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Gut Bacteria Could Impact Aging – R & D Magazine
Posted: June 15, 2017 at 8:50 pm
A bacteria in the gut may could hold the key to slowing down the aging process.
Scientists from Baylor College of Medicine and the University of Texas Health Science Center at Houston have found bacterial genes and compounds that extend the life of and slow down the progression of tumors and the accumulation of amyloid-beta, which is associated with Alzheimers disease.
The scientific community is increasingly aware that our body's interactions with the millions of microbes in our bodies, the microbiome, can influence many of our functions, such as cognitive and metabolic activities and aging, corresponding author Meng Wang, Ph.D., associate professor of molecular and human genetics at Baylor and the Huffington Center On Aging, said in a statement.
In this work we investigated whether the genetic composition of the microbiome might also be important for longevity, she added.
The researchers have identified the genes and compounds in C. elegans, a laboratory worm that is a transparent, simple organism that share essential characteristics with human biology.
The worm only lives two-to-three weeks and feeds on bacteria. However, it does progressively age to develop into an adult, while also reproducing.
We think that C. elegans is a wonderful system in which to study the connection between bacterial genes and aging because we can very fine tune the genetics of microbes and test many genes in the worm in a relatively short time, Wang said. We fed C. elegans each individual mutant bacteria and then looked at the worms' life span.
Of the nearly 4,000 bacterial genes we tested, 29, when deleted, increased the worms' lifespan. Twelve of these bacterial mutants also protected the worms from tumor growth and accumulation of amyloid-beta, a characteristic of Alzheimer's disease in humans.
The researchers then discovered that some of the bacterial mutants increased longevity by acting on some of the worms known processes linked to aging. After providing purified colonic acid to the worms, the researchers found that they lived longer.
Based on these results the researchers believe it is possible to design preparations of bacteria or their compounds that could help slow down the aging process.
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A new video shows you exactly what it looks like when DNA replicates – Mashable
Posted: at 8:49 pm
Mashable | A new video shows you exactly what it looks like when DNA replicates Mashable Scientists at the University of California, Davis, captured DNA replication on video for the first time. The 11-second clip which kind of looks like something pulled from a 1970s video game shows glowing strands of DNA stretching from left to ... Scientists Watch DNA Copy And Paste Itself For The First Time |
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A new video shows you exactly what it looks like when DNA replicates - Mashable
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To Keep DNA Lounge Open, Owner Closes Two Other Businesses … – Eater SF
Posted: at 8:49 pm
The SoMa all-ages venue Codeword and its adjoining pizza restaurant DNA Pizza will close at the end of July according to owner Jamie Zawinski. The nightclub proprietor, who also owns and operates the larger DNA Lounge, revealed the news on his blog yesterday, explaining that closing Codeword and DNA Pizzeria could help the already embattled DNA Lounge survive.
Zawinksi signed the lease on his second, smaller venue Codeword at 917 Folsom (5th and Folsom) in 2015 amid better business at his flagship club, DNA Lounge. Since then, things have taken a bad turn for the businesses generally, as Zawinski first confided in a December blog post.
Formerly a software engineer, Zawinski opened DNA Lounge with his winnings in the Startup Lottery, but after spending an estimated $5 million on it without turning a profit, hes run out of money. Now, unless he sees an uptick in attendance at DNA Lounge and support in the form of donations from patrons, Zawinski says hell have to close his club. But first, the ax is coming down for its spinoff, Codeword.
Rather than blaming high rent as a cause of Codewords closure, Zawinski actually thanks his landlord, who even lowered the rent and allowed Zawinski to break his lease when he couldnt find anyone to buy the business and take over the lease. Most of all, Zawinski thanked all of the artists and promoters who made a go of it at the club.
But will closing Codeword and DNA Pizzeria save DNA Lounge? Zawinski doesnt sound optimistic. Overall, we're still pretty fucked, he writes. Getting rid of Codeword staunches the flow, but we're still bleeding out, every damned day.
To help, you can donate to the clubs Patreon account, or go dance at Bootie, the weekly dance/sweat party held at DNA Lounge.
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To Keep DNA Lounge Open, Owner Closes Two Other Businesses ... - Eater SF
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New concerns raised over value of genome-wide disease studies – Nature.com
Posted: at 8:49 pm
Sandor Csudai/Getty Images
Genome-wide association studies search through huge groups of people to find DNA variants linked to diseases or traits.
Compare the genomes of enough people with and without a disease, and genetic variants linked to the malady should pop out. So runs the philosophy behind genome-wide association studies (GWAS), which researchers have used for over a decade to find genetic ties to diseases such as schizophrenia and rheumatoid arthritis. But a provocative analysis now calls the future of that strategy into question and raises doubts about whether funders should pour more money into these experiments.
GWAS are fast expanding to encompass hundreds of thousands even millions of patients (see 'The genome-wide tide'). But biologists are likely to find that larger studies turn up more and more genetic variants or 'hits' that have minuscule influences on disease, says Jonathan Pritchard, a geneticist at Stanford University in California. It seems likely, he argues, that common illnesses could be linked by GWAS to hundreds of thousands of DNA variants: potentially, to every single DNA region that happens to be active in a tissue involved in a disease.
In a paper published in Cell on 15 June1, Pritchard and two other geneticists suggest that many GWAS hits have no specific biological relevance to disease and wouldnt serve as good drug targets. Rather, these 'peripheral' variants probably act through complex biochemical regulatory networks to influence the activity of a few core genes that are more directly connected to an illness.
The implicit assumption of GWAS has been that when you find hits, they should be directly involved in the disease youre studying, he says. When you start to think that all of the expressed genes in a tissue can matter, it becomes untenable that theres a simple biological story for each one.
Many geneticists say they think Pritchard's view could be correct and that he articulates widely-held concerns about the difficulty of interpreting GWAS findings because of gaps in understanding about biochemical networks. I think its pretty plausible, says Joe Pickrell, a human geneticist at the New York Genome Center in New York City. We might not actually be learning anything hugely interesting until we understand how these networks are connected.
Rather than more and bigger GWAS, researchers and funders should devote their efforts to mapping regulatory networks in cells, Pritchard argues. Biologists that aim to link genes with diseases, he says, should focus on identifying the mutations that directly cause disorders; some of these variants are so rare that they aren't picked up in GWAS.
GWAS experiments have identified some genes that contribute to the risk of developing conditions such as obesity, but they have also thrown up plenty of vexing problems. Most of the hits found in GWAS dont seem to encode genes that make proteins, so it is hard to interpret their connection to a disease or trait. And even for traits that are known to be highly heritable suggesting that they have a large genetic influence the cumulative influence of all the DNA variants spotted by GWAS doesnt fully explain the variation seen between people. A 2014 study of 250,000 people, for example, identified nearly 700 DNA variants linked to height: but together, they explain only about 16% of differences in height across a population2.
In the Cell paper, Pritchards team re-analysed the data from the 2014 study. The researchers estimate that as many as 100,000 single-letter DNA variants can influence a persons height, but each one has a minuscule impact; on average just about one-tenth of a millimetre. These variants tend to lie in regions that do not themselves encode genes but which influence the activity of regions that do.
The researchers also re-analysed data from GWAS of schizophrenia, rheumatoid arthritis and Crohns disease. They found GWAS hits in DNA regions that are expressed in the particular cells relevant to the disease: neurons for schizophrenia, and immune cells for the two autoimmune diseases. But regions of DNA active in many types of body tissue were just as likely to be hits as those that were active only in neurons or immune cells, the team found. That lends credence to the idea that large GWAS are simply picking up most of the DNA variants that have an influence on gene regulation, and that happen to be active in broad functions of disease-relevant cells, rather than in particular activities linked to illness.
This doesnt mean that researchers should stop carrying out GWAS studies, some geneticists say. Although GWAS hits might be peripheral to a disease, identifying more of them enables scientists to knit together the biological networks implicated in a disease and understand how they interact, says Mark McCarthy, a human geneticist at the University of Oxford, UK, who is working on a GWAS of type 2 diabetes involving around 1 million participants. Those of us who do ever bigger GWAS, we dont just simply crank the handle, he says. Were motivated by lots of biological insights coming out of GWAS.
And Joel Hirschhorn, a human geneticist at Children's Hospital Boston, says that not all hits uncovered by very large GWAS are peripheral. The 2014 height study, which Hirschhorn co-led, uncovered an association to an important growth factor that wasn't picked up in a smaller GWAS study of height, he points out.
But Aravinda Chakravarti, a human geneticist at Johns Hopkins University in Baltimore, Maryland, hopes that the paper will challenge what he terms a cowboy attitude in genomics research that emphasizes collecting ever more genetic associations over understanding the deeper biology behind them. This is a nice paper simply because its going to kick people in the shin, which, as scientists, we need from time to time.
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Healthspanners and Immortalists: A Philosophy of Longevity – The Daily Meal
Posted: at 8:48 pm
My Uncle Phil, who drank himself into his mid-60s before his liver gave out, always claimed that he wasnt much interested in longevity. Whoever said, hed ask rhetorically as he sipped his eighth or ninth lunchtime Scotch and water, that the point of life was to make it last as long as possible?
This brings to mind the old joke about the man whose doctor tells him that he has to stop smoking, drinking, eating rich foods, and having sex. If I give up all that, the man asks, will I live a lot longer? Probably not, the doctor replies, but it will seem a lot longer.
In an article this spring in The New Yorker called Silicon Valleys Quest to Live Forever which was basically about how all those billionaire titans of the digital universe dont see why they should have to actually, you know, die, considering their dazzling disruptive genius the writer Tad Friend divided longevity scientists into two groups:
healthspanners, whose ideal (I paraphrase) is a healthy life snuffed out quickly and painlessly after a good long run, and immortalists, who think we (or at least they) ought to be able to pretty much live forever. (Friend further separated the latter category into two factions, the Meat Puppets, who believe that we can retool our biology and remain in our bodies, and the RoboCops, who believe that well eventually merge with mechanical bodies and/or with the cloud the latter only slightly sillier, I'd venture, than the former.)
Immortal is a funny word when you stop to think about it, deriving from the joining of the Latin prefix im ("un-") with the Latin noun mortalis ("mortal," in the sense of a mortal being) which of course is in turn derived from mortem, death.. It's more or less a synonym for not human, in other words. If you're immortal, then, you're not really one of us.
Ever since it first dawned on the human mind that human bodies apparently didnt last forever, though, people have been desperately looking for the loophole. Well, yeah, the lights might go out and the body turn to compost, but surely our spirits would survive, finding new homes in a cat, a tree, an Egyptian princess maybe even in Shirley MacLaine. Or else wed ascend to the heavenly realm where we would indeed live forever, even though we were, paradoxically, dead. Or on a more interventionist level, maybe if we drank enough of that mercury-and-honey cocktail the mixologist down at the alchemists shop was brewing up we could actually stay around in more or less the same form. Or maybe if we sold our soul to the.
Of the possibility of reincarnation or heavenly repose, both of them widely held as religious tenets around the world, the best that can be said is that, well, maybe I guess well find out if and when we get there. On the subject of alchemical elixirs, theres no need to equivocate: They didn't work, and were quite possibly poisonous to boot (see heavenly realm). And that selling-the-soul stuff never seems to work out too well in the end.
Ultimately, I think we just have to face it: Death and taxes. And I just got a letter from the IRS.
If death is inevitable, then, as the smart money certainly says it is, what about keeping it at bay for a while longer? That we can talk about. Average life expectancy worldwide increased about seven years for men and 10 years for women between 1990 and 2013. If it were to keep going at that rate indefinitely.
But it won't. Methuselah lived 900 years, according to Ira Gershwin (and 969 according to Genesis 5:27), but the oldest documented human being in modern times was Jeanne Calment, a Frenchwoman who died at the age of 122in 1997 and researchers believe that the absolute limit for human life is probably 125. Different researchers believe that it might be possible for a human being to run as fast as 40 miles an hour (Usain Bolt manages about 28). Needless to say, the chances of you or me achieving either milestone are mighty slim.
Does that mean we shouldn't try at least for the 125 years thing? Well, no, I guess not. Eating right, exercising, avoiding tobacco and non-prescription opioids and too much alcohol all those things you've been being told to do since you were old enough to care are probably well worth trying. At least in moderation. At least as long as they don't turn our lives into existential scut work, an anhedonic slog.
It would be nice to think that we can just keep going, but of course we can't. We know what's coming. We can rage or pray or turn to crackpot remedies or feed ourselves reassuring fantasies about post-cryogenic resurrection or downloading our spirits into cyberspace, but it isn't going to do any good.
Through his haze of Cutty Sark, Uncle Phil had a point. Maybe we should consider the possibility that longevity isn't everything. Maybe we should consider the possibility that as they used to say in those old commercials for Winston cigarettes (speaking of things we're supposed to avoid) it's not how long you make it, it's how you make it long.
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Healthspanners and Immortalists: A Philosophy of Longevity - The Daily Meal
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The ultimate Father’s Day gift: a longer, healthier life – Kitsap Sun
Posted: at 8:48 pm
Kitsap 1:59 p.m. PT June 15, 2017
Ginny Sugimoto, MD(Photo: Kitsap Sun)
This Fathers Day, you could give your dad a tie or a watch, but I have another suggestion: How about giving him the gift of a long, healthy life?
Over the years, researchers, mysticsand even science fiction writers have sought the key to longevity, but no one has found one perfect answer. One challenge is that many factors that affect human longevity are mostly beyond an individuals control, such as a persons genetic makeup, or their exposure to environmental pollution. On the other hand, research indicates that our actions have more influence over our life expectancy than we may think. Results of a study of Danish twins, for instance, suggested that 25 percent of our aging is determined by our genetics, while 75 percent is determined by lifestyle and medical conditions.
This is good news because it means we can have a big effect on healthy aging by changing how we live. Scientists in a range of fields are finding that we can live longer, healthier lives through basic daily attention to such things as avoiding smoking, eating well, exercising, and getting regular checkups and enough sleep. While these lifestyle choices apply to both females and males, women worldwide already live longer than men do on average about three to seven years longer, depending on location. There are several reasons for this, including the extra risks men are more likely to take when young due in part frontal lobes in the male brain that develop later than in females and the fact that men are much more likely to skip doctors visits and health screens than women are.
With that in mind, here are five science-backed ways to increase the odds of a long, healthy life, for your father, or anyone you care about:
1.Get treated. Everyone should start with making sure they are getting and following effective treatments for any chronic conditions, especially individuals with diabetes, hypertension, sleep apnea and/or obesity. If undiagnosed and untreated, these conditions are sure ways to shorten a life and to deteriorate health in older age. See the doctor for regular screenings to diagnose and treat medical problems before they further affect your quality of life. Those screenings include not just blood pressure checks and cancer screenings, such as colonoscopies, but also screenings for depression and other mental health concerns. Men are more likely to commit suicide than women, even though women seem to be more likely to have depression and to make suicide attempts.
2. Focus on diet. Diet and longevity have been linked in numerous studies. A Mediterranean-style diet, for instance, is associated with heart health, brain health and longer life. That diet is high in olive oil and fresh vegetables, particularly leafy greens, fruits, whole grains, nuts, and legumes such as chickpeas and lentils; moderate in fish, dairy, and wine, and low in red meat, eggs and sugar. Another possible longevity diet is that of people who live in the Okinawan Islands of Japan, which boasts a large number of centenarians. The Okinawans eat several servings of fish a week, and also consume copious whole grains, vegetables, soy products, and seaweed, as well as a kind of native sweet potato that is rich in beneficial nutrients. Another community known for longevity, the Seventh Day Adventist Community in Southern California, also has a high intake of fresh fruits, vegetables, and whole grains, as well as nuts which have been shown to benefit heart health. They eat little or no meat or fish. These individuals also eschew smoking and drinking. If you smoke, quit. If you drink, follow guidelines for moderation.
Other dietary research is focused on specific vitamins for instance, some research suggests that Vitamins C and E may provide health benefits as we age, functioning primarily as antioxidants to protect against damage to cells. But research suggests the best way to get these vitamins is in a plant-based diet. Sources high in Vitamin C include red peppers, kale, broccoli, spinach, strawberries, cabbage, and oranges. Foods high in Vitamin E include wheat germ, sunflower seeds, almonds, whole wheat, spinach, and cabbage. Eating fish twice a week protects against inflammation and atherosclerosis hardening and narrowing of arteries. There is increasing evidence that foods which contain live, beneficial bacteria, called probiotics, may also have an anti-aging effect. Good sources of probiotics include certain yogurts (make sure the label says they contain live bacteria), kefir, aged cheeses, and sauerkraut, kimchi and pickles all of which will only contain probiotics if they are sold in the refrigerated section those sold on store shelves at room temperature have been pasteurized, removing the bacteria.
3. Stick to a sleep schedule. We often have disrupted sleep as we age, and if it disrupts our internal circadian rhythm that manages our hormones, body temperature, and other functions it can be damaging to our health. Older adults still need seven to nine hours of sleep a night. Try to go to sleep and get up at the same time, and avoid napping if it affects sleep. Avoid screen time in bed, as it can also disrupt sleep. Some people believe alcohol helps them fall asleep, however, alcohol makes it harder to stay asleep once you do nod off. Talk to your doctor if you have trouble falling asleep or staying asleep.
4. Keep your body active. Physical activity is associated with a higher quality of life and a longer life, with benefits such as reducing insulin resistance, reducing inflammation and promoting brain health, particularly in areas associated with memory and learning. Daily activity also improves sleep and mood. All adults should aim for at least 150 minutes a week of at least moderate physical activity that gets your heart pumping thats about 30 minutes most days of the week. Walking is an excellent activity for overall health. Participants in a study that improved memory walked briskly for one hour, twice a week.
5. Engage your mind and be social. Learning new skills, doing the crosswords, reading, working and volunteering can all help to stimulate the brain in ways that may help to protect it from age-related changes. Connecting with others socially also activates your brain, and improves emotional health. Staying connected with friends and family keeps life stimulating and fun. it also helps you maintain a network of caring and support when you need it. Try a new hobby, find a new walking buddy, and try to hold an attitude of openness to new thoughts and adventures.
Its a great day to start on these steps to a healthier, longer life or to help your father do so.
Resources: The website of the National Institute on Aging offers many health and aging resources: http://www.nia.nih.gov
Ginny Sugimoto, MD, is a board-certified family practice doctor at Kaiser Permanente Port Orchard Medical Center. Her philosophy of care includes a emphasizing a preventive lifestyle and shared decision-making in partnership with her patients.
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The ultimate Father's Day gift: a longer, healthier life - Kitsap Sun
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Elixir of youth? New anti-ageing hope with pill made from human GUT bacteria – Express.co.uk
Posted: at 8:48 pm
GETTY
The elusive 'elixir of youth' pill is a major step nearer after the discovery of bacterial genes and compounds that not only extended life, but slowed down tumour growth and the build up of amyloid-beta, a compound associated with Alzheimer's disease.
Scientists at Baylor College of Medicine and the University of Texas Health Science Centre in the US hope one day a simple pill could play a vital role in slowing down ageing.
Dr Meng Wang, an Associate Professor of molecular and human genetics at Baylor, said: "The scientific community is increasingly aware that our body's interactions with the millions of microbes in our bodies, the microbiome, can influence many of our functions, such as cognitive and metabolic activities and ageing.
"In this work we investigated whether the genetic composition of the microbiome might also be important for longevity."
The study used the laboratory worm C. elegans, a transparent, simple organism that is as long as a pinhead and shares essential characteristics with human biology.
We think that C. elegans is a wonderful system in which to study the connection between bacterial genes and aging
Dr Meng Wang
During its two to three week long lifespan, the worm feeds on bacteria, develops into an adult, reproduces, and progressively ages, loses strength and health and dies.
Prof Wang explained: "We think that C. elegans is a wonderful system in which to study the connection between bacterial genes and aging because we can very fine tune the genetics of microbes and test many genes in the worm in a relatively short time."
To test the effect of individual bacterial genes on the lifespan of the worms they employed a complete gene-deletion library of bacterium E. coli. These each lacked one of close to 4,000 genes.
Prof Wang said: "We fed C. elegans each individual mutant bacteria and then looked at the worms' life span.
"Of the nearly 4,000 bacterial genes we tested, 29, when deleted, increased the worms' lifespan.
"Twelve of these bacterial mutants also protected the worms from tumour growth and accumulation of amyloid-beta, a characteristic of Alzheimer's disease in humans."
Further experiments found some of the bacterial mutants increased longevity by acting on some of the worm's known processes linked to ageing.
Other mutants encouraged longevity by over-producing the polysaccharide colanic acid.
When the purified colanic acid was given to C. elegans, the worms also lived longer.
Colanic acid also showed similar effects in the laboratory fruit fly and in mammalian cells cultured in the lab.
GETTY
She suggested it might be possible in the future to design preparations of bacteria or their compounds that could help slow down the ageing process.
Colanic acid mediates crosstalk between bacteria and mitochondria.
In particular colanic acid regulated the fusion-fission dynamics of mitochondria, the structures that provide the energy for the cell's functions.
Prof Wang added: "These findings are also interesting and have implications from the biological point of view in the way we understand host-microbe communication
"Mitochondria seem to have evolved from bacteria that millions of years ago entered primitive cells.
"Our finding suggests that products from bacteria today can still chime in the communication between mitochondria in our cells.
"We think that this type of communication is very important and here we have provided the first evidence of this.
"Fully understanding microbe-mitochondria communication can help us understand at a deeper level the interactions between microbes and their hosts."
The study was published in the journal Cell.
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Novartis (NVS) Announced Positive Data on Psoriasis Cosentyx – Zacks.com
Posted: at 8:48 pm
Novartis AG (NVS - Free Report) announced positive data on arthritis drug Cosentyx from two phase III studies at the Annual European Congress of Rheumatology (EULAR 2017), in Madrid.
Cosentyx, fully human monoclonal antibody, is already approved in the U.S. and EU for the treatment of moderate-to-severe plaque psoriasis. The drug is also approved in the EU for the treatment of adults with ankylosing spondylitis (AS) who have responded inadequately to conventional therapy, such as non-steroidal anti-inflammatory drugs. The drug is also instrumental for the treatment of active psoriatic arthritis (PsA) in adults when the response to disease modifying anti-rheumatic drug therapy is unsatisfactory.
In Jan 2016, Cosentyx obtained the FDA approval for the treatment of adults with active ankylosing spondylitis and for the treatment of adults with active psoriatic arthritis.
The data shows sustained improvement in the signs and symptoms for active AS at three years. The new data also revealed that Cosentyx provides rapid and sustained pain relief in patients with PsA out to 2 years.
Data from the phase III study, MEASURE 1 extension study, showed 80% of AS patients consistently achieved an ASAS 20 response at 3 years, in tandem with previous findings from the FUTURE 1 study on Cosentyx for active PsA. Additionally, a 2-year post-hoc analysis of the FUTURE 2 study evaluated Cosentyx in PsA, where 99% patients reported moderate-to-extreme pain or discomfort before initiating treatment. At week 3, half of the treated with Cosentyx reported clinically meaningful improvements in pain of over 20%, as measured by Visual Analogue Scale.
Meanwhile, patient recruitment is underway for the new head-to-head clinical trial, EXCEED, to evaluate the superiority of Cosentyx versus AbbVies (ABBV - Free Report) Humira in PsA.
Novartis has outperformed the Zacks classified industry over the last six months. The stock has rallied 12.2% compared with the Large Cap Pharmaceuticals industrys gain of 4.5%.
The uptake of Cosentyx has been strong and the company has grabbed market shares from rivals, Humira and Amgens (AMGN - Free Report) Enbrel. Cosentyx achieved blockbuster status in 2016 recording over $1 billion of sales.
Novartis expects the next growth phase to begin in 2018 driven by Cosentyx (in all three indications psoriasis, psoriatic arthritis and ankylosing spondylitis) Entresto, and Kisqali and a deep pipeline with candidates like CTL019, BAF312, AMG 334, RTH258. Going forward, we expect that the approval of new drugs and label expansion of existing ones will bode well for Novartis.
Zacks Rank & Key Pick
Novartis currently carries a Zacks Rank #3 (Hold).
A better-ranked stock in healthcare sector include VIVUS, Inc. (VVUS - Free Report) which sports a Zacks Rank #1 (Strong Buy). You can seethe complete list of todays Zacks #1 Rank stocks here.
VIVUSs loss per share estimates lessened from 50 cents to 39 cents for 2017 in the last 30 days. The company posted positive earnings surprises in all four trailing quarters with average beat of 233.69%.
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Novartis (NVS) Announced Positive Data on Psoriasis Cosentyx - Zacks.com
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Analyses of liver cancer reveals unexpected genetic players – Baylor College of Medicine News (press release)
Posted: at 8:47 pm
Liver cancer has the second-highest worldwide cancer mortality, and yet there are limited therapeutic options to manage the disease. To learn more about the genetic causes of this cancer, and to identify potential new therapeutic targets for HCC, a nation-wide team of genomics researchers co-led by David Wheeler, Director of Cancer Genomics and Professor in the Human Genome Sequencing Center (HGSC) at Baylor College of Medicine, and Lewis Roberts, Professor of Medicine at the Mayo Clinic, analyzed 363 liver cancer cases from all over the world gathering genome mutations, epigenetic alteration through DNA methylation, RNA expression and protein expression. The research appears in Cell.
Part of the larger Cancer Genome Atlas project (TCGA), this work represents the first large scale, multi-platform analysis of HCC looking at numerous dimensions of the tumor. There have been large-cohort studies in liver cancer in the past, but they have been limited mainly to one aspect of the tumor, genome mutation. By looking at a wide variety of the tumors molecular characteristics we get substantially deeper insights into the operation of the cancer cell at the molecular level, Wheeler said.
The research team made a number of interesting associations, including uncovering a major role of the sonic hedgehog pathway. Through a combination of p53 mutation, DNA methylation and viral integrations, this pathway becomes aberrantly activated. The sonic hedgehog pathway, the role of which had not been full appreciated in liver cancer previously, is activated in nearly half of the samples analyzed in this study.
We have a very active liver cancer community here at Baylor, so we had a great opportunity to work with them and benefit from their insights into liver cancer, Wheeler said. Among the many critical functions of the liver, hepatocytes expend a lot of energy in the production of albumin and urea. It was fascinating to realize how the liver cancer cell shuts these functions off, to its own purpose of tumor growth and cell division.
Intriguingly, we found that the urea cycle enzyme carbamyl phosphate synthase is downregulated by hypermethylation, while cytoplasmic carbamyl phosphate synthase II is upregulated, said Karl-Dimiter Bissig, Assistant Professor of Molecular and Cellular Biology at Baylor and co-author of the study. This might be explained by the anabolic needs of liver cancer, reprogramming glutamine pathways to favor pyrimidine production potentially facilitating DNA replication, which is beneficial to the cancer cell.
Albumin and apolipoprotein B are unexpected members on the list of genes mutated in liver cancer. Although neither has any obvious connection to cancer, both are at the top of the list of products that the liver secretes into the blood as part of its ordinary functions, explained Dr. David Moore, professor of molecular and cellular biology at Baylor. For the cancer cell, this secretion is a significant loss of raw materials, amino acids and lipids that could be used for growth. We proposed that mutation of these genes would give the cancer cells a growth advantage by preventing this expensive loss.
Multiple data platforms coupled with clinical data allowed the researchers to correlate the molecular findings with clinical attributes of the tumor, leading to insights into the roles of its molecules and genes to help design new therapies and identify prognostic implications that have the potential to influence HCC clinical management and survivorship.
This is outstanding research analyzing a cancer thats increasing in frequency, especially in Texas. Notably, the observation of gene expression signatures that forecast patient outcome, which we validate in external cohorts, is a remarkable achievement of the study. The results have the potential to mark a turning point in the treatment of this cancer, said Dr. Richard Gibbs, director of the HGSC at Baylor. The HGSC was also the DNA sequence production Center for the project.
Wheeler says they expect the data produced by this TCGA study to lead to new avenues for therapy in this difficult cancer for years to come. There are inhibitors currently under development for the sonic hedgehog pathway, and our results suggest that those inhibitors, if they pass into phase one clinical trials, could be applied in liver cancer patients, since the pathway is frequently activated in these patients, added Wheeler.
This work was supported by the National Institutes of Health and represents the last major cancer to be analyzed in the TCGA program. See a full list of contributors.
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Analyses of liver cancer reveals unexpected genetic players - Baylor College of Medicine News (press release)
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Newly identified method of gene regulation challenges accepted … – Phys.Org
Posted: at 8:47 pm
June 15, 2017
Researchers at the Stanford University School of Medicine have discovered an unexpected layer of the regulation of gene expression. The finding will likely disrupt scientists' understanding of how cells regulate their genes to develop, communicate and carry out specific tasks throughout the body.
The researchers found that cellular workhorses called ribosomes, which are responsible for transforming genes encoded in RNA into proteins, display a never-before-imagined variety in their composition that significantly affects their function. In particular, the protein components of a ribosome serve to tune the tiny machine so that it specializes in the translation of genes in related cellular pathways. One type of ribosome, for example, prefers to translate genes involved in cellular differentiation, while another specializes in genes that carry out essential metabolic duties.
The discovery is shocking because researchers have believed for decades that ribosomes functioned like tiny automatons, showing no preference as they translated any and all nearby RNA molecules into proteins. Now it appears that broad variation in protein production could be sparked not by changes in the expression levels of thousands of individual genes, but instead by small tweaks to ribosomal proteins.
'Broad implications'
"This discovery was completely unexpected," said Maria Barna, PhD, assistant professor of developmental biology and of genetics. "These findings will likely change the dogma for how the genetic code is translated. Until now, each of the 1 to10 million ribosomes within a cell has been thought to be identical and interchangeable. Now we're uncovering a new layer of control to gene expression that will have broad implications for basic science and human disease."
Barna is the senior author of the study, which will be published online June 15 in Molecular Cell. Postdoctoral scholars Zhen Shi, PhD, and Kotaro Fujii, PhD, share lead authorship. Barna is a New York Stem Cell Robertson Investigator and is also a member of Stanford's Bio-X and Child Health Research Institute.
The work builds upon a previous study from Barna's laboratory that was published June 1 in Cell. The lead author of that study was postdoctoral scholar Deniz Simsek, PhD. It showed that ribosomes also differ in the types of proteins they accumulate on their outer shells. It also identified more than 400 ribosome-associated proteins, called RAPs, and showed that they can affect ribosomal function.
Every biology student learns the basics of how the genetic code is used to govern cellular life. In broad strokes, the DNA in the nucleus carries the building instructions for about 20,000 genes. Genes are chosen for expression by proteins that land on the DNA and "transcribe" the DNA sequence into short pieces of mobile, or messenger, RNA that can leave the nucleus. Once in the cell's cytoplasm, the RNA binds to ribosomes to be translated into strings of amino acids known as proteins.
Every living cell has up to 10 million ribosomes floating in its cellular soup. These tiny engines are themselves complex structures that contain up to 80 individual core proteins and four RNA molecules. Each ribosome has two main subunits: one that binds to and "reads" the RNA molecule to be translated, and another that assembles the protein based on the RNA blueprint. As shown for the first time in the Cell study, ribosomes also collect associated proteins called RAPs that decorate their outer shell like Christmas tree ornaments.
'Hints of a more complex scenario'
"Until recently, ribosomes have been thought to take an important but backstage role in the cell, just taking in and blindly translating the genetic code," said Barna. "But in the past couple of years there have been some intriguing hints of a more complex scenario. Some human genetic diseases caused by mutations in ribosomal proteins affect only specific organs or tissues, for example. This has been very perplexing. We wanted to revisit the textbook notion that all ribosomes are the same."
In 2011, members of Barna's lab showed that one core ribosomal protein called RPL38/eL38 is necessary for the appropriate patterning of the mammalian body plan during development; mice with a mutation in this protein developed skeletal defects such as extra ribs, facial clefts and abnormally short, malformed tails.
Shi and Fujii used a quantitative proteomics technology called selected reaction monitoring to precisely calculate the quantities, or stoichiometry, of each of several ribosomal proteins isolated from ribosomes within mouse embryonic stem cells. Their calculations showed that not all the ribosomal proteins were always present in the same amount. In other words, the ribosomes differed from one another in their compositions.
"We realized for the first time that, in terms of the exact stoichiometry of these proteins, there are significant differences among individual ribosomes," said Barna. "But what does this mean when it comes to thinking about fundamental aspects of a cell, how it functions?"
To find out, the researchers tagged the different ribosomal proteins and used them to isolate RNA molecules in the act of being translated by the ribosome. The results were unlike what they could have ever imagined.
"We found that, if you compare two populations of ribosomes, they exhibit a preference for translating certain types of genes," said Shi. "One prefers to translate genes associated with cell metabolism; another is more likely to be translating genes that make proteins necessary for embryonic development. We found entire biological pathways represented by the translational preferences of specific ribosomes. It's like the ribosomes have some kind of ingrained knowledge as to what genes they prefer to translate into proteins."
The findings dovetail with those of the Cell paper. That paper "showed that there is more to ribosomes than the 80 core proteins," said Simsek. "We identified hundreds of RAPs as components of the cell cycle, energy metabolism, and cell signaling. We believe these RAPs may allow the ribosomes to participate more dynamically in these intricate cellular functions."
"Barna and her team have taken a big step toward understanding how ribosomes control protein synthesis by looking at unperturbed stem cells form mammals," said Jamie Cate, PhD, professor of molecular and cell biology and of chemistry at the University of California-Berkeley. "They found 'built-in' regulators of translation for a subset of important mRNAs and are sure to find more in other cells. It is an important advance in the field." Cate was not involved in the research.
Freeing cells from micromanaging gene expression
The fact that ribosomes can differ among their core protein components as well as among their associated proteins, the RAPs, and that these differences can significantly affect ribosomal function, highlights a way that a cell could transform its protein landscape by simply modifying ribosomes so that they prefer to translate one type of genesay, those involved in metabolismover others. This possibility would free the cell from having to micromanage the expression levels of hundreds or thousands of genes involved in individual pathways. In this scenario, many more messenger RNAs could be available than get translated into proteins, simply based on what the majority of ribosomes prefer, and this preference could be tuned by a change in expression of just a few ribosomal proteins.
Barna and her colleagues are now planning to test whether the prevalence of certain types of ribosomes shift during major cellular changes, such as when a cell enters the cell cycle after resting, or when a stem cell begins to differentiate into a more specialized type of cell. They'd also like to learn more about how the ribosomes are able to discriminate between classes of genes.
Although the findings of the two papers introduce a new concept of genetic regulation within the cell, they make a kind of sense, the researchers said.
"About 60 percent of a cell's energy is spent making and maintaining ribosomes," said Barna. "The idea that they play no role in the regulation of genetic expression is, in retrospect, a bit silly."
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Again we're shocked to discover that the higher energy environment our solar system experiences, the greater the tightening and finite organizing we see at the cellular level. What will we find only to lose it as our system passes out of higher energy is astonishing. Looking thru this lens of higher energy in past cycles reforms myths into potential truths.
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Newly identified method of gene regulation challenges accepted ... - Phys.Org
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