Editor’s choice: recent research highlights from the International Journal of Nanomedicine – Dove Medical Press

Farooq A Shiekh,1 Abdul-Rahman M Abu-Izzah,2 Vivian J Lee,2 Syed Mudassar1

1Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences (SKIMS), Srinagar, India; 2Department of Basic Medical Sciences, Avalon University School of Medicine, Curacao, the Netherlands Is nanomedicine really less harmful? Evaluation of: Thakkar A, Chenreddy S, Thio A, Khamas W, Wang J, Prabhu S. Preclinical systemic toxicity evaluation of chitosan-solid lipid nanoparticle-encapsulated aspirin and curcumin in combination with free sulforaphane in BALB/c mice. Int J Nanomedicine. 2016;11:32653276. Nanomedicine1 has increasingly received a tremendous attention over the past two decades as a potential multidimensional field, developing nano-applications that are transforming a host of medical products and services,2,3 including drug delivery4 and health-monitoring devices, and the possibility of gaining new insights about undruggable targets and treatment through atomic-scale precision is increasing rapidly.5 Although it is uncertain as to which of the new delivery platforms will become the most effective and useful, it is certain that many new approaches will be investigated in the years to come.4,6

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

More:

Editor's choice: recent research highlights from the International Journal of Nanomedicine - Dove Medical Press

Researcher awarded grant for HIV/AIDS drug study – FIU News

Rahul Dev Jayant, PhD

Rahul Dev Jayant, assistant professor in the Department of Immunology, has received a $25,000 grant from The Campbell Foundation in Ft. Lauderdale to continue his research on sustained-release nanoformulation to deliver antiretroviral (ARV) medication for patients living with HIV/AIDS.

Using FIU patented nanotechnology, Jayant, a researcher at the Herbert Wertheim College of Medicines Center for Personalized Nanomedicine, has successfully integrated Tenofovir, an antiretroviral drug used to fight HIV, into a long-active nanoformulation thatcan release the medication for up to one week.

Now, with the generous help from The Campbell Foundation, we will be working toward the development of single-dose formulation that can release the ARV drugs up to one month, Jayant said.

Bill Venuti and Ken Rapkin (first and third from right) of The Campbell Foundation present the $25K check to the Immunology Department team.

Sustained release of antiretroviral medication has the potential to be a game changer for many people living with HIV/AIDS who may have trouble adhering to the daily pill dosing that current treatments require.

The Campbell Foundation has been funding cutting-edge research into a cure for HIV since its creation in 1995 by the late Richard Campbell Zahn, the chemist who developed Herpecin-L Lip Balm for the treatment of cold sores and fever blisters.

These fast-track grants to South Florida-based researchers show our Board of Directors ongoing commitment to addressing HIV/AIDS right here in our own backyard, said Campbell Foundation Trustee Bill Venuti.

If you're new here, you may want to subscribe to our newsletter. Thanks for visiting!

Here is the original post:

Researcher awarded grant for HIV/AIDS drug study - FIU News

MNE 2012 16 > 20 September 2012 38th International …

The MNE2012 Organizing Committee is pleased to announce that the 38th International Micro & Nano Engineering Conference (MNE 2012) will be held in Toulouse-France at the Pierre Baudis Congress Centre from 16 to 20 September 2012.

The MNE Conference focuses on micro and nano-fabrication and manufacturing using lithography and other nano-patterning related approaches. The Conference brings together engineers and scientists from all over the world to discuss recent progress and future trends in the fabrication, manufacturing and application of micro and nano-structures and devices. Applications in electronics, photonics, electromechanics, environment and life sciences are discussed.

MNE attracts about 700 delegates (>500 papers) and is the first international micro-nanotechnology Conference in Europe on the following subjects :

1. Micro and Nanolithography

2. Micro and Nanofabrication/Micro and Nanoengineering

3. Micro and Nano Systems

4. Micro ans Nano Devices and Systems for Biology, Chemistry and Medicine

We host a technical exhibition which remains continuously opened during the four days of the Conference.

The Conference program and layout have been structured to maximize the opportunity for delegates to visit the technical exhibition.

Welcome to Southern France, in Toulouse, the pink city. In our region, nature can be beautiful and majestuous, tormented or peaceful. The monuments, churches, abbeys, castles and palaces built by our ancestors to protect themselves or to pay tribute to their faith are in tune with natural beauty. Toulouse, a rich and beautiful city, is famous for its aeronautical and space achievements, its university founded in 1229, its laboratories and research centres. Today, more than 97,000 students attend its three universities, institutes and schools. This city owes its name Ville Rose to the colour of the bricks covering the walls, which glitter Under the blazing sun.

It combines a strong living spirit with a brilliant past and can unveil the gist of its beauties while jealously hiding less familiar treasures. Toulouse is constantly building the future but is also a real heaven for the strolling passer-by who just wants to muse in a cloister or on a terrace outside a caf or a restaurant till very late at night. Toulouse also lives within the sound of rhythm and music, with a subtle mix of Italian and Spanish influences.

By organizing this meeting, we will provide you with an excellent opportunity for scientific and social interaction.

We look forward to welcoming you in Toulouse!

Yours sincerely

Conference Chair: Ch.VIEU

Conference Co-Chairs: J. PERROCHEAU Ch. CERCLIER

Program Chair and Co-Chairs: G. BEN ASSAYAG Y. CHEN J. GRISOLIA

See the original post here:

MNE 2012 16 > 20 September 2012 38th International ...

Careers in the future world – The Nation

Taking place at Bangkok Convention Hall (BCC Hall) on the fifth floor of Central Plaza Lat Phrao on July 15, the event will showcase careers that will suit their skills and interests and help them make decisions about further education and professional life. Participants will also learn and find out about the real world of work.

The overall aim of this campaign is to give teenagers an opportunity to explore the 24 most promising jobs of the future from Thailands leading companies. By participating in the event, teenagers will also get inspired to develop their potential, starting with understanding themselves, realising their capabilities, choosing careers that match their interests as well planning fot the future, says Siriporn Nopwattanapong, KTBs executive vice president and director of communication and branding group.

KTB is well aware of the importance of building strong developmental foundations in education for Thai children at all levels. Additionally, the Digital Transformation has a significant impact on jobs and gives rise to new professional opportunities and, more importantly, Thai teenagers are being pressed to pursue career paths that have little bering on their capability, skills and interests. In the midst of all of this, teenagers fail to finish their degree courses, while some lack the skills or knowledge to perform their job responsibilities, which is detrimental to their careers, she adds.

The career guidance event is divided into three parts. The first part is the 24 Trendy Career Insight Exhibition focusing on environment engineering, data science and nano-engineering, IT including software, application and game development, accounting & finance, medical fields (dermatologist, sports scientist and veterinarian), business ownership (start-up owner, digital entrepreneur and smart farmer), design (augmented reality, architect and creative) and alternative careers (acting coach, fitness trainer, supplementary businessman, cover artist and beauty blogger etc).

The second part is Job Tour and will take 100 teenagers selected from the Next-Gen Career by KTB event on a private visit to Thailands leading companies, which cover four different career groups such as engineering, IT, design and business owner. The third part is Workshop during which the 100 participants will be coached over two days in identifying their dreams, developing their potential and thinking skills and encouraged to gain hands-on experience.

Those who attend the event will gain insight into the 24 promising jobs of the future and career advice from professionals in various fields. The event will also features talks by successful role models who will share and exchange their experience. Interested teenagers can register for this Next-Gen Careers by KTB at http://www.ktb.co.th/csr. The first 500 to registered will be eligible for giveaways at the event.

The rest is here:

Careers in the future world - The Nation

Rutgers Researchers Invent Sensor that Could Improve Treatment of … – TAPinto.net

NEW BRUNSWICK, NJ Rutgers University-New Brunswick scientists have created a graphene-based sensor that could lead to earlier detection of looming asthma attacks and improve the management of asthma and other respiratory diseases, preventing hospitalizations and deaths.

The sensor paves the way for the development of devices possibly resembling fitness trackers like the Fitbit which people could wear and then know when and at what dosage to take their medication.

Our vision is to develop a device that someone with asthma or another respiratory disease can wear around their neck or on their wrist and blow into it periodically to predict the onset of an asthma attack or other problems, said Mehdi Javanmard, an assistant professor in the Department of Electrical and Computer Engineering. It advances the field of personalized and precision medicine.

Sign Up for E-News

Javanmard and a diverse team of Rutgers-New Brunswick experts describe their invention in a study recently published online in the journal Microsystems & Nanoengineering.

Asthma, which causes inflammation of the airway and obstructs air flow, affects about 300 million people worldwide. About 17.7 million adults and 6.3 million children in the United States were diagnosed with asthma in 2014. Symptoms include coughing, wheezing, shortness of breath, and chest tightness. Other serious lung ailments include chronic obstructive pulmonary disease (COPD), which encompasses emphysema and chronic bronchitis.

Todays noninvasive methods for diagnosing and monitoring asthma are limited in characterizing the nature and degree of airway inflammation, and require costly, bulky equipment that patients cannot easily keep with them. The methods include spirometry, which measures breathing capacity, and testing for exhaled nitric oxide, an indicator of airway inflammation. Theres an urgent need for improved, minimally invasive methods for the molecular diagnosis and monitoring of asthma, according to the study.

Measuring biomarkers in exhaled breath condensate tiny liquid droplets discharged during breathing can contribute to understanding asthma at the molecular level and lead to targeted treatment and better disease management.

The Rutgers researchers miniaturized electrochemical sensor accurately measures nitrite in exhaled breath condensate using reduced graphene oxide. Reduced graphene oxide resists corrosion, has superior electrical properties and is very accurate in detecting biomarkers. Graphene is a thin layer of the graphite used in pencils.

Nitrite level in breath condensate is a promising biomarker for inflammation in the respiratory tract. Having a rapid, easy method to measure it can help an asthmatic determine if air pollutants are affecting them so they can better manage use of medication and physical activity, said Clifford Weisel, study co-author and professor at Rutgers Environmental and Occupational Health Sciences Institute (EOHSI). It could also be used in a physicians office and emergency departments to monitor the effectiveness of various anti-inflammatory drugs to optimize treatment.

Increases in airway inflammation may be an early warning sign of increased risk of an asthma attack or exacerbation of COPD, allowing for earlier and more-effective preventive measures or treatment, said Robert Laumbach, study co-author and an occupational and environmental medicine physician at EOHSI.

Just looking at coughing, wheezing and other outward symptoms, diagnosis accuracy is often poor, so thats why this idea of monitoring biomarkers continuously can result in a paradigm shift, said Javanmard, who works in the School of Engineering. The ability to perform label-free quantification of nitrite content in exhaled breath condensate in a single step without any sample pre-treatment resolves a key bottleneck to enabling portable asthma management.

The next step is to develop a portable, wearable system, which could be commercially available within five years, he said. The researchers also envision expanding the number of inflammation biomarkers a device could detect and measure.

In the U.S. alone, allergy inflammation, asthma and various respiratory conditions are all on the rise, so devices that can help diagnose, monitor and manage these conditions will be in high demand, Javanmard said.

Todd B. Bates is a science communicator with Public and Media Relations at Rutgers University-New Brunswick.

Originally posted here:

Rutgers Researchers Invent Sensor that Could Improve Treatment of ... - TAPinto.net

What Is the Future of Computers? | Moore’s Law

Integrated circuit from an EPROM memory microchip showing the memory blocks and supporting circuitry.

In 1958, a Texas Instruments engineer named Jack Kilby cast a pattern onto the surface of an 11-millimeter-long "chip" of semiconducting germanium, creating the first ever integrated circuit. Because the circuit contained a single transistor a sort of miniature switch the chip could hold one "bit" of data: either a 1 or a 0, depending on the transistor's configuration.

Since then, and with unflagging consistency, engineers have managed to double the number of transistors they can fit on computer chips every two years. They do it by regularly halving the size of transistors. Today, after dozens of iterations of this doubling and halving rule, transistors measure just a few atoms across, and a typical computer chip holds 9 million of themper square millimeter. Computers with more transistors can perform more computations per second (because there are more transistors available for firing), and are therefore more powerful. The doubling of computing power every two years is known as "Moore's law," after Gordon Moore, the Intel engineer who first noticed the trend in 1965.

Moore's law renders last year's laptop models defunct, and it will undoubtedly make next year's tech devices breathtakingly small and fast compared to today's. But consumerism aside, where is the exponential growth in computing power ultimately headed? Will computers eventually outsmart humans? And will they ever stop becoming more powerful?

The singularity

Many scientists believe the exponential growth in computing power leads inevitably to a future moment when computers will attain human-level intelligence: an event known as the "singularity." And according to some, the time is nigh.

Physicist, author and self-described "futurist" Ray Kurzweil has predicted that computers will come to par with humans within two decades. He told Time Magazine last year that engineers will successfully reverse-engineer the human brain by the mid-2020s, and by the end of that decade, computers will be capable of human-level intelligence.

The conclusion follows from projecting Moore's law into the future. If the doubling of computing power every two years continues to hold, "then by 2030 whatever technology we're using will be sufficiently small that we can fit all the computing power that's in a human brain into a physical volume the size of a brain," explained Peter Denning, distinguished professor of computer science at the Naval Postgraduate School and an expert on innovation in computing. "Futurists believe that's what you need for artificial intelligence. At that point, the computer starts thinking for itself." [How to Build a Human Brain]

What happens next is uncertain and has been the subject of speculation since the dawn of computing.

"Once the machine thinking method has started, it would not take long to outstrip our feeble powers," Alan Turing said in 1951 at a talk entitled "Intelligent Machinery: A heretical theory," presented at the University of Manchester in the United Kingdom. "At some stage therefore we should have to expect the machines to take control." The British mathematician I.J. Good hypothesized that "ultraintelligent" machines, once created, could design even better machines. "There would then unquestionably be an 'intelligence explosion,' and the intelligence of man would be left far behind. Thus the first ultraintelligent machine is the last invention that man need ever make," he wrote.

Buzz about the coming singularity has escalated to such a pitch that there's even a book coming out next month, called "Singularity Rising" (BenBella Books), by James Miller, an associate professor of economics at Smith College, about how to survive in a post-singularity world. [Could the Internet Ever Be Destroyed?]

Brain-like processing

But not everyone puts stock in this notion of a singularity, or thinks we'll ever reach it. "A lot of brain scientists now believe the complexity of the brain is so vast that even if we could build a computer that mimics the structure, we still don't know if the thing we build would be able to function as a brain," Denning told Life's Little Mysteries. Perhaps without sensory inputs from the outside world, computers could never become self-aware.

Others argue that Moore's law will soon start to break down, or that it has already. The argument stems from the fact that engineers can't miniaturize transistors much more than they already have, because they're already pushing atomic limits. "When there are only a few atoms in a transistor, you can no longer guarantee that a few atoms behave as they're supposed to," Denning explained. On the atomic scale, bizarre quantum effects set in. Transistors no longer maintain a single state represented by a "1" or a "0," but instead vacillate unpredictably between the two states, rendering circuits and data storage unreliable. The other limiting factor, Denning says, is that transistors give off heat when they switch between states, and when too many transistors, regardless of their size, are crammed together onto a single silicon chip, the heat they collectively emit melts the chip.

For these reasons, some scientists say computing power is approaching its zenith. "Already we see a slowing down of Moore's law," the theoretical physicist Michio Kaku said in a BigThink lecture in May.

But if that's the case, it's news to many. Doyne Farmer, a professor of mathematics at Oxford University who studies the evolution of technology, says there is little evidence for an end to Moore's law. "I am willing to bet that there is insufficient data to draw a conclusion that a slowing down [of Moore's law] has been observed," Farmer told Life's Little Mysteries. He says computers continue to grow more powerful as they become more brain-like.

Computers can already perform individual operations orders of magnitude faster than humans can, Farmer said; meanwhile, the human brain remains far superior at parallel processing, or performing multiple operations at once. For most of the past half-century, engineers made computers faster by increasing the number of transistors in their processors, but they only recently began "parallelizing" computer processors. To work around the fact that individual processors can't be packed with extra transistors, engineers have begun upping computing power by building multi-core processors, or systems of chips that perform calculations in parallel."This controls the heat problem, because you can slow down the clock," Denning explained. "Imagine that every time the processor's clock ticks, the transistors fire. So instead of trying to speed up the clock to run all these transistors at faster rates, you can keep the clock slow and have parallel activity on all the chips." He says Moore's law will probably continue because the number of cores in computer processors will go on doubling every two years.

And because parallelization is the key to complexity, "In a sense multi-core processors make computers work more like the brain," Farmer told Life's Little Mysteries.

And then there's the future possibility of quantum computing, a relatively new field that attempts to harness the uncertainty inherent in quantum states in order to perform vastly more complex calculations than are feasible with today's computers. Whereas conventional computers store information in bits, quantum computers store information in qubits: particles, such as atoms or photons, whose states are "entangled" with one another, so that a change to one of the particles affects the states of all the others. Through entanglement, a single operation performed on a quantum computer theoretically allows the instantaneous performance of an inconceivably huge number of calculations, and each additional particle added to the system of entangled particles doubles the performance capabilities of the computer.

If physicists manage to harness the potential of quantum computers something they are struggling to do Moore's law will certainly hold far into the future, they say.

Ultimate limit

If Moore's law does hold, and computer power continues to rise exponentially (either through human ingenuity or under its own ultraintelligent steam), is there a point when the progress will be forced to stop? Physicists Lawrence Krauss and Glenn Starkman say "yes." In 2005, they calculated that Moore's law can only hold so long before computers actually run out of matter and energy in the universe to use as bits. Ultimately, computers will not be able to expand further; they will not be able to co-opt enough material to double their number of bits every two years, because the universe will be accelerating apart too fast for them to catch up and encompass more of it.

So, if Moore's law continues to hold as accurately as it has so far, when do Krauss and Starkman say computers must stop growing? Projections indicate that computer will encompass the entire reachable universe, turning every bit of matter and energy into a part of its circuit, in 600 years' time.

That might seem very soon. "Nevertheless, Moore's law is an exponential law," Starkman, a physicist at Case Western University, told Life's Little Mysteries. You can only double the number of bits so many times before you require the entire universe.

Personally, Starkman thinks Moore's law will break down long before the ultimate computer eats the universe. In fact, he thinks computers will stop getting more powerful in about 30 years. Ultimately, there's no telling what will happen. We might reach the singularity the point when computers become conscious, take over, and then start to self-improve. Or maybe we won't. This month, Denning has a new paper out in the journal Communications of the ACM, called "Don't feel bad if you can't predict the future." It's about all the people who have tried to do so in the past, and failed.

This story was provided by Life's Little Mysteries, a sister site to LiveScience. Follow Natalie Wolchover on Twitter @nattyoveror Life's Little Mysteries @llmysteries. We're also on Facebook & Google+.

Read this article:

What Is the Future of Computers? | Moore's Law

CereScan Demos CereMetrix at Society for Nuclear Medicine … – Business Wire (press release)

DENVER--(BUSINESS WIRE)--CereScan, a leading provider of neuro-diagnostics solutions, presented the newest features, capabilities and use cases of its CereMetrix platform during the Society for Nuclear Medicine and Molecular Imaging (SNMMI) Annual Conference at the Colorado Convention Center last week. CereMetrix is a patented, statistically-correlated, normative and scalable medical database designed to aid in the diagnosis and treatment of the human brain.

CereMetrix will provide the healthcare community with the most robust resource on conditions like traumatic brain injury, toxic brain injury, Alzheimers Disease and other dementias, PTSD, bipolar disorder, ADHD, anxiety, autism and depression. Its a brain focused medical analytics platform that may accelerate the accurate and effective diagnosis of complex brain-related disorders to improve treatment and outcomes for patients.

We see SNMMI members as core stakeholders for CereMetrix and wanted to engage them to both share our vision and get feedback on the solution. Im happy to report that the response was overwhelmingly favorable and we now feel that we are innovating in the right direction, said John Kelley Jr., Chairman and CEO of CereScan.

The key attributes of CereMetrix include:

About CereScan

CereScan combines state-of-the-art brain imaging technologies with a patient-centered model of care to provide the highest level of neuro-diagnostics available. CereScan utilizes state-of-the-art gamma camera technology, new generation imaging software and a proprietary process to produce comprehensive medical reports including voxel level images of brain function and physiology. Our functional brain imaging technologies are the most sophisticated in the world today. Additional information about the company is available at https://cerescan.com.

CereScan and CereMetrix are registered trademark of CereHealth Corp.

Read the original post:

CereScan Demos CereMetrix at Society for Nuclear Medicine ... - Business Wire (press release)

Top Biomedical Journal Is Edited at Wayne State University and the Perinatology Research Branch of NICHD/NIH – Newswise (press release)

Newswise DETROIT The medical journal publishing original research in the field of obstetrics and gynecology with the highest impact factor is edited on the campus of the Wayne State University School of Medicine.

Thomson Reuters announced June 14 the 2016 impact factor of biomedical journals on its Journal Citation Reports, the world's most influential resource for evaluating peer-reviewed publications and the authoritative source of annual journal metrics, including the renowned Impact Factor of Journals.

The American Journal of Obstetrics & Gynecology ranked second in the discipline of obstetrics and gynecology with an impact factor of 5.574. Human Reproduction Update, which publishes only reviews and not original research, ranked first; therefore, for all intents and purposes, the American Journal of Obstetrics & Gynecology is the leading journal in impact factor in obstetrics and gynecology publishing original research.

Roberto Romero, M.D., D.Med.Sci., chief of the Perinatology Research Branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health, is editor in chief for Obstetrics of the American Journal of Obstetrics & Gynecology. The journal, the oldest in obstetrics and gynecology, which celebrates its 150th anniversary in 2019, is edited at the PRB, on the campus of the WSU School of Medicine and the Detroit Medical Center.

The American Journal of Obstetrics & Gynecology has the highest number of citations of any journal in obstetrics and gynecology, said Dr. Romero, who also serves as director of the Division of Obstetrics and Maternal-Fetal Medicine for the NIH and is a professor of Molecular Obstetrics and Genetics in the Center of Molecular Medicine and Genetics for Wayne State University.

Throughout its distinguished history, the journal has changed the lives of women and their families, and the practice of obstetrics and gynecology.

Dr. Romero offered numerous examples of landmark papers published on the pages of the journal, including:

The impact factor, published independently by Thomson Reuters, is used to assess a journal's standing in scholarly literature through the objective evaluation of quantifiable, statistical information. The analysis comprises citation data, impact and influence metrics, and millions of cited and citing journal data points from the Web of Science, the industry's leading citation indices in the sciences, social sciences, and arts and humanities.

The American Journal of Obstetrics & Gynecology, Dr. Romero noted, has introduced innovations in biomedical publishing and is committed to bringing information to physicians, scientists, midwives, nurses and patients, and has promoted changes to favor wide dissemination of its content with videos, PowerPoint presentations and other features. The journal has a new section to celebrate Giants in Obstetrics and Gynecology, recognizing the protagonists of the field and the stories behind the headlines.

The journal is published by Elsevier, the largest publisher in the world. The American Journal of Obstetrics & Gynecology has a printed circulation of 42,000 in the United States, and is present in every major biomedical library and maternity hospital around the world. Its electronic presence and international footprint and influence have made it the premier academic journal in obstetrics and gynecology.

###

About Wayne State University

Wayne State University is one of the nations pre-eminent public research universities in an urban setting. Through its multidisciplinary approach to research and education, and its ongoing collaboration with government, industry and other institutions, the university seeks to enhance economic growth and improve the quality of life in the city of Detroit, state of Michigan and throughout the world. For more information about research at Wayne State University, visit research.wayne.edu.

The rest is here:

Top Biomedical Journal Is Edited at Wayne State University and the Perinatology Research Branch of NICHD/NIH - Newswise (press release)

Awards for the Wellcome community in the Queen’s Birthday Honours – Wellcome Trust

News / Published: 19 June 2017

Several members of the Wellcome community have been named in the Queens Birthday Honours list. The list, which was announced over the weekend, includes over 1,000 people who are recognised for their achievements and contributions to society.

Members of the Wellcome community recognised in the honours list include:

Our warmest congratulations to all those who have been honoured this year.

Dr Jeremy Farrar, Wellcomes Director, said: "The Queens Birthday Honours is a wonderful way to celebrate the achievements and contribution to society of so many from Wellcomes broad community. I am delighted for everyone who was recognised, but a very special mention and congratulations to Beth Thompson who led Wellcomes work on EU data protection, which allowed critical research to proceed, ensured cross border collaboration and protected individual privacy. A huge achievement!"

A full list of all those who have been recognised can be found on the Government website.

Read more from the original source:

Awards for the Wellcome community in the Queen's Birthday Honours - Wellcome Trust

A Couple’s Quest To Stop A Rare Disease Before It Takes One Of Them – Maine Public

In 2010, Sonia Vallabh watched her mom, Kamni Vallabh, die in a really horrible way.

First, her mom's memory started to go, then she lost the ability to reason. Sonia says it was like watching someone get unplugged from the world. By the end, it was as if she was stuck between being awake and asleep. She was confused and uncomfortable all the time.

"Even when awake, was she fully or was she really? And when asleep, was she really asleep?" says Sonia.

The smart, warm, artistic Kamni just 51 years old was disappearing into profound dementia.

"I think until you've seen it, it's hard to actually imagine what it is for a person to be alive and their body is moving around, but their brain is not there anymore," says Eric Minikel, Sonia's husband.

In less than a year, Sonia's mom died.

An autopsy showed Kamni had died from something rare -- a prion disease. Specifically, one called fatal familial insomnia because in some patients it steals the ability to fall asleep.

Basically, certain molecules had started clumping together in Kamni's brain, killing her brain cells. It was all because of one tiny error in her DNA an "A" where there was supposed to be a "G," a single typo in a manuscript of 6 billion letters.

Sonia sent a sample of her own blood to a lab, where a test confirmed she inherited the same mutation. The finding threw the family into grief all over again.

"But that grieving period sort of started to resolve within about a week or so," she says. "And we weren't in crisis anymore. We were finding our way toward a new normal, where this was something that we were going to have to live with and deal with and learn more about."

Today, Sonia and her husband live and work in Cambridge, Mass., where they are both doctoral students in the lab of Stuart Schreiber, a Harvard professor of chemistry and chemical biology. Over the past several years, the couple has completely redirected their careers and their lives toward this single goal: to prevent prion disease from ever making Sonia sick.

The two wear bright colors and laugh easily. When they answer my questions, they look at each other instead of at me. They like complicated board games, urban walks and efficient cooking. They are thinkers and problem solvers, which is why, when Sonia got her genetic test results, it changed everything.

The change

"It didn't happen all at once," Sonia says. "There wasn't a day when we woke up and said, 'OK let's change everything about our lives.'"

At the time, Sonia, who has a Harvard law degree, had just started a new job as a legal consultant. Eric was a transportation analyst.

But they couldn't stop thinking about Sonia's test result. They started researching prion diseases online, and invited over friends who are biologists and chemists, to help them understand the science.

"And around that time," Sonia says, "we both enrolled in night classes as well," in subjects like biology and neuroscience.

They were hungry to learn more as quickly as possible; the night classes weren't enough.

"I was basically fresh out of law school and started walking into classes at MIT during the day because this was kind of all I could think about," says Sonia, who at the time wore sneakers every day so that she could rush between work, classes, and a neuroscience lab at Massachusetts General Hospital. She'd started volunteering there, thanks to a professor from one of her classes, and mentors in the lab who helped her learn everything from how to use a pipette to how to work with human brain cells.

"And from there, this is where things happened surprisingly quickly," Sonia says.

The couple started a nonprofit, Prion Alliance, in hopes of raising money for research. Sonia left her legal job to work in the Mass General lab full-time as a technician. Then, Eric left his job and joined a genetics lab, applying his skills in coding to analyzing genetic data, rather than transportation data.

"I was getting left behind!" he says. "Sonia was out there doing all this science. It was her day job now and I was still in my old career and, you know, it was a good job and all, it was meaningful, but it wasn't the mission that it was increasingly clear that we were going to be on."

Just months after they'd finished grad school in law and urban planning, the pair went back to graduate school, this time in biomedical sciences to study prion diseases.

"You are talking to two third-year graduate students," says Eric.

Life as scientists

The two now share an office and a lab bench, under Schreiber's supervision, at the Broad Institute of MIT and Harvard.

"There's a date in the future when Sonia will get the first dose of the drug that's going to save her life," Eric says. "What can I do today that brings that date closer to the present?"

A posted printout of an email says: "Let's just blast forward and solve problems as they become real and as they need immediate solutions." It's a note Schreiber sent the pair at one point when they were worrying about bureaucratic hoops they had to jump through.

"I thought it was a good philosophy, so we printed it out and put it on the wall," says Eric.

Sonia and Eric are "the best of humanity" Schreiber tells Shots. "Their story is, of course, remarkable, and they personify the concept of patientscientists. But their deep understanding of science and ability to innovate and execute on one of the hardest challenges in biomedical science are breathtaking."

Schreiber says that his lab, like many others in biomedicine, has long included researchers who are physicians as well as scientists; that dual training and experience brings an important perspective to the research, he says.

"But the last decade has seen the emergence of patientscientists including Sonia and Eric, but also others in my lab," he says. "And this has had an even greater impact on the lab. They remind us of our mission to understand and treat human disease."

Still, it's really hard to cure diseases especially conditions like this one, because the usual way scientists look for a treatment isn't going to work.

Sonia is 33 years old. On average, people with the kind of genetic mutation she has usually start to show symptoms at age 50. But they could surface at any time. Symptoms of fatal familial insomnia have set in as early as age 12 and as late as 84. Once they do, it's a rapid decline like Alzheimer's disease on fast-forward.

"You're healthy, you're healthy, you're healthy and then you're falling off a cliff," says Sonia. "You wait a little bit too long, and that patient is gone. We need to get out ahead of it aggressively."

The challenge

They need to keep Sonia from getting sick in the first place. And they need to do it quickly. But right now, Sonia appears to be just fine, and that's actually one of the first obstacles.

Across medicine, there is an understandable resistance to testing experimental drugs on healthy people. That's why, traditionally, drug trials go something like this: Take a group of people who are sick, give some of them an experimental medicine, and wait to see if it makes them get better, live longer, or decline more slowly than people who didn't get the drug.

But Sonia has to convince the medical establishment that, especially in the age of genetics, some people who seem perfectly healthy should be considered patients.

"We have to be willing to act upstream of what we would traditionally call 'illness'," she says.

It's a shift in mindset that she had to come to grips with, personally.

"I feel very lucky to be healthy today," she says. "But I hold a sort of dual reality understanding of my own health, which is that I'm healthy today but very seriously at risk for a very serious disease."

Others in the medical field, like Dr. Reisa Sperling, who studies Alzheimer's disease, are making the same mental shift as they think about the best time to intervene.

"Alzheimer's disease is a terrible disease. Many people fear it more than cancer," says Sperling, a neurologist with Brigham and Women's Hospital and Massachusetts General Hospital.

Like Sonia and Eric, she, too, is on a quest to prevent even the first symptoms of a terrible brain disease.

Sperling is now enrolling people whose brain scans show they might be in the very early stages of Alzheimer's in a clinical trial to test an experimental drug treatment. And she's planning another study in people as young as 50 who have no noticeable symptoms, but are at high risk of developing them.

"It really does primarily come down to thinking about disease as beginning years before symptoms," says Sperling. "If we can shift that thinking not just in Alzheimer's disease, but in rarer diseases like prion diseases I think this is the way we win the war."

But before any of that can happen with a prion disease, there's the problem of actually doing the science to find a good candidate drug.

The plan

Researchers don't have one in hand yet, but they have a clear idea of what it should look like, based on studies in mice. Sonia and Eric already are talking to pharmaceutical companies that may be involved in running human trials in the future, and have requested a meeting with the Food and Drug Administration to talk about what a trial should involve.

Other efforts at treating prion disease have focused on preventing the misfolded proteins from killing brain cells, or on preventing them from accumulating. Sonia and Eric have a different approach.

"We're really interested in preventing the misfolding in the first place," says Sonia.

"Sonia's brain is producing this mutant protein," Eric says. "But as far as we know it's not misfolded yet, and the disease process hasn't started. I want her brain to be producing half or less of the amount of that protein as she is [producing] right now, because we know that less is better."

Essentially, they want to muffle the faulty gene in order to reduce the amount of prion protein floating around in Sonia's brain.

But a key question right now is this: Say they make the right drug and give it to Sonia and others with her type of mutation. If the goal is to change nothing about her current health, then how will they know it's actually working?

A traditional clinical trial is out of the question, Eric says.

It would be unethical and untenable he says, to "just treat half of the people with a drug and half with placebo and then wait 30 years to see when they die."

Not only would that kind of experiment condemn some patients to terrible death, it would also be wildly expensive and require thousands of participants. There are only a few hundred people in the U.S. with prion disease mutations.

"Instead, we need a biomarker," Eric says. "We need some laboratory test that we can run on a living human to see if the drug is having its effect."

The answer, Sonia and Eric hope, could be in a very cold refrigerator in the lab where they work. It's full of samples of spinal fluid. In mouse studies, at least, reducing prion protein in the brain seems to delay disease progression.

So, Sonia and Eric are now studying samples of spinal fluid from all sorts of people from people who already have symptoms of prion disease, from others like Sonia (who have mutations for prion disease but no symptoms yet) and from healthy controls. The aim is to establish how the levels of protein in the samples change over time, to figure out if protein levels would be a good enough measure to say, "Yes, this drug works."

"We have strong evidence that 50 percent [reduction] if we could achieve that would be protective," says Sonia, based on preliminary findings in mice.

Others are optimistic, too

Sonia and Eric are organized, hardworking, and efficient. Ultimately, for them, failure is not an option. But on a day-to-day basis, failure is what science is all about.

"In biology, if everything you did one day goes wrong, and then you figure out why it went wrong, that was a good day," says Eric, who chronicles their struggles on a blog.

It's an achingly slow process. But Eric thinks they will do it they'll find a drug.

"I'm an optimist that we'll get there in our lifetime," he says, "but not this year and not next year."

He's not alone in his optimism. Sonia and Eric have some powerful colleagues who believe the couple can pull it off colleagues like Eric Lander, a renowned mathematician, geneticist and molecular biologist. He started the Human Genome Project and founded the Broad Institute where Sonia and Eric now work.

"This is not pie in the sky," says Lander. "I see a path forward for multiple shots on goal. All you have to do is get one through."

Fifteen years ago, he says, solving this puzzle would have seemed impossible. But now he believes the science, the technology, and the knowledge about what certain mutations mean for a person's health have made defeating prion disease possible.

"Human genetics and molecular medicine are reaching a point of maturity where they're becoming much more powerful," he says. "It's exciting and important and there's nobody who's more motivated than somebody who's going to be affected by the disease themselves."

One small success

In one way, Sonia and Eric have already stopped the disease in its tracks.

Sonia is very pregnant. She's due in July to have a daughter a daughter without a mutation for prion disease. That's something the couple made sure of by screening embryos after in vitro fertilization.

So, they've stopped the transmission of prion disease in Sonia's line of the family. And in a way, that's a gift from Sonia's mom, Kamni, the couple says.

"If my mom was still alive, we wouldn't know any of this and we wouldn't have had the opportunity to choose to have a mutation-negative baby," says Sonia. "But, tragically, it also means that they'll never meet."

Sonia and Eric hope that, by the time their daughter is in elementary school, Sonia will be taking an experimental drug that could keep her as healthy as she is today.

Read more:

A Couple's Quest To Stop A Rare Disease Before It Takes One Of Them - Maine Public

Molecular mechanism underlies anxiety, autism – Medical Xpress

June 19, 2017 by Joseph Bonner The top image shows the movement of a mouse in a behavioral test that measures social interaction. The blue to green color represents least to most time spent interacting with another mouse. The bottom set of images measures anxiety-like behavior exhibited by a mouse. The amount of filling in the vertical bars represents levels of anxiety. Credit: Dr. Zeeba Kabir/Weill Cornell Medicine

A calcium-dependent molecular mechanism discovered in the brain cells of mice by Weill Cornell Medicine investigators may underlie the impaired social interactions and anxiety found in neuropsychiatric disorders including schizophrenia and autism.

The study, published June 6 in Molecular Psychiatry, reports that reduced function of a calcium channel at synapses, the site of contact essential for communication between neurons, impairs social behavior and heightens anxiety. The findings also illuminate how this occurs: overactivation of a molecule within protrusions in neurons, called spines, which receive communicating signals from adjacent neurons. Blocking the action of this molecule in adult mice repaired the abnormal social interactions and elevated anxiety, a finding that may lead to the development of new treatments for patients with certain neuropsychiatric and anxiety disorders.

"Our study suggests that if we can repair malfunctioning synapses in humans, we can reverse behavioral abnormalities and potentially treat specific symptoms, such as social impairment and anxiety, in patients with these neuropsychiatric disorders," said senior study author Anjali Rajadhyaksha, associate professor of neuroscience in pediatrics and of neuroscience in the Feil Family Brain and Mind Research Institute, and director of the Weill Cornell Autism Research Program at Weill Cornell Medicine. "We believe that targeting this molecule and its pathway may provide us with a molecular framework for future exploration of treatment of patients."

Rajadhyaksha and her colleagues focused on a calcium channel gene called CACNA1C that has emerged as a significant risk gene across major forms of neuropsychiatric disorders: schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders and attention deficit hyperactivity disorder. Impaired social behavior and elevated anxiety are common symptoms observed in patients with these disorders.

Studies using mice lacking CACNA1C production in neurons in a part of the brain, called the prefrontal cortex, which is responsible for cognition, personality and decision-making, made mice less social and more anxious. This finding seemingly confirms those of human studies, which suggests that defects in protein production may underlie the symptoms of patients with neuropsychiatric disorders and autism.

The investigators then identified the culprit for the social impairments and elevated anxiety: increased activity of a molecule called eIF2alpha that has been linked to cognitive deficits in neurodegenerative disorders like Alzheimer's disease.

Zeeba Kabir, the study's first author and a postdoctoral researcher in Rajadhyaksha's lab, tested a small molecule called ISRIB, which had previously been shown to block the action of eIF2alpha and improve learning and memory in mice, in rodents missing the CACNA1C gene. ISRIB reversed the aberrant behavior found in these mice, improving their social interactions and reducing anxiety.

"Some studies have revealed that ISRIB has side effects that may be harmful to human cells," Rajadhyaksha said, "but research shows that there are two alternative small molecule inhibitors of eIF2alpha that may be safer for use in humans. A next step is to study these ISRIB alternatives in mice to determine whether they have a similar effect."

"Neuropsychiatric disorders are complex and treatments remain suboptimal," Rajadhyaksha said. "To be able to treat specific symptoms that are common across multiple disorders is an exciting possibility. We would also like to determine whether alterations in the eIF2alpha pathway are held in common among other rodent models displaying social deficits and anxiety that result from risk genes other than CACNA1C. If so, molecules like ISRIB could be widely applicable for treating these symptoms, in general."

Explore further: Study may explain gene's role in major psychiatric disorders

A new study shows the death of newborn brain cells may be linked to a genetic risk factor for five major psychiatric diseases, and at the same time shows a compound currently being developed for use in humans may have therapeutic ...

Children with autism spectrum disorder (ASD) experience internalizing and externalizing problems at higher rates than typically developing children, which could worsen social impairment, according to researchers with the ...

Alterations in social behaviour, including aggression, are associated with a number of neuropsychiatric disorders such as schizophrenia and bipolar disorder. Along with DiGeorge syndrome and velo-cardio-facial syndrome, these ...

A study of a new mouse model identifies a drug target that has the potential to increase social interaction in individuals with some forms of autism spectrum disorder (ASD), according to researchers in the Perelman School ...

Autism spectrum disorders (ASDs) are characterized by impaired social interactions and repetitive behaviors, often accompanied by abnormal reactions to sensory stimuli. ASD is generally thought to be caused by deficits in ...

Reducing the function of the autism-associated gene Pcdh10 leads to impairments in social behavior, according to a study published in Biological Psychiatry. Reducing Pcdh10 function also disrupted the structure and function ...

We may be inclined to think that a fun experiencesay, watching a movie or indulging in a tasty treatwill be all the more enjoyable if we save it until we've finished our work or chores, but new research shows that this ...

A calcium-dependent molecular mechanism discovered in the brain cells of mice by Weill Cornell Medicine investigators may underlie the impaired social interactions and anxiety found in neuropsychiatric disorders including ...

As language develops over time, its limits have forced us to economize. In the evolution of English, the most common way this is accomplished is through imbuing existing words with multiple meanings.

One of the well-known challenges of marriage is keeping the passion alive after years of partnership, as passions tend to cool even in very happy relationships. In a new study, a team of psychological scientists led by James ...

"Alexa, who am I?" Amazon Echo's voice-controlled virtual assistant, Alexa, doesn't have an answer to that yet. However, for other applications of speech technology, computer algorithms are increasingly able to discriminate, ...

A new iPhone app developed by University of Illinois at Chicago researchers aims to track and predict mood episodes through keystrokes.

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Read the original post:

Molecular mechanism underlies anxiety, autism - Medical Xpress

Research shows bone-building protein can be used in therapy – Baylor College of Medicine News (press release)

The WNT1 ligand has previously been identified in bone disease, but its role in bone homeostasis, its cellular source and targets in bone have only just recently been identified.The research, led by Dr. Brendan Lee at Baylor College of Medicine, appears in the Journal of Clinical Investigation.

To determine the bone-specific function of WNT1, the mutation that has been associated with recessive forms of Osteogenesis Imperfecta (OI) and other forms of early-onset osteoporosis, Lee, chair of the Department of Molecular and Human Genetics at Baylor, generated mouse models to study the consequences of both the loss and gain of WNT1 function in a specialized bone cell called the osteocyte.

This research builds on previous work that identified WNT1s role in coordination and its known effect on brain development. Now, we understand how this molecule works in bone, and this paper tells us that WNT1 is produced by osteocytes to control the activity of the bone-forming cell, the osteoblast, said Lee, also the Robert and Janice McNair Endowed Chair and professor of molecular and human genetics at Baylor.

The role of osteocytes, blasts and clasts

The over- or underexpression of WNT1 is controlled by osteocytes, or bone embedded cells. The osteocytes produce WNT1 to signal to bone-forming cells called osteoblasts that reside on the surface of bone via a biochemical pathway called mTORC1. When WNT1 is overexpressed by the osteocyte, bone formation is stimulated due to an increase in osteoblast numbers and collagen production following the activation of the mTORC1 pathway in these cells.

Osteocytes are embedded in the bone, with osteoblasts and osteoclasts sitting on the surface adding or removing bone, respectively, explained Lee. It turns out, osteocytes are actually the master controllers of this balance of bone formation and resorption in part by acting as either a receiver or sender of WNT signals.

We knew previously from others work that osteocytes could inhibit bone formation by producing the protein sclerostin, which represses osteoblast function. This research brings the cycle of information full circle by showing that while sclerostin turns the osteoblasts off, WNT1 from osteocytes turns them on, Lee said.

On the other hand, loss of WNT1 function resulted in low bone mass and spontaneous fracturing, similar to that seen in patients with OI. In this case, the osteocyte is not producing WNT1. However, osteocytes also can receive WNT signals themselves, leading them to control the activity of bone-removing cells, the osteoclasts.

Therapeutic impact

Primary therapies traditionally used to treat OI have shown limited efficacy in combating WNT1-related OI and osteoporosis. However, Lee and his research team identified anti-sclerostin antibody (Scl-Ab) treatment is effective in augmenting the action of other WNT ligands to improve bone mass and to significantly decrease the number of fractures in swaying mice, a model of WNT1 related OI and osteoporosis.

The results of this study, while conducted in mice, have important implications for the treatment of OI and osteoporosis in humans down the road, Lee said. By blocking sclerostin, the bone can be repaired effectively in diseases related to loss of WNT1 suggesting a personalized therapy. This is exciting especially as a promising anti-sclerostin drug is already in clinical development.

This work was supported by the Baylor College of Medicine Intellectual and Developmental Disabilities Research Center from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the Baylor College of Medicine Advance Cores with funding from the National Institutes of Health, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rolanette and Berdon Lawrence Bone Disease of Texas and the Center for Skeletal Medicine and Biology at Baylor College of Medicine.

Other contributors to this work include Kyu Sang Jeong, Yi-Chien Lee, Yuqing Chen, Ming-Ming Jiang and Elda Munivez, all of whom are with Baylor, and Catherine Ambrose with the University of Texas Health Science Center at Houston.

Original post:

Research shows bone-building protein can be used in therapy - Baylor College of Medicine News (press release)

Fastest Mobile Networks 2017 – PCMag

We tested data speeds on AT&T, Sprint, T-Mobile, and Verizon Wireless in 30 US cities. Find out which network is the fastest where you live.

Our drive through the Southeast took us from the Triangle to the Triad, down I-85 to Charlotte and Atlanta with a stop in Greenville, down I-75 to Orlando, over to Tampa, and then back across on FL-70 to West Palm Beach and Miami.

As we saw in the Northeast, AT&T did the best on our Southeastern segment, in this case with the best upload and download speeds. Verizon, long renowned for excellent coverage, came a close second.

But in my mind, the big news here is that T-Mobile is now a viable player in North Carolina, where it struggled with coverage for a while. T-Mobile was in the green all though our NC drive, while Sprint coverage dropped a few times north of Charlotte.

Verizon may be a better choice than AT&T in Florida, because of coverage. AT&T's LTE network struggled a bit on our cross-Florida drive, with dropouts in the swampy middle of the state along FL-70. Verizon kept on truckin' with LTE the whole time.

PCMag.com's lead mobile analyst, Sascha Segan, has reviewed hundreds of smartphones, tablets and other gadgets in more than 9 years with PCMag. He's the head of our Fastest Mobile Networks project, one of the hosts of the daily PCMag Live Web show and speaks frequently in mass media on cell-phone-related issues. His commentary has appeared on ABC, the BBC, the CBC, CNBC, CNN, Fox News, and in newspapers from San Antonio, Texas to Edmonton, Alberta. Segan is also a multiple award-winning travel writer, having contributed... More

Read more:

Fastest Mobile Networks 2017 - PCMag

‘The One Device’: How the iPhone changed our lives – USA TODAY

Jefferson Graham , USA TODAY 12:04 p.m. EDT June 19, 2017

by Brian Merchant

(Little, Brown and Company)

in Non-Fiction

In the last 10years, the Apple iPhone has changed our lives in more ways than we can imagine.

Remember when we went to restaurants and walked down the street without staring at oursmartphones? How we checked our e-mail once or twice a day instead of every minute and had a work-free weekend without touching basewith co-workers and bosses?

Thank the iPhone for the always-on culture, for building the app economy that brought ride-hailing cab alternatives, visual dating tools and the constant sharing of upload-from-anywhere travel photos.

As we approach the 10th anniversary of the iPhoneon June 29, there's a great book in this, and not just the birth of the iPhone, but how it's evolved in the last decadeas well.

The One Device: The Secret History of the iPhone(Little, Brown, 380pp., **out of four stars) by Brian Merchant, an editor at Motherboard, isn't it, unfortunately.

In a nutshell, Merchant's bookdwells on Apple's penchant for secrecy (old news,don't we all know this?) and expands beyond the basic story of the device's birth with long passages on the history of touch screen, gyroscopes and other smartphone features.

In this Jan. 9, 2007, file photo, Apple CEO Steve Jobs holds up an iPhone at the Macworld Conference in San Francisco.(Photo: Paul Sakuma, AP)

The iPhone wasn't just Apple co-founder Steve Jobs' idea. Credit goes to an overworked and under-appreciatedteam of engineers who did the grunt work and came up with many of the features. When Merchant focuses on the basic history, he's in good territory. It's a great story with Jobs changing his mind on several key details at the last minute, andthe iPhone not being finished and looking like it wouldn't make the planned Jan.7, 2007 reveal at the Macworldconference. (It went on sale six months later.)

Merchant connected with many of the key engineers from the iPhone team, which isn't an easy thing to do, as Apple frowns oncurrent and past employees talking in an un-controlled environment. He expands the story by spending time in China, where more than200 million iPhones are mass-produced yearly, at the Foxconn plants. He somehow manages to sneak in to the ultra-secretive facility, where many workers have responded to the crushing hours and mind-numbing work by committing suicide from the top of the building.

But I missed the parts of the story that Merchant left out. Hedecided not to focus on the birthand growth of Google's Android operating system, which now has an 85 percentmarket share, or the rise of Apple's chief rival Samsung, and the Galaxy S line of smartphones.

Author Brian Merchant.(Photo: Cara Robbins)

He skipsout on how Tim Cook, who took over as CEO of Apple after Jobs' death in 2011, has been skimpy on innovation, but has built the iPhone into an even bigger business that now represents two-thirds of Apple's revenues. Nary a word is said about the iPad, the Apple Watchor what Apple will do when the inevitable happensand the life cycle for the iPhone comes to an end.

Well, the material is there. Perhaps it's time to get to work on the sequel.

See the rest here:

'The One Device': How the iPhone changed our lives - USA TODAY

Jodie Marsh’s fans left shocked by her ‘stunning’ 69-year-old mum – The Sun

The pair went out for a meal in identical outfits

JODIE Marshs Twitter followers have been left stunned by the glamour girls age-defying mum.

The busty beauty, 38, shared four pictures of herself hanging out with her mum Kristina and fans wasted no time in praising her youthful good looks.

Jodie Marsh

Her first upload read: I took my parents out for a meal today & by coincidence my mum and I both wore black wide leg jumpsuits. We look like twins

When a fan retweeted it, calling Jodies mum a sort, she added: And can I just point out that my mum is nearly 70!!! (She wont mind me saying). Shes bloody amazing and beautiful what a woman

With the surprising age revealed, her Twitter followers went into overdrive, with one writing: 70?????? Have you checked her birth certificate??

Jodie Marsh

Another said: She looks amazing. What fantastic genes you have

Your mom looks stunning for nearly 70 and @JodieMarsh you are always stunning , gushed one.

ITV

A fourth enthused: Your mum is gorgeous Jodie, can see where you get your looks from

Earlier this month Jodie said she considers herself seven-years celibate and doesnt count the fumbles she had during her short marriage to James Placido.

In a revealing chat, the star explained that she was celibate for the five years prior to tying-the-knot with her now ex-husband and doesnt rate the passionate moments that occurred during their short marriage.

ITV

I dont count the blip I had when I married that t***** because the sex was so s***, so Id say its been seven years now, Jodie told Heat magazine.

She added she doesnt miss sex, saying: I dont think about it and I dont miss it. I think Im dead from the waist down. I dont have any urges or feelings. I honestly get more excited about a cheese souffle.

Got a story? email digishowbiz@the-sun.co.uk or call us direct on 02077824220

Follow this link:

Jodie Marsh's fans left shocked by her 'stunning' 69-year-old mum - The Sun

Elon Musk’s brain-computer interface plans are creepy and exactly the kind of AI you dread – BGR India

Humans are driven by emotions and sentiments. Their outlook to the surrounding is quite subjective rather than being driven algorithms or binary codes like 01101100011010010110011001100101. Being the most intelligent species on this blue planet, humans have sporadically played God. From cloning to genetic-level modifications, there are numerous such instances. Of late, the focus has shifted toArtificial Intelligence (AI). Perhaps your first-level interactions with AI have already happened. From Apples Siri to Amazons Alexa, the so-called assistants are actually your personal assistants, assisting you in your daily lives with bare minimum distraction.

Ask some silly questions to Siri, get some witty responses, and no harm done. Right? Of course, AI is at a very nascent stage but quite smart or dumb, as you may perceive, even in its budding years. The different forms of AI around us are constantly improving, getting upgrades and more importantly getting smarter. Like most of you, even I dread the day AIs get better than us and then get better of us. Even though I hail accomplishments like Google DeepMinds victory over Go Player champion, I seriously dont want AIs to peak after a certain level, where we have lost control only to be left as the second most intelligent species on this planet.

Even as tech companies are working, at surprisingly good pace, to improve the current AI, a few have envisioned slightly different versions. Elon Musk, the man who is known for his ambitious plans like electric cars, solar-powered homes, reusable rockets, sending people to Mars and so on, has also joined the fray with Neuralink. His idea of AI is building an interface between your brains and the computer. Elon Musks AI is more of an extension of yourself that is most probably bit more smart and efficient. I am sure youre already wondering if its something like The Matrix. Perhaps. Musk hopes to build something that will keep a check on AI an apprehension raised by the likes of Stephen Hawking and Bill Gates.

via GIPHY

According to Tim Urban of Wait But Why, Musk is working to merge human brains and AI that will cope with the super-intelligent AIs. He [Musk] believes that the solution to reduce existential risk is to be able to high bandwidth interface with AI. He thinks that if we can think with AI, it allows AI to function as a third layer in our brain, where we could have AI thats built for us. So we have human intelligence and then we have artificial intelligence, and theyre both us and so we become AI in a way, Urban is quoted as saying. ALSO READ: Neuralink and the Brains Magical Future

Urban admits this is indeed creepy but hopes that with everyone having his own AI, there will be nothing for the AI to conquer anything. Its much safer in a weird way, even though it gives us all a lot more power. Its like you dont want one Superman on earth, but if you have a billion Supermen then everything is okay because they check and balance each other, he adds.ALSO READ: A quick guide to Elon Musks new brain-implant company, Neuralink

Essentially, Urban is saying that if each country on the planet had a nuclear bomb, thered be no nuclear war ever. Well, the AI is not like the nuclear bomb, but the fear from it, in my opinion, is quite at the same level. At the moment, when we think about the AIs, we think of a smarter holographic image of a person that has all the answers and knowledge. But would we want to give away everything that our brains have to create a smarter version of yourself? I would not, for one. Perhaps I am okay to see an AI as a third person and neutral face rather blended with my personal history, dark desires, and fears that Id never acknowledged or even document. Most probably Id be livid and submerged into inferiority complex after seeing a smarter version of myself.

In case youre wondering, brain-computer interface concept is not really new. The basic versions of the interface are already lending support to people with disabilities, allowing hearing capabilities to auditory impaired, letting visually challenged to see, and lending a limb with prosthetics. Researchers are already working to connect the 100 billion neurons in our brain to make us do things that seem super human at the moment. Making an AI out of the brain-computer interface, of course, seems plausible but will be an overkill.

Fortunately, Musks plans dont involve connecting wires to the back of your neck to summon the AI, but wirelessly with the cloud. That being said, Musks few observations about us are quite intriguing. One of them is that we are already becoming a cyborg. Youre already a different creature than you would have been 20 years ago, or even 10 years ago. I think people theyre already kind of merged with their phone and their laptop and their applications and everything, he mentioned.ALSO READ: Google I/O 2017: Artificial Intelligence-first finally becomes a thing

Contrary to his opinion, Id like to believe our dependence on internet, smartphones, and applications is more based on our necessities rather the novelty. The apps and the magical world of the internet are just filling gaps that we perhaps had overlooked for a while. For an example, before Facebook, there was Orkut or Myspace, and after Facebook, therell be something else. But I doubt we are ready now or will ever be in at least the next decade, to give away everything we possess to upload our brains to the cloud. Had the Man of Steel been real, and I were the Kal-El, Id be freaked out to see my dead father, wandering around in the abandoned ship. Perhaps, I am okay to talk to an invisible AI with robotic-accent.Mind uploading in fiction Wikipedia

via GIPHY

See the article here:

Elon Musk's brain-computer interface plans are creepy and exactly the kind of AI you dread - BGR India

Medicine information leaflets ‘too scary’, say experts – BBC News


BBC News
Medicine information leaflets 'too scary', say experts
BBC News
There is too much focus on the potential side-effects of medicines on information leaflets inside packs and not enough on their benefits, says the Academy of Medical Sciences. Its new report calls for them to be rewritten to give a more balanced view ...
Medicine information leaflets 'must be clearer' say expertsITV News

all 3 news articles »

Read the original here:

Medicine information leaflets 'too scary', say experts - BBC News

University of Chicago Medicine will remain in UnitedHealthcare’s network – Chicago Tribune

University of Chicago Medicine and insurer UnitedHealthcare have reached a contract agreement that will keep the academic medical system and its doctors in the insurer's network.

The agreement will spare about 8,000 patients from having to either switch doctors or pay significantly more for care.

The new contract agreement comes shortly after patients received letters saying that University of Chicago Medicine and University of Chicago Physicians Group could be out of UnitedHealthcare's network starting June 30.

The letter raised fear among patients that they would have to scramble to find new physicians or face higher costs for medical care.

"This renewed contract means UChicago Medicine's relationship with patients who carry UnitedHealthcare insurance remains unchanged and they will not face any additional out-of-pocket health costs," University of Chicago Medicine said in a statement Monday.

lschencker@chicagotribune.com

Twitter @lschencker

Read the original here:

University of Chicago Medicine will remain in UnitedHealthcare's network - Chicago Tribune

A hit on alternative medicine – Washington Post

June 19 at 6:51 PM

The June 16 Politics & the Nation article Risky Lyme treatments on the rise read like another hit on alternative medicine by the Centers for Disease Control and Prevention. It had all the key words favored by the CDC: risky, dangerous, expensive, unorthodox and its standard phrases, according to a new report, Officials ... are alarmed. Then there was the CDCs gold-standard complaint: unproven treatments. Well, not to put too fine a point on it, but proof is reserved for mathematics and logic.

The article said, Many of the treatments ... have no evidence of effectiveness. Thats better. Talk about evidence rather than proof. But it didnt list all of the many treatments with no evidence of effectiveness. Obviously, the clinicians using unorthodox therapies would not be able to stay in business if they were not getting positive results from some of the treatments. The article mentioned a few anecdotal accounts of doom but didnt provide information about other factors that could have played a role in the unfortunate outcomes. Nor did it cite any cases in which people were cured or their health improved by the unorthodox therapies.

And since when did garlic supplements become dangerous and expensive?

William Cates, Charlottesville

Originally posted here:

A hit on alternative medicine - Washington Post