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Monday, 27 February 2012

Too Much Tweeting Bad for Health

Spending hours on twitter is unhealthy, says Twitter's creative director.
Biz Stone, who is also the creative director the micro-blogging site, said users should visit the site for information but leave once they had found it.
Speaking at a business conference in Montreal, Canada, Stone said that using Twitter for hours at a time "sounds unhealthy".
"I like the kind of engagement where you go to the website and you leave because you've found what you are looking for or you found something very interesting and you learned something," the Guardian quoted him as telling the Board of Trade of Metropolitan Montreal on Wednesday.
"I think that's a much healthier engagement. Obviously, we want you to come frequently," he stated.
As reported by Montreal Gazette, the social networking guru also said there were no plans to increase Twitter's 140-character limit.
Source-ANI

The animal products in your medicine cabinet

Most of us put a good deal of thought into the food we put in our bodies. But do we ever consider the food in our medicine?
That's right, the food in our medicine.
While television and print ads alike are loaded with messages about potential serious side effects, prescription drug disclaimers are issued to warn against possible unintended consequences resulting from a drug’s active ingredient(s).
But what you may not know is that the bulk of your prescription pill is made up of inactive ingredients, known as “excipients," and that your drugs couldn’t be made without them. Quite simply, excipients are what encapsulates your capsule or forms your pill into a solid as opposed to a powder.
Here’s the rub: One of the most common excipients used is gelatin, which is almost universally of animal origin. This presents a problem, as you might imagine, to those living within religious or dietary restrictions.
According to a new study released Monday in the BMJ Postgraduate Medical Journal, 43.2% of the study population “would prefer not to take animal product-containing medication, even if no alternative were available.” 500 people participated in the study.
Of the study participants with dietary restrictions, 88% said they would prefer to take oral medication containing only vegetable products. Of the patients who preferred vegetarian-only treatment, 85.2% said they would not take any oral medication which contained animal products, though more than half said they would do so if no alternatives were available.
Perhaps most surprising, less than a quarter of those patients with dietary restrictions specifically asked the doctor who prescribed the drug or the pharmacist who dispensed it about its composition.
Previous studies have shown that doctors do not regularly discuss a medication's inactive ingredients with their patients, and very few patients think to ask.
Of the participants who were surveyed, those who followed a Halal diet and those who designated themselves as pure vegetarian/vegan were far more like to ask about a drug’s constituents than those who avoided only certain animal foods, such as chicken, beef, or pork.
The data from the study shows that the majority of the people who were surveyed found it completely acceptable that their medications contained gelatin, an animal by-product. But if it's important for you to know and to control exactly what food is entering your body, the takeaway here is simple: ask your doctor - or your pharmacist.
Source:CNN

Sunday, 26 February 2012

Report: Women have rare egg-producing stem cells

For 60 years, doctors have believed women were born with all the eggs they'll ever have. Now Harvard scientists are challenging that dogma, saying they've discovered the ovaries of young women harbor very rare stem cells capable of producing new eggs.
If Sunday's report is confirmed, harnessing those stem cells might one day lead to better treatments for women left infertile because of disease — or simply because they're getting older.
"Our current views of ovarian aging are incomplete. There's much more to the story than simply the trickling away of a fixed pool of eggs," said lead researcher Jonathan Tilly of Harvard's Massachusetts General Hospital, who has long hunted these cells in a series of controversial studies.
Tilly's previous work drew fierce skepticism, and independent experts urged caution about the latest findings.
A key next step is to see whether other laboratories can verify the work. If so, then it would take years of additional research to learn how to use the cells, said Teresa Woodruff, fertility preservation chief at Northwestern University's Feinberg School of Medicine.
Still, even a leading critic said such research may help dispel some of the enduring mystery surrounding how human eggs are born and mature.
"This is going to spark renewed interest, and more than anything else it's giving us some new directions to work in," said David Albertini, director of the University of Kansas' Center for Reproductive Sciences. While he has plenty of questions about the latest work, "I'm less skeptical," he said.
Scientists have long taught that all female mammals are born with a finite supply of egg cells, called ooctyes, that runs out in middle age. Tilly, Mass General's reproductive biology director, first challenged that notion in 2004, reporting that the ovaries of adult mice harbor some egg-producing stem cells. Recently, Tilly noted, a lab in China and another in the U.S. also have reported finding those rare cells in mice.
But do they exist in women? Enter the new work, reported Sunday in the journal Nature Medicine.
First Tilly had to find healthy human ovaries to study. He collaborated with scientists at Japan's Saitama Medical University, who were freezing ovaries donated for research by healthy 20-somethings who underwent a sex-change operation.
Tilly also had to address a criticism: How to tell if he was finding true stem cells or just very immature eggs. His team latched onto a protein believed to sit on the surface of only those purported stem cells and fished them out. To track what happened next, the researchers inserted a gene that makes some jellyfish glow green into those cells. If the cells made eggs, those would glow, too.
"Bang, it worked — cells popped right out" of the human tissue, Tilly said.
Researchers watched through a microscope as new eggs grew in a lab dish. Then came the pivotal experiment: They injected the stem cells into pieces of human ovary. They transplanted the human tissue under the skin of mice, to provide it a nourishing blood supply. Within two weeks, they reported telltale green-tinged egg cells forming.
That's still a long way from showing they'll mature into usable, quality eggs, Albertini said.
And more work is needed to tell exactly what these cells are, cautioned reproductive biologist Kyle Orwig of the University of Pittsburgh Medical Center, who has watched Tilly's work with great interest.
But if they're really competent stem cells, Orwig asked, then why would women undergo menopause? Indeed, something so rare wouldn't contribute much to a woman's natural reproductive capacity, added Northwestern's Woodruff.
Tilly argues that using stem cells to grow eggs in lab dishes might one day help preserve cancer patients' fertility. Today, Woodruff's lab and others freeze pieces of girls' ovaries before they undergo fertility-destroying chemotherapy or radiation. They're studying how to coax the immature eggs inside to mature so they could be used for in vitro fertilization years later when the girls are grown. If that eventually works, Tilly says stem cells might offer a better egg supply.
Further down the road, he wonders if it also might be possible to recharge an aging woman's ovaries.
The new research was funded largely by the National Institutes of Health. Tilly co-founded a company, OvaScience Inc.,to try to develop the findings into fertility treatments.
Source:AP

Pioneering lab work aims to smash women's fertility barrier

An experiment that produced human eggs from stem cells could one day be a boon for women who are desperate to have a baby, according to a study published on Sunday.
The work sweeps away the belief that a woman has only a limited stock of eggs and replaces it with the theory that the supply is continuously replenished from precursor cells in the ovary, its authors said.
"The prevailing dogma in our field for the better part of the last 50 or 60 years was that young girls at birth were given a bank account of eggs at birth that's not renewable," said Jonathan Tilly, director of the Vincent Center for Reproductive Biology at Massachusetts General Hospital, who led the research.
"As they become mature and become a woman, they use those eggs up (and) the ovaries will fail when they enter menopause."
Tilly first challenged the "bank account" doctrine eight years ago, suggesting female mammals continue producing egg-making cells into adulthood rather than from a stock acquired at birth.
His theory ran into a firestorm.
Other scientists challenged the accuracy of his experiments or dismissed their conclusions as worthless, given that they had only been conducted on lab mice.
But the new work, said Tilly, not only confirms his controversial idea, but takes it farther.
In it, his team isolated egg-producing stem cells in human ovaries and then coaxed them into developing oocytes, as eggs are called.
Building on a feat by Chinese scientists, they pinpointed the oocyte stem cells by using antibodies which latched onto a protein "handle" located on the side of these cells.
The team tagged the stem cells with a fluorescent green protein -- a common trick to help figure out what happens in lab experiments.
The cells were injected into biopsied human ovarian tissue which was then grafted beneath the skin of mice.
Within 14 days, the graft had produced a budding of oocytes. Some of the eggs glowed with the fluorescent tag, proving that they came from the stem cells. But others did not, which suggested they were already present in the tissue before the injection.
Tilly said "the hairs were standing up on my arm" when he saw time-elapse video showing the eggs maturing in a lab dish.
Further work needs to be done to test the viability of the eggs, and little is known about the hormones or other mechanisms by which oocytes emerge from the stem cells.
But the impact could be far-reaching, Tilly said.
"If we can guide the process correctly, I think it opens up a chance that sometime in the future, we might get to the point of actually having an unlimited source of human eggs," Tilly said in a video recording released to the press.
"A woman could come in, have a small biopsy taken from her ovary for us to retrieve these cells. Once we get these cells out, we can take a hundred of them and make a million of them.
"If we can get to the stage of generating functional human eggs outside the body, it would rewrite essentially human assisted reproduction."
According to a press release issued by Massachusetts General Hospital, Tilly's team are already exploring the idea of banks where oocyte stem cells can be frozen and stored, and then retrieved when a woman wants to have a baby.
Human eggs are extremely delicate and likely to suffer damage when frozen and thawed, but this risk does not apply to the egg cells that make them, it said.
Previous work has shown that around one in 10 women of reproductive age is at risk of premature ageing of the ovaries, a finding with repercussions in societies where women opt ever later to become mothers.
Source:AFP

CCHMC scientists develop a unique compound that stops disease-fuelling inflammation in lab tests

Scientists from Cincinnati Children’s Hospital Medical Center (CCHMC) have developed a unique compound that in laboratory tests blocks inflammation-causing molecules in blood cells known to fuel ailments like cancer and cardiovascular disease without causing harmful toxicity.
Past attempts to identify new compounds that tamp down so-called reactive oxygen species (ROS) molecules in cells have been complicated by toxicity issues and a lack of specificity in targeting molecular processes. Researchers from Cincinnati Children’s Hospital Medical Center report in the February 24 Chemistry & Biology (a Cell Press publication) they have overcome this problem.
They did so by using computer-assisted drug design – verified by laboratory tests on human and mouse inflammatory cells – to precisely target a single component of an enzyme network called NOX2. The enzyme network drives ROS production in immune system white blood cells known as neutrophils. The eventual goal, researchers say, is establishing new small-molecule inhibiting drugs that can stop excessive inflammation and treat a number of inflammation-mediated diseases that need improved therapies.
“Drugs that potently and specifically target ROS production by NOX2 enzyme are an unmet clinical need that will have far-reaching implications for treatment of disease,” said Yi Zheng, PhD, a lead investigator on the study and director of Experimental Haematology/Cancer Biology at Cincinnati Children’s. “The lead candidate we developed, Phox-I, shows promising inflammation inhibiting activity in cells and mouse models.”

The production of ROS in cells is a normal part of the body’s immune system, as oxidative enzymes are generated by white blood cells to attack illness-causing microorganisms. In a number of pathologic conditions, however, various environmental stressors (like acute ischemia, chronic infections, etc.) can help trigger an overabundance of biochemical signalling. The signaling occurs through a regulatory pathway involving Rac GTPases, a family of intracellular signal transducers that amplify ROS production by the NOX2 enzyme network.

Normally, Rac GTPases maintain cell growth and survival programs in the body, including the NOX enzyme network and its activation of ROS production in cells. When signalling miscues occur they cause an unusually high burst of ROS production and release harmful superoxide chemicals. This up-regulation creates excessive inflammation that damages tissues and drives the onset of diseases like Chronic Obstructive Pulmonary Disease, ischemia-induced lung and brain damage and hypertension, among others.
Previous attempts to create compounds that target and stop harmful ROS production, including an earlier compound developed by Dr. Zheng’s laboratory, have been able to reduce inflammation in cells. Unfortunately, the compounds were not specific or efficient enough in targeting the Rac GTPase regulatory pathway. This meant the compounds inhibited several different cellular processes – including some that are necessary and beneficial – leading to toxicity.
Zheng and his colleagues achieved greater specificity and efficiency through their design of small molecular inhibitors they named Phox-I1 and Phox-I2. The inhibitors precisely target and block the binding of a signal sensor for the NOX2 enzyme called p67-phox to Rac GTPase. P67-phox has to bind with Rac GTPase to activate the oxidase enzyme complex of NOX2 (known as NADPH) that produces superoxide and causes inflammation.
In laboratory tests involving normal human blood cells, leukaemic cells and mouse blood cells, Phox-l1blocked p67-phox binding with Rac. It did so in a dose-dependent manner with enough precision to shut down ROS production without causing unwanted toxicity in the cells, the researchers report. In unpublished test results on mouse models of lung inflammation, Zheng said the investigators found that the Phox-I lead compounds are effective in blocking neutrophil mediated inflammation and damage.
The results are part of a patient application filed by Cincinnati Children’s with the United States Patent Office for Phox-I inhibitors. The medical centre’s Center for Technology Commercialization is exploring opportunities to rapidly advance continuing research and development of the compounds that could possibly accelerate their transition to future clinical testing.
Zheng said that although the study data describe an innovative approach that shows promise, a significant amount of additional research is needed before the Phox-I can be tested in humans. The research team continues to experiment with structural alterations to Phox-I to make the compounds more potent in inhibiting excessive ROS and superoxide production without being toxic to normal cells. Researchers are also expanding their tests in mouse models to see how effective the compounds are in safely shutting down the onset of simulated human diseases caused by inflammation.
The research was funded by an innovation grant from CincyTech USA, and a National Institutes of Health Small Business Technology Transfer Grant.
Source:Pharmabiz

`2`, Forever the Loneliest

People living alone are perhaps happier and more socially active in comparison to their cohabiting counterparts, suggests a new research.
A new book, Going Solo - The Extraordinary Rise and Surprising Appeal of Living Alone by Eric Klinenberg, argues that rather than the single-individual householder being "sad, lonely old baby boomers" as demographer Bernard Salt put it, we are increasingly learning to fly solo and, in the process, devising new ways of living.
"Today the majority of people who live alone are actually more socially active with friends and neighbours than their married counterparts," the Sydney Morning Herald quoted Klinenberg, a Professor of Sociology at New York University as saying.
"They do get lonely sometimes, but the people I interviewed said that there's nothing lonelier than living with the wrong person," he stated.
Klinenberg conducted more than 300 in-depth interviews of 'singletons' (his term) across all ages and classes in the US and came to the conclusion that this way of life can help us discover things about ourselves as well as appreciate the pleasure of good company.
"Living in a city makes it much easier for singletons to get out into the public realm and contribute to the common good," he explained.
He found that those living solo are more likely to eat out, exercise, attend extracurricular classes, public events and lectures, and volunteer.
It's a way of living that is growing at an unprecedented rate.
The Australian Bureau of Statistics estimate that by 2031, 3.6 million people will live in lone person households.
Klinenberg puts the growing trend down to a four major factors.
"The rising status of women has been essential to the change, because their economic independence and personal freedom allowed women to delay marriage or escape failing ones," he noted.
"Then there's the communications revolution, beginning with the telephone and continuing to Facebook and Skype, because these technologies allow people to be connected even while they're home alone.
"Urbanisation is a third force, because it created booming subcultures of singles who live alone, together in particular urban neighbourhoods throughout the world. Finally, there's the longevity revolution, which has made ageing alone a common experience too," he added.
In his research, Klinenberg learned that people go solo at all stages of life.
But he was surprised to find that the fastest-growing group of singletons is people under 35.
It seems the lure of shared households - where bills are itemised and fought over and food sometimes labeled in the fridge - is an option that no longer appeals. As the song goes 'Two can be as bad as one, it's the loneliest number since the number one.'
Source-ANI

How Cancer Cells Change Once They Spread to Other Areas in the Body

Cancer cells must transform themselves so they can detach from a tumor before spreading to a distant organ.Now, scientists at Weill Cornell Medical College have revealed critical steps in what happens next -- how these cells reverse the process, morphing back into classical cancer that can now grow into a new tumor.
Their findings, now published online and in a upcoming issue of Cancer Research and funded through a National Cancer Institute grant to the Cornell Center on the Microenvironment and Metastasis and the Neuberger Berman Foundation, show that a single protein, versican, is key to this process in breast cancer, the tumor they studied. When researchers stopped versican from functioning in mice, breast cancer could not "seed" themselves into the lungs and form secondary tumors.
"Our findings both help us understand how breast cancer metastasizes to the lungs and ways to possibly prevent that deadly spread," says the study's senior investigator, Dr. Vivek Mittal, an associate professor of cell and developmental biology in cardiothoracic surgery and director of the Neuberger Berman Lung Cancer Laboratory at Weill Cornell Medical College.
"These are exciting insights into a poorly investigated area," Dr. Mittal says. "There are no clinically approved drugs now that can effectively target metastatic lesions, which is why more than 90 percent of human cancer-related deaths come from spread of the disease from a primary tumor."
"The results of this study are a critical step in deconstructing the process of metastases -- which is critical to curing our patients," says co-author Dr. Linda T. Vahdat, professor of medicine, chief of the Solid Tumor Service and director of the Breast Cancer Research Program at Weill Cornell. "As a direct result of this study, we are working on ways to interrupt the process by which tumors co-opt the infrastructure in our bodies to grow and spread."
This important study starts to unravel the mechanistic basis of cancer metastases, not only in breast cancer but possibly in other types of cancer, says Dr. Nasser Altorki, the David B. Skinner Professor of Thoracic Surgery at Weill Cornell Medical College and director of the division of thoracic surgery at NewYork-Presbyterian/Weill Cornell. "The need for a prepared and receptive soil may be required for cancer cell seeding regardless of the primary cancer's site of origin."
The Seed and the Soil
Cancer researchers have believed that for a cancer to spread, its "seed" must find the right "soil" in a distant organ in order to thrive. And they have hypothesized that this seed is formed through a process known as epithelial-mesenchymal transition (EMT), in which cancer cells lose their sticky grip to other cells in a primary tumor and become more mobile, able to travel through the blood to a distant organ.
But what happens next is conjecture. Scientists have speculated that the cells undergo a reverse process, called mesenchymal-epithelial transition (MET), in which the cancer seeds morph back into epithelial cells that can make contact with tissue and integrate in the new organ. Little is known about MET compared to EMT.
In this study, Dr. Mittal, along with his colleagues at Weill Cornell, studied mouse models of spontaneous breast cancer development. They first discovered that primary breast tumors send a signal that forces bone-marrow-derived hematopoietic cells to move into the lungs of the mice. "This appears to be the soil the cancer seeds need," says Dr. Mittal. The next question was obvious: What is it about the soil that helps the seed?
The team found that a subtype of these bone marrow cells expressed versican, which allowed the cancer cells, once they traveled to the lungs, to morph back into epithelial cells. "The primary tumor sets up the lung microenvironment to promote metastasis," he says. "MET resulted not from properties within the cancer cell itself, but due to a unique crosstalk between the microenvironment and tumor cells in the lung."

In their next experiment, the researchers blocked versican production by injecting small interfering RNAs (siRNAs) in the bone marrow that silenced the versican gene, which prevented MET and blocked tumor outgrowth in the lung.
Human Tumors Express Versican
Next, they investigated human breast metastases to the lung, utilizing lung samples obtained from breast cancer patients contributed by researchers at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University. "We found versican was highly expressed in those lung tumors, which matched what we found in our mice," Dr. Mittal says. "This all made sense to us, because versican has been linked to cancer progression, although no one knew why.
"This is the first study demonstrating the significance of MET in the formation of macrometastases in distant organs," Dr. Mittal says. "Given the findings, we now have a potential strategy to stop cancer spread before it starts, or to shut it down if it has already occurred."
Source-Eurekalert

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