Medicinezine.com - Reviews and articles in Wellness & Lifestyle, Child & Teen Health, Women’s Health, Men's Health, Mental Health, Natural Medicine, Drugs and Medication, Sexual Health.

Counting Carbs? Understanding Glycemic Index and Glycemic Load

Editor — Sat, 26 Jan 2013 01:58:56 +0000

Counting Carbs? Understanding Glycemic Index and Glycemic Load

You’ve probably heard of glycemic index and glycemic load. Some studies suggest that sticking to foods with a low glycemic index may help prevent diabetes, cardiovascular disease and cancer. Some claim it helps with weight loss. The truth is, we don’t know all the answers yet. Here’s what you need to know.

The glycemic index and load concern carbohydrates, or carbs—one of the main types of nutrients in our diets. Carbs with a simple chemical structure are called sugars. Sugars are found naturally in foods like fruits, vegetables and milk products. They’re also added to many foods and drinks. Complex carbs, like starches and fiber, are found in whole-grain breads and cereals, starchy vegetables and legumes.

Click on the image to find the tastiest Low Glycemic Diet Plan ever!

Your digestive system changes the carbs you eat into glucose, a type of sugar that your body uses for energy. Simple carbs are more quickly digested and absorbed than complex ones, so simple carbs can raise your blood glucose levels faster and higher.

People with diabetes need to manage their blood glucose levels. High blood glucose can damage tissues and organs. In time, it can lead to heart disease, blindness, kidney failure and other problems. If you have diabetes, controlling your blood glucose will prevent or delay these health complications. So it’s important to understand how foods and drinks affect your blood sugar.

“The evidence seems to support the concept that the more complex carbohydrates will lead to better blood sugar control than the more simple sugars,” says Dr. Myrlene Staten, an NIH diabetes expert.

Researchers developed the glycemic index to measure the quality of carbs in foods. It shows how the carbs in different foods raise blood sugar. White rice, for example, has a higher glycemic index than brown rice, which has more complex carbs.

But it’s not just the types of carbs that matter. The more carbs you eat, the more your blood sugar rises. “The glycemic index really doesn’t take into consideration how much you eat.

Dr. Somdat Mahabir

That’s why researchers came up with the concept of glycemic load. It captures both the types of carbs in a food and the amount of carbs in a serving. Essentially, it shows how a portion of food affects your blood sugar. Many things affect the glycemic load, including food processing, how ripe a fruit is, how a food is prepared and how long it’s been stored.

Glycemic index and glycemic load aren’t things you’ll see on a label, so they’re not easy to use. But labels do show helpful information: calories, total carbohydrates, sugars and fiber.

“It makes sense for everybody, not only diabetics, to eat the more complex carbohydrates because they will be more gradually absorbed, and blood sugar highs and lows will be smaller,” Staten says. Whole foods with complex carbs will give you more minerals and vitamins, too, and are usually good sources of fiber.

The Low Glycemic Index (Low GI) Diet

Do you want a sure fire way to lose weight and keep it off?

If you want a solution that just works, and tackles all the factors responsible for weight gain then look no further than www.fitium.com

Fitium is an online weight loss system, which provides you with your very own personalised diet plan, designed to help you get to your ideal weight.

Fitium helps you tackle the nutrition, lifestyle, mindset, and fitness elements that will supercharge your weight loss, and help you look & feel great.

Counting Carbs? Understanding Glycemic Index and Glycemic Load is an article review from: Medicinezine.com

- MedicinEzine.com is a carefully selected collection of articles about alternative or complementary forms of medicine products. MedicinEzine.com provides free registration, customer reviews and information, allows customer comments, user comments. MedicinEzine.com
- MedicinEzine.com is a World Journal of medicine articles and reviews, product reviews, customer reviews and opinions. MedicinEzine.com provides the latest medical news and headlines from the world of medicine and healthcare today and tomorrow. MedicinEzine.com News

Fitium: What’s Inside? How Will It Help You Lose Weight? Fitium Review.

Editor — Fri, 25 Jan 2013 22:05:33 +0000

If you’re looking for the official Fitium diet website – click here

What is Fitium?

Fitium is a revolutionary online weight loss system which has helped thousands not only lose weight, but live a healthier lifestyle.

How does Fitium work?

The key idea behind Fitium is that there is “no one size fits all diet”. Our genetics, lifestyle, age, fitness, health and diet mean that the same diet can help someone lose weight, whilst making another gain weight!
Fitium takes a different approach, and seeks to understand how your body works, in order to provide a personalised plan designed to help your body lose weight naturally, and keep it off!

Let’s see how it works:
Understanding why you are gaining weight
When you first sign up, you’ll complete a short 8-minute assessment which help Fitium understand how your body works, and pinpoint areas which are causing you to gain weight.

Your personalised diet plan
Fitium then helps you identify your ideal weight, and creates a personalised plan to help you reach it. Your plan will feature an easy to follow blueprint which includes:

How many calories you need to consume
Which calories to prioritise
Which foods to avoid (including recommended substitutes)
Specific recommendations to address your key weight gain factors
Tailored advice to help blast your stubborn fat zones

Lose weight from the first week
Starting a new habit or change is not easy, and there are many factors that can derail your progress. So Fitium have developed the 7 Day Accelerator course to guide you through the first week, help you avoid common pitfalls, turbocharge your results and ensure you have the best strategies for long term success too.

Take the guesswork out of what to eat
Fitium takes the pain out of creating tasty yet healthy meals by providing breakfast, lunch, snack and dinner meals tailored to your exact diet needs. These meals are filling, packed with nutrients and are designed to help you lose weight naturally.

Get support and stay on track each step of the way
Making lifestyle and diet changes can be overwhelming, especially if you are balancing family life and work. So our team has developed weekly coaching challenges to help you implement your new diet plan, one step at a time, and get closer to looking and feeling great.

Tackle the real reasons you gain weight
Don’t let your environment or lifestyle sabotage your weight loss. Fitium has developed tried and tested strategies to help you deal with emotional eating, social occasions, stress and day to day situations which can get in the way of your progress.

Monitor your progress and reach your diet goals
Fitium provides an easy to follow dashboard to help you monitor your progress, track your meals, review your activity and keep an eye on your health vitals. This results in improved accountability and has been proven to double weight loss in many studies.

Fitium Review. Who is behind Fitium?

Fitium was designed with the help of a doctor, nutritionist and personal trainer, distilling years of experience into an easy to follow system, you can access online 24/7 from the comfort of your home.

Click here to read more about the team

Fitium is not just a diet but a lifestyle

Many diets focus on the symptoms, instead of tackling the root causes of weight gain they offer “band aid” solutions which tend to be short term, and unsustainable in the long term.

Fitium works differently by first understanding what is causing your weight gain, and by helping you tackle the nutrition, mindset and lifestyle changes you need to not only lose weight, but improve your health for the long term.
By completing the accelerator course, and the ongoing coaching challenges you will unlock the keys to sustainable weight loss as well as look and feel great.

Need some help to make weight loss dieting work?
If you seek expert advice on losing weight naturally, click here.

The Fitium.com website: What’s inside the Membership Area?

7 day accelerator course to provide you with everything you need to get started fast, and ease you into your new lifestyle + Weekly coaching challenges developed by the team to help you stay on track and get ongoing improvements

Optional video workouts to workout at home

A personalised diet plan based on your body’s requirements to maximise your weight loss

Meal Planner – ATailored meal plans based on your diet plan, featuring tasty meals you can create from home, and exact serving sizes to support your weight loss goals

A health dashboard to help you monitor your progress, and keep track of your physical activity

Ongoing support from the expert team through hundreds of practical guides (with more added on a monthly basis) and Q&A sessions

A food diary to help you track your meals, calorie intake and analyse key nutritional stats

Fitium Review. Fitium Plans and Pricing

There are 3 different plans available for you – a month-by-month plan, a 6 month/bi-annual plan and a yearly plan.

We would recommend starting right out with the yearly plan. Why, you ask?

Well, not only is it the yearly plan give the best value by far – at $2.48 per week!! – but having a yearly membership will make you stick to the plan and finally accomplish your weight loss goal! Plus, there is an iron-clad 30-day Money Back Guarantee. So if you aren’t satisfied with what Fitium has to offer you, just ask for a refund. But if you love it, as we know you will, you get to stay at the lowest price possible.

A little sneaky but a great tactic, don’t you think?

Click here to see the plans and sign up now

Monthly plan$19.95

$4.59 per week
Savings

6-month plan$74.99

$2.87 per week
37% Savings

1-year plan$129.50

$2.48 per week
45% Savings

Fitium Review. Customer reviews of Fitium

Some Customer reviews of Fitium Diet Plan found on the web

For those who have been overweight for a long time, this is the program for you. There are no pills, no supplements and no contracts to keep paying for so that they work. This is a lifestyle change that is best suited for those who need to lose the weight and keep it off for the rest of their lives.
What is more important is that Fitium also encourages you to exercise to help you get into shape which in turn helps keep the weight off as well. The more muscle you build, the more fat will burn away when you exercise.
Fitium may be the most obvious solution for millions of people, yet they do not have the information themselves to carry out the simple, straightforward meal plans that Fitium has in store.
We wholeheartedly recommend Fitium as the program to help people lose weight and keep it off for good.

“Fitium is good if you follow the challenges.To get the most of the site you need to follow the coaching challenges which I found really motivating, especially as I have a tendency to easily get bored.

I lost 3 stones in two months on this plan and actually enjoyed the process. I didn’t have to make drastic changes to my diet, and the suggested meals were tasty and filling. On other diets I have always felt hungry or would get aches and pains in the middle of the day, but with the Fitium diet plan I sometimes couldn’t finish my plate!

I recommend opting for the three or six month package deal, as it works out much cheaper than the monthly payment option.”

Perhaps one of the most thrilling aspects of this weight loss dieting program is that you get your own and personalized fitness coach. To be honest, this is something that you will definitely not come across with any other program out there.

In fact, as online health sites go, this is one of the best performers we have seen in terms of providing their customers with the capability to shed weight and improve their fitness. The end result is a great looking body, slim and toned figure and a much healthier aspect.

Visit the the official Fitium website

Customer reviews of Fitium submitted by our visitors

Fitium: What’s Inside? How Will It Help You Lose Weight? Fitium Review. is an article review from: Medicinezine.com

Genomic Technology Detects Fetal Problems

Editor — Mon, 17 Dec 2012 18:48:51 +0000

Genomic Technology Detects Fetal Problems

Two new studies show the potential of a genomic technique to help spot abnormalities in fetuses that conventional methods can’t. One research team used the technology in prenatal testing. Another showed that it could help detect the reasons for stillbirths. The approach might allow better planning for early interventions.

Some pregnant women have their fetuses tested for birth defects prenatally (while still in the womb). The testing is most often used by women who are older than 35 years of age, those in whom screening tests reveal particular risks and those with a family history of certain conditions. Doctors typically examine an individual’s set of chromosomes—the structures that contain our DNA—under a microscope. The technique, called karyotyping, can reveal abnormalities in chromosome shapes or numbers. Karyotyping is also used to investigate the reason for pregnancies that end in stillbirth—the death of a fetus in the womb at or after the 20th week of pregnancy.

Karyotyping, however, requires cells to be grown in culture and is often not possible in a stillbirth, so researchers have been seeking an alternative. In the new studies, scientists supported by NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) tested a different approach, called microarray analysis. DNA microarray chips are used to detect missing segments of chromosomes (deletions) or additional segments (duplications) that may be too small to be seen by karyotype. The studies appeared together on December 6, 2012, in the New England Journal of Medicine.

One team led by Dr. Ronald J. Wapner of Columbia University Medical Center enrolled over 4,400 women for prenatal testing. The women were selected because of advanced age, an abnormal result in Down’s syndrome screening, anomalies on sonograms or other reasons. Microarray analysis, the researchers found, revealed genetic conditions in 2.5% of the pregnancies with a normal karyotype. Among cases with sonogram anomalies, microarrays detected genetic problems in 6% of those with a normal karyotype.

Another group led by Dr. Uma Reddy of NICHD compared microarrays to karyotypes in more than 500 stillbirths. Shortly after each stillbirth, blood was collected from the umbilical cord and tissue collected from the fetus and placenta. Microarray analysis yielded results in 87% of the stillbirths, compared to 70% for karyotype analysis. Microarrays revealed more cases with genetic abnormalities than karyotyping (8% vs. 6%). Among stillbirths with a major birth defect, microarrays detected about 54% more abnormalities than karyotyping (30% vs. 19%).

“Previous studies suggest that 25% to 60% of stillbirths are unexplained,” Reddy says. “Microarray may explain genetic causes of stillbirths that previously were not identifiable by karyotype.”

These studies demonstrate how microarrays might help parents and health professionals better plan and manage both current and future pregnancies. However, the technique is more expensive than karyotyping. In prenatal testing, microarrays may be especially useful when sonograms detect a problem in the fetus. For stillbirths, it might best be used when the karyotype has failed or when there is a birth defect.

The studies also revealed genetic variants that haven’t yet been examined. Wapner’s group will follow the children in their study to understand the significance of these variants. Reddy and other researchers continue to investigate how genetic variations contribute to stillbirth.

By Harrison Wein, Ph.D.

###

* The above story is reprinted from materials provided by National Institutes of Health (NIH)
** The National Institutes of Health (NIH) , a part of the U.S. Department of Health and Human Services, is the nation’s medical research agency—making important discoveries that improve health and save lives. The National Institutes of Health is made up of 27 different components called Institutes and Centers. Each has its own specific research agenda. All but three of these components receive their funding directly from Congress, and administrate their own budgets.

Genomic Technology Detects Fetal Problems is an article review from: Medicinezine.com

Brain Changes as Trust Rises With Age

Editor — Mon, 17 Dec 2012 18:35:07 +0000

Brain Changes as Trust Rises With Age

Older adults are more likely than younger ones to perceive dishonest faces as trustworthy, according to a new study of social judgments and brain activity. The findings may help explain why older people are more likely to fall victim to fraud.

Up to 80% of scam victims are over 65, according to the U.S. Federal Trade Commission (FTC). Some experts suspect that older people are more vulnerable to fraud because they are more trusting than younger adults. But it hadn’t been clear whether the differences might have a biological basis.

A team led by Dr. Shelley Taylor at the University of California, Los Angeles, set out to explore whether older adults perceive facial cues related to trustworthiness differently from younger adults. The researchers showed photographs of faces selected to look trustworthy, neutral or untrustworthy to a group of 119 older adults (ages 55 to 84) and 24 younger adults (ages 20 to 42). Signs of untrustworthiness included averted eyes, insincere smiles and a backward tilt of the head. The participants were asked to rate each face based on how trustworthy or approachable it seemed.

A smaller group of participants performed the same task while the scientists used functional MRI to look at changes in brain activity. The study was funded by NIH’s National Institute on Aging (NIA) and appeared online on December 3, 2012, in the Proceedings of the National Academies of Sciences.

Neutral faces and faces high in trust cues were rated similarly by both groups. However, the older adults were significantly more likely than the younger ones to rate untrustworthy faces as trustworthy. “Most of the older adults showed this effect,” Taylor says. “They missed facial cues that are pretty easily distinguished.”

The functional MRI scans revealed significant differences in brain activity between the age groups. An area known as the anterior insula, which is associated with “gut feelings,” became more active in the younger subjects at the sight of an untrustworthy face. Older subjects, however, showed little to no activation in this area.

“The older adults do not have as strong an anterior insula early-warning signal; their brains are not saying ‘be wary,’ as the brains of the younger adults are,” Taylor says. Future research is needed to determine whether this is because older adults are paying less attention to important social signals or whether their brains are somehow unable to process those signals.

Misplaced trust can have severe consequences for older adults, especially when it comes to financial fraud. “Older adults seem to be particularly vulnerable to interpersonal solicitations, and their reduced sensitivity to cues related to trust may partially underlie this vulnerability,” Taylor says.

By Meghan Mott, Ph.D.

###

Brain Changes as Trust Rises With Age is an article review from: Medicinezine.com

Source of New Heart Cell Growth Discovered

Editor — Mon, 17 Dec 2012 18:24:58 +0000

Source of New Heart Cell Growth Discovered

A study in mice suggests that new heart cells arise from pre-existing heart cells and that the renewal process slows with age. The findings may lead to improved regenerative therapy for people with heart damage.

Dividing heart cells in newborn mice incorporate a tracer that can be seen in the cells’ nuclei. The color scale at the bottom shows the intensity of the tracer signal, with higher intensity toward the right side. Image by Senyo et al., courtesy of Nature.

The heart’s muscle cells, called cardiomyocytes, don’t readily replenish themselves. So an injured heart isn’t easy to mend. After a heart attack, a significant number of cardiomyocytes die. This jeopardizes heart function and can lead to chronic heart failure and possibly death. To help heal damaged hearts, scientists have been searching for a group of cells in the heart that can replenish damaged tissue.

Recent research has shown that the human heart generates new cardiomyocytes throughout its lifespan, but how frequently the cells are generated and where they come from is still debated. Studying heart tissue and cell turnover rate is technically very challenging. Some research has hinted that new cells can arise from progenitor cells at a fairly high rate. Other work has suggested that pre-existing cardiomyocytes divide at a fairly low rate to give rise to new cells.

A team led by Dr. Richard T. Lee of Brigham and Women’s Hospital and Harvard Medical School applied novel technology to investigate heart cell regeneration in mice. They used a technique called multi-isotope imaging mass spectrometry (MIMS). MIMS can detect nonradioactive stable isotope tracers. In contrast to most other tracers, these don’t alter biochemical reactions and aren’t harmful to the organism.

The scientists incorporated a rare stable isotope of nitrogen, nitrogen-15 (¹⁵N), into thymidine—one of the building blocks of DNA. When cells divide, the [¹⁵N] thymidine is taken up and added to new DNA. It can then be seen in the cells’ nuclei using MIMS. The work was supported in part by several NIH institutes, including the National Institute on Aging (NIA) and National Heart, Lung and Blood Institute (NHLBI). The study appeared online on December 5, 2012, in Nature.

To study cell turnover at different ages, the scientists gave 3 groups of mice [¹⁵N] thymidine for 8 weeks starting at day 4 (newborn), 10 weeks (young adult) or 22 months (old adult). To distinguish which types of cells created new cardiomyocytes, they performed similar experiments in mice genetically engineered with fluorescent tags to mark cardiomyocytes.

The scientists found that new heart cells were generated from pre-existing cardiomyocytes rather than progenitor cells. They estimated a yearly renewal rate of less than 1% during normal, healthy conditions. The rate of cell regeneration, they found, declined with age.

The team next used MIMS to study cell turnover following a heart attack. In the 8 weeks after the damage, roughly 3% of heart cells regenerated in the area next to the injured site. However, the researchers also noted that many cells had taken up ¹⁵N but not completed cell division.

“Our data show that adult cardiomyocytes are primarily responsible for the generation of new cardiomyocytes and that as we age, we lose some capacity to form new heart cells,” Lee says. “This means that we are losing our potential to rebuild the heart in the latter half of life, just when most heart disease hits us. If we can unravel why this occurs, we may be able to unleash some heart regeneration potential.”

By Miranda Hanson, Ph.D.

###

Source of New Heart Cell Growth Discovered is an article review from: Medicinezine.com

Forecasting Flu Outbreaks

Editor — Mon, 10 Dec 2012 18:10:22 +0000

Forecasting Flu Outbreaks

Scientists were able to forecast seasonal flu outbreaks using an approach common to weather prediction. The accomplishment lays the groundwork for systems to help public officials better predict and prepare for outbreaks.

In temperate regions, people become sick from influenza infections most often during winter. Dry air appears to be a factor. People also spend more time indoors together when it’s colder, giving flu viruses more opportunity to spread. But beyond this general trend, our ability to make real-time predictions of the timing, duration and magnitude of local seasonal flu outbreaks remains limited.

Dr. Jeffrey Shaman at Columbia University teamed up with Dr. Alicia Karspeck of the National Center for Atmospheric Research to develop a way to more precisely predict the course of seasonal flu outbreaks. They used an approach similar to that employed by meteorologists to forecast weather. In weather prediction, new data must continually be taken into account as atmospheric conditions change. Prediction of disease outbreak, they reasoned, also needs to continually incorporate new information.

Shaman had previously developed a mathematical model of flu transmission that takes into account how humidity levels affect susceptibility to infection. In the new study, the researchers incorporated Google Flu Trends data into the model. Google researchers—working with scientists at the Centers for Disease Control and Prevention—have shown a close relationship between how many people search for flu-related topics and how many actually have flu symptoms. Google Flu Trends uses search data to estimate current flu activity in numerous countries. It also tracks activity by district, province, state or municipality.

The researchers incorporated these web-based estimates for the 2003–2008 influenza seasons in New York City into their model of influenza transmission dynamics. Their study was funded by NIH’s National Institute of General Medical Sciences (NIGMS) and National Institute of Environmental Health Sciences (NIEHS), along with the Department of Homeland Security. Results appeared online on November 26, 2012, in Proceedings of the National Academy of Sciences.

The scientists assimilated weekly flu activity estimates into the simulations. They then generated weekly forecasts using the optimized model. They showed that, by using this method, they were able to make accurate real-time predictions of flu outbreak peaks more than 7 weeks in advance of the actual peaks.

The ability to predict the timing and severity of seasonal flu outbreaks can help health officials and the general public better prepare. “Flu forecasting has the potential to significantly improve our ability to prepare for and manage the seasonal flu outbreaks that strike each year,” says Dr. Irene Eckstrand of NIGMS.

The scientists expect the accuracy of their model’s predictions to rise as more years of Google Flu Trends data and more locations become available. The approach can also be adapted to develop predictions for other seasonally recurring respiratory diseases, such as respiratory syncytial virus—a major cause of respiratory infections in children—and rhinovirus, which causes the common cold.

By Harrison Wein, Ph.D.

###

Forecasting Flu Outbreaks is an article review from: Medicinezine.com

Gene Variations Linked to Lung Cancer in Non-Smokers

Editor — Mon, 10 Dec 2012 18:03:40 +0000

Gene Variations Linked to Lung Cancer in Non-Smokers

Researchers identified 3 genetic regions that predispose Asian women who’ve never smoked to lung cancer. The finding provides evidence that lung cancer among never-smokers can differ on a fundamental level from lung cancer in smokers.

Up to 90% of lung cancer deaths can be attributed to smoking. But lung cancer in people who never smoked is still the seventh leading cause of cancer deaths worldwide. Many women in Eastern Asia who’ve been diagnosed with lung cancer have never smoked. Environmental factors, such as secondhand smoke or exhaust from indoor cooking, likely account for some cases. But in most regions of Eastern Asia, they explain only a small proportion of these cases.

To gain a better understanding of lung cancer in Asian females who never smoked, researchers from NIH’s National Cancer Institute (NCI) partnered with colleagues from several other countries to conduct the largest genome-wide association studies (GWAS) in female never-smokers to date. GWAS scan the genomes of large numbers of people to find genetic variations associated with a particular disease or trait.

The scientists combined data from 14 studies from mainland China, South Korea, Japan, Singapore, Taiwan and Hong Kong that involved a total of about 14,000 Asian women (6,600 with lung cancer and 7,500 without the disease). Some of these studies included data on environmental factors, such as exposure to secondhand smoke. The results were published in the December 2012 issue of Nature Genetics.

The researchers found that variations at 3 locations in the genome—2 on chromosome 6 and another on chromosome 10—were associated with lung cancer in Asian females who’d never smoked. The discovery on chromosome 10 was particularly noteworthy, since it hadn’t been identified in any previous GWAS of lung cancer.

Variations at a location on chromosome 15 have been linked to lung cancer risk in many previous GWAS of lung cancer that were conducted primarily in smokers. In the new study, however, the researchers didn’t detect an association with this region. The finding suggests that the variations associated with lung cancer on chromosome 15 may be smoking-related.

The researchers did find evidence that Asian women with one of the newly identified genetic variants may be more susceptible to the effects of environmental tobacco smoke. However, more research will be needed to prove the connection.

“This study is the first large-scale genome-wide association study of lung cancer among never-smoking females anywhere in the world,” says lead investigator Dr. Qing Lan of NCI. The findings illustrate how GWAS can yield insights into inherited genetic risk in populations with unique characteristics or environmental exposures.

“Our study provides strong evidence that common inherited genetic variants contribute to an increased risk of lung cancer among Asian women who have never smoked,” says coauthor Dr. Nathaniel Rothman of NCI. “These variants may also increase lung cancer risk associated with environmental factors, such as environmental tobacco smoke.”

###

Gene Variations Linked to Lung Cancer in Non-Smokers is an article review from: Medicinezine.com

Old Habits Gone But Not Forgotten

Editor — Mon, 10 Dec 2012 17:53:31 +0000

Old Habits Gone But Not Forgotten

Scientists have identified a small region of the rat brain that seems to control whether certain habits will continue or be replaced by new habits. The finding offers insights into the brain pathways that help us shift between fixed and flexible behaviors.

Habits are a powerful force in our lives. Repeated activities—like tooth brushing or driving the same route to work—can become ingrained behaviors performed with little conscious thought. Such automatic habits can be helpful. Others can become harmful routines, such snacking on sweets, smoking, or abusing drugs or alcohol.

Scientists have long searched for the brain circuitry that creates, controls and overwrites our habits. Earlier research hinted that a specific brain area—known as the infralimbic cortex in rats—plays an important role.

To learn more, Drs. Ann Graybiel and Kyle Smith of the Massachusetts Institute of Technology and their colleagues used a technique called optogenetics to turn the infralimbic cortex off and on in rats with ingrained habits. The approach uses flashes of laser light to temporarily shut down genetically altered cells in specific brain regions. The study was supported in part by NIH’s National Institute of Mental Health (NIMH).

As reported in the November 13, 2012, edition of the Proceedings of the National Academy of Sciences, the scientists trained rats to run a T-shaped maze. As rats approached the crossroad, differing audio tones signaled which of 2 possible rewards awaited—sugar water might lay in one direction or chocolate milk in the other. Choosing the wrong direction meant no reward. Eventually, running the maze correctly became nearly automatic for the rats.

To confirm that the behavior had become a habit, the scientists then “devalued” one of the rewards by pairing it with an unpleasant substance. Despite their new aversion to one of the rewards, the rats continued to run the maze as before, turning toward the now-distasteful reward when cued by a certain tone.

Using optogenetics, the scientists then briefly disabled the infralimbic cortex as rats approached the crossroad. With that brain area offline, the rats appeared to act more thoughtfully, turning away from the unpleasant reward and toward the untainted treat. Over time, they continued this new habit, automatically turning in the same direction regardless of the cue or reward.

Once the new habit was firmly established, the infralimbic cortex was again disrupted via optogenetics. Surprisingly, the new habit was blocked, and the rats returned to their original habit of following the audio cues, even if it led to an unpleasant reward.

“This habit was never really forgotten,” Smith says. “It’s lurking there somewhere, and we’ve unmasked it by turning off the new one.”

These results suggest that the brain can quickly toggle between old and new habits, and that the infralimbic cortex plays a key role in mediating these behaviors. “To us, what’s really stunning is that habit representation still must be totally intact and retrievable in an instant, and there’s an online monitoring system controlling that,” Graybiel says.

By Vicki Contie

###

Old Habits Gone But Not Forgotten is an article review from: Medicinezine.com

A Little Exercise Might Lengthen Life

Editor — Mon, 03 Dec 2012 17:45:44 +0000

A Little Exercise Might Lengthen Life

A little physical activity can go a long way toward extending your life, regardless of your weight, a new study found. People who walked briskly or did other activity at only half the recommended amount gained nearly 2 years in life expectancy compared to inactive people. Those who exercised even more gained up to 4.5 years of life.

Researchers have long known that physical activity can enhance health. Exercise can help with weight control; strengthen bones, muscles and joints; and reduce the risk for heart disease and other disorders. Despite these known benefits, most Americans are sitting or inactive for more than half of each day, and about one-third of U.S. adults are obese.

Earlier studies identified a relationship between longevity and both physical activity and body mass index (BMI, a ratio of weight to height). But it was unclear how different levels of activity and BMI might affect life expectancy.

To take a closer look, an international team of scientists led by Dr. Steven C. Moore at NIH’s National Cancer Institute (NCI) analyzed data on more than 650,000 adults who were followed for about 10 years. These people, mostly age 40 and older, were drawn from 6 studies originally designed to assess cancer risk. The studies relied on self-reported activity levels and BMIs. The work was funded in part by NCI, along with NIH’s National Institute on Aging (NIA) and National Heart, Lung and Blood Institute (NHLBI).

As reported in the November 2012 issue of PLoS Medicine, the researchers found that people who said they exercised at recommended levels gained 3.4 years of life compared to those who were inactive. The U.S. Department of Health and Human Services recommends that adults engage in physical activity for 2.5 hours at moderate intensity—or 75 minutes at vigorous intensity—each week.

Participants who were physically active at twice the recommended level gained 4.2 years in life expectancy. Those who said they got half the recommended amount of physical activity added 1.8 years to their lives.

The researchers also found that obesity was linked to a shorter lifespan. However, physical activity across all BMI levels helped to lengthen life. People who were active and moderately obese gained about 3 years of life expectancy compared to those who were normal weight but inactive.

The combination of obesity and inactivity led to the worst outcomes. People who were obese and inactive had a life expectancy that was between 5 and 7 years shorter than those who were normal weight and moderately active.

“In this study we saw that if you don’t do any activity, doing some will give you a benefit in terms of life expectancy. And if you currently do some activity, doing more will probably give you even greater benefits,” says Moore. “Regular exercise extended the lives in every group that we examined in our study—normal weight, overweight, or obese.”

###

A Little Exercise Might Lengthen Life is an article review from: Medicinezine.com

Gene Therapy for Salivary Gland Shows Promise

Editor — Mon, 03 Dec 2012 17:39:17 +0000

Gene Therapy for Salivary Gland Shows Promise

An experimental trial showed that gene therapy can be performed safely in the human salivary gland. The accomplishment may one day lead to treatments to help head and neck cancer survivors who battle with chronic dry mouth.

A mouse embryonic salivary gland.Credit: Melinda Larsen et al., Developmental Biology 255: 178-191, 2003.

People with head and neck cancer often receive radiation therapy to shrink their tumors. The radiation can damage salivary glands, reducing their ability to secrete saliva into the mouth. Saliva is needed for taste, swallowing and speech. It also helps prevent infection and tooth decay. Salivary glands may partly recover after radiation therapy, but recovery is usually not complete. Doctors have limited options to offer most patients.

In the early 1990s, as the first gene therapy studies entered research clinics, Dr. Bruce Baum of NIH’s National Institute of Dental and Craniofacial Research (NIDCR) saw the potential of gene therapy to restore saliva secretion in salivary glands. He and his colleagues have been working for years to restore saliva secretion in animal models. By delivering the gene for a protein called aquaporin-1 into salivary gland cells, they restored saliva secretion in animal models. Aquaporin-1 forms pore-like water channels in cell membranes to help move fluid—such as when salivary gland cells secrete saliva into the mouth.

In 2008, the scientists treated the first patients in a small clinical trial designed to assess safety, work out dosage and identify side effects. The team included investigators from NIDCR, NIH’s National Cancer Institute (NCI) and the NIH Clinical Center.

Eleven head and neck cancer survivors received a single-dose infusion directly into one of their 2 parotid salivary glands, the largest of the major salivary glands. The aquaporin-1 gene was packaged in a disabled adenovirus, which causes the common cold when intact. The disabled virus served as a delivery vehicle, or vector, entering cells that line the salivary gland and transferring the gene within. Once inside, the gene is turned on, or expressed, and directs the cells to make aquaporin-1.

The scientists reported on November 20, 2012, in Proceedings of the National Academy of Sciences that 6 of the 11 treated participants had increased levels of saliva secretion. Five also reported a renewed sense of moisture and lubrication in their mouths over the initial 42-day study period. There were no serious side effects.

The researchers tested 4 different doses of virus in the trial. Neither of the 2 people receiving the highest dose showed any benefit from the procedure. This and other observations suggest that higher doses of this virus may backfire, causing the immune system to launch an attack and prevent gene transfer.

“It is time to evaluate a different vector to deliver the aquaporin-1 gene, one that will cause only a minimal immune response,” Baum says.

Because of safety concerns, the researchers used a virus that causes only short-lived gene expression. Future research will be needed to develop methods that not only avoid an immune response but are also capable of longer-lived expression in salivary glands.

“These data will serve as stepping stones for other scientists to improve on this first attempt in the years ahead,” says Baum. “The future for applications of gene therapy in the salivary gland is bright.”

###

Gene Therapy for Salivary Gland Shows Promise is an article review from: Medicinezine.com

Technique Selectively Represses Immune System

Editor — Mon, 03 Dec 2012 17:25:43 +0000

Technique Selectively Represses Immune System

Researchers devised a way to successfully treat symptoms resembling multiple sclerosis in a mouse model. With further development, the technique might be used to treat multiple sclerosis and other autoimmune disorders.

Myelin (green) encases and protects nerve fibers (brown). A new technique prevents the immune system from attacking myelin in a mouse model of multiple sclerosis. / Credit: Dr David Furness, Wellcome Images. All rights reserved by Wellcome Images.

Multiple sclerosis is an autoimmune disease—a type of disease in which the immune system mistakenly attacks the body’s own tissues. In multiple sclerosis, immune system T cells attack myelin, the insulating material that encases nerve fibers. Resulting nerve damage in the brain and spinal cord can cause muscle weakness, loss of vision, numbness or tingling, and difficulty with coordination and balance. It can also lead to paralysis.

Current treatments for autoimmune disorders involve the use of immunosuppressant drugs. These work by tamping down immune system activity. However, they can also leave patients susceptible to infections and increase their risk of cancer. Drs. Stephen Miller and Lonnie Shea at Northwestern University teamed up with researchers at the University of Sydney and the Myelin Repair Foundation in California to come up with a more targeted approach. They aimed to repress only the part of the immune system that causes autoimmune disorders while leaving the rest of the system intact.

Their new approach takes advantage of a natural safeguard used by the body to deactivate T cells that have the potential to attack the body’s healthy tissues. Apoptotic, or dying, cells release chemicals that attract immune system cells called macrophages. Macrophages gobble up the dying cells and deliver them to the spleen, where they present self-antigens—tiny portions of proteins from the dying cells—to a pool of T cells. To ensure that T cells don’t attack the body’s own tissues, the macrophages initiate the repression of any T cells that bind to the self-antigens.

In previous work, Miller’s group was able to couple specific self-antigens such as myelin to apoptotic cells to tap into this natural mechanism and suppress T cells that would normally attack the body’s own tissue. However, using apoptotic cells as a vehicle proved to be a costly, difficult and time-consuming procedure.

In the new study, the team linked myelin antigens to microscopic, biodegradable particles in the hope that these would be similarly taken up by circulating macrophages. Their work was partly supported by NIH’s National Institute of Biomedical Imaging and Bioengineering (NIBIB) and National Institute of Neurological Disorders and Stroke (NINDS). The study appeared online on November 18, 2012, in Nature Biotechnology.

The myelin-bound particles proved to be just as good as apoptotic cells, if not better, at inducing T-cell tolerance in a mouse model of multiple sclerosis. The particles both prevented symptoms and slowed their progression when injected at first detection of disease symptoms.

The team is hoping to begin phase I clinical trials in the near future. The material that makes up the particles has already been approved by the U.S. Food and Drug Administration for other uses. The researchers are also exploring the approach to treat other autoimmune diseases such as type 1 diabetes and food allergies.

“I think we’ve come up with a very potent way to induce tolerance that can be easily translated into clinical practice,” Miller says. “We’re doing everything we can now to take this forward.”

###

Technique Selectively Represses Immune System is an article review from: Medicinezine.com

Cataloging Human Genetic Variation

Editor — Mon, 19 Nov 2012 18:55:43 +0000

Cataloging Human Genetic Variation

The world’s largest, most detailed catalog of human genetic variation—used by disease researchers around the world—has more than doubled in size. The newly published information will provide deeper insights into the genomic basis of human disease.

Genetically, people are more than 99% alike. Although most of the variations between us have little or no effect, others can contribute to disease. The goal of the 1000 Genomes Project is to identify and compile variants in the human genome that are harbored by at least 1 in 50 people. NIH’s National Human Genome Research Institute (NHGRI) helps fund and direct this international public-private consortium of scientists.

In the November 1, 2012, issue of Nature, the scientists described their latest map of genetic variation. They combined whole-genome sequencing with more detailed sequencing of the protein-coding regions of the genome—the “exome.” So far, the consortium has sequenced the genomes of over 1,000 people from 14 populations in Europe, East Asia, sub-Saharan Africa and the Americas. Ultimately, the scientists will study more than 2,500 people from 26 populations.

The new map includes 38 million single differences in DNA sequence, known as single nucleotide polymorphisms, or SNPs. It also includes 1.4 million short insertions or deletions of DNA (as small as a single base or as large as 50 bases) and 14,000 large deletions of DNA.

The researchers found that people from different populations have different profiles of rare variants. The patterns of rare variants differed by geography.

“Project researchers discovered that each person carries a handful of rare variants that would currently be recognized as disease-causing and a few hundred more rare variants that are likely to have a detrimental effect on how genes work,” says Dr. Gilean McVean of the University of Oxford in England, co-leader of the project’s analysis group. “It’s fortunate that most of us usually carry only 1 copy of these variants since 2 copies might lead to disease.”

All of the 1000 Genomes Project information is freely available on the Internet through public databases. The 2012 dataset will be followed by the last addition in 2013. This growing catalog will continue to help researchers pinpoint genetic variants associated with disease. Identifying the genetic underpinnings of disease can help lead to new diagnostic tests and treatments.

“With this project, we have succeeded in making sure that information about our shared genetic heritage, and the common DNA variants we carry, are freely available for researchers to use to benefit patients around the world,” says project co-leader Dr. David Altshuler of Massachusetts General Hospital and the Broad Institute. “Moreover, the tools and methods that this project has helped foster are being used now in disease-oriented genetics research and will be used increasingly in clinical care.”

###

Cataloging Human Genetic Variation is an article review from: Medicinezine.com

Brain Wave Synchronization Key to Working Visual Memory

Editor — Mon, 19 Nov 2012 17:50:23 +0000

Brain Wave Synchronization Key to Working Visual Memory

Short-term memories are stored as synchronized signals between 2 key brain hubs, according to a new study in monkeys. The findings show for the first time how the brain stores visual information for working memory tasks.

Plots showing the coherence between activity of cells in different brain regions for objects the monkey saw over several trials. Red indicates that the brain waves were highly in-sync, and presumably involved in holding short-term memory about that object. The memory of each object is represented by its own unique mix of neurons oscillating in-sync. Image courtesy of Dr. Charles Gray, Montana State University.

Working memory is the ability to hold information in mind and quickly process that information in order to act on it. The visual working memory system has been extensively studied in monkeys and humans. Previous research showed that 2 brain areas, the prefrontal cortex and the parietal cortex, are activated when working memory is used. Electrical signals between neurons in this circuit become synchronized during an identity-matching task in which the subject is asked to match a previously seen object after a time delay.

In the new study, a team led by Dr. Charles Gray at Montana State University analyzed signals from groups of neurons in the prefrontal and parietal brain regions in monkeys performing visual working memory tasks. To earn a juice reward, the monkeys had to correctly identify an object (or its location) that had been previously shown to them on a computer screen. The study was funded by NIH’s National Institute of Mental Health (NIMH) and National Institute of Neurological Disorders and Stroke (NINDS). It appeared online on November 1, 2012, in Science.

The researchers expected to see increases in synchronous activity, or coherence, between the 2 brain hubs when the object disappeared from the screen and the monkeys had to hold that information in mind. Surprisingly, they found that the degree of coherence depended on the identity of the object. For example, neurons were more in-sync in response to an image of bananas than to an image of a teddy bear. This suggests that these neurons may be selective for particular visual features and that synchronized signals in this circuit carry content-specific information.

“This work demonstrates, for the first time, that there is information about short-term memories reflected in in-sync brainwaves,” says Gray.

Previously, many researchers had thought that the firing rate of single neurons in the prefrontal cortex, the brain’s executive hub, is the major player in working memory. The study found, however, that the parietal cortex was more influential in governing the patterns of synchronization.

The coherence patterns were different for each image that the monkeys saw. This suggests that it may be possible to determine the identity of an object and its location by analyzing these brain waves. Scientists might thus be able to predict the image seen by a monkey, in essence ‘seeing’ their short-term visual memories.

“The Holy Grail of neuroscience has been to understand how and where information is encoded in the brain. This study provides more evidence that large scale electrical oscillations across distant brain regions may carry information for visual memories,” says NIMH Director Dr. Thomas R. Insel.

###

Brain Wave Synchronization Key to Working Visual Memory is an article review from: Medicinezine.com

Dozens of Genes Linked to Bowel Diseases

Editor — Mon, 19 Nov 2012 16:08:20 +0000

Dozens of Genes Linked to Bowel Diseases

Researchers found 71 new human genes associated with Crohn’s disease and ulcerative colitis—forms of chronic inflammatory bowel disease (IBD) that affect nearly 2.5 million people worldwide. The study brings the total number of genes linked with IBD to 163.

The most common signs of IBD are diarrhea and abdominal pain. Its exact causes are unclear. Researchers believe an unknown factor or agent triggers an abnormal reaction by the body’s immune system. Genes play some role, as the disease tends to run in families. People of Jewish heritage, particularly Ashkenazi Jews of Eastern European descent, have an increased risk of developing IBD.

A consortium of researchers from the United States, Canada and Europe set out to find common genetic variants that influence the risk for IBD. They did a meta-analysis of 15 previous genome-wide association studies. Led by Dr. Judy H. Cho of Yale School of Medicine, their analysis included data from more than 6,000 people with Crohn’s disease, 7,000 with ulcerative colitis and 35,000 unaffected people.

The scientists also analyzed DNA samples using a custom chip called the Immunochip. This chip includes almost 200,000 small genetic variations selected from past studies of autoimmune and inflammatory diseases. The team examined more than 60,000 samples from over 20,000 people with Crohn’s disease, 15,000 people with ulcerative colitis, and 25,000 people with neither disease. The study was partly funded by several NIH institutes, led by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the November 1, 2012, issue of Nature.

The scientists found 71 new genes associated with IBD. Of the 163 genes now linked to IBD, 110 are associated with Crohn’s disease and ulcerative colitis, 30 are specific to Crohn’s and 23 are specific to ulcerative colitis. For 134 of the genes, the variants associated with disease aren’t predicted to cause changes in protein structure. These variants may affect when and to what extent the genes are turned on and off, known as gene expression.

The team found that many of the genes tied to IBD were previously linked with other inflammatory diseases, such as ankylosing spondylitis (spine inflammation) and the skin disorder psoriasis. “Performing the meta-analysis on these large datasets provides the statistical power and integrity to confirm the associations of these genes to IBD and identifies gene variants that until now, were only suspected to overlap with other inflammatory diseases,” Cho says.

The researchers also found considerable overlap between the genes linked to IBD and those responsible for resisting infections by mycobacteria, which can cause diseases such as tuberculosis and leprosy. “The marked extent to which the findings make clear the overlap between IBD and mycobacterial infections was rather unexpected,” Cho says.

These findings will help investigators further explore the pathways that lead to IBD and other inflammatory diseases. This knowledge may help lead to better, more targeted treatments. Nevertheless, even this large number of genes explains only a fraction of the risk for IBD. Further study will be needed to reveal other factors involved, both genetic and environmental.

###

Dozens of Genes Linked to Bowel Diseases is an article review from: Medicinezine.com

Healthy Diet May Fend Off Type 2 Diabetes After Gestational Diabetes

Editor — Wed, 31 Oct 2012 20:43:07 +0000

Healthy Diet May Fend Off Type 2 Diabetes After Gestational Diabetes

By keeping a healthy diet in the years after pregnancy, women who develop diabetes during pregnancy can greatly reduce their risk for type 2 diabetes, a new study found.

About 5% of pregnant women nationwide develop high blood sugar levels even though they didn’t have diabetes before pregnancy. This condition, called gestational diabetes, significantly raises a woman’s risk for type 2 diabetes later in life. In type 2 diabetes, cells don’t respond properly to insulin, a hormone that signals cells to take the sugar glucose in from the blood. If left untreated, blood sugar levels can soar and cause problems. Complications of type 2 diabetes include heart disease, stroke, kidney disease, blindness and amputation.

Research has shown that, among the general population, healthy eating can reduce the risk of developing type 2 diabetes. A team led by Dr. Cuilin Zhang of NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) aimed to explore how a healthy diet affects the risk for type 2 diabetes among women who’ve had gestational diabetes. The study was supported by NICHD along with NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and National Cancer Institute (NCI). Results appeared online on September 17, 2012, in the Archives of Internal Medicine.

The researchers studied over 4,400 women who developed gestational diabetes between 1991 and 2001. The women were taking part in a long-term study of nurses called the Nurses’ Health Study II. As part of the ongoing study, the nurses filled out questionnaires every other year on lifestyle and health. They completed a questionnaire every 4 years about their intake of several common food items during the previous year.

The researchers ranked the women’s diets by how closely they matched 3 widely studied diets: a Mediterranean-style diet, the Dietary Approaches to Stop Hypertension (DASH) diet and healthy eating guidelines developed by the U.S. Department of Agriculture (the Healthy Eating Index). All 3 diets promote eating fruits, vegetables, nuts, legumes and whole grains.

The researchers found that 491 of the women developed type 2 diabetes. The women who adhered most closely to the diets lowered their risk for type 2 diabetes considerably when compared to the least compliant. Women who followed the Mediterranean diet most closely had a 40% lower risk of developing type 2 diabetes. Those who followed the DASH diet most closely had a 46% lower risk. Those who adhered most closely to the Healthy Eating Index had a 57% lower risk.

“Our findings indicate that women with gestational diabetes aren’t necessarily preordained to develop type 2 diabetes,” Zhang says. “It appears they may have some degree of control. Sticking to a healthy diet may greatly reduce their chances for developing diabetes later in life.”

Dr. Zhang said her team is now evaluating other factors—such as genes, physical activity and other lifestyle variables—that might affect a woman’s diabetes risk in a large, ongoing study of U.S. and Danish women called the Diabetes and Women’s Health Study.

###

Healthy Diet May Fend Off Type 2 Diabetes After Gestational Diabetes is an article review from: Medicinezine.com

Improved COPD Detection

Editor — Wed, 31 Oct 2012 15:33:09 +0000

Improved COPD Detection

A new technique can distinguish between different types of chronic obstructive pulmonary disease (COPD) and track disease progression. The method could allow for more accurate diagnoses and lead to more effective treatments for COPD.

PRM images can help distinguish healthy lung areas (green) from those with early-stage damage (yellow) and emphysema (red). Image courtesy of University of Michigan Center for Molecular Imaging.

COPD is a lung disease that makes it hard to breathe. In people who have COPD, airway tubes to the lungs narrow, making it hard to get air in and out. COPD can cause wheezing, shortness of breath, chest tightness and coughing that produces large amounts of mucus. Cigarette smoking is the leading cause of COPD in the United States, but the disease can have other roots as well.

COPD can involve damage to the small airways of the lungs (functional small airways disease) as well as destruction of lung tissue (emphysema). The ability to diagnose the extent of lung damage could help doctors track disease progression and personalize COPD treatments. Current CT scan methods can assess the extent of emphysema, but measuring functional small airways disease has remained a challenge.

Researchers at the University of Michigan led by Dr. Brian D. Ross set out to address the problem by adapting an image analysis technique called parametric response mapping (PRM) that they’d first developed to track tumors. In PRM, a computer matches voxels—the smallest measureable unit of volume in an image data set—between CT scans. Voxels in scans taken during a full inhalation are matched with equivalent voxels in scans taken during a full exhalation. The density of healthy lung tissue changes more between the 2 states than the density of diseased lung tissue. By comparing densities in each voxel pair, a computer program can create 3-D maps of damage throughout the entire lung.

The scientists analyzed whole-lung CT scans of 194 people with COPD acquired at both full inhalation and full exhalation in the COPDGene study, which is funded by NIH’s National Heart, Lung and Blood Institute (NHLBI). Additional funding was provided by NIH’s National Cancer Institute (NCI) and National Institute of Biomedical Imaging and Bioengineering (NIBIB). Results appeared online on October 7, 2012, in Nature Medicine.

The researchers showed that PRM could successfully identify the extent of both functional small airways disease and emphysema. They also observed a pattern in the data suggesting that functional small airways disease may precede emphysema in the progression of COPD.

To investigate whether PRM could be used to track disease progression, the researchers analyzed images from people who had undergone inspiratory/expiratory CT scanning over a period of time. They found that PRM could be used to monitor COPD progression.

“Essentially, with the PRM technique, we’ve been able to tell sub-types of COPD apart, distinguishing functional small airway disease from emphysema and normal lung function,” Ross says. “We believe this offers a new path to more precise diagnosis and treatment planning and a useful tool for precisely assessing the impact of new medications and other treatments.”

By Harrison Wein, Ph.D.

###

Improved COPD Detection is an article review from: Medicinezine.com

Gene Tied to Hearing Loss and Usher Syndrome

Editor — Wed, 31 Oct 2012 15:25:51 +0000

Gene Tied to Hearing Loss and Usher Syndrome

Scientists discovered mutations in a gene that lead to hearing loss and also contribute to Usher syndrome. The finding adds to a growing body of knowledge about the biological pathways involved in these disorders.

CIB2 (green and yellow) is found in inner ear hair cells, including the tips of stereocilia. Image by the authors.

Usher syndrome is the most common condition that affects both hearing and vision. There are 3 clinical types of Usher syndrome. In the United States, types 1 and 2 are the most prevalent.

Researchers had previously linked a region on chromosome 15 to type 1 Usher syndrome in 2 families. The region was also tied to hearing impairment not linked with other symptoms (nonsyndromic deafness) in 5 large Pakistani families. The researchers later found 52 more Pakistani families with hearing impairment linked to the genetic region.

In their new report, the team worked to pinpoint the specific mutations responsible. The study was led by Drs. Zubair Ahmed and Saima Riazuddin of the University of Cincinnati and Dr. Thomas B. Friedman of NIH’s National Institute on Deafness and Other Communication Disorders (NIDCD). The results appeared in the November 2012 issue of Nature Genetics.

The researchers found that the mutations responsible were in a gene calledCIB2. These mutations are among the major causes of hearing impairment in the Pakistani population. The scientists also linked a mutation in the gene with deafness in a Turkish family.

CIB2 belongs to a family of proteins that bind calcium and integrins, a type of protein that is thought to regulate calcium concentration in specific places inside the cell. Experiments revealed that the newly identified mutations affect the way CIB2 binds calcium.

The researchers hypothesized that CIB2 plays a role in mechanotransduction—the process by which sound waves are transformed into the electrical signals that the brain recognizes as sound. CIB2 joins a growing list of genes associated with Usher syndrome. The proteins these genes produce are thought to interact to influence the structure and function of stereocilia, bristly structures that sit atop sensory “hair” cells in the inner ear. Most scientists believe that as stereocilia move, microscopic tethers between them open ion channels, the tiny holes in the cell that let electrically charged molecules (ions) pass in and out. The ions rushing inside begin an electrical signal that travels to the brain. CIB2, the researchers reasoned, may play a role in how calcium ions modulate these signals in hair cells.

Experiments in mice revealed CIB2 in the stereocilia of inner ear hair cells. Consistent with the protein playing a role in Usher syndrome, CIB2 also showed up in retinal photoreceptor cells, which convert light into electrical signals in the eye. Experiments in zebrafish and fruit flies found that CIB2 is essential for the function and proper development of both hair cells and retinal photoreceptor cells.

Taken together, these results suggest that CIB2 helps regulate calcium in the mechanotransduction process that enables us to hear. “With this knowledge, we are one step closer to understanding the mechanism of mechano-electrical transduction,” Ahmed says.

By Harrison Wein, Ph.D.

###

Gene Tied to Hearing Loss and Usher Syndrome is an article review from: Medicinezine.com

Cell Phones Track Malaria’s Spread

Editor — Mon, 22 Oct 2012 18:48:49 +0000

Cell Phones Track Malaria’s Spread

Researchers used mobile phone data to track malaria parasite movements across Kenya. The results may help guide the design of more effective disease control programs.

Nearly a million people die of malaria each year—mostly infants, young children and pregnant women, and most of them in Africa. The disease is caused by a single-cell parasite called Plasmodium. Female mosquitoes can become infected after feeding on an infected human. They, in turn, can infect a new person when they feed again. Malaria may bring fever, chills and flu-like illness. Left untreated, it can cause life-threatening complications.

Both the parasites that cause malaria and the mosquitoes that carry them have been extensively studied. Less well understood has been how human travel affects the spread of the disease. A team of researchers led by Dr. Caroline Buckee at the Harvard School of Public Health set out to use mobile phone data to better understand how people help spread the parasite.

The researchers estimated the daily locations of almost 15 million mobile phone subscribers in Kenya between June 2008 and June 2009. They mapped every call or text made by each person to one of almost 12,000 cell towers. They then compared the mobile users’ movements with a malaria prevalence map from 2009. Their study was supported in part by NIH’s National Institute of General Medical Sciences (NIGMS) and National Institute of Allergy and Infectious Diseases (NIAID). The results appeared on October 12, 2012, in Science.

As expected, the Kenyan travel network was dominated by the capital Nairobi, which forms a hub for human movement to and from all regions of the country. The parasite routes show that the Lake Victoria region serves as a major source of malaria. Main destinations for the parasite lay around the Lake Victoria region and in the Nairobi area.

Areas in the highly urbanized center of Nairobi had a low ratio of clinical cases to phone data estimates of imported parasites. In contrast, hospitals on the periphery of the city had a higher ratio of clinical cases to estimates based on the phone data. These patterns suggest that there is some local transmission in the residential and less developed areas, but less within the urban city center.

“This is the first time that such a massive amount of cell phone data—from millions of individuals over the course of a year—has been used, together with detailed infectious disease data, to measure human mobility and understand how a disease is spreading,” Buckee says.

Officials can employ mosquito control programs, medications and other measures such as bed nets to combat malaria. Understanding the roles that different regions play in the spread of disease can help them decide where best to direct their limited resources. Officials might also target human travel itself, encouraging travelers to alter their behaviors and focusing their surveillance efforts along high-risk routes.

By Harrison Wein, Ph.D.

###

Cell Phones Track Malaria’s Spread is an article review from: Medicinezine.com

Bacterial Protein in House Dust May Spur Asthma

Editor — Mon, 22 Oct 2012 18:40:52 +0000

Bacterial Protein in House Dust May Spur Asthma

A bacterial protein in common house dust may worsen allergies that could lead to asthma, according to a new report. The finding gives insight into the link between allergic asthma and the environment.

Asthma is caused by swelling and inflammation of the airways. When airways narrow, less air gets through to the lungs, causing wheezing, coughing, chest tightness and trouble breathing. Asthma can be triggered by allergy-causing substances in the environment called allergens. Indoor allergens from dust mites, cockroaches, dogs, cats, rodents, molds and fungi been linked to asthma.

Previous studies in mice have found that house dust extracts can promote asthma-like responses to inhaled proteins that normally wouldn’t trigger allergic reactions. A research team led by Dr. Donald Cook of NIH’s National Institute of Environmental Health Sciences (NIEHS) set out to explore whether microbial products in house dust might trigger these asthma-like responses. Their study appeared online on October 14, 2012, in Nature Medicine.

The scientists used an innocuous protein called ovalbumin for their screen. Mice inhaling either ovalbumin alone or any of a series of microbial products alone didn’t have airway reactions. However, when given together, certain products caused some mice to become sensitized to ovalbumin and develop airway inflammation when later exposed.

The scientists saw particularly strong allergic airway responses in mice receiving ovalbumin together with a bacterial protein called flagellin. Flagellin is a major component of structures called flagella that certain bacteria have on their surfaces. The mice displayed all the common symptoms of allergic asthma, including more mucus production, airway obstruction and airway inflammation.

Past studies have shown that a specific immune system receptor called Toll-like receptor 5 (TLR5) recognizes flagellin. TLR5 helps detect bacteria and activate a branch of the immune system called the innate immune system. The researchers explored how mice lacking the gene for TLR5 reacted in their inhalation tests. They found that both flagellin and house dust extracts primed weaker allergic airway responses in these mice than in mice that had the gene for TLR5. The results suggest that flagellin, through TLR5, may prime the immune system to react to allergens in house dust.

The researchers tested house dust extracts for flagellin and detected significant amounts of the protein. They also discovered that people with asthma have higher levels of antibodies against flagellin in their blood than people without asthma.

“All of these data suggest that flagellin in common house dust can promote allergic asthma by priming allergic responses to common indoor allergens,” says co-author Dr. Darryl Zeldin of NIEHS.

“More work will be required to confirm our conclusions, but it’s possible that cleaning can reduce the amount of house dust in general, and flagellated bacteria in particular, to reduce the incidence of allergic asthma,” Cook says.

###

Bacterial Protein in House Dust May Spur Asthma is an article review from: Medicinezine.com

Brain Protein Structure Offers Clues for Drug Design

Editor — Mon, 22 Oct 2012 16:15:21 +0000

Brain Protein Structure Offers Clues for Drug Design

Researchers have published the first highly detailed picture of how neurotensin, a molecule that plays an important role in the brain, interacts with its receptor. The achievement may help scientists design better drugs for certain disorders.

Neurotensin (see arrow) in the binding pocket of NTSR1. Image by Grisshammer and Tate labs, courtesy of Nature.

Neurotensin is a peptide of just 13 amino acids (too short to be called a protein). Because it acts on neurons, or nerve cells, it’s called a neuropeptide. When neurotensin binds its receptor, neurotensin receptor (NTSR1), it initiates a series of reactions. The neuropeptide plays many roles in the brain and also regulates digestive processes in the gut. Previous studies have shown that neurotensin may be involved in Parkinson’s disease, schizophrenia, temperature regulation, pain and cancer cell growth.

NTSR1 belongs to a class of membrane proteins called G-protein coupled receptors (GPCRs). The molecules that activate these receptors are called ligands. Previous X-ray crystallography studies showed that smaller ligands, such as adrenaline and retinal, bind in the middle of their respective GPCRs and well below the receptor’s surface.

A research team led by Dr. Reinhard Grisshammer of NIH’s National Institute of Neurological Disorders and Stroke (NINDS) set out to use X-ray crystallography to show what NTSR1 looks like in atomic detail when bound to neurotensin. Their study was supported by NINDS, NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and others. The report appeared online on October 10, 2012, in Nature.

In X-ray crystallography, scientists shoot X-rays at crystallized molecules to determine a molecule’s shape and structure. The X-rays change directions, or diffract, as they pass through the crystals. They then hit a detector where they form a pattern that is used to calculate the atomic structure of the molecule.

Forming well-diffracting neuropeptide-bound GPCR crystals is very difficult, and the researchers spent many years on the project. A group led by Dr. Christopher Tate at the MRC Laboratory of Molecular Biology in Cambridge, England, collaborated on the project. Tate’s lab used recombinant gene technology to create a stable version of NTSR1. Grisshammer’s lab employed the latest methods to crystallize the receptor bound to a short version of neurotensin.

The results suggest a novel binding mechanism for a neuropeptide to activate its target GPCR. Neurotensin binds to the outer part of its receptor, just at the receptor surface.

Atomic structures can guide the way scientists think about how proteins work. This finding may change the way scientists develop drugs targeting similar neuropeptide receptors.

“The knowledge of how the peptide binds to its receptor should help scientists design better drugs,” Grisshammer says. Nonetheless, he adds, more work will be needed to fully understand the detailed signaling mechanism of this GPCR.

###

Brain Protein Structure Offers Clues for Drug Design is an article review from: Medicinezine.com