Researchers create compounds that boost antibiotics’ effectiveness

Researchers create compounds that boost antibiotics’ effectiveness Inhibitor compounds developed by biologists and chemists have been shown to bolster the ability of antibiotics to treat deadly bacterial diseases such as MRSA and anthrax. via ScienceDaily: Top Health News: Nov. 25, 2013 — Inhibitor compounds developed by UC Irvine structural biologists and Northwestern University chemists have been shown to bolster the ability of antibiotics to treat deadly bacterial diseases such as MRSA and anthrax.The discovery by UC Irvine’s Thomas Poulos and Northwestern’s Richard Silverman builds on previous work in which they created compounds that inhibit an enzyme called neuronal nitric oxide synthase. These have demonstrated the potential to treat neurodegenerative diseases by blocking overproduction of cell-killing nitric oxide within neurons.Now the researchers are learning that the compounds may have another important function. After Poulos and Silverman read a study suggesting that nitric oxide synthase helped pathogenic bacteria resist antibiotics, their laboratory teams paired the inhibitor compounds with currently used antibiotics to see if they could suppress NOS — and increase the antibiotics’ effectiveness.”We found that NOS inhibitors were extremely successful at inhibiting neurodegeneration in an animal model, and if they could be successful combating other diseases, we wanted to identify that as quickly as possible to help other people,” said Poulos, Chancellor’s Professor of biochemistry, chemistry and pharmaceutical sciences at UC Irvine.The researchers tested their compounds on Bacillus subtilis, nonpathogenic bacteria very similar to Staphylococcus aureus (known as MRSA), and Bacillus anthracis, which causes anthrax. Bacteria treated with the NOS inhibitors and an antibiotic were killed off more efficiently and completely than bacteria treated with only an antibiotic. The scientists then compared the three-dimensional structure of the inhibitors bound to the bacterial NOS with those bound to the neuronal NOS and determined that they bonded quite differently.”Now that we know which region of the NOS to target, we should to be able to develop compounds that selectively bind to bacterial NOS,” Poulos said, adding that his team will also need to try out those compounds in animal models. For more info: Researchers create compounds that boost antibiotics’ effectiveness ScienceDaily: Top Health News Researchers create compounds that boost antibiotics’ effectiveness L’articolo Researchers create compounds that boost antibiotics’ effectiveness sembra essere il primo su My Biologica.

Study pinpoints cell type, brain region affected by gene mutations in autism

Study pinpoints cell type, brain region affected by gene mutations in autism Researchers have identified the disruption of a single type of cell — in a particular brain region and at a particular time in brain development — as a significant factor in the emergence of autism. via ScienceDaily: Top Science News: Nov. 21, 2013 — A team led by UC San Francisco (UCSF) scientists has identified the disruption of a single type of cell — in a particular brain region and at a particular time in brain development — as a significant factor in the emergence of autism.The finding, reported in the Nov. 21 issue of Cell, was made with techniques developed only within the last few years and marks a turning point in autism spectrum disorders (ASDs) research.Large-scale gene-sequencing projects are revealing hundreds of autism-associated genes. Scientists have begun to leverage new methods to decipher how mutations in these disparate genes might converge to exert their effects in the developing brain.The new research focused on just nine genes, those most strongly associated with autism in recent sequencing studies, and investigated their effects using precise maps of gene expression during human brain development.Led by Jeremy Willsey, a graduate student in the laboratory of senior author Matthew W. State, MD, PhD, of UCSF, the group showed that this set of genes contributes to abnormalities in brain cells known as cortical projection neurons in the deepest layers of the developing prefrontal cortex, during the middle period of fetal development.Though a range of developmental scenarios in multiple brain regions is surely at work in ASDs, the researchers said the ability to place these specific genetic mutations in one specific set of cells — among hundreds of cell types in the brain, and at a specific point in human development — is a critical step in beginning to understand how autism comes about.”Given the small subset of autism genes we studied, I had no expectation that we would see the degree of spatiotemporal convergence that we saw,” said State, an international authority on the genetics of neurodevelopmental disorders.”This strongly suggests that, though there are hundreds of autism risk genes, the number of underlying biological mechanisms will be far fewer,” he said. “This is a very important clue to advance precision medicine for autism toward the development of personalized and targeted therapies.”Complex Genetic Architecture of ASDsASDs, which are marked by deficits in social interaction and language development, as well as by repetitive behaviors and/or restricted interests, are known to have a strong genetic component.But these disorders are exceedingly complex, with considerable variation in symptoms and severity, and little consistency in the mutations among affected individuals.Instead, with the rise of new sequencing methods over the past several years, researchers have identified many rare, non-inherited, spontaneous mutations that appear to act in combination with other genetic and non-genetic factors to cause ASDs. According to some estimates, mutations in as many as 1,000 genes could play a role in the development of these disorders.While researchers have been heartened that specific genes are now rapidly being tied to ASDs, State said the complex genetic architecture of ASDs is also proving to be challenging.”If there are 1,000 genes in the population that can contribute to risk in varying degrees and each has multiple developmental functions, it is not immediately obvious how to move forward to determine what is specifically related to autism,” State said. “Without this, it is very difficult to think about how to develop new and better medications,” he said.Focusing on Nine GenesTo begin to grapple with those questions, the researchers involved in the new study first selected as “seeds” the nine genes that have been most strongly tied to ASDs in recent sequencing research from their labs and others.Importantly, these nine genes were chosen solely because of the statistical evidence for a relationship to ASDs, not because their function was known to fit a theory of the cause of ASDs. “We asked where the leads take us, without any preconceived idea about where they should take us,” said State.The team then took advantage of BrainSpan, a digital atlas assembled by a large research consortium, including co-author Nenad Šestan, MD, PhD, and colleagues at Yale School of Medicine. Based on donated brain specimens, BrainSpan documents how and where genes are expressed in the human brain over the lifespan.The scientists, who also included Bernie Devlin, PhD, of The University of Pittsburgh School of Medicine; Kathryn Roeder, PhD, of Carnegie-Mellon University; and James Noonan, PhD, of Yale School of Medicine, used this tool to investigate when and where the nine seed genes join up with other genes in “co-expression networks” to wire up the brain or maintain its function.The resulting co-expression networks were then tested using a variety of pre-determined criteria to see whether they showed additional evidence of being related to ASDs. … For more info: Study pinpoints cell type, brain region affected by gene mutations in autism ScienceDaily: Top Science News Study pinpoints cell type, brain region affected by gene mutations in autism L’articolo Study pinpoints cell type, brain region affected by gene mutations in autism sembra essere il primo su My Biologica.

Two human proteins found to affect how ‘jumping gene’ gets around

Two human proteins found to affect how ‘jumping gene’ gets around Using a new method to catch elusive “jumping genes” in the act, researchers have found two human proteins that are used by one type of DNA to replicate itself and move from place to place. The discovery breaks new ground in understanding the arms race between a jumping gene driven to colonize new areas of the human genome and cells working to limit the risk posed by such volatile bits of DNA. via ScienceDaily: Top Health News: Nov. 21, 2013 — Using a new method to catch elusive “jumping genes” in the act, researchers have found two human proteins that are used by one type of DNA to replicate itself and move from place to place. The discovery, described in the Nov. 21 issue of Cell, breaks new ground, they say, in understanding the arms race between a jumping gene driven to colonize new areas of the human genome and cells working to limit the risk posed by such volatile bits of DNA.Jumping genes, more formally known as transposons or transposable elements, are DNA segments with the blueprints for proteins that help to either copy the segment or remove it, then insert it into a new place in the genome. Human genomes are littered with the remnants of ancient jumping genes, but because cells have an interest in limiting such trespasses, they have evolved ways to regulate them. Most jumping genes have mutated and can no longer move, but these “rusting hulks” are still passed down from generation to generation.One exception is a jumping gene called L1, which has been so successful that copies of it make up about 20 percent of human DNA. While many of these copies are now mutated and dormant, others are still active and thus the subject of much interest from geneticists.”Human cells have evolved ways of limiting jumping genes’ activity, since the more frequently they move, the more likely they are to disrupt an important gene and cause serious damage,” says Lixin Dai, Ph.D., a postdoctoral associate at the Johns Hopkins Institute for Basic Biomedical Sciences, who led the study. To find out more about how cells control L1 and what tricks the jumping gene uses to get around these defenses, Dai and others in the laboratory of Jef Boeke, Ph.D., first induced lab-grown human cells to make large amounts of the proteins for which L1 contains the blueprints. As expected, the two types of L1 protein joined with human proteins and genetic material called RNA to form so-called ribonucleoprotein particle complexes, which L1 uses to “jump.”To find out which human proteins interact with ribonucleoproteins — and are therefore likely to have a role in either tamping down its activity or helping it along — Boeke’s team collaborated with researchers at The Rockefeller University who had developed a technique for fast-freezing yeast with liquid nitrogen, then grinding it up for analysis with steel balls and very rapidly pulling out the ribonucleoproteins with tiny magnetic particles. “It’s a good way of preserving the interactions,” Dai says.Adapting this powerful technique to human cells, the team found 37 proteins that appear to interact with the ribonucleoprotein, and they selected two for further analysis. … For more info: Two human proteins found to affect how ‘jumping gene’ gets around ScienceDaily: Top Health News Two human proteins found to affect how ‘jumping gene’ gets around L’articolo Two human proteins found to affect how ‘jumping gene’ gets around sembra essere il primo su My Biologica.

Protein coding ‘junk genes’ may be linked to cancer

Protein coding ‘junk genes’ may be linked to cancer By using a new analysis method, researchers have found close to one hundred novel human gene regions that code for proteins. A number of these regions are so-called pseudogenes, which may be linked to cancer. The expectation is now that this recently developed protein analysis method will open up a whole new field of research. via ScienceDaily: Top Health News: Nov. 17, 2013 — By using a new analysis method, researchers at Karolinska Institutet and Science for Life Laboratory (SciLifeLab) in Sweden have found close to one hundred novel human gene regions that code for proteins. A number of these regions are so-called pseudogenes, which may be linked to cancer. The expectation is now that this recently developed protein analysis method, published in the scientific journal Nature Methods, will open up a whole new field of research.All information about the human genome is stored in the DNA sequence in the cell nucleus, and was mapped in the early 2000s. Genes are defined sections of DNA encoding different types of proteins. In recent decades, researchers have been able to define around 21,000 protein coding human genes, using DNA analysis, for example. In the different cell types of the body, different protein producing genes are active or inactive, and many medical conditions also depend on altered activity of specific genes.In humans, only about 1.5% of the human genome or DNA consists of protein-coding genes. Of the remaining DNA, some sequences are used to regulate the genes’ production of proteins, but the bulk of the DNA is considered to lack any purpose and is often referred to as ‘junk DNA’. Within this junk DNA there are so-called called pseudogenes. Pseudogenes have been considered as non-functional genes, which are believed to be gene remnants that lost their function during evolution.In the current paper in Nature Methods, researchers present a new proteogenomics method, which makes it possible to track down protein coding genes in the remaining 98.5% of the genome, something that until now has been an impossible task to pursue. … For more info: Protein coding ‘junk genes’ may be linked to cancer ScienceDaily: Top Health News Protein coding ‘junk genes’ may be linked to cancer L’articolo Protein coding ‘junk genes’ may be linked to cancer sembra essere il primo su My Biologica.

Anthrax bacteria play hide and seek

Anthrax bacteria play hide and seek An anthrax infection can be fatal even when the infectious agent is no longer detected. Research reveals the way its lethal factor manages to turn invisible to the immune system. via ScienceDaily: Top Health News: Nov. 14, 2013 — An anthrax infection can be fatal even when the infectious agent is no longer detected. Research carried out at EPFL reveals the way its lethal factor manages to turn invisible to the immune system.The bacterium responsible for anthrax develops a strategy reminiscent of the Trojan horse tale. Its pathogenic factor is able to penetrate inside a cell in such a way that it becomes completely invisible to both the immune system and medical analysis. Furthermore, it manages to exit the cell several days later, and then it continues to poison other cells.This mechanism was discovered by researchers from EPFL, the University of California at Berkeley and the National Institute of Health in Washington. It finally explains the reason why some living organisms succumb to the disease up to two weeks after the disappearance of the last signs of bacterial presence. “This remained a mystery for more than 50 years, said Gisou van der Goot, who heads a research unit at EPFL’s Global Health Institute. The bacteria would disappear after the administration of antibiotics, but the subject still died a few days later.”Under the host cell’s skinThe researchers focused in the way the anthrax toxin was able to get inside the cell. Composed of two elements — a “protective antigen” and a “lethal factor,” the toxin does not merely create a passage across the cellular membrane. Instead, it introduces itself by endocytosis, a process by means of which the pathogen is “swallowed” by the cell.The intoxication does not stop there. … For more info: Anthrax bacteria play hide and seek ScienceDaily: Top Health News Anthrax bacteria play hide and seek L’articolo Anthrax bacteria play hide and seek sembra essere il primo su My Biologica.

Nanotech drug smugglers

Nanotech drug smugglers Tiny capsules of carbon are invisible to the chemical gatekeeper that flushes potentially harmful substances out of our bodies’ cells, according to new research. The finding might allow a pharmaceutical to be smuggled into cells even when multidrug resistance has evolved. via ScienceDaily: Top Health News: Nov. 11, 2013 — Tiny capsules of carbon are invisible to the chemical gatekeeper that flushes potentially harmful substances out of our bodies’ cells, according to research published in the International Journal of Computational Biology and Drug Design. The finding might allow a pharmaceutical to be smuggled into cells even when multidrug resistance has evolved.Share This:Sergey Shityakov and Carola Förster of the University of Würzburg, Germany, explain that the protein, P-glycoprotein, acts as a gatekeeper, flushing out potentially harmful chemicals that enter the body as well as the naturally-occurring products of metabolism. The protein thus plays a vital role in the health of the cell. Unfortunately, it is a strong modulator of chemical traffic across the cell membrane that it can also prevent therapeutic agents from working properly, flushing them out as if they were simply harmful compounds. This process underpins the emergence of multidrug resistance in several diseases, including various forms of cancer.Shityakov and Förster have revealed recently that if there were a way to mask the presence of the therapeutic agent, later the gatekeeper would not see them as “unwanted molecular entities” to be eradicated, and therefore, these drugs might be able to carry out their job unhindered and so overcome drug resistance. However, some of the chemical substances have turned to the realm of nanotechnology, and in particular, tiny capsules of carbon atoms known as fullerenes and the related molecules, the carbon nanotubes. The latter synthetic materials are not recognized by P-glycoprotein and so can penetrate lipid membranes moving freely in and out of cells.The team has investigated whether it might be possible to carry drug molecules inside these nanocapsules so that they are unimpeded by interactions with P-glycoprotein or other receptors. They used high-power computational techniques to demonstrate that carbon nanotubes are not able to “dock” with the gatekeeper protein. Moreover, their analysis of the binding energy needed to push a nanotube into P-glycoprotein shows that the process is unfavourable and so rather than “docking” with this gatekeeper protein these peculiar materials are repelled by it to maintain the interior of the cell and so have the potential to act as a molecular drug smuggler.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is based on materials provided by Inderscience, via AlphaGalileo. … For more info: Nanotech drug smugglers ScienceDaily: Top Health News Nanotech drug smugglers L’articolo Nanotech drug smugglers sembra essere il primo su My Biologica.

Social symptoms in autistic children may be caused by hyper-connected neurons

Social symptoms in autistic children may be caused by hyper-connected neurons The brains of children with autism show more connections than the brains of typically developing children do. What’s more, the brains of individuals with the most severe social symptoms are also the most hyper-connected. The findings reported in two independent studies are challenge the prevailing notion in the field that autistic brains are lacking in neural connections. via ScienceDaily: Top Health News: Nov. 7, 2013 — The brains of children with autism show more connections than the brains of typically developing children do. What’s more, the brains of individuals with the most severe social symptoms are also the most hyper-connected. The findings reported in two independent studies published in the Cell Press journal Cell Reports on November 7th are challenge the prevailing notion in the field that autistic brains are lacking in neural connections.The findings could lead to new treatment strategies and new ways to detect autism early, the researchers say. Autism spectrum disorder is a neurodevelopmental condition affecting nearly 1 in 88 children.”Our study addresses one of the hottest open questions in autism research,” said Kaustubh Supekar of Stanford University School of Medicine of his and his colleague Vinod Menon’s study aimed at characterizing whole-brain connectivity in children. “Using one of the largest and most heterogeneous pediatric functional neuroimaging datasets to date, we demonstrate that the brains of children with autism are hyper-connected in ways that are related to the severity of social impairment exhibited by these children.”In the second Cell Reports study, Ralph-Axel Müller and colleagues at San Diego State University focused specifically on neighboring brain regions to find an atypical increase in connections in adolescents with a diagnosis of autism spectrum disorder. That over-connection, which his team observed particularly in the regions of the brain that control vision, was also linked to symptom severity.”Our findings support the special status of the visual system in children with heavier symptom load,” Müller said, noting that all of the participants in his study were considered “high-functioning” with IQs above 70. He says measures of local connectivity in the cortex might be used as an aid to diagnosis, which today is based purely on behavioral criteria.For Supekar and Menon, these new views of the autistic brain raise the intriguing possibility that epilepsy drugs might be used to treat autism.”Our findings suggest that the imbalance of excitation and inhibition in the local brain circuits could engender cognitive and behavioral deficits observed in autism,” Menon said. That imbalance is a hallmark of epilepsy as well, which might explain why children with autism so often suffer with epilepsy too.”Drawing from these observations, it might not be too far fetched to speculate that the existing drugs used to treat epilepsy may be potentially useful in treating autism,” Supekar said. For more info: Social symptoms in autistic children may be caused by hyper-connected neurons ScienceDaily: Top Health News Social symptoms in autistic children may be caused by hyper-connected neurons L’articolo Social symptoms in autistic children may be caused by hyper-connected neurons sembra essere il primo su My Biologica.

Did inefficient cellular machinery evolve to fight viruses and jumping genes?

Did inefficient cellular machinery evolve to fight viruses and jumping genes? It might seem obvious that humans are elegant and sophisticated beings in comparison to lowly bacteria, but when it comes to genes, a scientist wants to turn conventional wisdom about human and bacterial evolution on its head. via ScienceDaily: Top Science News: Nov. 7, 2013 — It might seem obvious that humans are elegant and sophisticated beings in comparison to lowly bacteria, but when it comes to genes, a UC San Francisco scientist wants to turn conventional wisdom about human and bacterial evolution on its head.Far from being sleekly performing and fine-tuned athletes, the molecules guiding the activity of our genes are like sour bureaucrats that clog up the works and create unnecessary inefficiency, asserts Hiten Madhani, MD, PhD, a professor of biochemistry and biophysics at UCSF. In contrast, bacteria carry out these processes efficiently with less frustration for the gene to express itself.Madhani presented his viewpoint in an essay entitled “The Frustrated Gene: Origins of Eukaryotic Gene Expression,” published online November 7, 2013 in the journal Cell.Although his thinking was stimulated by his own research findings, Madhani described his Cell essay as a “just so” story, a conjecture that challenges conventional thinking, but that so far is without data to back it up. He paraphrased a source of inspiration, the renowned scientist Sydney Brenner, who won a Nobel Prize for his own studies of gene regulation. “Biology is awash in a sea of data, but it needs new theories,” Madhani said.Most scientists believe that the complexity of the molecular mechanisms that guide the expression of genes and the production of proteins within a human cell is needed to allow for flexible responses that drive the development and maintenance of multifaceted organism, Madhani said.But he proposes that this complexity in genetic regulatory machinery did not originally evolve to allow for the development of the whole human. Instead, he suggested, complexity in gene expression might have first evolved in early eukaryotes to thwart infection by “parasitic DNA,” such as retroviruses, that would otherwise invade the cell nucleus and disrupt normal genes.In contrast to humans, bacteria control their genes and have adaptively evolved in myriad ways without complex mechanisms like those that guide human gene expression. In fact, humans, whose cells number in the many trillions, and disease-causing bacteria, which are but a single cell, have been doing battle and evolving together for ages, with multidrug-resistant bacteria perhaps being latest type of villain to emerge in this epic struggle.Bacteria have persisted despite their simplicity. They have only one gene-bearing chromosome and lack any kind of cell nucleus. The bacterial chromosome itself lacks the modifiable, protective sheath known as chromatin. Many other details of gene expression differ between human and bacterial cells. … For more info: Did inefficient cellular machinery evolve to fight viruses and jumping genes? ScienceDaily: Top Science News Did inefficient cellular machinery evolve to fight viruses and jumping genes? L’articolo Did inefficient cellular machinery evolve to fight viruses and jumping genes? sembra essere il primo su My Biologica.

New model for organ repair

New model for organ repair Researchers have a new model for how the kidney repairs itself, a model that adds to a growing body of evidence that mature cells are far more plastic than had previously been imagined. via ScienceDaily: Top Health News: Nov. 1, 2013 — Harvard Stem Cell Institute (HSCI) researchers have a new model for how the kidney repairs itself, a model that adds to a growing body of evidence that mature cells are far more plastic than had previously been imagined.After injury, mature kidney cells dedifferentiate into more primordial versions of themselves, and then differentiate into the cell types needing replacement in the damaged tissue. This finding conflicts with a previously held theory that the kidney has scattered stem cell populations that respond to injury. The research appears online in PNAS Early Edition.HSCI Kidney Diseases Program Leader Benjamin Humphreys, MD, PhD, a Harvard Medical School assistant professor at Brigham and Women’s Hospital, was suspicious of the kidney stem cell repair model because his previous work suggested that all kidney cells have the capacity to divide after injury. He and his colleagues decided to test conventional wisdom by genetically tagging mature kidney cells in mice that do not express stem cell markers; the hypothesis being that the mature cells should do nothing or die after injury. The results showed that not only do these fully differentiated cells multiply, but they can multiply several times as they help to repair the kidney.”What was really interesting is when we looked at the appearance and expression patterns of these differentiated cells, we found that they expressed the exact same ‘stem cell markers’ that these other groups claimed to find in their stem cell populations,” said Humphreys. “And so, if a differentiated cell is able to express a ‘stem cell marker’ after injury, then what our work shows is that that’s an injury marker — it doesn’t define a stem cell.”This new interpretation of kidney repair suggests a model by which cells reprogram themselves; similar to the way mature cells can be chemically manipulated to revert to an induced pluripotent state. The research echoes a study published last month by HSCI Principal Faculty member David Breault, MD, PhD, who showed that cells in the adrenal glands also regenerate by means of natural lineage conversion.”One has to remember that not every organ necessarily is endowed with clear and well-defined stem cell populations, like the intestines or the skin,” Humphreys explained. “I’m not saying that kidney stem cells don’t exist, but in tissues where cell division is very slow during homeostasis, there may not have been an evolutionary pressure for stem cell mechanisms of repair.”He plans to apply his kidney repair discovery to define new therapeutic targets in acute kidney injury. The goal would be to find drugs that accelerate the process of dedifferentiation and proliferation of mature kidney cells in response to injury, as well as slow down pathways that impair healing or lead to scar tissue formation. For more info: New model for organ repair ScienceDaily: Top Health News New model for organ repair L’articolo New model for organ repair sembra essere il primo su My Biologica.

Molecule that orients neurons for high definition sensing identified

Molecule that orients neurons for high definition sensing identified Many animals have highly developed senses, such as vision in carnivores, touch in mice, and hearing in bats. New research has uncovered a brain molecule that can explain the existence of such finely-tuned sensory capabilities, revealing how brain cells responsible for specific senses are positioned to receive incoming sensory information. via ScienceDaily: Top Health News: Oct. 31, 2013 — Many animals have highly developed senses, such as vision in carnivores, touch in mice, and hearing in bats. New research from the RIKEN Brain Science Institute has uncovered a brain molecule that can explain the existence of such finely-tuned sensory capabilities, revealing how brain cells responsible for specific senses are positioned to receive incoming sensory information.The study, led by Dr. Tomomi Shimogori and published in the journal Science, sought to uncover the molecule that enables high acuity sensing by examining brain regions that receive information from the senses. They found that areas responsible for touch in mice and vision in ferrets contain a protein called BTBD3 that optimizes neuronal shape to receive sensory input more efficiently.Neurons have a highly specialized shape, sending signals through one long projection called an axon, while receiving signals from many branch-like projections called dendrites. The final shape and connections to other neurons are typically completed after birth. Some neurons have dendrites distributed equally all around the cell body, like a starfish, while in others they extend only from one side, like a squid, steering towards axons that are actively bringing in information from the peripheral nerves. It was previously unknown what enables neurons to have highly oriented dendrites.”We were fascinated by the dendrite patterning changes that occurred during the early postnatal stage that is controlled by neuronal input,” says Dr. Shimogori. “We found a fundamental process that is important to remove unnecessary dendrites to prevent mis-wiring and to make efficient neuronal circuits.”The researchers searched for genes that are active exclusively in the mouse somatosensory cortex, the brain region responsible for their sense of touch, and found that the gene coding for the protein BTBD3 was active in the neurons of the barrel cortex, which receives input from their whiskers, the highly sensitive tactile sensors in mice, and that these neurons had unidirectional dendrites.Using gene manipulations in embryonic mouse brain the authors found that eliminating BTBD3 made dendrites uniformly distribute around neurons in the mouse barrel cortex. … For more info: Molecule that orients neurons for high definition sensing identified ScienceDaily: Top Health News Molecule that orients neurons for high definition sensing identified L’articolo Molecule that orients neurons for high definition sensing identified sembra essere il primo su My Biologica.

Brain regions can be specifically trained with video games

Brain regions can be specifically trained with video games Video gaming causes increases in the brain regions responsible for spatial orientation, memory formation and strategic planning as well as fine motor skills. This has been shown in a new study. The positive effects of video gaming may also prove relevant in therapeutic interventions targeting psychiatric disorders. via ScienceDaily: Top Health News: Oct. 30, 2013 — Video gaming causes increases in the brain regions responsible for spatial orientation, memory formation and strategic planning as well as fine motor skills. This has been shown in a new study conducted at the Max Planck Institute for Human Development and Charité University Medicine St. Hedwig-Krankenhaus. The positive effects of video gaming may also prove relevant in therapeutic interventions targeting psychiatric disorders.Share This:In order to investigate how video games affect the brain, scientists in Berlin have asked adults to play the video game “Super Mario 64″ over a period of two months for 30 minutes a day. A control group did not play video games. Brain volume was quantified using magnetic resonance imaging (MRI). In comparison to the control group the video gaming group showed increases of grey matter, in which the cell bodies of the nerve cells of the brain are situated. These plasticity effects were observed in the right hippocampus, right prefrontal cortex and the cerebellum. These brain regions are involved in functions such as spatial navigation, memory formation, strategic planning and fine motor skills of the hands. … For more info: Brain regions can be specifically trained with video games ScienceDaily: Top Health News Brain regions can be specifically trained with video games L’articolo Brain regions can be specifically trained with video games sembra essere il primo su My Biologica.

Why plants usually live longer then animals

Why plants usually live longer then animals Stem cells are crucial for the continuous generation of new cells. Although the importance of stem cells in fuelling plant growth and development still many questions on their tight molecular control remain unanswered. Plant researchers have now discovered a new step in the complex regulation of stem cells. via ScienceDaily: Top Science News: Oct. 24, 2013 — Stem cells are crucial for the continuous generation of new cells. Although the importance of stem cells in fuelling plant growth and development still many questions on their tight molecular control remain unanswered. Plant researchers at VIB and Ghent University discovered a new step in the complex regulation of stem cells.Today, their results are published online in this week’s issue of Science Express.Lieven De Veylder said, “Our data suggest that certain organizing stem cells in plant roots are less sensitive for DNA-damage. Those cells hold an original and intact DNA copy which can be used to replace damaged cells if necessary. Animals rely on a similar mechanism but most likely plants have employed this in a more optimized manner. This could explain why many plants can live for more than hundreds of years, while this is quite exceptional for animals.”Quiescent organisers of plant growthPlant growth and development depend on the continuous generation of new cells. A small group of specialized cells present in the growth axes of a plant is driving this. These so-called stem cells divide at a high frequency and have the unique characteristic that the original mother cell keeps the stem cell activity while the daughter cell acquires a certain specialization. Besides these stem cells, plant roots also harbor organizing cells. … For more info: Why plants usually live longer then animals ScienceDaily: Top Science News Why plants usually live longer then animals L’articolo Why plants usually live longer then animals sembra essere il primo su My Biologica.

Mesothelioma Chemotherapy – What Are the Six Commonly Used Chemotherapy Agents?

Mesothelioma Chemotherapy – What Are the Six Commonly Used Chemotherapy Agents? Mesothelioma cancer, can be treated by the use of anti cancer drug therapies. These anti cancer drugs act by inhibiting tumor growth through the blocking of cell division and multiplication. This mode of action also unfortunately affects other rapidly replicating cells in the body, cells of the hair and the lining of the intestine are particularly vulnerable, thus leading to the common side effects of anti cancer drugs like hair loss and nausea. Mesothelioma is notoriously resistant to common anti cancer chemotherapy as result of some reasons. The cancer takes a long time to mature and show symptoms, by the time these symptoms appear the tumor will be well formed with a lot of layers of dead cells that the anti cancer drugs will find it difficult to penetrate, and also by the time a diagnosis of mesothelioma is made, most victims have but a short time left to live so the drugs do not have enough time to exert their maximal effect. New drugs that have been designed to overcome these challenges and have fewer and lesser side effects include: Alimta (Pemetrexed) Alimta was approved by The Food and Drug Administration in February 2004 as a new anti cancer drug for the treatment of mesothelioma. Its mode of action is by inhibiting the creation of thymidine and purine , two enzymes that are vital to cell growth. This stops the mesothelioma cancer cells from multiplying at a very fast rate. Its side effects include nausea and vomiting, diarrhea, fatigue, mouth sores and low blood counts. Patients are usually placed on vitamin B12 and folic acid supplements to reduce the severity of the side effects. Cisplatin This is a platinum-based chemotherapy drug that prevents the reproduction of DNA and is used to treat a number of different cancers including mesothelioma. The FDA approved it in 1978 to treat a number of cancers, and has proved somewhat effective on mesothelioma. Cisplatin however has some very serious side effects which inlude ear damageototoxicity leading to hearing loss, kidney damage, nerve damage, and nausea, and so some oncologist are very reluctant to prescribe this drug to patients. Tomudex (Raltitrexed) This drug prevents cancer cells from replicating the DNA that is needed for multiplication and spread of cancer. This drug can be used as a monotherapy or in combination with onconase. Vinorelbine This anticancer drug was initially approved by the FDA in 1994 for the treatment of small lung cancer and breast cancer, but recent studies have shown that it could also be effective against mesothelioma, and the drug has little side effect profile. It can also be used in combination with some other chemotherapy drugs. Onconase (Ranpirnase/P-30 Protein) Onconase is a chemical taken from the eggs of the leopard frog that blocks protein synthesis which leads to blockage of tumor cell division and growth. It has shown promise as becoming one of the more effective drugs for treating cancer, as survival rates for one and two years are 34.4% and 21.6 respectively, as opposed to six to eight months without treatment. Veglin This is an anticancer chemotherapy drug that blocks the growth of tumors in people suffering from lymphoma, Kaposi’s sarcoma, and colon and lung cancers. Many oncologists believe that it could be effective in fighting mesothelioma, as Veglin inhibits vascular endothelial growth factor (VEGF), a substance that is usually found in very high concentrations in mesothelioma patients. VEGF helps tumors grow new blood vessels which help to supply nutrients to the new tumor cells. This drug inhibits this process thus starving the new cancer cells of their much needed nutrients, leading to their ultimate death Bello Kamorudeen.http://www.mesotheliomacorner.blogspot.com via Mesothelioma arena: Mesothelioma cancer, can be treated by the use of anti cancer drug therapies. These anti cancer drugs act by inhibiting tumor growth through the blocking of cell division and multiplication. This mode of action also unfortunately affects other rapidly replicating cells in the body, cells of the hair and the lining of the intestine are particularly vulnerable, thus leading to the common side effects of anti cancer drugs like hair loss and nausea.Mesothelioma is notoriously resistant to common anti cancer chemotherapy as result of some reasons. The cancer takes a long time to mature and show symptoms, by the time these symptoms appear the tumor will be well formed with a lot of layers of dead cells that the anti cancer drugs will find it difficult … For more info: Mesothelioma Chemotherapy – What Are the Six Commonly Used Chemotherapy Agents? Mesothelioma arena Mesothelioma Chemotherapy – What Are the Six Commonly Used Chemotherapy Agents? L’articolo Mesothelioma Chemotherapy – What Are the Six Commonly Used Chemotherapy Agents? sembra essere il primo su My Biologica.

Physical cues help mature cells revert into embryonic-like stem cells

Physical cues help mature cells revert into embryonic-like stem cells Bioengineers have shown that physical cues can help reprogram mature cells back into pluripotent stem cells. The study demonstrates for the first time that biomaterials can help regulate the memory of a cell’s identity. via ScienceDaily: Top Health News: Oct. 21, 2013 — Bioengineers at the University of California, Berkeley, have shown that physical cues can replace certain chemicals when nudging mature cells back to a pluripotent stage, capable of becoming any cell type in the body.The researchers grew fibroblasts cells taken from human skin and mouse ears on surfaces with parallel grooves measuring 10 micrometers wide and 3 micrometers high. After two weeks of culture in a special cocktail used to reprogram mature cells, the researchers found a four-fold increase in the number of cells that reverted back to an embryonic-like state compared with cells grown on a flat surface. Growing cells in scaffolds of nanofibers aligned in parallel had similar effects.The study, published online Sunday, Oct. 20, in the journal Nature Materials, could significantly enhance the process of reprogramming adult cells into embryonic-like stem cells that can differentiate, or develop, into any type of tissue that makes up our bodies.The 2012 Nobel Prize in Physiology or Medicine was awarded to scientists who discovered that it was possible to reprogram cells using biochemical compounds and proteins that regulate gene expression. These induced pluripotent stem cells have since become a research mainstay in regenerative medicine, disease modeling and drug screening.”Our study demonstrates for the first time that the physical features of biomaterials can replace some of these biochemical factors and regulate the memory of a cell’s identity,” said study principal investigator Song Li, UC Berkeley professor of bioengineering. “We show that biophysical signals can be converted into intracellular chemical signals that coax cells to change.”The current process for reprogramming cells relies on a formula that uses a virus to introduce gene-altering proteins into mature cells. Certain chemical compounds, including valproic acid, that can dramatically affect global DNA structure and expression are also used to boost the efficiency of the reprogramming process.”The concern with current methods is the low efficiency at which cells actually reprogram and the unpredictable long-term effects of certain imposed genetic or chemical manipulations,” said study lead author Timothy Downing, who did this research as a graduate student in the UC Berkeley-UC San Francisco Joint Graduate Program in Bioengineering. “For instance, valproic acid is a potent chemical that drastically alters the cell’s epigenetic state and can cause unintended changes inside the cell. Given this, many people have been looking at different ways to improve various aspects of the reprogramming process.”Previous studies have shown that physical and mechanical forces can influence cell fate, but the effect on epigenetic state and cell reprogramming had not been clear.The new study found that culturing cells on micro-grooved biomaterials improved the quality and consistency of the reprogramming process, and was just as effective as valproic acid.”Cells elongate, for example, as they migrate throughout the body,” said Downing, who is now a research scientist in Li’s lab. … For more info: Physical cues help mature cells revert into embryonic-like stem cells ScienceDaily: Top Health News Physical cues help mature cells revert into embryonic-like stem cells L’articolo Physical cues help mature cells revert into embryonic-like stem cells sembra essere il primo su My Biologica.

Watching the heartbeat of molecules

Watching the heartbeat of molecules A team of scientists now report on a new method of rapidly identifying different molecular species under a microscope. Their technique of coherent Raman spectro-imaging with two laser frequency combs takes a big step towards the holy grail of real-time label-free biomolecular imaging. via ScienceDaily: Top Science News: Oct. 17, 2013 — A team of scientists around Prof. Theodor W. Hänsch and Dr. Nathalie Picqué at the Laser Spectroscopy Division of the Max Planck Institute of Quantum Optics (Garching), in a collaboration with the Ludwig-Maximilians-Universität Munich and the Institut des Sciences Moléculaires d’Orsay (France) now report on a new method of rapidly identifying different molecular species under a microscope. Their technique of coherent Raman spectro-imaging with two laser frequency combs takes a big step towards the holy grail of real-time label-free biomolecular imaging, as published recently in Nature.How does a drug influence a living cell? In which way can signal molecules change the cell metabolism? Such questions are difficult to answer, since cells are highly complex “chemical factories” which constantly manufacture and break down a large number of different molecular species. Biologists have learnt to attach fluorescent dye labels to certain proteins so that they can distinguish them under a microscope. However, such labels can alter the cell functions. … For more info: Watching the heartbeat of molecules ScienceDaily: Top Science News Watching the heartbeat of molecules L’articolo Watching the heartbeat of molecules sembra essere il primo su My Biologica.

MesoMark: Progress in the Diagnosis and Monitoring of Mesothelioma

MesoMark: Progress in the Diagnosis and Monitoring of Mesothelioma Among the many challenges of managing mesothelioma are the difficulties in diagnosing and then following the disease for progression or response to treatments administered. One of the potential tools to help in this regard is an assay of soluble mesothelin related peptides, now a commercially available test called Mesomark. Mesothelin is a glycoprotein (a protein with sugar molecules attached to it) that is expressed on normal mesothelial cells but also over-expressed in patients with malignant pleural mesothelioma (MPM) as well as potentially in patients with peritoneal mesothelioma or ovarian cancer. Soluble mesothelin-related peptides (SMRPs) are believed to be either peptide fragments of mesothelin (peptides being pieces of larger proteins) or variant versions of mesothelin that don’t remain bound to the cell surface. These SMRPs can then end up in serum or pleural fluid. The two main ways in which SMRPs, or the Mesomark assay, might be used is to make the diagnosis of mesothelioma or to follow the course of the disease. What we’ve learned is that while the Mesomark assay shows an abnormal elevation in some patients with mesothelioma, that proportion has varied from 19% to 68% of the patients tested 1, less commonly elevated in patients with earlier stage (I or II) MPM or in the minority of patients with sarcomatoid histology. On the other hand, when the Mesomark assay is found to be elevated in a patient with a suspicion of MPM, the vast majority of the time (88-100% in different studies), the diagnosis was ultimately confirmed. Another approach is to look at SMRP in pleural fluid 2, since patients with MPM are often initially diagnosed after presenting with shortness of breath caused by a large pleural effusion. However, results with pleural fluid are similarly infallible, with a substantial proportion of patients with MPM failing to demonstrate abnormally elevated SMRPs in pleural fluid. At this time, it is appropriate to send blood or potentially pleural fluid for the Mesomark assay, though it is necessary to recognize that an abnormal test does not replace a tissue diagnosis from a biopsy, and also that many patients with MPM will not have an abnormal Mesomark test. Another setting in which the Mesomark assay could be helpful is for following the course of the disease in patients known to have SMRPs elevated at diagnosis 3. Here, the Mesomark assay serves a similar function as Prostate Specific Antigen, or PSA, another blood test that is controversial in its role for diagnosing cancer, but PSA testing is the most common and readily available way to monitor the course of prostate cancer. Both prostate cancer and MPM are diseases in which imaging is often not especially reliable, as there is often no obviously measurable discrete lesion or collection of lesions to follow on imaging scans. In these situations, having a blood test that can be monitored can be quite helpful. After surgery, where post-operative scarring can make it extremely difficult to interpret scan findings, is the previously elevated Mesomark continuing to remain low, or has it begun to rise after initially dropping after surgery? In the much larger proportion of MPM patients who aren’t candidates for surgery, SMRPs declining over time typically correlate with scan findings, offering an option between scans for monitoring response to often difficult therapy, and potentially providing a more reliable index of activity than imaging when there is extensive scarring after a pleurodesis or other ambiguous scan findings. While the Mesomark assay isn’t abnormal in enough patients to be a conclusive indicator of mesothelioma in patients who are undergoing an initial workup and are still awaiting a diagnosis, it is now a helpful tool to add for the significant subset of patients who are found to have abnormally elevated SMRPs. — References: 1. Hollevoet K, Reitsma JB, Creaney J, et al. Serum mesothelin for diagnosing malignant pleural mesothelioma: An individual patient data meta-analysis. J Clin Oncol 30: 1541-1549, 2012. 2. Creaney J, Yeoman D, Naumoff LK, et al. Soluble mesothelin in effusions: a useful tool for the diagnosis of malignant mesothelioma. Thorax 62: 569-573, 2007. 3. Wheatley-Price P, Yang B, Patsios D, et al. Soluble mesothelin-related peptide and osteopontin as markers of response in malignant mesothelioma. J Clin Oncol 28: 3316-3322, 2010. via Mesothelioma Cancer Alliance Blog: For more info: MesoMark: Progress in the Diagnosis and Monitoring of Mesothelioma Mesothelioma Cancer Alliance Blog MesoMark: Progress in the Diagnosis and Monitoring of Mesothelioma L’articolo MesoMark: Progress in the Diagnosis and Monitoring of Mesothelioma sembra essere il primo su My Biologica.

How a ubiquitous herpesvirus sometimes leads to cancer

How a ubiquitous herpesvirus sometimes leads to cancer Most of us are infected with the herpesvirus known as Epstein-Barr virus. For most of us, the virus will lead at worst to a case of infectious mononucleosis, but sometimes, and especially in some parts of the world, those viruses are found in association with cancer. Now, researchers have found that the difference between a relatively harmless infection and a cancer-causing one lies at least partly in the viral strain itself. via ScienceDaily: Top Health News: Oct. 10, 2013 — You might not know it, but most of us are infected with the herpesvirus known as Epstein-Barr virus (EBV). For most of us, the virus will lead at worst to a case of infectious mononucleosis, but sometimes, and especially in some parts of the world, those viruses are found in association with cancer. Now, researchers reporting in the Cell Press journal Cell Reports on October 10 have found that the difference between a relatively harmless infection and a cancer-causing one lies at least partly in the viral strain itself.Share This:The results offer some of the first evidence for the existence of distinct EBV subtypes with very different public health risks. The researchers say that vaccination or other strategies for preventing EBV infection will need to be designed with these most pathogenic, cancer-causing strains in mind.”EBV is an important but neglected pathogen,” said Henri-Jacques Delecluse of the German Cancer Research Centre in Heidelberg, Germany. “We have made an important step in recognizing that EBV is actually a family of viruses that have different properties, some of which are very likely to cause disease. So, the consequences of being infected with EBV might be different, depending on the strain one carries.”Delecluse and his colleagues made the discovery by sequencing the DNA of a viral strain dubbed M81 isolated from a Chinese patient with nasopharyngeal carcinoma (NPC). Their analyses revealed that M81 is highly similar to other viruses isolated from NPCs and profoundly different from Western strains in terms of its ability to infect and replicate within cells.The M81 strain can infect epithelial cells and multiply spontaneously at a very high level in all cells it infects, including B lymphocytes, the cells in which the viruses hide, the researchers report. It remains to be seen exactly how infected epithelial cells become cancerous.”Our results have made me radically change my strategy to address the problem of EBV-associated diseases,” Delecluse said. “The current view is that the virus is essentially the same all over the world and that local conditions explain the different consequences of EBV infection. … For more info: How a ubiquitous herpesvirus sometimes leads to cancer ScienceDaily: Top Health News How a ubiquitous herpesvirus sometimes leads to cancer L’articolo How a ubiquitous herpesvirus sometimes leads to cancer sembra essere il primo su My Biologica.

Fluorescent compounds allow clinicians to visualize Alzheimer’s disease as it progresses

Fluorescent compounds allow clinicians to visualize Alzheimer’s disease as it progresses What if doctors could visualize all of the processes that take place in the brain during the development and progression of Alzheimer’s disease? Such a window would provide a powerful aid for diagnosing the condition. Now, researchers have developed a new class of imaging agents that enables them to visualize tau protein aggregates, a pathological hallmark of Alzheimer’s disease and related neurodegenerative disorders, directly in the brains of living patients. via ScienceDaily: Top Health News: Sep. 18, 2013 — What if doctors could visualize all of the processes that take place in the brain during the development and progression of Alzheimer’s disease? Such a window would provide a powerful aid for diagnosing the condition, monitoring the effectiveness of treatments, and testing new preventive and therapeutic agents. Now, researchers reporting in the September 18 issue of the Cell Press journal Neuron have developed a new class of imaging agents that enables them to visualize tau protein aggregates, a pathological hallmark of Alzheimer’s disease and related neurodegenerative disorders, directly in the brains of living patients.Share This:In the brains of patients with Alzheimer’s disease, tau proteins aggregate together and become tangled, while fragments of another protein, called amyloid beta, accumulate into deposits or plaques. Tau tangles are not only considered an important marker of neurodegeneration in Alzheimer’s disease but are also a hallmark of non-Alzheimer’s neurodegenerative disorders, tauopathies that do not involve amyloid beta plaques. While imaging technologies have been developed to observe the spread of amyloid beta plaques in patients’ brains, tau tangles were previously not easily monitored in the living patient.In this latest research in mice and humans, investigators developed fluorescent compounds that bind to tau (called PBBs) and used them in positron emission tomography (PET) tests to correlate the spread of tau tangles in the brain with moderate Alzheimer’s disease progression. “PET images of tau accumulation are highly complementary to images of senile amyloid beta plaques and provide robust information on brain regions developing or at risk for tau-induced neuronal death,” says senior author Dr. Makoto Higuchi, of the National Institute of Radiological Sciences in Japan. “This is of critical significance, as tau lesions are known to be more intimately associated with neuronal loss than senile plaques.”The advance may also be helpful for diagnosing, monitoring, and treating other neurological conditions because tau tangles are not limited to Alzheimer’s disease but also play a role in various types of dementias and movement disorders.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is based on materials provided by Cell Press, via EurekAlert!, a service of AAAS. Note: Materials may be edited for content and length. … For more info: Fluorescent compounds allow clinicians to visualize Alzheimer’s disease as it progresses ScienceDaily: Top Health News Fluorescent compounds allow clinicians to visualize Alzheimer’s disease as it progresses L’articolo Fluorescent compounds allow clinicians to visualize Alzheimer’s disease as it progresses sembra essere il primo su My Biologica.

A protein that can mean life or death for cells

A protein that can mean life or death for cells Scientists have discovered that the protein Mitofusin 2 plays a crucial role in correctly measuring stress levels, and also makes sure the pathways of cell repair or cell death are effective. via ScienceDaily: Top Health News: Sep. 17, 2013 — Each cell in an organism has a sensor that measures the health of its “internal” environment. This “alarm” is found in the endoplasmic reticulum (ER), which is able to sense cellular stress and trigger either rescue responses or the death of the cell. A team from the Institute for Research in Biomedicine (IRB), in Barcelona, has discovered that the protein Mitofusin 2 (Mfn2) plays a crucial role in correctly measuring stress levels, and also makes sure the pathways of cell repair or cell death are effective.The researchers reveal some of the molecular mechanisms that connect Mfn2 to endoplasmic reticulum stress in the latest edition of the scientific journal, EMBO Journal, from the Nature Group, published by the European Molecular Biology Organization.When the scientists removed Mfn2 from the cell under conditions of cell stress, the endoplasmic reticulum responded by over-activating the repair pathways. By doing so, it contradictorily functioned worse, reducing the capacity of cells to overcome the stress insult and promoting to a lesser degree apoptotic cell death. “When Mfn2 is removed, the cellular stress response pathways are completely disrupted,” says Antonio Zorzano, coordinator of IRB’s Molecular Medicine Programme and leader of the group “Heterogenic and polygenic diseases.”Not only diabetesMfn2 is a mitochondrial protein whose deficiency is related to diabetes. In an earlier publication in Proceedings of the National Academy of Sciences (PNAS), Dr. Zorzano’s research team demonstrated that without Mfn2, tissues become resistant to insulin, a characteristic of diabetes and the so-called metabolic syndrome. In this study, they also observed that the cells had higher endoplasmic reticulum stress.The current study investigates the relationship between mitochondria and the endoplasmic reticulum, and indicates that changes in mitochondria, caused by the loss of the Mfn2 protein, directly affect the endoplasmic reticulum function. “We have shown that Mfn2 is important for cell viability and has implications for numerous diseases, such as neurodegeration, cancer, cardiovascular disease, in addition to diabetes,” says postdoctoral researcher Juan Pablo Muñoz, first author of the study.Is Mitofusin 2 a good therapeutic target?”The fact that we can modulate cell damage response with Mfn2 opens a wide window of possible therapeutic avenues for further study,” says Muñoz. … For more info: A protein that can mean life or death for cells ScienceDaily: Top Health News A protein that can mean life or death for cells L’articolo A protein that can mean life or death for cells sembra essere il primo su My Biologica.

Mesothelioma: diagnosis

Mesothelioma: diagnosis Mesothelioma is a rare disease and for this reason there are no screening for early diagnosis in people at risk. In the case of persons exposed to asbestos for longer or shorter periods, some doctors recommend periodic examinations ( x-rays or computed tomography) to monitor changes over time in the structure of the lungs that might indicate the presence of mesothelioma or lung cancer. However it is not yet clear whether this strategy could lead to an early diagnosis . The first step towards a correct diagnosis is still a visit from your primary care physician or a specialist who ask questions about your medical history to determine a possible exposure to asbestos and assess the presence of fluid in the abdomen or in the cavity around the heart . In case of suspected mesothelioma then proceed with some more specific tests : Chest X-ray : may show abnormalities in the mesothelium of the chest cavity , called the pleura (change of thickness or the presence of calcium deposits ) , or lungs . Tomography of the chest ( TC): allows you to determine the presence of the tumor, its exact location and its possible spread to other organs , while also helping the surgeon to determine the most appropriate type of intervention . Recently it has been developed the so-called spiral CT , which, compared to the traditional one is faster and allows to obtain more detailed images . PET is used to identify the cells that are growing faster and which correspond to cancer cells. The images obtained are not as detailed as those of the TC but they can help doctors understand whether anomalies of the mesothelium are actually tumors or other lesions and whether the cancer has spread to lymph nodes or other parts of the body. Today, there are tools that can perform in a single session for both CT and PET . Magnetic resonance: it allows to obtain detailed images of soft tissues of the body, such as CT scans , but without using X-ray In case of mesothelioma may be useful for assessing the health of the diaphragm , the thin membrane muscle below the lungs , essential for respiration . Biopsy: is the most effective tool to confirm the suspicion of mesothelioma. In some cases with a long thin needle samples are taken of fluid present in the chest ( thoracentesis ) , abdomen ( paracentesis ) or in the cavity around the heart ( pericardiocentesis ) and occurs at the microscope the presence of tumor cells. In other cases, however , it is necessary to withdraw small portions of mesothelial tissue with a thin needle inserted under the skin or with the insertion of a probe equipped with a video camera through a small cut in the skin : in this way, the doctor can see suspicious areas and withdraw samples which are then analyzed under a microscope. To distinguish with certainty mesothelioma from other tumor types , the samples taken by biopsy may be subjected to immunohistochemical analysis ( to see the proteins present on the cell surface ) or genetic ( to detect the expression of genes typical of mesoelioma ) . – Blood tests : they are not typically used to arrive at a diagnosis , but may be useful to confirm a obtained by other techniques or to follow the course of the disease during and after treatment. Are measured in particular the levels of osteopontin and SMRP , molecules present in higher doses in case of mesothelioma L’articolo Mesothelioma: diagnosis sembra essere il primo su My Biologica.

Cell death protein could offer new anti-inflammatory drug target

Cell death protein could offer new anti-inflammatory drug target Scientists have revealed the structure of a protein that is essential for triggering a form of programmed cell death called necroptosis, making possible the development of new drugs to treat chronic inflammatory diseases such as Crohn’s disease and rheumatoid arthritis. via ScienceDaily: Top Health News: Sep. 5, 2013 — Scientists in Melbourne, Australia, have revealed the structure of a protein that is essential for triggering a form of programmed cell death called necroptosis, making possible the development of new drugs to treat chronic inflammatory diseases such as Crohn’s disease and rheumatoid arthritis.Dr James Murphy, Associate Professor John Silke, Dr Joanne Hildebrand, Dr Peter Czabotar, Professor Warren Alexander and colleagues from the Walter and Eliza Hall Institute have shown that the protein MLKL plays a crucial role in the signalling pathways that trigger a recently discovered cell death pathway called necroptosis. The results were published today in the journal Immunity.Usually, when a cell detects that it is infected by a virus or bacteria or has other irreparable damage it self-destructs through a process called apoptosis. But Associate Professor Silke said some bacteria and viruses had developed ways of preventing this cell suicide, also allowing the invaders to survive. It is at this point that the ‘back up’ necroptosis pathway might be activated.”During necroptosis the cell still self-destructs but in doing so it also sends an ‘SOS’ to the immune system to tell it that something has gone wrong with the cell’s normal cell death process of apoptosis. So internally, the cell is still doing its best to self-destruct in an orderly and programmed way, but it is simultaneously sending signals to the immune system to mount a response to the invaders.”However there are times when the necroptosis pathway may be inappropriately activated, sending messages to the immune system that promote inflammation and the development of inflammatory diseases.Dr Murphy said the discovery of MLKL’s role in activating the necroptosis pathway was an important step in understanding this cell death pathway and its role in disease. “Necroptosis has only been defined in the past 10 years and the role MLKL plays was only discovered in 2012,” Dr Murphy said. “This study provides the first genetic proof that MLKL is required for necroptosis as well as the first full-length, atomic level, three-dimensional structure of a protein that regulates necroptosis. These discoveries are really exciting because they give us a new target to look at for developing treatments for people who suffer from an inflammatory disease.”The three-dimensional images of MLKL, which were obtained using the Australian Synchrotron, revealed an interesting detail about the protein, Dr Murphy said. “The structure revealed that MLKL is a ‘dead enzyme’, making it different from the other proteins in the signalling pathway,” Dr Murphy said. … For more info: Cell death protein could offer new anti-inflammatory drug target ScienceDaily: Top Health News Cell death protein could offer new anti-inflammatory drug target L’articolo Cell death protein could offer new anti-inflammatory drug target sembra essere il primo su My Biologica.

Bismuth-carrying nanotubes show promise for CT scans

Bismuth-carrying nanotubes show promise for CT scans Scientists are placing bismuth in nanotubes to tag stem cells for efficient tracking with CT scanners. via ScienceDaily: Top Health News: Sep. 4, 2013 — Scientists at Rice University have trapped bismuth in a nanotube cage to tag stem cells for X-ray tracking.Bismuth is probably best known as the active element in a popular stomach-settling elixir and is also used in cosmetics and medical applications. Rice chemist Lon Wilson and his colleagues are inserting bismuth compounds into single-walled carbon nanotubes to make a more effective contrast agent for computed tomography (CT) scanners.Details of the work by Wilson’s Rice team and collaborators at the University of Houston, St. Luke’s Episcopal Hospital, and the Texas Heart Institute appear in the Journal of Materials Chemistry B.This is not the first time bismuth has been tested for CT scans, and Wilson’s lab has been experimenting for years with nanotube-based contrast agents for magnetic resonance imaging (MRI) scanners. But this is the first time anyone has combined bismuth with nanotubes to image individual cells, he said.”At some point, we realized no one has ever tracked stem cells, or any other cells that we can find, by CT,” Wilson said. “CT is much faster, cheaper and more convenient, and the instrumentation is much more widespread (than MRI). So we thought if we put bismuth inside the nanotubes and the nanotubes inside stem cells, we might be able to track them in vivo in real time.”Experiments to date confirm their theory. In tests using pig bone marrow-derived mesenchymal stem cells, Wilson and lead author Eladio Rivera, a former postdoctoral researcher at Rice, found that the bismuth-filled nanotubes, which they call Bi@US-tubes, produce CT images far brighter than those from common iodine-based contrast agents.”Bismuth has been thought of before as a CT contrast agent, but putting it in nanotube capsules allows us to get them inside cells in high concentrations,” Wilson said. “That lets us take an X-ray image of the cell.”The capsules are made from a chemical process that cuts and purifies the nanotubes. When the tubes and bismuth chloride are mixed in a solution, they combine over time to form Bi@US-tubes.The nanotube capsules are between 20 and 80 nanometers long and about 1.4 nanometers in diameter. … For more info: Bismuth-carrying nanotubes show promise for CT scans ScienceDaily: Top Health News Bismuth-carrying nanotubes show promise for CT scans L’articolo Bismuth-carrying nanotubes show promise for CT scans sembra essere il primo su My Biologica.

TB and Parkinson’s disease linked by unique protein

TB and Parkinson’s disease linked by unique protein A protein at the center of Parkinson’s disease research now also has been found to play a key role in causing the destruction of bacteria that cause tuberculosis, according to microbiologists. via ScienceDaily: Top Health News: Sep. 4, 2013 — A protein at the center of Parkinson’s disease research now also has been found to play a key role in causing the destruction of bacteria that cause tuberculosis, according to scientists led by UC San Francisco microbiologist and tuberculosis expert Jeffery Cox, PhD.The protein, named Parkin, already is the focus of intense investigation in Parkinson’s disease, in which its malfunction is associated with a loss of nerve cells. Cox and colleagues now report that Parkin also acts on tuberculosis, triggering destruction of the bacteria by immune cells known as macrophages. Results appear online today (September 4, 2013) in the journal Nature.The finding suggests that disease-fighting strategies already under investigation in pre-clinical studies for Parkinson’s disease might also prove useful in fighting tuberculosis, according to Cox. Cox is investigating ways to ramp up Parkin activity in mice infected with tuberculosis using a strategy similar to one being explored by his UCSF colleague Kevan Shokat, PhD, as a way to ward off neurodegeneration in Parkinson’s disease.Globally, tuberculosis kills 1.4 million people each year, spreading from person to person through the air. Parkinson’s disease, the most common neurodegenerative movement disorder, also affects millions of mostly elderly people worldwide.Cox homed in on the enzyme Parkin as a common element in Parkinson’s and tuberculosis through his investigations of how macrophages engulf and destroy bacteria. In a sense the macrophage — which translates from Greek as “big eater” — gobbles down foreign bacteria, through a process scientists call xenophagy.Mycobacterium tuberculosis, along with a few other types of bacteria, including Salmonella and leprosy-causing Mycobacterium leprae, are different from other kinds of bacteria in that, like viruses, they need to get inside cells to mount a successful infection.The battle between macrophage and mycobacterium can be especially intense. M. tuberculosis invades the macrophage, but then becomes engulfed in a sac within the macrophage that is pinched off from the cell’s outer membrane. The bacteria often escape this intracellular jail by secreting a protein that degrades the sac, only to be targeted yet again by molecular chains made from a protein called ubiquitin. … For more info: TB and Parkinson’s disease linked by unique protein ScienceDaily: Top Health News TB and Parkinson’s disease linked by unique protein L’articolo TB and Parkinson’s disease linked by unique protein sembra essere il primo su My Biologica.

Life without insulin is possible, study suggests

Life without insulin is possible, study suggests Several millions of people around the world suffer from insulin deficiencies. Insulin is a hormone, secreted by the beta cells in the pancreas, which plays a major role in the regulation of energy substrates such as glucose. This insufficiency, primarily caused by diabetes (types 1 and 2), has lethal consequences if it is not treated. As of now, only daily insulin injections allow certain patients to survive. via ScienceDaily: Top Health News: Sep. 3, 2013 — Several millions of people around the world suffer from insulin deficiencies. Insulin is a hormone, secreted by the beta cells in the pancreas, which plays a major role in the regulation of energy substrates such as glucose. This insufficiency, primarily caused by diabetes (types 1 and 2), has lethal consequences if it is not treated. As of now, only daily insulin injections allow patients to survive.Several millions of people around the world suffer from insulin deficiencies. Insulin is a hormone, secreted by the beta cells in the pancreas, which plays a major role in the regulation of energy substrates such as glucose. This insufficiency, primarily caused by diabetes (types 1 and 2), has lethal consequences if it is not treated. As of now, only daily insulin injections allow patients to survive. This approach, however, brings on serious side effects. Thanks to their research which was published in the journal Cell Metabolism, the University of Geneva (UNIGE) scientists identified the underlying mechanisms, proving that life without insulin is possible, and paving the way for new diabetes treatments.While life without insulin was inconceivable, a group of researchers, led by Roberto Coppari, professor in the Department of Cell Physiology and Metabolism at UNIGE, has just demonstrated that insulin is not vital for survival. … For more info: Life without insulin is possible, study suggests ScienceDaily: Top Health News Life without insulin is possible, study suggests L’articolo Life without insulin is possible, study suggests sembra essere il primo su My Biologica.

Bad to the bone: Some breast cancer cells are primed to thrive

Bad to the bone: Some breast cancer cells are primed to thrive Scientists have discovered that some loose breast cancer cells, have a leg up on survival —- the genes they express make them more likely to prosper in bone tissue. The team also found that whether or not cancer cells turn on those genes depends on what their surroundings were like in the primary breast tumor. If the breast tumor had molecular patterns similar to those found in bone, the tumor is more likely to spread to bone later. via ScienceDaily: Top Health News: Aug. 29, 2013 — When a cancer cell sloughs off the edge of a tumor in the breast, it faces a tough road to survive. The cell must not only remain physically intact as it rushes through blood vessels, but it also must find a new organ to lodge itself in, take in enough nutrients and oxygen to stay alive, and begin dividing, all while escaping notice by the body’s immune system.A team of Howard Hughes Medical Institute (HHMI) scientists has discovered that some loose breast cancer cells, have a leg up on survival — the genes they express make them more likely to prosper in bone tissue. The team also found that whether or not cancer cells turn on those genes depends on what their surroundings were like in the primary breast tumor. If the breast tumor had molecular patterns similar to those found in bone, the tumor is more likely to spread to bone later.”It’s like in society — who you hang out with shapes who you are,” says HHMI investigator Joan Massagué of Memorial Sloan-Kettering Cancer Center. “And that might make you better or worse equipped to handle situations you’ll encounter.”The new findings, published August 29, 2013 in the journal Cell, could eventually lead to new drugs that block cancers from spreading to bone or other organs, he says.When cells from a primary tumor circulate through the body and begin growing in a new organ, a metastatic tumor is formed. Such metastases are often harder to treat than primary tumors; the vast majority of people who die of cancer have not only a primary tumor but also metastatic disease. So a major goal of cancer researchers is to not only find ways to treat primary tumors, but stop cancer from metastasizing.Massagué’s lab group discovered in 2009 that by looking at the genetics of breast cancer cells, they could predict which were most likely to spread to bone. A set of genes dubbed the Src response signature (SRS) was more often turned on in the cells that metastasized to the bone. But the researchers didn’t know why.”What was really a conundrum was how this pathway got turned on in the first place,” says Massagué. … For more info: Bad to the bone: Some breast cancer cells are primed to thrive ScienceDaily: Top Health News Bad to the bone: Some breast cancer cells are primed to thrive L’articolo Bad to the bone: Some breast cancer cells are primed to thrive sembra essere il primo su My Biologica.

Scientists map molecular mechanism that may cause toxic protein buildup in dementing disorders

Scientists map molecular mechanism that may cause toxic protein buildup in dementing disorders There is no easy way to study diseases of the brain. Extracting brain cells, or neurons, from a living patient is risky, while examining a patient’s brain post-mortem only reveals the disease’s final stages. And animal models, while incredibly informative, have fallen short during the crucial drug-development stage of research. But scientists have taken a potentially more powerful approach: An advanced stem-cell technique that creates a human model of degenerative disease in a dish. via ScienceDaily: Top Health News: Aug. 29, 2013 — There is no easy way to study diseases of the brain. Extracting neurons from a living patient is both difficult and risky, while examining a patient’s brain post-mortem usually only reveals the disease’s final stages. And animal models, while incredibly informative, have frequently fallen short during the crucial drug-development stage of research. The result: we are woefully unprepared to fight — and win — the war against this class of diseases.But scientists at the Gladstone Institutes and the University of California, San Francisco (UCSF) are taking a potentially more powerful approach: an advanced stem-cell technique that creates a human model of degenerative disease in a dish.Using this model, the team uncovered a molecular process that causes neurons to degenerate, a hallmark sign of conditions such as Alzheimer’s disease and frontotemporal dementia (FTD). The results, published in the latest issue of Stem Cell Reports, offer fresh ammunition in the continued battle against these and other deadly neurodegenerative disorders.The research team, led by Gladstone Investigator Yadong Huang, MD, PhD, identified an important mechanism behind tauopathies. A group of disorders that includes both Alzheimer’s and FTD, tauopathies are characterized by the abnormal accumulation of the protein Tau in neurons. This buildup is thought to contribute to the degeneration of these neurons over time, leading to debilitating symptoms such as dementia and memory loss. But while this notion has been around for a long time, the underlying processes have largely remained unclear.”So much about the mechanisms that cause tauopathies is a mystery, in part because traditional approaches — such as post-mortem brain analysis and animal models — give an incomplete picture,” explained Dr. Huang. … For more info: Scientists map molecular mechanism that may cause toxic protein buildup in dementing disorders ScienceDaily: Top Health News Scientists map molecular mechanism that may cause toxic protein buildup in dementing disorders L’articolo Scientists map molecular mechanism that may cause toxic protein buildup in dementing disorders sembra essere il primo su My Biologica.

Scientists detail critical role of gene in many lung cancer cases

Scientists detail critical role of gene in many lung cancer cases Scientists have shown that a well-known cancer-causing gene implicated in a number of malignancies plays a far more critical role in non-small cell lung cancer, the most common form of the disease, than previously thought. via ScienceDaily: Top Health News: Aug. 29, 2013 — Scientists from the Florida campus of The Scripps Research Institute (TSRI) have shown that a well-known cancer-causing gene implicated in a number of malignancies plays a far more critical role in non-small cell lung cancer, the most common form of the disease, than previously thought.These findings establish the gene as a critical regulator of lung cancer tumor growth. This new information could turn out to be vital for the design of potentially new therapeutic strategies for a group of patients who represent almost half of non-small cell lung cancer cases.In the study, published online ahead of print by the journal Cancer Research, the scientists found that presence of known oncogene Notch 1 is required for survival of cancer cells. In both cell and animal model studies, disabling Notch 1 leads to a rise in cancer cell death.”While Notch signaling has emerged as an important target in many types of cancer, current methodologies that target that pathway affect all members of the Notch family, and this has been associated with toxicity,” said Joseph Kissil, a TSRI associate professor who led the study. “We were able to identify Notch 1 as the critical oncogene to target, at least in a common form of lung cancer.”The new findings show that Notch1 is required for initial tumor growth, as it represses p53, a well-known tumor suppressor protein that has been called the genome’s guardian because of its role in preventing mutations. The p53 protein can repair damaged cells or force them to die through apoptosis — programmed cell death.Using animal models, the study shows that inhibition of Notch1 signaling results in a dramatic decrease in initial tumor growth. Moreover, disruption of Notch 1 induces apoptosis by increasing p53 stability — substantially increasing its biological half-life, for example.These findings provide important clinical insights into the correlation between Notch1 activity and the poor prognosis of non-small cell lung cancer patients who carry the non-mutated form of the p53 gene. “If you look at lung cancer patient populations, Notch signaling alone isn’t a prognostic indicator, but if you look at p53-positive patients it is,” Kissil said. For more info: Scientists detail critical role of gene in many lung cancer cases ScienceDaily: Top Health News Scientists detail critical role of gene in many lung cancer cases L’articolo Scientists detail critical role of gene in many lung cancer cases sembra essere il primo su My Biologica.

‘Mini human brains’ created: Scientists grow human brain tissue in 3-D culture system

‘Mini human brains’ created: Scientists grow human brain tissue in 3-D culture system Complex human brain tissue has been successfully developed in a three-dimensional culture system. The method allows pluripotent stem cells to develop into cerebral organoids — or “mini brains” — that consist of several discrete brain regions. via ScienceDaily: Top Science News: Aug. 29, 2013 — Complex human brain tissue has been successfully developed in a three-dimensional culture system established in an Austrian laboratory. The method described in the current issue of Nature allows pluripotent stem cells to develop into cerebral organoids — or “mini brains” — that consist of several discrete brain regions.Instead of using so-called patterning growth factors to achieve this, scientists at the Institute of Molecular Biotechnology (IMBA) of the Austrian Academy of Sciences (OeAW) fine-tuned growth conditions and provided a conducive environment. As a result, intrinsic cues from the stem cells guided the development towards different interdependent brain tissues. Using the “mini brains,” the scientists were also able to model the development of a human neuronal disorder and identify its origin — opening up routes to long hoped-for model systems of the human brain.The development of the human brain remains one of the greatest mysteries in biology. Derived from a simple tissue, it develops into the most complex natural structure known to man. Studies of the human brain’s development and associated human disorders are extremely difficult, as no scientist has thus far successfully established a three-dimensional culture model of the developing brain as a whole. Now, a research group lead by Dr. Jürgen Knoblich at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA) has just changed that.Brain Size MattersStarting with established human embryonic stem cell lines and induced pluripotent stem (iPS) cells, the group identified growth conditions that aided the differentiation of the stem cells into several brain tissues. While using media for neuronal induction and differentiation, the group was able to avoid the use of patterning growth factor conditions, which are usually applied in order to generate specific cell identities from stem cells. … For more info: ‘Mini human brains’ created: Scientists grow human brain tissue in 3-D culture system ScienceDaily: Top Science News ‘Mini human brains’ created: Scientists grow human brain tissue in 3-D culture system L’articolo ‘Mini human brains’ created: Scientists grow human brain tissue in 3-D culture system sembra essere il primo su My Biologica.

Scientists ‘spike’ stem cells to generate myelin

Scientists ‘spike’ stem cells to generate myelin Stem cell technology has long offered the hope of regenerating tissue to repair broken or damaged neural tissue. via ScienceDaily: Top Health News: Aug. 28, 2013 — Stem cell technology has long offered the hope of regenerating tissue to repair broken or damaged neural tissue. Findings from a team of UC Davis investigators have brought this dream a step closer by developing a method to generate functioning brain cells that produce myelin — a fatty, insulating sheath essential to normal neural conduction.”Our findings represent an important conceptual advance in stem cell research,” said Wenbin Deng, principal investigator of the study and associate professor at the UC Davis Department of Biochemistry and Molecular Medicine. “We have bioengineered the first generation of myelin-producing cells with superior regenerative capacity.”The brain is made up predominantly of two cell types: neurons and glial cells. Neurons are regarded as responsible for thought and sensation. Glial cells surround, support and communicate with neurons, helping neurons process and transmit information using electrical and chemical signals. One type of glial cell — the oligodendrocyte — produces a sheath called myelin that provides support and insulation to neurons. Myelin, which has been compared to insulation around electrical wires that helps to prevent short circuits, is essential for normal neural conduction and brain function; well-recognized conditions involving defective myelin development or myelin loss include multiple sclerosis and leukodystrophies.In this study, the UC Davis team first developed a novel protocol to efficiently induce embryonic stem cells (ESCs) to differentiate into oligodendroglial progenitor cells (OPCs), early cells that normally develop into oligodendrocytes. Although this has been successfully done by other researchers, the UC Davis method results in a purer population of OPCs, according to Deng, with fewer other cell types arising from their technique.They next compared electrophysiological properties of the derived OPCs to naturally occurring OPCs. They found that unlike natural OPCs, the ESC-derived OPCs lacked sodium ion channels in their cell membranes, making them unable to generate spikes when electrically stimulated. … For more info: Scientists ‘spike’ stem cells to generate myelin ScienceDaily: Top Health News Scientists ‘spike’ stem cells to generate myelin L’articolo Scientists ‘spike’ stem cells to generate myelin sembra essere il primo su My Biologica.

Mother’s genes can impact aging process

Mother’s genes can impact aging process Researchers have shown that aging is determined not only by the accumulation of changes during our lifetime, but also by the genes we acquire from our mothers. via ScienceDaily: Top Science News: Aug. 21, 2013 — As we age, our cells change and become damaged. Now, researchers at Karolinska Institutet and the Max Planck Institute for Biology of Aging have shown that aging is determined not only by the accumulation of changes during our lifetime but also by the genes we acquire from our mothers. The results of the study are published in the journal Nature.There are many causes of aging that are determined by an accumulation of various kinds of changes that impair the function of bodily organs. Of particular importance in aging, however, seems to be the changes that occur in the cell’s power plant — the mitochondrion. This structure is located in the cell and generates most of the cell’s supply of ATP which is used as a source of chemical energy.”The mitochondria contains their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the aging process,” said Nils-Göran Larsson, Ph.D., professor at the Karolinska Institutet and principal investigator at the Max Planck Institute for Biology of Aging, and leader of the current study alongside Lars Olson, Ph.D., professor in the Department of Neuroscience at the Karolinska Institutet. “Many mutations in the mitochondria gradually dis-able the cell’s energy production,” said Larsson.For the first time, the researchers have shown that the aging process is influenced not only by the accumulation of mitochondrial DNA damage during a person’s lifetime, but also by the inherited DNA from their mothers.”Surprisingly, we also show that our mother’s mitochondrial DNA seems to influence our own aging,” said Larsson. “If we inherit mDNA with mutations from our mother, we age more quickly.”Normal and damaged DNA is passed down between generations. However, the question of whether it is possible to affect the degree of mDNA damage through lifestyle intervention is yet to be investigated. All that the researchers know now is that mild DNA damage transferred from the mother contributes to the aging process.”The study also shows that low levels of mutated mDNA can have developmental effects and cause deformities of the brain,” said lead author Jaime Ross, Ph.D., at the Karolinska Institutet.”Our findings can shed more light on the aging process and prove that the mitochondria play a key part in aging; they also show that it’s important to reduce the number of mutations,” said Larsson.”These findings also suggest that therapeutic interventions that target mitochondrial function may influence the time course of aging,” said Barry Hoffer, M.D., Ph.D., a co-author of the study from the Department of Neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine. … For more info: Mother’s genes can impact aging process ScienceDaily: Top Science News Mother’s genes can impact aging process L’articolo Mother’s genes can impact aging process sembra essere il primo su My Biologica.

New findings on how the ear hears could lead to better hearing aids

New findings on how the ear hears could lead to better hearing aids A healthy ear is much better at detecting and transmitting sound than even the most advanced hearing aid. But now researchers have uncovered new insights into how the ear — in particular, the cochlea — processes and amplifies sound. The findings could be used for the development of better devices to improve hearing. via ScienceDaily: Top Health News: Aug. 20, 2013 — A healthy ear is much better at detecting and transmitting sound than even the most advanced hearing aid. But now researchers reporting in the August 20 issue of the Biophysical Journal, a Cell Press publication, have uncovered new insights into how the ear — in particular, the cochlea — processes and amplifies sound. The findings could be used for the development of better devices to improve hearing.Share This:Sound-sensing cells within the cochlea — called hair cells due to the presence of cilia on their membrane surfaces — vibrate strongly at different sound frequencies depending on their location. To examine the cochlear electro-mechanics responsible for this process, Dr. Elizabeth Olson and Dr. Wei Dong, both of Columbia University, designed tiny sensors that could simultaneously measure small pressure fluctuations and cell-generated voltages at specific locations within the ears of live gerbils.It was previously shown that the pivoting of cilia on a hair cell mechanically opens ion channels in the cell membrane, allowing the current to flow and generate voltage. This sends a signal to a nerve cell, which relays the specific sound frequency signal to the brain. In addition, energy released by hair cell voltage feeds back to amplify the motion specific to that location’s frequency, thus driving additional movement of the local hair cells.Dr. Dong and Dr. … For more info: New findings on how the ear hears could lead to better hearing aids ScienceDaily: Top Health News New findings on how the ear hears could lead to better hearing aids L’articolo New findings on how the ear hears could lead to better hearing aids sembra essere il primo su My Biologica.

Biomarker could help scientists choose the right cell line when conducting stem cell experiments

Biomarker could help scientists choose the right cell line when conducting stem cell experiments Stem cells that strongly express a gene called WNT3 are biased to develop into cells and tissues including pancreas, liver and bladder. This discovery suggests that other genes may serve as biomarkers for selecting stem cells with a preference for turning into different tissue types. Such markers would make it easier for stem cell scientists to choose the right cell line to start with when generating specific tissues for study. via ScienceDaily: Top Health News: June 4, 2013 — According to researchers at Boston Children’s Hospital, stem cells that strongly express a gene called WNT3 are biased to develop into cells and tissues including pancreas, liver and bladder. This discovery suggests that other genes…

Genetic signature of deadly brain cancer identified

Genetic signature of deadly brain cancer identified A multi-institutional team of researchers have pinpointed the genetic traits of the cells that give rise to gliomas — the most common form of malignant brain cancer. The findings provide scientists with rich new potential set of targets to treat the disease. via ScienceDaily: Top Health News: June 3, 2013 — A multi-institutional team of researchers have pinpointed the genetic traits of the cells that give rise to gliomas — the most common form of malignant brain cancer. The findings, which appear in the journal Cell Reports, provide scientists with rich new potential set of targets to treat the disease.”This study identifies a core set of genes and pathways that are dysregulated during both the early and late…