Category: Health

{A study of more than 196,000 children found no association between a mother having an influenza infection anytime during pregnancy and an increased risk of autism spectrum disorders (ASDs) in children, according to a new study published online by JAMA Pediatrics.}

The study by Ousseny Zerbo, Ph.D., of Kaiser Permanente Northern California, Oakland, and coauthors included 196,929 children born in the health system from 2000 through 2010 at a gestational age of at least 24 weeks.

Within the group, there were 1,400 mothers (0.7 percent) diagnosed with influenza and 45,231 mothers (23 percent) who received an influenza vaccination during pregnancy. There were 3,101 children (1.6 percent) diagnosed with ASD.

The authors report no association between increased risk of ASD and influenza vaccination during the second and third trimesters of pregnancy. There was a suggestion of increased risk of ASD with maternal vaccination in the first trimester but the authors explain the finding was likely due to chance because it was not statistically significant after adjusting for multiple comparisons.

The study cannot establish causality and has several limitations, including ASD status determined by diagnoses on medical records and not validated by standardized clinical assessment for all cases. Also, the authors could not control for other possible unmeasured mitigating factors.

“We found no association between ASD risk and influenza infection during pregnancy or influenza vaccination during the second to third trimester of pregnancy. However, there was a suggestion of increased ASD risk among children whose mothers received influenza vaccinations early in pregnancy, although the association was insignificant after statistical correction for multiple comparisons. While we do not advocate changes in vaccine policy or practice, we believe that additional studies are warranted to further evaluate any potential associations between first-trimester maternal influenza vaccination and autism,” the study concludes.

{Heart disease is a leading cause of early death in the world today, and many people spend a lot of their day in sedentary position, which isn’t good either. Many hours spent in the office are in sedentary positions and it’s also the same when you get home.
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Research has shown that it’s bad for your heart, and if you want to live longer you should start walking more, every day.

What if you find that just a simple walking regime every day would make you live longer?

Researchers at Binghamton University, State University of New York found that moderately intensive walking improves cardiovascular risk factors in the short-term.

A team of researchers led by Pamela Stewart Fahs conducted the study on a group of 70 women. The Participants were given a programmable pedometer to wear for waking hours over a 10-week period and asked to walk briskly for at least 150 minutes per week. Two days later, they returned to record pre-test data. Next, a web-based risk assessment tool was used to determine the participant’s risk of a heart attack within the next 10 years.

After five weeks, participants were invited to attend a talk about heart health and to have their pedometer data downloaded. Researchers reviewed the activity data with the participants and discussed increasing their aerobic steps. Participants were also offered a challenge in an effort to increase aerobic activity as well as to improve retention to study completion. This challenge included an increase their total daily average of aerobic steps by at least 10 percent for the remainder of the study.

Finally, on completion of the program, participants’ weight, BMI, blood pressure, and cholesterol were measured. They were also asked to complete a survey about their physical activity, food choices, personal characteristics and behaviors from the 10-week period.

The results of their post-test confirmed the team’s initial hypothesis that walking would improve cardiovascular risk factors in the short term.

The study, titled “Walking for Heart Health: A Study of Adult Women in Rural New York,” was published in Creative Nursing.

{If you’ve not been eating eggs, you don’t know what you’ve been missing out on; eggs are about the healthiest foods you can eat as a person. They have a lot of nutrients that are designed to keep you in proper health.}

Take a look at some of the benefits you stand to enjoy from eating enough eggs.

{{ Eggs raise the HDL level }}

Also known as ‘good cholesterol’, HDL can be found in the blood stream. Its job is to move around the blood, looking for bad cholesterol and fat to eliminate from the blood stream. In doing this, the HDL ensures you are safe from heart attack. The higher the HDL, the safer you are, and the lower, the less safe.

{{Healthier bones }}

Eggs have the right combination of vitamins required to give you stronger, healthier bones. So the more eggs you eat, the stronger your bones are.

{{They promote weight loss }}

If you’re looking to eat less calories, and lose some weight, you have no reason not to eat eggs.

According to a new research from the Rochester Centre for Obesity in America, eating eggs for breakfast could help limit your calorie intake throughout the rest of the day, by more than 400 calories.

{{Healthier brain }}

Just like with your bones, eggs have all the right nutrients your brain requires to stay in top condition. You end up being smarter, think faster, and even more.

{{They are rich in protein }}

If you didn’t know that eggs have one of the highest levels of protein you’ll find in any food, now you know. Protein is very important for your general well being. So eat more eggs to stay healthier.

{{Protection from eye diseases }}

Eggs have the right nutrients to ward off harmful eye conditions like cataract, and make your eyesight sharper and better.

{{Healthier hair and nails }}

And the list goes on. Eating eggs can also give you healthier hair and nails.

Eat right, and stay healthy.

{Scientists at the Universities of York and Texas have found that a component of cancer cells, which acts like a ‘cellular post office’, could be the key to preventing the spread of lung cancer to other parts of the body.}

The findings could point towards new therapeutics, targeted at a particular communication mechanism in the cell. This communication triggers a change in the scaffolding of the cell perimeter — altering from a fixed shape, attached to an organ, to a less stable one, moving freely around the body.

The ‘post office’ of the cell, or the Golgi apparatus as it is more commonly known, has the ability to package proteins in order to transport them to other parts of the cell or to deliver them to areas outside of the cell.

Researchers identified that a protein, called PAQR11, inside the ‘cellular post office’, receives a signal from another protein, called Zeb1; the communication between the two proteins prompts the transport of membrane sacks inside the Golgi.

These sacks, or vesicles, change their delivery routes and fundamentally alter the perimeter of the cancer cells making it possible for the cell to detach from its fixed position in the lung and travel to other areas of the body.

Dr Daniel Ungar, from the University of York’s Department of Biology, said: “If we think of the cancer cell like a tent structure; it has fixed sides to hold its shape and is firmly anchored to the ground in order to secure its contents. It cannot conceivably be moved until its architecture is altered somehow.

“In order to move the tent, we have to rearrange its contents and collapse its sides in order to lift it out of its anchored position and carry it away. A similar process happens with cancer when it metastasises — its outer edges are altered resulting in it becoming un-anchored.”

The Golgi, which is the delivery centre for communications between proteins, hence the name ‘cellular post office’, receives the communication between two proteins, which signals that the movement of membrane sacks around the cell should be changed. This change in movement alters the perimeter of the cancer cell and, much like a tent’s sides collapsing, allows it to move from its original resting place to anywhere in body.

Dr Ungar added: “Now that we recognise this system, there is the potential to develop a drug that interferes with this communication and prevents the Golgi apparatus from facilitating the movement of the membrane sacks. The next stage of this study will be to look at how we target this process without interrupting normal cellular functions of non-cancerous cells.”

The research, funded by the National Institutes of Health, the American Cancer Society, and the Cancer Prevention Research Institute of Texas, is published in The Journal of Clinical Investigation.

{Do air-borne allergens in schools affect students’ asthma symptoms?

A new article by Wanda Phipatanakul, M.D., M.S., of Boston’s Children’s Hospital and Harvard Medical School, Boston, and coauthors examined that question in a study that included 284 students (ages 4 to 13) enrolled at 37 inner-city schools in the northeastern United States.}

Classroom and home dust samples linked to the students were collected and analyzed for common indoor allergens, including rat, mouse, cockroach, cat, dog and dust mites. Associations between school exposure to allergens and asthma outcomes were adjusted for exposure to the allergens at home.

Mouse allergen was the most commonly detected allergen in schools and homes. Higher exposure to mouse allergen at school was associated with increased asthma symptoms and lower lung function, according to the results.

None of the other airborne allergens were associated with worse asthma outcomes. While cat and dog allergens were commonly detected in the schools, dust mite levels were low and cockroach and rat allergens were mostly undetectable in schools and homes.

Limitations of the study include results that may not be generalizable to other cities where other allergens may be predominant in schools.

“These findings suggest that exposure reduction strategies in the school setting may effectively and efficiently benefit all children with asthma. Future school-based environmental intervention studies may be warranted,” the authors conclude.

{Mental disorders and physical diseases frequently go hand in hand. For the first time, psychologists at the University of Basel and Ruhr University Bochum have identified temporal patterns in young people: arthritis and diseases of the digestive system are more common after depression, while anxiety disorders tend to be followed by skin diseases.}

Physical diseases and mental disorders affect a person’s quality of life and present a huge challenge for the healthcare system. If physical and mental disorders systematically co-occur from an early age, there is a risk that the sick child or adolescent will suffer from untoward developments.

{{Data from 6,500 teenagers}}

In a project financed by the Swiss National Science Foundation, a research group led by PD Dr. Marion Tegethoff in collaboration with Professor Gunther Meinlschmidt from the University of Basel’s Faculty of Psychology has now examined the temporal pattern and relationship between physical diseases and mental disorders in children and young people. In the journal PLOS ONE, they analyzed data from a representative sample of 6,483 teenagers from the US aged between 13 and 18.

The researchers noted that some physical diseases tend to occur more frequently in children and adolescents if they have previously suffered from certain mental disorders. Likewise, certain mental disorders tend to occur more frequently after the onset of particular physical diseases. Affective disorders such as depression were frequently followed by arthritis and diseases of the digestive system, while the same relationship existed between anxiety disorders and skin diseases. Anxiety disorders were more common if the person had already suffered from heart disease. A close association was also established for the first time between epileptic disorders and subsequent eating disorders.

{{Epilepsy and eating disorders}}

The results offer important insights into the causal relationship between mental disorders and physical diseases. The newly identified temporal associations draw attention to processes that could be relevant both to the origins of physical diseases and mental disorders and to their treatment. In an earlier study, the same authors had already provided evidence for the relationship between mental disorders and physical diseases in young people.

“For the first time, we have established that epilepsy is followed by an increased risk of eating disorders — a phenomenon, that had previously been described only in single case reports. This suggests that approaches to epilepsy treatment could also have potential in the context of eating disorders,” explains Marion Tegethoff, the study’s lead author. From a health policy perspective, the findings underscore that the treatment of mental disorders and physical diseases should be closely interlinked from an early age on.

{How highly potent antibody neutralizes Zika infection discovered.
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As Zika spreads throughout the world, the call for rapid development of therapeutics to treat Zika rings loud and clear. Taking a step further in identifying a possible therapeutic candidate, a team of researchers at Duke-NUS Medical School (Duke-NUS), in collaboration with scientists from the University of North Carolina, have discovered the mechanism by which C10, a human antibody previously identified to react with the Dengue virus, prevents Zika infection at a cellular level.

Previously, C10 was identified as one of the most potent antibodies able to neutralise Zika infection. Now, Associate Prof Lok Shee-Mei and her team at the Emerging Infectious Disease Programme of Duke-NUS have taken it one step further by determining how C10 is able to prevent Zika infection.

To infect a cell, virus particles usually undergo two main steps, docking and fusion, which are also common targets for disruption when developing viral therapeutics. During docking, the virus particle identifies specific sites on the cell and binds to them. With Zika infection, docking then initiates the cell to take the virus in via an endosome — a separate compartment within the cell body. Proteins within the virus coat undergo structural changes to fuse with the membrane of the endosome, thereby releasing the virus genome into the cell, and completing the fusion step of infection.

Using a method called cryoelectron microscopy, which allows for the visualisation of extremely small particles and their interactions, the team visualised C10 interacting with the Zika virus under different pHs, so as to mimic the different environments both the antibody and virus will find themselves in throughout infection. They showed that C10 binds to the main protein that makes up the Zika virus coat, regardless of pH, and locks these proteins into place, preventing the structural changes required for the fusion step of infection. Without fusion of the virus to the endosome, viral DNA is prevented from entering the cell, and infection is thwarted.

“Hopefully, these results will further accelerate the development of C10 as a Zika therapy to combat its effects of microcephaly and Guillain-Barré syndrome. This should emphasise the need for further studies of the effect of C10 on Zika infection in animal models,” commented Dr Lok.

“By defining the structural basis for neutralization, these studies provide further support for the idea that this antibody will protect against Zika infection, potentially leading to a new therapy to treat this dreaded disease,” says Ralph Baric, PhD, professor in the Department of Epidemiology at UNC’s Gillings School of Global Public Health.

These findings suggest that C10 may be developed as a therapy for Zika infection, and should be further explored. In addition, disrupting fusion with C10 may prove to be more effective in preventing Zika infection compared with therapies that attempt to disrupt docking. This is because the fusion step is critical for Zika infection, while the virus may develop other mechanisms to overcome disruptions to the docking step. With the call for rapid development of Zika therapies, C10 has emerged as a front runner to answer this call.

{Since 1980, the incidence of hepatocellular carcinoma, the most common type of liver cancer, has nearly tripled, and obesity related liver disease is one of the driving forces behind the increasing number of cases. Baylor College of Medicine researchers are now examining how other lifestyle factors may affect your health. Using mice, the scientists show that repeated jet lag increases both obesity related liver disease and the risk of liver cancer. The study appears November 23 in Cancer Cell.}

“Liver cancer is on the rise worldwide, and in human studies we’ve now seen that patients can progress from fatty liver disease to liver cancer without any middle steps such as cirrhosis,” says David Moore, a professor of molecular and cellular biology, who led the study with Associate Professor Loning Fu, both at Baylor. “We knew we needed an animal model to examine this connection, and studies in the Fu Lab found that chronically jet-lagged mice developed liver cancer in a very similar way as that described for obese humans.”

When we are exposed to light, our bodies’ central circadian clock in the brain resets. When we constantly travel through different time zones, work night shifts, or push ourselves to stay awake at the regular sleep time, our central clock is being chronically disrupted. This disruption also extends to clocks in other tissues that are controlled by the central clock.

By changing the times the lights went on and off during the night each week, the researchers modeled the effects of chronic jet lag in normal mice who were fed a healthy diet. They found that the mice gained weight and fat, and developed fatty liver disease, which progressed to chronic inflammation and eventually liver cancer in some cases

The jetlagged mice lost normal control of liver metabolism. This included not only the buildup of fat, but also increased production of bile acids, which are produced by the liver to help us digest our food. Earlier studies have linked high bile acid levels to liver cancer, not only in mice but also in humans.

The researchers found that circadian clock disruption activated two nuclear receptors that help regulate liver bile acid metabolism. Jetlagged mice lacking a receptor called FXR, which keeps bile acid level in the liver within a normal physiological range, had higher bile acid levels and much more liver cancer. Mice lacking a receptor called CAR that regulates bile acid breakdown and is also known to promote liver cancer, did not get any liver tumors.

In humans, these receptors work in a similar manner. The Baylor College of Medicine scientists didn’t directly study jetlag in humans. But there is evidence that sleep disruption increases both fatty liver disease and liver cancer risk in humans, and they hypothesize that lifestyle changes that generate chronic jet lag can also disrupt the body’s internal homeostasis and increase liver cancer risk in humans.

“Recent studies have shown that more than 80 percent of the population in the United States adopt a lifestyle that leads to chronic disruption in their sleep schedules,” says Loning Fu. “This has also reached an epidemic level in other developed countries, which is coupled with the increase in obesity and liver cancer risk.”

The scientists hope to continue their research to further examine whether drugs interacting with the nuclear receptors can help to prevent jet lag from affecting bile acid levels in the liver, with the ultimate goal of potentially using them as pharmaceutical strategies to prevent liver cancer in humans.

“This experiment allowed us to take several threads that were already there and put them together to come to this conclusion,” says Moore. “We think most people would be surprised to hear that chronic jet lag was sufficient to induce liver cancer.”

“To us, our results are consistent with what we already knew about these receptors, but they definitely show that chronic circadian disruption alone leads to malfunction of these receptors,” Fu adds. “And thus, maintaining internal physiological homeostasis is really important for liver tumor suppression.”