Biochemistry and Molecular Biology Official Blog

Would you mind for a second

Sunday, 15 October 2017

Immunology A Short Course

1388
Richard CoicoImmunology: A Short Course (Coico, Immunology)2015-04-27Medicine5/9/2015 6:53:51 PMgestalt



Download here

Saturday, 14 October 2017

lodish Molecular Cell Biology 8th edition



Harvey Lodish, Arnold Berk, Chris A. KaiserMolecular Cell Biology (8th edition)2016Biology5/24/2016 2:37:57 PM

Molecular Cell Biology (8th edition)

Download 

Tuesday, 16 May 2017

Detailed Studies of Activity of Gene of protein coded by unknown gene

Basically there is an unknown Gene that makes up a Protein with specific function and by deleting that part of the gene and leaving the rest part of the gene which is still performing that function, so to check whether that gene is still performing all the functions right or not....

This is done through the process call Site Directed Mutagenesis or Invitro Mutagenesis.


  • So After Mutagenesis, the gene is inserted in the host 
  • Afterwards via Homologous recombination Gene Replaces the existing copy of gene
  • Still we have no idea what cells have undergone Homologous Recombination.
  • So we use a Marker's Gene [ Antibiotic Resistant ]
  • If marker gene is present, so will be the mutated gene
  • But now the problem is if the That Marker gene is incorporated in genome instead of mutated
so we use a system called a Two step Gene Replacement
  • First two Target gene is replaced by Marker Gene on its own.
  • The Cells which undergo Recombination are identified by selecting Marker Gene phenotype.
  • There cell's are then used in 2nd step where Marker gene is replaced by Mutated Gene.
Afterwards the success is monitored by the looking for the cells that have lost the Marker gene phenotype.
Now the cells contain the Mutated gene and their phenotype can be examined to verify the effect of direct mutated Gene.

Tuesday, 2 May 2017

Biochemistry By D.Voet & J. Voet 4E

About Author:-
Donald Herman Voet (born November 29, 1938) is an associate professor of chemistry at the University of Pennsylvania. His laboratory utilizes x-ray crystallography to understand structure-function relationships in proteins.He and his wife, Judith G. Voet, are authors of biochemistry text books that are widely used in undergraduate and graduate curricula.


Download 



Friday, 28 April 2017

Working human forebrain circuits assembled in a lab dish

Date:
April 26, 2017
Source:
Stanford University Medical Center
Summary:
Peering into laboratory glassware, researchers have watched stem-cell-derived nerve cells arising in a specific region of the human brain migrate into another brain region. This process recapitulates what's been believed to occur in a developing fetus, but has never previously been viewed in real time.
FULL STORY

After spheroids representing two different brain regions fuse in a dish, neurons from one spheroid (green) migrate into the second and forge connections with neurons residing there.
Credit: Courtesy of the Pasca lab
Peering into laboratory glassware, Stanford University School of Medicine researchers have watched stem-cell-derived nerve cells arising in a specific region of the human brain migrate into another brain region. This process recapitulates what's been believed to occur in a developing fetus, but has never previously been viewed in real time.
The investigators saw the migrating nerve cells, or neurons, hook up with other neurons in the target region to form functioning circuits characteristic of the cerebral cortex.
These observations showcase neuroscientists' newfound ability to monitor, assemble and manipulate so-called neural spheroids, generated from human induced pluripotent stem cells, to study the normal development of the human forebrain during late pregnancy.
"We've never been able to recapitulate these human-brain developmental events in a dish before," said the study's senior author, Sergiu Pasca, MD, assistant professor of psychiatry and behavioral sciences. "The process happens in the second half of pregnancy, so viewing it live is challenging. Our method lets us see the entire movie, not just snapshots."
The findings, and the techniques used to obtain them, carry potential for the personalized study of individuals' psychiatric disorders. In the study, to be published online April 26 in Nature, the scientists were able to attribute, for the first time, defects in neuronal migration to Timothy syndrome, a rare condition that predisposes people to autism, epilepsy and cardiac malfunction. Postdoctoral scholars Fikri Birey, PhD, Jimena Andersen, PhD, and Chris Makinson, PhD, share lead authorship.
The need for 3-D models
Culturing neurons in a lab dish is old hat. But the two-dimensional character of life lived atop a flat glass coverslip doesn't sit well with cells designed for three-dimensional existence. Neurons cultured in monolayers mature only partially, tend to die fairly quickly and interact suboptimally.
In a 2015 study, Pasca and his colleagues described their method for producing neural spheroids. Neural precursor cells generated from iPS cells are placed in culture dishes whose bottoms are coated to make it impossible for neurons to attach. The cells float freely in a nutrient-rich broth, ultimately developing into hundreds of almost perfectly round balls approaching 1/16 of an inch in diameter and consisting of over 1 million cells each. These neurons can live for up to two years, and they mature fully.
The spheroids created in the 2015 study recapitulated the human cerebral cortex's six-layer-thick architecture, and the neurons they contained were of the type that arise in and dominate the cerebral cortex. They're called glutamatergic neurons because they secrete the excitatory chemical glutamate.
But the cerebral cortex's glutamatergic neurons don't remain alone for long. During fetal development, they are eventually joined by neurons of another type that originate in a slightly deeper region of the developing forebrain. These neurons secrete a neuromodulatory -- and usually inhibitory -- substance called GABA, so they're deemed GABAergic. It's known that GABAergic cells migrate from their region of origin to the cortex, where they interlace with its resident glutamatergic cells and with one another to form the circuitry responsible for the brain's most advanced cognitive activities. But no one had been able to watch this happen with human cells in a dish.
In the new study, the researchers separated their spheroids into two batches and coaxed them to become different regions of the human brain. They cultured one batch in a medium that induces cortexlike spheroids containing glutamatergic neurons. They placed the second batch in dishes whose broth steers the spheroids toward resembling the underlying brain region where GABAergic neurons originate.
Then, the investigators juxtaposed the two distinct types of spheroids. Within three days, the two spheroids fused, and GABAergic neurons from one spheroid began migrating into the glutamatergic-neuron-rich spheroid. Their migration pattern, the scientists noted, was halting: They would move toward the target spheroid for a little while, then stop for an extended period, then start up again in stuttering jumps.
On reaching their destination, the GABAergic travelers underwent a transformation, sprouting dendrites -- branching, foliage-like "tails" that receive inputs from other neurons -- and forming working connections with the glutamatergic neurons. Electrophysiological tests revealed that GABAergic and glutamatergic neurons were successfully forming circuits and signaling to one another.
Insight into Timothy syndrome
The scientists had access to tissue samples from patients with Timothy syndrome, an extremely rare and historically lethal condition caused by a mutation in the gene coding for a type of calcium channel -- a protein containing a pore that responds to different voltage levels by opening or closing, respectively permitting or blocking the flow of calcium across otherwise impermeable membranes. Such calcium channels are essential to many cellular processes. Timothy syndrome patients' severe cardiac abnormalities once spelled ultra-short life expectancies, but now can be ameliorated with pacemakers. However, survivors usually have autism and frequently have epilepsy.
The investigators generated both types of neural spheroids from their Timothy-syndrome tissue samples, fused them and watched to see what would happen. What they saw was this: The GABAergic neurons, which seemed to develop normally, exhibited aberrant start-and-stop migration patterns. Their forward movements were more frequent, but far less efficient, than those of normal neurons.
The mutation behind Timothy syndrome increases the likelihood that the calcium channel for which it codes will let calcium ions flow through it. So, the researchers reasoned, a drug impeding the channel's activity might reverse the aberration. Indeed, two different drugs that block this type of calcium channel restored normal migratory activity to the Timothy-syndrome-derived GABAergic neurons.
Diverse variants in the same gene responsible for Timothy syndrome are associated with schizophrenia, other forms of autism spectrum disorder and bipolar disorder. Pasca said he suspects these variants may affect GABAergic neurons' integration with cortical glutamatergic neurons, resulting in a cognition-altering imbalance between excitation and inhibition in the cortex and laying the groundwork for these disorders.
"Our method of assembling and carefully characterizing neuronal circuits in a dish is opening up new windows through which we can view the normal development of the fetal human brain," said Pasca. "More importantly, it will help us see how this goes awry in individual patients."
Stanford's Office of Technology Licensing has filed for a patent on the intellectual property involving the generation of brain-region-specific neural spheroids and their assembly for studying development and disease.
###
Other Stanford study co-authors are postdoctoral scholars Saiful Islam, PhD, and Nina Huber, PhD; senior research scientists Nancy O'Rourke, PhD, and Wu Wei, PhD; high school lab intern Nicholas Thom; Lars Steinmetz, PhD, professor of genetics; Jonathan Bernstein, MD, PhD, associate professor of pediatrics; Joachim Hallmayer, MD, professor of psychiatry and behavioral sciences; and John Huguenard, PhD, professor of neurology and of neurosurgery.
The study was funded by the National Institutes of Health (grants R01MH100900, R01MH100900, R01MH107800 and P01HG00020526), the California Institute for Regenerative Medicine, the MQ Foundation, the Donald E. and Delia B. Baxter Foundation, the Kwan Research Fund, the Stanford Child Research Health Institute, the Wishes for Elliot Foundation, a Walter V. and Idun Berry Postdoctoral Fellowship, the Stanford School of Medicine Dean's Office, the UC-San Francisco Program for Breakthrough Biomedical Research and the Sandler Foundation.
Stanford's Department of Psychiatry and Behavioral Sciences and the Stanford Center for Sleep Sciences and Medicine also supported the work.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://med.stanford.edu/school.html. The medical school is part of Stanford Medicine, which includes Stanford Health Care and Stanford Children's Health. For information about all three, please visit http://med.stanford.edu.
Print media contact: Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu) Broadcast media contact: Becky Bach at (650) 724-2454 (retrout@stanford.edu)

Story Source:
Materials provided by Stanford University Medical Center. Original written by Bruce Goldman. Note: Content may be edited for style and length.

Tuesday, 25 April 2017

Brain stimulation during training boosts performance

Date:
April 24, 2017
Source:
DOE/Sandia National Laboratories
Summary:
New research shows that working memory training combined with a kind of noninvasive brain stimulation can lead to cognitive improvement under certain conditions. Improving working memory or cognitive strategies could be very valuable for training people faster and more efficiently.
FULL STORY

Sandia National Laboratories cognitive scientist Mike Trumbo adjusts the placement of a transcranial direct current stimulation unit on cognitive scientist Laura Matzen's head. Though Trumbo has tried tDCS dozens of times, he does not use it to boost his own brain.
Credit: Photo by Randy Montoya
Your Saturday Salsa club or Introductory Italian class might be even better for you than you thought.
According to Sandia National Laboratories cognitive scientist Mike Trumbo, learning a language or an instrument or going dancing is the best way to keep your brain keen despite the ravages of time. Not only do you enhance your cognition but you also learn a skill and have fun.
Several commercial enterprises have claimed you can get cognitive benefits from brain training games intended to enhance working memory. Working memory is the amount of information you can hold and manipulate in your mind at one time, said cognitive scientist Laura Matzen. However, a burgeoning body of research shows working memory training games don't provide the benefits claimed. A study by Trumbo, Matzen and six colleagues published in Memory and Cognition shows evidence that working memory training actually impairs other kinds of memory.
On the other hand, studies have shown that learning another language can help school-age children do better in math and can delay the onset of dementia in older adults. Also going dancing regularly is the best protection against dementia compared to 16 different leisure activities, such as doing crossword puzzles and bicycling. Playing board games and practicing a musical instrument are the next best activities for keeping the mind sharp. Dancing is probably so effective because it combines cognitive exertion, physical exercise and social interaction, said Trumbo.
New research from Sandia published in Neuropsychologia shows that working memory training combined with a kind of noninvasive brain stimulation can lead to cognitive improvement under certain conditions. Improving working memory or cognitive strategies could be very valuable for training people faster and more efficiently.
"The idea for why brain stimulation might work when training falls short is because you're directly influencing brain plasticity in the regions that are relevant to working memory task performance. If you're improving connectivity in a brain region involved in working memory, then you should get transfer to other tasks to the extent that they rely on that same brain region," said Trumbo. "Whereas when you're having people do tasks in the absence of brain stimulation, it's not clear if you're getting this general improvement in working memory brain areas. You might be getting very selective, task kind of improvements."
Matzen cautioned that research using transcranial direct current stimulation (tDCS) to improve cognitive performance is relatively new, and the field has produced mixed results. More research is needed to understand how best to use this technology.
Neurons that fire together wire together
Using more than 70 volunteers divided into six groups, the researchers used different combinations of working memory training with transcranial direct current stimulation. Then they assessed the volunteers' performance on working memory tests and a test of problem-solving ability.
Using electrodes placed on the scalp and powered by a 9-volt battery, a tDCS unit delivers weak constant current through the skull to the brain tissue below. According to Trumbo, most people feel some mild tingling, itching or heat under the electrode for the first few minutes. There are well-established safety guidelines for tDCS research, ensuring that the procedure is safe and comfortable for participants and this research was approved by Sandia's Human Studies Board and the University of New Mexico's Institutional Review Board. There are commercial tDCS devices already on the market.
Researchers think tDCS makes neurons a little bit more likely to fire, which can help speed up the formation of neuronal connections and thus learning, said Matzen. Though the exact mechanisms aren't well understood, its potential is. According to studies, tDCS can help volunteers remember people's names, is better than caffeine at keeping Air Force personnel awake and may even help fight depression.
Brain stimulation and brain training: better together?
In the Sandia-led study, the volunteers played verbal or spatial memory training games for 30 minutes while receiving stimulation to the left or right forehead. That part of the brain is called the dorsolateral prefrontal cortex and is involved in working memory and reasoning. Since the right hemisphere is involved in spatial tasks and the left hemisphere is involved in verbal tasks, the researchers thought volunteers who received stimulation on the right side while training on spatial tasks would improve on spatial tests and those who received stimulation on the left side while training on verbal tasks would improve on verbal tests.
The verbal task involved remembering if a letter had appeared three letters back in a string of letters, for instance A-C-B-A-D. The spatial task was similar but involved remembering the sequence that blocks appear in a grid.
As expected, the spatial/right group got better at the spatial test but not verbal or reasoning tests. The spatial/left group performed about the same as the volunteers that received mock stimulation. The verbal/left group got better at the verbal test but not spatial or reasoning tests.
However, the results from the verbal/right group were surprising, said Trumbo. This group got better at the trained task -- remembering strings of letters -- as well as the closely related task -- remembering the sequence of boxes in a grid. They also improved on a reasoning test. The sample size was small, with only 12 volunteers, but the improvements were statistically significant, said Matzen.
One explanation Trumbo offered is that the right dorsolateral prefrontal cortex is particularly involved in strategy use during tasks. By stimulating the right side during the verbal task, the volunteers might get better at using a strategy. The tDCS improves the connections of these neurons, which leads to enhanced ability to use this strategy, even on other tasks.
He added, "We did not explicitly collect data related to strategy use, so it is kind of an open question. I'd really like to do some follow-up work."
If tDCS can reliably enhance working memory or cognitive strategies, it could be very useful for training people faster and more efficiently. Matzen said, "This could benefit many mission areas at Sandia where people must learn complex tools and systems. Reducing training time and improving cognitive performance would have substantial benefits to overall system performance."

Story Source:
Materials provided by DOE/Sandia National LaboratoriesNote: Content may be edited for style and length.

Journal Reference:
  1. Michael C. Trumbo, Laura E. Matzen, Brian A. Coffman, Michael A. Hunter, Aaron P. Jones, Charles S.H. Robinson, Vincent P. Clark. Enhanced working memory performance via transcranial direct current stimulation: The possibility of near and far transferNeuropsychologia, 2016; 93: 85 DOI: 10.1016/j.neuropsychologia.2016.10.011

Genetics, environment combine to give everyone a unique sense of smell

FULL STORY

Genetically identical mice exposed to different smells as they grow up develop different olfactory receptors in their noses.
Credit: © Marion Wear / Fotolia
Researchers from the Wellcome Trust Sanger Institute and their collaborators have shown that receptors in the noses of mice exposed to certain smells during life are different to genetically similar mice that lived without those smells. Published today in eLife, the study found it is this combination of genetics and experience that gives each individual a unique sense of smell.
Our sense of smell comes from the olfactory organ in the nose, which is made up of sensory neurons containing receptors that can detect odours. There are about one thousand types of olfactory receptors in the nose, compared with only three types of visual receptors in the eye, and 49 types of taste receptors on the tongue. Of our senses, the olfactory system is the most complex, and combinations of signals from different olfactory receptors allow people to smell an enormously large repertoire of odours. However, how different people vary in their smelling abilities is not well understood.
To investigate the sense of smell the researchers used laboratory mice as a model, comparing the olfactory neurons from genetically identical animals that grew up in different environments. They also compared animals that grew up in the same environment but were genetically different.
The team used RNA sequencing to see which receptor genes were active. The researchers found that genetics controlled which receptors were present in the mice. Crucially however, they found that the environment that the individual had lived in had a significant effect on the number of cells able to identify each smell.
Professor Fabio Papes, an author on the paper from the University of Campinas in Brazil, said: "It became clear that the role of genes, especially those that encode olfactory receptors in the genome, is very important in the construction of nasal tissue, but there was a very remarkable contribution of the environment, something that has not been previously described to this extent. We found the cellular and molecular construction of the olfactory tissue at a given moment is prepared not only by the organism's genes but also by its life history."
Olfactory neurons are formed throughout an individual's lifetime, and the study showed the olfactory system adapted to the environment, leading to more cells capable of detecting scents to which there has been greater exposure. As a consequence, different individuals, even if genetically similar, may have completely different olfactory abilities. This could contribute to the individuality of the sense of smell, even in humans.
The knowledge that an individual's history can affect the structure of olfactory tissue neurons may have implications for personalised medicine as different people's sense organs could be constructed differently and respond in different ways. Studying olfactory neurons can also provide information about how the neurons in the brain are organised and function.
Dr Darren Logan, the lead author on the study from the Wellcome Trust Sanger Institute, said: "The neurons in the olfactory system are highly connected to the neurons in the brain and studying these can help us understand neuronal development. We have shown that each individual has a very different combination of possible olfactory neurons, driven by genetics. In this study we also show that, with experience of different smells, these combinations of neurons change, so both genetics and environment interplay to give every individual a unique sense of smell."

Story Source:
Materials provided by Wellcome Trust Sanger InstituteNote: Content may be edited for style and length.

Journal Reference:
  1. Ximena Ibarra-Soria, Thiago S Nakahara, Jingtao Lilue, Yue Jiang, Casey Trimmer, Mateus AA Souza, Paulo HM Netto, Kentaro Ikegami, Nicolle R Murphy, Mairi Kusma, Andrea Kirton, Luis R Saraiva, Thomas M Keane, Hiroaki Matsunami, Joel Mainland, Fabio Papes, Darren W Logan. Variation in olfactory neuron repertoires is genetically controlled and environmentally modulatedeLife, 2017; 6 DOI: 10.7554/eLife.21476
FULL STORY

Genetically identical mice exposed to different smells as they grow up develop different olfactory receptors in their noses.
Credit: © Marion Wear / Fotolia
Researchers from the Wellcome Trust Sanger Institute and their collaborators have shown that receptors in the noses of mice exposed to certain smells during life are different to genetically similar mice that lived without those smells. Published today in eLife, the study found it is this combination of genetics and experience that gives each individual a unique sense of smell.
Our sense of smell comes from the olfactory organ in the nose, which is made up of sensory neurons containing receptors that can detect odours. There are about one thousand types of olfactory receptors in the nose, compared with only three types of visual receptors in the eye, and 49 types of taste receptors on the tongue. Of our senses, the olfactory system is the most complex, and combinations of signals from different olfactory receptors allow people to smell an enormously large repertoire of odours. However, how different people vary in their smelling abilities is not well understood.
To investigate the sense of smell the researchers used laboratory mice as a model, comparing the olfactory neurons from genetically identical animals that grew up in different environments. They also compared animals that grew up in the same environment but were genetically different.
The team used RNA sequencing to see which receptor genes were active. The researchers found that genetics controlled which receptors were present in the mice. Crucially however, they found that the environment that the individual had lived in had a significant effect on the number of cells able to identify each smell.
Professor Fabio Papes, an author on the paper from the University of Campinas in Brazil, said: "It became clear that the role of genes, especially those that encode olfactory receptors in the genome, is very important in the construction of nasal tissue, but there was a very remarkable contribution of the environment, something that has not been previously described to this extent. We found the cellular and molecular construction of the olfactory tissue at a given moment is prepared not only by the organism's genes but also by its life history."
Olfactory neurons are formed throughout an individual's lifetime, and the study showed the olfactory system adapted to the environment, leading to more cells capable of detecting scents to which there has been greater exposure. As a consequence, different individuals, even if genetically similar, may have completely different olfactory abilities. This could contribute to the individuality of the sense of smell, even in humans.
The knowledge that an individual's history can affect the structure of olfactory tissue neurons may have implications for personalised medicine as different people's sense organs could be constructed differently and respond in different ways. Studying olfactory neurons can also provide information about how the neurons in the brain are organised and function.
Dr Darren Logan, the lead author on the study from the Wellcome Trust Sanger Institute, said: "The neurons in the olfactory system are highly connected to the neurons in the brain and studying these can help us understand neuronal development. We have shown that each individual has a very different combination of possible olfactory neurons, driven by genetics. In this study we also show that, with experience of different smells, these combinations of neurons change, so both genetics and environment interplay to give every individual a unique sense of smell."

Story Source:
Materials provided by Wellcome Trust Sanger InstituteNote: Content may be edited for style and length.

Journal Reference:
  1. Ximena Ibarra-Soria, Thiago S Nakahara, Jingtao Lilue, Yue Jiang, Casey Trimmer, Mateus AA Souza, Paulo HM Netto, Kentaro Ikegami, Nicolle R Murphy, Mairi Kusma, Andrea Kirton, Luis R Saraiva, Thomas M Keane, Hiroaki Matsunami, Joel Mainland, Fabio Papes, Darren W Logan. Variation in olfactory neuron repertoires is genetically controlled and environmentally modulatedeLife, 2017; 6 DOI: 10.7554/eLife.21476

Saturday, 1 April 2017

Blood test unlocks new frontier in treating depression

Date:
March 29, 2017
Source:
UT Southwestern Medical Center
Summary:
For the first time, doctors can determine which medication is more likely to help a patient overcome depression, according to research that pushes the medical field beyond what has essentially been a guessing game of prescribing antidepressants.
FULL STORY

A study from Dr. Madhukar Trivedi (front) demonstrated that measuring a depressed patient’s C-reactive protein level can help doctors prescribe an antidepressant that is more likely to work.
Credit: Image courtesy of UT Southwestern Medical Center
Doctors for the first time can determine which medication is more likely to help a patient overcome depression, according to research that pushes the medical field beyond what has essentially been a guessing game of prescribing antidepressants.
A blood test that measures a certain type of protein level provides an immediate tool for physicians who until now have relied heavily on patient questionnaires to choose a treatment, said Dr. Madhukar Trivedi, who led the research at UT Southwestern Medical Center's Center for Depression Research and Clinical Care.
"Currently, our selection of depression medications is not any more superior than flipping a coin, and yet that is what we do. Now we have a biological explanation to guide treatment of depression," said Dr. Trivedi, Director of the depression center, a cornerstone of UT Southwestern's Peter O'Donnell Jr. Brain Institute.
The study demonstrated that measuring a patient's C-reactive protein (CRP) levels through a simple finger-prick blood test can help doctors prescribe a medication that is more likely to work. Utilizing this test in clinical visits could lead to a significant boost in the success rate of depressed patients who commonly struggle to find effective treatments.
A major national study Dr. Trivedi led more than a decade ago (STAR*D) gives insight into the prevalence of the problem: Up to a third of depressed patients don't improve during their first medication, and about 40 percent of people who start taking antidepressants stop taking them within three months.
"This outcome happens because they give up," said Dr. Trivedi, whose previous national study established widely accepted treatment guidelines for depressed patients. "Giving up hope is really a central symptom of the disease. However, if treatment selection is tied to a blood test and improves outcomes, patients are more likely to continue the treatment and achieve the benefit."
The new research published in Psychoneuroendocrinology measured remission rates of more than 100 depressed patients prescribed either escitalopram alone or escitalopram plus bupropion. Researchers found a strong correlation between CRP levels and which drug regimen improved their symptoms:
  • For patients whose CRP levels were less than 1 milligram per liter, escitalopram alone was more effective: 57 percent remission rate compared to less than 30 percent on the other drug.
  • For patients with higher CRP levels, escitalopram plus bupropion was more likely to work: 51 percent remission rate compared to 33 percent on escitalopram alone.
Dr. Trivedi noted that these results could readily apply to other commonly used antidepressants.
"These findings provide evidence that a biological test can immediately be used in clinical practice," he said.
Dr. Trivedi identified CRP as a potential marker for depression treatments because it has been an effective measure of inflammation for other disorders such as cardiovascular disease and diabetes.
While previous research to establish CRP as an antidepressant marker used levels three to five times higher than the latest study, "my theory was that you don't need that high of an inflammation to experience the sickness of depression," Dr. Trivedi said. "Even a little inflammation may be sufficient for the patients to experience some of these symptoms of depression."
The next step is to conduct larger studies to verify CRP's role with other antidepressants and find alternative markers where CRP does not prove effective. Dr. Trivedi said these studies could lead to additional useful biological tests that can be used in practice.
"Both patients and primary-care providers are very desperately looking for markers that would indicate there is some biology involved in this disease. Otherwise, we are talking about deciding treatments from question-and-answer from the patients, and that is not sufficient," said Dr. Trivedi, a Professor of Psychiatry who holds the Betty Jo Hay Distinguished Chair in Mental Health and is the inaugural holder of the Julie K. Hersh Chair for Depression Research and Clinical Care.
The data reviewed for the study came from the CO-MED trial, which was funded by the National Institute of Mental Health. The work was also supported through UT Southwestern's Center for Depression Research and Clinical Care and The Hersh Foundation.
Other UT Southwestern researchers include Dr. Manish Jha, Dr. Abu Taher Minhajuddin, Dr. Bharathi Gadad, Dr. Tracy Greer, Bruce Grannemann, Dr. Abigail Soyombo and Taryn Mayes. Dr. A. John Rush, Professor Emeritus, Duke-National University of Singapore also collaborated on the publication.
"With advances in technology and our understanding of the biology of depression, our ongoing work with additional biomarkers is likely to yield tests for other subtypes of depression," said Dr. Jha, Assistant Professor of Psychiatry.

Story Source:
Materials provided by UT Southwestern Medical CenterNote: Content may be edited for style and length.

Journal Reference:
  1. Manish K. Jha, Abu Minhajuddin, Bharathi S. Gadad, Tracy Greer, Bruce Grannemann, Abigail Soyombo, Taryn L. Mayes, A. John Rush, Madhukar H. Trivedi. Can C-reactive protein inform antidepressant medication selection in depressed outpatients? Findings from the CO-MED trialPsychoneuroendocrinology, 2017; 78: 105 DOI: 10.1016/j.psyneuen.2017.01.023

Saturday, 24 December 2016

Scientists build bacteria-powered battery on single sheet of paper

Researchers have created a bacteria-powered battery on a single sheet of paper that can power disposable electronics. The manufacturing technique reduces fabrication time and cost, and the design could revolutionize the use of bio-batteries as a power source in remote, dangerous and resource-limited areas.
FULL STORY

Researchers at Binghamton University, State University of New York have created a bacteria-powered battery on a single sheet of paper that can power disposable electronics.
Credit: Seokheun
Instead of ordering batteries by the pack, we might get them by the ream in the future. Researchers at Binghamton University, State University of New York have created a bacteria-powered battery on a single sheet of paper that can power disposable electronics. The manufacturing technique reduces fabrication time and cost, and the design could revolutionize the use of bio-batteries as a power source in remote, dangerous and resource-limited areas.
"Papertronics have recently emerged as a simple and low-cost way to power disposable point-of-care diagnostic sensors," said Assistant Professor Seokheun "Sean" Choi, who is in the Electrical and Computer Engineering Department within the Thomas J. Watson School of Engineering and Applied Science. He is also the director of the Bioelectronics and Microsystems Lab at Binghamton.
"Stand-alone and self-sustained, paper-based, point-of-care devices are essential to providing effective and life-saving treatments in resource-limited settings," said Choi.
On one half of a piece of chromatography paper, Choi and PhD candidate Yang Gao, who is a co-author of the paper, placed a ribbon of silver nitrate underneath a thin layer of wax to create a cathode. The pair then made a reservoir out of a conductive polymer on the other half of the paper, which acted as the anode. Once properly folded and a few drops of bacteria-filled liquid are added, the microbes' cellular respiration powers the battery.
"The device requires layers to include components, such as the anode, cathode and PEM (proton exchange membrane)," said Choi. "[The final battery] demands manual assembly, and there are potential issues such as misalignment of paper layers and vertical discontinuity between layers, which ultimately decrease power generation."
Different folding and stacking methods can significantly improve power and current outputs. Scientists were able to generate 31.51 microwatts at 125.53 microamps with six batteries in three parallel series and 44.85 microwatts at 105.89 microamps in a 6x6 configuration.
It would take millions of paper batteries to power a common 40-watt light bulb, but on the battlefield or in a disaster situation, usability and portability is paramount. Plus, there is enough power to run biosensors that monitor glucose levels in diabetes patients, detect pathogens in a body or perform other life-saving functions.
"Among many flexible and integrative paper-based batteries with a large upside, paper-based microbial fuel cell technology is arguably the most underdeveloped," said Choi. "We are excited about this because microorganisms can harvest electrical power from any type of biodegradable source, like wastewater, that is readily available. I believe this type of paper biobattery can be a future power source for papertronics."
The innovation is the latest step in paper battery development by Choi. His team developed its first paper prototype in 2015, which was a foldable battery that looked much like a matchbook. Earlier this year they unveiled a design that was inspired by a ninja throwing star.
The current work is available online in the journal Advanced Materials Technologies and will be presented at the IEEE MEMS 2017 conference in Las Vegas, Nevada on Jan. 22-26.

Story Source:
Materials provided by Binghamton University, State University of New YorkNote: Content may be edited for style and length.

Journal Reference:
  1. Yang Gao, Seokheun Choi. Stepping Toward Self-Powered Papertronics: Integrating Biobatteries into a Single Sheet of PaperAdvanced Materials Technologies, 2016; 1600194 DOI: 10.1002/admt.201600194

Jobsmag.inIndian Education BlogThingsGuide

like us