Survival numbers for progeria draw optimism from some, skepticism from others.Despite an unpromising start for development of farnesyltransferase inhibitors (FTIs) in cancer indications, lonafarnib is now providing new hope for children with the rare and life-threatening genetic disease, progeria. Results from the first-ever clinical trial in children with progeria have recently been published, with every child showing an improvement in her symptoms (weight gain, bone structure, hearing and/or vascular stiffness).Affecting one in eight million live births, progeria (also known as Hutchinson-Gilford Progeria Syndrome or HGPS), is a rare and fatal disease characterized by symptoms of premature aging in children.Children with the disorder appear healthy at birth, but then fail to thrive. By the age of 18–24 months, symptoms such as limited growth, whole-body alopecia and distinctive facial features, become apparent. As the children age, signs and symptoms get progressively worse, with kidney failure, loss of eyesight and cardiovascular problems commonly reported.Similarly to elderly people, affected children develop musculoskeletal degeneration with a loss of body fat and muscle, stiff joints, osteoporosis and often dislocation of the hips. The average lifespan of children with progeria is 13 (range 8–20) years, with death usually a consequence of heart attack or stroke caused by atherosclerosis.Rarely inherited, progeria is caused by a sporadic, single-base mutation at position 1824 in the lamin A (LMNA) gene, resulting in substitution of thymine instead of cytosine. Lamin A is the structural scaffold that holds the cell nucleus together. Specifically, this occurs when a farnesyl functional group is attached to prelamin A, allowing temporary attachment to the nuclear rim and subsequent removal of the farnesyl group to produce lamin A.The mutated lamin A protein that causes progeria is called progerin. Permanent farnesylation in progerin results in irreversible attachment to the nuclear membrane, causing inadequate structural support and interference with mitosis and other such processes.In 2005, a study led by researchers at the University of California, Los Angeles, showed that a class of drugs called farnesyltransferase inhibitors (FTIs), which block the attachment of a molecule to the faulty protein that allows it to accumulate around the nucleus, restored normal shape to cells from kids with progeria. Several groups working with mice having the same mutation next established that the drug also reduced signs of premature aging in those rodents. Because FTIs had already been tested in children with cancer, with no significant side effects, PRF quickly pushed to start a trial of the FTI lonafarnib in 2007. Gordon, working with a team led by oncologist Mark Kieran of the Dana-Farber Cancer Institute in Boston, initially followed 25 children as they received the drug for at least 2 years. The trial results, published in 2012, showed that many of the patients had small weight gains and reductions in the stiffness of their blood vessels, though some scientists found the results inconclusive and hard to interpret.In the new analysis, Gordon and her colleagues wanted to see whether children treated so far—including those in the first lonafarnib trial and those in an ongoing trial that adds two other drugs to the treatment—survived longer than untreated kids. But because there are so few children with progeria, and the disease is invariably fatal, PRF and the study designers had agreed not to create a group receiving a placebo; all who participated in the study received the drug, including Gordon’s son. For a comparison group, Gordon and her colleagues instead collected data about untreated children from historical records in the foundation’s international registry, previously published case reports, and public databases.The finding “is very gratifying and encouraging,” says physician-geneticist Francis Collins, who is director of the National Institutes of Health in Bethesda, Maryland, and whose research team has studied the mechanisms of and potential treatments for progeria. Collins acknowledges that the lack of a direct control group enrolled in the trial is “not ideal,” but he notes “there really wasn’t much of an alternative to what was done—namely, to do an open-label trial where all of the kids were given the chance to have access to the drug.”
Via Dr. Stefan Gruenwald
A gas giant has been added to the short list of exoplanets discovered through direct imaging. It is located around GU Psc, a star three times less massive than the Sun and located in the constellation Pisces.
Via José Gonçalves
Electronic devices that become soft when implanted inside the body and can deploy to grip 3-D objects, such as large tissues, nerves and blood vessels have been created by researchers from The University of Texas at Dallas and the University of Tokyo.These biologically adaptive, flexible transistors might one day help doctors learn more about what is happening inside the body, and also could be used to stimulate the body for treatments.The research, published in Advanced Materials, is one of the first demonstrations of transistors that can change shape and maintain their electronic properties after they are implanted in the body, said Jonathan Reeder, a graduate student in materials science and engineering and lead author of the work.“Scientists and physicians have been trying to put electronics in the body for a while now, but one of the problems is that the stiffness of common electronics is not compatible with biological tissue,” he said.“You need the device to be stiff at room temperature so the surgeon can implant the device, but soft and flexible enough to wrap around 3-D objects so the body can behave exactly as it would without the device. By putting electronics on shape-changing and softening polymers, we can do just that.”Shape memory polymers (plastics) developed by Dr. Walter Voit, assistant professor of materials science and engineering and mechanical engineering and an author of the paper, are key to enabling the technology.The polymers respond to the body’s environment and become less rigid when they’re implanted. In addition to the polymers, the electronic devices are built with layers that include thin, flexible electronic foils first characterized by a group including Reeder in work published last year in Nature.The Voit and Reeder team from the Advanced Polymer Research Lab in the Erik Jonsson School of Engineering and Computer Science fabricated the devices with an organic semiconductor but used adapted techniques normally applied to create silicon electronics that could reduce the cost of the devices.“We used a new technique in our field to essentially laminate and cure the shape memory polymers on top of the transistors,” said Voit, who is also a member of the Texas Biomedical Device Center. “In our device design, we are getting closer to the size and stiffness of precision biologic structures, but have a long way to go to match nature’s amazing complexity, function and organization.”
Via Dr. Stefan Gruenwald
Synergistic action of compounds isolated from the hexane extract of Ardisia crispa root against tumour-promoting effect, in vitro. . « An isomeric mixture of α,β-amyrin (triterpene) and 2-methoxy-6-undecyl-1,4-benzoquinone (quinone) isolated from the Ardisia crispa root hexane (ACRH) extract was reported to possess anti-inflammatory properties in vivo. Considering the close association between inflammation and cancer, on top of the lack of antitumour study on those compounds, this study aimed to determine the potential of both compounds against tumour promotion in vitro, either as single agent or in combination. Triterpene and quinone compounds, as well as triterpene–quinone fraction (TQF) and ACRH were subjected to inhibition of Epstein–Barr virus-early antigen (EBV-EA) activation assay for that purpose. Compared with curcumin (positive control), inhibition against EBV-EA activation occurred in the order: ACRH>TQF ≥ curcumin>α,β-amyrin ≥ 2-methoxy-6-undecyl-1,4-benzoquinone. These findings reported, for the first time, the antitumor-promoting effect of α,β-amyrin and 2-methoxy-6-undecyl-1,4-benzoquinone from the roots of A. crispa, which was enhanced when both compounds act in synergy. »Looi Ting Yeong, Roslida Abdul Hamid, Latifah Saiful Yazan, Huzwah Khaza'ai & Dayang Erna Zulaikha Awang Hamsin
- Received: 9 Mar 2014 - Accepted: 15 Apr 2014 - Published online: 16 May 2014
Natural Product Researchdoi: 10.1080/14786419.2014.917415
One of the most significant decisions we face as scientists comes at the end of our formal education. Choosing between industry and academia is easy for some, incredibly fraught for others. The author has made two complete cycles between these career destinations, including on the one hand 16 years in academia, as grad student (twice, in biology and in computer science), post-doc, and faculty, and on the other hand 19 years in two different industries (computer and pharmaceutical). The following rules reflect that experience, and my own opinions.
“ Japan's quest to tap the natural gas beneath the ocean floor The Conversation The methane that it contains is usually formed by the work of tiny microbes that consume organic material buried in seafloor sediments.”
Via Catherine Russell
US researchers have built a wirelessly powered pacemaker the size of a grain of rice and implanted it in a rabbit. They were able to hold a metal plate a few centimetres above the rabbit's chest and use it to regulate the animal's heartbeat. If such medical implants could be made to work in humans, it could lead to smaller devices that are safer to fit. The findings are published in the journal PNAS.The researchers from Stanford University hope their development could also eventually dispense with the bulky batteries and clumsy recharging systems that are currently a feature of such devices.The central discovery was a new type of wireless power transfer that could safely penetrate deep inside the body, using roughly the same power as a cell phone."We need to make these devices as small as possible to more easily implant them deep in the body," said co-author Dr Ada Poon, from Stanford's department of electrical engineering. Near-field waves can be safely used, but they can only transfer power over short distances.The researchers were able to design a device that blends the safety of near-field waves with the reach of far-field waves. "With this method, we can safely transmit power to tiny implants in organs like the heart or brain, well beyond the range of current near-field systems," said John Ho, a graduate student in Dr Poon's lab.
Via Dr. Stefan Gruenwald
How can an ant lift objects many times heavier than its own body? Engineers at The Ohio State University combined computational modeling at the Ohio Supercomputer Center (OSC) and lab experiments to find out.They focused on the ant’s neck — the single joint of soft tissue that bridges the stiff exoskeleton of the ant’s head and thorax. When an ant carries food or any other object, the neck joint supports the full weight of the load.The researchers reverse-engineered the biomechanics of the neck by developing 3-D models of the of the ant’s internal and external anatomy from X-ray cross-section images (microCT) of ant specimens and loading the data into a modeling program (ScanIPþFE) that assembled the segments and converted them into a mesh frame model of more than 6.5 million elements.The model then was loaded into a finite element analysis program (Abaqus), an application that creates accurate simulations of complex geometries and forces, and the data was processed on the powerful Oakley Cluster, an array of 8,300 processor cores (Intel Xeon) at the Ohio Supercomputer Center.The experiments, published in the Journal of Biomechanics, revealed that the neck joints could withstand loads of about 5,000 times the ant’s body weight, and that the ant’s neck-joint structure produced the highest strength when its head was aligned straight, as opposed to turned to either side.“Loads are lifted with the mouthparts, transferred through the neck joint to the thorax, and distributed over six legs and tarsi that anchor to the supporting surface,” explainedCarlos Castro, assistant professor of mechanical and aerospace engineering at Ohio State.“While previous research has explored attachment mechanisms of the tarsi (feet), little is known about the relation between the mechanical function and the structural design and material properties of the ant.”“Our results accurately pinpoint the stress concentration that leads to neck failure and identify the soft-to-hard material interface at the neck-to-head transition as the location of failure,” said Castro.“The design and structure of this interface is critical for the performance of the neck joint. The unique interface between hard and soft materials likely strengthens the adhesion and may be a key structural design feature that enables the large load capacity of the neck joint.”The simulations confirmed the joint’s directional strength and, consistent with the experimental results, indicated that the critical point for failure of the neck joint is at the neck-to-head transition, where soft membrane meets the hard exoskeleton.
Via Dr. Stefan Gruenwald
Rising global demand for meat will result in increased environmental pollution, energy consumption, and animal suffering. Cultured meat, produced in an animal-cell cultivation process, is a technically feasible alternative lacking these disadvantages, provided that an animal-component-free growth medium can be developed. Small-scale production looks particularly promising, not only technologically but also for societal acceptance. Economic feasibility, however, emerges as the real obstacle.In a paper in the Cell Press journal Trends in Biotechnology, Cor van der Weele of Wageningen University in The Netherlands and coauthor Johannes Tramper describe a potential meat manufacturing process, starting with a vial of cells taken from a cell bank and ending with a pressed cake of minced meat.Cor van der Weele point out that the rising demand for meat around the world is unsustainable in terms of environmental pollution and energy consumption, in addition to animal suffering associated with factory farming.Fortunately, it’s already possible to make meat from stem cells, as demonstrated by Mark Post, a professor of tissue engineering at Maastricht University who created the first lab-grown hamburger in 2013.There will be challenges when it comes to maintaining a continuous stem cell line and producing cultured meat that’s cheaper than meat obtained in the usual way, they say.However, “cultured meat has great moral promise,” write van der Weele and Tramper. “Worries about its unnaturalness might be met through small-scale production methods that allow close contact with cell-donor animals, thereby reversing feelings of alienation. From a technological perspective, ‘village-scale’ production is also a promising option.”
Via Dr. Stefan Gruenwald
When scientists transplanted human neural stem cells into mice with multiple sclerosis (MS), within a remarkably short period of time, 10 to 14 days, the mice had regained motor skills.Six months later, they showed no signs of slowing down.Results from the study demonstrate that the mice experience at least a partial reversal of symptoms. Immune attacks are blunted, and the damaged myelin is repaired, explaining their dramatic recovery.The finding, which uncovers potential new avenues for treating MS, was published May 15, 2014 in the journal Stem Cell Reports (open access).How they did it: Ronald Coleman (a graduate student of Jeanne Loring, Ph.D., co-senior author and director of the Center for Regenerative Medicine at The Scripps Research Institute and co-first author on the publication) changed the normal protocol and grew the neural stem cells so they were less crowded on a Petri dish than usual.That yielded a human neural stem cell type that turned out to be extremely potent. The experiments have since been successfully repeated with cells produced under the same conditions, but by different laboratories.The human neural stem cells send chemical signals that instruct the mouse’s own cells to repair the damage caused by MS. Experiments by Lane’s team suggest that TGF-beta proteins comprise one type of signal, but there are likely others. This realization has important implications for translating the work to clinical trials in the future.“Rather than having to engraft stem cells into a patient, which can be challenging from a medical standpoint, we might be able to develop a drug that can be used to deliver the therapy much more easily,” said Tom Lane, Ph.D., a professor of pathology at the University of Utah.With clinical trials as the long-term goal, the next steps are to assess the durability and safety of the stem cell therapy in mice. “We want to try to move as quickly and carefully as possible,” he said. “I would love to see something that could promote repair and ease the burden that patients with MS have.”“The aspect I am most interested is to define what is being secreted from the human cells that influence demyelination,” Lane told KurzweilAI in an email interview. “Other studies have shown either effects on neuroinflammation or demyelination; ours is one of a select few to show that stem cells influence both.”However, it is too soon to say when can we expect this innovation to be available for MS patients, Lane added.
Via Dr. Stefan Gruenwald
A spiraling, green high-rise designed by Paris-based Belgian architect Vincent Callebaut is currently under construction in Taipei, Taiwan. It will add interest to XinYi District’s existing mixture of buildings which range from LEED Platinum EBOM-rated Taipei 101, the world’s tallest green building, to a traditionally Chinese-styled Sun Yat-sen Memorial Hall built in 1972.
Via Lauren Moss
“Neurogenesis interferes with past learning in infant and adult mice.”For anyone fighting to save old memories, a fresh crop of brain cells may be the last thing they need. Research published today in Sciencesuggests that newly formed neurons in the hippocampus — an area of the brain involved in memory formation — could dislodge previously learned information1. The work may provide clues as to why childhood memories are so difficult to recall.“The finding was very surprising to us initially. Most people think new neurons mean better memory,” says Sheena Josselyn, a neuroscientist who led the study together with her husband Paul Frankland at the Hospital for Sick Children in Toronto, Canada.Humans, mice and several other mammals grow new neurons in the hippocampus throughout their lives — rapidly at first, but more and more slowly with age. Researchers have previously shown that boosting neural proliferation before learning can enhance memory formation in adult mice2, 3. But the latest study shows that after information is learned, neuron growth can degrade those memories.Although seemingly counterintuitive, the disruptive role of these neurons makes some sense, says Josselyn. She notes that some theoretical models have predicted such an effect4. “More neurons increase the capacity to learn new memories in the future,” she says. “But memory is based on a circuit, so if you add to this circuit, it makes sense that it would disrupt it.” Newly added neurons could have a useful role in clearing old memories and making way for new ones, says Josselyn.
Via Dr. Stefan Gruenwald
Whitehead Institute scientists have identified a genetic cause of a facial disorder known as hemifacial microsomia (HFM). The researchers find that duplication of the geneOTX2 induces HFM, the second-most common facial anomaly after cleft lip and palate. HFM affects approximately one in 3,500 births. While some cases appear to run in families, no gene had been found to be causative. That is until Whitehead Fellow Yaniv Erlich and his lab set out to do just that. Their work is described in this week’s issue of the journal PLOS ONE.Patients with HFM tend to have asymmetrical faces—typically with one side of the upper and lower jaws smaller than the opposite side—a smaller or malformed ear on the affected side, and, in some cases, neurological or developmental abnormalities. Thought to be brought on by circulation difficulties during embryonic development, HFM is also thought to be sporadic—meaning that it occurs spontaneously rather than through inheritance. However, one family in northern Israel has more than its share of the anomaly.To identify the origin of this family’s disorder, Erlich and lab technician Dina Zielinski began studying the genomes of a five-year-old female member of the family, along with those of her mother, grandmother, and male cousin, who all exhibited traits of HFM. Later, the genetic information from the grandmother’s Russian cousin, who resides in the Philadelphia area, was recruited to the study.“What’s unique here is that this is the largest family with this disorder described in the literature,” says Erlich. “Most of the time, you see one person affected, or perhaps two people—a parent and a child. Such a large family increases the power of the genetic study and clearly signals that there is a genetic component to a disease.”Within this large piece of DNA, Zielinski identified eight candidate genes that could cause the type of HFM running in this family. She then used two algorithms to compare the molecular signatures of these eight genes to other genes known to be responsible for various facial malformations with features similar to HFM. After this analysis, the gene OTX2 that codes for a transcription factor rose above the seven other candidates.These results are supported by what is known of OTX2’s function. Previous data indicates that the gene codes for a protein that is expressed in the heads and pharyngeal arches of mouse embryos in developmental stages corresponding to the periods when HFM abnormalities are thought to arise in humans.Although this is a tantalizing hint as to OTX2’s activity during development, Zielinski cautions that little is known about its overall role, in part because it serves as a transcription factor that regulates other genes.“OTX2’s activity is very complicated,” says Zielinski, who is first author of the PLOS ONE paper. “Development is dependent on tight control of these transcription factors that turn other genes on and off. The feedback between OTX2 and other transcription factors is complex but we know thatOTX2 plays a critical role in craniofacial patterning.”
Via Dr. Stefan Gruenwald
“ Daily Mail World's oldest sperm discovered in 17m-year-old Queensland fossil Daily Mail The fossilised sperm is estimated to be about 1.3 millimetres long, about the same length or slightly longer than the ostracod itself.”
Via Catherine Russell
Researchers at The University of Akron are again spinning inspiration from spider silk—this time to create more efficient and stronger commercial and biomedical adhesives that could, for example, potentially attach tendons to bones or bind fractures.
Via José Gonçalves
The green rice leafhopper is never alone. When a female’s egg and a male’s sperm fuse into a new cell, that cell is already infected with bacteria. As the newly conceived leafhopper grows from one cell into millions, its internal bacteria—its endosymbionts—go along for the ride. Right from the start, the leafhopper isn’t an individual in its own right, but a collection of animal and microbes that live together.Many insects and other animals inherit endosymbionts from their parents, but almost all of them do so from their mothers. There’s good reason for this. An egg cell is big. Its central nucleus, which contains its DNA, is surrounded by a spacious and roomy cytoplasm, which can house lots of bacteria. But a sperm cell has no cytoplasm, and its tiny head is all nucleus. This streamlined shape is good for swimming, but it’s terrible for packaging bacterial heirlooms. That’s why males almost never pass on endosymbionts to their kids, while females often do. Sperm just isn’t very good packing material.But try telling that to the green rice leafhopper. This small green bug is a serious pests of rice plants in East Asia, and its cells are filled with at least three species of bacteria. And one of them—Rickettsia—can infect the insect’s sperm.Kenji Watanabe and Hiroaki Noda from the National Institute of Agrobiological Sciences in Japan found that almost every one of the leafhopper’s sperm cells contains several copies of Rickettsia, with up to 23 microbes per head. The team have no idea how the bacteria gain entry, or why their presence doesn’t seem to harm or disable the sperm in any way. But they do know that if these infected sperm fertilise eggs, they can pass their copies of Rickettsia into the next generation.This unique ability to transmit microbes via sperm could completely change the usual relationship between the insects and the bacteria. These partnerships are fairly straightforward if microbes are only passed down the maternal line. Every individual inherits a single strain of microbe, and they co-evolve in neat tandem. Buchnera, for example, lives inside the cells of aphids, and has been co-evolving with them for over 150 million years. If you draw the family tree ofBuchnera strains, it would look almost identical to the family tree of their aphid hosts.But in the leafhopper, both males and females can pass Rickettsia to their offspring, so each individual could end up with different bacterial strains. “Co-infections are likely to introduce more conflict with the host” as strains compete with each other, says Nancy Moran from the University of Texas in Austin. Conflicts between harmless bacteria can potentially harm their hosts, as the adaptations that allow one microbe to best another can sometimes allow them to cause disease. If that’s true here, Rickettsia may flip from being a harmless (or even beneficial) partner into an enemy.Jack Werren from Rochester University, who studies Wolbachia, says that the Japanese team found irrefutable evidence for sperm transmission, but their study also raises many questions. How doesRickettsia function inside the nucleus? And with its host’s DNA within easy reach, could it be manipulating the leafhopper’s genes?And what’s Rickettsia doing inside its host? Is it a benign parasite, or is it actually helpful? Many endosymbionts provide their hosts with nutrients or defend them against parasites and diseases. Aphids, for example, cannot survive without Buchnera. Rickettsia, however, seems to be dispensable. When Watanabe and Noda cured the leafhoppers of their infections, the adult insects seemed fine.But as Werren points out, the team only studied small numbers of the insects in their laboratory. It’s possible that Rickettsia might help the leafhoppers by protecting them from parasites, or even bydetoxifying pesticides in their environment—benefits that would only reveal themselves in the wild.
Via Dr. Stefan Gruenwald
“ Chances are when you hear the term social network your mind immediately refers to one of the many social networking platforms available today. A less thought of context for the term is one that relates to bats.”
Via caroline jezierski
“Study counters notion that placenta is sterile, suggests oral hygiene may be important for healthy pregnancy”Researchers have discovered a small community of bacteria living in a most unlikely place: the placenta, the organ that nourishes a developing fetus through the umbilical cord. The finding overturns the conventional wisdom that the placenta is sterile. The study also suggests that these microbes may come from the mouth, affirming that good oral hygiene may be important for a healthy pregnancy.Medical experts have long assumed that any bacteria found in the organ must have been picked up when it passed through the vagina after delivery. But more recently, researchers have realized that a baby has a community of bacteria in its gut when it is born. And these bacteria don’t match those in the vagina, suggesting some other source, such as the placenta, says fetal medicine specialist Kjersti Aagaard of Baylor College of Medicine in Houston, Texas.Aagaard and co-workers are collaborators on the U.S. Human Microbiome Project, which is studying microbiomes—communities of bacteria, fungi, and viruses—that live in various places on and in our bodies. They looked for a placental microbiome by analyzing carefully collected placentas from 320 pregnancies. The researchers extracted DNA from the placentas and sequenced it for snippets and entire bacterial genomes in order to identify and quantify microbial species and the genes they carried. This analysis revealed low levels of a diverse set of bacteria, mostly nondisease causing strains of Escherichia coli, which dominate our intestinal tracts, but also others from five broad groups, or phyla. Most were benign species known to provide services such as metabolizing vitamins.Surprisingly, the mix of bacteria in the placenta looked more like the microbiome in an adult human’s mouth than the vaginal, skin, gut, or other body microbiomes, Aagaard’s team reports today in Science Translational Medicine. The researchers think the microbes may get to the placenta from the mother’s mouth through her bloodstream, perhaps when she brushes her teeth and dislodges them into the blood. That possibility is intriguing, because there’s a well-known correlation between gum disease and preterm birth. Indeed, the array of bacteria in the placenta differed in women who gave birth early, before 37 weeks.
Via Dr. Stefan Gruenwald
Researchers at the University of North Carolina (UNC) School of Medicine have found a new target for treating chronic pain: an enzyme called PIP5K1C. In a paper published May 21 in the journal Neuron, a team of researchers led by Mark Zylka, PhD, Associate Professor of Cell Biology and Physiology, shows that PIP5K1C controls the activity of cellular receptors that signal pain.By reducing the level of the enzyme, researchers showed that the levels of a crucial lipid called PIP2in pain-sensing neurons is also lessened, thus decreasing pain.They also found a compound that could dampen the activity of PIP5K1C. This compound, currently named UNC3230, could lead to a new kind of pain reliever for the more than 100 million people who suffer from chronic pain in the United States alone.In particular, the researchers showed that the compound might be able to significantly reduce inflammatory pain, such as arthritis, as well as neuropathic pain – damage to nerve fibers. The latter is common in conditions such as shingles, back pain, or when bodily extremities become numb due to side effects of chemotherapy or diseases such as diabetes.Brittany Wright, a graduate student in Zylka’s lab, found that the PIP5K1C kinase was expressed at the highest level in sensory neurons compared to other related kinases. Then the researchers used a mouse model to show that PIP5K1C was responsible for generating at least half of all PIP2 in these neurons.“That told us that a 50 percent reduction in the levels of PIP5K1C was sufficient to reduce PIP2levels in the tissue we were interested in – where pain-sensing neurons are located” Zylka said. “That’s what we wanted to do – block signaling at this first relay in the pain pathway.”Once Zylka and colleagues realized that they could reduce PIP2 in sensory neurons by targeting PIP5K1C, they teamed up with Stephen Frye, PhD, the Director of the Center for Integrative Chemical Biology and Drug Discovery at the UNC Eshelman School of Pharmacy.They screened about 5,000 small molecules to identify compounds that might block PIP5K1C. There were a number of hits, but UNC3230 was the strongest. It turned out that Zylka, Frye, and their team members had come upon a drug candidate. They realized that the chemical structure of UNC3230 could be manipulated to potentially turn it into an even better inhibitor of PIP5K1C. Experiments to do so are now underway at UNC.
Via Dr. Stefan Gruenwald
Andrew Thompson is CEO and co-founder of Proteus Digital Health, a California-based company building tiny ingestible sensors that can be incorporated into pills to let doctors know when patients take them. This is one of several connected products the company has in the pipeline that should help improve current diagnosis and treatment methods. Andrew was speaking at Wired Health on 29 April, 2014.What we've created is a new category of therapeutic products. Today you have generic products, branded products and soon we'll have digital products". We're in an early phase of commercial release of these products and that will start to expand fairly dramatically over the next couple of years. We created an FDA De Novo device category for an ingestible sensor and we have permission to make use of that technology either as a co-ingested, co-packaged or encapsulated dose form. We've also created a new pathway for what I'm going to call a digital NDA [new drug approval], which could lead to a new class of therapeutic product. The first of these digital NDAs will start to appear in 2015. Andrew Thomson states, "What we've created is a new category of therapeutic products. Today you have generic products, branded products and soon we'll have digital products. And digital products are going to by far the most valuable and biggest category -- over time."Video talk: https://www.youtube.com/watch?v=3aId6jSDSg0Proteus Digital Health
Via Dr. Stefan Gruenwald
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