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Tuesday 25 November 2014

7 Of The Most Powerful Medicinal Plants

From Cannabis to Mint, there are hundreds of common herbs, flowers, berries and plants that serve all kinds of medical and health purposes.
Here are seven of the top medicinal plants that can help with: anti-inflammatory, anti-fungal, insect repellent, antibacterial, detoxification, fever reduction, antihistamine and pain relief.

Cannabis

Mostly legal until 1970 when it became classified as a hard drug. No one thought of it as a dangerous or illicit drug until the 20th century. In fact, the Declaration of Independence is written on it.
Hemp is a remarkable and renewable plant, offering all kinds product and food uses that surpass cotton and plastic. Health benefits are well documented, from depression, anxiety relief, reduced blood pressure, pain alleviation and even glaucoma treatment. It is not addictive, does not kill brain cells and is not a “gateway” drug – in fact, when pot is more available, studies show that the use of hard drugs like heroin and cocaine actually decreases.

Lady Ferns

Grab some and roll it up between your palms. The juices released will quickly ease stinging burns and can also ease minor cuts and burns. Bracken fern are similar to lady fern and will work as well.

Tansy

Tansy is an old-world aster and remedy, used for flavoring beer and stews as well as repelling insects.
Rubbing the leaves on the skin provides an effective bug repellent, but tansy can also be used to treat worms.
It is said to be poisonous when extracted, but a few leaves are not harmful if ingested.

Mint-leaves-2007Mint

Mint is famous for soothing headaches, fighting nausea, calming the stomach and reducing nervousness and fatigue.
Korean mint, also called Indian mint and hyssop, is a fairly effective antiviral, making it useful for fighting colds and the flu.
Whatever continent you’re on, some type of mint is usually to be found. Eat whole, garnish food or make tea to get the all purpose health benefits.

alfalfa

 Alfalfa

Alfalfa is incredibly rich in minerals and health-promoting nutrients and compounds. With roots that grow 20 to 30 feet deep, alfalfa is considered the “father of all plants”. (It also contains a high amount of protein for a green.) It can treat morning sickness, nausea, kidney stones, kidney pain and urinary discomfort.
It is a powerful diuretic and has a bit of stimulant power, helping to energize after a bout with illness. It’s a liver and bowel cleanser and long-term can help reduce cholesterol.

Sage

Sage is an incredibly useful herb, It is anti-inflammatory, anti-oxidant, antifungal, aids digestion, relieves cramps, reduces diarrhea, dries up phlegm, fights colds, reduces inflammation and swelling and kills bacteria. Sage apparently even brings color back to gray hair.
red-clover

 Red Clover

The plant’s reddish pink blossoms can be used for coughs and colds, but they are an excellent detoxifier and blood cleanser as well.
For more valuable plant related content be sure to check two other articles previously featured on Collective Evolution:

Source:CE

Metabolic Syndrome can be Prevented With Healthy Gut Microbiota

Metabolic syndrome can be treated or prevented by promoting healthy gut microbiota, the bacteria that live in the intestine. Metabolic syndrome is a combination of risk factors that increases a person's risk for heart disease, diabetes and stroke, suggest researchers at Georgia State University and Cornell University. Their findings are published in the journal Gastroenterology.


 


The study, a follow-up to the research team's previous paper in Science, uses an improved technical approach, making the results more significant. 

The research team includes Dr. Andrew Gewirtz, a professor in the Institute for Biomedical Sciences at Georgia State; Dr. Benoit Chassaing, a post doctoral fellow at Georgia State; and Dr. Ruth Ley of the departments of Microbiology and Molecular Biology at Cornell. 

"These results suggest that developing a means to promote a more healthy microbiota can treat or prevent metabolic disease," Gewirtz said. "They confirm the concept that altered microbiota can promote low-grade inflammation and metabolic syndrome and advance the underlying mechanism. We showed that the altered bacterial population is more aggressive in infiltrating the host and producing substances, namely flagellin and lipopolysaccharide, that further promote inflammation." 

Metabolic syndrome is a serious health condition that affects 34 percent of American adults, according to the American Heart Association. A person is diagnosed with metabolic syndrome when they have three of these risk factors: a large waistline, high triglyceride (type of fat found in the blood) level, low HDL cholesterol level, high blood pressure and high fasting blood sugar. A person with metabolic syndrome is twice as likely to develop heart disease and five times as likely to develop diabetes, according to the National Institutes of Health. 

Because metabolic syndrome is becoming more common, scientists are exploring possible causes. In their previous study in Science, Gewirtz, Ley and other researchers showed altered gut microbiota plays a role in promoting metabolic syndrome. 

Gut microbiota performs key functions in health and when it becomes dysregulated it can promote chronic inflammatory diseases such as Crohn's disease and ulcerative colitis. In addition, altered gut microbiota promotes inflammation that leads to metabolic syndrome. 

"We've filled in a lot of the details about how it works," Gewirtz said. "It's the loss of TLR5 on the epithelium, the cells that line the surface of the intestine and their ability to quickly respond to bacteria. That ability goes away and results in a more aggressive bacterial population that gets closer in and produces substances that drive inflammation." 

Normally, the bacteria are in the mucous layer at a certain distance away from epithelial cells. The researchers showed altered gut microbiota is more aggressive in infiltrating the host and gets very close to the epithelium. This altered population produces flagellin and lipopolysaccharide, which further promote inflammation. 

The research team improved the study by comparing mice that were siblings and littermates, making all conditions in the study the same. The mice only differed by whether they were missing a specific gene, TLR5. Previously, the researchers studied mice that were from two different strains and lived in separate environments. In this study, they found the absence of TLR5 on the intestinal surface leads to alterations in bacteria that drive inflammation, leading to metabolic syndrome. 
 Source:National Institutes of Health.

Envisioning Better Healthcare in India for the Future Through Collective Innovations

Mr. Sunil Wadhwani, a philanthropist and angel investor based in Pittsburgh, USA, and Chairman and Co-founder of IGATE Corporation USA founded the Wadhwani Initiative for Sustainable Healthcare or WISH Foundation. Recently, the SCALE Healthcare Innovations summit convened by the WISH Foundation was held in Delhi.

 
The summit brought together over three hundred national, state, community, and international leaders from government, private sector, and development partners, social enterprises, healthcare innovators, academia and media, who form the healthcare ecosystem, to support the scale up. The goals for the summit included learning how to scale up, promising healthcare innovations capable of changing the healthcare paradigm for the poor and significantly contributing to achieve the commitment of India to ensure health for all. The timing was impeccable as news reports indicate the Union Government's keen interest in inviting private stakeholders under the National Rural Heath Mission. 

Addressing the summit, Dr. Vishwa Mohan Katoch, Secretary, Department of Health Research & Director General, ICMR, said, "We must ensure that affordable technologies benefit a large number of people. As a representative of the government, we assure you our partnership." Niraj Kumar Pawan, an IAS officer and Director of National Health Mission, Rajasthan, while sharing his experiences, said that it was high time we give up on the age old procedures. He also discussed the social and cultural prejudices that affect a girl child in India and the need to tackle these issues adding that every time a girl child is born to a family, a greeting signed by the Chief Minister of Rajasthan is despatched to the home of the newborn. Another one of Rajasthan's initiatives, the mother and child tracking system, which started out on a simple spreadsheet, has been scaled up and undertaken by the National Health Mission. The model, now popularly known as Mother and Child Tracking System (MCTS), is being replicated across the country. 

A 2012 study by Federation of Indian Chambers of Commerce Industry (FICCI), an association of business organization, and the consultants Ernst and Young, estimated that the universal health coverage of India was feasible in a decade and this required the Government's expense on health to rise to 3.7-4.5 percent of India's GDP. While it is important for the Government to provide primary healthcare facilities to its citizens, the issues of affordability and accessibility should be addressed and resolved. At present, 39 million people are pushed below the poverty line every year because of the unaffordability of healthcare. Public Private Partnerships (PPP) in the healthcare sector definitely seems like a feasible solution to tackle the burden of expenditure on the poor and the public sector. Sanjeev K Chaudhury, Managing Director, SRL Diagnostics said, "We need to add a fourth pillar to the PPP model, that is, Philanthropy. It is important to provide cost-effective and quality healthcare to the poor." 

Some of the key components and aspects discussed in the summit include the following:
  • s  Innovation in technology and processes is required for the deliverance of inexpensive and quality healthcare services for a rapidly changing India.
  • s  Scaling up Healthcare Innovations to strengthen Preventive and Primary Healthcare Delivery in India.
  • s  Bringing out specific action points to address the challenges of scaling up promising healthcare innovations to revitalize primary healthcare delivery in India.
  • s  An Innovation Showcase where innovators and enterprises displayed their innovations.
  • s  If quality healthcare services are implemented properly, 42 of every 1000 infants will be prevented from dying before their first birthday and 58 of 1000 infants before their fifth. And an estimated 178 of 100,000 pregnant women will be saved from pregnancy and childbirth related deaths.
  • s  Path-breaking ideas such as the health ATMs that are automatic kiosk-typed diagnostic center, designed holistically to address primary healthcare requirements were discussed. The health vending machines will have an attached cabin to provide diagnostic services like testing body vitals etc.
ACCESS Health International, Center for Health Market Innovation's (CHMI) partner in India, was present at the summit to collaborate on the SCALE Rajasthan project. With CHMI's support, ACCESS and WISH aim to build relationships between private health providers and government officials for effective public-private partnership formation. Mr. Wadhwani said, "WISH commits to raise a $100 million healthcare innovation fund which would accelerate the scale up of 50-100 innovators over the next 10 years." If the innovative ideas and collaborations of this summit are successful, then the Indian healthcare sector will receive the much-needed improvement that it has been craving for.
 Source:Desk

Stem cells that help regrow nails found

Stem cells that help regrow nails found
Researchers have found out the stem cells that will aid the nails in coming back after they are lost.A team of USC Stem Cell researchers led by principal investigator Krzysztof Kobielak and co-first authors Yvonne Leung and Eve Kandyba has discovered nail stem cells, which undergo differentiation to form multiple tissues. 

"That was a very surprising discovery, since the dual characteristic of these nail stem cells to regenerate both the nail and skin under certain physiological conditions is quite unique and different from other skin stem cells, such as those of the hair follicle or sweat gland," principal investigator Krzysztof Kobielak said in a university news release.

Usually, the stem cells help both the nails and nearby skin to grow. But as per the study, if a nail is damaged or destroyed, the stem cells only help in nail repair.

According to the researchers, these stem cells could be used to grow tissue for other body parts and this could mean that someday doctors can work on getting back lost limbs or organs.

If the nail is injured or lost, a protein called bone morphogenic protein, or BMP, signals to the stem cells to function only for nail repair. 

 Source:USC


 

Monday 24 November 2014

Read:What Ayurveda says from thosuand of years:The Gut-Brain Connection, Mental Illness, and Disease

 We are never truly alone. On our skin, in our gums, and in our guts live 100 trillion organisms, altogether known as the microbiome. These beasties comprise 90% of the cells of our bodies, though these cells are so tiny in size that it appears our own human cells predominate. It is only recently that we have begun to study these organisms with any depth. Most of them live within the gut, and cannot be cultured, and only with the advent of advanced genetic testing have we been able to have a better understanding of the variety and numbers of microbes we’re dealing with. They are Bacteria, and
What do they have to do with psychiatry? It turns out way more than we might have suspected. The gut and brain have a steady ability to communicate via the nervous system, hormones, and the immune system. Some of the microbiome can release neurotransmitters, just like our own neurons do, speaking to the brain in its own language via the vagus nerve.
To have a full understanding of how the whole gut-brain connection works, you need robust knowledge of endocrinology, immunology, pathology, and neurology, which is a bit beyond the scope of a blog article. However, to break it down to simplistic terms, here are the basic links:
1) The body responds to stress (mental or physical) via the hypothalamic-pituitary-adrenal axis. For example, if you are eating lunch and a lion jumps into the middle of your picnic table, your “fight or flight” system is fired into full gear, your heart pounds, your pupils dilate, your hair stands on end, natural steroids and adrenaline flood your system to strengthen your muscles and give you an extra burst of speed. Even your platelets change shape so they are more sticky, leaving you less likely to bleed out if you are attacked. Naturally, our bodies have negative feedback that can tone down the fight or flight response once the danger is past (assuming you survive). Under conditions of chronic stress, however, mental or physical, the feedback tends to get messed up, leading to symptoms of chronic stress (which includes mental issues such as anxiety or clinical depression, but also physical problems such as chronic gut problems, headaches, high blood pressure, etc.). What does all of that have to do with the gut?
2) While the hormonal system that regulates fight-or-flight, rest-and-recovery, and everything in between is easy to conceptualize, the second underlying system, the immune system, is far more complex and works at a cellular level. Our bodies aren’t particularly sophisticated when it comes to facing off against stress. Our stress response doesn’t readily distinguish between mental and physical distress; your heart pounds and you tremble with anxiety when you are in an uncomfortable meeting with your boss, when such a reaction is not helpful in that situation, though it might have helped with the lion. And not only to we respond to the tough day on the job with a hormonal response, but also an immunological one. When our body is under stress, it releases what are called inflammatory cytokines, little chemical messengers that bring a certain part of our immune system into high alert. In a sense, our body reacts to all stress as if it were an infection, and to chronic stress as if it were a chronic infection.* Now the immune system works wonders and inflammation saves your life nearly every day from all the pathogens out there like the flu and strep, but chronic levels of inflammatory response also lead to all sorts of chronic disease, for example depressive disorders, high blood pressure, atherosclerosis, autoimmune diseases such as ulcerative colitis and multiple sclerosis. Immune system activation can also determine whether or not we develop cancer. Where does the gut get involved? Well, it turns out the gut microbiome plays a key role in regulating our immune response. Thus the make-up of our gut microbiome could make the difference as to whether we are sick or well, both mentally and physically.
3) Animal and human studies support the theory that pathogenic bacteria in the gut, such as C. Difficile, or in certain circumstances, H. Pylori, lead to human disease, and not just the obvious direct illnesses,pseudomembranous colitis and ulcers. These bacteria also interact with the immune system in the gut to cause the release of inflammatory cytokines, stress steroids, and a systemic stress response (similar in most ways to the lion attack). Some of the responses of the gut even have an effect on our pain response…yes, people with certain unfavorable gut bacteria might be more sensitive to pain than others. However, other commensal organisms in the gut seem to have the opposite effect, the most studied being certain strains of Bifidobacteriumand Lactobacillus. The right sort of commensal bacteria keep the numbers of pathogenic bacteria low, and also interact with the immune system in a way to turn off that chronic stress response. The “right” gut bacteria also interact on a hormonal level, helping to turn off the cortisol and adrenaline response that can cause long-term harm to the body. However, each large group of gut bacteria (and Archaea, which have a big influence on digestion and help us ferment and breakdown otherwise indigestible plant fibers) have many different strains, and each of these strains may have differential effects, some of them synergistic or antagonistic. The scope of complexity of the problem is mind-bending. In general, it is felt that more variety in the gut microbiome is probably better, and studies of hunter-gatherers show us they seem to have both more mass and more variety of gut bacteria than do modern Westernized humans.
What is the direct evidence these gut microbes affect the brain? Most of the evidence is in mice or rats, but scientists have shown that rats raised germ-free have different production of key brain neuron fertilizers that help with neuroregeneration, neuroplasticity, and repair than do rats that are (like most animals) colonized with gut bacteria. This same brain fertilizer, BDNF, is necessary in the human brain as well. BDNF being low in the wrong place at the wrong time is implicated in clinical depression, chronic anxiety syndromes, and other psychiatric disease. Other differences in germ free mice include changes in the shape and expression of certain neurotransmitter receptors, NMDA and 5HT1A. These receptors are also important in the regulation of mood, anxiety, and a malfunctioning NMDA receptor is part of the pathology of psychosis, as seen in schizophrenia or bipolar disorder. Certain strains of probiotics can increase the availability of tryptophan, the key precursor to making serotonin.
There is also evidence stress can affect the microbiome. Mice exposed to early parental loss have an immediate reduction in the amount of lactobacilli in the feces. Some of these microbiota changes are long term, including decreasing some “friendly” bacteria and increasing the relative abundance of pathogenic bacteria such as Clostridium.
To add complexity to the whole question, most of these studies are about certain bacterial species among many thousands of bacteria species, and beyond the commensal bacteria, the human immune system is also profoundly affected by so-called pseudocommensal organisms (such asM vaccae) found in soil and water that don’t stay in our guts, but regularly passed through them in human history as we ate wild foods and drank spring and pond water. In modern times, those who have been vaccinated with Bacille-Calmette-Guerin (BCG) as protection against tuberculosis have, in a sense, been chronically infected with a pseudocommensal somewhat similar to M vaccae. Along with some protection against tuberculosis, those who have received the vaccine are also less likely to develop melanoma (and some other cancers) than those who haven’t, suggesting the effect of the vaccine on the immune system helps T cells of our immune system in cancer surveillance and elimination of neoplastic cells. In addition, those infected with chronic parasites such as hookworms seem to have a much lower incidence of autoimmune disease than do modern, Western, mostly parasite-free humans. Since our immune system co-evolved with these parasites, it would make sense that their absence would have a profound effect on immune regulation, leading to all sorts of consequences, both physical and psychiatric.
How can we affect the gut microbiome and the immune system? Changing the diet will have immediate effects, with folks who eat highly refined diets having a different gut composition than those who eat more whole foods, fruits and vegetables. We can also take probiotics, though the research is preliminary, and probiotics only help temporarily (that is, as long as you take them). Some probiotic formulations now include soil bacteria, giving the benefits (and risks?) of both commensal and pseudocommensal exposure. Strains of bacteria that affect the brain or behavior are called psychobiotics. Fecal transplants will cause a permanent change in the microbiota. BCG and vaccinia injections could be something to look at as well. Also, some studies are being done on infection with hookworm and pig whipworm eggs in autoimmune conditions to replicate exposure to the complex eukariotic parasites.
All in all, the gut is a terrific place to start helping humans be as healthy,resilient, and robust as we have evolved to be.
Sources: Dinan, T., Cryan, J., Regulation of the stress response by the gut microbiota: Implications for psychoneuroimmunology. Psychoneuroimmunology (2012) 37, 1369-1378
Wang, Y. Kasper, LH. The role of micro biome in central nervous system disorders. Brain Behav. Immun. (2014),http://dx.doi.org/10.1016/j.bbi.2013.12.015
Krone, B. et al, Protection against melanoma by vaccination with Bacille-Calmette-Guerin (BCG) and/or vaccinia: an epidemiology-based hypothesis on the nature of a melanoma risk factor and its immunological control. European Journal of Cancer. 41 (2005) 107-107.
*Some very bright people believe that chronic diseases are all caused by chronic infections, and in some cases this may be true, for example, toxoplasma infection is associated with a higher risk of developing schizophrenia, but I think the body’s stress response, once it is out of balance, can explain many chronic illnesses without invoking a chronic infection in every case.
Courtesy:Psychology Today

Schizophrenia may be triggered by excess protein during brain development

Rutgers researcher says too much causes abnormalities and faulty connections in laboratory studies

A gene associated with schizophrenia plays a role in brain development and may help to explain the biological process of the disease, according to new Rutgers research.
In the study, published in Biological Psychiatry, Bonnie Firestein, professor in the Department of Cell Biology and Neuroscience, says too much protein expressed by the NOS1AP gene, which has been associated with schizophrenia, causes abnormalities in brain structure and faulty connections between nerve cells that prevent them from communicating properly.
Firestein's research indicates that an overabundance of a protein in the NOS1AP gene resulted in the dendrites -- tree-like structures that allow cells to talk to each other and are essential to the functioning of the nervous system -- being stunted in the developing brains of rats.
She and her colleagues found that too much of the NOS1AP protein in brain cells didn't allow them to branch out and kept them deep within the neocortex, the portion of the brain responsible for higher functioning skills, such as spatial reasoning, conscious thought, motor commands, language development and sensory perception.
In the control group of rats in which NOS1AP chemical protein was not overexpressed, the cellular connections developed properly, with cells moving out to the outer layers of the neocortex and enabling the nerve cells to communicate.
"When the brain develops, it sets up a system of the right type of connectivity to make sure that communication can occur," says Firestein. "What we saw here was that the nerve cells didn't move to the correct locations and didn't have dendrites that branch out to make the connections that were needed."
Although scientists can't pinpoint for certain the exact cause of schizophrenia, they have determined that several genes, including NOS1AP, are associated with an increased risk for the disabling brain disorder and believe that when there is an imbalance of the chemical reactions in the brain, development can be disrupted.
Firestein has been working with Rutgers geneticist Linda Brzustowicz, professor and chair of the Department of Genetics, who co-authored the paper and first began investigating the genetic link between NOS1AP and schizophrenia a decade ago.
While about 1 percent of the general population suffers from schizophrenia, the risk increases to about 10 percent in the first degree relatives of an individual with the disease. NOS1AP has been identified as a risk factor in some families with multiple individuals affected with schizophrenia.
Since the prefrontal cortex, the part of the brain that is associated with schizophrenia, matures through adulthood, Firestein says it is possible that drug treatment therapies could be developed to target the disease in adolescents when schizophrenia is thought to develop and when symptoms appear.
"The next step would be to let the disease develop in the laboratory and try to treat the over expression of the protein with an anti-psychotic therapy to see if it works," says Firestein.
Source:Biological Psychiatry

Tiny Patient Prompts Advance in Neuro-genetics

Take a deep breath and hold it. Keep holding it. Keep waiting … wait … don’t breathe yet … Feel that burning in your lungs?
That’s your brain telling you to breathe. Or rather, that’s a tiny group of cells in the brain stem telling you to breathe. Those cells can sense the buildup of carbon dioxide in your blood, thanks in part to a protein called connexin. Carbon dioxide latches onto connexin, which then spurs cells to signal “it’s time to breathe!” Neurons fire, your diaphragm moves down, and you inhale.
Babies start breathing in the womb, inhaling and exhaling irregularly at first, and then gradually more and more, until the day when they’re born and have to do it all the time. But premature babies sometimes have trouble. They stop breathing periodically, sometimes for 20 or 30 seconds at a time. Sometimes they’re fine, and sometimes they’re not, and doctors struggle to help them.
That may soon change, however, thanks to a two-month-old patient at UConn Health with a rare connexin mutation, and his doctor’s willingness to call for help.An infant breathes with the help of a respirator in an isolette in a Neonatal Intensive Care Unit. (Shutterstock/UConn Photo)
An infant breathes with the help of a respirator in a Neonatal Intensive Care Unit isolette. (Shutterstock/UConn Photo)
The patient was just two months old, deaf, blind, and covered in thick, leathery, cracked skin. And he had odd, disordered breathing that left his oxygen levels too low. He had been referred to UConn Health for his skin condition, but neonatal research director Naveed Hussain was startled by the baby’s breathing troubles. Premature babies often have trouble breathing, but two-month-olds rarely do.
Hussain began searching for information about the baby’s mutation, which was at a spot on the genome called connexin26. Related mutations are known to result in deafness, blindness, or skin trouble. But no one had ever reported disordered breathing, at least not in humans. So Hussain began reading about animals with connexin mutations. Which is how he discovered that Daniel Mulkey, a UConn associate professor of physiology and neurobiology, had looked at just this type of mutation-related breathing disruption in rats. Hoping that Mulkey might be able to suggest a therapy for the patient, Hussain picked up the phone.
Daniel Mulkey, associate professor of physiology and neurobiology, looks at tissue under a microscope at his lab. (Peter Morenus/UConn Photo)
Daniel Mulkey, associate professor of physiology and neurobiology, looks at tissue under a microscope at his lab. (Peter Morenus/UConn Photo)
Mulkey was intrigued. He knew that a common connexin mutation blocked expression of the protein altogether. Having one copy of that mutation is a common cause of inherited deafness; having two copies is lethal in utero. But Hussain’s patient had one normal copy, and one connexin26 mutation. So why was he in such bad shape?
Mulkey asked Nick Dale, an expert on connexin protein at the University of Warwick, UK, to express the connexin26 mutation in human astrocytes. Astrocytes are the most abundant cells in the brain and do many things, including signaling to neurons. Dale found that astrocytes with the connexin26 mutation couldn’t bind to carbon dioxide. This specific connexin mutation was dominant, and suppressed expression of the normal protein. Such mutant cells were oblivious to dangerously high carbon dioxide levels, and this almost certainly explained the baby’s disordered breathing. It was also the first time a direct link between the connexin channel, carbon dioxide, and respiration had been shown in humans.
Carbon dioxide-sensing astrocytes are found in the retrotrapezoid nucleus (RTN) area on the brainstem. These astrocytes help trigger breathing when blood levels of carbon dioxide rise too high. (Daniel Mulkey/UConn Image)
Carbon dioxide-sensing astrocytes are found in the retrotrapezoid nucleus (RTN) area on the brainstem. These astrocytes help trigger breathing when blood levels of carbon dioxide rise too high. (Daniel Mulkey/UConn Image)
While Dale and Mulkey were looking at the mutation’s effect on human cells, Hussain began to review recordings of the breathing patterns of his patient, trying to see if there was anything that could give advance warning of a bad breathing episode. There’s not much in the medical literature about the breathing patterns of newborn infants, and Hussain and his colleagues began to wonder if they were even looking at the right things. He invited Mulkey and Xinnian Chen, a UConn assistant professor-in-residence in physiology and neurobiology who specializes in biosignal processing, to examine the recordings.
“They pointed out things we at the hospital hadn’t paid any attention to. We invited them to speak at one of our conferences, and that led to a discussion with fellows, and faculty questioning if we maybe could do more with breathing patterns in babies” to help them, Hussain says.
Xinnian Chen, assistant professor-in-residence in physiology and neurobiology, looks at a graph showing the respiration pattern of an infant. (Peter Morenus/UConn Photo)
Xinnian Chen, assistant professor-in-residence in physiology and neurobiology, looks at a graph showing the respiration pattern of an infant. (Peter Morenus/UConn Photo)
Chen began carefully sifting the data, looking at records of normal breathing, of bad breathing, and most importantly at the recordings taken minutes before the start of a bad breathing episode. She was searching for subtle differences that could serve as warning signs.
What she has found so far has been suggestive. It looks like healthy breathing rhythms are similar to healthy heartbeats. Both of them have slight blips and variations here and there. Heart rhythms have been studied extensively, and cardiologists know that if a heart starts to beat too simplistically regularly, a heart attack is likely in the coming hours. With Hussain’s help, the team is gathering recordings of many more premature infants and developing an algorithm that should eventually be able to pinpoint when a baby’s breathing pattern goes south.
Sadly, the findings couldn’t help Hussain’s patient, but the researchers hope their early warning system will be able to save other infants, alerting health care providers to dangerous breathing patterns before a baby gets into serious trouble.
Source: eLife

Sunday 23 November 2014

Newspaper from Facebook may Hit Media Hard

 Newspaper from Facebook may Hit Media Hard
The ailing news media is likely to face an acid test with Facebook's move to fulfill its ambition to be the personal "newspaper" for its billion-plus members.

The huge social network has become a key source of news for many users, as part of a dramatic shift in how people get information in the digital age. 

Company founder Mark Zuckerberg told a forum in early November that his goal is to make Facebook's news feed "the perfect personalized newspaper for every person in the world." 

Zuckerberg said that while a newspaper provides the same information to every reader, Facebook can tailor its feed to the interests of the individual, delivering a mix of world news, community events and updates about friends or family. 

"It's a different approach to newspapering," said Ken Paulson, a former editor of USA Today who is now dean of communications at Middle Tennessee State University. 

"It's neither good nor bad, but it's something a traditional newspaper can't do." 

With Facebook, editorial decisions about what members see are made not by a journalist, but an algorithm that determines which items are likely to be of greatest interest to each person. 

This may concern the traditional journalism community, but even some media experts acknowledge that Facebook appears to be able to deliver more of what people want to see, in an efficient way. 

"It's intimate, it's relevant, it's extraordinarily timely and it's about you. That's more than any newspaper can do," said Alan Mutter, a former Chicago daily newspaper editor who is now a consultant for digital media ventures. 

Mutter said that as newspapers cling to their "ancient" business model, organizations like Facebook are making the news more personal. 

And he said the trend will continue as younger readers shun print in favor of digital and mobile platforms. 

- Algorithm as editor? - 

Nikki Usher, a George Washington University journalism professor specializing in new media, said Facebook configures its news feed using an algorithm taking into account tens of thousands of factors. 

"Facebook has all the data to tell you what all of your friends are reading, so you have a better chance of seeing things that you are interested in," she said. 

"The reason Facebook has so many engineers and data scientists is to continually make the algorithm better. The algorithm gets stronger as more people use it." 

Facebook is a source of news for at least 30 percent of Americans, and a major driver of traffic to news websites, according to a Pew Research Center study. 

This gives the social network enormous power over the news media, which is increasingly dependent on traffic from Facebook and other social platforms. 

Even though Facebook is known for its computer coding, it still must make editorial decisions, Usher points out. 

"What's scary is how reactive a position it puts news organizations, which are trying to guess Facebook's next move," she said. "That's a lot of power to put in a single organization." 

Facebook, Google and other tech firms jealously guard their algorithmic formulas. But observers note that a single tweak of that formula can have important consequences for news organizations. 

"News organizations are trying to build their strategy around trying to guess the algorithm, and ultimately that's a losing strategy," Usher said. 

- Getting 'soul' - 

But with traditional news media hurting, it remains unclear how the industry can support the kind of journalism needed to keep people informed as it has in the past. 

Mutter said what people read may change -- it may be sponsored or subsidized in a way that may or may not be transparent. 

"It won't necessarily be real journalism, but it will be content," he said. 

Paulson said that while Facebook can deliver much of the information from newspapers, "it would be hard pressed to capture the soul" of traditional print news. 

"Freedom of the press was established to keep an eye on people in power and inform the community," he added. "There's a tremendous public spirit component that you can't address with an algorithm." 

Paulson said that while Facebook is a useful platform for sharing, it will not underwrite the kind of investigative journalism upon which newspapers often pride themselves. With journalism retrenching, that weakens the entire democratic process. 

"We get the kind of news we deserve and are willing to pay for," Paulson added.

 Source:
 Pew Research Center 

  

Saturated Fat in Blood Does Not Increase on Doubling Saturated Fat in Diet: Study

Total levels of saturated fat in the blood are not increased on doubling or tripling saturated fat in the diet, revealed researchers.


However, increasing levels of carbohydrates in the diet during the study promoted a steady increase in the blood of a fatty acid linked to an elevated risk for diabetes and heart disease. 

The finding "challenges the conventional wisdom that has demonized saturated fat and extends our knowledge of why dietary saturated fat doesn't correlate with disease," said senior author Jeff Volek, a professor of human sciences at The Ohio State University. 

In the study, participants were fed six three-week diets that progressively increased carbs while simultaneously reducing total fat and saturated fat, keeping calories and protein the same. 

The researchers found that total saturated fat in the blood did not increase - and went down in most people - despite being increased in the diet when carbs were reduced. Palmitoleic acid, a fatty acid associated with unhealthy metabolism of carbohydrates that can promote disease, went down with low-carb intake and gradually increased as carbs were re-introduced to the study diet. 

"It's unusual for a marker to track so closely with carbohydrate intake, making this a unique and clinically significant finding. As you increase carbs, this marker predictably goes up," Volek said. 

When that marker increases, he said, it is a signal that an increasing proportion of carbs are being converted to fat instead of being burned as fuel. Reducing carbs and adding fat to the diet in a well-formulated way, on the other hand, ensures the body will promptly burn the saturated fat as fuel - so it won't be stored. 

"When you consume a very low-carb diet your body preferentially burns saturated fat," Volek said. "We had people eat 2 times more saturated fat than they had been eating before entering the study, yet when we measured saturated fat in their blood, it went down in the majority of people. Other traditional risk markers improved, as well." 

Volek and colleagues recruited 16 adults for the study, all of whom had metabolic syndrome, defined as the presence of at least three of five factors that increase the risk for heart disease and diabetes (excess belly fat, elevated blood pressure, low "good" cholesterol, insulin resistance or glucose intolerance, and high triglycerides). 

After getting them to a baseline reduced-carb diet for three weeks, researchers fed the participants the exact same diets, which changed every three weeks, for 18 weeks. The diets started with 47 grams of carbs and 84 grams of saturated fat each day, and ended with 346 carb grams per day and 32 grams daily of saturated fat. 

Each day's meals added up to 2,500 calories and included about 130 grams of protein. The highest-carb level represented 55 percent of daily calories, which roughly matches the estimated daily percentage of energy provided by carbs in the American diet. 

Compared to baseline, there were significant improvements in blood glucose, insulin and blood pressure that were similar across diets. Participants, on average, lost almost 22 pounds by the end of the trial. 

When looking at palmitoleic acid, however, the scientists found that it consistently decreased on the high-fat/low-carb diet in all participants. The fatty acid then showed a step-wise increase in concentration in the blood as carbs were progressively added to the diet. Elevated levels of palmitoleic acid in the blood have been linked to obesity and higher risk for inflammation, insulin resistance, impaired glucose tolerance, metabolic syndrome, type-2 diabetes, heart disease and prostate cancer. 

The study does not address what happens to palmitoleic acid levels when high carbs are combined with a diet high in saturated fat. Instead, Volek hoped to identify the carb-intake point at which participants began to store fat. 

Saturated Fat in Blood Does Not Increase on Doubling Saturated Fat in Diet: Study"That turned out to be highly variable," he said. "Everyone showed increased palmitoleic acid levels as carbs increased, but values varied widely between individuals, especially at the highest carb intake. This is consistent with the idea that people vary widely in their tolerance to carbohydrates." 

Participants' existing health risks were not a factor in the study because everyone ate the exact same diet for 18 weeks. Their bodies' responses to the food were the focus of the work. 

"There is widespread misunderstanding about saturated fat. In population studies, there's clearly no association of dietary saturated fat and heart disease, yet dietary guidelines continue to advocate restriction of saturated fat. That's not scientific and not smart," Volek said. "But studies measuring saturated fat in the blood and risk for heart disease show there is an association. Having a lot of saturated fat in your body is not a good thing. The question is, what causes people to store more saturated fat in their blood, or membranes, or tissues? 

"People believe 'you are what you eat,' but in reality, you are what you save from what you eat," he said. "The point is you don't necessarily save the saturated fat that you eat. And the primary regulator of what you save in terms of fat is the carbohydrate in your diet. Since more than half of Americans show some signs of carb intolerance, it makes more sense to focus on carb restriction than fat restriction." 

Volek sees this palmitoleic acid as a potential biomarker to signal when the body is converting carbs to fat, an early event that contributes to what he calls "metabolic mayhem." 

"There is no magical carb level, no cookie-cutter approach to diet, that works for everyone," he said. "There's a lot of interest in personalized nutrition, and using a dynamically changing biomarker could provide some index as to how the body is processing carbohydrates." 
 Source:The Ohio State University.

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