A new study has found that chronic cigarette use affects your posture because it affects the brain systems. Postural instability is pretty common among alcohol dependent (AD) individuals, because alcohol damages that parts of the brain systems that maintain postural stability.
Thomas Paul Schmidt, a research associate in the department of radiology and biomedical imaging at the University of California San Francisco, and San Francisco Veterans Affairs Medical Center, said that anecdotal and empirical findings revealed that postural instabilities with eyes open or closed is common in treatment-seeking AD individuals.
During the study, Schmidt and his colleagues recruited AD participants from substance-abuse outpatient clinics and controls from the local community. To assess postural stability and balance, they administered an ataxia battery to 115 smoking and non-smoking AD individuals and to 74 smoking and non-smoking light/non-drinking controls. The researchers assessed subgroups of AD individuals at three testing sessions during abstinence from alcohol: one week, five weeks, and 34 weeks of abstinence.
They assessed all controls once, and a subset of the non-smoking controls was re-tested after 40 weeks. The researchers then used this data to find out if cigarette smoking affected postural stability in both the control and AD groups, and if postural stability is affected by smoking during alcohol abstinence.
Schmidt remarked that during the research it was revealed that non-smoking AD individuals showed marked improvement on a measure of postural stability over the course of eight months of abstinence.
The study has been published online in the journalism Alcoholism: Clinical and Experimental Research
Anopheles gambiae mosquitoes are the main transmitters of malaria, which affects around 200 million people every year. The females mate only once during their lives.
They store the sperm from this single mating in an organ called the spermatheca, from which they repeatedly take sperm over the course of their lifetime to fertilise the eggs that they lay. The female needs the sperm to stay healthy whilst they are in storage in the spermatheca, so that they are viable each time she uses them to reproduce.
The new research shows that the sperm are partly protected by the actions of an enzyme called HPX15. When the researchers interfered with HPX15 in female A gambiae mosquitoes in the laboratory, the females fertilised fewer eggs and therefore produced fewer offspring. This is the first time that scientists have discovered a mechanism that preserves the function of sperm in A gambiae.
The researchers, from Harvard School of Public Health, the University of Perugia and Imperial College London, believe that their insight could ultimately lead to a new weapon in the fight against malaria. This would work by disabling HPX15 to reduce female fertility and through that, reduce the number of malaria-carrying mosquitoes in circulation.
“Malaria kills over 650,000 people every year and we need to find new ways of tackling it, partly because mosquitoes continue to evolve ways of resisting our efforts,” Dr Robert Shaw, one of the lead authors of the research, said. “We are interested in cutting the numbers of malarial mosquitoes by impairing their ability to reproduce, and our new study suggests a way that we might be able to do this.
“There is no single magic bullet for tackling malaria, but making mosquitoes less fertile could provide us with a valuable weapon against the disease,” said Shaw. The study suggests that HPX15 may protect the stored sperm against potentially damaging molecules called free radicals, which are particularly abundant after a female takes a blood feed.
Ensuring that the sperm are healthy after blood-feeding is important for the female’s fertility as she reproduces after each feed, fertilising her eggs with sperm released from the spermatheca. The study was published in the journal Proceedings of the National Academy of Sciences.
Investigators analyzed 25 genes in postmortem brain tissue of children with and without autism. These included genes that serve as biomarkers for brain cell types in different layers of the cortex, genes implicated in autism and several control genes.
Their findings are published in the online edition of the New England Journal of Medicine.
“Building a baby’s brain during pregnancy involves creating a cortex that contains six layers,” said Eric Courchesne, Ph.D., professor of neurosciences and director of the Autism Center of Excellence at University of California, San Diego (UC San Diego).
“We discovered focal patches of disrupted development of these cortical layers in the majority of children with autism.”
The findings confirm the hypothesis that for some children with autism, the brain can sometimes rewire connections and the child can improve abilities — especially with early therapeutic intervention.
Rich Stoner, Ph.D., of the UC San Diego Autism Center of Excellence created a unique three-dimensional model visualizing brain locations where patches of cortex had failed to develop the normal cell-layering pattern.
“The most surprising finding was the similar early developmental pathology across nearly all of the autistic brains, especially given the diversity of symptoms in patients with autism, as well as the extremely complex genetics behind the disorder,” said Ed S. Lein, Ph.D.
During early brain development, each cortical layer develops its own specific types of brain cells, each with specific patterns of brain connectivity that perform unique and important roles in processing information.
As a brain cell develops into a specific type in a specific layer with specific connections, it acquires a distinct genetic signature or “marker” that can be observed.
The study found that in the brains of children with autism, key genetic markers were absent in brain cells in multiple layers.
“This defect,” Courchesne said, “indicates that the crucial early developmental step of creating six distinct layers with specific types of brain cells — something that begins in prenatal life — had been disrupted.”
“Equally important,” said the scientists, “these early developmental defects were present in focal patches of cortex, suggesting the defect is not uniform throughout the cortex.”
The brain regions most affected by focal patches of absent gene markers were the frontal and the temporal cortex, possibly illuminating why different functional systems are impacted across individuals with the disorder.
The frontal cortex is associated with higher-order brain function, such as complex communication and comprehension of social cues. The temporal cortex is associated with language.
The disruptions of frontal and temporal cortical layers seen in the study may underlie symptoms most often displayed in autistic spectrum disorders. The visual cortex — an area of the brain associated with perception that tends to be spared in autism — displayed no abnormalities.
“The fact that we were able to find these patches is remarkable, given that the cortex is roughly the size of the surface of a basketball, and we only examined pieces of tissue the size of a pencil eraser,” said Lein.
“This suggests that these abnormalities are quite pervasive across the surface of the cortex.”
Researching the origins of autism is challenging because it typically relies upon studying adult brains and attempting to extrapolate backwards.
“In this case,” Lein said, “we were able to study autistic and control cases at a young age, giving us a unique insight into how autism presents in the developing brain.”
“The finding that these defects occur in patches rather than across the entirety of cortex gives hope as well as insight about the nature of autism,” added Courchesne.
According to the scientists, such patchy defects, as opposed to uniform cortical pathology, may help explain why many toddlers with autism show clinical improvement with early treatment and over time.
The findings support the idea that in children with autism the brain can sometimes rewire connections to circumvent early focal defects, raising hope that understanding these patches may eventually open new avenues to explore how that improvement occurs.
Source: University of California, San Diego
Reviewed by John M. Grohol, Psy.D. on April 7, 2014
“This is a welcome discovery whatever the origin,” Mark Hulett from La Trobe Institute for Molecular Science in Melbourne was quoted as saying.
The molecule, found in nicotiana sylvestris (flowering tobacco) plant, forms a pincer-like structure that grips onto lipids present in the membrane of cancer cells.
It then effectively rips them open, causing the cell to expel its contents and explode.
According to researchers, this universal defence process could also potentially be harnessed for the development of antibiotic treatment for microbial infections.
The pre-clinical work is being conducted by the Melbourne biotechnology company Hexima. “The preliminary trials have looked promising,” said Hulett.
The study was published in the journal eLife.
Researchers found that cocoa, the basic ingredient in chocolate and one of the most flavanol-rich foods, can actually prevent people from gaining excess weight and lower blood sugar levels.
According to sources, the scientists found that one particular type of antioxidant in cocoa called oligomeric procyanidins, when added to the food fed to laboratory mice, made a big difference in keeping the mice’s weight down and also improved their glucose tolerance level which could potentially help prevent type-2 diabetes.
Researchers reportedly also stated that Oligomeric procyanidins possess the greatest antiobesity and antidiabetic bioactivities of the flavanols in cocoa.
Previous studies have also linked chocolate to health benefits such as improved thinking, decreased appetite and lower blood pressure. The study is published in American Chemical Society’s Journal of Agricultural & Food Chemistry.
A latest research paper shows a diet low in nutrients might help increase the lifespan of humans.
The research conducted on laboratory animals argues that dietary restrictions can result in higher rates of cellular recycling and repair mechanisms in the body. But, according to them, this effect evolved to help organisms during famines.
The authors explain that animals need less food for survival as the stored nutrients in the cells can be recycled and reused.
“This is the most intriguing aspect, from a human health stand point. Although extended lifespan may simply be a side effect of dietary restriction, a better understanding of these cellular recycling mechanisms that drive the effect may hold the promise of longer, healthier lives for humans,” said lead study author, Dr Margo Adler, an evolutionary biologist at UNSW Australia in a press release.
“This effect has been demonstrated in laboratories around the world, in species ranging from yeast to flies to mice. There is also some evidence that it occurs in primates,” Adler said
“But we think that lifespan extension from dietary restriction is more likely to be a laboratory artifact,” said Adler. She further explained that the most commonly believed theory is that this effect evolved to enhance the survival chances during times of famine.
The authors explained why no extension in lifespan is seen in the wild. This is because restricted diets lower the ability of the immune system to fight diseases and reduce the muscle strength necessary to defend against predators.
“Unlike in the benign conditions of the lab, most animals in the wild are killed young by parasites or predators,” Adler explained
“Since dietary restriction appears to extend lifespan in the lab by reducing old-age diseases, it is unlikely to have the same effect on wild animals, which generally don’t live long enough to be affected by cancer and other late-life pathologies,” she added.
The paper is published in the journal ‘BioEssays.’
Around 600 million people worldwide have some kind of kidney ailment and chronic kidney diseases are predicted to increase by 17 per cent over the next decade if not detected early, said a nephrologist in Mumbai on Thursday.
Speaking on the occasion of World Kidney Day, Vivekanand Jha, Executive Director, George Institute for Global Health, India said chronic kidney diseases are considered to be a global health problem but many cases go undiagnosed as people ignore the symptoms of the disease in the early stages.
“In kidney diseases if detected early and treated properly, the deterioration in kidney functioning can be slowed or even stopped,” Jha said.
“Though it is an undeniable fact that chronic kidney disease prevalence rises with age and exceeds 40-50 per cent amongst elders, people should visit doctors at least twice a month for a check up,” said Jha, who is also the secretary of the Indian Society of Nephrology.
“Early detection and prevention will lead not only to improved outcomes, better quality of life, but huge cost-savings on treatment,” said Jha.
Early stage kidney disease is not being identified and diagnosed as early and often as is necessary. Patients are frequently told not to worry until kidney damage has progressed to near failure. Furthermore, patients do not have the necessary education or resources to manage their own risk factors and lifestyle to prevent initial kidney damage and progression of the disease.
Primary care practitioners will know which tests to order and how to recognise early-stage kidney disease, which will increase the total number of diagnoses of kidney disease. In addition, primary care practitioners have the knowledge and tools to treat early-stage kidney disease in order to slow its progression, and refer their patients to nephrologists when they need more specialised care.
WASHINGTON: In a breakthrough, scientists have discovered a new class of antibiotics to fight deadly bacteria such as methicillin-resistant Staphylococcus aureus and other drug-resistant bacteria that threaten public health.
The new class, called oxadiazoles, was discovered by University of Notre Dame researchers led by Mayland Chang and Shahriar Mobashery in silico (by computer) screening and has shown promise in the treatment of MRSA in mouse models of infection.
Researchers who screened 1.2 million compounds found that the oxadiazole inhibits a penicillin-binding protein, PBP2a, and the biosynthesis of the cell wall that enables MRSA to resist other drugs.
The oxadiazoles are also effective when taken orally. This is an important feature as there is only one marketed antibiotic for MRSA that can be taken orally, researchers said.
MRSA has become a global public-health problem since the 1960s because of its resistance to antibiotics.
In the US alone, 278,000 people are hospitalised and 19,000 die each year from infections caused by MRSA, said researchers.
Only three drugs currently are effective treatments, and resistance to each of those drugs already exists.
The researchers have been seeking a solution to MRSA for years.
“Professor Mobashery has been working on the mechanisms of resistance in MRSA for a very long time,” Chang said.
“As we understand what the mechanisms are, we can devise strategies to develop compounds against MRSA,” said Chang.
“Mayland Chang and Shahriar Mobashery’s discovery of a class of compounds that combat drug resistant bacteria such as MRSA could save thousands of lives around the world. We are grateful for their leadership and persistence in fighting drug resistance,” said Greg Crawford, dean of the College of Science at the University of Notre Dame.
The research is published in the Journal of the American Chemical Society.
WASHINGTON: Scientists have discovered how the immune system makes a powerful antibody that blocks HIV infection of cells by targeting a key site, paving way for an effective vaccine for the deadly virus.
Researchers believe that if a vaccine could elicit potent antibodies to a specific conserved site in the V1V2 region of the virus, one of a handful of sites that remains constant on the fast-mutating virus, then the vaccine could protect people from HIV infection.
Analyses of the results of a clinical trial of the only experimental HIV vaccine to date to have modest success in people suggest that antibodies to sites within V1V2 were protective.
The new findings point the way towards a potentially more effective vaccine that would generate V1V2-directed HIV neutralising antibodies, researchers said.
The study led by the National Institute of Allergy and Infectious Diseases ( NIAID) scientists began by identifying an HIV-infected volunteer who naturally developed V1V2-directed HIV neutralising antibodies, named CAP256-VRC26, after several months of infection.
Using techniques similar to those employed in an earlier study of HIV-antibody co-evolution, the researchers analysed blood samples donated by the volunteer between 15 weeks and 4 years after becoming infected.
This enabled the scientists to determine the genetic make-up of the original form of the antibody; to identify and define the structures of a number of the intermediate forms taken as the antibody mutated towards its fullest breadth and potency.
It also allowed them to describe the interplay between virus and antibody that fostered the maturation of CAP256-VRC26 to its final, most powerful HIV-fighting form.
The study showed that after relatively few mutations, even the early intermediates of CAP256-VRC26 can neutralise a significant proportion of known HIV strains.
This improves the chances that a V1V2-directed HIV vaccine developed based on the new findings would be effective, according to scientists, who have begun work on a set of vaccine components designed to elicit V1V2 neutralising antibodies and guide their maturation.