Global Community Marks World AIDS Day Today 1 December

The international community can end the AIDS epidemic by 2030 by working together, according to the Executive Director of the Joint UN Programme on HIV/AIDS (UNAIDS).

Speaking ahead of World Aids Day, marked annually on 1 December Michel Sidibé said health systems need to be strengthened.

He added that more should be done to reach people left behind, including young women and girls, men who have sex with men, prisoners and sex workers.

Now, Mr Sidibé said, is the time to break the AIDS epidemic for good as it could "spring" back and be impossible to end.

“I want to say to the world that it's time for us to redouble our effort, to fast track our actions, to make sure that we quicken the pace. Together I am sure we can end AIDS epidemic by 2030.”

Mr Sidibé added that this day is an opportunity to reflect on the lives lost to Ebola given the outbreak's similarities to the beginning of the AIDS epidemic.

He explained that Ebola sufferers were hiding, scared, and facing widespread stigma and discrimination of the type encountered by the first people to contract AIDS.

In a related development, the President of Bridging the Gap foundation,an NGO Emmanuel Quainoo, says for Ghana to make meaningful headway in the fight against HIV/AIDS, it is imperative that students are included in all aspects of the education drive.

He said if students get the message on HIV and AIDS and make healthy lifestyle choices, they will in turn disseminate the information among their peers, parents, siblings and other relatives.

Mr Quainoo appealed to NGOs dealing in HIV/AIDS prevention in Ghana to endeavour to promote the adoption of healthy lifestyle choices among students.


GBC/United Nations.

5 ways how we are letting stress affect our cells

Although you experience it in the head, your body is the first to react to stress.

With sudden onset of stress, the muscles get tense all at once, and then release their tension when the trigger passes.Chronic stress causes the muscles in your body to remain in a constant state of caution. When muscles stay tense for long, they can lead to other reactions in the body and even promote stress-related disorders. Both, tension headache and migraine headaches are associated with chronic muscle tension in the shoulders, neck and head. Then, the heart rate speeds up, muscles tighter, face turns red and there's a general sense of uneasiness and helplessness. But stress can also seep into your cells.Rising temperatures, toxins, infections, and resource shortages threaten how cells function and impact your health. Here are five ways you may be letting stress affect your cell.

PASS IT ON

Environmental stress can reach deep into the cells' interiors and alter the genetic material held within their nuclei. And the changes can be inherited. A study showed that limited food availability during a man's lifetime was linked to his grandchildren's risk of diabetes, obesity and cardiovascular disease.Another research at an American school showed that when male mice were fed a low-protein diet, the activity of hundreds of genes in the animals' offspring changed. In particular, genes that manufacture fats were more active. While making more fats might be a protective stress response, it also could lead to obesity and related diseases.Genomic (discipline in genetics that applies recombinant DNA) research suggests a potential link between changes transmissible from parent to offspring in patterns of gene activity and changes in chemical markers, affixed to certain genes.Scientists are trying to understand the nature of these changes and how they occur.

PRODDING THEM TO TANGLE

Increased temperature can stress out cells. Expose them to temperatures just three degrees than they are used to, and the proteins in the cell begin to unravel and stop functioning. If they unravel too much, they tangle up with each other and form a clump that can kill the cell. To prevent this, cells rely on a set of molecules called heat shock proteins that work in many different ways. Some tuck the sticky, carbonrich regions of unfolded proteins into a small pocket; others form barrels that sequester unravelled proteins away from any potential tangling partners. Once the body cools down, heat shock proteins help refold into proper shapes. THEY EVOLVE Cells can adapt to stressful conditions in a short period. They use intricate mechanisms to maintain the stability of their genetic DNA material. For example, yeast -an organism commonly used to study human genetics -quickly gained or lost entire chromosomes when researchers stressed it with exposure to different chemicals.After prolonged exposure, colonies of yeast with chromosome changes evolved resistance to certain chemicals, including an antibiotic. Under stressful conditions, however, they relax these controls.


AGEING THEM PREMATURELY

Doctors say, every cell in your body has its own doomsday clock, ticking down the number of times it can safely divide. This clock takes the form of a cap on the ends of each chromosome. Telomeres (a compound structure at the end of a chromosome) keep the chromosome from fraying. But they get shorter each time the cell divides. Shortened telomeres have been linked to agerelated diseases, such as arthritis, hypertension, and diabetes.Research suggests that chronic stress can dramatically shorten telomere length, causing cells to age and die prematurely. As a countermeasure, certain cells respond to temporary stressors like fear or infection by upping their production of the enzyme, telomerase, that helps telomeres maintain their length.

LEADING THEM TO SUICIDE

At the cellular level, death is essential for life. Apoptosis is a normal, programmed process of cellular self-destruction. It is called cellular suicide. And although it involves cell death, apoptosis serves a healthy and protective role in our bodies. It, in fact, helps shape our physical features and organs before birth and rids our bodies of unneeded or potentially harmful cells. This strategy sidesteps the destructive effects of a cell dying from the stressful conditions, which can kill nearby healthy cells by triggering inflammation. And since cell death plays a role in a number of neurological and cardiovascular diseases, medical experts believe understanding how cells make the life-or-death decision might lead to ways to reduce the damage caused by these types of conditions.

-TOI

Why do people cry even though they are happy

"Tears flow when people are overwhelmed with strong positive emotions and people who do this seem to recover better from those strong emotions," said psychologist Oriana Aragon at the Yale University in the US.

People overcome strong positive emotions with tears of joy, says a study, adding that crying actually helps them recover from the situation.

Aragon and her colleagues at Yale ran participants through some emotional scenarios such as cute babies or a crying spouse who is reunited with her soldier husband returning from war, and measured their responses.

"People restore emotional equilibrium with these expressions," she added.

They found that individuals who express negative reactions to positive news were able to moderate intense emotions more quickly.

They also found people, who are most likely to cry at their child's graduation are most likely to want to pinch a cute baby's cheeks.

There is also some evidence that strong negative feelings may provoke positive expressions.

For example, nervous laughter appears when people are confronted with a difficult or frightening situations, and we also smile during extreme sadness.

"The new discoveries begin to explain common things that many people do but do not even understand themselves," Aragon said.

"These insights advance our understanding of how people express and control their emotions, which is importantly related to mental and physical health, the quality of relationships with others, and even how well people work together," she concluded.

The paper was published in the journal Psychological Science.

Promising target for HIV treatment identified

Like a slumbering dragon, HIV can lay dormant in a person's cells for years, evading medical treatments only to wake up and strike at a later time, quickly replicating itself and destroying the immune system.

Now, scientists at the Salk Institute for Biological Studies have uncovered a new protein that participates in active HIV replication.

The protein, called Ssu72, is part of a switch used to awaken HIV-1 (the most common type of HIV) from its slumber.

The team began by identifying a list of 50 or so proteins that interact with a well-known protein HIV creates called Tat.

"The virus cannot live without Tat," said Katherine Jones, Salk professor in the Regulatory Biology Laboratory and senior author of the study.

Tat acts as a lookout in the cell for the virus, telling the virus when the cellular environment is favourable for its replication.

When the environment is right, Tat kicks off the virus' transcription, the process by which HIV reads and replicates its building blocks (RNA) to spread throughout the body.

One of the proteins on the list that caught Jones' eye was Ssu72 (a phosphatase).

This enzyme had been shown in yeast to affect the transcription machinery. Her team found that Ssu72 binds directly to Tat and not only begins the transcription process, but also creates a feedback loop to ramp up the process.

"Tat is like an engine for HIV replication and Ssu72 revs up the engine," said Lirong Zhang, one of the first authors.

"If we target this interaction between Ssu72 and Tat, we may be able to stop the replication of HIV," said Zhang.

The team found that Ssu72 is not required for making RNA for most host cell genes in the way it is used by HIV, making it a potentially promising target for drug therapy.

"Many proteins that Tat interacts with are essential for normal cellular transcription so those can't be targeted unless you want to kill normal cells," said co-first author Yupeng Chen, a Salk researcher.

"Ssu72 seems to be different - at least in the way it is used by HIV," said Chen.

The study was published in the journal Genes and Development.

Walnuts help prevent Alzheimer disease

The study was published in the Journal of Alzheimer's Disease.

Having a walnut-enriched diet every day may help reduce the risk, delay the onset, slow the progression of, or prevent Alzheimer's disease all together, found a study led by an Indian-origin researcher.

"study adds to the growing body of research that demonstrates the protective effects of walnuts on cognitive functioning," said Abha Chauhan from the New York State Institute for Basic Research in Developmental Disabilities (IBR).

The research group examined the effects of dietary supplementation on mice with six percent and nine percent walnuts, that is equivalent to one ounce (28.3 gram) and 1.5 ounces (42.5 gram) per day, respectively.

The researchers found significant improvement in learning skills, memory, reducing anxiety and motor development in mice fed a walnut-enriched diet.

Oxidative stress and inflammation are prominent features in the disease.

The high antioxidant content of walnuts (3.7 mmol/ounce) may have been a contributing factor in protecting the mouse's brain from the degeneration typically seen in Alzheimer's disease, the researchers suggested.

This research stemmed from a previous cell culture study led by Chauhan that highlighted the protective effects of walnut extract against the oxidative damage caused by amyloid beta protein.

"These findings are very promising and could help lay the groundwork for future human studies on walnuts and Alzheimer's disease - a disease for which there is no known cure," Chauhan added.

The protein is the major component of amyloid plaques that form in the brains of those with Alzheimer's disease.

Artificial sweeteners may alters body blood sugar controls

Scientists have found that artificial sweeteners alter the microbiome, the population of bacteria that is in the digestive system.

Artificial sweeteners may disrupt the body’s ability to regulate blood sugar, causing metabolic changes that can be a precursor to diabetes, researchers are reporting.

That is “the very same condition that we often aim to prevent” by consuming sweeteners instead of sugar, said Dr Eran Elinav, an immunologist at the Weizmann Institute of Science in Israel, at a news conference to discuss the findings.

The scientists performed a multitude of experiments, mostly on mice, to back up their assertion that the sweeteners alter the microbiome, the population of bacteria that is in the digestive system.

The different mix of microbes, the researchers contend, changes the metabolism of glucose, causing levels to rise higher after eating and to decline more slowly than they would.

The findings by Dr Elinav and his collaborators in Israel, including Eran Segal, a professor of computer science and applied mathematics at Weizmann, were published in September by the journal Nature.

Cathryn R Nagler, a professor of pathology at the University of Chicago who was not involved with the research but did write an accompanying commentary in Nature, called the results “very compelling.”

She noted that many conditions, including obesity and diabetes, had been linked to changes in the microbiome. “What the study suggests,” she said, “is we should step back and reassess our extensive use of artificial sweeteners.”

Previous studies on the health effects of artificial sweeteners have come to conflicting and confusing findings. Some found that they were associated with weight loss; others found the exact opposite, that people who drank diet soda actually weighed more.

Some found a correlation between artificial sweeteners and diabetes, but those findings were not entirely convincing: Those who switch to the products may already be overweight and prone to the disease.

While acknowledging that it is too early for broad or definitive conclusions, Dr Elinav said he had already changed his own behavior.

“I’ve consumed huge amounts of coffee, and extensively used sweeteners, thinking like many other people that they are at least not harmful to me and perhaps even beneficial,” he said. “Given the surprising results that we got in our study, I made a personal preference to stop using them.

“We don’t think the body of evidence that we present in humans is sufficient to change the current recommendations,” he continued. “But I would hope it would provoke a healthy discussion.”

In the initial set of experiments, the scientists added saccharin (the sweetener in the pink packets of Sweet’N

-fe

Lung cancer can stay hidden for over 20 years

A new U.K. study reveals that lung cancer can remain inactive for almost 20 years before suddenly appearing as an aggressive form of the disease.
Lung cancers can lie dormant for over 20 years before suddenly turning into an aggressive form of the disease, according to a study published Thursday in the U.S. journal Science.

Lung cancer is known as the leading type of deadly cancer among U.S. men and women, and the second most common cancer diagnosed in the U.S. Cigarette smoking is listed as the leading cause of lung cancer, which can also be caused by using other types of tobacco. The American Cancer Society estimates that in the United States, for the year 2014, there will be about 224,210 new cases of lung cancer and nearly 159,260 deaths from it. This disease accounts for 27 percent of all cancer deaths.

The latest study, conducted by the Cancer Research UK's London Research Institute and the UCL Cancer Institute, found that lung cancer can remain hidden for over 20 years. This was based on the study conducted on lung cancers from seven patients that included smokers, ex-smokers and never smokers.

The researchers hoped this study will help improve early detection of the disease.

Professor Nic Jones, Cancer Research UK's chief scientist, said: "This fascinating research highlights the need to find better ways to detect lung cancer earlier when it's still following just one evolutionary path. If we can nip the disease in the bud and treat it before it has started travelling down different evolutionary routes we could make a real difference in helping more people survive the disease..."

It was noticed that after the first genetic mistake that triggered cancer, it can continue to exist undetected for several years until the novel additional defect triggers the rapid growth of the disease. It is during this expansion a sudden gush of different genetic faults that appear in separate region of the tumors. Each of the different sections comes from various paths indicating that every part of the tumor is genetically unique.

This study shows the need for advanced method to detect the disease earlier. Nearly two-thirds of the patients are being diagnosed with advanced form of cancers during which treatment is not successful. Based on this finding, the researchers hope for some improvement in the early detection of the disease.

Study author Professor Charles Swanton, at Cancer Research UK's London Research Institute and the UCL Cancer Institute, said: "Survival from lung cancer remains devastatingly low with many new targeted treatments making a limited impact on the disease. By understanding how it develops we've opened up the disease's evolutionary rule book in the hope that we can start to predict its next steps."

The finding was documented in Science today.