Alcohol can cut risk of men's heart problem

Good morning friends. Most men usually drink alcohol. Even young ones do that. Some parents advice their children especially boys that they should not get use to drink alcohol as it is bad in the body. But there is a study that alcohol can cut risk of men’s heart problem.

Alcohol lovers have now one more excuse to say 'cheers' every day, as a new research said it can cut the risk of heart problems by almost a third in men.

The Spanish research involving more than 15,500 men and 26,000 women found that those who have about four to ten units a day can apparently even halve their risk – regardless of whether they opt for beer, wine or spirits.

Women can get some benefits too, said the study published in Heart journal, although more testing is needed.

The research involved men and women aged between 29 and 69, who were asked to document their lifetime drinking habits and followed for 10 years.

Crucially the research team claim to have eliminated the "sick abstainers" risk by differentiating between those who had never drunk and those whom ill-health had forced to quit.

This has been used in the past to explain fewer heart-related deaths among drinkers on the basis that those who are unhealthy to start with are less likely to drink, the BBC reported.
The exact mechanisms are as yet unclear, but it is known that alcohol helps to raise high-density lipoproteins, sometimes known as good cholesterol, which helps stop so-called bad cholesterol from building up in the arteries.

The study was conducted in Spain, a country with relatively high rates of alcohol consumption and low rates of coronary heart disease.

However, British experts warn the claims must not be seen as a green light to over-indulge.
Cathy Ross, of the British Heart Foundation, said:

"While alcohol could offer limited protection to one organ, abuse of it can damage the heart and other organs, such as the liver, pancreas and brain."

Robert Sutton, professor of surgery at Liverpool University, said the study had "several flaws" and must not be taken to mean high levels of alcohol can improve health.

They warned that heavy drinking can increase the risk of other diseases, as alcohol responsible for 1.8 million deaths globally per year. – Indian Express

Faulty fibres linking brain areas cause muscle disorders

Good morning friends. I’m reading some articles here and also health concerns are one of my favorite article to read. With reference to The Times of India there are faulty fibers linking in our brain areas which causes muscle disorders.

Muscle disorders like writer's cramp may result from abnormalities in fibres connecting different brain areas, according to a study.

Dr Christine Delmaire, of Centre Hospitalier Regional Universitaire Roger Salengro, Lille, France, and Institut National de la Sante et de la Recherche Medicale, Paris, came to this conclusion after studying 26 right-handed patients with writer's cramp and 26 right-handed control participants, who were the same sex and age.

All subjects underwent diffusion-tensor magnetic resonance imaging (DTI) that assesses the status of white matter, coated nerve fibres that allow impulses to travel through the brain.

Christine said that the DTI scans of the writer's cramp patients revealed areas of abnormalities in the white matter of nerve pathways connecting the main sensorimotor cortex to brain areas below the cortex, such as the thalamus.

The researchers further revealed that the same abnormalities were not observed in healthy controls.

"In conclusion, this study suggests that writer's cramp is associated with microstructural changes involving fibers that carry afferents (information from senses to the brain) and efferents (motor information from the brain to the muscles) to the primary sensorimotor cortex. However, it is unknown how these changes relate to the physiopathology of the disease," the authors write.

The study has been published in the Archives of Neurology, one of the JAMA/Archives journals.

New therapy 'can reverse Alzheimer's memory loss

Good morning friends. There is this new therapy that can reverse Alzheimer’s memory loss. This is a tough sickness which usually’s the target are older people. Everyone has the mentality that when you got this kind of disease, you will never be cured.

Scientists have developed a new therapy which they claim can prevent and even reverse memory loss in Alzheimer's patients.

It could repair some of the damage caused by the disease by treating patients with a naturally occurring protein in the body, called brain-derived neurotrophic factor.

"The effects of BDNF were potent. When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the disease.

"We have shown that BDNF targets the cells themselves, preventing their death, stimulating their function, improving learning and memory. BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping disease progression in the cortical regions that receive treatment." The scientist found BDNF treatment can slow or stop the progression of Alzheimer's in the animals.

And, compared to animals not treated with the protein they had significant improvement in their memory and learning skills.

It seems to show that another protein, BDNF, may protect and restore memory. This research offers insight into the way in which Alzheimer's progresses and alternative avenues of research."

Reference: indianexpress

Single brain cell can hold memories

Good morning friends. We all know that brain is the most important part of our body. It is the brain who command us what to do. As it is very useful

Individual nerve cells in the front part of the brain can hold traces of memories on their own for as long as a minute and possibly longer.

This is the first time that a study has recognized the specific signal that establishes nonpermanent cellular memory, and revealed how the brain holds temporary information. The new finding has implications for addiction, attention disorders and stress-related memory loss. Permanent memories are known to be stored when the excitatory amino acid glutamate activates in channels on nerve cells in the brain to reorganize and strengthen the cells’ connections with one another.

This process takes minutes to hours to turn on and off and is too slow to buffer, or temporarily hold, rapidly incoming information.

It shows that rapid-fire inputs less than a second long initiate a cellular memory process in single cells lasting as long as minute, a process called metabotropic glutamate transmission.

It has been said that this transmission in the most highly evolved brain region holds moment-to-moment information.

These cellular findings have implications for how the human brain stores rapidly changing information, like the temporary memory a card shark uses when counting cards in a game of Black Jack and, as casinos have figured out. It is the memory that is most sensitive to the disruptive effects of alcohol and noisy distractions.

ref: The times of India

Studying how nitric oxide alters brain function can lead to Alzheimer's treatment

Good morning friends. These is one of the illness many wouldn’t want to have. I hope we don’t all get any of this.
A team of British researchers has found that nitric oxide (NO) can change the computational ability of the brain.
Experts at the Medical Research Council (MRC) Toxicology Unit at the University of Leicester say that their new finding has implications for the treatment of neurodegenerative diseases like Alzheimer's Disease.
Professor Ian Forsythe, who led the study at the university, said that the new findings might also help advance scientists' understanding of brain function more generally.
"It is well known that nerve cells communicate via the synapse - the site at which chemical messengers (neurotransmitters such as acetylcholine or glutamate) are packaged and then released under tight control to influence their neighbours," Professor Forsythe, of the MRC Toxicology Unit, said in a research paper published in the journal Neuron.
"Nitric oxide is a chemical messenger which cannot be stored and can rapidly diffuse across cell membranes to act at remote sites (in contrast to conventional neurotransmitters which cannot pass across cell membranes).
"It is broadly localized in the central nervous system, where it influences synaptic transmission and contributes to learning and memory mechanisms. However, because it is normally released in such minute quantities and is so labile, it is very difficult to study.
"We have exploited an in vitro preparation of a giant synapse -called the calyx of Held, developed here at the University of Leicester in the 1990s- and its target in the auditory pathway to explore nitric oxide signalling in the brain.
"We show that NO is made in response to incoming synaptic activity (activity generated by sound received by the ear) and that it acts to suppress a key potassium ion-channel (Kv3). Normally these ion-channels keep electrical potentials very short-lived, but nitric oxide shifts their activity, slowing the electrical potentials and reducing information passage along the pathway, acting as a form of gain control.
"Surprisingly, the whole population of neurons were affected, even those neurons which had no active synaptic inputs, so indicating that nitric oxide is a 'volume transmitter' passing information between cells without the need for a synapse. Such a function is ideal for tuning neuronal populations to global activity. On the other hand, too much nitric oxide is extremely toxic and will cause death of nerve cells; so within the kernel of this important signalling mechanism are the potential seeds for neurodegeneration, which if left unchecked contribute to the pathologies of stroke and dementias," the researcher added.
Professor Forsythe revealed that his research team will be trying to understand how these signalling mechanisms are applicable elsewhere in the brain, and how aberrant signalling contributes to neurodegenerative disease processes such as in Alzheimer's disease. (ANI)

Studying how nitric oxide alters brain function can lead to Alzheimer's treatment

Good morning friends. These is one of the illness many wouldn’t want to have. I hope we don’t all get any of this.

A team of British researchers has found that nitric oxide (NO) can change the computational ability of the brain.

Experts at the Medical Research Council (MRC) Toxicology Unit at the University of Leicester say that their new finding has implications for the treatment of neurodegenerative diseases like Alzheimer's Disease.

Professor Ian Forsythe, who led the study at the university, said that the new findings might also help advance scientists' understanding of brain function more generally.

"It is well known that nerve cells communicate via the synapse - the site at which chemical messengers (neurotransmitters such as acetylcholine or glutamate) are packaged and then released under tight control to influence their neighbours," Professor Forsythe, of the MRC Toxicology Unit, said in a research paper published in the journal Neuron.

"Nitric oxide is a chemical messenger which cannot be stored and can rapidly diffuse across cell membranes to act at remote sites (in contrast to conventional neurotransmitters which cannot pass across cell membranes).

"It is broadly localized in the central nervous system, where it influences synaptic transmission and contributes to learning and memory mechanisms. However, because it is normally released in such minute quantities and is so labile, it is very difficult to study.

"We have exploited an in vitro preparation of a giant synapse -called the calyx of Held, developed here at the University of Leicester in the 1990s- and its target in the auditory pathway to explore nitric oxide signalling in the brain.

"We show that NO is made in response to incoming synaptic activity (activity generated by sound received by the ear) and that it acts to suppress a key potassium ion-channel (Kv3). Normally these ion-channels keep electrical potentials very short-lived, but nitric oxide shifts their activity, slowing the electrical potentials and reducing information passage along the pathway, acting as a form of gain control.

"Surprisingly, the whole population of neurons were affected, even those neurons which had no active synaptic inputs, so indicating that nitric oxide is a 'volume transmitter' passing information between cells without the need for a synapse. Such a function is ideal for tuning neuronal populations to global activity. On the other hand, too much nitric oxide is extremely toxic and will cause death of nerve cells; so within the kernel of this important signalling mechanism are the potential seeds for neurodegeneration, which if left unchecked contribute to the pathologies of stroke and dementias," the researcher added.

Professor Forsythe revealed that his research team will be trying to understand how these signalling mechanisms are applicable elsewhere in the brain, and how aberrant signalling contributes to neurodegenerative disease processes such as in Alzheimer's disease. (ANI)