Feeling sleepy after a sleepless night?

In many cases, people spend sleepless night. Especially, if we consider the case of students during exam time. Many of the students have a habit of studying throughout the night prior to exams and then they feel sleepy while writing them. Have you not experienced during your student life? And in some cases you may also get a feedback from them that even though he studied he was not able to recollect it during the exams. And I am sure it must have been the case with you as well at some stage in your life. 

Have you wondered why is it so? 

A recent study published in Nature has answers to these questions?

A recent study on rats have suggested that sleep deprived neurons may shut down even when awake. As a result, sleep-deprived selves are so cognitively challenged: we are, if not precisely half-asleep, partially asleep.

“After a long period in an awake state, cortical neurons can go briefly ‘offline,’” wrote researchers led by University of Wisconsin neuroscientists Vladyslav Vyazovskiy and Giulio Tononi in a study published April 27 in Nature. “Although both EEG and behavior indicate wakefulness, local populations of neurons in the cortex may be falling asleep, with negative consequences for performance.” To study rats’ neurology, Tononi’s team wired their brains to an EEG machine, kept them awake longer than usual, and looked for patterns in readouts of their brains’ electrical activity.

They found that scattered neurons throughout the rats’ brains gradually alternated between periods of activity and inactivity — a pattern associated with deep sleep, not wakefulness. But unlike their synchronization during sleep, these oscillations were brief and disjointed.When the researchers tested the rats in a sugar-pellet-reaching task, performance declined in proportion to their neurons’ “offline” status, suggestive of how sleep-deprived people have trouble functioning.

Sleepwalkers, for example, seem to inhabit “a twilight state between sleep and wakefulness,” wrote Colwell. Many animals also alternate between shutting down their brains’ left and right hemispheres, allowing for rest while maintaining vigilance.“These observations also suggest that single neurons can move into a rest state,” wrote Colwell. 

“The ability to control behavior actively with some neural circuits while others may be idling could be evolutionarily advantageous.” However, Colwell cautioned against assuming that the patterns seen by Tononi in rats are responsible for short-of-sleep human grouchiness, distraction and poor judgment. For now that’s “arguably an intellectual stretch,” he wrote — but the the data supports further investigations. “And although it is only anecdotal evidence,” Colwell concluded, “I could swear that some of my students can sleep with their eyes wide open.”

 I am sure that after reading this article, many students would avoid spending sleepless nights during exams.

Source:  University of California, Los Angeles

Tips for CSIR NET JRF Life sciences students

Syllabus

•  If you take a quick look at the syllabus for CSIR NET JRF life sciences, you would notice that not only topics related to Biotechnology but whole of the life sciences has been included. Well that is unfair on the syllabus part but yes when it is common to all life sciences candidates it does makes sense.
• Try to cover almost of the entire syllabus, but its obviously difficult, in that case you may restrict yourself to certain topics which appear interesting to you. But remember you must have knowledge of the topic to its minute levels. This will help you in clearing your interview, I remember when I had interview in IISC Bangalore, I was asked to choose my strongest topic & questions were asked in a brain storming forty five minute session.
• Some of the topics related to botany or zoology may appear boring to you, in that case try to first make your Biotech topics stronger, then only move to these topics.  

Preparation

• Ideally the preparation should start three months before exam, but that means you must stick to a particular schedule. If you are an appearing candidate I would suggest starting in the third semester itself (provided if you wanna clear JRF).
• Solve sample papers as much as you can, well that is a typical advice to any competition aspirant, I would suggest to get in to the details ( theory part) as soon as you come through the questions.
• If you are a appearing candidate, then try to co-relate the questions from the theory part, Remember, it doesn’t matter how much your university awards you, rather a JRF would Really MATTER, so devote as much time as possible to get in to the subjects & concepts. They emphasize concepts rather than mugging up & vomiting data.

Exam

• Again comes the question which one to stress for more, Paper 1 or 2? Well I would suggest you to concentrate more on paper 2 but remember passing in Paper 1 is very important, so make sure you strike a fair balance.
• During exam- I would suggest not to panic rather stick to your basics while answering, coz most questions are from basics but we tend to complicate it.
• Try not to solve all questions rather try to gain confidence by answering questions which you know first in case of paper 1. In paper 2 just cram through the paper what it contains and how much you know, don’t panic if you don’t Know, try to stick to the word limit while answering, be to the point and quote examples

How to Avoid a Disaster?

Though we cannot say anything about the cut off marks, experience tells that one has to score well in Paper I to get JRF. At the same time leave your thoughts about the performance in the Paper I back and do well in the afternoon session with a clear and sound mind. Some may have a tendency to throw it up feeling dejected about your performanceduring the day. 

Let us wait the results to come before making disastrous assumptions to spoil your day. Also be cool in your approach to the exam and never give up during the examination by doing things like answering all the multiple choice questions randomly based on luck feeling dejected of your performance. There is plenty of time to be prepared and perform well. And from experience, many have come out successfully even after believing that they did perform very poorly.

In examination with objective type multiple choice questions (MCQs), there is a tendency called the ‘Red Wire Syndrome’ which means to answer all questions whether one knows the correct answer or not. If we can classify the questions into three categories, viz. 1) Sure, 2) Not So Sure and 3) Never, indicating whether one knows the correct answer, possible but some doubt still prevails and almost impossible, respectively. The ‘red wire syndrome’ means that one will have tendency to answer all the questions, which is disastrous, just like a child who touches a ‘red hot wire’ seeing its beauty. The key to success lies in answering all the ‘Sure’ types, and leaving out the ‘Never’ types. It is imperative to learn the art of intelligent guessing to answer the type 2. 

This evidently comes from one’s experience and basic knowledge of the subject. So never ever find it insulting to go back to your basics (atleast refer to some of the basic books in the list below). So never forget practice well using previous question papers of NET JRF to make you come out with flying colours.

After Exam

Well your work is not yet over, try to recollect  the questions and write it down, if that is not possible try to demarcate the topics which were stressed specifically, this would of immense help in case if you do not clear.

How to utilize INTERNET for CSIR UGC NET EXAM?

Well the answer lies in exploiting this resource as much as possible to gain subject material. I would suggest joining CSIR NET JRF discussion groups to interact with other aspirants and ask questions.

This article was submitted By a successful candidate who did his MSC Biotechnology from IIT  and further got JRF and got calls from IISC Bangalore, CDRI Lucknow and many more. Due to our Privacy policy we are unable to reveal the identity of the scholar.

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Malarial Mosquitoes Are Evolving Into New Species, Say Researchers

Two strains of the type of mosquito responsible for the majority of malaria transmission in Africa have evolved such substantial genetic differences that they are becoming different species, according to researchers behind two new studies published in the journal Science.

Over 200 million people globally are infected with malaria, according to the World Health Organisation, and the majority of these people are in Africa. Malaria kills one child every 30 seconds.

The international research effort, co-led by scientists from Imperial College London, looks at two strains of the Anopheles gambiae mosquito, the type of mosquito primarily responsible for transmitting malaria in sub-Saharan Africa. These strains, known as M and S, are physically identical. However, the new research shows that their genetic differences are such that they appear to be becoming different species, so efforts to control mosquito populations may be effective against one strain of mosquito but not the other.

The scientists argue that when researchers are developing new ways of controlling malarial mosquitoes, for example by creating new insecticides or trying to interfere with their ability to reproduce, they need to make sure that they are effective in both strains.

The authors also suggest that mosquitoes are evolving more quickly than previously thought, meaning that researchers need to continue to monitor the genetic makeup of different strains of mosquitoes very closely, in order to watch for changes that might enable the mosquitoes to evade control measures in the future.

Professor George Christophides, one of the lead researchers behind the work from the Division of Cell and Molecular Biology at Imperial College London, said: "Malaria is a deadly disease that affects millions of people across the world and amongst children in Africa, it causes one in every five deaths. We know that the best way to reduce the number of people who contract malaria is to control the mosquitoes that carry the disease. Our studies help us to understand the makeup of the mosquitoes that transmit malaria, so that we can find new ways of preventing them from infecting people."

Dr Mara Lawniczak, another lead researcher from the Division of Cell and Molecular Biology at Imperial College London, added: "From our new studies, we can see that mosquitoes are evolving more quickly than we thought and that unfortunately, strategies that might work against one strain of mosquito might not be effective against another. It's important to identify and monitor these hidden genetic changes in mosquitoes if we are to succeed in bringing malaria under control by targeting mosquitoes."

The researchers reached their conclusions after carrying out the most detailed analysis so far of the genomes of the M and S strains of Anopheles gambiae mosquito, over two studies. The first study, which sequenced the genomes of both strains, revealed that M and S are genetically very different and that these genetic differences are scattered around the entire genome. Previous studies had only detected a few 'hot spots' of divergence between the genomes of the two strains. The work suggested that many of the genetic regions that differ between the M and S genomes are likely to affect mosquito development, feeding behaviour, and reproduction.

In the second study, the researchers looked at many individual mosquitoes from the M and S strains, as well as a strain called Bamako, and compared 400,000 different points in their genomes where genetic variations had been identified, to analyse how these mosquitoes are evolving. This showed that the strains appear to be evolving differently, probably in response to factors in their specific environments -- for example, different larval habitats or different pathogens and predators. This study was the first to carry out such detailed genetic analysis of an invertebrate, using a high density genotyping array.

As a next step in their research, the Imperial researchers are now carrying out genome-wide association studies of mosquitoes, using the specially designed genotyping chip that they designed for their second study, to explore which variations in mosquito genes affect their propensity to become infected with malaria and other pathogens.

Both of the studies just published were collaborations between researchers at Imperial and international colleagues, involving researchers from institutions including the University of Notre Dame, the J. C. Venter Institute, Washington University and the Broad Institute. Funding for the projects was provided by the National Human Genome Research Institute, the National Institutes of Health, the BBSRC, and the Burroughs Welcome Fund.

Vaccines could help elephantiasis spread

PARASITIC worms can adjust their survival strategy based on their host's immune response. This means potential vaccines against elephantiasis might make the infection spread more easily through communities.

Elephantiasis infects 120 million people a year in Africa and Asia. Tiny filaria worms carried by mosquitoes block the lymph vessels that normally drain fluid from limbs or genitals, which then swell to grotesque proportions. The only prevention is a yearly dose of worming drugs, but fewer than half the people at risk receive them.

Work is under way on a vaccine, but Simon Babayan at the University of Edinburgh, UK, and colleagues, have discovered that some vaccines may make the worms worse. When filaria worms in mice sense that the mouse is mounting a strong immune reaction, they change their life cycle, producing more offspring in the blood earlier. This helps the worm ensure that it will be picked up and transmitted by another mosquito despite the immune attack (PLoS Biology, DOI: 10.1371/journal.pbio.1000525).

Unfortunately, experimental vaccines rely on the very immune reactions that warn the worms, Babayan says. People who get such a vaccine may defeat their own infection, but the worms' early response means they will pass on more infections.

Babayan says potential vaccines should be tested for whether their targets adapt to them in this way.

Universal cancer marker shows new treatment options

A single screening method that can force a wide range of cancers to reveal themselves has been discovered. The universal cancer marker could help doctors find and treat tumours, and provide surgeons with a "dotted line" to cut them out.

The key to the technique is the receptor for follicle-stimulating hormone (FSH). This receptor – typically involved in controlling women's reproductive cycles – appears in unusually large amounts in prostate tumours. So Aurelian Radu at Mount Sinai School of Medicine in New York and colleagues looked for it in 1336 human tumour samples, including prostate, breast, lung and liver cancers.

The group applied colour-labelled antibodies for the FSH receptor to the samples. They found that in every sample, the antibodies bound to blood vessels around the periphery of the tumour.

Radu doesn't yet know why tumour blood vessels express the receptor, though he thinks it might play a role in the formation of new vessels.

 

One-stop screening

 

The marker could be useful in pinpointing and treating tumours, says Radu. Currently, different imaging techniques are used to identify different types of tumour. "Using this marker, we can use one imaging technique for the whole body," says Radu. He hopes broader screening will enable earlier detection of secondary tumours.

Kairbaan Hodivala-Dilke at Barts and The London School of Medicine and Dentistry's Institute of Cancer agrees: "It's certainly a good marker, and could be especially useful in surgery, which is a bit hit-and-miss at the moment," she says. Using colour-labelled antibodies to highlight the edges of a tumour could enable surgeons to "cut along the dotted line".

Additionally, by attaching a cancer drug to an FSH receptor antibody, "we have the potential to target therapy exclusively to the tumour", says Radu.

Drugs that inhibit the FSH receptor are already in development as potential contraceptives, says Radu. He hopes that some might be trialled as anti-cancer drugs in the future.

Gene therapy proposed to treat depression

A NOVEL treatment for depression may soon get the go ahead: injecting genes directly into the brain. It would be the first attempt to treat a psychiatric illness with gene therapy.

A gene called p11 is vital for enabling neurons to respond to the neurotransmitter serotonin. A lack of p11 has been shown to lead to depression in humans.

To test whether gene therapy could help, Michael Kaplitt of the Weill Cornell Medical College in New York City and colleagues first demonstrated that mice lacking p11 showed symptoms of depression, failing to respond with the same vitality as healthy mice when exposed to challenges, such as showing decreased effort when having to swim to an island.

Next they injected viruses containing p11 directly into the nucleus accumbens of the mice lacking p11. This part of the brain is where a lack of p11 manifests itself as depression in humans. The team found this reversed the depression in the mice (Science Translational Medicine, DOI: 10.1126/scitranslmed.3001079).

Although the proposal to do the same in humans sounds drastic, Kaplitt points out that a similar procedure has already been used to deliver genes to the brain's of people with Parkinson's disease.

"We're already doing a primate study to support a potential human trial, so this is moving ahead very rapidly," says Kaplitt.

 

“Injecting a virus containing the missing gene into a mouse's brain reversed its depression”

Low levels of vitamin B12 linked to Alzheimer's

People with low levels of vitamin B₁₂ may be at greater risk of developing Alzheimer's disease. The finding supports previous research showing large doses of B vitamins might halve the rate of brain shrinkage.

Babak Hooshmand and colleagues at the Karolinska Institute in Stockholm, Sweden, followed 271 healthy people aged 65 to 79 for seven years. The researchers measured the blood concentration of the amino acid homocysteine, high levels of which have been linked to negative effects on the brain, such as stroke. They also measured levels of active vitamin B₁₂, which can decrease homocysteine levels.

By the end of the study, 17 people had developed Alzheimer's. A level of homocysteine moderately above average corresponded to a 16 per cent higher risk of developing Alzheimer's, while a level of active B₁₂ slightly above average meant a 2 per cent lower risk.

"This is a very convincing study," says David Smith of the University of Oxford, who has investigated the effect of B-vitamin supplements on brain shrinkage. He says it is the first to show that low levels of active vitamin B₁₂ are a risk factor for developing dementia several years later.

Although B₁₂ deficiency is common among elderly people, more evidence is needed before recommending B₁₂ supplements to stave off dementia, says Hooshmand.

Replication of Prions

If prions lack their own nucleic acids and are merely proteins, a very important question requires an answer. How can a protein enter a host cell and direct the process of replication? To answer this question a large number of hypotheses have been put forward. An interesting hypothesis has been given by a group of scientists from the MRC Neuropathogenesis Unit at Edinburg. This hypothesis states that the existence of small piece of DNA gene (also called prp gene) is necessary to encode the amino acid sequence of prion protein at the time of its replication. This DNA gene is a component of the host genetic material (host DNA). The prion protein presumably serves as a promoter of DNA gene expression.

Recent studies indicate that prions represent a changed conformation of proteins normally found in cells. Once prions are produced, they somehow persuade the normal versions of the corresponding protein to assume the altered conformation and, thereby, become prions.

What is the Origin of Viruses?

Origin of Viruses
Three theories have been put forward to explain the origin of viruses. These theories are highly speculative and are as follows :

Survivors of Pre-Cellular First Living Inhabitants of the Earth
This theory intimately rests on the theory of origin of life on Earth. Life, according to this theory, originated from simple inorganic compounds by a slow biochemical evolution of “ordinary” chemical reactions spread over millions and millions of years.

It is speculated that during the course of origin of life on Earth somewhere at the stage when complex chemical molecules united to form still more complex molecules which could mate with still other metastable molecules till a relatively large molecule (like nucleoprotein) capable of growth and division, a simple virus or a protovirus may have originated (Haldane, 1954; Fraser, 1967). This theory, however, enjoys some insurmountable objections.

Present day viruses are all obligate parasites and it is difficult to conceive of their origin before the origin of their hosts (cells) which are at a far higher scale of evolution. Viruses use the same genetic code as cellular organisms and depend solely and entirely on ribosomes, transfer RNAs and enzymes of the host cell for protein biosynthesis. Moreover, viral nucleic acid has the same properties and the same mode of replication as the nucleic acid of cellular organisms.

Regression from More Highly Evolved Free-Living Microorganisms/Cells
Viruses are considered to have originated by retrogressive evolution from free-living cells, according to this theory. A parasite evolves retrogressively as it takes the ready made metabolites from its host instead of synthesizing them himself.

If the parasite continues to evolve retrogressively then, to save labour and energy, it would slowly loss some of its physiological, morphological and even genetical functions that become super-numerary in its new ecological niche and new mode of biological existence. A parasite would, therefore, get regressed to a much simpler organism. Obligate intracellular parasitism is the most specialized type of parasitism and such a parasite would ultimately possess only the bare minimum and this minimum is the possession of a nuclei acid (to ensure genetic continuity) enclosed within a protein shell (to ensure safety of the nucleic acid).

Shedding of all unnecessary morphological, physiological and genetical materials would necessarily reduce the size. A formerly free-living organism would thus be transformed into a virus. Green (1935), Laidlow (1938) and Burnet (1945) support the theory of retrogressive origin of viruses but the same is opposed by Luria and Darnell (1967) and Fenner (1968).

Derived from Normal Constituents of the Cell
An eukaryotic cell possesses organelles like chloroplasts and mitochondria which self-replicating semi-autonomous structures and reproduce their like. Chloroplasts and mitochondria increase in size and then divide while kinetosome is synthesized near a pre-existing one by assembly from the tubular materials. Besides they possess DNA which is functional and possesses its own mutational history, codes for the synthesis of mRNA and also presumably for protein.

Mitochondria mutate to non­functional forms in Neurospora and yeasts, while chloroplasts mutate to undeveloped, colourless proplastids in algae and higher plants. These mutations are based on genetic changes. Cells also contain certain organelles that exceptionally undergo autonomous unrestricted replications; examples are the centrioles in Marsilea and sperms and nuclear genes in the amphibian oocytes.

Viruses resemble above mentioned cellular organelles in chemical composition, possession of nucleic acid, genetic continuity of genome, independent mutational history, capacity to replicate independently under their own genetic control and also under the overall regulatory control of and within the premises of the host cell.

Many of the cellular organelles or factors possess some of the distinctive characters of viruses, or more specifically, of viral genetic determinant (reproductive independence, evolutionary independence, independent cell to cell transfer and infectivity and pathogenicity) while others could be conferred on them by a specific arrangement of nucleotides. Viruses could, therefore, be derived from any or several of these cellular components and it is possible that different viruses have originated differently. Some of the possibilities are given below:

1. Primordial self-replicating molecules may have mutated to regain the capacity to enter ('infect') the cell and then integrate with it. Such a molecule would be a 'virus'.

2. Some plasmids or even chromosomal segments may have evolved by merging of some primitive self-replicating molecules with the cellular genome. If this s true then it conceivable that some of the genes or groups of genes may revert to their ancestral habit and may have regained/evolved the genetic independence and independence and independent transfer of this genetic material. This would result in the ‘virus’.

3. Some genes of the cell could have escaped of the control mechanisms of the cell and may have acquired the capacity of autonomous replication independent of the division of the cell and capacity of independent transfer. Integration of these genes with the host genome would give us a prophage. Origin of bacteriophage from such prophage DNA has been outlined by Lindegren (1962). Luria and Darnell (1967) also suggest that bacteriophages containing DNA may have evolved from a number of genetic transfer elements (like F factor, bacteriocinogenic factor, etc.) occurring in the prokaryotic cells.

4. DNA viruses of eukaryotic cells may have originated from the functional DNA of cellular organelles (e.g., mitochondria and chloroplast) rather than for nuclear DNA (Matthews, 1970).

5. Origin of DNA plant viruses is somewhat more difficult to understand since there is no definite information with respect to the integration of plant viral nucleic acid into the genome of the plant cell. There is, however, some suggestive evidence in this connection. Some experimental evidence suggests that cut surfaces of barley seeds take up the DNA of the bacterium Micrococcus lysodeikticus and that it integrates into nuclear DNA of barley and replicates (Ledous and Huort, 1968).

In short, therefore, viruses may have originated from cell constituents which escape the control mechanisms of the cell, regained/developed the capacity of autonomous self-replication and ability to mediate their own independent cell to cell transfer and could enter or infect cells to which they did not belong.

Sleep Disorders in living things@biohunting.blogspot.com

At least 40 million Americans each year suffer from chronic, long-term sleep disorders each year, and an additional 20 million experience occasional sleeping problems. These disorders and the resulting sleep deprivation interfere with work, driving, and social activities. They also account for an estimated $16 billion in medical costs each year, while the indirect costs due to lost productivity and other factors are probably much greater. Doctors have described more than 70 sleep disorders, most of which can be managed effectively once they are correctly diagnosed.

The most common sleep disorders include

• insomnia,
• sleep apnea,
• restless legs syndrome, and
• narcolepsy.

Insomnia:
Almost everyone occasionally suffers from short-term insomnia. This problem can result from stress, jet lag, diet, or many other factors. Insomnia almost always  affects job performance and well-being the next day. About 60 million Americans a year have insomnia frequently or for extended periods of time, which leads to even more serious sleep deficits. Insomnia tends to increase with age and affects about 40 percent of women and 30 percent of men. It is often the major disabling symptom of an underlying medical disorder.

For short-term insomnia, doctors may prescribe sleeping pills. Most sleeping pills stop working after several weeks of nightly use, however, and long-term use can actually interfere with good sleep. Mild insomnia often can be prevented or cured by practicing good sleep habits (see "Tips for a Good Night's Sleep"). For more serious cases of insomnia, researchers are experimenting with light therapy and other ways to alter circadian cycles.

Sleep Apnea
Sleep apnea is a disorder of interrupted breathing during sleep. It usually occurs in association with fat buildup or loss of muscle tone with aging. These changes allow the windpipe to collapse during breathing when muscles relax during sleep. This problem, called obstructive sleep apnea, is usually associated with loud snoring (though not everyone who snores has this disorder). Sleep apnea also can occur if the neurons that control breathing malfunction during sleep.

During an episode of obstructive apnea, the person's effort to inhale air creates suction that collapses the windpipe. This blocks the air flow for 10 seconds to a minute while the sleeping person struggles to breathe. When the person's blood oxygen level falls, the brain responds by awakening the person enough to tighten the upper airway muscles and open the windpipe. The person may snort or gasp, then resume snoring. This cycle may be repeated hundreds of times a night. The frequent awakenings that sleep apnea patients experience leave them continually sleepy and may lead to personality changes such as irritability or depression. Sleep apnea also deprives the person of oxygen, which can lead to morning headaches, a loss of interest in sex, or a decline in mental functioning. It also is linked to high blood pressure, irregular heartbeats, and an increased risk of heart attacks and stroke. Patients with severe, untreated sleep apnea are two to three times more likely to have automobile accidents than the general population. In some
high-risk individuals, sleep apnea may even lead to sudden death from respiratory arrest during sleep.

An estimated 18 million Americans have sleep apnea. However, few of them have had the problem diagnosed. Patients with the typical features of sleep apnea, such as loud snoring, obesity, and excessive daytime sleepiness, should be referred to a specialized sleep center that can perform a test called polysomnography. This test records the patient's brain waves, heartbeat, and breathing during an entire night. If sleep apnea is diagnosed, several treatments are available. Mild sleep apnea frequently can be overcome through weight loss or by preventing the person from sleeping on his or her back. Other people may need special devices or surgery to correct the obstruction. People with sleep apnea should never take sedatives or sleeping pills, which can prevent them from awakening enough to breathe.

Restless Legs Syndrome
Restless legs syndrome (RLS), a familial disorder causing unpleasant crawling, prickling, or tingling sensations in the legs and feet and an urge to move them for relief, is emerging as one of the most common sleep disorders, especially among older people. This disorder, which affects as many as 12 million Americans, leads to constant leg movement during the day and insomnia at night. Severe RLS is most common in elderly people, though symptoms may develop at any age. In some cases, it may be linked to other conditions such as anemia, pregnancy, or diabetes.

Many RLS patients also have a disorder known as periodic limb movement disorder or PLMD, which causes repetitive jerking movements of the limbs, especially the legs. These movements occur every 20 to 40 seconds and cause repeated awakening and severely fragmented sleep. In one study, RLS and PLMD accounted for a third of the insomnia seen in patients older than age 60. RLS and PLMD often can be relieved by drugs that affect the neurotransmitter dopamine, suggesting that dopamine abnormalities underlie these disorders' symptoms. Learning how these disorders occur may lead to better therapies in the future.

Narcolepsy
Narcolepsy affects an estimated 250,000 Americans. People with narcolepsy have frequent "sleep attacks" at various times of the day, even if they have had a normal amount of night-time sleep. These attacks last from several seconds to more than 30 minutes. People with narcolepsy also may experience cataplexy (loss of muscle control during emotional situations), hallucinations, temporary paralysis when they awaken, and
disrupted night-time sleep. These symptoms seem to be features of REM sleep that appear during waking, which suggests that narcolepsy is a disorder of sleep regulation.

The symptoms of narcolepsy typically appear during adolescence, though it often takes years to obtain a correct diagnosis. The disorder (or at least a predisposition to it) is usually hereditary, but it occasionally is linked to brain damage from a head injury or neurological disease. Once narcolepsy is diagnosed, stimulants, antidepressants, or other drugs can help control the symptoms and prevent the embarrassing and dangerous effects of falling asleep at improper times. Naps at certain times of the day also may reduce the excessive daytime sleepiness. In 1999, a research team working with canine models identified a gene that causes narcolepsy–a breakthrough that brings a cure for this disabling condition within reach. The gene, hypocretin receptor 2, codes for a protein that allows brain cells to receive instructions from other cells.

The defective versions of the gene encode proteins that cannot recognize these messages, perhaps cutting the cells off from messages that promote wakefulness. The researchers know that the same gene exists in humans, and they are currently searching for defective versions in people with narcolepsy.

How Much Sleep Do We Need?

The amount of sleep each person needs depends on many factors, including age. Infants generally require about 16 hours a day, while teenagers need about 9 hours on average. For most adults, 7 to 8 hours a night appears to be the best amount of sleep, although some people may need as few as 5 hours or as many as 10 hours of sleep each day.

Women in the first 3 months of pregnancy often need several more hours of sleep than usual. The amount of sleep a person needs also increases if he or she has been  eprived of sleep in previous days. Getting too little sleep creates a "sleep debt," which is much like being overdrawn at a bank. Eventually, your body will demand that the debt be repaid. We don't seem to adapt to getting less sleep than we need; while we may get used to a sleep-depriving schedule, our judgment, reaction time, and other functions are still impaired.

People tend to sleep more lightly and for shorter time spans as they get older, although they generally need about the same amount of sleep as they needed in early adulthood. About half of all people over 65 have frequent sleeping problems, such as insomnia, and deep sleep stages in many elderly people often become very short or stop completely.

This change may be a normal part of aging, or it may result from medical problems that are common in elderly people and from the medications and other treatments for those
problems. Experts say that if you feel drowsy during the day, even during boring activities, you haven't had enough sleep. If you routinely fall asleep within 5 minutes of lying down, you probably have severe sleep deprivation, possibly even a sleep disorder. Microsleeps, or very brief episodes of sleep in an otherwise awake person, are another mark of sleep deprivation. In many cases, people are not aware that they are experiencing microsleeps.

The widespread practice of "burning the candle at both ends" in western industrialized societies has created so much sleep deprivation that what is really abnormal sleepiness is now almost the norm. Many studies make it clear that sleep deprivation is dangerous. Sleep-deprived people who are tested by using a driving simulator or by performing a hand-eye coordination task perform as badly as or worse than those who are intoxicated.

Sleep deprivation also magnifies alcohol's effects on the body, so a fatigued person who drinks will become much more impaired than someone who is well-rested. Driver fatigue is
responsible for an estimated 100,000 motor vehicle accidents and 1500 deaths each year, according to the National Highway Traffic Safety Administration. Since drowsiness is the brain's last step before falling asleep, driving while drowsy can – and often does – lead to disaster.

Caffeine and other stimulants cannot overcome the effects of severe sleep deprivation. The National Sleep Foundation says that if you have trouble keeping your eyes focused, if you can't stop yawning, or if you can't remember driving the last few miles, you are probably too drowsy to drive safely.

Water Electrolysis experiment is one of the best experiment

Problem:
How can you perform Electrolysis of water to produce Hydrogen and Oxygen?

Research the Problem:
Electrolysis is Chemical change, especially decomposition, produced in an electrolyte by an electric current. Electrolytes dissolve by dissociation. That is when the molecules of the substance break down into charged particles called ions. An ion with a negative charge is called an anion because it is drawn through the solution to the positive charge on the anode. A particle with a positive charge is called a cation. It moves through the solution to the cathode. Water has its solvent properties because it is polar. The molecule has charged ends (+ and -). These charged ends react with charges on other polar substances to dissolve them. They do so by taking hydrogen atoms from the substance to form hydronium ions. The word electrolysis means the process of breaking molecules to smaller components by using an electric current. Positive and negative poles of a DC electric source such as a battery can absorb opposite ions of an electrolyte causing separation of ions and creation of a new substance.

Hypothesis: Adding some Sulfuric Acid as electrolyte will increase conductivity of water and creation of Hydrogen and Oxygen gases.

Experiment:
In this experiment, initially we used two copper wires, one twelve-volt battery, and some drinking water to do the tests. The process was slow and caused excessive amounts of corrosion on the copper wires and discoloration in the water. To avoid corrosion of electrodes and discoloration of water, we repeated the test using Graphite Rods as electrodes. Also to speed up the process we added some Sulfuric Acid to the water as electrolyte.

Materials Used:
Copper Wire, Graphite Rods, Sulfuric Acid, Test Tubes, Beaker, Water

Procedure:
Fillup ¼ of beaker with clear water, secure two test tubes filled with water in the beaker in a way that test tubes are up-side down over the beaker. Mount the wires or electrodes that you have prepared and then connect the electricity.

Check the produced hydrogen and oxygen gasses in five minutes. Repeat the test with different electrodes and different amounts of electrolytes and record the results in the table below. You may want to repeat the experiment with different electrods. (Electrode is only the area that has contact with water, not the part that has insulator or plastic cover. In the above picture electrodes are identified with yellow color).

Now, Analyze your data and come up with your own conclusion.

Make Electricity from fruits are made easy

Introduction: 

This project is one of the most famous electricity projects that can be performed successfully by most students in the age of 10 to 16. Since the same method is used to get energy from many fruits and chemicals, this project has many names. Following are some of the other names or titles for this project:

• Fruit power or fruit battery
• Convert Chemical energy to electrical energy
• Potato battery or Lemon battery

Procedure:

           Making electricity from chemicals is based on the same scientific principles on which all modern batteries work. You insert copper and zinc electrodes in an acidic liquid and produce some electricity from the chemical reaction between your electrodes and electrolyte. The electricity produced in this way can be displayed with a multi-meter that can show millivolts. It may also be able to power up a 1.2 Volts light bulb. Making electricity experiment can be used for many different science projects.

List of Bioinformatics Courses offered in India

Azyme Biosciences, Bangalore ( Karnataka )
1188/20,3rd Floor, 26th Main, Opp. Ragigudda Temple Arch , Bangalore ( Bangalore (Bengaluru) Dist. )- 560069, Phone : 080-65467596 

Apeejay Svran Institute for Biosciences and Clinical Research, Gurgaon( Haryana )
Sector-32, Plot-26 , Gurgaon ( Gurgaon Dist. ) - 122001

bioCampus, Hyderabad( Andhra Pradesh )
gvk bioSciences Private Limited, #S-1, Phase -1, Technocrats Industrial Estate Balanagar , Hyderabad ( Hyderabad Dist. ) - 500037

Bioinformatics Institute of India (B.I.I.), Noida( Uttar Pradesh)
C-56A/28, Sector - 62 , Noida ( Gautam Buddha Nagar Dist. ) - 201301

Biosys Biotech Lab and Research Centre, Chennai( Tamil Nadu )
63/32, IInd Floor, Kamaraj colony, Ist street Kodambakkam , Chennai ( Chennai Dist. ) - 600024

C.M.S. College of Science and Commerce, Coimbatore( Tamil Nadu )
Chinnavedampatty , Coimbatore ( Coimbatore Dist. ) - 641006

Center for Bioinformatics Research Institute, Chennai( Tamil Nadu )
203/1,Arcot Road, NSK Salai, Vadapalani , Chennai ( Chennai Dist. ) - 600026

Devi Ahilya Vishwavidyalaya : School of Biotechnology, Indore( Madhya Pradesh )
Devi Ahilya University, Khandwa Road , Indore ( Indore Dist. ) - 452001

Dolphin (P.G.) Institute of Bio-Medical and Natural Sciences, Dehradun( Uttarakhand )
Manduwala, Chakrata Road , Dehradun ( Dehradun Dist. ) - 248007

Dr. N.G.P. Arts and Science College, Coimbatore( Tamil Nadu )
Kalapatti Road , Coimbatore ( Coimbatore Dist. ) - 641048

Holy Matha College of Modern Technology, Ernakulam( Kerala )
Manakkapadi, North Paravur , Ernakulam ( Ernakulam Dist. ) - 683511

Institute of Bioinformatics and Applied Biotechnology, Bangalore( Karnataka )
G-05, Tech Park Mall,International Technology Park Bangalore (ITPB), Whitefield Road , Bangalore ( Bangalore (Bengaluru) Dist. ) - 560066

Integral University, Lucknow( Uttar Pradesh )
Dasauli, P.O. Bas-ha Kursi Road , Lucknow ( Lucknow Dist. ) - 226026

iPower Solutions India Ltd, Adyar( Tamil Nadu )
9/5, IInd Floor, II Main Road , Karpagam Gardens , Adyar ( Chennai Dist. ) - 600020

Jamia Millia Islamia, New Delhi( Delhi )
Maulana Mohammad Ali Johar Marg, Jamia Nagar , New Delhi ( Delhi ) – 110025

Karpagam University, Coimbatore( Tamil Nadu )
Pollachi Main Road, Eachanari Post , Coimbatore ( Coimbatore Dist. ) - 641021

M.S. (Maharaja Sayajirao) University of Baroda : Faculty of Technology and Engineering, Vadodara( Gujarat )
Kalabhavan Rajmahal Road, Nr. Kirtistambh , Vadodara ( Vadodara (Baroda) Dist. ) - 390001

Madurai Kamaraj University, Madurai( Tamil Nadu )
Palkalai Nagar , Madurai ( Madurai Dist. ) - 625021

Mar Athanasius College, Kothamangalam( Kerala )
Kothamangalam ( Ernakulam Dist. ) - 686666

Muthayammal College of Arts and Science, Namakkal( Tamil Nadu )
Rasipuram , Namakkal ( Namakkal Dist. ) - 637408

Pondicherry University : Bioinformatics Centre, Puducherry( Puducherry )
School of Life Sciences, Pondicherry University , Puducherry ( Puducherry ) - 605014

S.R.M. University, Chennai( Tamil Nadu )
3 Veerasamy Street, West Mambalam , Chennai ( Chennai Dist. ) - 600033

Satyam Sri Services, Bangalore( Karnataka )
143, 5th Main, 100 Ft Ring Road, KEB Layout, BTM 1st Stage , Bangalore ( Bangalore (Bengaluru) Dist. ) - 560030

Singhania University, Jhunjhunu( Rajasthan )
V.P.O.Pacheri Bari , Jhunjhunu ( Jhunjhunu Dist. ) - 333515

University of Calcutta, Kolkata( West Bengal )
Senate House, 87 /1 College Street , Kolkata ( Kolkata Dist. ) - 700073

University of Hyderabad, Hyderabad( Andhra Pradesh )
P O Central University , Hyderabad ( Hyderabad Dist. ) - 500046

University of Pune : Bioinformatics Centre, Pune( Maharashtra )
The Director, University of Pune , Pune ( Pune Dist. ) - 411007

Vishwa Bioservices, Hyderabad( Andhra Pradesh )
2-3-512/134/1/B, Bapu Nagar, Amberpet , Hyderabad ( Hyderabad Dist. ) - 500029