Global Symposium for Natural Products Development Organized in India by Amity University

India’s first International Society for the Development of Natural Products (ISDNP) symposium was organized by Amity University, Uttar Pradesh, along with the National Society of Ethnopharmacology, India (NSE) and Phytochemical Society of Asia (PSA). 
Several foreign delegates, 29 Indian delegates and 23 delegates from various institutions of Amity University are attending the symposium.Researchers, students and industry representatives from various countries are discussing the application of analytical methods, phytochemistry, biotechnological, pharmacological and genetics for the development of natural products, taking part in lectures, poster sessions and the round table discussion. The symposium is an ideal platform for networking with international communities to industries, pharmaceutical firms, herbal pharma etc. Brand awareness and building international relationships particularly by advancing company's business opportunities is also an extra advantage to the companies. 
At Amity Campus, the Committee of the International Society for the Development of Natural Products has also announced its next venue for its 8th International Symposium i.e. Dhaka University, Bangladesh. 
Welcoming the august gathering, Prof. P. Pushpangadan, Padama Shree, DG, Amity Institute for Herbal and Biotech Products Development, President, National Society of Ethnopharmacology (NSE) India and Chairman, 7th ISDNP said that it is for the first time that ISDNP Symposium is being held in India, which is a very apt venue keeping in view its rich biodiversity. He discussed about Herbal drugs, Nutraceuticals, Allopathy and moreover he said that more than 40% allopathic drugs are plant based. 
Professor Yoshinori Asakawa, President, PSA, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Japan traced the history of PSA and shared its mission and objectives, which is to educate and promote natural sciences amongst the global audience. He called upon the students and faculty members of Amity University to become members of PSA and contribute towards the development and promotion of natural products across the globe. 
During the three day symposium, a host of technical sessions will unfold highlighting issues of contemporary relevance.
Source-ANI
 
 

Scientists Reveal Exact Cause of Depression

Scientists have provided fresh insights into the cause of major depressive disorder. In organisms as complex as humans, the neural mechanisms that help answer the question, "Is it worth my effort?" can fail, leading to debilitating mental illnesses. Major depressive disorder, for instance, which affects nearly 20 percent of people at some point in life, is correlated with underperformance in the parts of the brain involved in motivation.But Karl Deisseroth, MD, PhD, a professor of bioengineering and of psychiatry and behavioral sciences at Stanford University, and postdoctoral scholar Melissa Warden, PhD, have struggled to work out the exact cause and effect. 
Clinicians refer to this slowing down of motivation in depressed patients as "psychomotor retardation." According to Deisseroth, who is also a practicing psychiatrist, patients may experience this symptom mentally, finding it hard to envision the positive results of an action, or, he said, they may feel physically heavy, like their limbs just do not want to move. 
Psychiatrists, Deisseroth included, believe the will to act may be born in the prefrontal cortex - the foremost part of the brain that helps plan and coordinate action. It then zips through the brain as a series of electrical signals, passing from neuron to neuron along countless branching pathways until it reaches the nerves that directly implement movement. 
Until this study, however, it was not clear which of these pathways might control the willingness to meet challenges, or the anticipation that action might be worthwhile in a difficult situation. 
To isolate these pathways relevant to depression, Deisseroth's team needed to stimulate specific brain cells in rodents and observe changes in their behavior. They used optogenetics, a technique Deisseroth developed at Stanford in 2005, which has since revolutionized the fields of bioengineering and neuroscience. 
The secret is as old as green algae. These single-celled organisms produce a protein called channelrhodopsin that makes them sensitive to sunlight. Borrowing and engineering the gene for this protein, Deisseroth has been able to create neurons that respond to light delivered from fiber-optic cables. He can turn the neurons on and off by sending bursts of light to activate different areas of the brain and then observe the effects on behavior. 
Surprisingly, the researchers found that simply stimulating the prefrontal cortices of rodents didn't motivate them to try any harder in a laboratory challenge. It turns out that motivation is not as simple as stimulating a region of the brain. Instead of one switch in the prefrontal cortex that turns motivation on, multiple switches work in concert. Some neurons excite motivated activity and others inhibit it. Broadly stimulating the executive part of the brain will not generate a simple effect on behavior. 
"It's one step more subtle" said Deisseroth, "but this is something that optogenetics was very well-suited to resolve." 
An optogenetic method called projection targeting allowed the scientists to work backward from the brain stem and find the exact pathway from neurons in the prefrontal cortex that signal motivation. 
The researchers first introduced their light-sensitive protein into cells in the prefrontal cortex. The light sensitivity then spread out like the branches of a tree through all the outgoing connections and eventually made its way to the brain stem, making those regions light sensitive, too. 
Then, illuminating the newly light-sensitive regions of the brain stem thought to control motivational movement, Deisseroth and Warden watched the behavioral effects as a subgroup of neurons in the prefrontal cortex that sent connections to brain stem were activated. They could see not only which cells are possibly involved in motivation, but the way motivation moves from one brain region to another. 
The researchers suspected that one part of the brain stem in particular, the dorsal raphe nucleus, might be crucial to behaviors that control effort. This cluster of cells is a production hub for serotonin - a chemical messenger that changes the firing behavior of other cells. Serotonin is associated with mood modulation; many antidepressant drugs, for instance, may act by increasing serotonin concentration in the brain. 
When the pathway between the prefrontal cortex and the dorsal raphe nucleus was stimulated, rodents facing a challenge in the lab showed an immediate and dramatic surge in motivation. 
Curiously, however, when the rodents were relaxing in their home environment, the same stimulation had no effect. The pathway was not merely linked to any action, or to agitation; it was, more specifically, helping to "set the effort that the organism was willing to put forth to meet a challenge," Deisseroth said. 
Researchers were also able to produce the opposite effect - reduced effort in response to challenge - by stimulating prefrontal neurons that project to the lateral habenula, a region perched atop the brain stem that is thought to play a role in depression. When this region was getting signals driven optogenetically from the prefrontal cortex, rodents put forward less effort. 
Connecting depressive symptoms with brain pathways may be helpful in the development of drugs, but according to Deisseroth, the most important part of this research is its insight into how motivation works in both depressed and healthy people. 
The study has been published online in Nature.
Source-ANI  

Research shows diabetes drug improves memory

An FDA-approved drug initially used to treat insulin resistance in diabetics has shown promise as a way to improve cognitive performance in some people with Alzheimer's disease.
Working with genetically engineered mice designed to serve as models for Alzheimer's, University of Texas Medical Branch at Galveston researchers found that treatment with the anti-insulin-resistance drug rosiglitazone enhanced learning and memory as well as normalized insulin resistance. The scientists believe that the drug produced the response by reducing the negative influence of Alzheimer's on the behavior of a key brain-signaling molecule.
The molecule, called extracellular signal-regulated kinase (ERK), becomes hyperactive both in the brains of Alzheimer's patients and in the mice at a disease stage corresponding to mild cognitive impairment in human Alzheimer's. This excessive activity leads to improper synaptic transmission between neurons, interfering with learning and memory.
Rosiglitazone brings ERK back into line by activating what's known as the peroxisome proliferator-activated receptor gamma (PPARγ) pathway, which interacts with genes that respond to both PPARγ and ERK.
"Using this drug appears to restore the neuronal signaling required for proper cognitive function," said UTMB professor Larry Denner, the lead author of a paper describing this work now online in the Journal of Neuroscience. "It gives us an opportunity to test several FDA-approved drugs to normalize insulin resistance in Alzheimer's patients and possibly also enhance memory, and it also gives us a remarkable tool to use in animal models to understand the molecular mechanisms that underlie cognitive issues in Alzheimer's."
ERK dysfunction in the Alzheimer's mouse model was discovered several years ago by UTMB associate professor Kelly Dineley, senior author of theJournal of Neuroscience paper. But putting together the protein, gene and memory pieces of the puzzle required a multidisciplinary translational research team including animal cognitive neuroscientists, biochemists, molecular biologists, mass spectrometrists, statisticians and bioinformaticists.
"We were extraordinarily lucky to have this diverse group of experts right here on our campus at UTMB that could coalesce to bring such different ways of thinking to bear on a common problem," Denner said. "It was quite a challenge to get all of these experts communicating in a common scientific language. But now that we have this team working, we can move on to even more detailed and difficult questions."
Now the UTMB research team and other investigators across the world are starting clinical trials to investigate the value of therapies for insulin resistance in early-stage Alzheimer's disease in humans.
Source:University of Texas Medical Branch at Galveston 

New noninvasive tool helps target Parkinson’s disease

 Health professionals may soon have a new method of diagnosing Parkinson’s disease, one that is noninvasive and inexpensive, and, in early testing, has proved to be effective more than 90 percent of the time.In addition, this new method has the potential to track the progression of Parkinson’s, as well as measure the effectiveness of treatments for the disorder, said Rahul Shrivastav, professor and chairperson of Michigan State University’s Department of Communicative Sciences and Disorders and a member of the team developing the new method.It involves monitoring a patient’s speech patterns – specifically, movement patterns of the tongue and jaw.“In Parkinson’s disease, a common limitation is that the movements become slow and have a reduced range,” said Shrivastav. “We believe we see this pattern in speech too – the tongue doesn’t move as far as it should, doesn’t move as quickly as it should and produces subtle changes in speech patterns.”This method is particularly sensitive to Parkinson’s disease speech and, Shrivastav said, is effective with only two seconds of speech.“That’s significant in several ways: The detection methodology is noninvasive, easy to administer, inexpensive and capable of being used remotely and in telemedicine applications,” he said.Presently there are no tried-and-true methods for diagnosing Parkinson’s. Shrivastav said if a person is showing early symptoms of the disease, which include tremors, slower movements or rigid muscles, he or she is given a drug to treat the disease.“If the symptoms go away,” he said, “then it’s assumed you must have Parkinson’s disease.”In more advanced cases, he said, symptoms are usually prominent enough that it is fairly easy to diagnose.Parkinson’s disease is a neurological disorder affecting a half million people in the United States, with 50,000 newly diagnosed cases every year. It occurs when nerve cells in the brain stop producing a chemical called dopamine, which helps control muscle movement. Without dopamine, the nerve cells cannot properly send messages, leading to the loss of muscle function.While there is no cure for Parkinson’s disease, early detection is particularly important since the treatments currently available for controlling symptoms are most effective at that stage.Shrivastav and his colleagues from the University of Florida’s Department of Speech, Language and Hearing Sciences, recently presented their findings at the Acoustical Society of America Conference.

Source:MSU

New Study Confirms Link Between Job and Breast Cancer Risk

In a recent study it was found that certain jobs pose a higher risk of breast cancers, particularly those that expose the worker to potential carcinogens. The findings of the study were published in BioMed Central's open access journal Environmental Health. 
Breast cancer is the most frequent cancer diagnosis among women in industrialized countries, and North American rates are among the highest in the world. Endocrine-disrupting chemicals and carcinogens, some of which may not have yet been classified as such, are present in many working environments and could increase breast cancer risk. In their study, James T Brophy and his colleagues set out to characterize the possible links between breast cancer and occupation, particularly in farming and manufacturing.The population-based case-control study was conducted in Southern Ontario, Canada, and included 1006 breast cancer cases (referred by the Windsor Regional Cancer Centre) with 1147 randomly selected and matched community controls.
 Using interviews and surveys, the team collected data on participants' occupational and reproductive histories. All jobs were coded for their likelihood of exposure to carcinogens and endocrine disruptors, and patients' tumor pathology regarding endocrine receptor status was assessed. The authors found in this group of participants that, across all sectors, women in jobs with potentially high exposures to carcinogens and endocrine disrupters had an elevated breast cancer risk. Sectors with increased risk included agriculture, bar/gambling, automotive plastics manufacturing, food canning and metal-working. 
Importantly, premenopausal breast cancer risk was highest in the automotive plastics and food canning industries.The findings also suggested that women with lower socioeconomic status had an elevated risk of breast cancer, which may result from higher exposures to endocrine-disrupting chemicals in the lower-income manufacturing and agricultural industries of the study area.The results lend weight to hypotheses linking breast cancer risk and exposures likely to include carcinogens and endocrine disrupters. Lead author Brophy said, "Our results highlight the importance of occupational studies in identifying and quantifying environmental risk factors and illustrates the value of taking detailed occupational histories of cancer patients. Mounting evidence suggests that we need to re-evaluate occupational exposure limits in regulatory protection."
Soure: BioMed 
 

Melatonin Helps Treat Sleep Disorders in Neuro-Developmentally Challenged Children

Melatonin is an important hormone concerned with the sleep-wake cycle in human beings. And, children with neuro-developmental ailments show higher prevalence of sleep disturbances as compared to their peers without these problems. 
Paul Gringras and his colleagues conducted a randomized placebo controlled trial to examine the efficacy of melatonin in treating sleep disorders in kids with neuro-developmental problems. The study was published in BMJ 2012.
 The researchers enrolled 146 children from 19 hospitals across Wales and England, ranging in age from 3 years to 15 years 8 months, and having neurological and developmental problems. The children also had deranged sleep patterns. 
Sleep problem was defined in the study as ‘the child not falling asleep within one hour of lights out or having less than six hours of continuous sleep’. 
Just 45 minutes before retiring to bed, the children were given immediate-release melatonin or matching placebo capsules for 12 weeks. The dose was started with 0.5mg and was subsequently increase to 2mg, 6mg and 12mg depending upon the response. The parents were asked to maintain a record of their children’s sleep. The child’s sleep pattern was reviewed at four weekly intervals and the dose was increased to the next dose increment if the child - 

• fulfilled the sleep disorder eligibility criteria; 

• had received at least 5 of the possible 7 doses in the preceding week; and 

• had no serious adverse events. 

The scientists observed the factors such as sleep onset latency, family functioning, adverse effects and assessment of child behavior. Nature and duration of sleep was assessed from parent’s record diaries and actigraphy. Actigraphy is a ‘non-invasive method of monitoring human rest / activity cycles’. 

It was found that melatonin increased total sleep time and decreased sleep onset latency. Melatonin was very effective in children with long sleep latency. 
The researchers observed that melatonin induced little extra sleep in children. They fell asleep faster and woke up earlier. However the family functioning outcomes and child behavior did not show significant improvement. The scientists were of the opinion that further comparisons with melatonin analogues or slow-release melatonin were needed. 
Anant Dave, child psychiatrist from West Midlands, while commending the study however feels that ‘the frequency with which Melatonin is prescribed is quite high when one considers its modest effect on sleep as described in this study’. He suggested that the care-givers of children with neuro-developmental disorders should be given better support as well as ‘more specific non-pharmacological approaches towards sleep problems, using a range of therapeutic modalities’. 
Reference: Melatonin for sleep problems in children with neurodevelopmental disorders: randomised double masked placebo controlled trial; Gringras et al; BMJ 2012 
 

Gene That Can Help Predict The Time of Death Identified

Researchers have for the first time identified a common gene variant that helps determine the time a person will wake up each day. 
Furthermore, this new discovery not only demonstrates this common polymorphism influences the rhythms of people's day-to-day lives -- it also finds this genetic variant helps determine the time of day a person is most likely to die.The surprising findings, which appear in the November 2012 issue of the Annals of Neurology, could help with scheduling shift work and planning medical treatments, as well as in monitoring the conditions of vulnerable patients. 
"The internal 'biological clock' regulates many aspects of human biology and behavior, such as preferred sleep times, times of peak cognitive performance, and the timing of many physiological processes. It also influences the timing of acute medical events like stroke and heart attack," says first author Andrew Lim, MD, who conducted the work as a postdoctoral fellow in the Department of Neurology at Beth Israel Deaconess Medical Center (BIDMC). 
"Previous work in twins and families had suggested that the lateness or earliness of one's clock may be inherited and animal experiments had suggested that the lateness or earliness of the biological clock may be influenced by specific genes," adds Lim, who is currently an Assistant Professor in the Division of Neurology at the University of Toronto. 
The work originated several years ago while Lim was working in the laboratory of BIDMC Chief of Neurology Clifford Saper, MD, PhD. Lim and the other lab members were studying why older people have trouble sleeping and had joined a research project based at Rush University in Chicago involving 1,200 people who signed on as healthy 65-year-olds and would receive annual neurological and psychiatric examinations. 
The cohort's original intent was to determine if there were identifiable precursors to the development of Parkinson's disease or Alzheimer's disease. As part of the research the subjects were undergoing various sleep-wake analyses using a wristband called an actigraph, which provides a reliable record of an individual's pattern of activity. Additionally, in order to provide the scientists with information on sleep-wake patterns within a year of death, the participants had agreed to donate their brains after they died. 
But the investigation took a new turn when Lim learned that the same group of subjects had also had their DNA genotyped. Teaming up with investigators from Brigham and Women's Hospital (BWH), Lim and his colleagues compared the wake-sleep behavior of these individuals with their genotypes. These findings were later verified in a group of young volunteers. 
They soon discovered a single nucleotide near a gene called "Period 1" that varied between two groups that differed in their wake-sleep behavior. At this particular site in the genome, 60 percent of individuals have the nucleotide base termed adenine (A) and 40 percent have the nucleotide base termed guanine (G). Because we have two sets of chromosomes, in any given individual, there's about a 36 percent chance of having two As, a 16 percent chance of having two Gs, and a 48 percent chance of having a mixture of A and G at this site. 
"This particular genotype affects the sleep-wake pattern of virtually everyone walking around, and it is a fairly profound effect so that the people who have the A-A genotype wake up about an hour earlier than the people who have the G-G genotype, and the A-Gs wake up almost exactly in the middle," explains Saper, who is also the James Jackson Putnam Professor of Neurology and Neuroscience at Harvard Medical School. Also, expression of the Period 1 gene was lower in the brains and white blood cells of people with the G-G genotype than in people with the A-A genotype, but only in the daytime, which is when the gene is normally expressed. 
This discovery marks the biggest contribution of a single genotype in a large population to determine the time of day when people wake up or go to sleep. But could the variant also affect other aspects of the body's circadian rhythm? 
"Virtually all physiological processes have a circadian rhythm, meaning that they occur predominantly at certain parts of the day. There's even a circadian rhythm of death, so that in the general population people tend on average to be most likely to die in the morning hours. Sometime around 11 am is the average time," says Saper. 
When the investigators went back and looked at the people in the study (many of whom had enrolled more than 15 years ago at age 65) who had died, they found that this same genotype predicted six hours of the variation in the time of death: those with the AA or AG genotype died just before 11 a.m., like most of the population, but those with the GG genotype on average died at just before 6 p.m. 
"So there is really a gene that predicts the time of day that you'll die. Not the date, fortunately, but the time of day," says Saper. 
Lim says that additional work is needed to determine the mechanisms by which this and other gene variants influence the body's biological clock. In addition to helping people optimize their schedules, the research could eventually lead to novel therapies to treat disturbances of this clock as seen in jet lag or shift work. 
"Also, working out which causes of death are influenced by gene variants like the one we identified may eventually lead to rational timed interventions—such as taking heart medications at particular times depending on which version of the gene variant one carries—to provide protection during an individuals' period of greatest risk," says Lim. The potential clinical applications may be as diverse as the many processes that the circadian clock controls. 
Source:Beth Israel Deaconess Medical Center (BIDMC).