The Hindu | Curcumin nanoparticles found to shorten TB treatment time The Hindu Gobardhan Das from the Special Centre for Molecular Medicine, Jawaharlal Nehru University (JNU) Delhi and his team found nanoparticle curcumin to be five times more bioavailable (which is the proportion of drug that enters circulation after ... |
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Curcumin nanoparticles found to shorten TB treatment time - The Hindu
eGov Magazine | Elets | Precision medicine: The unfolding revolution in healthcare eGov Magazine | Elets Healthcare experts say that drivers of precision medicine would be quality patient care, improved quality of life and reduced cost of treatment. Studies have already shown that if treatment strategy is based on patients' molecular profile it leads to ... |
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Precision medicine: The unfolding revolution in healthcare - eGov Magazine | Elets
Professor Anne Ridley FMedSci FRS has been confirmed as the new Head of the School for Cellular and Molecular Medicine.
Professor Ridley is currently Head of the Cell Motility and Cytoskeleton Section in the Randall Division of Cell and Molecular Biophysics at Kings College London. She will succeed Professor Chris Paraskeva as Head of School when she takes up her post in January 2018.
Professor Ridleys academic career has included postdoctoral research at MIT and at the Institute of Cancer Research in London, a professorship at the Ludwig Institute for Cancer Research at UCL and, since 2007, a post as Professor of Cell Biology at Kings College London. Her awards include the British Society of Cell Biologys Hooke Medal and the Lilian-Bettencourt Prize for the Life Sciences.
She became a fellow of the Royal Society of Biology in 2009, and a fellow of the Academy of Medical Sciences in 2012. She became an honorary fellow of the Royal Microscopical Society in 2014 and a fellow of the Royal Society in 2017.
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China-focused venture capital firm Qiming Venture Partners has led a RMB175 million (US$25 million) series A round in QIAGEN (Suzhou) Translational Medicine Co., a Chinese precision medicine solutions provider.
New Horizon Capital, Quanchuang Capital and Shanghai Anjie Medical Equipment Company also participated in the round, according to a company announcement.
"QIAGEN Suzhou is an innovative start-up providing precision medicine solutions. The company's president, Dr. Nick Zhang and the team are dedicated to push the clinical development of new medicines based on their knowledge and experience in the industry," said Nisa Leung, managing partner of Qiming. "We are glad to participate in the company's growth, and we hope that we can help its development with our investments."
Founded in 2013 by NASDAQ-listed molecular diagnostics firm QIAGEN and Suzhou-based BioBay, a Suzhou-based innovative science and technology park, QIAGEN Suzhou specializes in the fields of medicine laboratory testing and molecular diagnostics.
It provide solutions containing biomarker validation and diagnosis product development, integrating the translational medicine and molecular diagnostics platform, including DNA sequencing technology, enzyme-linked immunosorbent assay and electro-chemiluminescence immunoassay.
The firm plans to use the latest proceeds to establish a factory, and enhance its research and development team. It plans to transition from a research-focused institution to a fully commercialized firm, providing molecular diagnostics solutions based on artificial intelligence for cancer targeted therapy and immunotherapy.
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Qiming Leads $25M Round In Precision Medicine Solutions Firm QIAGEN Suzhou - China Money Network
July 6, 2017 Cancer Histopathologic image of colonic carcinoid. Credit: Wikipedia/CC BY-SA 3.0
Poor diet is associated with 80% of colorectal cancer cases, but the exact pathways by which diet leads to cancer are not known.
In a newly published study, Cleveland Clinic researchers have identified a specific molecular pathway that plays a key role in the link between a high-fat diet and tumor growth in the colon.
In the July 6 issue of Stem Cell Reports, the team showed in pre-clinical models that cancer stem cell growth in the colon was enhanced by a high-fat, Western diet. Cancer stem cells are a subset of resilient, aggressive malignant cells that are believed to be partially responsible for spread and recurrence of cancer.
Furthermore, when the researchers blocked the JAK2-STAT3 cellular signaling pathway, a widely studied pathway known to promote tumor growth, the spike in cancer stem cell growth caused by the high-fat diet declined.
This study provides more insight into how the JAK2-STAT3 pathway is linked to diet-related cancer. Pinpointing the exact mechanism can help researchers develop therapeutics to counteract the negative effects of a Western diet on colorectal cancer.
Colorectal cancer is the third most common cancer in the United States with more than 130,000 cases reported annually. The disease arises as a result of a combination of several genetic, epigenetic and environmental causes, such as diet.
"We have known the influence of diet on colorectal cancer. However, these new findings are the first to show the connection between high-fat intake and colon cancer via a specific molecular pathway," said Matthew Kalady, M.D., co-author of the study, colorectal surgeon, and Co-Director of the Cleveland Clinic Comprehensive Colorectal Cancer Program. "We can now build upon this knowledge to develop new treatments aimed at blocking this pathway and reducing the negative impact of a high-fat diet on colon cancer risk."
The team analyzed human colorectal cancer-free survival data in the Cancer Genome Atlas and evaluated primary and metastasized colorectal cancer specimens via microarray analysis. They further verified the link between high-fat diet and stem cell maintenance in obesity-resistant mice.
"These findings also provide a new way in which cancer stem cells are regulated and provide insight into how environmental influences, such as diet, can alter cancer stem cell populations in advanced cancers," said Justin D. Lathia, Ph.D., Associate Professor in the Department of Cellular and Molecular Medicine, Lerner Research Institute, and co-author of the study.
Explore further: Grape-based compounds kill colon cancer stem cells in mice
More information: Stem Cell Reports (2017). http://www.cell.com/stem-cell-reports 2213-6711(17)30265-5
Journal reference: Stem Cell Reports
Provided by: Cleveland Clinic
Colorectal cancer has been linked to carbohydrate-rich western diets, but the underlying mechanisms have been unclear. A study published by Cell Press July 17th in the journal Cell shows that gut microbes metabolize carbohydrates ...
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Researchers publish new findings on influence of high-fat diet on colorectal cancer - Medical Xpress
Raj Atikkuke, a molecular medicine and genetics researcher and founder of ITOS Oncology, speaks to reporters following a media event discussing the latest cancer research technology at Hotel-Dieu Grace Healthcare, July 5, 2017. Dax Melmer / Windsor Star
Bladder cancer progresses quickly in some patients but not in others. Why? The answer is probably in the cancer cell genes.
Somewhere in each cancer cell are genes that have mutated. If those genes and their mutations can be identified, they can be targeted with treatment that is more effective and has fewer side-effects.
Its personalized cancer treatment.
This is the future of cancer diagnosis, of cancer treatment, of cancer management, of cancer prognosis, molecular medicine and genetics researcher Raj Atikkuke said Wednesday, surrounded by local oncologists and other researchers as he launched his company ITOS Oncology at Hotel-Dieu Grace Healthcare.
Raj Atikkuke, a molecular medicine and genetics researcher and founder of ITOS Oncology, speaks to reporters following a media event discussing the latest cancer research technology at Hotel-Dieu Grace Healthcare, July 5, 2017. Dax Melmer / Windsor Star
Atikkuke and others hope that Windsor, where the rate of new cancer cases and cancer mortality are higher than the rest of Ontario, can become a leader in the rapid transformation of care.
It might be that we develop one profile that works really well in one disease site and everybody in the world sends it to us, said Dr. Caroline Hamm, clinical director of the Windsor Cancer Research Group. Were looking for what we can do better than anybody else and be the centre of cancer therapy for that particular disease.
Cancer is caused by mutations in key genes, called oncogenes. So every cancer can be defined by its genomic profile. Cancer drugs are most effective when they target the oncogene mutations. For example, there is a specific mutation that occurs in one gene in melanoma, a deadly skin cancer. A drug has been developed that targets that mutation and is known to work best in those patients.
ITOS, which stands for Its The Oncogene Signature, extracts DNA from cancer cells and searches for signature genetic mutations.
When we have that information, it becomes easier to target those cancer cells, said Atikkuke, who is collaborating with the University of Windsor and Windsor Regional Cancer Centre.
Researchers can also look for mutations in genes that make people susceptible to cancer. For example, there are a number of inherited genetic mutations that predispose women to breast cancer,
ITOS is the only centre in Ontario west of London that sequences cancer genes and one of few in North America that will provide a complete genetic profile of a cancer.
Ontario pays for testing for a limited number of proven genetic markers in certain cancers, such as lung cancer. But the testing isnt done here. Samples are sent to London, Hamilton and Toronto. The government also pays for a fuller genetic profile of breast cancers. That testing is done in California. The information sent back from across Ontario and California tells doctors what treatment is likely to work best. Performing a genetic profile of a cancer at ITOS will cost about $1,000. Research is expected to be paid for by grants.
Eventually, every cancer patient is expected to receive a genetic profile. It will save money, said Atikkuke. Now, most patients require a cocktail of chemotherapy drugs. In the future, theyll need only one, targeted drug.
Its important for Windsor, which has a burgeoning health care research sector, to do this kind of work, said Hamm.
Were very far away from things in Ontario. There are people that forego therapy because of the travel. Their families cant take them. Theyre not healthy enough to travel. We have to realize that we have a unique need here. We need to develop our clinical and research facilities here because if we dont, patient outcomes will be compromised.
ITOS will do laboratory research first here, said Hamm. Windsor has archived tissue and data bases with information on thousands of local cancer patients what stage cancer they had, what chemotherapy they received, how long they lived. Beginning with a subset of patients, for example those with a certain type of breast cancer, researchers can study the genetic profiles of the cancers.
We can see, Oh, this is why that group of people didnt do as well as the other group, said Hamm. Because they have this pattern on their genetic profile. This pattern is a group we need to focus on. Is there something in this pattern that we can target? If we did this a little bit differently, maybe we could have more people live. Thats what its about.
Clinical trials could be conducted eventually, the data could be published, and if the world says yes, that is valid data, everyone with that type of cancer will send their tissue to ITOS Oncology and say we need this tested.
There are many steps, she acknowledged, but this is where it starts.
Atikkuke will also travel to India this month to try to get hospitals and cancer centres there to send their patients DNA here for testing.
The difficult thing about treating cancer, said Hamm, is it isnt all one disease, as genetic profiling has shown. Advances in treatment have been unbelievable, she said. The ability to target treatment means some patients have been cured without chemotherapy or can live normal lifespans despite having cancer and receiving treatment.
Thats the beauty of targeted therapy, she said. Its not just, Lets kill everything and hope healthy stuff grows back.'
But, referring to ITOS, she said, this is the stuff we need to continue moving it forward.
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Jarvis: New Windsor company aims to personalize cancer treatment ... - Windsor Star
July 5, 2017 Credit: University of Oxford
Researchers from the University of Oxford are using a unique blend of virtual reality and innovative genetic techniques to understand the causes of diseases such as diabetes and anaemia.
The team, working in collaboration with physicists from Universita' di Napoli and software developers and artists at Goldsmiths, University of London, are using the state-of-the-art technology to investigate the 3-D structure of DNA. The way in which DNA is arranged in 3-D space has huge consequences for human health and disease. Subtle changes in DNA folding impact on whether genes can be switched on or off at particular times dictating what a cell can do. It is this process that the team are trying to get to the bottom of in the hunt for the causes of disease, and potential new treatments.
The scientists are presenting their research at the Royal Society's annual Summer Science Exhibition.
Prof Jim Hughes, Associate Professor of Genome Biology, University of Oxford, said: "It's becoming increasingly apparent that the way that a cell fits two metres of DNA into a structure more than ten times smaller than a human hair, is more than just a random process. We are dissecting this intricate folding to understand which parts of our immense genome are interacting at any one time, helping us understand whether changes in this process can cause disease."
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CSynth the software on show at the Royal Society's Summer Science Exhibition is designed to provide an engaging way to explore and understand the complex structure of the genome in 3-D, by integrating data from genome sequencing, computer modelling and high powered microscopy. Scientists are now hoping to use virtual reality to visualise the huge amounts of data they can generate in the laboratory.
Speaking about the software, Stephen Taylor, Head of the Computational Biology Research Group at the MRC Weatherall Institute of Molecular Medicine, University of Oxford, said: "With advances in genetic techniques, we can now harness more information than ever before from biological data provided by patients and volunteers. With the CSynth software we can integrate data from different experiments into something more tangible to help researchers understand how DNA folds. In addition, using the Virtual Reality mode in CSynth is helping us visualise these complex 3-D structures in a more intuitive way."
Prof William Latham from the Department of Computing, Goldsmiths, University of London, said: "I'm fascinated by the way we can use art to better understand and envision scientific concepts. In CSynth we've created something that not only accelerates research progress, but also allows the public to share in unravelling some of the mesmerising and intricate structures inside our body."
Prof Frederic Fol Leymarie from Goldsmiths, said: "By combining maths and physics together with computer games technologies, we can program realistic molecular interactions, and immerse people in the dynamic world of DNA. CSynth takes you on a close encounter with the very fabric of life."
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Researchers use virtual reality to unpack causes of common diseases - Medical Xpress
ANN ARBOR, Mich. -- After 12 weeks of taking an anti-inflammatory asthma drug, obese patients with type 2 diabetes showed a clinically significant drop in blood glucose.
The drug amlexanox, prescribed in Japan to treat asthma, appeared to free the metabolic system to burn more energy. A subset of patients had improved fatty liver disease and insulin sensitivity, a response seen among those who started the clinical trial with higher levels of inflammation in their fat tissue than others.
While the discovery at Michigan Medicine and the University of California at San Diego is not ready for the clinic, it reveals an inflammatory link between obesity and type 2 diabetes.
Inflammation is the bodys natural response to injury and illness, but chronic inflammation caused by obesity is believed to promote insulin resistance, a main feature of diabetes.
We are beginning to understand the role this form of internal inflammation plays in the development of chronic diseases like diabetes, says lead study author Elif Oral, M.D., director of the MEND Obesity and Metabolic Disorder Program at Michigan Medicine. Ultimately we may be able to personalize therapy based on the degree of inflammation present at baseline which is a new concept.
Oral is an endocrinologist and translational scientist at Michigan Medicine, the University of Michigans academic medical center where the clinical trial was conducted and analyzed.
Tissue analysis was led by study author Alan R. Saltiel, Ph.D., at U-C San Diego, along with scientists at the Salk Institute for Biological Sciences.
In the Cell Metabolism study, researchers identified a molecular signature in obese patients with type 2 diabetes who responded to the drug amlexanox.
When we looked at the drug-treated group we saw a bimodal distribution, that is, there were some responders and some nonresponders. We didnt understand why, so we did a molecular analysis from biopsies of fat cells we took from patients at the beginning and end of the study, says Saltiel, director of the Institute for Diabetes and Metabolic Health at U-C San Diego
In the responder group, the level of inflammation in fat was higher than in the nonresponder group at the beginning of the study, indicating that there is something about inflammation that predisposes a person to respond. And, what was really amazing was that there were more than 1,100 gene changes that occurred exclusively in the responders.
The glucose-lowering effects of amlexanox were first discovered in mice during research at the University of Michigan where Saltiel served as director of the Life Sciences Institute at the U-M.
Promising results
Amlexanox is an inhibitor of two enzymes, IKK and TBK1. In previous studies, Saltiel and U-M researchers discovered that these two enzymes are induced in obese mice, causing a drop in energy expenditure or reduction in calories burned.
This prompted them to look for inhibitors of these enzymes by screening a library of 150,000 chemicals. They found amlexanox. Giving obese mice the inhibitor caused them to lose weight, while their sensitivity to insulin increased, improving their diabetes and fatty liver disease.
The human trial revealed that gene changes that occurred in the mouse model also happened in the human responder group. Blood sugar in the clinical trial patients went down as genes involved in the expenditure of energy changed.
The proof of concept trial began with an unblinded safety trial of six patients. It was followed by a controlled trial of 42 obese patients with type 2 diabetes.
Half of the patients were randomized to a placebo group while the other half received amlexanox for three months. Blood sugar, insulin sensitivity, weight and liver fat were measured. A biopsy of fat cells from each patients midsection was taken before and after the trial to measure changes in gene expression.
The most exciting part of this is that we have a new drug that has never been studied before, says Saltiel. Its a new mechanism for a diabetes and fatty liver drug. Its promising, but there are a lot of questions that need to be answered still.
Among them: Which gene changes are the most important to target? Whats the right drug dosage? What time of day should it be administered? How often should patients take the drug? Can the percentage of responders be increased? Will the beneficial effects of the drug be sustained for a longer time?
One-third of the participants in the blinded study responded. Among responders with nonalcoholic fatty liver disease, an improvement was also seen.
Researhers are planning follow-up trialsto look at whether its possible tostratify patients who are likely to respond based on the degree of underlying inflammation, and explore if other drug combinations can be used with amlexanox.
We are grateful for patient participation and hope that our patients will respond with the same enthusiasm to our new trials. Without patients volunteering, the sort of study can never happen, says Oral.
Primary support for the research came from the National Institutes of Health High Risk High Reward grant R21DK098776.
Additional authors include Shannon M. Reilly, Andrew V. Gomez, Rasimcan Meral, Laura Butz, Nevin Ajluni, Thomas C. Chenevert, Evgenia Korytnaya, Adam H. Neidert, Rita Hench, Diana Rus, Jeff Horowitz, BreAnne Poirier, Peng Zhao, Kim Lehmann, Mohit Jain, Ruth Yu, Christopher Liddle, Maryam Ahmadian, Michael Downes and Ronald M. Evans.
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AsianScientist (July 4, 2017) - Once assumed to be little more than a simple pH buffer, uterine fluid is now thought to play an important role in preparing fetuses for life outside the womb. These findings have been published in Trends in Molecular Medicine.
A developing fetus bathes in a mixture of cellular secretions and proteins unique to its mothers uterus. Before fertilization, the pH of uterine fluid creates a conducive environment for sperm migration. Thereafter, its volume supports the embryo as it implants onto the wall of the uterus.
Studies in livestock, rodents, and humans have shown that information from a mothers environment (e.g., food availability, stress, and pollutant exposure) can leave epigenetic tags on the DNA of her fetus, potentially influencing the progression and long-term health of the developing embryo.
Scientists have hypothesized that blood flow via the placenta might constitute one way the body communicates the mothers condition to the fetus. However, there is evidence that the fetus reacts to changes such as those stemming from the mothers diet, long before the establishment of the placenta.
This suggests the involvement of uterine fluid as the communication medium to transfer information between the maternal environment and the floating embryo, said senior author Dr. Duan En-Kui, a reproductive biologist at the Institute of Zoology, Chinese Academy of Sciences. The preimplantation period is a critical time for programming offspring health, and thus, expecting mothers should keep a good diet and good mood, and stay away from harmful chemicals during this critical window.
While there is much to be learned about how mother-fetus communication takes place, the theory is that information in extracellular vesicles (molecular packages that move from cell to cell) within uterine fluid and tissue deliver cargo such as microRNAs and amino acids to the fetus. These molecules may be tagging fetal cell DNA in ways that alter gene expression, and thus, they program how the embryo and placenta develop.
Consequently, researchers are interested in learning which specific maternal environmental exposures and behaviors could change the composition of molecules transported via the uterine fluid to the fetus.
For example, mouse studies have shown that a low-protein maternal diet can reduce the level of certain amino acids in uterine fluid and affect gene expression of nutrition- and transport-related genes. While these changes might prevent malnutrition in the developing embryo, once grown, the mouse offspring are more predisposed to heart disease when compared to animals on a regular diet.
Dr. Wang Hongmei, co-senior author of the paper, speculates that uterine fluid could someday be used to analyze or even manipulate what signals are being received by a fetus.
For now, uterine fluid collection is not a standard biomarker, yet many studies have revealed its potential role for non-invasive analysis, and we also see great potential in it, she said. One, it can be screened by using ultrasound recording coupled with computational or biomechanical analysis; and two, uterine fluid can also be collected during an endometrial examination.
The article can be found at: Zhang et al. (2017) Uterine Fluid in Pregnancy: A Biological and Clinical Outlook.
Source: Chinese Academy of Sciences; Photo: Shutterstock. Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.
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How Uterine Fluid Informs The Fetus - Asian Scientist Magazine
The team, working in collaboration with physicists from Universita' di Napoli and software developers and artists at Goldsmiths, University of London, are using the state-of-the-art technology to investigate the 3D structure of DNA. The way in which DNA is arranged in 3D space has huge consequences for human health and disease. Subtle changes in DNA folding impact on whether genes can be switched on or off at particular times dictating what a cell can do. It is this process that the team are trying to get to the bottom of in the hunt for the causes of disease, and potential new treatments.
Prof Jim Hughes, Associate Professor of Genome Biology, University of Oxford, said: Its becoming increasingly apparent that the way that a cell fits two metres of DNA into a structure more than ten times smaller than a human hair, is more than just a random process. We are dissecting this intricate folding to understand which parts of our immense genome are interacting at any one time, helping us understand whether changes in this process can cause disease.
CSynth the software on show at the Royal Societys Summer Science Exhibition is designed to provide an engaging way to explore and understand the complex structure of the genome in 3D, by integrating data from genome sequencing, computer modelling and high powered microscopy. Scientists are now hoping to use virtual reality to visualise the huge amounts of data they can generate in the laboratory.
Speaking about the software, Stephen Taylor, Head of the Computational Biology Research Group at the MRC Weatherall Institute of Molecular Medicine, University of Oxford, said: With advances in genetic techniques, we can now harness more information than ever before from biological data provided by patients and volunteers. With the CSynth software we can integrate data from different experiments into something more tangible to help researchers understand how DNA folds. In addition, using the Virtual Reality mode in CSynth is helping us visualise these complex 3D structures in a more intuitive way.
Prof William Latham from the Department of Computing, Goldsmiths, University of London, said: Im fascinated by the way we can use art to better understand and envision scientific concepts. In CSynth weve created something that not only accelerates research progress, but also allows the public to share in unravelling some of the mesmerising and intricate structures inside our body.'
Prof Frederic Fol Leymarie from Goldsmiths, said: By combining maths and physics together with computer games technologies, we can program realistic molecular interactions, and immerse people in the dynamic world of DNA. CSynth takes you on a close encounter with the very fabric of life.
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Researchers use virtual reality to unpick causes of common diseases - ETHealthworld.com
UNIVERSITY boffins are using virtual reality to unpick the causes of conditions such as diabetes and anaemia.
Researchers from Oxford University have blended VR and genetic techniques, using state-of-the-art technology to show the 3D structure of DNA.
Newly-created software CSynth has been developed along with physicists from Universita di Napoli in Italy and developers and artists at Goldsmiths, University of London, to explore the structure of the genome in 3D.
Subtle changes to DNA can dictate what a cell can do, and it is hoped that studying this process can get to the bottom of causes and potential new treatments.
CSynth will be one of 22 exhibits on show at the Royal Societys annual Summer Science Exhibition y in London from today.
Visitors to the exhibition will be able to manipulate DNA in virtual reality, seeing first-hand how changes in DNA folding influence the way bodies work.
Stephen Taylor, head of the research group at Oxfords MRC Weatherall Institute of Molecular Medicine, said: With advances in genetic techniques, we can now harness more information than ever before from biological data provided by patients and volunteers.
Using the virtual reality mode in CSynth is helping us visualise these complex 3D structures in a more intuitive way.
Professor Frederic Fol Leymarie, of Goldsmiths, added: By combining maths and physics with computer games technologies, we can program realistic molecular interactions and immerse people in the dynamic world of DNA.
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Virtual reality unpicks causes of healthy conditions (From The Oxford ... - The Oxford Times
Earlier this year, theNorth American Association of Central Cancer Registriesestimated that 1.69 million people in the U.S. alone will be diagnosed with some form of cancer in 2017. With such a huge number of people being diagnosed with complex diseases, such as cancer, the industry must continue to step up efforts to improve the outcomes. One option showing considerable potential is taking a precision medicine approach to determine the patients optimal treatment based on their personal molecular makeup and genomic profile.
Precision medicine gained significant attention following the launch of thePrecision Medicine Initiative, which saw the White House under President Obama invest $215 million, to broadly support research, development, innovation into the area.Similar projects, such as the Precision Medicine Catapult in the UK, added to the buzz. This interest, combined with technological developments and advances in data mining, has started to show promising results.
The life sciences industry, however, is facing a roadblock when it comes to turning promising research into a practical treatment option. Clinicians and researchers alike are finding it difficult to understand the data available to them and then translate the findings into treatments that will significantly improve clinical outcomes for patients. So, what can the life science industry do to turn precision medicine into reality?
What is holding back advances?
The emergence of new technology, combined with the use of huge knowledge databases, has been largely credited for recent advances in precision medicine. By using Next Generation Sequencing tools alongside gene expression profiling, physicians and researchers can better understand the makeup of the disease and how it is affecting the patient, within minutes.
By using data and research from previous laboratory experiments, researchers can identify the drug on the market with the highest chances of being effective against the particular proliferation mechanism driving the disease. This type of approach will revolutionize the treatment of complex diseases such as cancer, and in theory could saves countless lives around the globe. However, this requires a blend of deep technical and scientific skills, technical know-how to crunch the data, and scientific understanding to draw accurate clinical inferences. Without this blended approach, precision therapy for cancer will remain promising yet impractical.
Case study: Wake Forest Hospital and Elseviers R&D Solutions
Elsevier completed a precision medicine pilot with Dr. Francisco Castillos from Wake Forest, a small oncology practice in Winston-Salem, North Carolina (NC). The pilot aimed to treat three late-stage cancer patients, who had exhausted all standard-of-care treatment options, using a two-pronged precision medicine approach.
Castillos was able to understand in detail the pathways activated in the individuals cancer using Elseviers Pathway Studio tools. Then, he could point to what FDA-approved drugs that would be effective for the particular molecular mechanism driving the disease, or point to the relevant clinical trials. These analyses were reached through a combination of aggregating and harmonizing data, and Castillos scientific understanding and insight. While this study proves the viability of precision medicine in cancer, it is not an approach that can be replicated at scale.
A better use of data is key to precision medicine success
To achieve successful precision medicine at scale and to be able to offer it as an everyday treatment option, researchers in drug R&D need to better understand and manage the reams of unstructured data available to them. The data generated from understanding disease mechanisms is vital to successful drug development. Researchers need to find actionable insights relating to a particular gene, disease or biomarker, which requires searching the relevant published scientific literature, abstracts and clinical trial data and connecting the disparate pieces of information.
The type of approach conducted by Castillos, combining the use of molecular profiling and data mining tools, will help researchers tap into the existing repository of therapeutic drugs already on the market. In the last 25 years, hundreds of FDA-approved drugs have become available, with well-known mechanisms of action. With this approach, it would be possible to identify which approved therapies may be the best choice for a given patient or patient group/sub-group, based on what is driving their disease at a molecular level.
Not limited to the treatment of cancer
Precision medicine is the face of 21st-century medicine and can be used to treat many complex diseases, even at the earliest of stages, when a tissue biopsy is available and a genomics profile can be evaluated. The one treatment fits all approach is no longer the only viable option. Those suffering from complex diseases such as multiple sclerosis, schizophrenia, and depression are prescribed medication every day that proves ineffective due to their genetic makeup and individual factors which determine patient response. According toNNT,the 10 top-selling drugs in the U.S. help at best one in four of the patients using them, or in the worst case just one in 24 patients benefit from the drug theyre taking.
There is no denying that challenges involved with precision medicine are complex and there is lots of work to be done by the life science industry. Despite this, precision medicine will inevitably become the expected method of treatment for many diseases. Back in 2006, there were only13 examplesof precision medicine drugs, treatments and diagnostics products available. By 2014, this number had increased to 113, and is only set to grow following a better understanding of what the data generated by technology actually means, and how it can be used.
To do this, physicians and clinical researchers need to better understand the data available to them using digital solutions that accelerate patient analysis and accurately mine the data. Only then can they can match patients to an FDA-approved drug, and improve outcomes for patients all over the world.
Photo: Getty Images
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Richard Pops
Alkermes $ALKS has one shot at making ALKS-3831 a standout in the schizophrenia field. For years now, investigators expected to be able to show that the drug performs pretty much the same as the generic olanzapine in terms of efficacy, but significantly better in terms of preventing the weight gain and all the risks that come with it that afflicts patients on the old drug.
But in the first of two Phase III readouts on Thursday evening, investigators were only able to point to a similar efficacy with olanzapine without the benefit on weight gain.
Elliot Ehrich
Alkermes CEO Richard Pops and R&D chief Elliot Ehrich were sticking with the top line and heralded the data as a success. But in a wrap on side effects the company also noted that weight gain was similar for both drugs.
The stock dropped 5% as the data hit Thursday evening, carving out more than a billion dollars in market cap.
Those rates were similar, noted Ehrich during the Q&A with analysts Thursday evening.
The two execs, though, insisted that the 4-week study was simply too short to expect a separation on weight gain. That key question, they say, will have to wait for a 6-month study where patients will have a chance to balance the scale in favor of the Alkermes drug.
Based on its earlier work, says Pops, it clearly takes time three to six months for the weight gain advantage to demonstrate itself.
Many physicians recognize the powerful efficacy profile of olanzapine, but are hesitant to prescribe it given the severe weight gain and metabolic side effects commonly associated with its use, said Christoph Correll, M.D., professor of Psychiatry and Molecular Medicine at Hofstra Northwell School of Medicine. A new antipsychotic with robust efficacy and a favorable weight and metabolic profile compared to olanzapine would be a welcome addition to the schizophrenia treatment landscape. This study confirms a key element of this profile, with a clear demonstration of efficacy in a large, well-conducted clinical trial.
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NEEDHAM, MA--(Marketwired - June 30, 2017) - Cambridge Healthtech Institute, a division of Cambridge Innovation Institute, announces the opening of the call for speakers for the 25th International Molecular Medicine Tri-Conference, taking place February 11-16, 2018 at the Moscone South Convention Center in San Francisco, CA.
Since its debut in 1993, the annual Molecular Medicine Tri-Conference has become one of the world's leading international events in the field of drug discovery, development and diagnostics. The Tri-Conference unites an ecosystem of 3,700 innovative thinkers and thought leaders throughout biotech, pharma and academia from around the world.
Spanning five days, the 2018 meeting includes 16 parallel conference tracks, 7 Symposia, Training Seminars, and 25 in-depth short courses. Compelling talks, including best practice case studies and joint partner presentations, will feature over 500 industry and academic colleagues discussing themes of cancer research, big data, molecular diagnostics, precision medicine, data science, human microbiome, point-of-care diagnostics, infectious diseases, and more.
Showcase your research and work at this influential meeting and help your colleagues and peers stay abreast of important updates and advances in the field.
Submit a speaking proposal online at http://www.TriConference.com/speaker-proposal -- deadline for submission is July 7th.
For more information about the event, including pricing, exhibiting and sponsoring, visit: http://www.TriConference.com
About Cambridge Healthtech Institute (www.healthtech.com)Cambridge Healthtech Institute (CHI), a division of Cambridge Innovation Institute, is the preeminent life science network for leading researchers and business experts from top pharmaceutical, biotech, CROs, academia, and niche service providers. CHI is renowned for its vast conference portfolio held worldwide including PepTalk, Molecular Medicine Tri-Conference, SCOPE Summit, Bio-IT World Conference & Expo, PEGS Summit, Drug Discovery Chemistry, Biomarker World Congress, World Preclinical Congress, Next Generation Dx Summit and Discovery on Target. CHI's portfolio of products includes Cambridge Healthtech Institute Conferences, Barnett International, Insight Pharma Reports, Cambridge Marketing Consultants, Cambridge Meeting Planners, Knowledge Foundation, Bio-IT World, Clinical Informatics News and Diagnostics World.
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The premier event on Molecular Medicine & Diagnostics, uniting 3,700 innovative thinkers and thought leaders throughout biotech, pharma and academia, is accepting speaker proposals
NEEDHAM, MA--(Marketwired - June 30, 2017) - Cambridge Healthtech Institute, a division of Cambridge Innovation Institute, announces the opening of the call for speakers for the 25th International Molecular Medicine Tri-Conference, taking place February 11-16, 2018 at the Moscone South Convention Center in San Francisco, CA.
Since its debut in 1993, the annual Molecular Medicine Tri-Conference has become one of the world's leading international events in the field of drug discovery, development and diagnostics. The Tri-Conference unites an ecosystem of 3,700 innovative thinkers and thought leaders throughout biotech, pharma and academia from around the world.
Spanning five days, the 2018 meeting includes 16 parallel conference tracks, 7 Symposia, Training Seminars, and 25 in-depth short courses. Compelling talks, including best practice case studies and joint partner presentations, will feature over 500 industry and academic colleagues discussing themes of cancer research, big data, molecular diagnostics, precision medicine, data science, human microbiome, point-of-care diagnostics, infectious diseases, and more.
Showcase your research and work at this influential meeting and help your colleagues and peers stay abreast of important updates and advances in the field.
Submit a speaking proposal online at http://www.TriConference.com/speaker-proposal -- deadline for submission is July 7th.
For more information about the event, including pricing, exhibiting and sponsoring, visit: http://www.TriConference.com
About Cambridge Healthtech Institute (www.healthtech.com) Cambridge Healthtech Institute (CHI), a division of Cambridge Innovation Institute, is the preeminent life science network for leading researchers and business experts from top pharmaceutical, biotech, CROs, academia, and niche service providers. CHI is renowned for its vast conference portfolio held worldwide including PepTalk, Molecular Medicine Tri-Conference, SCOPE Summit, Bio-IT World Conference & Expo, PEGS Summit, Drug Discovery Chemistry, Biomarker World Congress, World Preclinical Congress, Next Generation Dx Summit and Discovery on Target. CHI's portfolio of products includes Cambridge Healthtech Institute Conferences, Barnett International, Insight Pharma Reports, Cambridge Marketing Consultants, Cambridge Meeting Planners, Knowledge Foundation, Bio-IT World, Clinical Informatics News and Diagnostics World.
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June 30, 2017
Cleveland Clinic researchers have uncovered a biological link between gut bacteria metabolism and obesity. The team showed that blocking a specific intestinal microbial pathway can prevent obesity and insulin resistance, as well as cause fat tissue to become more metabolically active. The study was recently published in Cell Reports.
The research team, led by J. Mark Brown, Ph.D., of Cleveland Clinic's Lerner Research Institute, studied the metabolic pathway that creates trimethylamine oxide (TMAO), a chemical produced by gut bacteria during digestion of key nutrients - choline, lecithin and carnitine - found abundantly in animal products, such as red meat, processed meats, egg yolks and liver.
Dr. Brown's colleague on the current study - Stanley Hazen, M.D., Ph.D. - previously showed that high levels of TMAO are associated with a higher risk of severe cardiovascular events, such as heart attack and stroke.
Since cardiovascular disease and obesity are so closely linked, the team hypothesized that TMAO may also be involved in metabolic pathways that lead to obesity. They focused on a host enzyme called flavin-containing monooxygenase 3(FMO3), which converts TMAO into its active form. They discovered that mice that had a missing or deactivated FMO3 gene were protected from obesity, even when fed a high-fat, high-calorie diet. Furthermore, the FMO3-negative mice showed higher expression of genes associated with beige or brown fat cells, which are more metabolically active than white fat cells.
The study confirmed in 435 patients that high levels of TMAO are associated with higher incidence of Type 2 diabetes.
"Obesity, diabetes and cardiovascular disease are strongly linked. While the microbiome has been shown to affect cardiovascular disease, there is as yet no concrete evidence of precisely how gut bacteria influence obesity," Brown said. "These findings shed light on a possible way to manipulate the microbiome with therapeutics to combat our obesity and diabetes epidemic."
Brown is a member of the scientific staff in the Lerner Research Institute's Department of Cellular & Molecular Medicine. Rebecca Schugar, PhD, is first author on the publication in Cell Reports.
"Given the numerous strong associations of the gut microbe-driven TMAO pathway with human disease, this work has broad implications for drug discovery efforts targeting gut microbes themselves," said Dr. Hazen, chair of the Department of Cellular & Molecular Medicine for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart & Vascular Institute at Cleveland Clinic. "However, additional work is needed to better understand the entire pathway and the links between TMA, FMO3, TMAO and human health."
TMAO is a byproduct of bacterial digestion of choline, lecithin and carnitine, nutrients that are especially abundant in animal products such as red meat, processed meats and liver. Dr. Hazen, who also holds the Jan Bleeksma Chair in Vascular Cell, has previously linked TMAO to an increased risk of cardiovascular disease and has shown it can be a powerful tool for predicting future heart attacks, stroke and death in multiple patient populations. Dr. Hazen is an inventor of a test for TMAO that was licensed to Cleveland HeartLab, Inc., a Cleveland Clinic spin-off company. Dr. Hazen and Cleveland Clinic would benefit financially from sales of the test.
Explore further: Researchers show dietary choline and TMAO linked with increased blood clotting
Journal reference: Cell Reports
Provided by: Cleveland Clinic
Cleveland Clinic researchers have shown, for the first time in humans, that choline is directly linked to increased production of a gut bacteria byproduct that increases the risk of blood-clotting events like heart attack ...
Cleveland Clinic researchers have demonstrated - for the first timethat targeting microbes in the gut may prevent heart disease brought on by nutrients contained in a diet rich in red meat, eggs and high-fat dairy products.
Cleveland Clinic researchers have, for the first time, linked trimethylamine N-oxide (TMAO) - a gut metabolite formed during the digestion of egg-, red meat- or dairy-derived nutrients choline and carnitine - to chronic kidney ...
A chemical byproduct of intestinal bacteria-dependent digestion, TMAO (trimethylamine N-oxide) already proven to contribute to heart disease and to be an accurate tool for predicting future heart attacks, stroke and death ...
A microbial byproduct of intestinal bacteria contributes to heart disease and serves as an accurate screening tool for predicting future risks of heart attack, stroke and death in persons not otherwise identified by traditional ...
Cleveland: In a combination of both clinical studies of over 4,000 patients and animal model studies, Cleveland Clinic researchers have demonstratedfor the first timethat gut microbes alter platelet function and risk ...
Cleveland Clinic researchers have uncovered a biological link between gut bacteria metabolism and obesity. The team showed that blocking a specific intestinal microbial pathway can prevent obesity and insulin resistance, ...
The endothelial cells that comprise blood vessels are uniquely responsive to cues from other organs, since their role is to integrate intimately into tissues and provide a means for delivery of oxygen and nutrients and waste ...
Although the basic outlines of human hearing have been known for years - sensory cells in the inner ear turn sound waves into the electrical signals that the brain understands as sound - the molecular details have remained ...
A new antiviral drug candidate inhibits a broad range of coronaviruses, including the SARS and MERS coronaviruses, a multi-institutional team of investigators reports this week in Science Translational Medicine. The findings ...
The billion-year-old primordial system by which early life forms protected themselves against viral infection can still be found in human cells, despite the presence of the much more sophisticated and powerful defense system ...
Mucus is important for maintaining healthy lungs. Inhaled particles, including bacteria and viruses, get trapped in mucus and then ciliatiny hair like projections on the surface of the airway cellssweep the mucus out ...
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Altering gut bacteria pathways may stimulate fat tissue to prevent ... - Medical Xpress
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Discovery provides potential target for vaccines, treatments
Scientists have solved the structure of a protein that helps a common respiratory virus evade the immune system. The researchers have identified critical parts of the protein that could be targeted with drugs or vaccines, opening up the possibility of preventing or treating an infection that sickens thousands of babies and elderly people every year.
By age 2, most children have been infected with respiratory syncytial virus (RSV), which usually causes only mild cold symptoms. But people with weakened immune systems, such as infants and the elderly, can face serious complications, including pneumonia and in some cases death.
Now, scientists studying the virus, led by researchers at Washington University School of Medicine in St. Louis, have found clues to how RSV causes disease. They mapped the molecular structure of an RSV protein that interferes with the bodys ability to fight off the virus. Knowing the structure of the protein will help them understand how the virus impedes the immune response, potentially leading to a vaccine or treatment for this common infection.
We solved the structure of a protein that has eluded the field for quite some time, said Daisy Leung, PhD, an assistant professor of pathology and immunology, and of biochemistry and molecular biophysics at Washington University School of Medicine in St. Louis, and the studys co-senior author. Now that we have the structure, were able to see what the protein looks like, which will help us define what it does and how it does it. And that could lead, down the road, to new targets for vaccine or drug development.
The study is published June 30 in Nature Microbiology.
Each year in the United States, more than 57,000 children younger than 5 years old are hospitalized due to RSV infection, and about 14,000 adults older than 65 die from it.
There is no approved vaccine for RSV and treatment is limited the antiviral drug ribavirin is used only in the most severe cases because it is expensive and not very effective so most people with RSV receive supportive care to make them more comfortable while their bodies fight off the virus.
For people with weakened immune systems, though, fighting RSV can be tough because the virus can fight back. Scientists have long known that a non-structural RSV protein is key to the viruss ability to evade the immune response. However, the structure of that protein, known as NS1, was unknown. Without seeing what the protein looked like, scientists were unable to determine exactly how NS1 interfered with the immune system.
Its an enigmatic protein. Everybody thinks it does many different things, but weve never had a framework to study how and why the protein does what it does, said co-senior author Gaya Amarasinghe, PhD, an associate professor of pathology and immunology.
Leung, Amarasinghe and colleagues used X-ray crystallography a technique that involves crystallizing the protein, bouncing X-rays off it, and analyzing the resulting patterns to determine the 3-D structure of NS1. Then, in a detailed analysis of the structure, they identified a piece of the protein, known as the alpha 3 helix, which might be critical for suppressing the immune response.
To test their hypothesis, the researchers created different versions of the NS1 protein, some with the alpha 3 helix region intact, and some with it mutated. In collaboration with others Rohit Pappu, PhD, the Edwin H. Murty Professor of Biomedical Engineering, Michael Holtzman, MD, the Selma and Herman Seldin Professor of Medicine, Maxim Artyomov, PhD, an assistant professor of pathology and immunology, and Christopher Basler, PhD, of Georgia State University they tested the functional impact of helix 3 and created a set of viruses containing the original or the mutant NS1 genes, and measured the effect on the immune response when they infected cells with these viruses.
They found that the viruses with the mutated helix region did not suppress the immune response while the ones with the intact helix region did.
One of the surprising things we found was that this protein does not target just one set of genes related to the immune response, but it globally modulates the immune response, said Amarasinghe, also an associate professorof molecular microbiology, and of biochemistry and molecular biophysics.
The findings show that the alpha 3 helix region is necessary for the virus to dial the bodys immune response down. By suppressing the immune response, the virus gives itself a better chance of surviving and multiplying, or in other words, of causing disease. RSV usually can only cause disease in people whose immune systems are already weak, so a vaccine or treatment that targets the alpha 3 helix to prevent immune suppression may be just what people need to be able to successfully fight off the virus, the researchers said.
Chatterjee S, Luthra P, Esaulova E, Agapov E, Yen BC, Borek DM, Edwards MR, Mittal A, Jordan DS, Ramanan P, Moore ML, Pappu RV, Holtzman MJ, Artyomov M, Basler CF, Amarasinghe GK, Leung DW. Structural basis for human respiratory syncytial virus NS1-mediated modulation of host responses. Nature Microbiology. June 30, 2017.
This study was supported by the National Institutes of Health, grant numbers R01AI107056, R01AI123926, R01AI114654, U191099565, U19AI109945, U19AI109664, U19AI070489, R01AI111605, R01AI130591, R01AI087798, U19AI095227, and T32-CA09547-37; the Defense Threat Reduction Agency of the Department of Defense, grant numbers HDTRA1-16-0033 and HDTRA1-16-0033; the National Science Foundation, grant number MCB-1121867; the Childrens Discovery Institute, a partnership between Washington University School of Medicine and St. Louis Childrens Hospital, grant number PD-II-2013-272; and the American Heart Association, 15POST25140009.
Washington University School of Medicines 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is one of the leading medical research, teaching and patient-care institutions in the nation, currently ranked seventh in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.
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Alkermes announced positive preliminary topline results from ENLIGHTEN-1, the first of two key phase 3 studies in the ENLIGHTEN clinical development program for ALKS 3831, an investigational, novel, once-daily, oral atypical antipsychotic drug candidate for the treatment of schizophrenia. ENLIGHTEN-1 was a multinational, double-blind, randomized, phase 3 study that evaluated the antipsychotic efficacy, safety and tolerability of ALKS 3831 compared to placebo over four weeks in 403 patients experiencing an acute exacerbation of schizophrenia. The study also included a comparator arm of olanzapine, an established atypical antipsychotic agent with proven efficacy. The study met the prespecified primary endpoint, with ALKS 3831 demonstrating statistically significant reductions from baseline in Positive and Negative Syndrome Scale (PANSS) scores compared to placebo (p<0.001). Data from the study also showed that olanzapine achieved similar improvements from baseline PANSS scores, compared to placebo (p=0.004). The study also met its key secondary endpoint of improvement on the Clinical Global Impression Severity (CGI-S) scale for ALKS 3831 versus placebo (p=0.002). ALKS 3831 is designed to provide the strong antipsychotic efficacy of olanzapine and a differentiated safety profile with favorable weight and metabolic properties.
The positive results of ENLIGHTEN-1 provide clear evidence of the safety, tolerability and antipsychotic efficacy of ALKS 3831 in a large, randomized registration trial, saidElliot Ehrich, M.D., Executive Vice President of Research and Development atAlkermes. The results of this phase 3 study also provide additional evidence of the antipsychotic properties of ALKS 3831 relative to olanzapine, an agent well known to clinicians. We look forward to completing our analysis of this large study and presenting the data at a future medical meeting.
Many physicians recognize the powerful efficacy profile of olanzapine, but are hesitant to prescribe it given the severe weight gain and metabolic side effects commonly associated with its use, saidChristoph Correll, M.D., Professor of Psychiatry and Molecular Medicine atHofstra Northwell School of Medicine. A new antipsychotic with robust efficacy and a favorable weight and metabolic profile compared to olanzapine would be a welcome addition to the schizophrenia treatment landscape. This study confirms a key element of this profile, with a clear demonstration of efficacy in a large, well-conducted clinical trial.
Overall, 91% of patients who received ALKS 3831 completed the study, compared to 89% of patients who received olanzapine and 83% of patients who received placebo. The most common adverse events for both the ALKS 3831 and olanzapine treatment groups were weight gain, somnolence and dry mouth.
Alkermeswill present comprehensive data from the ENLIGHTEN-1 study at an upcoming medical meeting and submit the results for publication in a peer-reviewed journal. ENLIGHTEN-2, a six-month phase 3 study evaluating the weight gain profile of olanzapine compared to ALKS 3831, is ongoing with data expected in 2018.
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Alkermes Announces Positive Preliminary Phase 3 Results for ... - Drug Discovery & Development
Marco Solmi,1,2 Andrea Murru,3 Isabella Pacchiarotti,3 Juan Undurraga,4,5 Nicola Veronese,2,6 Michele Fornaro,7,8 Brendon Stubbs,2,911 Francesco Monaco,2 Eduard Vieta,3 Mary V Seeman,12 Christoph U Correll,13,14 Andr F Carvalho2,15
1Neuroscience Department, University of Padua, 2Institute for Clinical Research and Education in Medicine, Padua, Italy; 3Bipolar Disorders Unit, Institute of Neuroscience, Hospital Clnic, University of Barcelona, IDIBAPS, CIBERSAM, Barcelona, Catalonia, Spain; 4Department of Psychiatry, Faculty of Medicine, Clnica Alemana Universidad del Desarrollo, 5Early Intervention Program, J. Horwitz Psychiatric Institute, Santiago, Chile; 6National Research Council, Ageing Section, Padua, 7Laboratory of Molecular and Translational Psychiatry, Department of Neuroscience, School of Medicine, University Federico II, Naples, Italy; 8New York State Psychiatric Institute, Columbia University, New York, NY, USA; 9Health Service and Population Research Department, Institute of Psychiatry, Psychology and Neuroscience, Kings College London, 10Physiotherapy Department, South London and Maudsley NHS Foundation Trust, London, 11Faculty of Health, Social Care and Education, Anglia Ruskin University, Chelmsford, UK; 12Institute of Medical Science, Toronto, ON, Canada; 13Department of Psychiatry Research, Zucker Hillside Hospital, Northwell Health, Glen Oaks, 14Department of Psychiatry and Molecular Medicine Hempstead, Hofstra Northwell School of Medicine, Hempstead, NY, USA; 15Translational Psychiatry Research Group and Department of Clinical Medicine, Faculty of Medicine, Federal University of Cear, Fortaleza, Cear, Brazil
Abstract: Since the discovery of chlorpromazine (CPZ) in 1952, first-generation antipsychotics (FGAs) have revolutionized psychiatric care in terms of facilitating discharge from hospital and enabling large numbers of patients with severe mental illness (SMI) to be treated in the community. Second-generation antipsychotics (SGAs) ushered in a progressive shift from the paternalistic management of SMI symptoms to a patient-centered approach, which emphasized targets important to patients psychosocial functioning, quality of life, and recovery. These drugs are no longer limited to specific Diagnostic and Statistical Manual of Mental Disorders (DSM) categories. Evidence indicates that SGAs show an improved safety and tolerability profile compared with FGAs. The incidence of treatment-emergent extrapyramidal side effects is lower, and there is less impairment of cognitive function and treatment-related negative symptoms. However, treatment with SGAs has been associated with a wide range of untoward effects, among which treatment-emergent weight gain and metabolic abnormalities are of notable concern. The present clinical review aims to summarize the safety and tolerability profile of selected FGAs and SGAs and to link treatment-related adverse effects to the pharmacodynamic profile of each drug. Evidence, predominantly derived from systematic reviews, meta-analyses, and clinical trials of the drugs amisulpride, aripiprazole, asenapine, brexpiprazole, cariprazine, clozapine, iloperidone, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, sertindole,ziprasidone, CPZ, haloperidol, loxapine, and perphenazine, is summarized. In addition, the safety and tolerability profiles of antipsychotics are discussed in the context of the behavioral toxicity conceptual framework, which considers the longitudinal course and the clinical and therapeutic consequences of treatment-emergent side effects. In SMI, SGAs with safer metabolic profiles should ideally be prescribed first. However, alongside with safety, efficacy should also be considered on a patient-tailored basis. Keywords: antipsychotics, side effects, tolerability, safety, psychosis, psychiatry
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.
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Healing the lungs of patients with chronic obstructive pulmonary disease (COPD) could save millions of lives each year yet the frustrating condition remains poorly understood and lacks any substantive therapy.
As physicians, we would love to understand better what is going on with COPD so that we can precisely target our therapies to patients, said Stephanie Christenson, MD, an assistant professor of medicine at UC San Francisco.
Her team hopes to tease apart the complexity of COPD and create treatments specific to each variant of the disease. One of Christensons collaborations will be taking findings from studies in mice to see if the same holds true in humans.
Ours is certainly a risky proposal, but it potentially could have huge rewards if we find ways to regenerate destroyed lungs, she said.
Christenson is one of 26 UCSF investigators who received funding from the 2017 cycle of the Marcus Program in Precision Medicine Innovation to help generate understanding of human disease. The program, supported by a gift from longtime UCSF supporters George and Judy Marcus, specifically supports high-risk projects that would likely yield high-impact benefits to patients.
COPD is a huge burden on the health care system, and the funding from the Marcus Program helps us drill down into the mechanisms of the disease to figure out how to treat patients better, Christenson said.
In its first two years, the Marcus Program has awarded more than $3.5 million, supporting 66 UCSF researchers in 17 departments across four UCSF schools. Projects all employ innovative research approaches to better understand why disease presentation and response to treatment are different for each individual, with the goal of developing specialized therapies to improve patient care the cornerstone of precision medicine.
The 10 projects funded this year include precision diagnoses of infectious diseases and autoimmune encephalitis, a therapy for Parkinsons Disease and development of a molecular medicine consult service for patients with rare and undiagnosed diseases.
Investing in the future of health by encouraging teams of diverse scientists to solve modern medical problems was the vision of George and Judy Marcus when they initiated the Marcus Program last year. George Marcus serves on the UCSF Foundation Board of Overseers and is a former UC Regent.
The wonderful thing about the Marcuses is that they recognized the enormous need for funding basic science research especially where it has clear ties to translation into improved patient care and they had a real interest in helping fill that funding gap with their support, said Gretchen Kiser, PhD, the executive director of the UCSF Research Development Office.
The program has two award categories to allow funding of early ideas that dont have much data as well as support for more established studies. The Seeding Bold Ideas program enables initial exploration of untested hypotheses with funding up to $75,000, while the Transformative Integrated Research award supports new directions for established basic science-driven translational studies with funds up to $400,000.
The Marcus Program emphasizes speed in bridging basic and translational research by supporting projects that will generate specific results within one year. Those findings may include the discovery that the proposed idea was incorrect.
The bottom line is that our researchers cant wait to get started, but while their ideas are scientifically sound, they lack the preliminary data that more traditional funders require, said Chancellor Sam Hawgood, MBBS. The Marcus Program provides the type of funding that is critical to enabling those high-risk projects to happen quickly. Often it is projects like these that lead us beyond more incremental, albeit valuable, advances, resulting in significant leaps forward in improved patient care.
For more campus news and resources, visitPulse of UCSF.
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Marcus Program Funds COPD Research, Other Projects to Improve Patient Care - UCSF News Services