyone to experience in the metaverse and also enable downloadable blueprints for build in the physical world via NFTs.

"ChopraVerse is creating homes for multidimensional living, nourishing the body, mind, spirit and environment as a unified experience in awareness. It will give everyone an opportunity to generate their own abode for the return to wholeness and healing," says Deepak Chopra, world-renowned pioneer in integrative medicine, NY Times best selling author and co-founder of Seva.Love.

Utopia, which recently acquired Virtual Voyagers, has carried out more than 230 projects related to the metaverse for major brands such as META and Vodafone, winning more than 20 awards for innovation and creativity. "The opportunity Web3 technology currently presents to creators, developers and businesses is exciting on many levels. Utopia is born from the dream, duty, and vision of achieving a connection between the tangible and virtual world - in which we will live in an ethical, inclusive, and responsible way," says Nino Saez, co-founder and CEO of Utopia.

"The ChopraVerse will transform how we interact and experience wellbeing in the digital and physical world. Our collaboration with Utopia will enable us to experience interoperable metaverse experiences in real-time, 3D virtual worlds that can be experienced synchronously, maintain presence and have a collaborative experience," says Poonacha Machaiah, co-founder and CEO of SEVA.LOVE. "While the NFT world is incredible, it is still evolving, and we saw a gap in the market to build a wellbeing community and make real social impact via the metaverse."

"The Utopia and ChopraVerse collaboration will enable an ecosystem in the digital world for impactful collaborations within the metaverse, where we aim to bring global action to educate the world, connecting philanthropists, embracing brands and businesses using the power of the blockchain to raise awareness on building a more ethical and transparent world, a community of philanthropreneur's, spreading kindness fast to where it's needed," says Maria Bravo, co-founder Utopia and Global Gift Foundation.

The ChopraVerse roadmap has planned NFT drops which will serve as access tokens to the ChopraVerse in Utopia. Additionally, there will also be a limited number of NFTs that will integrate blueprints and wellbeing design principles, by licensure through the Architect, Vera Iconica Architecture, that can be leveraged to build homes in the physical world. "The House of Enlightenment was designed both to be built in the physical world and to be experienced by many in the digital world as a home that optimizes health and wellbeing in harmony with nature. It is an education and awareness tool that anyone can go into to learn meditation or how your surroundings are impacting your health and behavior and what you can do to elevate your state of being," says Veronica Schreibeis Smith, CEO & Founding Principal, Vera Iconica Architecture.

The ChopraVerse platform has built on its partnership with Deepak Chopra and is collaborating with other global wellbeing experts, products and services within its own metaverse while also integrating with brands and experiences in the Utopia metaverse.

For more information please visit: http://www.chopraverse.io

About Seva.Love

Seva.Love is the metaverse for wellbeing initiative that has been founded by serial technology entrepreneur Pooancha Machaiah and world-renowned pioneer in integrative medicine, personal transformation and NY Times bestselling author Deepak Chopra, MD.

Seva.Love is championing wellbeing and social impact in Web3 by curating leading artists, influencers, wellbeing experts and creating conscious communities. Seva.Love has exclusive access to Deepak Chopra web3 content and the ChopraVerse will enable transmedia storytelling and engage communities in the metaverse and IRL. Access to the Seva ecosystem will be via NFTs and the Seva token. For more information please visit https://www.seva.love/ and follow us at twitter: @sevaislove instagram: @sevaislove discord: https://discord.seva.love/

About Utopia

Utopia Group is a Web3 ecosystem brought together by four founders, Alejandro Saez, Maria Bravo, Eva Longoria, and Javier Garcia - with the mission of disrupting how businesses operate and innovate using the power of blockchain technology.

The Utopia Group's vision is to focus on bridging the gap between the physical and digital worlds. Through Utopia's acquisition of Virtual Voyageurs, the group will offer strategic consulting services, particularly developing metaverse applications and experiences, as well as educational programs and initiatives in the world of Web3.

About Vera Iconica Architecture

Founded in 2010 in Jackson by Wyoming native and Wellness Architecture pioneer, Veronica Schreibeis Smith, Vera Iconica specializes in Architecture, Interior Design, and Real Estate Development and is known globally for its Wellness Kitchen. Based in the Mountain West with offices in Jackson and Denver, Vera Iconica's highly flexible, international team of experts merges cultural, spiritual, and qualitative elements with hard science to create highly customized solutions that elevate healthy, conscious living. For more information please visit https://veraiconica.com/ and follow at instagram: @veraiconicaarchitecture

SOURCE SEVA.LOVE

Read the original here:
Deepak Chopra & Seva.Love Announce "ChopraVerse: House of Enlightenment," the Metaverse for Wellbeing in Collaboration with Utopia - PR...

Allergic to the world: can medicine help people with severe intolerance to chemicals? – The Guardian

Sharon calls herself a universal reactor. In the 1990s, she became allergic to the world, to the mould colonising her home and the paint coating her kitchen walls, but also deodorants, soaps and anything containing plastic. Public spaces rife with artificial fragrances were unbearable. Scented disinfectants and air fresheners in hospitals made visiting doctors torture. The pervasiveness of perfumes and colognes barred her from in-person social gatherings. Even stepping into her own back garden was complicated by the whiff of pesticides and her neighbours laundry detergent sailing through the air. When modern medicine failed to identify the cause of Sharons illness, exiting society felt like her only solution. She started asking her husband to strip and shower every time he came home. Grandchildren greeted her through a window. When we met for the first time, Sharon had been housebound for more than six years.

When I started medical school, the formaldehyde-based solutions used to embalm the cadavers in the human anatomy labs would cause my nose to burn and my eyes to well up representing the mild, mundane end of a chemical sensitivity spectrum. The other extreme of the spectrum is an environmental intolerance of unknown cause (referred to as idiopathic by doctors) or, as it is commonly known, multiple chemical sensitivity (MCS). An official definition of MCS does not exist because the condition is not recognised as a distinct medical entity by the World Health Organization or the American Medical Association, although it has been recognised as a disability in countries such as Germany and Canada.

Disagreement over the validity of the disease is partially due to the lack of a distinct set of signs and symptoms, or an accepted cause. When Sharon reacts, she experiences symptoms from seemingly every organ system, from brain fog to chest pain, diarrhoea, muscle aches, depression and odd rashes. There are many different triggers for MCS, sometimes extending beyond chemicals to food and even electromagnetic fields. Consistent physical findings and reproducible lab results have not been found and, as a result, people such as Sharon not only endure severe, chronic illness but also scrutiny over whether their condition is real.

The first reported case of MCS was published in the Journal of Laboratory and Clinical Medicine in 1952 by the American allergist Theron Randolph. Although he claimed to have previously encountered 40 cases, Randolph chose to focus on the story of one woman, 41-year-old Nora Barnes. She had arrived at Randolphs office at Northwestern University in Illinois with a diverse and bizarre array of symptoms. A former cosmetics salesperson, she represented an extreme case. She was always tired, her arms and legs were swollen, and headaches and intermittent blackouts ruined her ability to work. A doctor had previously diagnosed her with hypochondria, but Barnes was desperate for a real diagnosis.

Randolph noted that the drive into Chicago from Michigan had worsened her symptoms, which spontaneously resolved when she checked into her room on the 23rd floor of a hotel where, Randolph reasoned, she was far away from the noxious motor exhaust filling the streets. In fact, in his report Randolph listed 30 substances that Barnes reacted to when touched (nylon, nail polish), ingested (aspirin, food dye), inhaled (perfume, the burning of pine in fireplace) and injected (the synthetic opiate meperidine, and Benadryl).

He posited that Barnes and his 40 other patients were sensitive to petroleum products in ways that defied the classic clinical picture of allergies. That is, rather than an adverse immune response, such as hives or a rash where the body is reacting to a particular antigen, patients with chemical sensitivities were displaying an intolerance. Randolph theorised that, just as people who are lactose-intolerant experience abdominal pain, diarrhoea and gas because of undigested lactose creating excess fluid in their gastrointestinal tract, his patients were vulnerable to toxicity at relatively low concentrations of certain chemicals that they were unable to metabolise. He even suggested that chemical sensitivity research was being suppressed by the ubiquitous distribution of petroleum and wood products. MCS, he believed, was not only a matter of scientific exploration, but also of deep-seated corporate interest. Randolph concludes his report with his recommended treatment: avoidance of exposure.

In that one-page abstract, Randolph cut the ribbon on the completely novel but quickly controversial field of environmental medicine. Nowadays, we hardly question the ties between the environment and wellbeing. The danger of secondhand smoke, the realities of climate change and the endemic nature of respiratory maladies such as asthma are common knowledge. The issue was that Randolphs patients lacked abnormal test results (specifically, diagnostic levels of immunoglobulin E, a blood marker that is elevated during an immune response). Whatever afflicted them were not conventional allergies, so conventional allergists resisted Randolphs hypotheses.

Randolph was in the dark. Why was MCS only now rearing its head? He also asked another, more radical question: why did this seem to be a distinctly American phenomenon? After all, the only other mention of chemical sensitivities in medical literature was in the US neurologist George Miller Beards 1880 textbook A Practical Treatise on Nervous Exhaustion (Neurasthenia). Beard argued that sensitivity to foods containing alcohol or caffeine was associated with neurasthenia, a now-defunct term used to describe the exhaustion of the nervous system propagated by the USs frenetic culture of productivity. Like Beard, Randolph saw chemical sensitivities as a disease of modernity, and conceived the origin as wear-and-tear as opposed to overload.

Randolph proposed that Americans, propelled by the post-second world war boom, had encountered synthetic chemicals more and more in their workplaces and homes, at concentrations considered acceptable for most people. Chronic exposure to these subtoxic dosages, in conjunction with genetic predispositions, strained the body and made patients vulnerable. On the back of this theory, Randolph developed a new branch of medicine and, with colleagues, founded the Society for Clinical Ecology, now known as the American Academy of Environmental Medicine.

As his professional reputation teetered, his popularity soared and patients flocked to his care. Despite this growth in interest, researchers never identified blood markers in MCS patients, and trials found that people with MCS couldnt differentiate between triggers and placebos. By 2001, a review in the Journal of Internal Medicine found MCS virtually nonexistent outside western industrialised countries, despite the globalisation of chemical use, suggesting that the phenomenon was culturally bound.

MCS subsequently became a diagnosis of exclusion, a leftover label used after every other possibility was eliminated. The empirical uncertainty came to a head in 2021, when Quebecs public health agency, the INSPQ, published an 840-page report that reviewed more than 4,000 articles in the scientific literature, concluding that MCS is an anxiety disorder. In medicine, psychiatric disorders are not intrinsically inferior; serious mental illness is, after all, the product of neurological dysfunction. But the MCS patients I spoke to found the language offensive and irresponsible. Reducing what they felt in their eyes, throats, lungs and guts to anxiety was not acceptable at all.

As a woman I will call Judy told me: I would tell doctors my symptoms, and then theyd run a complete blood count and tell me I looked fine, that it must be stress, so theyd shove a prescription for an antidepressant in my face and tell me to come back in a year. In fact, because MCS is so stigmatising, such patients may never receive the level of specialised care they need. In the wake of her treatment, Judy was frequently bedbound from crushing fatigue, and no one took her MCS seriously. I think a lot of doctors fail to understand that we are intelligent, she said. A lot of us with chemical sensitivities spend a good amount of our time researching and reading scientific articles and papers. I probably spent more of my free time reading papers than most doctors.

Judy grew up in Texas, where she developed irritable bowel syndrome and was told by doctors that she was stressed. Her 20s were spent in Washington state where she worked as a consultant before a major health crash left her bedbound for years (again, the doctors said she was stressed). Later, after moving to Massachusetts, a new paint job at her home gave her fatigue and diarrhoea. She used to browse the local art museum every Saturday, but even fumes from the paintings irritated her symptoms. She visited every primary care doctor in her city, as well as gastroenterologists, cardiologists, neurologists, endocrinologists and even geneticists. Most of them reacted the same way: with a furrowed brow and an antidepressant prescription in hand. Not one allopathic doctor has ever been able to help me, Judy said.

Morton Teich is one of the few physicians who diagnoses and treats patients with MCS in New York. The entrance to his integrative medicine private practice is hidden away behind a side door in a grey-brick building on Park Avenue. As I entered the waiting room, the first thing to catch my eye was the monstrous mountain of folders and binders precariously hugging a wall, in lieu of an electronic medical record. I half-expected Teichs clinic to resemble the environmental isolation unit used by Randolph in the 1950s, with an airlocked entrance, blocked ventilation shafts and stainless-steel air-filtration devices, books and newspapers in sealed boxes, aluminium walls to prevent electromagnetic pollution, and water in glass bottles instead of a cooler. But there were none of the above. The clinic was like any other family medicine practice I had seen before; it was just very old. The physical examination rooms had brown linoleum floors and green metal chairs and tables. And there were no windows.

Although several of Teichs patients were chemically sensitive, MCS was rarely the central focus of visits. When he introduced me, as a student writing about MCS, to his first patient of the day, a petrol-intolerant woman whose appointment was over the phone because she was housebound, she admitted to never having heard of the condition. You have to remember, Teich told me, that MCS is a symptom. Its just one aspect of my patients problems. My goal is to get a good history and find the underlying cause. Later, when I asked him whether he had observed any patterns suggesting an organic cause of MCS, he responded: Mould. Almost always.

Many people with MCS I encountered online also cited mould as a probable cause. Sharon told me about her first episode in 1998, when she experienced chest pain after discovering black mould festering in her familys trailer home. A cardiac examination had produced no remarkable results, and Sharons primary care physician declared that she was having a panic attack related to the stress of a recent miscarriage. Sharon recognised that this contributed to her sudden health decline, but also found that her symptoms resolved only once she began sleeping away from home.

She found recognition in medical books such as Toxic (2016) by Neil Nathan, a retired family physician who argued that bodily sensitivities were the product of a hyper-reactive nervous system and a vigilant immune system that fired up in reaction to toxicities, much as Randolph had said. The conditions that Nathan describes are not supported by academic medicine as causes of MCS: mould toxicity and chronic Lyme disease are subject to the same critique.

Sharon went to see William Rea, a former surgeon (and Teichs best friend). Rea diagnosed her with MCS secondary to mould toxicity. Mould is everywhere, Teich told me. Not just indoors. Mould grows on leaves. Thats why people without seasonal allergies can become chemically sensitive during autumn. When trees shed their leaves, he told me, mould spores fly into the air. He suspected that American mould is not American at all, but an invasive species that rode wind currents over the Pacific from China. He mentioned in passing that his wife recently died from ovarian cancer. Her disease, he speculated, also had its roots in mould.

In fact, Teich commonly treats patients with nystatin, an antifungal medication used to treat candida yeast infections, which often infect the mouth, skin and vagina. I have an 80% success rate, he told me. I was dubious that such a cheap and commonplace drug was able to cure an illness as debilitating as MCS, but I could not sneer at his track record. Every patient I met while shadowing Teich was comfortably in recovery, with smiles and jokes, miles apart from the people I met in online support groups who seemed to be permanently in the throes of their illness.

However, Teich was not practising medicine as I was taught it. This was a man who believed that the recombinant MMR vaccine could trigger acute autism traditionally an anti-science point of view. When one of his patients, a charismatic bookworm Ill call Mark, arrived at an appointment with severe, purple swelling up to his knees and a clear case of stasis dermatitis (irritation of the skin caused by varicose veins), Teich reflexively blamed mould and wrote a prescription for nystatin instead of urging Mark to see a cardiologist. When I asked how a fungal infection in Marks toes could cause such a bad rash on his legs, he responded: We have candida everywhere, and its toxins are released into the blood and travel to every part of the body. The thing is, most people dont notice until its too late.

Moulds and fungi are easy scapegoats for inexplicable illnesses because they are so ubiquitous in our indoor and outdoor environments. A great deal of concern over mould toxicity (or, to use the technical term, mycotoxicosis) stems from the concept of sick-building syndrome, in which visible black mould is thought to increase sensitivity and make people ill. This was true of Mark, who could point to the demolition of an old building across the street from his apartment as a source of mould in the atmosphere. Yet in mainstream medicine, diseases caused by moulds are restricted to allergies, hypersensitivity pneumonitis (an immunologic reaction to an inhaled agent, usually organic, within the lungs) and infection. Disseminated fungal infections occur almost exclusively in patients who are immunocompromised, hospitalised or have an invasive foreign body such as a catheter. Furthermore, if clinical ecologists such as Teich are correct that moulds such as candida can damage multiple organs, then it must be spreading through the bloodstream. But I have yet to encounter a patient with MCS who reported fever or other symptoms of sepsis (the traumatic, whole-body reaction to infection) as part of their experience.

Teich himself did not use blood cultures to verify his claims of systemic candidiasis, and instead looked to chronic fungal infection of the nails, common in the general population, as sufficient proof.

I dont need tests or blood work, he told me. I rarely ever order them. I can see with my eyes that he has mould, and thats enough. It was Teichs common practice to ask his patients to remove their socks to reveal the inevitable ridges and splits on their big toenails, and thats all he needed.

Through Teich, I met a couple who were both chemically sensitive but otherwise just regular people. The wife, an upper-middle-class white woman I will call Cindy, had a long history of allergies and irritable bowel syndrome. She became ill whenever she smelled fumes or fragrances, especially laundry detergent and citrus or floral scents. Teich put both her and her husband on nystatin, and their sensitivities lessened dramatically.

What struck me as different about her case, compared with other patients with MCS, was that Cindy was also on a course of antidepressants and cognitive behavioural therapy, the standard treatment for anxiety and depression. It really helps to cope with all the stress that my illness causes. You learn to live despite everything, she said.

In contemporary academic medicine, stress and anxiety cause MCS, but MCS can itself cause psychiatric symptoms. Teich later told me, unexpectedly, that he had no illusions about whether MCS is a partly psychiatric illness: Stress affects the adrenals, and that makes MCS worse. The mind and the body are not separate. We have to treat the whole person.

Lose yourself in a great story: from politics to psychology, food to technology, culture to crime

To understand this case, I also spoke to Donald Black, associate chief of staff for mental health at the Iowa City Veterans Administration Health Care. He co-authored a recent article on idiopathic environmental intolerance that took a uniform stance on MCS as a psychosomatic disorder. In 1988, when Black was a new faculty member at the University of Iowa, he interviewed a patient entering a drug trial for obsessive-compulsive disorder. He asked the woman to list her medications, and watched as she started unloading strange supplements and a book about environmental illness from her bag.

The woman had been seeing a psychiatrist in Iowa City a colleague of Blacks who had diagnosed her with systemic candidiasis. Black was flummoxed. If that diagnosis was true, then the woman would be very ill, not sitting calmly before him. Besides, it was not up to a psychiatrist to treat a fungal infection. How did he make the diagnosis? Did he do a physical or run blood tests? No, the patient told him, the psychiatrist just said that her symptoms were compatible with candidiasis. These symptoms included chemical sensitivities. After advising the patient to discard her supplements and find a new psychiatrist, Black made some phone calls and discovered that, indeed, his colleague had fallen in with the clinical ecologists.

Black was intrigued by this amorphous condition that had garnered an endless number of names: environmentally induced illness, toxicant-induced loss of tolerance, chemical hypersensitivity disease, immune dysregulation syndrome, cerebral allergy, 20th-century disease, and mould toxicity. In 1990, he solicited the aid of a medical student to find 26 subjects who had been diagnosed by clinical ecologists with chemical sensitivities and to conduct an emotional profile. Every participant in their study filled out a battery of questions that determined whether they satisfied any of the criteria for psychiatric disorders. Compared with the controls, the chemically sensitive subjects had 6.3 times higher lifetime prevalence of major depression, and 6.8 times higher lifetime prevalence of panic disorder or agoraphobia; 17% of the cases met the criteria for somatisation disorder (an extreme focus on physical symptoms such as pain or fatigue that causes major emotional distress and problems functioning).

In my own review of the literature, it was clear that the most compelling evidence for MCS came from case studies of large-scale initiating events such as the Gulf war (where soldiers were uniquely exposed to pesticides and pyridostigmine bromide pills to protect against nerve agents) or the terrorist attacks on the US of 11 September 2001 (when toxins from the falling towers caused cancers and respiratory ailments for years). In both instances, a significant number of victims developed chemical intolerances compared with populations who were not exposed. From a national survey of veterans deployed in the Gulf war, researchers found that up to a third of respondents reported multi-symptom illnesses, including sensitivity to pesticides twice the rate of veterans who had not deployed. Given that Gulf war veterans experienced post-traumatic stress disorder at levels similar to those in other military conflicts, the findings have been used to breathe new life into Randolphs idea of postindustrial toxicities leading to intolerance. The same has been said of the first responders and the World Trade Centres nearby residents, who developed pulmonary symptoms when exposed to cigarette smoke, vehicle exhaust, cleaning solutions, perfume, or other airborne irritants after 9/11, according to a team at Mount Sinai.

Black, who doubts a real disease, has no current clinical experience with MCS patients. (Apart from the papers he wrote more than 20 years ago, he had seen only a handful of MCS patients over the course of his career.) Despite this, he had not only written the article about MCS, but also a guide in a major online medical manual on how to approach MCS treatment as a psychiatric disease. When I asked him if there was a way for physicians to regain the trust of patients who have been bruised by the medical system, he simply replied: No. For him, there would always be a subset of patients who are searching for answers or treatments that traditional medicine could not satisfy. Those were the people who saw clinical ecologists, or who left society altogether. In a time of limited resources, these were not the patients on which Black thought psychiatry needed to focus.

It became clear to me why even the de facto leading professional on MCS had hardly any experience actually treating MCS. In his 1990 paper, Black then a young doctor rightly observed that traditional medical practitioners are probably insensitive to patients with vague complaints, and need to develop new approaches to keep them within the medical fold. The study subjects clearly believed that their clinical ecologists had something to offer them that others did not: sympathy, recognition of pain and suffering, a physical explanation for their suffering, and active participation in medical care.

I wondered if Black had given up on these new approaches because few MCS patients wanted to see a psychiatrist in the first place.

Physicians on either side of the debate agreed that mental illness is a crucial part of treating MCS, with one I spoke to believing that stress causes MCS, and another believing that MCS causes stress. To reconcile the views, I interviewed another physician, Christine Oliver, a doctor of occupational medicine in Toronto, where she has served on the Ontario Task Force on Environmental Health. Oliver believes that both stances are probably valid and true. No matter what side youre on, she told me, theres a growing consensus that this is a public health problem.

Oliver represents a useful third position, one that takes the MCS illness experience seriously while sticking closely to medical science. As one of few MCS-agnostic physicians, she believes in a physiological cause for MCS that we cannot know and therefore cannot treat directly due to lack of research. Oliver agrees with Randolphs original suggestion of avoiding exposures, although she understands that this approach has resulted in traumatising changes in patients abilities to function. For her, the priority for MCS patients is a practical one: finding appropriate housing. Often unable to work and with a limited income, many of her patients occupy public housing or multi-family dwellings. The physician of an MCS patient must act like a social worker. Facilities such as hospitals, she feels, should be made more accessible by reducing scented cleaning products and soaps. Ultimately, finding a non-threatening space with digital access to healthcare providers and social support is the best way to allow the illness to run its course.

Whether organic or psychosomatic or something in between, MCS is a chronic illness. One of the hardest things about being chronically ill, wrote the American author Meghan ORourke in the New Yorker in 2013 about her battle against Lyme disease, is that most people find what youre going through incomprehensible if they believe you are going through it. In your loneliness, your preoccupation with an enduring new reality, you want to be understood in a way that you cant be.

A language for chronic illness does not exist beyond symptomatology, because in the end symptoms are what debilitate normal human functioning. In chronic pain, analgesics can at least deaden a patients suffering. The same cannot be said for MCS symptoms, which are disorienting in their chaotic variety, inescapability and inexpressibility. There are few established avenues for patients to completely avoid triggering their MCS, and so they learn to orient their lives around mitigating symptoms instead, whether that is a change in diet or moving house, as Sharon did. MCS comes to define their existence.

As a housebound person, Sharons ability to build a different life was limited. Outside, the world was moving forward, yet Sharon never felt left behind. What allowed her to live with chronic illness was not medicine or therapy, but the internet. On a typical day, Sharon wakes up and prays in bed. She wolfs down handfuls of pills and listens to upbeat music on YouTube while preparing her meals for the day: blended meats and vegetables, for easier swallowing. The rest of the day is spent on her laptop computer, checking email and Facebook, watching YouTube videos until her husband returns home in the evening. Then bed. This is how Sharon has lived for the past six years, and she does not expect anything different from the future. When I asked her if being homebound was lonely, I was taken aback at her reply: No.

In spite of not having met most of her 15 grandchildren (with two more on the way), Sharon keeps in daily contact with all of them. In fact, Sharon communicates with others on a nearly constant basis. Some people are very much extroverts, Sharon wrote. I certainly am. But there are also people who need physical touch and I can understand why they might need to see real people then but its very possible to be content with online friends. This is my life! The friendships that Sharon formed online with other housebound people with chronic illnesses were the longest-lasting and the most alive relationships she had ever known. She had never met her best friend of 20 years their relationship existed completely through letters and emails, until two years ago, when the friend died. That was very hard for me, Sharon wrote.

The pandemic changed very little of Sharons life. If anything, Covid-19 improved her situation. Sharons local church live-streamed Sunday service, telehealth doctor appointments became the default, YouTube exploded in content, and staying indoors was normalised. Sharon saw her network steadily expand as more older adults became isolated in quarantine.

People within the online MCS community call themselves canaries, after the birds historically used as sentinels in coalmines to detect toxic levels of carbon monoxide. With a higher metabolism and respiratory rate, the small birds would theoretically perish before the less-sensitive human miners, providing a signal to escape. The question for people with MCS is: will anyone listen?

Us canaries, said a woman named Vera, who was bedbound from MCS for 15 years after a botched orthopaedic surgery, we struggle and suffer in silence. Now, in the information age, they have colonised the internet to find people like themselves. For our part, we must reimagine chronic illness which will become drastically more common in the aftermath of the pandemic where what matters to the patient is not only a scientific explanation and a cure, but also a way to continue living a meaningful life. This calls into action the distinction between illness and disease that the psychiatrist and anthropologist Arthur Kleinman made in his 1988 book The Illness Narratives. Whereas a disease is an organic process within the body, illness is the lived experience of bodily processes. Illness problems, he writes, are the principal difficulties that symptoms and disability create in our lives.

By centring conversations about MCS on whether or not it is real, we alienate the people whose illnesses have deteriorated their ability to function at home and in the world. After all, the fundamental mistrust does not lie in the patient-physician relationship, but between patients and their bodies. Chronic illness is a corporeal betrayal, an all-out assault on the coherent self. Academic medicine cannot yet shed light on the physiological mechanisms that would explain MCS. But practitioners and the rest of society must still meet patients with empathy and acceptance, making space for their narratives, their lives, and their experience in the medical and wider world.

This essay was originally published in Aeon

Follow the Long Read on Twitter at @gdnlongread, listen to our podcasts here and sign up to the long read weekly email here.

Read this article:
Allergic to the world: can medicine help people with severe intolerance to chemicals? - The Guardian

Genetic footprints of assortative mating in the Japanese population – Nature.com

Study cohort description

We used data on a total of 172,270 individuals of Japanese and East Asian ancestry. Of these, data on 165,098 individuals were obtained from BBJ, which has enrolled 200,000 participants to date. BBJ is a multi-institutional hospital-based genome cohort that collected participants affected with at least one of 47 diseases20. We excluded (1) individuals with low genotyping call rates (<98%), (2) closely related individuals (PI_HAT0.125 by PLINK, v.1.90b4.4; https://www.cog-genomics.org/plink/) and (3) outliers from the Japanese cluster based on principal component analysis (PCA) using PLINK2 (v.2.00a2.3 and v.2.00a3; https://www.cog-genomics.org/plink/2.0/) with samples of the 1000 Genomes Projects. Further, we separated the BBJ individuals into two Japanese clusters22,27 the mainland cluster (n=156,151) and Ryukyu cluster (n=8,947), by visual inspection based on the PCA plot (Supplementary Fig. 1). All the participants provided written informed consent approved from ethics committees of RIKEN Center for Integrative Medical Sciences, and the Institute of Medical Sciences, the University of Tokyo.

The Japanese subjects in replication cohorts were collected from three Japanese population-based cohorts (the Nagahama cohort study, JBIC and the Osaka University healthy cohort). The Nagahama cohort study is a community-based cohort in Nagahama city, Shiga prefecture, Japan. The study recruited healthy individuals between the ages of 30 and 74 (ref. 46). JBIC consists of EpsteinBarr virus-transformed B lymphoblast cell lines of unrelated Japanese individuals47. Osaka University healthy cohort is a volunteer-based cohort study recruited from the Osaka University Graduate School of Medicine, the University of Tokyo and the University of Tsukuba48. For each cohort, we also excluded individuals with a low genotyping call rate, a high heterozygosity rate, closely related individuals (PI_HAT0.125) and PCA outliers from EAS populations28,48,49. In addition, we extracted the EAS individuals from UKB. UKB is a population-based cohort that recruited approximately 500,000 individuals between 40 and 69 years of age from across the United Kingdom50. We obtained EAS individuals from unrelated UKB individuals based on PCA visualization combined with the 1000 Genomes Projects (Supplementary Fig. 2). Finally, we included 16,119 individuals in the replication study (n=8,947 from BBJ Ryukyu, n=1,275 from Osaka University healthy cohort, n=2,945 from the Nagahama cohort study, n=1,110 from JBIC and n=1,842 from UKB EAS). This study was approved by the ethical committee of Osaka University Graduate School of Medicine.

BBJ collected baseline clinical information and dietary and activity habits information through interviews and reviews of medical records using a standardized questionnaire. We selected 81 traits (57 anthropometric traits and biomarkers, 11 dietary habits, six behavioural traits, six diseases and one dummy; Supplementary Tables 24). We used these data from participants above the age of 18, and drinking and smoking traits from those above the age of 20. We normalized each anthropometric trait and biomarker traits by applying rank-based inverse normal transformation as previously reported (Supplementary Table 8)51,52,53. For each dietary habit, the participants were asked to clarify the frequency of consumption on a four-point scale, and we assigned the corresponding values to their responses as previously described26, where almost every day=7, 34 days per week=3.5, 12 days per week=1.5 and rarely=0. Behavioural traits included ever versus never drinking and ever versus never smoking54 as binary traits, and the frequency of four PAs (light-PA, gymnastics, walking and sports). For each PA, participants were also asked for the frequency and the length of time per week on a seven-point scale, and we quantified the activity by converting the responses to total minutes of activity time per week (minweek1), where 30 (15) minday1=210 (105), <30 (15) minday1=140 (70), three to four times a week for 30 (15) min=105 (52.5), three to four times a week for <30 (15) min=70 (35), one to two times a week for 30 (15) min=45 (22.5), one to two times a week for <30 (15) min=30 (15) and rarely=0 (the number in parentheses indicates gymnastics time).

For disease phenotypes, cases with myocardial infarction, stable angina and unstable angina were reclassified as CAD. We then selected six diseases from the target disease of BBJ (T2D, dyslipidaemia, cataract, CAD, arrhythmia and ischaemic stroke), where the number of cases exceeded 10,000 individuals55.

In addition, we set a dummy phenotype as a negative control. We generated a phenotype with heritability (h2=0.5) from 10,000 causal variants randomly sampled from BBJ GWAS data using GCTA GWAS simulation56. The phenotype followed the model yj=gj+ej, where gj=i(Wiji) and Wij=(xij2pi)[2pi(1pi)]1/2, where xij is the genotype for the ith causal variant of the jth individual, pi is the allele frequency of the ith causal variant within a population and ej is the residual effect generated from a normal distribution with mean 0 and variance Var(gj)(1h2)/h2. i is the effect size of the ith causal variant generated from a normal distribution with mean 0 and variance 1 (ref. 57). The values were normalized by applying a rank-based inverse normal transformation.

The BBJ GWAS data were genotyped using the Illumina HumanOmniExpressExome BeadChip or a combination of the Illumina HumanOmniExpress and HumanExome BeadChips. The quality control of the genotypes was described elsewhere51. In brief, we excluded variants satisfying the following criteria: (1) call rate <99%, (2) P value for HWE<1.0106, (3) number of heterozygotes <5 and (4) a concordance rate <99.5% or a non-reference concordance rate between the GWAS array and whole genome sequencing. The genotype data were phased by Eagle (v.2; https://alkesgroup.broadinstitute.org/Eagle/), and imputed with the 1000 Genomes Project Phase3 (v.5) and BBJ1K using Minimac3 software (v.2.0.1; https://genome.sph.umich.edu/wiki/Minimac3). After imputation, we excluded variants with an imputation quality of R-square (Rsq)<0.7 and those with a minor allele frequency (MAF)<1%.

As for the other Japanese datasets, JBIC was genotyped using Illumina HumanCoreExome Beadchip. As stringent quality control filters, we excluded the variants that satisfied (1) call rate<0.99, (2) MAF<1% and (3) HWE P<1.0107 (ref. 47). Osaka University healthy cohort was genotyped using Illumina Infinium Asian Screening Array. We excluded the variants that satisfied (1) call rate<0.99, (2) minor allele count<5 and (3) HWE P<1.0105 (ref. 48). The Nagahama cohort study was genotyped using six genotype arrays. We then selected two platforms (Illumina Human610-Quad Beadchip and Illumina HumanOmni2.5-4v1 Beadchip) with a large number of samples. For each of the two datasets, we excluded variants with (1) call rate<0.98, (2) MAF<1% and (3) HWE P<1.0106 (ref. 28). Genotype data were phased by Shapeit (v.2; https://mathgen.stats.ox.ac.uk/genetics_software/shapeit/shapeit.html) or Eagle, and imputed with the reference panel from the 1000 Genomes Project Phase3 (v.5) and BBJ1K using Mimimac3. After imputation, we excluded variants with an imputation quality of Rsq<0.7 and MAF<1%.

The UKB project was genotyped using either Applied Biosystems UK BiLEVE Axiom Array or Applied Biosystems UKB Axiom Array. The genotypes were imputed using the Haplotype Reference Consortium, UK10K and the 1000 Genomes Phase 3 reference panel by IMPUTE4. The detailed characteristics of the cohort and genotypephenotype data were described elsewhere50. We extracted EAS individuals and excluded variants with INFO score 0.8 and MAF1%.

As independent external reference GWASs or genotype data of Japanese ancestry were not publicly available, we adopted a tenfold LOGO meta-analysis to maintain both the accuracy of the GWAS statistics and the statistical power in PGS21. We first randomly split the BBJ mainland samples into the 10 target subsets. GWAS was performed on 81 complex traits for samples excluding the target subset using GCTA-fastGWA (v.1.93.3beta2; https://cnsgenomics.com/software/gcta/#Overview) as a MLM approach with 7,401,847 autosomal variants23,24. For GCTA-fastGWA, we computed a sparse genetic relationship matrix (GRM) for BBJ participants (n=182,961) using slightly LD-pruning variants (LD-pruning parameters in PLINK: indep-pairwise 1000 100 0.9, and MAF1%, sparse GRM parameter: make-bK-sparse 0.05). Regarding the 57 anthropometric traits and biomarkers, the 11 dietary traits, the four PA traits and the two binary traits in the behavioural traits, we fitted age, age-squared, sex, the top 20 PCs and 47 disease status as covariates. For the six diseases, we also fitted age, age-squared, sex and the top 20 PCs as covariates. We also performed GWAS using GCTA-fastGWA for all individuals in the BBJ mainland cluster to apply to other Japanese or EAS datasets. LD score regression (LDSC, v.1.0.0; https://github.com/bulik/ldsc) was applied to the summary statistics of the whole-sample GWAS to estimate potential population stratification. We adopted the HapMap3 SNPs, excluding the human leukocyte antigen region, using precomputed LD scores from 1KG EAS downloaded from the LDSC software website (Supplementary Table 5)58.

To estimate phenotypic variances explained by imputed data for some of the traits, we applied GREML-LDMS using GCTA (v.1.93.2beta; https://cnsgenomics.com/software/gcta/#Overview)57. We created the GRM using all variants for BBJ mainland samples. We estimated LD scores using default parameters in GCTA, and stratified SNPs into LD score quartiles. Next, we divided the SNPs within each LD score quartile into six MAF groups (MAF<5%, 5%MAF<10%, 10%MAF<20%, 20%MAF<30%, 30%MAF<40%, 40%MAF) and generated 24 GRMs. We calculated the phenotypic variance for each GRM and summed them to derive the total phenotypic variance (Supplementary Table 7). In the calculations, we randomly sampled 50,000 unrelated individuals (GRM<0.05) randomly downsampled from BBJ mainland individuals to avoid computational burden and used the same normalized values for quantitative traits and covariates for binary traits as used in the GWAS analysis.

To derive PGSs of individuals in each of the target subsets, we applied PRS-CS (https://github.com/getian107/PRScs) to construct PGSs that included genome-wide HapMap3 variants. PRS-CS is one of the beta shrinkage methods, which applies a Bayesian regression framework to identify posterior variant effect sizes based on continuous shrinkage before using both GWAS summary data and the external LD reference panel25. When the training sample size was large enough and the casecontrol imbalance was small, the automated optimization model (PRS-CS-auto) had the same precision as the grid model59,60. Therefore, for each of the target folds, we estimated the posterior mean effects of SNPs from the MLM-GWAS summary data of all training samples using PRS-CS-auto with the precomputed HapMap3 SNP LD reference panel from 1KG EAS downloaded from the PRS-CS website. We calculated PGSodd and PGSeven of individuals within the target subset using the estimated posterior effect of SNPs by PLINK2 score function. We normalized the calculated PGSs for each trait in each target subset to compare the effect sizes across the phenotypes.

We quantified the trait variance explained by the derived PGSs in individuals within one withheld subgroup. Each trait was modelled as a combination of PGS and all covariates. The null hypothesis used the same model without the PGS term. We calculated the adjusted R2 for quantitative traits and the Nagelkerkes R2 for binary traits (Supplementary Table 5).

For GPD estimation, we performed PCA of even and odd number chromosomes for each of the target subsets. We then estimated GPD using a linear regression method following the formula based on the original study18:

$${mathrm{PGS}_{rm{odd}}}approx theta _{mathrm{{even}}_{mathrm{to}}_{mathrm{odd}}}{mathrm{PGS}_{rm{even}}} + 20{mathrm{PCs}_{rm{even}}}$$

$${mathrm{PGS}_{rm{even}}}approx theta _{mathrm{{odd}}_{mathrm{to}}_{mathrm{even}}}{mathrm{PGS}_{rm{odd}}} + 20{mathrm{PCs}_{rm{odd}}}$$

where PGS is the scaled polygenic score, PCs are the results of the PCA and is the estimate of GPD. We further meta-analysed the GPD estimate from each of the ten subsets using the fixed effect method using metafor (v.1.9-9; http://www.metafor-project.org/doku.php/metafor) implemented in R (v.3.4.0; https://www.r-project.org/). We also estimated the GPD for the other Japanese and EAS datasets using the summary results of the whole BBJ sample GWASs by PRS-CS-auto. Finally, we performed a meta-analysis on the GPD estimates from the BBJ and other Japanese and EAS datasets by the fixed effect method using metafor. We estimated the P value of meta-analysed GPD using the Wald test.

To assess the robustness of our analysis to the chosen grouping of chromosomes, we altered the combinations of chromosomes such that the number of SNPs was the same in the two groups: (1) first half and second half; chromosomes 18 versus chromosomes 922, and (2) pseudo-random chromosomes; chromosomes 1, 3, 5, 6, 9, 10, 13, 14, 17 and 18 versus chromosomes 2, 4, 7, 8, 11, 12, 15, 16, 19, 20, 21 and 22. Using the two alternative combinations, we estimated the GPD for each cohort and meta-analysed the results.

We also calculated the theoretical GPD derived in the original study18. The theoretical value () followed the formula,

$$theta = frac{{rho f_0}}{{2 - rho (2 - f_0)}}left[ {1 + frac{{M(1 - rho )}}{{nh_{mathrm{{eq}}}^2}}left{ {1 + frac{{rho f_0}}{{2(1 - rho )}}} right}^{ - 3}} right]^{ - 1}$$

where (rho = rh_{mathrm{{eq}}}^2), r is a phenotypic correlation between spouses, (h_{mathrm{eq}}^2) is an equilibrium heritability of the phenotype, (f_0 approx f_{mathrm{{eq}}}/(1 - rho )), (f_{{rm{eq}}} = h_{{rm{snp}}}^2/h_{{rm{eq}}}^2,) (h_{{rm{snp}}}^2) is a SNP-based heritability, M is the number of causal variants and n is the sample size of the GWAS.

We analysed individuals of white British ancestry determined by PCA (n=337,139) from UKB by adopting the tenfold LOGO approach to the six available traits (adult height, BMI, T2D, CAD, duration of light-PA and yoghurt consumption)50. When adult height and BMI were measured multiple times, we adopted the mean value to obtain a single value per participant and normalized the values using the rank-based inverse normal transformation method. Regarding T2D, the case was defined following the ICD-10 codes and probable T2D and possible T2D in a T2D inference algorithm based on Eastwood et al.61. We also defined individuals without any diabetes status as the T2D control based on ICD-10 and the inference algorithm. As for CAD, the case was extracted following ICD-10 codes, surgical procedure recodes, self-reported illness codes and self-reported operation codes based on Fall et al.62. Regarding the duration of light-PA (Data-Field 104920), we extracted the data from instance 0 (n=70,692) and converted the coding to categorical values. Regarding the consumption of yoghurt, we extracted data from instance 0 within consumers of yoghurt/ice cream as binary traits (n=70,692 and Data-Field 102080). From the imputed GWAS data, we excluded the variants that satisfied MAF1% and INFO score 0.8, and fastGWA conducted generalized MLM approaches for nine subset samples with adjustment for age, age-squared, sex, top 20 PCs, ascertainment centre information and batch information as covariates. For the six phenotypes, we estimated the PGSs for odd and even chromosomes by PRS-CS-auto using genome-wide HapMap SNPs and the 1KG EUR LD reference panel, and the GPD was estimated in the same way as described in the Japanese study. We further meta-analysed the GPD estimate from each of the ten subgroups by the fixed effect method using metafor.

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

See the original post:
Genetic footprints of assortative mating in the Japanese population - Nature.com

PsiQuantum Has A Goal For Its Million Qubit Photonic Quantum Computer To Outperform Every Supercomputer On The Planet – Forbes

PsiQuantum

In 2009, Jeremy O'Brien, a professor at the University of Bristol, published a research paper describing how to repurpose on-chip optical components originally developed by the telecom industry to manipulate single particles of light and perform quantum operations.

By 2016, based on the earlier photonic research, OBrien and three of his academic colleagues, Terry Rudolph, Mark Thompson, and Pete Shadbolt, created PsiQuantum.

The founders all believed that the traditional method of building a quantum computer of a useful size would take too long. At the companys inception, the PsiQuantum team established its goal to build a million qubit, fault-tolerant photonic quantum computer. They also believed the only way to create such a machine was to manufacture it in a semiconductor foundry.

Early alerts

PsiQuantum first popped up on my quantum radar about two years ago when it received $150 million in Series C funding which upped total investments in the company to $215 million.

That level of funding meant there was serious interest in the potential of whatever quantum device PsiQuantum was building. At that time, PsiQuantum was operating in a stealth mode, so there was little information available about its research.

Finally, after receiving another $450 million in Series D funding last year, PsiQuantum disclosed additional information about its technology. As recently as few weeks ago, a small $25 million US government grant was awarded jointly to PsiQuantum and its fabrication partner, GlobalFoundries, for tooling and further development of its photonic quantum computer. Having GlobalFoundries as a partner was a definite quality signal. GF is a high-quality, premiere fab and only one of the three tier one foundries worldwide.

With a current valuation of $3.15 Billion, PsiQuantum is following a quantum roadmap mainly paved with stepping stones of its own design with unique technology, components, and processes needed to build a million-qubit general-purpose silicon photonic quantum computer.

Technology

Classical computers encode information using digital bits to represent a zero or a one. Quantum computers use quantum bits (qubits), which can also represent a one or a zero, or be in a quantum superposition of some number between zero and one at the same time. There are a variety of qubit technologies. IBM, Google, and Rigetti use qubits made with small loops of wire that become superconductors when subjected to very cold temperatures. Quantinuum and IonQ use qubits formed by removing an outer valence electron from an atom of Ytterbium to create an ion. Atom Computing makes neutral atom spin qubits using an isotope of Strontium.

Light is used for various operations in superconductors and atomic quantum computers. PsiQuantum also uses light and turns infinitesimally small photons of light into qubits. Of the two types of photonic qubits - squeezed light and single photons - PsiQuantums technology of choice is single-photon qubits.

Using photons as qubits is a complex process. It is complicated to determine the quantum state of a single photon among trillions of photons with a range of varied frequencies and energies.

Dr. Pete Shadbolt is the Co-founder and Chief Science Officer of PsiQuantum. His responsibilities include overseeing the application and implementation of technology and scientific-related policies and procedures that are vital to the success of PsiQuantum. After earning his PhD in experimental photonic quantum computing from the University of Bristol in 2014, he was a postdoc at Imperial College researching the theory of photonic quantum computing. While at Bristol, he demonstrated the first-ever Variational Quantum Eigensolver and the first-ever public API to a quantum processor. He has been awarded the 2014 EPSRC "Rising Star" by the British Research Council; the EPSRC Recognizing Inspirational Scientists and Engineers Award; and the European Physics Society Thesis Prize.

Dr. Shadbolt explained that detecting a single photon from a light beam is analogous to collecting a single specified drop of water from the Amazon river's volume at its widest point.

That process is occurring on a chip the size of a quarter, Dr. Shadbolt said. Extraordinary engineering and physics are happening inside PsiQuantum chips. We are constantly improving the chips fidelity and single photon source performance.

Just any photon isnt good enough. There are stringent requirements for photons used as qubits. Consistency and fidelity are critical to the performance of photonic quantum computers. Therefore, each photon source must have high purity, proper brightness, and generate consistently identical photons.

The right partner

GlobalFoundries facility in Essex, Vermont

When PsiQuantum announced its Series D funding a year ago, the company revealed it had formed a previously undisclosed partnership with GlobalFoundries. Out of public view, the partnership had been able to build a first-of-its-kind manufacturing process for photonic quantum chips. This manufacturing process produces 300-millimeter wafers containing thousands of single photon sources, and a corresponding number of single photon detectors. The wafer also contains interferometers, splitters, and phase shifters. In order to control the photonic chip, advanced electronic CMOS control chips with around 750 million transistors were also built at the GlobalFoundries facility in Dresden, Germany.

Photon advantages

Every quantum qubit technology has its own set of advantages and disadvantages. PsiQuantum chose to use photons to build its quantum computer for several reasons:

Another major advantage of photon qubits worth highlighting is the ability to maintain quantum states for a relatively long time. As an example of lights coherence, despite traveling for billions of years, light emitted by distant stars and galaxies reaches earth with its original polarization intact. The longer a qubit can maintain its polarized quantum state, the more quantum operations it can perform, which makes the quantum computer more powerful.

Why start with a million qubits?

We believed we had cracked the code for building a million-qubit quantum computer, Dr. Shadbolt said. Even though that's a huge number, the secret seemed simple. All we had to do was use the same process as the one being used to put billions of transistors into cell phones. We felt a large quantum computer wouldnt exist in our lifetime unless we figured out how to build it in a semiconductor foundry. That idea has been turned into reality. We are now building quantum chips next to laptops and cell phone chips on the GlobalFoundries 300-millimeter platform.

According to Dr. Shadbolt, PsiQuantums custom fabrication line has made much progress. Surprisingly, building a million-qubit quantum machine in a foundry has many of the same non-quantum issues as assembling a classical supercomputer, including chip yields, reliability, high-throughput testing, packaging, and cooling albeit to cryogenic temperatures.

From the time that our first GlobalFoundries announcement was made until now, we've produced huge amounts of silicon, Dr. Shadbolt said. Weve done seven tapeouts in total and were now seeing hundreds and hundreds of wafers of silicon coming through our door. We are investing heavily in packaging, assembly systems, integration, and fiber attachment to ensure the highest efficiency of light flowing in and out of the chip.

PsiQuantum is performing a great deal of ongoing research as well as continually improving the performance of photonic components and processes. In addition to high-performance optical components, the technologies that enable the process are also very important. A few enablers include optical switches, fiber-to-chip interconnects, and bonding methods.

We have greatly improved the efficiency of our photon detectors over the last few tapeouts at GlobalFoundries, Dr. Shadbolt explained. Were constantly working to prevent fewer and fewer photons from being lost from the system. We also have driven waveguide losses to extremely low levels in our recent chips.

There is much innovation involved. Our light source for single photons is a good example. We shine laser light directly into the chip to run the single photon sources. The laser is about a trillion times more intense than the single photons we need to detect, so we must attenuate light on that chip by a factor of about a trillion.

Dr. Shadbolt attributes PsiQuantums manufacturing success to GlobalFoundries. From experience, he knows there is a significant difference between a second-tier foundry and a first-tier foundry like GlobalFoundries. Building chips needed by PsiQuantum can only be built with an extremely mature manufacturing process.

PsiQuantum has two demanding requirements. We need a huge number of components, and we need those components to consistently meet extremely demanding performance requirements. There are very few partners in the world who can reliably achieve something like this, and we always knew that partnering with a mature manufacturer like GlobalFoundries would be key to our strategy.

The partnership has also been beneficial for GlobalFoundries because it has gained additional experience with new technologies by adding PsiQuantums photonic processes to the foundry.

The end is in sight

According to Dr. Shadbolt, the original question of whether large numbers of quantum devices could be built in a foundry is no longer an issue as routinely demonstrated by its output of silicon. However, inserting new devices into the manufacturing flow has always been difficult. It is slow and it is very expensive. Nanowire single photon detectors are an example of a development that came directly from the university lab and was inserted into the manufacturing process.

PsiQuantums semiconductor roadmap only has a few remaining items to complete. Since a million qubits wont fit on a single chip, the quantum computer will require multiple quantum processor chips to be interconnected with optical fibers and facilitated by ultra-high-performance optical switches to allow teleportation and entanglement of single photon operations between chips.

What remains is the optical switch, Dr. Shadbolt said. You might ask why photonic quantum computing people have never built anything at scale? Or why they havent demonstrated very large entangled states? The reason is that a special optical switch is needed, but none exists. It must have very high performance, better than any existing state-of-the-art optical switch such as those used for telecom networking. Its a classical device, and its only function will be to route light between waveguides, but it must be done with extremely low loss and at very high speed. It must be a really, really good optical switch.

If it cant be bought, then it must be built

Implementing an optical switch with the right specs is a success-or-fail item for PsiQuantum. Since a commercial optical switch doesnt exist that fits the application needs, PsiQuantum was left with no choice but to build one. For the past few years, its management has been heavily investing in developing a very high-performance optical switch.

Dr. Shadbolt explained: I believe this is one of the most exciting things PsiQuantum is doing. Building an extremely high-performance optical switch is the next biggest thing on our roadmap. We believe it is the key to unlocking the huge promise of optical quantum computing.

Summary

PsiQuantum was founded on the belief that photonics was the right technology for building a fault tolerant quantum machine with a million qubits and that the proper approach was based on semiconductor manufacturing. In contrast to NISQ quantum computers, the founders wanted to avoid building incrementally larger and larger machines over time.

Considering the overall process needed to build a million-qubit quantum computer, its high degree of complexity, and the lack of proven tools and processes to do it with, PsiQuantum has made amazing progress since it first formed the company.

It established a true partnership with one of the best foundries in the world and produced seven tapeouts and funded a half dozen new tools to build a first-of-its-kind wafer manufacturing process, incorporating superconducting single photon detectors into a regular silicon-photonic chip.

And today, it is answering yet another challenge by building an optical switch to fill a void where the needed product doesnt exist.

It is no surprise that an ultra- high-performance optical switch is a key part of PsiQuantums plans to build a scalable million qubit quantum computer. Other quantum companies are also planning to integrate similar optical switching technology to scale modular QPU architectures within the decade. The high-performance optical switch PsiQuantum is developing could someday connect tens of thousands of quantum processing units in a future multi-million qubit quantum data center. As a standalone product, it could also be a source of additional revenue should PsiQuantum choose to market it.

Once the optical switch has been built, it will then need to be enabled into GlobalFoundries manufacturing flow. That is the last step needed to complete PsiQuantums foundry assembly process and then it will be ready to produce photonic quantum computer chips.

But even with a complete end-to-end manufacturing process, significantly more time will be needed to construct a full-blown fault-tolerant quantum computer. It will remain for PsiQuantum to build complete quantum computers around chips produced by GlobalFoundries. For that, it will need a trained workforce and a location and infrastructure where large qubit photonic quantum computers can be assembled, integrated, tested, and distributed.

Based on the amount of post-foundry work, development of the optical switch, and assembly that remains, and assuming no major technology problems or delays occur, I believe it will be after mid-decade before a photonic quantum computer of any scale can be offered by PsiQuantum.

Ill wrap this up with comments made by Dr. Shadbolt during our discussion about the optical switch. I believe it demonstrates why PsiQuantum has been, and will continue to be successful:

Even though the optical switch will obviously be a very powerful generic technology of interest to others, we are not interested in its generic usefulness. We are only interested in the fact that it will allow us to build a quantum computer that outperforms every supercomputer on the planet. That is our singular goal.

Paul Smith-Goodson is Vice President and Principal Analyst for quantum computing, artificial intelligence and space at Moor Insights and Strategy. You can follow him on Twitter for more current information on quantum, AI, and space.

Note: Moor Insights & Strategy writers and editors may have contributed to this article.

Moor Insights & Strategy, like all research and tech industry analyst firms, provides or has provided paid services to technology companies. These services include research, analysis, advising, consulting, benchmarking, acquisition matchmaking, and speaking sponsorships. The company has had or currently has paid business relationships with 88, Accenture, A10 Networks, Advanced Micro Devices, Amazon, Amazon Web Services, Ambient Scientific, Anuta Networks, Applied Brain Research, Applied Micro, Apstra, Arm, Aruba Networks (now HPE), Atom Computing, AT&T, Aura, Automation Anywhere, AWS, A-10 Strategies, Bitfusion, Blaize, Box, Broadcom, C3.AI, Calix, Campfire, Cisco Systems, Clear Software, Cloudera, Clumio, Cognitive Systems, CompuCom, Cradlepoint, CyberArk, Dell, Dell EMC, Dell Technologies, Diablo Technologies, Dialogue Group, Digital Optics, Dreamium Labs, D-Wave, Echelon, Ericsson, Extreme Networks, Five9, Flex, Foundries.io, Foxconn, Frame (now VMware), Fujitsu, Gen Z Consortium, Glue Networks, GlobalFoundries, Revolve (now Google), Google Cloud, Graphcore, Groq, Hiregenics, Hotwire Global, HP Inc., Hewlett Packard Enterprise, Honeywell, Huawei Technologies, IBM, Infinidat, Infosys, Inseego, IonQ, IonVR, Inseego, Infosys, Infiot, Intel, Interdigital, Jabil Circuit, Keysight, Konica Minolta, Lattice Semiconductor, Lenovo, Linux Foundation, Lightbits Labs, LogicMonitor, Luminar, MapBox, Marvell Technology, Mavenir, Marseille Inc, Mayfair Equity, Meraki (Cisco), Merck KGaA, Mesophere, Micron Technology, Microsoft, MiTEL, Mojo Networks, MongoDB, MulteFire Alliance, National Instruments, Neat, NetApp, Nightwatch, NOKIA (Alcatel-Lucent), Nortek, Novumind, NVIDIA, Nutanix, Nuvia (now Qualcomm), onsemi, ONUG, OpenStack Foundation, Oracle, Palo Alto Networks, Panasas, Peraso, Pexip, Pixelworks, Plume Design, PlusAI, Poly (formerly Plantronics), Portworx, Pure Storage, Qualcomm, Quantinuum, Rackspace, Rambus, Rayvolt E-Bikes, Red Hat, Renesas, Residio, Samsung Electronics, Samsung Semi, SAP, SAS, Scale Computing, Schneider Electric, SiFive, Silver Peak (now Aruba-HPE), SkyWorks, SONY Optical Storage, Splunk, Springpath (now Cisco), Spirent, Splunk, Sprint (now T-Mobile), Stratus Technologies, Symantec, Synaptics, Syniverse, Synopsys, Tanium, Telesign,TE Connectivity, TensTorrent, Tobii Technology, Teradata,T-Mobile, Treasure Data, Twitter, Unity Technologies, UiPath, Verizon Communications, VAST Data, Ventana Micro Systems, Vidyo, VMware, Wave Computing, Wellsmith, Xilinx, Zayo, Zebra, Zededa, Zendesk, Zoho, Zoom, and Zscaler. Moor Insights & Strategy founder, CEO, and Chief Analyst Patrick Moorhead is an investor in dMY Technology Group Inc. VI, Dreamium Labs, Groq, Luminar Technologies, MemryX, and Movandi.

Moor Insights & Strategy founder, CEO, and Chief Analyst Patrick Moorhead is an investor in dMY Technology Group Inc. VI, Dreamium Labs, Groq, Luminar Technologies, MemryX, and Movand

Read more from the original source:
PsiQuantum Has A Goal For Its Million Qubit Photonic Quantum Computer To Outperform Every Supercomputer On The Planet - Forbes

The Israel Innovation Authority is building a new quantum computing research center – what will the impact be? – Diginomica

In July 2022, the Israel Innovation Authority announced a budget of NIS 100 million ($29 million) to build a quantum computing research center headed by Israeli startup Quantum Machines, which will also help create a quantum computer.

Israels new quantum computing center is part of the NIS 1.25 billion ($390 million) Israel National Quantum Initiative, launched in 2018 to facilitate relevant quantum research, develop human capital in the field, encourage industrial projects, and invite international cooperation on R&D.

Israel has about two dozen startups and companies currently focused on quantum technologies, including Quantum Machines, whichraised $50 millionlast September. The company was founded in 2018, and went on to develop a standard universal language for quantum computers, as well as a unique platform that helps them run.

According to the Times of Israel, Defense Ministrys Directorate of Defense Research and Development (DDR&D) will issue a separate tender to finance the development of quantum technologies for military use for another NIS 100 million, the innovation authority said. According to their joint announcement Tuesday, the budget will fund two parallel avenues. The Israel Innovation Authority will focus on developing the infrastructure for quantum computational ability, which, it said, may include the use of technology from abroad. Meanwhile, the Defense Ministrys Directorate of Defense Research and Development (DDR&D) will establish a national center with quantum capabilities that will work with academia, industry, and government partners to develop a quantum processor and a complete quantum computer.

Tech giants like Google, Microsoft, IBM, and Intel are allracingto make quantum computing more accessible and build their systems. Countries such as China, the US, Germany, India, and Japanare pouring millionsinto developing their quantum abilities.

According to recent marketprojections, the global quantum computing market size was expected to have been worth $487.4 million in 2021, and reach $3.7 billion by 2030. Israels $29 million is minuscule compared to the governments above, and the tech elephants.

These government-funded initiatives to achieve dominance in critical technology remind me of Japans Fifth Generation, which never really reached its goals.

Itamar Sivan, co-founder and CEO of Quantum Machines, said in a company statement that the project's goal was to give Israeli companies access to the most advanced quantum technologies and services so that they can develop deep quantum expertise across industry and academia. This expertise will allow Israeli companies across various sectors and industries to gain a leading global position.

Quantum Machines, founded in 2018, has built a hardware and software solution Quantum Orchestration Platform (QOP) for operating quantum systems to facilitate research and enable future breakthroughs. The startup also developed the QUA, a standard universal language for quantum computers that will allow researchers and scientists to write programs for varied quantum computers with one unified code. Quantum Machines, together with a consortium of Israeli and international quantum tech companies at the center, will build a quantum computer to be made available to the commercial and research communities.

Israels $29 million is minuscule compared to the governments above and tech elephants. According torecent market projections, the global quantum computing market is expected to grow from about $470 million in 2021 to about $1.765 billion by 2026.

Quantum Machines is an exciting company. They possess no quantum computer of their own, and their products are somewhat unique. While most quantum computers are in labs as objects of experiments by scientists, Sivan explained something I didnt realize to me. According to Sivan, a quantum computer needs three elements: a quantum computer and an orchestration platform of (conventional) hardware and software. There is no software in a quantum computer. The platform manages the progress of its algorithm mainly through laser beam pulses. The logic needed to operate the quantum computer resides with and is controlled by the orchestration platform.

The crucial difference between Google's and Quantum Machines' strategy is that Google views the current NISQ state of affairs as a testbed for finding algorithms and applications for future development. At the same time, Sivan and his company produced an orchestration platform to put the current technology into play. Their platform is quantum computer agnostic it can operate with any of them. Sivan feels that focusing solely on the number of qubits is just part of the equation.

The center will offer access to research and development on three quantum processing technologies superconducting qubits, cold ions, and optic compute and provide services to the Israeli quantum computing community, the Israel Innovation Authority said Sunday. As per the Times of Israel:

Ami Appelbaum, chairman of the Israel Innovation Authority, said the new center was 'the answer to an existing strategic market failure and is part of the authoritys policy of enabling the industry to maintain its leading position at the forefront of breakthrough and disruptive technologies.'

'Quantum computing is a technology Israeli industry cannot ignore,' said Israel Innovation Authority CEO Dror Bin in a statement Tuesday. 'The industry must develop knowledge and access to infrastructure in which it can develop growth engines for activities it will decide to lead.'

I've always believed that action speaks louder than words. While Google is taking the long view, Quantum Machines provides the platform to see how far we can go with current technology. As I wrote in The unpredictable rise of quantum computing - have recent breakthroughs accelerated the timeline?

Google suggests the real unsolved problems in fields like optimization, materials science, chemistry, drug discovery, finance, and electronics will take machines with thousands of qubits and even envision one million on a planar array etched in aluminum. Major problems need solving, such as noise elimination, coherence, and lifetime (a qubit holds its position in a tiny time slice).

Googles tactics are familiar. Every time you use TensorFlow, it gets better. Every time you play with their autonomous car, it gets better. Their collaboration with a dozen technically advanced companies improves their quantum technology.

Follow this link:
The Israel Innovation Authority is building a new quantum computing research center - what will the impact be? - Diginomica

Gamaredon continues to target Ukraine. RedLine stealer disguised as game cheats. Emotet’s place in the malware landscape. Quantum computing risks. -…

At a glance.

Cisco Talos says the Russian threat actor Gamaredon (also known as Primitive Bear) continues to conduct espionage campaigns against Ukrainian organizations. The threat actor is using spearphishing emails to distribute malicious Microsoft Office documents:

"Cisco Talos discovered Gamaredon APT activity targeting users in Ukraine with malicious LNK files distributed in RAR archives. The campaign, part of an ongoing espionage operation observed as recently as August 2022, aims to deliver information-stealing malware to Ukrainian victim machines and makes heavy use of multiple modular PowerShell and VBScript (VBS) scripts as part of the infection chain. The infostealer is a dual-purpose malware that includes capabilities for exfiltrating specific file types and deploying additional binary and script-based payloads on an infected endpoint."

Kaspersky warns that the RedLine Trojan is being distributed with a bundle of malware that can spread itself by posting YouTube videos with malicious links. The researchers note that while this technique is unusual, it's achieved by "using relatively unsophisticated software":

"In addition to the payload itself, the discovered bundle is of note for its self-propagation functionality. Several files are responsible for this, which receive videos, and post them to the infected users YouTube channels along with the links to a password-protected archive with the bundle in the description. The videos advertise cheats and cracks and provide instructions on hacking popular games and software. Among the games mentioned are APB Reloaded, CrossFire, DayZ, Dying Light 2, F1 22, Farming Simulator, Farthest Frontier, FIFA 22, Final Fantasy XIV, Forza, Lego Star Wars, Osu!, Point Blank, Project Zomboid, Rust, Sniper Elite, Spider-Man, Stray, Thymesia, VRChat and Walken. According to Google, the hacked channels were quickly terminated for violation of the companys Community Guidelines."

Researchers at AdvIntel haveobservedmore than 1.2 million Emotet infections since the beginning of 2022. Most of the infections (35.7%) are located in the United States. The researchers also warn that the Quantum and BlackCat ransomware groups are now using the malware distribution botnet following the breakup of Conti in June 2022. BleepingComputeraddsthat significant spikes in Emotet activity were observed by both AdvIntel andESETin 2022.

According to Check Points visibility, however, the FormBook infostealer replaced Emotet as the most prevalent malware strain in August 2022, followed by the AgentTesla Trojan, the XMRig cryptominer, and the Guloader downloader.

Deloitte has published the results of a survey on awareness of cybersecurity risks related to quantum computing. The survey found that just over half (50.2%) of respondents are aware of harvest now, decrypt later attacks. These attacks involve stealing encrypted data and storing it until a quantum computer is developed that can break the encryption.

26.6% of respondents said their organization has already conducted a risk assessment on quantum computing risks, while 18.4% plan to conduct an assessment within one year.

Additionally, 27.7% of respondents said their organization would be most likely to address quantum risks following regulatory pressure, while 20.7% cited leadership demand within the organization to enable the cryptographic agility which can address the algorithms made obsolete by quantum computing.

Read more:
Gamaredon continues to target Ukraine. RedLine stealer disguised as game cheats. Emotet's place in the malware landscape. Quantum computing risks. -...

IonQ to Participate in IEEE International Conference on Quantum Computing and Engineering (QCE22) – Business Wire

COLLEGE PARK, Md.--(BUSINESS WIRE)--IonQ (NYSE: IONQ), an industry leader in quantum computing, today announced its participation in IEEE International Conference on Quantum Computing and Engineering (QCE22). The weeklong event will take place in Broomfield, Colorado, on September 18-23, 2022, and brings together some of the worlds leading quantum researchers, scientists, entrepreneurs, and academics to discuss and explore the latest advancements in the field of quantum.

IonQ co-founder and Chief Scientist Chris Monroe will keynote the event on September 19, where he will summarize the distinct advantages of trapped ion quantum computers in both academic and industrial settings, along with their uses in scientific and commercial applications. Fellow co-founder and Chief Technology Officer Jungsang Kim will also be participating in a workshop program on September 20, focused on constructing control systems for trapped ion quantum computers.

Additional IonQ team members will also be joining a number of workshops and panel discussions throughout the week, exploring topics like working with the Microsoft Azure Quantum Platform, the need for low-level programming to deliver quantum advantage, and the key challenges when scaling towards practical quantum computing. Fellow panelists and workshop participants include researchers and executives from Microsoft, IBM, Lawrence Berkeley National Laboratory, and more.

Visit the conference page here to learn more about QCE22, or click here to learn more about IonQs latest updates to its IonQ Aria system.

About IonQ

IonQ, Inc. is a leader in quantum computing, with a proven track record of innovation and deployment. IonQ's current generation quantum computer, IonQ Forte, is the latest in a line of cutting-edge systems, including IonQ Aria, a system that boasts industry-leading 23 algorithmic qubits. Along with record performance, IonQ has defined what it believes is the best path forward to scale. IonQ is the only company with its quantum systems available through the cloud on Amazon Braket, Microsoft Azure, and Google Cloud, as well as through direct API access. IonQ was founded in 2015 by Christopher Monroe and Jungsang Kim based on 25 years of pioneering research. To learn more, visit http://www.ionq.com.

IonQ Forward-Looking Statements

This press release contains certain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. Some of the forward-looking statements can be identified by the use of forward-looking words. Statements that are not historical in nature, including the words anticipate, expect, suggests, plan, believe, intend, estimates, targets, projects, should, could, would, may, will, forecast and other similar expressions are intended to identify forward-looking statements. These statements include those related to IonQs ability to further develop and advance its quantum computers and achieve scale; IonQs ability to optimize quantum computing results even as systems scale; the expected launch of IonQ Forte for access by select developers, partners, and researchers in 2022 with broader customer access expected in 2023; IonQs market opportunity and anticipated growth; and the commercial benefits to customers of using quantum computing solutions. Forward-looking statements are predictions, projections and other statements about future events that are based on current expectations and assumptions and, as a result, are subject to risks and uncertainties. Many factors could cause actual future events to differ materially from the forward-looking statements in this press release, including but not limited to: market adoption of quantum computing solutions and IonQs products, services and solutions; the ability of IonQ to protect its intellectual property; changes in the competitive industries in which IonQ operates; changes in laws and regulations affecting IonQs business; IonQs ability to implement its business plans, forecasts and other expectations, and identify and realize additional partnerships and opportunities; and the risk of downturns in the market and the technology industry including, but not limited to, as a result of the COVID-19 pandemic. The foregoing list of factors is not exhaustive. You should carefully consider the foregoing factors and the other risks and uncertainties described in the Risk Factors section of IonQs Quarterly Report on Form 10-Q for the quarter ended March 31, 2022 and other documents filed by IonQ from time to time with the Securities and Exchange Commission. These filings identify and address other important risks and uncertainties that could cause actual events and results to differ materially from those contained in the forward-looking statements. Forward-looking statements speak only as of the date they are made. Readers are cautioned not to put undue reliance on forward-looking statements, and IonQ assumes no obligation and does not intend to update or revise these forward-looking statements, whether as a result of new information, future events, or otherwise. IonQ does not give any assurance that it will achieve its expectations.

Link:
IonQ to Participate in IEEE International Conference on Quantum Computing and Engineering (QCE22) - Business Wire

Zapata Computing and The University of Hull Get Quantum-Ready For Ongoing Search for Life in Space – Business Wire

BOSTON--(BUSINESS WIRE)--Zapata Computing, the leading enterprise quantum software company, today announced that it has made significant headway in its mission to get the University of Hull quantum-ready for future space exploration. One year into the collaboration both teams have seen enough progress to extend their plans for expanding the search for indicators of life in deep space.

Together, Zapata and the University of Hull developed new techniques to extrapolate meaningful data from noisy quantum devices and used it to calculate the ro-vibrational spectrum of hydrogen to obtain results that are comparable with the state-of-the-art classical simulations, as well as the experimental results. The results obtained with these new quantum techniques can already be used to detect molecular hydrogen in space.

A big part of the progress is due to the University of Hulls successful migration of Big Compute capabilities from classical to quantum computers. Big Compute is Zapatas term for the market category for heterogeneous and distributed compute resources needed to address enterprise and other technologically advanced organizations most computationally complex problems. It builds on previous technical revolutions like Big Data and AI and leverages a wide spectrum of classical (e.g., GPU, TPU, CPU), high-performance (HPC) and quantum compute resources (e.g., quantum-inspired computers, NISQ devices, fault-tolerant quantum computers).

In practical terms, this means that when more powerful and fault-tolerant quantum computers are available, the team of scientists at the University of Hull will be able to greatly increase the range of their exploration, the complexity and number of molecules that they can search for, and the speed with which they analyze their findings as they search for life beyond planet Earth.

The scale of what we are trying to accomplish today is daunting, said Dr. David Benoit, senior lecturer in Molecular Physics and Astrochemistry at the University of Hull. There are over 16,000 different life-indicating molecules that were searching for in space, but we could increase our search significantly with quantum computers as they become more powerful in the future. And were going to need that power. Were not looking for a needle in a haystack here. That would be easy. This effort is more like looking for a speck of dust in a warehouse through a straw.

Throughout the project, the teams have achieved several new discoveries and scientific breakthroughs. These discoveries led them to expect that the quantum algorithm will scale better than the classical one in the future, making it possible to study larger molecules that would not be possible with a classical computer. Zapata Computing and the University of Hull also documented this research and recently published a paper regarding the findings titled, A pathway to accurate potential energy curves on NISQ devices. The teams will also share the overview of the project and the results of the first year of work at Quantum.Tech London in their presentation on September 20 titled, Using quantum computers to look for alien life in deep space.

The sheer scale of what the University of Hull is trying to accomplish technically is a clear indication that the need for Big Compute capabilities today are critical to prepare for the quantum future ahead, said Christopher Savoie, CEO and co-founder of Zapata Computing. Theres no question that the discovery of life in deep space is difficult, but its a challenge that is perfect for a quantum computer and there are steps that the University of Hull is taking, similar to those many enterprises are taking, to make iterative progress and prep for these more powerful machines as they come online.

For more information about the presentation at Quantum.Tech and Zapata Computing and its work with the University of Hull, please visit http://www.zapatacomputing.com or stop by the Zapata Computing Booth (A3) at Quantum.Tech London.

About Zapata Computing

Zapata Computing, Inc. is the leading enterprise quantum software company. The Companys Orquestra platform supports the research, development, and deployment of quantum-ready applications for enterprises most computationally complex problems. Zapata has pioneered new methods in ML, optimization, and simulation to maximize value from near-term quantum devices, and partners closely with ecosystem hardware providers such as Amazon, D-Wave, Google, Quantinuum, IBM, IonQ and Rigetti. Zapata was founded in 2017 and is headquartered in Boston, Massachusetts. For more information, visit http://www.zapatacomputing.com.

View original post here:
Zapata Computing and The University of Hull Get Quantum-Ready For Ongoing Search for Life in Space - Business Wire

Robots & Humans: Are we heading towards Singularity? – INDIAai

Imagine what will happen if we robots can process information, store data and transfer the same at a pace at which humans do, will they not be as good as humans? Just to let you know we will touch on one aspect in this article (Quantum Computing) which takes care of processing information, however there is tremendous progress already made to store information like our DNA and also transmit the same like our nervous system does.

As the smartest creatures on Earth, our journey from the analogue to the digital world has been at a tremendous pace in the past decades.

There was a time, few decades ago, when invention of electronic calculator marked a major breakthrough in the world of technology. The transformational advancements of processing information since then have been remarkable. Undoubtedly, we have come a long way with smartphones, wearable and smart devices, shifting from press the keys to touch, swipe and speak.

With Artificial Intelligence (AI), Virtual Reality (VR), Internet of Things (IoT) and Metaverse being technological realities today, we are also heading towards a new era of data & computation called quantum computing.

Now, Whats That?

Well, quantum computing is a futuristic technology which employs the power of quantum mechanics for solving extremely complex problems that are beyond the capacity of classical computers. To define it simply, this computer-based technology functions around the quantum theory principals where behaviours of matter and energy are studied on the atomic and subatomic levels.

Supercomputers designed on quantum theory consume comparative less energy while operating at an exponentially higher speed.

This quantum computer implements the laws of quantum mechanism for such complex calculation which are much beyond human comprehensions.

Tech titans envision that humans will be accelerated into the future by quantum computing through its impact on data analytics and artificial intelligence. Its massive speed and power shall help us crack even the complex challenges that we, human beings, face.

In the Next Decades, What If I Say That Robots Can Become a Challenge to the Humans?

If thats going to happen, it would be for AI and quantum technology. Scientists have already started to research on bridging the two avenues quantum physics having its strong algorithms and artificial intelligence coupled with autonomous machines. They are investigating the ways to use quantum technology for the advantage of learning robots. So far, the results show that robots can decide faster.

#Case Study:

A team of experimental physicists led by Philip Walther from The University of Vienna collaborated with theoreticians from German Aerospace Center, the Austrian Academy of Sciences and University of Innsbruck. Together, for the first time, they succeeded in proving the increase in actual learning time of a robot. Their experiment included the use of fundamental particles of light, single photons and integrated photonic quantum processor. The researchers implemented learning tasks by using this processor as a robot. The result showed significant reduction in the learning time, compared to the no quantum physics cases.

Hence, artificial intelligence devices that are integrated with quantum computing are capable of self-correction and learning through experience, much like humans.

Sounds interesting?Let me make it more intriguing for you.

As the speed of quantum computing is significantly higher than the traditional machines, this could result in quantum robots if rapid responses are recorded. Such robots are envisioned to be highly advanced and way more sophisticated, with unparalleled capabilities of multitasking. Not just that, but they will also be able to fully examine and adapt to various environments for survival, becoming independently more creative and data processing at a greater speed.

Scientists also opine that the concept of technological singularity will be possible, which signifies machines will be more progressive and smarter than humans.

Upcoming: Robots with Human Intelligence

Yes! You read that right.

Plans are already on to build robots that would share similar values as well as rights like us. They will have the ability to understand the world like humans, have same feelings as well as emotional spectrum. Such human-like technology will profoundly change our relationship with technology and the world around us.

What next?

Remember the movie titled Transcendence? The protagonist uploads his consciousness into quantum computer and outsmarts death! Well, what you might have thought to be unrealistic then may not be so today. Popular predictions say that humans will soon become transhumans through the concept of virtual or digital immortality. We already have quantum computer amongst us, though not a consumer product, but commercially available.

How would this technology make it happen?

Well, going back to its definition again, quantum computers utilise quantum bits or qubits. These tiny physical objects help them cope with highly complex problems and extremely large volumes of data in less than a second. Hence, storing a humans memories and personality would be an effortless job for the quantum computers.

Recent breakthroughs show that narrow AI can perform certain tasks much better than humans. It wont be surprising to say that artificial intelligence will emulate the human skill, i.e. responding to various tasks, and thereby, put our race at a challenge in the future.

Coming back to digital immortality, it is a theoretical concept of transferring and storing an individuals consciousness into a robot, a virtual body or a computer. The required technology with appropriate hardware for this transfer is expected to arrive soon in this decade, although several milestones are needed to be achieved yet.

Digital Immortality: How far are we?

Once a persons consciousness is uploaded, it can be stored in two different ways:

From there, it can easily interact with the physical as well as the virtual worlds. The fascinating result would be that the persons consciousness will remain alive in a virtual space for thousands and thousands of years to come. Thats not all. He can also travel to various virtual worlds and download content for enriched experience. Being still alive, he can work with his own digital clones to accomplish essential jobs in real life faster.

Quite a far future though, the second instance says human beings will possibly grow or build completely new bodies. While models may vary with the type of technology used, the least expensive one could be machine-like or robotic in appearance.

Fast forwarding many decades from today, we might have these machines as highly expensive synthetic bodies similar to the real human bodies using several hi-tech features to enhance their mental and physical capabilities. Moving thousands of years further, the world might have so advanced synthetic bodies that their capabilities would probably exceed our wildest imaginations today. If need be, new versions of these bodies can also come up.

According to the predictions of renowned futurist, Ray Kurzweil, uploading the human mind would be possible in the next quarter century, though perfection might need a lot of time.

In a major breakthrough in research a year ago, one of the most complex organs, eyes of mice, were reprogrammed in a lab. If a human goes blind when older, he/she never recovers the vision. Hence, the experiment was done on one-year old mice using gene therapy where their retinas were turned to be young again. Three out of the four reprogramming factors were implemented. Scientists successfully reversed aging in their retinas taking those backwards to around two months old in age. The mice could clearly see everything again much, like they saw when young. Additionally, the system can be turned on and off whenever required. Scientists confirmed that this can be done with any tissue to reverse aging, not going back too far though.

Probably, the concept of death will vanish in a century or so owing to the dynamic evolution of technology. Humans will just be moving from one body to another, with their memory and consciousness stored in the form of data.

To say so, its just the beginning for us to understand what possibilities artificial intelligence have. Every new and successful experiment, thus, adds to the development of the scope of quantum computing. IBM believes that quantum computing will become the mainstream technology in probably the next 5 years. At this point, can we look back to our mythology and sum up that our culture has been talking about it since eons?

Food for thought:

In simple terms, History for which we dont have documented proof is called Mythology. Do you think we will need to document or even speak 100 years from now? We have already moved from paper documents to speaking in a mic and recording the artefacts, why is it not possible to just transfer thoughts from one person (robot) to another without any speech or text?

Read the original here:
Robots & Humans: Are we heading towards Singularity? - INDIAai

A Study of Rucaparib in Patients With Metastatic Castration-resistant …

University of Alabama at Birmingham Birmingham, Alabama, United States, 35294 Mayo Clinc Phoenix, Arizona, United States, 85259 Arizona Oncology Associates Tucson, Arizona, United States, 85704 Alliance Research Centers Laguna Hills, California, United States, 92653 VA Greater Los Angeles Healthcare System Los Angeles, California, United States, 90073 University of Southern California Los Angeles, California, United States, 90211 Stanford University Palo Alto, California, United States, 94305 Sharp Memorial Hospital San Diego, California, United States, 92123 Pacific Hematology Oncology Associates San Francisco, California, United States, 94115 San Francisco VA Health Care System San Francisco, California, United States, 94143 UCSF Helen Diller Family Comprehensive Cancer Center San Francisco, California, United States, 94158 Redwood Regional Medical Group Santa Rosa, California, United States, 95406 Kaiser Permanente Medical Center (Vallejo) Vallejo, California, United States, 94589 Rocky Mountain Cancer Centers Aurora, Colorado, United States, 80012 Yale School of Medicine New Haven, Connecticut, United States, 06510 4701 Ogletown Stanton Rd. Newark, Delaware, United States, 19713 Georgetown University Medical Center Washington, District of Columbia, United States, 20007 Boca Raton Community Hospital, Inc. Boca Raton, Florida, United States, 33486 Florida Cancer Specialists Fort Myers, Florida, United States, 33980 University of Florida Health Cancer Center Orlando, Florida, United States, 32806 Moffitt Cancer Center Tampa, Florida, United States, 33612 Atlanta Urological Group Atlanta, Georgia, United States, 30312 University of Chicago Comprehensive Cancer Center Chicago, Illinois, United States, 60637 Ochsner Medical Center New Orleans, Louisiana, United States, 70121 University of Maryland Greenebaum Cancer Center Baltimore, Maryland, United States, 21201 Walter Reed Hospital Bethesda, Maryland, United States, 48202 Massachusetts General Hospital Boston, Massachusetts, United States, 02114 VA Ann Arbor Healthcare System Ann Arbor, Michigan, United States, 48105 Henry Ford Hospital Detroit, Michigan, United States, 48202 Fairview Hospital Edina, Minnesota, United States, 55435 Minnesota Oncology Hematology, P.A. Minneapolis, Minnesota, United States, 55404 Minnesota Veterans Research Institute Minneapolis, Minnesota, United States, 55417 HCA Midwest Division - Kansas City Kansas City, Missouri, United States, 64132 Alegent Health Bergan Mercy Hospital , GU Research Network Omaha, Nebraska, United States, 68130 Nebraska Cancer Specialists Omaha, Nebraska, United States, 68130 Comprehensive Cancer Centers of Nevada Las Vegas, Nevada, United States, 89119 Premier Urology Associates dba/AdvanceMed Research Lawrenceville, New Jersey, United States, 08648 Rutgers Cancer Institute of New Jersey New Brunswick, New Jersey, United States, 08901 Roswell Park Buffalo, New York, United States, 14263 NYU Perlmutter Cancer Center New York, New York, United States, 10016 Memorial Sloan Kettering CC New York, New York, United States, 10065 Weill Cornell Medical College/NewYork-Presbyterian Hospital New York, New York, United States, 10065 Premier Medical Group of the Hudson Valley PC Poughkeepsie, New York, United States, 12301 University of Rochester Rochester, New York, United States, 14642 SUNY Upstate Medical University Syracuse, New York, United States, 13210 Carolina Urology Partners Concord, North Carolina, United States, 28025 The Urology Group Cincinnati, Ohio, United States, 45212 Kettering Cancer Center Kettering, Ohio, United States, 45429 Clinical Research Solutions Middleburg Heights, Ohio, United States, 44130 VA Portland Health Care System Portland, Oregon, United States, 97219 Consultants in Medical Oncology Hematology Horsham, Pennsylvania, United States, 19044 SCRI - Tennessee Oncology Nashville, Tennessee, United States, 37203 Texas Oncology Medical City Dallas Dallas, Texas, United States, 75320 UT Southwestern Medical Center Dallas, Texas, United States, 75390 UT Health Science Center Houston, Texas, United States, 77030 Texas Oncology - Tyler Tyler, Texas, United States, 75702 Virginia Oncology Associates Norfolk, Virginia, United States, 23502 VA Puget Sound Seattle, Washington, United States, 98108 Northern Cancer Insitute, St. Leonards Saint Leonards, New South Wales, Australia, 2065 Royal Hobart Hospital Hobart, Tasmania, Australia, 7000 Peninsula & Southeast Oncology Frankston, Victoria, Australia, 3199 Barwon Health, University Hospital Geelong Geelong, Victoria, Australia, 3220 Cabrini Hospital Malvern, Victoria, Australia, 3144 Southside Cancer Care Centre Miranda, Australia, 2228 Orange Health Services Orange, Australia, 2800 St John of God Hospital, Subiaco Subiaco, Australia, 6008 Riverina Cancer Care Centre Wagga Wagga, Australia, 2650 ZNA Middelheim Antwerp, Belgium, 2020 Universitair Ziekenhuis Gent Gent, Belgium, B-9000 AZ Groeninge Kortrijk, Belgium, 8500 CHU Sart-Tilman Lige, Belgium, 4000 Equipe de Recherche Clinique, Dpartement d'Oncologie/Hmatologie Lige, Belgium, 4000 AZ DELTA Roeselare, Belgium, B-8800 Juravinski Cancer Centre Hamilton Health Services Hamilton, Ontario, Canada, L8V5C2 London Health Science Center - Victoria Hospital London, Ontario, Canada, N6A 4L6 The Ottawa Hospital Ottawa, Ontario, Canada, K1H8L6 Princess Margaret Hospital Toronto, Canada, M5G 2M9 Copenhagen University Hospital Copenhagen, Denmark, 2100 Herlev Hospital Herlev, Denmark, 2730 Vejle Sygehus Vejle, Denmark, 7100 Centre Franois Baclesse Caen, France, 14000 Centre Georges Franois Leclerc Dijon, France, 21079 Clinique Victor Hugo Centre Jean Bernard Le Mans, France, 72000 Hpital Priv La Louvire Lille, France, 59800 Polyclinique de Gentilly (Centre D'Oncologie De Gentilly) Nancy, France, 54100 Institut Curie Paris, France, 75248 Hpital Priv des Ctes d'Armor Plrin, France, 22190 CRLCC Eugene Marquis Rennes, France, 35042 Gemeinschaftspraxis fur Hamatologie & Onkologie Augsburg, Germany, 86150 Charite Universitatsmedizin Berlin Berlin, Germany, 12200 Universitatsklinikum Carl Gustav Carus Dresden, Germany, 01307 Universitatsklinikum Dusseldorf Dusseldorf, Germany, 40225 Urologische Gemeinschaftspraxis Emmendingen, Germany, 79312 Universitaetsklinikum Hamburg-Eppendorf (UKE) Hamburg, Germany, 20246 Universitaetsklinikum Heidelberg Heidelberg, Germany, 69120 Universitatsklinikum Jena Jena, Germany, 07747 Universittsklinik Kln Kln, Germany, 50937 Universittsklinikum Schleswig-Holstein Lbeck, Germany, 23538 Medizinischen Fakultt Mannheim der Universitt Heidelberg Mannheim, Germany, 68167 Studienpraxis Urologie Nrtingen, Germany, 72622 University of Tuebingen Tuebingen, Germany, 72076 Die Gesundhehitsunion DGU Wuppertal, Germany, 42103 Cork University Hospital Cork, Ireland, T12 DFK4 St. Vincent's University Hospital Dublin, Ireland, D04T6F4 St James's Hospital Dublin, Ireland, D08 NHY1 Adelaide & Meath Hospital, Incorporating the National Children's Hospital Dublin, Ireland, Dublin 24 Mater Misericordiae University Hospital Dublin, Ireland, Dublin 7 Rambam Health Care Campus (RHCC), Rambam Medical Center Haifa, Israel, 3109601 Hadassah University Hospital Jerusalem, Israel, 71120 Meir Medical Center Kfar Saba, Israel, 4428164 Rabin Medical Center-Beilinson Campus Petach Tikva, Israel, 4941492 Chaim Sheba Medical Center Ramat Gan, Israel, 52621 The Tel Aviv Sourasky Medical Center (Ichilov Hospital) Tel Aviv, Israel, 64231 Ospedale San Donato, Azienda USLSUDEST Arezzo, Italy, 52100 Ospedale Santa Maria delle Croci Faenza, Italy, 48018 IRCCS Istituto Nazionale dei Tumori (INT) Milano, Italy, 20133 IEO Instituto Europeo di Oncologia Milano, Italy, 20141 University of Modena and Reggio Emilia Medical Oncology Modena, Italy, 41124 Azienda Ospedaliera San Camillo-Forlanini Rome, Italy, 00152 Azienda Opsedaliera S. Maria di Terni Terni, Italy, 05100 Santa Chiara Hospital, Dept Medical Oncology Trento, Italy, 38122 Hospital Universitari Germans Trias i Pujol Badalona, Spain, 08916 Hospital del Mar, Servicio de Oncologa Barcelona, Spain, 08003 Hospital Clnic i Provincial de Barcelona-Oncology Barcelona, Spain, 08036 Instituto Catalan de Oncologia Barcelona, Spain, 08908 Hospital Universitari Germans Trias i Pujol Barcelona, Spain, 08916 Hospital General Universitario de Guadalajara Guadalajara, Spain, 19002 Hospital Universitario Lucus Augusti. Lugo, Spain, 27003 MD Anderson Cancer Center - Madrid Madrid, Spain, 28033 Hospital Universitario Ramn y Cajal Madrid, Spain, 28034 Hospital 12 de Octubre Madrid, Spain, 28041 Hospital Universitario La Paz Madrid, Spain, 28046 Hospital Puerta de Hierro-Majadahonda Madrid, Spain, 28222 Hospital Universitario Central de Asturias Oviedo, Spain, 33011 Corporacio Sanitaria Parc Tauli Sabadell, Spain, 8208 Marques de Valdecilla University Hospital (HUMV) Santander, Spain, 39008 Hospital Universitario Virgen del Roco Sevilla, Spain, 41013 Instituto Valenciano de Oncologia IVO Valencia, Spain, 46009 Wexham Park Hospital Slough, Berkshire, United Kingdom, SL2 4HL Mount Vernon Cancer Centre Northwood, England, United Kingdom, HA6 2RN Royal Marsden Hospital Sutton, Surrey, United Kingdom, SM2 5PT Oxford University Hospitals Headington, United Kingdom, OC3 7LJ Royal Liverpool Hospital Liverpool, United Kingdom, L7 8XP London Health Science Center - Victoria Hospital London, United Kingdom, N6A 4L6 Guy's Hospital London, United Kingdom, SE1 9RT Sarah Cannon Research Institutute - UK London, United Kingdom, W1G 6AD Southampton General Hospital Southampton, United Kingdom, SO16 6YD Musgrove Park Hospital Taunton, United Kingdom, TA1 5DA The Clatterbridge Cancer Centre NHS Foundation Trust Wirral, United Kingdom, CH63 4JY

Originally posted here:
A Study of Rucaparib in Patients With Metastatic Castration-resistant ...

Cellular & Gene Therapy Guidances | FDA

Should you find a link that does not work within any Guidance document, Rule or other document posted on the FDA Web site, please try searching for the document using the document title. If you need further assistance, please go to Contact FDA.

Considerations for the Development of Chimeric Antigen Receptor (CAR) T Cell Products; Draft Guidance for Industry3/2022

Human Gene Therapy Products Incorporating Human Genome Editing; Draft Guidance for Industry3/2022

Policy for Certain REMS Requirements During the Tocilizumab Shortage Related to the COVID-19 Public Health Emergency; Guidance for Industry and Health Care Professionals12/2021

Interpreting Sameness of Gene Therapy Products Under the Orphan Drug Regulations; Guidance for Industry9/2021

Studying Multiple Versions of a Cellular or Gene Therapy Product in an Early-Phase Clinical Trial; Draft Guidance for Industry9/2021

Manufacturing Considerations for Licensed and Investigational Cellular and Gene Therapy Products During COVID-19 Public Health Emergency; Guidance for Industry1/2021

Human Gene Therapy for Neurodegenerative Diseases; Draft Guidance for Industry1/2021

Chemistry, Manufacturing, and Control (CMC) Information for Human Gene Therapy Investigational New Drug Applications (INDs); Guidance for Industry1/2020

Long Term Follow-up After Administration of Human Gene Therapy Products; Guidance for Industry1/2020

Testing of Retroviral Vector-Based Human Gene Therapy Products for Replication Competent Retrovirus During Product Manufacture and Patient Follow-up; Guidance for Industry1/2020

Human Gene Therapy for Hemophilia; Guidance for Industry1/2020

Human Gene Therapy for Rare Diseases; Guidance for Industry1/2020

Human Gene Therapy for Retinal Disorders; Guidance for Industry1/2020

Evaluation of Devices Used with Regenerative Medicine Advanced Therapies;Guidance for Industry2/2019

Expedited Programs for Regenerative Medicine Therapies for Serious Conditions;Guidance for Industry2/2019

Regulatory Considerations for Human Cells, Tissues, and Cellular and Tissue-Based Products: Minimal Manipulation and Homologous Use; Guidance for Industry and Food and Drug Administration StaffUpdated: 12/2017

Same Surgical Procedure Exception under 21 CFR 1271.15(b): Questions and Answers Regarding the Scope of the Exception; Guidance for Industry11/2017

Deviation Reporting for Human Cells, Tissues, and Cellular and Tissue-Based Products Regulated Solely Under Section 361 of the Public Health Service Act and 21 CFR Part 1271; Guidance for Industry9/2017

Recommendations for Microbial Vectors Used for Gene Therapy; Guidance for Industry9/2016

Design and Analysis of Shedding Studies for Virus or Bacteria-Based Gene Therapy and Oncolytic Products; Guidance for Industry8/2015

Considerations for the Design of Early-Phase Clinical Trials of Cellular and Gene Therapy Products; Guidance for Industry6/2015

Determining the Need for and Content of Environmental Assessments for Gene Therapies, Vectored Vaccines, and Related Recombinant Viral or Microbial Products; Guidance for Industry3/2015

Guidance for Industry: BLA for Minimally Manipulated, Unrelated Allogeneic Placental/Umbilical Cord Blood Intended for Hematopoietic and Immunologic Reconstitution in Patients with Disorders Affecting the Hematopoietic System3/2014. (This guidance finalizes the draft guidance of the same title dated June 2013.)

IND Applications for Minimally Manipulated, Unrelated Allogeneic Placental/Umbilical Cord Blood Intended for Hematopoietic and Immunologic Reconstitution in Patients with Disorders Affecting the Hematopoietic System - Guidance for Industry and FDA Staff3/2014. (This guidance finalizes the draft guidance of the same title dated June 2013.)

Guidance for Industry: Preclinical Assessment of Investigational Cellular and Gene Therapy Products(This guidance finalizes the draft guidance entitled Guidance for Industry: Preclinical Assessment of Investigational Cellular and Gene Therapy Products dated November 2012) 11/2013

Guidance for Industry: Preparation of IDEs and INDs for Products Intended to Repair or Replace Knee Cartilage12/2011. (This guidance finalizes the draft guidance of the same title dated July 2007.)

Guidance for Industry: Clinical Considerations for Therapeutic Cancer Vaccines10/2011. (This guidance finalizes the draft guidance of the same title dated September 2009.)

Guidance for Industry: Potency Tests for Cellular and Gene Therapy Products1/2011. (This guidance finalizes the draft document of the same name, dated October 2008.)

Guidance for Industry: Cellular Therapy for Cardiac Disease(This guidance finalizes the draft guidance entitled Guidance for Industry: Somatic Cell Therapy for Cardiac Disease dated March 2009 (April 2, 2009, 74 FR 14992). 10/2010.

Guidance for Industry: Considerations for Allogeneic Pancreatic Islet Cell Products9/2009

Guidance for FDA Reviewers and Sponsors: Content and Review of Chemistry, Manufacturing, and Control (CMC) Information for Human Somatic Cell Therapy Investigational New Drug Applications (INDs)4/2008

Eligibility Determination for Donors of Human Cells, Tissues, and Cellular and Tissue-Based Products; Guidance for Industry8/2007

Guidance for Industry: Guidance for Human Somatic Cell Therapy and Gene Therapy3/1998

12/10/2021

See the rest here:
Cellular & Gene Therapy Guidances | FDA

NIH Funds Miller School Researchers Novel Work to Develop Gene Therapy for Hearing Loss-related Usher… – InventUM | University of Miami Miller…

Reading Time: 3 minutes

The National Institute on Deafness and Other Communication Disorders (NIDCD) has awarded Xue Zhong Liu, M.D., Ph.D., Marian and Walter Hotchkiss Endowed Chair in Otolaryngology at the University of Miami Miller School of Medicine, a five-year, $3.5 million R01 research grant to develop a precision medicine approach to treat hearing loss (HL) in Usher syndrome (USH).

There is no cure for USH, and current treatments inadequately address this inherited condition that can cause not only HL but also vision loss.

Todays treatment for Usher syndrome is limited to cochlear implants or hearing aids, which help to address the hearing loss, but there is no biological treatment for HL and the blindness. There is an unmet need to develop alternative treatment options, Dr. Liu said.

The NIH grant will fund Miller School research aimed at developing and testing novel therapy approaches with gene editing. Gene editing is a group of technologies that allow scientists to change an organism's DNA. CRISPR-Cas9 is a popular gene editing technology developed to treat genetic disorders.

The Miller School is one of a select few sites in the world conducting research to apply CRISPR/Cas9 gene editing for HL including Usher syndrome, said Dr. Liu, who also is vicechair of the Department of Otolaryngology and professor of otolaryngology, human genetics, biochemistry, and pediatrics at the Miller School.

Gene- and cell-based therapies using genome editing offer the promise of treatment for a variety of inherited disorders but have not been used successfully for human hereditary HL, including Usher syndrome.

Dr. Liu, along with his collaborator Dr. Zheng-Yi Chen from the Massachusetts Eye and Ear Infirmary, Department of Otolaryngology, Harvard Medical School, aim to pave the way for the development of gene therapy approaches that would address HL Usher syndrome patients hearing.

We will use CRISPR/Cas9 to correct mutations in three different Usher genes shown in our preliminary data to cause most inherited hearing loss in USH, he said. This will involve strategies to rescue hearing in transgenic USH mouse models and developing CRISPR/Cas9 editing strategies to disrupt USH mutations, using human inner ear organoids derived from patient-induced pluripotent stem cells.

The NIH-funded study could lead to patient-specific treatment, based on a patients USH genetic mutations. In the meantime, Dr. Liu has developed a collaborating program with the University of Miami Ear Institute and Bascom Palmer Eye Institute to provide better care for people with Usher syndrome.

Recent breakthroughs in genetic screening, gene- or cell-based therapeutics, and gene editing for the inner ear can lead to novel therapies for multiple classes of hereditary hearing loss. We are excited as this is the first gene therapy NIH grant using CRISPR/Cas9 at UM for common sensory disorders, said Fred Telischi, M.D., M.E.E., chair of otolaryngology, professor of neurological surgery and biomedical engineering, and the James R. Chandler Chair in Otolaryngology.

This grant was awarded by the NIDCD as part of its high-impact program to help meet an unmet patient need, Dr. Liu said. Our aim is to lay the foundation for moving genome editing approaches closer to clinical trials on humans with Usher syndrome, which accounts for about 50% of all hereditary deaf-blindness cases, including in children.

The Genetic Hearing Loss Clinic at University of Miami Ear Institute is a multi-disciplinary program that provides diagnostic, molecular testing, genetic counseling, and intervention options for patients and families who are dealing with various types of HL.

Read more from the original source:
NIH Funds Miller School Researchers Novel Work to Develop Gene Therapy for Hearing Loss-related Usher... - InventUM | University of Miami Miller...

CRISPR-Based HIV Gene Therapy Administered To First Human Patient – IFLScience

In a clinical trial, the first patient has received a single dose of a new human immunodeficiency virus (HIV) gene editing therapy, researchers at the Lewis Katz School of Medicine at Temple University and Excision BioTherapeutics, Inc have reported.

In a collaborative effort, the researchers are currently running aphase 1/2 clinical trial to evaluate the safety and efficacy of their therapy, calledEBT-101, which is based on gene editing technology known as CRISPR.

Nearly 40 million people worldwide suffer from the effects of HIV, and more than 40 years after the discovery of HIV/AIDS, there still are no curative treatments, said Professor Kamel Khalili, who helped lead the trial, in a statement.

EBT-101 can potentially address long-standing unmet needs of individuals living with HIV/AIDS by removing viral DNA from their cells, thereby eradicating infection.

When HIV infects, it takes long-term hold and hides from the immune system in cells, compromising the patient's immunity over time and eventually leading to the development of AIDS the progressive failure of a patient's immune system. There is currently no cure for HIV, but various treatments and medications can help manage the infection and slow or prevent the progression of the disease.

The therapy currently being trialed, which uses CRISPR gene editing to removeHIV viral DNA from infected cells, is a major step towardfinding a therapeutic cure.

We are well-positioned to collect key data that will enable our efforts to translate the success this approach has shown in animal models to human clinical trial participants, Khalili added. We look forward to investigating this hypothesis through the EBT-101 clinical program and are pleased that the EBT-101 Phase 1/2 trial is proceeding as planned.

The first patient to receive a single dose of EBT-101 in the current trial is currently under medical supervision and will soon be assessed to see if there is any viral rebound and whether the single curative treatment worked as planned. This will be a deciding factor in whether or not the patient is able to stop their current antiretroviral therapy in the future.

The official start of the Phase 1/2 clinical trials for EBT-101 brings us one extremely significant step closer to creating a potential cure for HIV/AIDS, said Dr Amy J. Goldberg, Interim Dean of the Katz School of Medicine. This amazing milestone speaks to the exceptional research acumen and scientific knowledge of Drs. Khalili and Burdo and their teams outstanding members of the Temple family.

For further details, you can view the clinical trial information at ClinicalTrials and follow its progress.

Read the original here:
CRISPR-Based HIV Gene Therapy Administered To First Human Patient - IFLScience

The New England Journal of Medicine Publishes Pivotal Tofersen Data that Show Benefits in Rare, Genetic Form of ALS – GlobeNewswire

CAMBRIDGE, Mass., Sept. 21, 2022 (GLOBE NEWSWIRE) -- Biogen Inc. (Nasdaq: BIIB) today announced that The New England Journal of Medicine(NEJM) has published detailed results from the Phase 3 VALOR study and the combined analysis of VALOR and its open label extension (OLE) study evaluating tofersen for the treatment of superoxide dismutase 1 (SOD1) amyotrophic lateral sclerosis (ALS). There is currently no treatment targeted for SOD1-ALS.

I see three key take home points from these data.First, tofersen clearly leads to lowering of SOD1 protein, as would be expected.Second there is substantial lowering of neurofilament levels, which I interpret as potentially slowing the underlying disease process. And third, there is a meaningful clinical benefit when looking at the later time points in the open label extension, said Timothy Miller, M.D., Ph.D., principal investigator of VALOR and ALS Center co-Director at Washington University School of Medicine, St. Louis. We are grateful to the dedication from participants, their families, and the sites for taking part in this important study.

Data from the combined analysis were previously presented at the European Network to Cure ALS (ENCALS) annual meeting and included within Biogens New Drug Application for tofersen that was recently accepted for priority review by the U.S. Food and Drug Administration. The application was given a Prescription Drug User Fee Act action date of January 25, 2023.

The ALS community has been actively pursuing new medicines for decades. To have data like these published in NEJM gives us energy and hope. We are now seeing in the data what we suspected about tofersen for a long time that it has the potential to make a clinical difference for people living with SOD1-ALS, said Merit Cudkowicz, M.D., co-principal investigator of the VALOR trial and co-founder of the Northeast ALS Consortium, Director of the Healey & AMG Center for ALS and Chair of Neurology at Massachusetts General Hospital and the Julieanne Dorn Professor of Neurology at Harvard Medical School. The lowering of neurofilament, a marker of axonal injury and neurodegeneration along with the clinical data, highlights the potential of tofersen.

About VALOR and the OLEVALOR was a six-month Phase 3, randomized, double-blind, placebo-controlled study to evaluate the effects of tofersen 100 mg in adults with ALS associated with a SOD1 mutation. In total, 108 participants were randomized in VALOR (n=72 to tofersen 100 mg and n=36 to placebo). Of these participants, 95 enrolled in the ongoing OLE. At the time of the analysis all participants had an opportunity for at least 12 months of follow-up, with a median exposure to tofersen of approximately 20 months (range: 1 34 months).

The primary endpoint of VALOR was change from baseline to week 28 in ALS Functional Rating Scale-Revised (ALSFRS-R) total score. Secondary endpoints included changes in total cerebrospinal fluid SOD1 protein concentration, plasma neurofilament light chain (NfL), slow vital capacity and handheld dynamometry in 16 muscles.

As previously reported in October 2021, VALOR did not meet the primary endpoint. However, trends of reduced disease progression across multiple secondary and exploratory endpoints were observed. The combined VALOR and OLE 12-month data, in which the clinical analyses adjusted for neurofilament levels as a marker of the disease progression rate at baseline, showed sustained reductions in SOD1 protein (a marker of target engagement) and neurofilament (a marker of neurodegeneration) and slowed decline in clinical function, respiratory function, strength, and quality of life with earlier initiation of tofersen.

In the 12-month data, the most common adverse events (AEs) in participants receiving tofersen in VALOR and the OLE study were procedural pain, headache, pain in the arms or legs, falls, and back pain. Most AEs in both VALOR and the OLE were mild to moderate in severity. Serious neurologic events including myelitis, chemical or aseptic meningitis, radiculitis, increased intracranial pressure and papilledema, were reported in 6.7 percent of participants receiving tofersen in VALOR and its OLE.

About TofersenTofersen is an antisense drug being evaluated for the potential treatment of SOD1-ALS. Tofersen binds and degrades SOD1 mRNA to reduce synthesis of SOD1 protein production. In addition to the ongoing open label extension of VALOR, tofersen is being studied in the Phase 3 ATLAS study designed to evaluate whether tofersen can delay clinical onset when initiated in presymptomatic individuals with a SOD1 genetic mutation and biomarker evidence of disease activity. Biogen licensed tofersen from Ionis Pharmaceuticals, Inc. under a collaborative development and license agreement.

About Amyotrophic Lateral Sclerosis and SOD1-ALSAmyotrophic lateral sclerosis (ALS) is a rare, progressive and fatal neurodegenerative disease that results in the loss of motor neurons in the brain and the spinal cord that are responsible for controlling voluntary muscle movement. People with ALS experience muscle weakness and atrophy, causing them to lose independence as they steadily lose the ability to move, speak, eat, and eventually breathe. Average life expectancy for people with ALS is three to five years from time of symptom onset.1

Multiple genes have been implicated in ALS. Genetic testing helps determine if a persons ALS is associated with a genetic mutation, even in individuals without a family history of the disease. Currently, there are no genetically targeted treatment options for ALS. Mutations in the SOD1 gene are responsible for approximately 2 percent of the estimated 168,000 people who have ALS globally (SOD1-ALS).2Life expectancy in SOD1-ALS varies widely with some patients surviving less than a year.3

Biogens Continuous Commitment to ALSFor over a decade, Biogen has been committed to advancing ALS research to provide a deeper understanding of all forms of the disease. The company has continued to invest in and pioneer research despite making the difficult decision to discontinue a late-stage ALS asset in 2013. Biogen has applied important learnings to its portfolio of assets for genetic and other forms of ALS, with the goal of increasing the probability of bringing a potential therapy to patients in need. These applied learnings include evaluating genetically validated targets in defined patient populations, pursuing the most appropriate modality for each target and employing sensitive clinical endpoints. Today, the company has a pipeline of investigational drugs being evaluated in ALS, including tofersen and BIIB105.

About BiogenAs pioneers in neuroscience, Biogen discovers, develops, and delivers worldwide innovative therapies for people living with serious neurological diseases as well as related therapeutic adjacencies. One of the worlds first global biotechnology companies, Biogen was founded in 1978 by Charles Weissmann, Heinz Schaller, Sir Kenneth Murray, and Nobel Prize winners Walter Gilbert and Phillip Sharp. Today, Biogen has a leading portfolio of medicines to treat multiple sclerosis, has introduced the first approved treatment for spinal muscular atrophy, and developed the first and only approved treatment to address a defining pathology of Alzheimers disease. Biogen is also commercializing biosimilars and focusing on advancing one of the industrys most diversified pipelines in neuroscience that will transform the standard of care for patients in several areas of high unmet need.

In 2020, Biogen launched a bold 20-year, $250 million initiative to address the deeply interrelated issues of climate, health, and equity. Healthy Climate, Healthy Lives aims to eliminate fossil fuels across the companys operations, build collaborations with renowned institutions to advance the science to improve human health outcomes, and support underserved communities.

We routinely post information that may be important to investors on our website atwww.biogen.com.Follow us on social media-Twitter,LinkedIn,Facebook,YouTube.

Biogen Safe HarborThis news release contains forward-looking statements, including statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, including statements about results from the Phase 3 VALOR study of tofersen or its OLE; the potential clinical effects of tofersen; the potential benefits, safety and efficacy of tofersen; the clinical development program for tofersen; the potential approval of tofersen; the identification and treatment of ALS; our research and development program for the treatment of ALS; the potential of our commercial business and pipeline programs, including tofersen; and risks and uncertainties associated with drug development and commercialization. These forward-looking statements may be accompanied by words such as aim, anticipate, believe, could, estimate, expect, forecast, intend, may, plan, potential, possible, will, would and other words and terms of similar meaning. Drug development and commercialization involve a high degree of risk and only a small number of research and development programs result in commercialization of a product. Results in early stage clinical trials may not be indicative of full results or results from later stage or larger scale clinical trials and do not ensure regulatory approval. You should not place undue reliance on these statements or the scientific data presented.

These statements involve risks and uncertainties that could cause actual results to differ materially from those reflected in such statements, including without limitation, uncertainty of success in the development and potential commercialization of tofersen; the risk that we may not fully enroll our clinical trials or enrollment will take longer than expected; unexpected concerns may arise from additional data, analysis or results obtained during our clinical trials; regulatory authorities may require additional information or further studies, or may fail or refuse to approve or may delay approval of our drug candidates, including tofersen; the occurrence of adverse safety events; the risks of unexpected hurdles, costs or delays; failure to protect and enforce our data, intellectual property and other proprietary rights and uncertainties relating to intellectual property claims and challenges; product liability claims; and the direct and indirect impacts of the ongoing COVID-19 pandemic on our business, results of operations and financial condition. The foregoing sets forth many, but not all, of the factors that could cause actual results to differ from our expectations in any forward-looking statement. Investors should consider this cautionary statement, as well as the risk factors identified in our most recent annual or quarterly report and in other reports we have filed with the U.S. Securities and Exchange Commission. These statements are based on our current beliefs and expectations and speak only as of the date of this news release.

We do not undertake any obligation to publicly update any forward-looking statements, whether as a result of new information, future developments or otherwise.

References:

See the article here:
The New England Journal of Medicine Publishes Pivotal Tofersen Data that Show Benefits in Rare, Genetic Form of ALS - GlobeNewswire

Alzheimer’s disease risk linked to newly discovered protein mutation – Medical News Today

Mitochondria are structures within the cell that convert energy from food into energy the cell can use. Each cell contains hundreds to thousands of mitochondria. Although most DNA is found inside the cells nucleus, mitochondria also contain a small amount of DNA, known as mitochondrial DNA.

In the early 2000s, researchers realized that short sections of mitochondrial DNA encode small (less than 100 amino acids long), biologically active proteins, now referred to as mitochondrial microproteins. The first mitochondrial microprotein to be discovered was called humanin.

There is growing evidence that humanin and other similar mitochondrial microproteins play a role in several age-related conditions, including Alzheimers disease.

Alzheimers disease is the most common type of dementia, characterized by progressive mental deterioration. According to the CDC, as many as 5.8 million Americans were living with Alzheimers disease in 2020.

The Cohen Laboratory at the University of Southern California (USC), one of the three laboratories that independently discovered humanin in 2003, has discovered a new microprotein connected to the risk of Alzheimers disease.

Their latest research, published in the journal of Molecular Psychiatry, revealed that a mutation in the newly discovered SHMOOSE microprotein is associated with a higher risk for Alzheimers disease across four cohorts. According to the researchers, nearly 1 in 4 individuals with European ancestry have the mutated version of the protein.

Dr. Pinchas Cohen, professor of gerontology, medicine, and biological sciences and senior author of the study, told Medical News Today:

The implications are not immediate, but we believe that [relatively soon], the SHMOOSE SNP [single nucleotide polymorphism] genetic variant that is found in over 20% of Europeans may guide both the classification of individuals that are at risk for Alzheimers that may benefit from certain preventive measures and also could inform the selection of medical interventions that will become available in the near future. A bit further ahead, SHMOOSE [protein] analogues may become available as therapeutics for individuals who carry the SNP and develop dementia, in a precision medicine approach.

Brendan Miller, Ph.D., first author of the study, studied mitochondrial DNA sequences from the Alzheimers Disease Neuroimaging Initiative (ADNI) database, searching for small variations in the genes called single nucleotide polymorphisms or SNPs. He found that a mutation in one particular mitochondrial SNP (rs2853499) was associated with a greater risk of Alzheimers disease and brain atrophy.

Dr. Miller and his colleagues then discovered that the mutated SNP causes a change in a mitochondrial microprotein, which they called SHMOOSE. The researchers used a technique called immunoprecipitation to isolate the SHMOOSE microprotein from the mitochondria of nerve cells.

When they analyzed this sample using mass spectrometry, they detected and identified two unique protein fragments from the SHMOOSE microprotein. The researchers reported that this is the first unique mass spectrometry-based detection of a mitochondrial-encoded microprotein to date.

Having identified a microprotein associated with a higher risk of Alzheimers disease, the researchers followed up on their discovery by carrying out studies in rats and cell culture experiments.

They found that the SHMOOSE microprotein accumulates in the mitochondria of neurons (nerve cells), where it binds to the inner mitochondrial membrane protein mitofilin. The SHMOOSE microprotein appears to act on the brain by influencing mitochondrial gene expression and boosting mitochondrial oxygen consumption. The researchers noted that mutated SHMOOSE microprotein was less effective at boosting oxygen consumption and impacted gene expression differently.

Dysregulated mitochondrial associated brain energetics is one of the multiple pathways thought to be important for Alzheimers disease, Andrew Saykin, PsyD, ABCN, Professor and Director of the Center for Neuroimaging and Indiana Alzheimers Disease Research Center, told MNT.

George Perry, Ph.D., Professor and Semmes Foundation Distinguished University Chair in Neurobiology at the University of Texas at San Antonio, told MNT that this study is very important as it links risk of [Alzheimers disease] to cellular metabolism. There are numerous cell biology and biochemical studies that highlight this [] and finding genetic data further support[s] this view.

Dr. Saykin observed that with further development and validation there could be implications of this and other microproteins for early detection, longitudinal monitoring, and potentially for therapeutic targeting.

MNT also discussed the studys findings with Tal Nuriel, Ph.D., Assistant Professor of Pathology and Cell Biology at Columbia University Irving Medical Center. Dr. Nuriel told MNT that most Alzheimers disease-related gene mutations discovered in the past are either very rare variants or common variants that confer a very small risk.

He said the mutation, or variant, in the SHMOOSE microprotein appears to confer a moderate risk for Alzheimers disease and is relatively common in the population and [this] alone makes it interesting.

Dr. Nuriel added that the fact that this is a microprotein that can theoretically be administered as a therapeutic agent is valuable. He cautioned that there will be a very long road ahead before any therapy derived from this microprotein could become a reality. Importantly, its unclear whether this SHMOOSE microprotein would enter the brain if given subcutaneously or intravenously. And if it doesnt enter the brain, this would greatly limit its ability to be used therapeutically.

When asked about the next step in the research following this discovery, Dr. Cohen told MNT, Our immediate plan is to treat mice that have been engineered to develop Alzheimers disease with SHMOOSE over several months and assess the improvement in their symptoms and performance. We will also work on developing longer acting analogues of the pep[t]ide.

The researchers noted in the study that SHMOOSE is yet another microprotein of a growing number that modify mitochondrial biology. According to a recent review, thousands of DNA sequences with microprotein-coding potential are currently unverified or functionally uncharacterized.

Read the rest here:
Alzheimer's disease risk linked to newly discovered protein mutation - Medical News Today

Epigenetic and transcriptomic alterations in offspring born to women with type 1 diabetes (the EPICOM study) – BMC Medicine – BMC Medicine

Hochberg Z, Feil R, Constancia M, Fraga M, Junien C, Carel JC, et al. Child health, developmental plasticity, and epigenetic programming. Endocr Rev. 2011;32:159224.

CAS PubMed Article Google Scholar

Clausen TD, Mathiesen ER, Hansen T, Pedersen O, Jensen DM, Lauenborg J, et al. High prevalence of type 2 diabetes and pre-diabetes in adult offspring of women with gestational diabetes mellitus or type 1 diabetes. Diabetes Care. 2008;31:34036.

PubMed Article Google Scholar

Rijpert M, Evers I, de Vroede MAMJ, de Valk HW, Heijnen CJ, Visser GHA. Risk factors for childhood overweight in offspring of type 1 diabetic women with adequate glycemic control during pregnancy. Diabetes Care. 2009;32:2099104.

PubMed PubMed Central Article Google Scholar

Manderson JG, Mullan B, Patterson CC, Hadden DR, Traub AI, McCance DR. Cardiovascular and metabolic abnormalities in the offspring of diabetic pregnancy. Diabetologia. 2002;45:9916.

CAS PubMed Article Google Scholar

Hjort L, Novakovic B, Grunnet LG, Maple-Brown L, Damm P, Desoye G, et al. Diabetes in pregnancy and epigenetic mechanismshow the first 9 months from conception might affect the childs epigenome and later risk of disease. Lancet Diabetes Endocrinol. 2019;7:796806.

PubMed Article Google Scholar

Illingworth RS, Bird AP. CpG islands--a rough guide. FEBS Lett. 2009;583:171320.

CAS PubMed Article Google Scholar

Szyf M, Bick J. DNA methylation: a mechanism for embedding early life experiences in the genome. Child Dev. 2013;84:4957.

PubMed Article Google Scholar

Jones PA. Functions of DNA methylation: Islands, start sites, gene bodies and beyond. Nat Rev Genet. 2012;13:48492.

CAS PubMed Article Google Scholar

Guo H, Zhu P, Yan L, Li R, Hu B, Lian Y, et al. The DNA methylation landscape of human early embryos. Nature. 2014;511:60610.

CAS PubMed Article Google Scholar

Opsahl JO, Moen GH, Qvigstad E, Bttcher Y, Birkeland KI, Sommer C. Epigenetic signatures associated with maternal body mass index or gestational weight gain: a systematic review. J Dev Orig Health Dis. 2020. https://doi.org/10.1017/S2040174420000811.

Jnsson J, Renault KM, Garca-Calzn S, Perfilyev A, Estampador AC, Nrgaard K, et al. Lifestyle Intervention in Pregnant Women With Obesity Impacts Cord Blood DNA Methylation, Which Associates With Body Composition in the Offspring. Diabetes. 2021;70(4):85466. https://doi.org/10.2337/db20-0487. Epub 2021 Jan 11. PMID: 33431374; PMCID: PMC7980200.

Kelstrup L, Hjort L, Houshmand-Oeregaard A, Clausen TD, Ninna S. Gene expression and DNA methylation of PPARGC1A in muscle and adipose tissue from adult offspring of women with diabetes in pregnancy. Diabetes. 2016;3:141.

Google Scholar

Hjort L, Martino D, Grunnet LG, Naeem H, Maksimovic J. Gestational diabetes and maternal obesity are associated with epigenome-wide methylation changes in children. JCI insight. 2018;3:e122572.

PubMed Central Article Google Scholar

Houshmand-Oeregaard A, Schrlkamp M, Kelstrup L, Hansen NS, Hjort L, Thuesen ACB, et al. Increased expression of microRNA-15a and microRNA-15b in skeletal muscle from adult offspring of women with diabetes in pregnancy. Hum Mol Genet. 2018;27:176371.

CAS PubMed Article Google Scholar

Hansen NS, Strasko KS, Hjort L, Kelstrup L, Houshmand-Regaard A, Schrlkamp M, et al. Fetal hyperglycemia changes human preadipocyte function in adult life. J Clin Endocrinol Metab. 2017;102:114150.

PubMed Article Google Scholar

Houshmand-Oeregaard A, Hansen NS, Hjort L, Kelstrup L, Broholm C, Mathiesen ER, et al. Differential adipokine DNA methylation and gene expression in subcutaneous adipose tissue from adult offspring of women with diabetes in pregnancy. Clin Epigenetics. 2017;9:112.

Article CAS Google Scholar

Houshmand-Oeregaard A, Hjort L, Kelstrup L, Hansen NS, Broholm C, Gillberg L, et al. DNA methylation and gene expression of TXNIP in adult offspring of women with diabetes in pregnancy. PLoS One. 2017;12:118.

Article CAS Google Scholar

Gautier JF, Porcher R, Abi Khalil C, Bellili-Munoz N, Fetita LS, Travert F, et al. Kidney Dysfunction in Adult Offspring Exposed In Utero to Type 1 Diabetes Is Associated with Alterations in Genome-Wide DNA Methylation. PLoS One. 2015;10(8):e0134654. https://doi.org/10.1371/journal.pone.0134654. PMID: 26258530; PMCID: PMC4530883.

Jensen DM, Damm P, Moelsted-Pedersen L, Ovesen P, Westergaard JG, Moeller M, et al. Outcomes in type 1 diabetic pregnancies: a nationwide, population-based study. Diabetes Care. 2004;27:281923.

PubMed Article Google Scholar

Vlachov Z, Bytoft B, Knorr S, Clausen TD, Jensen RB, Mathiesen ER, et al. Increased metabolic risk in adolescent offspring of mothers with type 1 diabetes: the EPICOM study. Diabetologia. 2015;58:145463.

PubMed Article CAS Google Scholar

Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:4129.

CAS PubMed Article Google Scholar

Aryee MJ, Jaffe AE, Corrada-Bravo H, Ladd-Acosta C, Feinberg AP, Hansen KD, et al. Minfi: a flexible and comprehensive Bioconductor package for the analysis of Infinium DNA methylation microarrays. Bioinformatics. 2014;30:13639.

CAS PubMed PubMed Central Article Google Scholar

Maksimovic J, Gordon L, Oshlack A. SWAN: Subset-quantile within array normalization for illumina infinium HumanMethylation450 BeadChips. Genome Biol. 2012;13:R44.

PubMed PubMed Central Article CAS Google Scholar

Du P, Zhang X, Huang C-C, Jafari N, Kibbe WA, Hou L, et al. Comparison of Beta-value and M-value methods for quantifying methylation levels by microarray analysis. BMC Bioinformatics. 2010;11:587.

CAS PubMed PubMed Central Article Google Scholar

Price ME, Cotton AM, Lam LL, Farr P, Emberly E, Brown CJ, et al. Additional annotation enhances potential for biologically-relevant analysis of the Illumina Infinium HumanMethylation450 BeadChip array. Epigenetics and Chromatin. 2013;6:115.

Article CAS Google Scholar

Houseman EA, Accomando WP, Koestler DC, Christensen BC, Marsit CJ, Nelson HH, et al. DNA methylation arrays as surrogate measures of cell mixture distribution. BMC Bioinformatics. 2012;13:86. https://doi.org/10.1186/1471-2105-13-86. PMID: 22568884; PMCID: PMC3532182.

Smyth GK. limma: Linear Models for Microarray Data. In: Gentleman R, Carey VJ, Huber W, Irizarry RA, Dudoit S, editors. Bioinformatics and Computational Biology Solutions Using R and Bioconductor. Statistics for Biology and Health. New York: Springer; 2005. https://doi.org/10.1007/0-387-29362-0_23.

Peters TJ, Buckley MJ, Statham AL, Pidsley R, Samaras K, Lord RV, et al. De novo identification of differentially methylated regions in the human genome. Epigenetics Chromatin. 2015;8:6. https://doi.org/10.1186/1756-8935-8-6. PMID: 25972926; PMCID: PMC4429355.

Trapnell C, Roberts A, Goff L, Pertea G, Kim D, Kelley DR, et al. Differential gene and transcript expression analysis of RNA-seq experiments with TopHat and Cufflinks. Nat Protoc. 2012;7:56278.

CAS PubMed PubMed Central Article Google Scholar

Anders S, Pyl PT, Huber W. HTSeq-A Python framework to work with high-throughput sequencing data. Bioinformatics. 2015;31:1669.

CAS PubMed Article Google Scholar

Robinson MD, McCarthy DJ, Smyth GK. edgeR: a Bioconductor package for differential expression analysis of digital gene expression data. Bioinformatics. 2010;26(1):13940. https://doi.org/10.1093/bioinformatics/btp616.

CAS Article PubMed Google Scholar

Yu G, Wang LG, Han Y, He QY. ClusterProfiler: an R package for comparing biological themes among gene clusters. Omi A J Integr Biol. 2012;16:2847.

CAS Article Google Scholar

Ren X, Kuan PF. methylGSA: a Bioconductor package and Shiny app for DNA methylation data length bias adjustment in gene set testing. Bioinformatics. 2019;35:19589.

CAS PubMed Article Google Scholar

Gentleman RC, Carey VJ, Bates DM, et al. Bioconductor: open software development for computational biology and bioinformatics. Genome Biol. 2004;5:R80. https://doi.org/10.1186/gb-2004-5-10-r80.

Gentleman R, Carey V, Huber W, Irizarry R, Dudoit S, Smyth GK. Bioinformatics and computational biology solutions using R and Biocunductor; 2015. p. 397420.

Google Scholar

Yu Y, Arah OA, Liew Z, Cnattingius S, Olsen J, Srensen HT, et al. Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring: population based cohort study with 40 years of follow-up. BMJ. 2019;367 Cvd:14.

Google Scholar

Chavey C, Fajas L. CXCL5 drives obesity to diabetes, and further. Aging (Albany NY). 2009;1:6747.

CAS PubMed PubMed Central Article Google Scholar

Maachi H, Fergusson G, Ethier M, Brill GN, Katz LS, Honig LB, et al. HB-EGF signaling is required for glucose-induced pancreatic -cell proliferation in rats. Diabetes. 2020;69:36980.

CAS PubMed PubMed Central Article Google Scholar

Kos K, Wilding JPH. SPARC: A key player in the pathologies associated with obesity and diabetes. Nat Rev Endocrinol. 2010;6:22535.

CAS PubMed Article Google Scholar

King GL, Park K, Li Q. Selective insulin resistance and the development of cardiovascular diseases in diabetes: The 2015 Edwin Bierman Award Lecture. Diabetes. 2016;65:146271.

CAS PubMed PubMed Central Article Google Scholar

Diz-Villanueva A, Sanz-Pamplona R, Carreras-Torres R, Moratalla-Navarro F, Henar Alonso M, Par-Brunet L, et al. DNA methylation events in transcription factors and gene expression changes in colon cancer. Epigenomics. 2020;12:1593610.

PubMed Article CAS Google Scholar

Prashanth G, Vastrad B, Tengli A, Vastrad C, Kotturshetti I. Identification of hub genes related to the progression of type 1 diabetes by computational analysis. BMC Endocr Disord. 2021;21:165.

Article CAS Google Scholar

Arnaboldi L, Ossoli A, Giorgio E, Pisciotta L, Lucchi T, Grigore L, et al. LIPA gene mutations affect the composition of lipoproteins: enrichment in ACAT-derived cholesteryl esters. Atherosclerosis. 2020;297(2019):815.

CAS PubMed Article Google Scholar

Savill SA, Leitch HF, Harvey JN, Thomas TH. Inflammatory adipokines decrease expression of two high molecular weight isoforms of tropomyosin similar to the change in type 2 diabetic patients. PLoS One. 2016;11:113.

Article CAS Google Scholar

Mazzarotto F, Tayal U, Buchan RJ, Midwinter W, Wilk A, Whiffin N, et al. Reevaluating the genetic contribution of monogenic dilated cardiomyopathy. Circulation. 2020;Dcm:38798.

Article CAS Google Scholar

Zhang SY, Lv Y, Zhang H, Gao S, Wang T, Feng J, et al. Adrenomedullin 2 improves early obesity-induced adipose insulin resistance by inhibiting the class II MHC in adipocytes. Diabetes. 2016;65:234255.

CAS PubMed Article Google Scholar

Fang M, Fan Z, Tian W, Zhao Y, Li P, Xu H, et al. HDAC4 mediates IFN- induced disruption of energy expenditure-related gene expression by repressing SIRT1 transcription in skeletal muscle cells. Biochim Biophys Acta - Gene Regul Mech. 2016;1859:294305.

CAS Article Google Scholar

Merid SK, Novoloaca A, Sharp GC, Kpers LK, Kho AT, Roy R, et al. Epigenome-wide meta-analysis of blood DNA methylation in newborns and children identifies numerous loci related to gestational age. Genome Med. 2020;12:117.

Article CAS Google Scholar

Waterland R, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol. 2003;23:5293300.

CAS PubMed PubMed Central Article Google Scholar

Li CCY, Young PE, Maloney CA, Eaton SA, Cowley MJ, Buckland ME, et al. Maternal obesity and diabetes induces latent metabolic defects and widespread epigenetic changes in isogenic mice. Epigenetics. 2013;8:60211.

CAS PubMed PubMed Central Article Google Scholar

Quilter CR, Cooper WN, Cliffe KM, Skinner BM, Prentice PM, Nelson L, et al. Impact on offspring methylation patterns of maternal gestational diabetes mellitus and intrauterine growth restraint suggest common genes and pathways linked to subsequent type 2 diabetes risk. FASEB J. 2014;28:486879.

CAS PubMed Article Google Scholar

Slieker RC, Bos SD, Goeman JJ, Bove JV, Talens RP, van der Breggen R, et al. Identification and systematic annotation of tissue-specific differentially methylated regions using the Illumina 450k array. Epigenetics Chromatin. 2013;6:26.

CAS PubMed PubMed Central Article Google Scholar

Byun HM, Siegmund KD, Pan F, Weisenberger DJ, Kanel G, Laird PW, et al. Epigenetic profiling of somatic tissues from human autopsy specimens identifies tissue- and individual-specific DNA methylation patterns. Hum Mol Genet. 2009;18:480817.

CAS PubMed PubMed Central Article Google Scholar

Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML, et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci U S A. 2005;102:106049.

Read more:
Epigenetic and transcriptomic alterations in offspring born to women with type 1 diabetes (the EPICOM study) - BMC Medicine - BMC Medicine

Adverum Biotechnologies to Participate in the Jefferies Cell and Genetic Medicine Summit – Adverum Biotec – Benzinga

REDWOOD CITY, Calif., Sept. 23, 2022 (GLOBE NEWSWIRE) -- Adverum Biotechnologies, Inc. ADVM, a clinical-stage company that aims to establish gene therapy as a new standard of care for highly prevalent ocular diseases, today announced that Peter Soparkar, chief operating officer of Adverum Biotechnologies, will present at the Jefferies Cell and Genetic Medicine Summit on September 29, 2022, at 9:30 a.m. ET.

The on-demand webcast corporate presentation may be accessed underEvents and Presentationsin the Investors section of Adverum's website. A replay of the webcast will be available on the website for 90 days following the presentation.

About Adverum Biotechnologies

Adverum Biotechnologies ADVM is a clinical-stage company that aims to establish gene therapy as a new standard of care for highly prevalent ocular diseases with the aspiration of developing functional cures to restore vision and prevent blindness. Leveraging the research capabilities of its proprietary, intravitreal (IVT) platform, Adverum is developing durable, single-administration therapies, designed to be delivered in physicians' offices, to eliminate the need for frequent ocular injections to treat these diseases. Adverum is evaluating its novel gene therapy candidate, ixoberogene soroparvovec (Ixo-vec, formerly referred to as ADVM-022), as a one-time, IVT injection for patients with neovascular or wet age-related macular degeneration. By overcoming the challenges associated with current treatment paradigms for these debilitating ocular diseases, Adverum aspires to transform the standard of care, preserve vision, and create a profound societal impact around the globe. For more information, please visitwww.adverum.com.

Corporate & Investor Inquiries

Anand ReddiVice President, Head of Corporate Strategy, External Affairs and EngagementAdverum Biotechnologies, Inc.T: 650-649-1358E:areddi@adverum.com

Media

Megan TalonAssociate Director, Corporate CommunicationsAdverum Biotechnologies, Inc.T: 650-649-1006E:mtalon@adverum.com

Go here to see the original:
Adverum Biotechnologies to Participate in the Jefferies Cell and Genetic Medicine Summit - Adverum Biotec - Benzinga

What exactly is precision medicine anyway? – health enews

Every person is unique, from their fingerprints to their DNA. Why then would a one-size-fits-all treatment program be appropriate for every person with a particular illness or condition?

Thats the basic idea behind the precision medicine, or personalized medicine, movement.

Precision medicine is a means of providing health care tailored to a patients individual characteristics, right down to the genetic level, says Dr. Antony Ruggeri, hematology and oncology physician at Aurora St. Lukes Medical Center.

When devising a targeted treatment, precision medicine considers not only a persons environment and lifestyle, but also their DNA. Each persons DNA is made up of unique gene patterns and variations that control their bodys functions.

In a sense, doctors have been personalizing medicine for years, Dr. Ruggeri says. We might not treat a middle-aged patient the same as an elderly patient. But where precision medicine has more recently taken a monumental step forward is in the use of molecular testing to determine a treatment course based on genetic makeup.

Modern molecular testing allows doctors to sequence, or identify, large portions of a persons DNA and then recommend a specific treatment based on a persons specific genetic variations.

Recent advances in precision medicine have led to powerful changes in disease treatment, particularly in the field of cancer care.

Cancer researchers have found that individual tumors also have unique molecular footprints, explains Dr. Ruggeri. Even among the same type of cancer, the genetic changes driving tumor growth will vary.

By taking a tumor tissue sample and comparing the tumors genetic makeup to those of other tumors recorded in an electronic database, doctors may find a treatment with a history of success against a tumor thats genetically similar.

For example, the American Society of Clinical Oncology Targeted Agent and Profiling Utilization Registry (TAPUR) study now underway at Advocate Aurora Health cancer clinics across Wisconsin is evaluating precision medicine cancer treatments with dozens of anticancer drugs that are already on the market.

The drugs available through the study are all approved by the U.S. Food and Drug Administration (FDA) for the treatment of a type of cancer but havent been FDA-approved to treat each study participants specific type of cancer. Researchers hope the study will help identify new treatments for many different types of advanced cancer.

Want to know more about research at Advocate Aurora Health? Visit aah.org/research.

ASCO, American Society of Clinical Oncology, and TAPUR are trademarks of the American Society of Clinical Oncology, Inc., used with permission.

Read more from the original source:
What exactly is precision medicine anyway? - health enews

Biological Links Identified Between an Aggressive Breast Cancer Type and African Ancestry – Weill Cornell Medicine Newsroom

Weill Cornell Medicine investigators have identified definitive biological links between African ancestry and disease processes that affect an aggressive cancer type called triple-negative breast cancer (TNBC). Their analysis of TNBC tumors from a diverse patient population yielded a large set of genes whose expression differed in patients with African ancestry compared with patients with European ancestry.

In the study, published Sept. 19 in Cancer Discovery, a journal of the American Association for Cancer Research, the scientists identify the expression of 613 genes associated with African ancestry and more than 2,000 genes associated with regional African ancestry in patients with TNBC. They also describe distinct patterns of immune responses in patients of African descent that may explain patterns of disease progression and outcomes. Together, these findings provide a foundation for future research into better treatment options for this cancer, which has the worst survival outcomes of all breast cancer types.

Many people are not aware of the geographic origins of their ancestors nor how much of their DNA was inherited from each source, known as genetic ancestry. Previous studies of racial differences in TNBC analyzed data from African American patients and relied on self-reported race, said senior author Dr. Melissa B. Davis, associate professor of cell and developmental biology research in surgery and director of health equity in the Englander Institute for Precision Medicine at Weill Cornell Medicine. Our study is the first to determine each individuals ancestry not only by African descent but also by specific regions within Africa.

TNBC tumor cells have no estrogen or progesterone receptors and scant amounts of HER2/neu protein on their surface, making them challenging to treat as they dont respond to hormone therapies or anti-HER2 drugs that block cell proliferation. The subtype represents about 33 percent of breast cancer diagnoses in African countries compared with less than 20 percent in other nations. African American women have twice the risk of developing TNBC and a higher risk of mortality than white Americans of European ancestry.

For their current study, the investigators performed ancestry estimation on breast tissue samples from 132 patients and RNA sequencing on a subset of 26 cases provided by the Englander Institute of Precision Medicine at Weill Cornell Medicine; the University of Alabama at Birmingham; and The International Center for the Study of Breast Cancer Subtypes (ICSBCS), now headquartered at Weill Cornell Medicine. The ICSBCS was established in 2004 and features partners across different regions of Africa as well as the Caribbean and Central America. This study drew samples from ICSBCS founding member The Komfo Anokye Teaching Hospital (KATH) in Kumasi, Ghana, as well as the Millennium Medical College St. Pauls Hospital in Addis Ababa, Ethiopia.

After identifying the expression of genes associated with African ancestry at the country and regional levels, the researchers examined the affected biological pathways and estimated proportions of immune cells in tumors. They discovered that women with TNBC with a high degree of African ancestry, primarily East Africans from Ethiopia, had significantly higher immune cell populations infiltrating tumors, than women with a lower degree of African ancestry who were mainly African Americans and West Africans from Ghana. Increased immune responses in TNBC tumors in women of regional African descent will be particularly interesting to researchers studying the benefits of immunotherapies, said lead author Dr. Rachel Martini, a postdoctoral associate in surgery at Weill Cornell Medicine.

This recent discovery gives us hope that we will continue to find answers and contribute to solutions for a disease which has long afflicted all ancestries, but shows greater burden in Africa, said Dr. Ernest Adjei, consulting pathologist at KATH. The ICSBCS provides a great platform for strong research collaborations into the future as we work together for improved outcomes in breast cancer management.

The investigators also found that several African ancestry-associated genes detected in normal breast tissue switched expressions in tumor tissue. These findings suggest that some ancestry-specific differences in gene expression may be in response to malignancies, said Dr. Martini.

Finally, the researchers examined the data by self-reported race and found some of the same pathways they had associated with ancestry. However, they also found others imprinted on tumors relating to diabetes and obesity that were not associated with ancestry. This finding suggests its essential to look at both race and ancestry when exploring disparities in TNBC development and outcomes, said Dr. Davis, who is an ethnicity scholar at the New York Genome Center and also serves as scientific director of ICSBCS. For example, we could potentially harness aspects of the diabetes or obesity pathways in tumors as targets to treat cancer patients with comorbidities.

The teams most recent findings add to a robust legacy of studies utilizing the ICSBCS biorepository that are clarifying the role of genetic ancestry related to breast cancer risk, added co-author Dr. Lisa Newman, chief of the Section of Breast Surgery at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center, professor of surgery at Weill Cornell Medicine and ICSBCS medical director and founder.

The investigators are now looking more deeply at gene expression differences to determine the master regulators of the pathways they identified and performing single cell analysis to learn more about the tumor microenvironment. We want to get to the bottom of the molecular features driving disparities in TNBC before we move our work into the clinical space, Dr. Davis said.

Read more:
Biological Links Identified Between an Aggressive Breast Cancer Type and African Ancestry - Weill Cornell Medicine Newsroom

Chroma Medicine Announces Formation of Scientific Advisory Board of Global Experts in Gene Editing and Cell and Gene Therapy – PR Newswire

Members Bradley Bernstein, M.D., Ph.D., Paula Cannon, Ph.D., Howard Chang, M.D., Ph.D., and Ahmad (Mo) Khalil, Ph.D., will guide advancement of the company's epigenetic editing platform and key programs

Scientific Advisors join Chroma Founders, Luke Gilbert, Ph.D., Keith Joung M.D., Ph.D., David Liu, Ph.D., Angelo Lombardo, Ph.D., Luigi Naldini, M.D., Ph.D., and Jonathan Weissman, Ph.D., expanding the company's world-class team of leaders in genomic medicine

CAMBRIDGE, Mass., Sept 20, 2022 /PRNewswire/ -- Chroma Medicine, Inc., (Chroma) a genomic medicine company pioneering single-dose epigenetic editing therapeutics, today announced the formation of a Scientific Advisory Board (SAB) comprising renowned leaders in epigenetics, cell and gene therapy, and synthetic biology: Bradley Bernstein, M.D., Ph.D., Paula Cannon, Ph.D., Howard Chang, M.D., Ph.D., and Ahmad (Mo) Khalil, Ph.D. The SAB members will provide key input to Chroma as the company advances its programs addressing a wide range of diseases.

"Each of these distinguished experts will be instrumental as we unlock the potential of epigenetic editing therapeutics," said Catherine Stehman-Breen, M.D., Chief Executive Officer of Chroma Medicine. "We are honored to welcome them to the Chroma team and eager to leverage their expertise as we build the future of genomic medicine."

"The SAB is composed of scientific leaders whose seminal research has significantly advanced the fields of genome editing and cell and gene therapy," said Vic Myer, Ph.D., President and Chief Scientific Officer of Chroma. "They bring a wealth of knowledge and experience to Chroma as we continue to advance our platform with the goal of bringing novel single-dose genomic therapeutics to patients."

Members of the Chroma Scientific Advisory Board include:

About Chroma Medicine

Chroma Medicine is a biotechnology company pioneering a new class of genomic medicines that harness epigenetics, nature's innate mechanism for gene regulation, to deliver single-dose therapeutics for patients with genetically driven diseases. The company was founded by the world's foremost experts in genomic research and is led by a veteran team of industry leaders and scientists with deep experience in genomic medicine, drug discovery, and development. For more information, please visit chromamedicine.com or follow the company on LinkedIn and Twitter.

SOURCE Chroma Medicine

Read more here:
Chroma Medicine Announces Formation of Scientific Advisory Board of Global Experts in Gene Editing and Cell and Gene Therapy - PR Newswire