Doctors make progress toward 'artificial pancreas'

Doctors are reporting a major step toward an "artificial pancreas," a device that would constantly monitor blood sugar in people with diabetes and automatically supply insulin as needed.
A key component of such a system — an insulin pump programmed to shut down if blood-sugar dips too low while people are sleeping — worked as intended in a three-month study of 247 patients.
This "smart pump," made by Minneapolis-based Medtronic Inc., is already sold in Europe, and the U.S. Food and Drug Administration is reviewing it now. Whether it also can be programmed to mimic a real pancreas and constantly adjust insulin based on continuous readings from a blood-sugar monitor requires more testing, but doctors say the new study suggests that's a realistic goal.
"This is the first step in the development of the artificial pancreas," said Dr. Richard Bergenstal, diabetes chief at Park Nicollet, a large clinic in St. Louis Park, Minn. "Before we said it's a dream. We have the first part of it now and I really think it will be developed."
He led the company-sponsored study and gave results Saturday at an American Diabetes Association conference in Chicago. They also were published online by the New England Journal of Medicine.
The study involved people with Type 1 diabetes, the kind usually diagnosed during childhood. About 5 percent of the 26 million Americans with diabetes have this type. Their bodies don't make insulin, a hormone needed to turn food into energy. That causes high blood-sugar levels and raises the risk for heart disease and many other health problems.
Some people with the more common Type 2 diabetes, the kind linked to obesity, also need insulin and might also benefit from a device like an artificial pancreas. For now, though, it's aimed at people with Type 1 diabetes who must inject insulin several times a day or get it through a pump with a narrow tube that goes under the skin. The pump is about the size of a cellphone and can be worn on a belt or kept in a pocket.
The pumps give a steady amount of insulin, and patients must monitor their sugar levels and give themselves more insulin at meals or whenever needed to keep blood sugar from getting too high.
A big danger is having too much insulin in the body overnight, when blood-sugar levels naturally fall. People can go into comas, suffer seizures and even die. Parents of children with diabetes often worry so much about this that they sneak into their bedrooms at night to check their child's blood-sugar monitor.
In the study, all patients had sensors that continuously monitored their blood sugar. Half of them had ordinary insulin pumps and the others had pumps programmed to stop supplying insulin for two hours when blood-sugar fell to a certain threshold.
Over three months, low-sugar episodes were reduced by about one-third in people using the pump with the shut-off feature. Importantly, these people had no cases of severely low blood sugar — the most dangerous kind that require medical aid or help from another person. There were four cases in the group using the standard pump.
"As a first step, I think we should all be very excited that it works," an independent expert, Dr. Irl Hirsch of the University of Washington in Seattle, said of the programmable pump.
The next step is to test having it turn off sooner, before sugar falls so much, and to have it automatically supply insulin to prevent high blood sugar, too.
Dr. Anne Peters, a diabetes specialist at the University of Southern California, said the study "represents a major step forward" for an artificial pancreas.
One participant, Spears Mallis, 34, a manager for a cancer center in Gainesville, Ga., wishes these devices were available now. He typically gets low-sugar about 8 to 10 times a week, at least once a week while he's asleep.
"I would set an alarm in the middle of the night just to be sure I was OK. That will cause you to not get a good night of rest," he said.
His "smart pump" stopped giving insulin several times during the study when his sugar fell low, and he wasn't always aware of it. That's a well-known problem for people with Type 1 diabetes — over time, "you become less and less sensitive to feeling the low blood sugars" and don't recognize symptoms in time to drink juice or do something else to raise sugar a bit, he said.
Besides Medtronic, Johnson & Johnson and several other research groups are working on artificial pancreas devices.

Source: AP

Health ministry to introduce medical electronics & devices bill in Parliament soon

The Ministry of Health & Family Welfare has proposed a new Bill bifurcating medical electronics and devices as separate entities from drugs. The new Bill will be presented in Parliament soon and once enacted as law it will give medical devices sector a new lease of life.
This was disclosed by Dr A K Panda, joint secretary, Ministry of Health & Family Welfare. He was addressing the global congress on ‘Investment Opportunities in Medical Electronics & Devices’ organised by FICCI recently in association with the Ministry of Health and Family Welfare on the theme ‘Harnessing Medical Technology for Inclusive Healthcare in India’.
The biggest challenge that the medical devices sector faces is in the realm of regulation as the Drug & Cosmetics (D&C) Act, 1940 does not define medical device anywhere in the Act. Hence, medical devices are currently notified as drugs under the current framework of the law. Therefore, all the attending rules and regulations of the D&C Act, which were designed for drugs (pharmaceuticals), were applicable to these medical devices, he said.
Dr Panda said that for the first time in the 12th Plan, the Government of India has allocated Rs.1800 crore to extend financial support to states and UTs to strengthen the regulatory system of medical electronics and devices in the country. The major part of this grant will be spent on procuring technically qualified manpower and establishing more laboratories, training academies, diagnostic labs, and capacity building.
He also proposed that an institutional mechanism should be set up where on a regular basis the relevant stakeholders from the sector could come together and deliberate on the latest developments in the medical devices field and also discuss the challenges and issues that arise with the fast changing technology.
India’s medical devices market is of almost $3 billion and is growing at a rate of 15 per cent. Hence the growth potential is immense and now healthcare is also a top priority for the government, said Dr Gautam Khanna, chairman, FICCI Medical Device Forum & executive director – Healthcare, 3M.
“Technology is making healthcare more accessible and popular. We also need to spread awareness about non-communicable diseases and PPP solutions must be explored further to strengthen the sector. The government has already launched few programmes in this regard but a greater push is needed,” Khanna added.
Sanjay Banerjee, co-chair, FICCI MDF & MD, Zimmer India, said there was an urgent need to address the issue of legislation and it was encouraging for the sector to know that the Ministry of Health & Family Welfare has proposed a new Bill in this regard in Parliament.
Dr A Didar Singh, secretary general, FICCI, said that India lacked technology and investment in this sector. “We should import technology from abroad and also look for ways to acquire investments from overseas. Then medical equipments and devices could be produced and manufactured in India and the cost of healthcare will eventually come down,” he added.

Source:Pharmabiz

Men Who Can't Produce Sperm Face Greater Cancer Risk: Study

Men who fail to produce sperm are more prone to developing cancer than the general population, says study. And a diagnosis of azoospermia before age 30 carries an eight-fold cancer risk, the study says.
"An azoospermic man's risk for developing cancer is similar to that for a typical man 10 years older," said Michael Eisenberg, MD, PhD, assistant professor of urology at the medical school and director of male reproductive medicine and surgery at Stanford Hospital & Clinics. Eisenberg is lead author of the study, which will be published online June 20 in Fertility and Sterility. Diagnoses of male infertility and azoospermia are surprisingly common in the United States. About 4 million American men — 15 percent of those ages 15-45 — are infertile. Of these, some 600,000 — about 1 percent of those of reproductive age — are azoospermic. "There is evidence that infertility may be a barometer for men's overall health," Eisenberg said, "and a few studies have found an association of male infertility with testicular cancer." The new study, he said, not only assigns the bulk of infertile men's increased cancer risk to those with azoospermia, but also suggests that this risk extends beyond testicular cancer. 
Eisenberg conducted most of the analysis for the study at Stanford, using data gathered from the Texas Cancer Registry and the Baylor College of Medicine in Houston, where he completed his medical training. The study's senior authors are Larry Lipshultz, MD, and Dolores Lamb, PhD, professors of urology at Baylor. 
The study population consisted of 2,238 infertile men who were seen at a Baylor andrology clinic from 1989 to 2009. Their median age was 35.7 when they were first evaluated for the cause of their infertility. Of those men, 451 had azoospermia, and 1,787 did not. There were otherwise no apparent initial differences between the two groups. 
Azoospermia can arise for two reasons. Obstructive azoospermia is caused by a blockage that prevents otherwise plentiful, fit sperm produced in the testes from reaching the ejaculate. But a screen of about one-fourth of the azoospermic men in the study population indicated that the vast majority suffered from the non-obstructive variety: Their testes didn't produce enough sperm for any to reach their ejaculate, most likely because of genetic deficiencies of one sort or another. Fully one-fourth of all the genes in the human genome play some role in reproduction, Eisenberg noted, so there are a lot of ways for the capacity to sire offspring to go astray. 
After undergoing a semen analysis, the men were followed for an average of 6.7 years to see which of them turned up in the Texas Cancer Registry. (Fortunately for the analysis, most people tend to stay in the state where they've grown up, said Eisenberg.) Their rates of diagnosed cancer incidence were then compared with age-adjusted cancer-diagnosis statistics of Texas men in general. 
In all, a total of 29 of the 2,238 infertile men developed cancer over a 5.8-year average period from their semen analysis to their cancer diagnosis. This contrasted with an expected 16.7 cases, on an age-adjusted basis, for the male Texas population in general (which, Eisenberg said, closely reflects cancer incidence rates for the entire U.S. population). This meant that infertile men were 1.7 times as likely to develop cancer as men in the general population. This is considered a moderately increased risk. 
But comparing the cancer risk of azoospermic and nonazoospermic infertile men revealed a major disparity: The azoospermic men were at a substantially elevated risk — nearly three times as likely to receive a diagnosis of cancer as men in the overall population. Infertile men who weren't azoospermic, in contrast, exhibited a statistically insignificant increased cancer risk of only 1.4 times that of men in the overall population. 
By excluding men whose cancer diagnosis came within two or three years of their infertility evaluation, the researchers were able to rule out the possibility that azoospermia caused by an undiagnosed cancer had affected the statistics. 
While the study wasn't large enough to delineate which specific types of cancer pushed azoospermic men's incidence rates up, the diagnoses they received covered a wide range of cancers: brain, prostate and stomach tumors, as well as melanoma, lymphoma, testicular cancer and cancer of the small intestine. The findings suggest that genetic defects that result in azoospermia may also broadly increase a man's vulnerability to cancer, Eisenberg said, supporting the notion that azoospermia and cancer vulnerability may share common genetic causes. 
The study, which was funded by the National Institute for Child Health and Human Development, is the first to examine the cancer risk of azoospermia in particular, or to link it to non-germ-cell cancers. Previous studies have failed to consistently identify any increased risk for nontesticular cancers in infertile men, whether azoospermic or otherwise. In those previous studies, however, azoospermic men couldn't be separately examined because sperm analyses weren't available. 
Most striking of all, said Eisenberg, was the cancer risk among azoospermic men who first had their semen analyzed before age 30. They were more than eight times as likely to subsequently develop cancer than Texas males in the general population of the same age. In contrast, there was no relationship between age of semen analysis and risk of cancer for nonazoospermic men. 
The good news, Eisenberg said, is that while the cancer risk among young azoospermic men was quite large compared to their same-age peers, their relative youth means that their absolute risk of contracting cancer during the follow-up period remained small. The bad news, he said, is that men in their 30s often don't have a primary health-care provider. He advised that young men who are diagnosed as azoospermic should be aware of their heightened risk and make sure to get periodic checkups with that in mind. 
SOURCE:Fertility and Sterility. 

 
 

Study Shows How Memories are Stored in the Brain

A new way to see where and how memories are stored in the brain has been developed by a team of scientists.

 The team, led by Don Arnold and Richard Roberts of USC, engineered microscopic probes that light up synapses in a living neuron in real time by attaching fluorescent markers onto synaptic proteins - all without affecting the neuron's ability to function. 
The fluorescent markers allow scientists to see live excitatory and inhibitory synapses for the first time - and, importantly, how they change as new memories are formed. 
The synapses appear as bright spots along dendrites (the branches of a neuron that transmit electrochemical signals). 
As the brain processes new information, those bright spots change, visually indicating how synaptic structures in the brain have been altered by the new data. 
"When you make a memory or learn something, there's a physical change in the brain. It turns out that the thing that gets changed is the distribution of synaptic connections," Arnold, associate professor of molecular and computational biology at the USC Dornsife College of Letters, Arts and Sciences, and co-corresponding author, said. 
The probes behave like antibodies, but bind more tightly, and are optimized to work inside the cell - something that ordinary antibodies can't do. 
To make these probes, the team used a technique known as "mRNA display," which was developed by Roberts and Nobel laureate Jack Szostak. 
The research is set to be published in the journal Neuron.
Source-ANI
 

Good Laugh can Boost Sex Life

Laughter can boost your sex life and help you live longer, say experts. 
Psychologist Stephanie Davies said that it's also the key to looking young and losing weight.Her book 'Laughology: Improve Your Life With The Science Of Laughter' is out on June 27 and reveals the many ways in which laughter can improve your life, the Sun reported. There is nothing sexier than someone who can make you laugh. Why do you think Russell Brand has ladies queuing up to become his next conquest? 
But laughter and humour are much more than aphrodisiacs. Studies have shown that they have a profound effect on our brains and bodies. 
They can make us healthier, they can help us make better decisions and they can help us cope with challenges. 
Laughter floods our brains with special chemicals - "happy hormones" that make us more positive, outgoing and sociable. 
Laughter and humour have also been shown to make us fitter and even look younger. 
A good belly-laugh gives our bodies a workout and if you dose yourself up on laughter and happiness, you can even shed pounds. 
Research has discovered that laughing hard for just ten or 15 minutes a day can help you shed several pounds a year. 
Laughter activates muscles around the body, from the tummy to the shoulders, and other studies have shown that a good laugh has the similar effect of a ten-minute session on a rowing machine. 
A study in the US also found that people who watched funny movies showed changes in levels of hormones regulating their appetite. 
Laughter also works on the mechanisms in the brain that make us eat too much of the wrong things. 
There is a major link between our emotions and the food choices we make. 
Many of us turn to chocolate or junk food when we are down, tired or stressed. We call it comfort eating. 
Laughter can act as a distraction to the cravings we experience before reaching for the Dairy Milk because it causes the brain to release serotonin, a hormone sometimes described as nature's appetite suppressant. 
This powerful chemical curbs cravings and makes you feel satisfied even if your stomach isn't full. 
Laughter is the best anti-ageing secret there is. 
It increases blood flow to the face, makes eyes sparkle and reduces stress, which has an effect on skin tone and its elasticity. 
The less stressed you are, the clearer your skin and the fewer wrinkles you get.
Source-ANI  

Must Know Top Ten Interesting Facts on Antioxidants

1. Antioxidants prevent cell destructions caused by the action of free radicals. Free radicals are unstable molecules that take away electrons from other molecules and damage them. This is the cause for many diseases.

2. Do you wonder how antioxidants work to prevent diseases? Antioxidants donate electrons to free radicals to stabilize them and this prevents free radicals from invading other cells and causing diseases.

3. Antioxidants play a vital role in anti-aging and keep you young.

4. Antioxidants protect you against heart disease, cancer and other diseases.

5. Your body can produce antioxidant enzymes on its own, which work along with the antioxidants that come with the food you eat.

6. Antioxidant defense system is the major reason why humans live longer than other living creatures.

7. Vitamin E is the powerful antioxidant commonly found in nuts, fortified cereals and sweet potatoes and it helps decrease the development of age-related macular degeneration and cataract.

8. Drinking 2 glasses of tomato juice a day fulfils your lycopene requirement. Lycopene, a powerful antioxidant is also present in watermelons, pink-grapefruits, apricots and pink-guavas.

9. Spices are highly rich in antioxidant content among all the food categories.

10. High beta-carotene intake may shoot up the risk for lung cancer in smokers; Increase in vitamin E intake may raise the risks of prostate cancer and a type of stroke.

References:
1. http://www.nlm.nih.gov/medlineplus/antioxidants.html
2. http://www.cancer.gov/cancertopics/factsheet/prevention/antioxidants
3. http://nccam.nih.gov/health/antioxidants/introduction.htm
4. http://www.aoa.org/x11817.xml
5. http://www.jacn.org/content/19/5/563.full
 

Are You Happy or Horny? A Brain Scan Can Tell

What are you feeling?  For the first time, a brain scan might be able to answer that question.
It’s not exactly mind reading, but a new program can identify emotional states— from happiness to sadness, lust to disgust— simply by analyzing brain activity, according to a recent study.
The technique isn’t just a parlor game; since emotional disturbances lie at the center of most psychiatric problems, a reliable way to detect feelings from brain scans could help researchers to better understand what goes wrong in cases of depression, autism, schizophrenia, anxiety disorders and many other conditions, as well as offer new insight into how emotions work.
The brain images represent the first time that scientists can “find neural signatures of different emotions,” says Karim Kassam, they study’s lead author and assistant professor of social and decision sciences at Carnegie Mellon University.
The research, which was published in the journal PLoS One, involved 10 method acting students, mainly women, who were part of the the Carnegie Mellon Drama Community at that university in Pittsburgh.  Method acting teaches students to embody the emotions of a character, fully immersing themselves in the experience by relying on personal feelings as a guide, so the scientists were confident that the students asked to display specific emotions would actually be feeling them.
Before having their brains scanned, the actors were asked to write scenarios so they could quickly evoke feelings generated by 18 words designating nine emotions: anger, disgust, fear, lust, happiness, pride, shame, envy and sadness. The actors also wrote a calm scenario that they used as a control when they were instructed not to act out intense feelings.
The volunteers were then placed in a scanner that recorded their brain activity as they saw the emotion-related words, flashed one at a time on a screen. After each appeared, each student had nine seconds to act out the emotion mentally, increasing its intensity over time. Afterward, they rated how deeply they had actually been able to feel the appropriate emotion. Each actor conducted multiple trials of each emotion.
To determine whether the acting differed substantially from actually feeling the emotion, the scientists also flashed 24 images, half of which were disgusting, the rest neutral, across the participants’ screens. The actors seemed to be pretty good at their method acting exercise, since their brains registered similar activity when viewing the disgusting images as when they were acting disgusted.
Based on the data collected on a particular actor’s brain activity, the scientists then developed an algorithm for predicting which patterns were related to which feelings. Around 84% of the time, the computer’s first guess as to what emotion was being displayed was correct, showing that individuals have predictable brain signatures for what they are feeling. These exact signatures may not be shared, however, since the program was less successful at predicting one person’s emotions by using data from other people’s scans. (It still performed better than chance, however, getting it right on the first time 71% of the time on average.) “Everyone feels like they understand anger, sadness or happiness and they think that they can define emotion, but it turns out to be very difficult to define and there’s not even a scientific consensus,” Kassam says.
What distinguished the varying feelings? Four factors emerged from the data. The most important involved whether the emotion was positive or negative. Positive valence made it highly unlikely that the computer would mistake happiness for shame or sadness for pride — indeed, those were the least likely mistakes it made. Arousal also played a role. “Sometimes we’re very energetic and sometimes we’re sluggish: anger looks very different from sadness on a dimension like arousal,” Kassam explains. An emotion’s social relevance also separated them — anger or envy, for instance, generally involves others while disgust is frequently more solitary.
Finally, the researchers say that lust appears to have a brain profile all its own, distinct from other emotions and therefore unlikely to be misread by the computer. “Lust looks like neither positive nor negative emotions,” Kassam says. The images showed that there were brain regions that were only activated by sexual desire. Why? Lust may stand out because of its critical role in reproduction — or because it can be either desirable or not, depending on the situation.  For example, lust may be perfectly pleasant when experienced at home with one’s spouse— but excruciatingly embarrassing and uncomfortable in other settings, especially when directed at inappropriate targets.
MORE: Scientists Predict Weight Gain and Sexual Activity by Peeking at the Brain
“[The study] basically shows that the differences between the emotions seem to be driven by valence, arousal, and social factors, along with their interesting lust factor,” says Russell Poldrack, professor of psychology and neuroscience at the University of Austin in Texas, who was not associated with the work. “There is nothing new about this, but these results are a nice confirmation, given that they didn’t design the study to find those factors but they instead fell out of the data.”
The fact that emotions may have some predictable brain signatures may also offer insight into how these emotions are formulated and, potentially, how they might be altered in cases of disease. “These results are important because it hasn’t been possible yet to move toward brain predictions of what people are feeling,” says Tor Wager, associate professor of neuroscience at the University of Colorado in Boulder, who was not associated with the research.  “It’s tremendously important for psychiatry because we have had not had markers for emotional processing and it is disturbed in virtually every psychiatric disorder and in some neurological diseases like Parkinson’s.”
MORE: Brain Scans Can Predict Which Criminals Are Likely to Get Re-Arrested
Emotions are also critical for many basic cognitive functions that we don’t often association with feelings. Some experts argue, for example, that emotions are biological programs for decision making, evolved to guide animals to make the best choices for successful survival and reproduction. They note that even the most apparently “rational” choice involves emotion because making a “good” choice requires seeing one option as preferable and preference involves desire. (This may be why depressed people so often have difficulty taking action:  if everything seems equally bleak, making a choice can become impossible.)
More research will be needed before the scans can be used to precisely answer questions like ‘How are you feeling?,’ but, if the results are confirmed and repeated, it may not be long before your brain gives your emotions away.
Source:TIME

Scientists Have Found Possible Cure for Gray Hair and Vitiligo

A team of European researchers developed a topical, UVB-activated compound called PC-KUS, which they claim can reverse oxidative stress responsible for causing gray hair and vitiligo.
 The pigment melanin determines the color of our skin, hair and eyes. Loss of melanin in the skin and hair causes vitiligo (white patches on the skin) and graying of hair. 
Our hair goes gray due to massive oxidative stress caused by accumulation of hydrogen peroxide in the hair follicle. This causes our hair to bleach itself from the inside out. Karin Schallreuter and colleagues, from the Institute for Pigmentary Disorders, E.M. Arndt University, Greifswald, Germany; and Centre of Skin Sciences, School of Life Sciences, University of Bradford, U.K, developed a photo-activated compound (PC-KUS) that could reverse this build up of hydrogen peroxide. This proprietary treatment works for vitiligo as well. 
'To date, it is beyond any doubt that the sudden loss of the inherited skin and localized hair color can affect those individuals in many fundamental ways,' said Schallreuter, the lead researcher of the study. 'The improvement of quality of life after total and even partial successful repigmentation has been documented.' 
This study analyzed the effects of the medication on an international group of 2,411 patients with vitiligo, where 2.4 percent were diagnosed with strictly segmental vitiligo (SSV), and 3.2 percent were diagnosed with mixed vitiligo (SSV plus non-segmental vitiligo NSV). 
Non-segmental vitiligo is the most common type of vitiligo in which the patches often become visible equally on both sides of the body, with some kind of symmetry. These symmetrical patches generally appear on skin that is exposed daily to the sun. 
Segmental vitiligo, on the other hand, is rare, non-symmetrical, and usually tends to affect dorsal roots of the spine. It is more stable, less erratic, and responds well to topical treatments. 
The researchers of this study found that patients who have SSV within a certain nerve distribution involving skin and eyelashes show the same oxidative stress as observed in the NSV, which is associated with decreased antioxidant capacities of enzymes like catalase and other antioxidants. 
The researchers treated the patients with PC-KUS (a modified pseudocatalase) and found that the treatment led to successful re-pigmentation in their skin and eyelashes, that is, the original color was restored. 
'For generations, numerous remedies have been concocted to hide gray hair, but now, for the first time, an actual treatment that gets to the root of the problem has been developed. While this is exciting news, what's even more exciting is that this also works for vitiligo. This condition, while technically cosmetic, can have serious socio-emotional effects of people. Developing an effective treatment for this condition has the potential to radically improve many people's lives,' said Gerald Weissmann, Editor-in-Chief of The FASEB Journal. 
This study is a follow up on a 2009 study published in the journal FASEB which described the cause of age-related graying of hair. According to the study findings, low levels of enzyme that breaks up hydrogen peroxide into water and oxygen (catalase) cause the build up of hydrogen peroxide. These hair follicles also have low levels of enzymes MSR A and B, which are used to repair the damage. Further complicating matters, the high levels of hydrogen peroxide and low levels of these enzymes, disrupt the formation of an enzyme tyrosinase (which produces melanin in hair follicles), thus causing graying of hair. 
References: 
http://www.fasebj.org/content/early/2013/04/29/fj.12-226779.abstract 
http://www.eurekalert.org/pub_releases/2013-05/foas-gha050313.php


 

Fermented Milk May Help Prevent Muscle Soreness After High Intensity Exercise

Researchers at Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Japan, report that fermented milk can prevent muscle damage associated with strenuous exercise.
Exercising increases the presence of free radicals that can damage tissues. Unaccustomed and high intensity exercise causes muscle damage known as delayed-onset muscle damage that involves protein degradation in the body. The damage occurs because of several factors, including mechanical stress, calcium accumulation, and oxidative stress. 
Fermented milk has several benefits including prolonged lifespan, antihypertensive effects, anti-tumorigenic effects, and immune system regulation. Some types of fermented milk also possess anti-inflammatory and antioxidant properties. In one of their earlier studies, Masayo Iwasa and colleagues have shown that Lactobacillus helveticus-fermented milk prevents muscle damage induced by acute exercise in experimental animals, suggesting that fermented milk may prevent the impairment of glucose metabolism associated with muscle damage. 
So, this time they conducted a trial to investigate the effect of fermented milk supplementation on glucose metabolism associated with muscle damage after acute exercise in humans. 
Eighteen healthy young men aged 20 to 22 years who were not habituated to a regular exercise regimen participated in this study. They participated in three trials of the study: rest with placebo intake (rest), exercise with placebo intake (placebo), and exercise with fermented milk intake (fermented milk). 
High intensity exercise included resistance exercise consisting of five sets of leg and bench presses at 70-100 percent 12 repetition maximum. Examination beverage (fermented milk or placebo) was taken before and after exercise. On the following day, respiratory metabolic performance, blood collection, and muscle soreness were assessed. 

The findings were- 
• Muscle soreness was significantly suppressed by the consumption of fermented milk compared with placebo. 

• Serum creatine phosphokinase was significantly increased by exercise, but this increase showed a tendency of suppression after the consumption of fermented milk. 

• Exercise significantly decreased the respiratory quotient, although this decrease was negated by the consumption of fermented milk. [Respiratory quotient (RQ) is a measurement of the ratio between oxygen intakes and carbon dioxide exhaled by an individual]. 

• Exercise significantly reduced the absorption capacity of serum oxygen radical, although this reduction was not observed with the consumption of fermented milk. 

These results indicate that dietary fermented milk improves the impairment of glucose metabolism associated with exercise-induced muscle damage in healthy people. 
'Previously, (studies have shown that) consumption of milk (unfermented) partially attenuates the muscle damage; therefore, the placebo trial, which used unfermented milk, may have also suppressed muscle damage to some extent. However, our results showed that fermented milk is more effective than milk,' says Wataru Aoi, one of the study authors. 
'The present study suggests that small digested peptides in fermented milk may contribute to increasing the level of antioxidants in muscle. In future studies, we will attempt to detect the specific small peptides present after the consumption of fermented milk,' they concluded. Source: Kyoto Prefectural University, Japan
 

National Medicinal Plants Board evaluating existing schemes for revision

Several States have failed to set up full-fledged State Medicinal Plants Boards (SMPBs), resulting in the lapse of Central funds notwithstanding the directions and persuasion by the Centre. Only eight states--Andhra Pradesh, Chattisgarh, Gujarat, Karnataka, Kerala, Maharashtra, Rajasthan and West Bengal — have full-time chief executives and full-fledged SMPBs, while other states were yet to take any pro-active measures in this regard. This has resulted in the lapse of funds for the preservation of medicinal plants in the States. Against this backdrop, the National Medicinal Plants Board (NMPB) is planning to overhaul itself to make the projects more effective in the coming years. At present, an evaluation of the schemes is underway and the programmes will be revised as per the outcome of the evaluation. The laxity on the part of the States and the status of programmes by the NMPB had recently come in for the scrutiny of the Parliamentary Standing Committee on Health also. “The Committee is of the view that full-fledged SMPBs with full-time chief executive officer will certainly lead to better implementation of the Schemes and programmes of NMPB and more efficient deployment of financial resources. The Committee, therefore, recommends to the Department to expedite its decision on increasing support for full fledged SMPBs,” the panel said. The panel also expressed concern over the amount of central funds remaining unaccounted. “The Committee notes with concern that a substantial amount of central funds for the previous years continues to remain unaccounted for under both the schemes of NMPB which is indicative of non-adherence to the basic financial norms. The Committee feels that the delay in timely submission of utilisation certificates would adversely affect execution of the projects,” it said. NMPB, established in 2000, is the apex national body which co-ordinates all matters relating to medicinal plants in the country and provides financial support to programmes relating to conservation, cultivation and the all-round development of the medicinal plants sector. The NMPB is also implementing a Centrally Sponsored Scheme of National Mission on Medicinal Plants since 2008-09. This Scheme is primarily aimed at supporting market driven medicinal plants cultivation on private land with backward linkages for establishment of nurseries, for supply of quality planting material and forward linkages for post-harvest management, marketing, infrastructure, certification, etc.  Source:Pharmabiz

Pluripotent cells from pancreatic cancer cells first human model of cancer's progression

Pancreatic cancer carries a dismal prognosis. According to the National Cancer Institute, the overall five-year relative survival for 2003-2009 was 6 percent.
Still, researchers and clinicians don't have a non-invasive way to even detect early cells that portent later disease. 'There's no PSA test for pancreatic cancer,' they say, and that's one of the main reasons why pancreatic cancer is detected so late in its course.
They have been searching for a human-cell model of early-disease progression. Now, Perelman School of Medicine, University of Pennsylvania scientists have used stem-cell technology to create a research cell line from a patient with advanced pancreatic ductal adenocarcinoma (PDAC).
This first-of-its-kind human-cell model of pancreatic cancer progression was published this week in Cell Reports from the lab of Ken Zaret, PhD, professor of Cell and Developmental Biology.
"It is the first example using induced pluripotent stem [iPS] cells to model cancer progression directly from a solid tumor, and the first human cell line that can model pancreatic cancer progression from early to invasive stages," says Zaret, also the associate director of the Penn Institute for Regenerative Medicine.
"We were able to predict the appearance of cellular features and protein markers in the intermediate stages of pancreatic cancer that are not evident in the terminal stages. This has given us new perspectives into what this deadly type of cancer looks like – something no one has seen before in human cells. Our analysis revealed known molecular networks that are activated during PDAC progression, as well as a new molecular network that is activated during the intermediate stages. This could provide a fresh outlook on biomarkers for early stages of the disease."
Source:Cell Reports

Men who can't produce sperm face increased cancer risk, Stanford-led study finds

Men who are diagnosed as azoospermic — infertile because of an absence of sperm in their ejaculate — are more prone to developing cancer than the general population, a study led by a Stanford University School of Medicine urologist has found. And a diagnosis of azoospermia before age 30 carries an eight-fold cancer risk, the study says.
"An azoospermic man's risk for developing cancer is similar to that for a typical man 10 years older," said Michael Eisenberg, MD, PhD, assistant professor of urology at the medical school and director of male reproductive medicine and surgery at Stanford Hospital & Clinics. Eisenberg is lead author of the study, which will be published online June 20 in Fertility and Sterility.
Diagnoses of male infertility and azoospermia are surprisingly common in the United States. About 4 million American men — 15 percent of those ages 15-45 — are infertile. Of these, some 600,000 — about 1 percent of those of reproductive age — are azoospermic. "There is evidence that infertility may be a barometer for men's overall health," Eisenberg said, "and a few studies have found an association of male infertility with testicular cancer." The new study, he said, not only assigns the bulk of infertile men's increased cancer risk to those with azoospermia, but also suggests that this risk extends beyond testicular cancer.
Eisenberg conducted most of the analysis for the study at Stanford, using data gathered from the Texas Cancer Registry and the Baylor College of Medicine in Houston, where he completed his medical training. The study's senior authors are Larry Lipshultz, MD, and Dolores Lamb, PhD, professors of urology at Baylor.
The study population consisted of 2,238 infertile men who were seen at a Baylor andrology clinic from 1989 to 2009. Their median age was 35.7 when they were first evaluated for the cause of their infertility. Of those men, 451 had azoospermia, and 1,787 did not. There were otherwise no apparent initial differences between the two groups.
Azoospermia can arise for two reasons. Obstructive azoospermia is caused by a blockage that prevents otherwise plentiful, fit sperm produced in the testes from reaching the ejaculate. But a screen of about one-fourth of the azoospermic men in the study population indicated that the vast majority suffered from the non-obstructive variety: Their testes didn't produce enough sperm for any to reach their ejaculate, most likely because of genetic deficiencies of one sort or another. Fully one-fourth of all the genes in the human genome play some role in reproduction, Eisenberg noted, so there are a lot of ways for the capacity to sire offspring to go astray.
After undergoing a semen analysis, the men were followed for an average of 6.7 years to see which of them turned up in the Texas Cancer Registry. (Fortunately for the analysis, most people tend to stay in the state where they've grown up, said Eisenberg.) Their rates of diagnosed cancer incidence were then compared with age-adjusted cancer-diagnosis statistics of Texas men in general.
In all, a total of 29 of the 2,238 infertile men developed cancer over a 5.8-year average period from their semen analysis to their cancer diagnosis. This contrasted with an expected 16.7 cases, on an age-adjusted basis, for the male Texas population in general (which, Eisenberg said, closely reflects cancer incidence rates for the entire U.S. population). This meant that infertile men were 1.7 times as likely to develop cancer as men in the general population. This is considered a moderately increased risk.
But comparing the cancer risk of azoospermic and nonazoospermic infertile men revealed a major disparity: The azoospermic men were at a substantially elevated risk — nearly three times as likely to receive a diagnosis of cancer as men in the overall population. Infertile men who weren't azoospermic, in contrast, exhibited a statistically insignificant increased cancer risk of only 1.4 times that of men in the overall population.
By excluding men whose cancer diagnosis came within two or three years of their infertility evaluation, the researchers were able to rule out the possibility that azoospermia caused by an undiagnosed cancer had affected the statistics.
While the study wasn't large enough to delineate which specific types of cancer pushed azoospermic men's incidence rates up, the diagnoses they received covered a wide range of cancers: brain, prostate and stomach tumors, as well as melanoma, lymphoma, testicular cancer and cancer of the small intestine. The findings suggest that genetic defects that result in azoospermia may also broadly increase a man's vulnerability to cancer, Eisenberg said, supporting the notion that azoospermia and cancer vulnerability may share common genetic causes.
The study, which was funded by the National Institute for Child Health and Human Development, is the first to examine the cancer risk of azoospermia in particular, or to link it to non-germ-cell cancers. Previous studies have failed to consistently identify any increased risk for nontesticular cancers in infertile men, whether azoospermic or otherwise. In those previous studies, however, azoospermic men couldn't be separately examined because sperm analyses weren't available.
Most striking of all, said Eisenberg, was the cancer risk among azoospermic men who first had their semen analyzed before age 30. They were more than eight times as likely to subsequently develop cancer than Texas males in the general population of the same age. In contrast, there was no relationship between age of semen analysis and risk of cancer for nonazoospermic men.
The good news, Eisenberg said, is that while the cancer risk among young azoospermic men was quite large compared to their same-age peers, their relative youth means that their absolute risk of contracting cancer during the follow-up period remained small. The bad news, he said, is that men in their 30s often don't have a primary health-care provider. He advised that young men who are diagnosed as azoospermic should be aware of their heightened risk and make sure to get periodic checkups with that in mind.
Source: Fertility and Sterility

Total amount of exercise important, not frequency, research shows

A new study by Queen’s University researchers has determined that adults who accumulated 150 minutes of exercise on a few days of the week were not any less healthy than adults who exercised more frequently throughout the week.Ian Janssen and his graduate student Janine Clarke studied 2,324 adults from across Canada to determine whether the frequency of physical activity throughout the week is associated with risk factors for diabetes, heart disease and stroke.“The findings indicate that it does not matter how adults choose to accumulate their 150 weekly minutes of physical activity,” says Dr. Janssen. “For instance, someone who did not perform any physical activity on Monday to Friday but was active for 150 minutes over the weekend would obtain the same health benefits from their activity as someone who accumulated 150 minutes of activity over the week by doing 20-25 minutes of activity on a daily basis.”Physical activity was measured continuously throughout the week by having research participants wear accelerometers on their waists. Accelerometers are tiny electrical devices (about the size of a small package of matches) that record how much a person moves every minute.Dr. Janssen divided the adults who met the physical activity guidelines (more than 150 minutes per week of aerobic activity) into those who were frequently active (active five to seven days of the week) and infrequently active (active one to four days of the week).“The important message is that adults should aim to accumulate at least 150 minutes of weekly physical activity in whatever pattern that works for their schedule.”

Source:The paper was published today in Applied Physiology, Nutrition and Metabolism

CNIO researchers discover a new gene involved in obesity

RAP1 is a gene that also protects telomeres. This is the first time that a link has been found between these structures that shorten with ageing and obesity

The discovery of an unexpected function for a gene that was associated to another process in the organism might be a solution in search of a problem, a clue to unsuspected connections. That is what has happened with RAP1, a gene that protects telomeres— the ends of chromosomes—after researchers from the Spanish National Cancer Research Centre (CNIO) surprisingly discovered its key role in obesity.
"We still don't know what evolutionary significance to attach to it, but it is at the very least interesting that a telomere gene is related to obesity", says Maria Blasco, CNIO director and co-author of the study published today in the journal Cell Reports.
RAP1 forms part of the shelterin complex, a group of proteins that make up the protective hood of telomeres—the DNA sequence at the ends of chromosomes that shortens with each cellular division and thus measures the ageing of the organism. There are six shelterins, and CNIO's Telomeres & Telomerase Group, which studies them in-depth, has discovered that RAP1, contrary to the rest, is not essential for the survival of the organism; but that does not mean RAP1 is not important. The reverse is rather the case: when comparing the genomes of different species, it can be observed that RAP1 is the most conserved shelterin of all. Despite the long history of evolutionary changes, RAP1 has not changed; it is present even in yeast. This normally implies an important role in the organism, but which one?
CNIO researchers had discovered that RAP1, in addition to being located in telomeres, is also present in the rest of the chromosome; they supposed it acts regulating the action of other genes. In order to analyse this other potential function, and its importance in the organism, CNIO researchers created a lineage of mice without RAP1 and, to their surprise, discovered a model for obesity.
Source:Cell Reports

Dietary fructose causes liver damage in animal model, study finds

The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories.
However, a new study conducted in an animal model at Wake Forest Baptist Medical Center showed that fructose rapidly caused liver damage even without weight gain. The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.
The study is published in the June 19 online edition of the American Journal of Clinical Nutrition.
"Is a calorie a calorie? Are they all created equal? Based on this study, we would say not," said Kylie Kavanagh, D.V.M., assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.
In a previous trial which is referenced in the current journal article, Kavanagh's team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period. Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group. They developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.
The big question for the researchers was what caused the liver damage. Was it because the animals got fat from eating too much, or was it something else?
To answer that question, this study was designed to prevent weight gain. Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference. Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.
Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.
Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain. At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through fecal samples and intestinal biopsies.
"What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor," Kavanagh said. "Six weeks in monkeys is roughly equivalent to three months in humans."
In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there. It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.
One of the limitations of the study was that it only tested for fructose and not dextrose. Fructose and dextrose are simple sugars found naturally in plants.
"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said. "What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.
"The liver damage began even in the absence of weight gain. This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems."
The Wake Forest Baptist team plans to begin a new study using the same controls but testing for both fructose and dextrose over a longer time frame.
Source:American Journal of Clinical Nutrition.

Brain Can Plan Actions Toward Things the Eye Doesn’t See

People can plan strategic movements to several different targets at the same time, even when they see far fewer targets than are actually present, according to a new study published in Psychological Science, a journal of the Association for Psychological Science.A team of researchers at the Brain and Mind Institute at the University of Western Ontario took advantage of a pictorial illusion — known as the “connectedness illusion” — that causes people to underestimate the number of targets they see.

“The Connectedness Illusion”: Connecting the circles creates the illusion of fewer circles on the right. But when our brain plans actions to these targets it computes the actual number of targets.

When people act on these targets, however, they can rapidly plan accurate and strategic reaches that reflect the actual number of targets.

Using sophisticated statistical techniques to analyze participants’ responses to multiple potential targets, the researchers found that participants’ reaches to the targets were unaffected by the presence of the connecting lines.Thus, the “connectedness illusion” seemed to influence the number of targets they perceived but did not impact their ability to plan actions related to the targets.These findings indicate that the processes in the brain that plan visually guided actions are distinct from those that allow us to perceive the world.“The design of the experiments allowed us to separate these two processes, even though they normally unfold at the same time,” explained lead researcher Jennifer Milne, a PhD student at the University of Western Ontario.“It’s as though we have a semi-autonomous robot in our brain that plans and executes actions on our behalf with only the broadest of instructions from us!”According to Mel Goodale, professor at the University of Western Ontario and senior author on the paper, these findings “not only reveal just how sophisticated the visuomotor systems in the brain are, but could also have important implications for the design and implementation of robotic systems and efficient human-machine interfaces.”

This work was supported by operating grants from the Natural Sciences and Engineering Research Council of Canada to J. C. Culham (Grant No. 249877 RGPIN) and M. A. Goodale (Grant No. 6313 2007 RGPIN).

Source:Association of Psychological Sciences

Low Levels of Vitamin D Linked to High Blood Pressure

A new study by researchers at the Institute of Child Health at University College London has found that low vitamin D levels can trigger high blood pressure.The researchers looked at the genetic link between vitamin D levels and the risk of hypertension or high blood pressure. The risk of developing high blood pressure fell by 8.1 percent for every 10 percent increase in the concentrations of the 25-hydroxyvitamin form of vitamin D, they reported. 
"Our new data provide further support for the important non-skeletal effects of vitamin D. We now intend to continue this work by examining the causal relationship between vitamin D status and other cardiovascular disease-related outcomes," said lead researcher Vimal Karani, from the Institute of Child Health at University College London. He added that some cases of cardiovascular disease can be prevented by taking vitamin D supplements. 
The study details were presented at the annual conference of the European Society of Human Genetics in Paris. 

Source: European Society of Human Genetics
 

Red Meat Ups Risk of Type 2 Diabetes

More red meat consumption is associated with a higher risk of type-2 diabetes mellitus, finds study published in JAMA Internal Medicine.
Red meat consumption has been consistently related to an increased risk of T2DM, but previous studies measured red meat consumption at a baseline with limited follow-up information. However, a person's eating behavior changes over time and measurement of consumption at a single point in time does not capture the variability of intake during follow-up, the authors note in the study background. 
An Pan, Ph.D., of the National University of Singapore, and colleagues analyzed data from three Harvard group studies and followed up 26,357 men in the Health Professionals Follow-up Study; 48,709 women in the Nurses' Health Study; and 74,077 women in the Nurses' Health Study II. Diets were assessed using food frequency questionnaires. 
During more than 1.9 million person-years of follow-up, researchers documented 7,540 incident cases of T2DM. 
"Increasing red meat intake during a four-year interval was associated with an elevated risk of T2DM during the subsequent four years in each cohort," according to the study. 
The results indicate that compared with a group with no change in red meat intake, increasing red meat intake of more than 0.50 servings per day was associated with a 48 percent elevated risk in the subsequent four-year period. Reducing red meat consumption by more than 0.50 servings per day from baseline to the first four years of follow-up was associated with a 14 percent lower risk during the subsequent entire follow-up. 
The authors note the study is observational so causality cannot be inferred. 
"Our results confirm the robustness of the association between red meat and T2DM and add further evidence that limiting red meat consumption over time confers benefits for T2DM prevention," the authors conclude.(JAMA Intern Med. Published online June 17, 2013. doi:10.1001/jamainternmed.2013.6633. Available pre-embargo to the media at http://media.jamanetwork.com.) 
Editor's Note: This work was supported by grants from the National Institutes of Health. An author also made a funding disclosure. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc. Commentary: Oxygen-Carrying Proteins in Meat and Risk of Diabetes Mellitus 
In an invited commentary, William J. Evans, Ph.D., of GlaxoSmithKline and Duke University, Durham, N.C., writes: "The article by Pan et al confirms previous observations that the consumption of so-called red meat is associated with an increased risk of type 2 diabetes mellitus (T2DM)." 
"Perhaps a better description of the characteristics of the meat consumed with the greatest effect on risk is the saturated fatty acid (SFA) content rather than the amount of oxygen-carrying proteins," Evans continues. 
"A recommendation to consume less red meat may help to reduce the epidemic of T2DM. However, the overwhelming preponderance of molecular, cellular, clinical and epidemiological evidence suggests that public health messages should be directed toward the consumption of high-quality protein that is low in total and saturated fat. … These public health recommendations should include cuts of red meat that are also low in fat, along with fish, poultry and low-fat dairy products. It is not the type of protein (or meat) that is the problem: it is the type of fat," Evans concludes.(JAMA Intern Med. Published online June 17, 2013. doi:10.1001/jamainternmed.2013.7399. Available pre-embargo to the media at http://media.jamanetwork.com.) 
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc. 
Source:JAMA Internal Medicine.

 

Talcum Powder Increases Risk of Ovarian Cancer

Regular use of talcum powder can increase the risk of developing ovarian cancer by 24 percent, finds new research.US scientists at Brigham and Women's Hospital in Boston have warned that powder particles applied to intimate areas after washing can seep into the body, the Daily Express reported. 
This can trigger inflammation, while increasing the risk of an ovarian tumour by 24 per cent. 
The study was published in the journal Cancer Prevention Research.
Source-ANI
 

Developmental Protein Serves as a Switch to Spread Cancer

A protein used by embryo cells during early development apparently serves as a switch in regulating the spread of cancer, known as metastasis and recently it is found in many different types of cancer.This is being reported by researchers at the University of California, San Diego School of Medicine and UC San Diego Moores Cancer Center in the June 15, 2013 issue of the journal Cancer Research. 
Metastasis is responsible for 90 percent of cancer-related deaths. More than 575,000 Americans die of cancer each year, the second leading cause of death in the United States after cardiovascular disease. 
The scientists, led by principal investigator Thomas Kipps, MD, PhD, Evelyn and Edwin Tasch Chair in Cancer Research at UC San Diego, discovered an association between the protein, called Receptor-tyrosine-kinase-like Orphan Receptor 1 or ROR1, and the epithelial-mesenchymal transition (EMT), a process that occurs during embryogenesis when cells migrate and then grow into new organs during early development.
In research published in 2012, Kipps and colleagues reported for the first time that ROR1 is expressed during embryogenesis and by many different types of cancers, but not by normal post-partum tissues. They also discovered that silencing the protein impaired the growth and survival of human breast cancer cells. 
In their latest work, the scientists found that high-level expression of ROR1 in breast cancer cells correlates to higher rates of relapse and metastasis in patients with breast adenocarcinoma, a type of cancer that originates in glandular tissue. Conversely, silencing expression of ROR1 reverses EMT and inhibits the metastatic spread of breast cancer cells in animal models. Moreover, the researchers found that treatment with a monoclonal antibody targeting ROR1 also could inhibit the growth and spread of highly metastatic tumors that express ROR1. 
"We might think of ROR1 as an oncogene," said study co-author Bing Cui, PhD, a postdoctoral fellow in Kipps' lab. "This means ROR1 has some tumor initiation functions. However, ROR1 also appears to allow transformed cells to invade other tissues and to promote tumor expansion in both the primary tumor site and in distant organs." 
Because ROR1 is expressed only in cancer cells, Kipps' team says it presents a singular, selective target for anti-cancer therapies that would leave normal cells unaffected. It's not yet clear how the monoclonal antibody approach, tested thus far only in culture and animal models, impacts primary tumors, said Cui, but it does offer promise for inhibiting the spread of cancer. The researchers are developing a humanized monoclonal antibody for potential clinical studies in patients with cancers that express ROR1.
Source:  Journal Cancer Research. 

 

Men Blamed For Menopause By Controversial Study

According to a controversial study by Canadian researchers published this week, men and their preference for younger female mates may have led to the phenomenon of menopause in women.
"If women were reproducing all along, and there were no preference against older women, women would be reproducing like men are for their whole lives," said evolutionary geneticist Rama Singh, a professor at McMaster University. 
Singh said the conventional "grandmother theory," which holds that older women grow infertile so that they can assist the survival of their kin by helping to raise their children's offspring, did not make sense to him. 
Instead of age leading to infertility, Singh theorized that the dwindling pool of male mates for older women -- because many older men seek to mate with younger women -- led to a lack of reproduction that gave rise to menopause. 
"If women were reproducing all along, and there were no preference against older women, women would be reproducing like men are for their whole lives." 
His work, backed up by computer models, suggests that a male mating preference for younger females could have led to the accumulation of genetic mutations that would harm female fertility and bring on menopause. 
The study was published on Thursday in the open-access, peer-reviewed journal PLOS Computational Biology. 
But while the assertion raised many eyebrows, not all experts are convinced by Singh, who questioned why menopause appears to be mainly a human phenomenon. 
"I cannot agree with the theory put forth," said Steven Goldstein, professor of obstetrics and gynecology at New York University School of Medicine. 
"There are other primates who do experience menopause, although life expectancy after menopause is extremely limited," said Goldstein, who was not involved in the research. 
"The same was true of humans until roughly the 1850s. In 1850 the average age of menopause was 46 and life expectancy was 50, which more closely parallels that of chimpanzees or gorillas." 
Rather, a more accurate explanation would be that scientific advances like water purification and antibiotics have led to much longer lives among humans, he said. 
"The cessation of reproductive capabilities in higher primates has always come shortly before the life span ends. It is only the advances of modern society that have women living so very long," he told AFP.
Source-AFP