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Bobby Murcer , New York Yankees announcer on the YES Network, has completed six weeks of chemotherapy and radiation treatment at a Houston hospital and is resting at his home in Oklahoma. Working there was a tremendous experience and gave me my first real taste of live television. Such cell reprogramming approaches may allow for the facile generation of replacement cells for some brain disorders. Augusto C Ochoa, M. According to reports, the veteran Turner and CNN reporter will be returning to ESPN where she will host her own program, serve as an anchor and reporter, contribute to SportsCenter and other platforms.

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NIH Director's Transformative Research Awards

Scott received his Ph. Rick Woychik's lab at the Oak Ridge National Laboratory where he cloned and molecularly characterized a classical coat-color gene in the mouse called the agouti locus. As a postdoctoral fellow in Dr.

As a PI, he has continued to develop and utilize mouse models of development and disease. Currently, his lab is particularly interested in identifying gut microbiota and microbial metabolites that influence colorectal cancer progression and elucidating their mechansims of action.

Dana Dolinoy is an Associate Professor of Environmental Health Sciences and Nutritional Sciences at the University of Michigan School of Public Health and leads the Environmental Epigenetics and Nutrition Laboratory, which investigates how nutritional and environmental factors interact with epigenetic gene regulation to shape health and disease.

Dolinoy holds a B. Her research focuses on examining the extent and implications of bacterial DNA integrations into animal genomes, including the human somatic genome. She has been at the forefront of research demonstrating that bacterial DNA integrations are extensive in invertebrates, sometimes encompassing multiple bacterial genomes.

Through an NIH New Innovator Award awarded in , her group used bioinformatics to demonstrate that such integrations are present in the human somatic genome where some are positioned in a manner where they could be oncogenic. He received his Eng. Research in his lab focuses on bioinformatics and computational systems biology, with particular emphasis on understanding the architecture and dynamics of gene-regulatory and signaling networks in human disease. Hetzer received his Ph.

He joined the faculty at the Salk as an Assistant Professor in and became Full Professor in His research focuses on fundamental aspects of organismal aging with a special focus on the heart and central nervous system. His laboratory has also made important contributions in the area of cancer research and cell differentiation. With a regenerative medicine focus, Scott conducted two post-doctoral fellowships, the first was to investigate the molecular pathogenesis of liver fibrosis and the second to define mechanisms driving neural stem cell maintenance.

His research program is broadly aimed at understanding single stem cell dynamics in the intestine and leveraging this information to develop physiologically relevant tissue constructs for cell-based therapies. Edward Mocarski started his career at Stanford University in where he served as Chairman of the Department of Microbiology and Immunology and Associate Dean for Research before becoming Professor Emeritus in as he accepted an appointment as Robert W.

He has made key contributions to the identification of replication functions, latent reservoir in myelomonocytic progenitors, immunomodulatory functions, and cellular response to viral infection. Recent studies of CMV-encoded inhibitors of cell death brought to light novel programmed cell death pathways that play out in mammals as alternatives to effectively eliminate pathogens that block apoptosis.

He has discovered that mammalian cell death machinery may become dysregulated to cause developmental failure as well as inflammatory disease. Saeed Tavazoie received his B. The main focus of his research is to understand how cells adapt to changes in their external environment. His lab studies this systems-level phenomenon across a range of timescales, from rapid transcriptional responses, to multi-generational epigenetic reprogramming, to long-term rewiring of signaling and regulatory networks over evolutionary timescales.

These studies have furthered our understanding of how environmental fluctuations are interpreted by cells; how global modulation of gene expression contributes to adaptation; how reprogramming of gene expression is encoded in DNA and RNA regulatory sequences; and how regulatory network rewiring underlies diverse phenomena of clinical relevance including antibiotic tolerance and cancer progression.

Zhang is a bioengineer focused on developing tools to better understand brain function and treat neurological and psychiatric disorders. Current research in the Zhang laboratory is centered on the development and application of the next generation of genome engineering tools to dissect the effects of genetic and epigenetic variation on the nervous system.

Redesigning the T cell: The proposed research will pursue improving cell and animal models for human brain disorders, as well as develop novel cell therapy strategies for brain diseases.

Recently, our group succeeded in the directed conversion of human patient skin fibroblasts to neurons, achieved by introducing a 'cocktail' of pro-neural factors. Such cell reprogramming approaches may allow for the facile generation of replacement cells for some brain disorders. The ultimate goal is to apply this technology to model Alzheimer disease pathology, with the intention of pursuing disease mechanisms and test potential therapies.

The evolution and ontogeny of lifespan at the species and individual level, the energetics of the organism in its environment, the storage of metabolizable energy as body fat, and socioeconomic disparities within populations all seem intricately related and yet the nature of these interrelations is poorly understood. Indeed questions as fundamental as why people age remain open and subsidiary questions such as why caloric restriction leads to increased lifespan and why lower socioeconomic status is related to obesity in developed countries also remain unanswered.

The research proposes a unified model informed by evolutionary thinking about life strategies which connects these phenomena. In this model, aging or more precisely senescence is not something that passively happens to people as the result of environmental insults or from metabolizing fuel.

That is, mortality rate or the rate of aging is seen as partially internally regulable phenomenon much like the control of body temperature in homeotherms in which the regulated rate is responsive to perceptions about the energetic state of the environment. From this perspective, it is perceptions of the energetic security of the environment that are a key factor in linking these phenomena.

We test this hypothesis using model organisms followed by mechanistic work involving internal clock regulation and other potential mechanisms. Development of new and more effective therapies for Type 2 diabetes T2DM and coronary artery disease CAD requires improved understanding of disease mechanisms.

Genome sequencing in human populations identifies genes and mutations underlying the inherited contribution to disease susceptibility, but progress is slowed by two central challenges: Our project addresses these challenges by integrating data and methods from human genetics, genome engineering, and stem cell biology, and is made possible by three recent advances: By engineering human stem cells to carry specific mutations, and by differentiating these engineered stem cells into physiologically relevant human metabolic cell types, we will make it possible to study the impact of large numbers of gene variants on human cell biology and function.

By relating the functions of gene mutations and cell biological processes with the phenotypes of human patients, we will provide pathophysiological insights and practical in vitro assays to guide development of therapeutics for these challenging diseases, which remain among the leading causes of morbidity and mortality in the United States and around the world.

Astrocytes are a major cell type in the brain long thought to be passive support cells, but our recent studies have shown that astrocytes powerfully control the formation and function synapses in the brain.

In this research we will test the hypothesis that the superior cognitive abilities of humans compared to rodents is, at least in part, the result of an evolutionary increase in the ability of human astrocytes to control synapse formation and function compared to rodent astrocytes. Telomeres comprise DNA sequences at the ends of chromosomes which shorten by about base pairs per year on average in humans due to oxidation and incomplete DNA replication during the cell cycle.

When telomeres become critically short, chromosomes form chromosome-chromosome fusions which can lead to cancer, and the exposed chromosome ends are recognized as double-stranded breaks that activate DNA damage repair responses that lead to cell death or senescence and consequent tissue and organ dysfunction.

Long telomeres protect the ends of chromosomes, and in our laboratory we have shown that short telomeres make the difference between a fatal and non-fatal muscular dystrophy. Thus, there is a strong motivation to develop methods to safely extend telomeres.

We propose to overcome current limitations in telomere extension with two high-impact and broadly-applicable tools: We will demonstrate the efficacy of these tools in cells from human Duchenne Muscular Dystrophy patients. Our ultimate goal is to develop telomere extension as a therapeutic tool to help prevent, delay, or treat the many diseases in which short telomeres play a major role. In the United States, more than , patients receive general anesthesia daily to safely undergo most surgical and many non-surgical procedures.

Use of anesthetic drugs by non-anesthesiologists in intensive care units and outpatient settings continues to grow. At the same time, anesthesia-related morbidity, including intra-operative awareness, altered neurological development and delirium in children and cognitive dysfunction in the elderly remain significant problems.

Despite the central role of anesthesiology in modern healthcare, research in this field is overly focused on deciphering the anesthetic and toxic mechanisms of current drugs with no attention to developing new approaches.

We propose to redesign general anesthesia by combining optogenetic, electrical and pharmacological manipulations in rodent models to create this behavioral- physiological state through precisely timed control of specific brain circuits. If successful this research will provide a new fundamental understanding of brain arousal control, and eventually, new anesthesiology practices including: Each year approximately three quarters of a million Americans will have a new myocardial infarction MI , and approximately half a million will have a recurrent MI.

No current therapies exist that directly address the negative left ventricular remodeling process that occurs post-MI and results in heart failure. There is therefore a strong clinical need to develop novel therapies to treat MI.

This research program will establish a new paradigm in the design of treatments for healing heart tissue post-MI. Specifically our plan is to develop self-assembling materials programmed to form a healing scaffold in damaged heart tissue immediately following MI. In the proposed, unprecedented approach, the materials will be designed to be injected intravenously rather than directly into heart tissue, and will target and self-assemble in the MI, providing a scaffold to recruit endogenous cells for cardiac repair.

This research proposes to change the current approach to understanding the molecular basis of memory. Our approach challenges the current focus on quantitative identification of synaptic RNAs by developing new technologies to address protein synthesis-dependent synaptic plasticity: These will allow us to redefine the problem from two new superimposed perspectives: Specific synapses will be studied: These complexes will be compared with a delineation of all ribosome-mRNA synaptic complexes present in the same dendrites, allowing us to validate interactions by identifying translationally regulated synaptic mRNAs synaptic translational profiling.

Regulated dendritic RNAs will be further validated by assessing for their translational state in well-studied paradigms of protein synthesis-dependent synaptic plasticity. Psychiatric disease represents the leading cause of disability both in the U.

In general, achieving high-resolution information on any biological system typically comes at the expense of the global perspective that is often essential to understanding.

This research project will directly address this challenge, in part by developing and applying new chemical engineering-based technologies to rapidly transform intact, impermeable and opaque biological tissue into macromolecule-permeable for labeling and interfacing and transparent form. The CLARITY technology will be developed with compatible readout methods for extracting volumetric activity and tissue history, information which can then be linked to global wiring and local molecular phenotypes obtained from the very same tissue or organism.

The approach will be developed in the vertebrate central nervous system, challenging for its low accessibility and high complexity, but CLARITY is applicable to any biological system including to the human brain and to models of neurological and psychiatric disease. Recently, an elegant technique was developed allowing for unprecedented control and specificity in mapping the molecular and cellular properties of neural circuits.

Some of the most burning questions in the neurobiology of pain, affect and addiction lend themselves particularly well to the implementation of optogenetic neural modulation techniques, yet these still require drastic miniaturization of circuits, power and light sources for full implementation in diverse neuroscience applications.

Enhancer Therapy Grant ID: Current efforts are to determine the biochemical and biological roles of sequence- specific transcription factors and their associated co-regulators at gene-specific and genome-wide scales.

This research project will use a combination of biochemical, cellular and genetic model systems are used, incorporating macrophage-specific knockouts, microarray technologies, massively parallel sequencing and bioinformatics approaches, to unravel the contributions of specific factors to the development of specialized macrophage functions in immunity and the pathogenesis of inflammatory diseases.

One of the primary focus areas of our research is working to integrate physiologically relevant sensory feedback with prosthetic limbs. To this end we employ a variety of approaches that interweave disciplines such as electrophysiology, psychophysics, biomedical engineering and cognition. Our research team is composed of an interconnected and communicative network of clinicians, engineers, and scientists.

This helps us to provide pathways from basic science discoveries that can be used to address clinical needs with transition directly to patient care. Pulmonary infections by microorganisms, such as Mycobacterium tuberculosis and Pseudomonas aeruginosa, are annually responsible for the morbidity and mortality of millions of immunocompromised individuals worldwide. Despite the availability of drugs that successfully eradicate these pathogens in vitro , they are far less successful in vivo.

Due to the challenges of working in situ , most studies of infectious disease agents IDA are conventionally performed with representative isolates and imperfect disease models in the laboratory; by necessity, they are highly reductionist. Very few direct measurements of the physiological state of drug-tolerant populations in the host exist, and little is known about which metabolic pathways are actually at play, much less how they change over time in response to co-evolving conditions within the lung.

We will tackle this critical knowledge gap using an approach inspired by geobiology. Geobiologists are experienced in studying the growth and metabolism of microbial populations in poorly accessible natural habitats by combining molecular biology and stable isotope geochemistry.

We propose to study IDA within infected lungs using these tools, with the goal of defining the composition, growth rate and metabolism of the microbial community at different stages in disease progression with high spatial resolution. The onset of distant metastasis marks the stage of cancer progression where the disease is no longer considered curable. Currently, clinicians are unable to determine when metastases have occurred until the cells have colonized one or more distal sites and often affected the function of the effected organ.

We propose an early detection system based on developing an implant that would recruit metastatic cancer cells and a sensor to identify when these cells have colonized the implant. Recruiting the metastatic cancer cells would initially function to reduce the burden of circulating tumor cells and limit their colonization in other tissues. Investigating the design of implants that recruit metastatic cancer cells is expected to further define the biology of the pre-metastatic niche.

Taken together, the development of an implant to recruit metastatic cells and a non-invasive technology to monitor growth could transform current clinical approaches to cancer treatment. With nearly 15 million units of red blood cells RBCs transfused to about 5 million patients in the U. During hypothermic storage, a significant fraction of stored RBCs becomes irreparably damaged and the storage medium accumulates known mediators of toxicity as byproducts of RBC metabolism and degradation.

The goal of this project is to develop technology for high-throughput removal of irreparably damaged cells and toxic mediators accumulating in the storage medium from RBC units during the transfusion process. In this project, we will systematically explore the design of smart nanobjects able to transduce molecular level sensing of indicators of health status a. Our results will lay groundwork for broadly applicable families of theranostic providing therapy upon diagnostics devices that would be able to autonomously monitor and correct disease states.

All mRNA molecules are subject to posttranscriptional gene regulation PTGR by hundreds of RNA-binding proteins RBPs involving sequence-dependent modulation of splicing, cleavage and polyadenylation, editing, transport, stability, and translation. The major goal of this application is to identify and characterize the interaction network of mRNA-binding transport and shuttling proteins at the sequence, structural, and functional level and to establish theoretical and experimental models that relate these features to RNA transport processes and PTGR.

Our approach involves deep sequencing methodologies suitable for broadly mapping interaction sites between RBPs and their RNA targets in human cells, followed by integrated annotation of binding sites on transcripts across libraries via a probabilistic graphical modeling approach to identify prevalent states reflecting particular site configurations. As computed interaction models emerge, these will be studied by biophysical and structural methods using natural, as well as designed RNA recognition element representing RNA ligands together with their respective recombinant proteins.

We anticipate the identification of numerous important regulatory regions in mRNAs, as well as uncover mRNAs and RBPs particularly vulnerable to mutation and deregulation in disease states. The role of the innate immune system in aging and AD has received limited study and is poorly understood.

This is due in part to confusion regarding microglial cells and how they relate to the peripheral innate immune system. This advance presents a unique opportunity to determine the functions and dysfunctions of innate immune cells in brain aging and the development of AD. We will study the innate immune system both in animal models and aging human subjects and in human postmortem tissue.

The existing health care system requires an individual to visit a health care facility to conduct point-in-time tests to monitor even the most basic health status markers, which can miss fluctuations in body chemistries that are vital to accurate diagnoses, particularly in high-risk populations.

Continuous multi-chemistry health sensors have the potential to dramatically change health care by paving the way for decentralization of health care delivery and shifting the focus away from reactive treatment to preventative maintenance. We propose to transform current testing paradigms by developing highly miniaturized, injectable, sensors for continuous and simultaneous monitoring of multiple body chemistries.

Sensor molecules that glow somewhat like fireflies when they come in contact with certain biomarkers are embedded into specially engineered tissue-like biomaterials. The sensor molecules are embedded in soft, tissue-like biomaterials that become part of the tissue in which they are injected, and do not cause the typical foreign body rejection response. The sensors are injected under the skin and monitored optically using a miniaturized, wireless, Band-Aid-like reader for continuous measurement or a hand-held wand for periodic self-measurement, depending on the clinical need.

The data may be viewed via cell phone or at a remote location, allowing the individual, physician, or other care providers to access medical data without the need for in-person examination until a critical threshold is met. The research project will develop a systematic in vivo discovery approach for identification of critical genes and pathways that limit the anti-tumor activity of cytotoxic T cells.

Our hypothesis is that shRNAs which target critical inhibitors in dysfunctional T cells can reprogram them to undergo substantial expansion in tumors. T cells will be genetically modified with shRNAs and then transferred into tumor-bearing mice so that enrichment of particular shRNAs within tumors can be quantified.

This in vivo approach will also be used to address a second related problem in oncology, the identification of combination therapies that act in a highly synergistic manner on defined cellular pathways. The therapeutic activity of these human T cells will be tested in a xenotransplant mouse model on human melanomas, as a key step towards translation of our discoveries into the clinic.

Figure describes a device that can manipulate small model nematodes worms in fluidic micro-channels. Populations of worms are treated with different drug compounds and then monitored for health of their entire nervous system at ultra-high speeds.

This device will enable the discovery of new drugs to delay or prevent the progression of neurodegenerative diseases and aging. Neural activity is recorded from channels distributed across two microelectrode arrays implanted in the premotor and primary cortex. Data are decoded in real time to control the cursor. Image shows a sirtuin enzyme catalyzing the removal of a protein modification lysine succinylation from metabolic enzymes.

This activity is required for the malignant growth of cancer cells. Small molecule inhibitors of the desuccinylation process may be a novel way to treat cancer. Image shows a schematic of genes being modified from bacteria, and then inserted into human immune cells. Image shows microscopic circuits that will enable monitoring of the brain's electrical activity using magnetic imaging techniques such as magnetic resonance imaging MRI.

Following injection into brains, the microdevices shown in green will convert neuronal voltage signals into tiny magnetic fields shown in dashed blue lines that will be detectable by MRI. Some of these memory T cells migrate into peripheral tissues, including skin, lung, and gastrointestinal tract, and become resident long-lived memory T cells TRM that protect against infection. Figure illustrates the key components of an innovative and non-pharmacologic treatment for Attention Deficit Hyperactivity Disorder ADHD that combines cognitive and physical exercises.

Part of the figure shows a child sitting at a classroom computer and doing one of the cognitive exercises. A second part of the figure shows a group of children engaged together in a group physical exercise in the gym that requires ball skills, concentration and memory. Last part of the figure shows a brain. Color-coded reconstruction of three pyramidal neurons in the mouse brain.

There are a number of axons making synapses on the beige neuron. Synapses are the sites of communication between neurons. Small, round particles, on the order of 10 microns, can be mixed with stem cells of the same approximate size to form aggregates of the cells and materials. As stem cells secrete growth factors, the entrapped particles can capture the secreted molecules. The aggregates can then be disrupted in order to retrieve the particles, now loaded with the stem cell-derived factors.

The stem cell factor-laden particles can then be injected at different sites of disease or injury in adult mammals in order to promote tissue repair and regeneration. Image displays a high-resolution, high magnification electron micrograph of mitochondria isolated from heart.

For high sensitivity and specificity in tumor detection, this system is equipped with 4 input channels, shown in 4 panels: Image shows a mesenchymal stem cell MSC on the bottom of the figure transferring red-dye labeled pieces of RNA into a target neuronal cell blue arrow. African trypanosomes are blood-borne parasites that use their surface coat as a decoy to trick the immune system into making long-lasting antibody responses. Image shows trypanosomes surrounded by immune cells B cells.

Trypanosome coats will be modified shown in the middle panel to trick the immune system into making therapeutic antibodies against disease-associated targets inserted epitope, shown in the right panel. Spina bifida is shown on the left, in magnetic resonance imaging MRI , showing the open spine and exposed spinal nerves arrow.

This and other Neural tube defects NTDs are due to a complex interaction of genetic predisposition and environmental factors, including the addition of methyl groups to DNA. A major source of methyl groups is the vitamin, folic acid. Such maps from patients with spina bifida will be compared with healthy controls to determine which genes are under- or over- methylated in affected patients and could contribute to their risk of having an NTD.

Structure of a Membrane Protein in a Lipid Membrane: Direct Conversion of Fibroblasts into Neurons: Microbes that cause disease are becoming resistant to antibiotics faster than we can find new ones, making many common infections untreatable and life threatening.

Innovative approaches are urgently needed to speed up the discovery of new anti-infectives. This project aims to achieve a paradigm shift in antimicrobial drug discovery by finding next generation anti-infectives that prevent disease by blocking pathogen adaptation to host physiology. Rather than simply preventing bacteria from growing, these new sophisticated drugs will prevent disease by interfering with a microbe's ability to interact with the human body.

The findings will help to identify drugs that cure otherwise lethal infections. A current paradigm in biology is that basal cells present in the epithelial lining of some organs never come into contact with the inner luminal side of the organ.

They will take this work one step further and create new model systems to determine the 3-D relationships and functions of different epithelial cell types as the basal cells detect and respond to various drugs, hormones, chemicals and pathogens that appear in the cavity of the organ. A better understanding of how these novel basal cells communicate with adjacent cells will help define disease mechanisms and suggest new diagnostic and therapeutic strategies for male infertility, and diseases of the lung, including asthma, chronic obstructive pulmonary disease COPD and cystic fibrosis CF.

High-throughput assays are indispensable for comprehensive functional proteome research. To accelerate research in this field, new protein capture tools for the detection and identification of specific proteins are needed. The reagents must be stable to thermal and proteolytic degradation, have high affinity, be easy to produce and present low cross-reactivity. This proposal presents an innovative approach for screening and selecting a new class of highly stable protein capture reagents and developing a new versatile approach for ligand immobilization that together enable rapid production of cyclotide-based microarrays for proteomics research.

These technologies have the potential to accelerate science discovery and to realize the diagnostic and prognostic benefits of clinical proteomics. Mitochondrial dysfunction has been associated with many diseases, including neurogegeneration, diabetes and cancer, although its exact role in the development of these diseases remains controversial.

This proposal tests the paradigm-shifting hypothesis that mitochondrial-derived proteins MPDs play a previously unappreciated role in the regulation of cellular and organismal function, and that disregulation of MDPs is important in disease development. Understanding the role of MPDs may lead to development of new therapeutic and diagnostic targets. This project aims to develop a revolutionary screening platform that will allow for the rapid isolation of hundreds of high affinity and specificity synthetic ligands for proteins in a highly parallel fashion.

The identification of large numbers of protein ligands is a high priority for biomedical research. Such ligands could be employed as reagents to construct tools for the discovery of diagnostically useful disease biomarkers. They could also serve as drug leads for a variety of therapeutically interesting targets. Because the ligands will be peptoids, which can be easily synthesized in large quantities by research laboratories lacking specialized organic chemistry skills, the ligands will be more widely accessible to the research community than would be most other classes of protein binding-molecules.

Tell your doctor if you have any side effect that bothers you or that does not go away. Call your doctor for medical advice about side effects. This site is published by Janssen Pharmaceuticals, Inc. The material on this site is intended only as informational or as an educational aid and it is not intended to be taken as medical advice. The ultimate responsibility for patient care resides with a healthcare professional.

This information is intended for the use of patients and caregivers in the United States and Puerto Rico only. Laws, regulatory requirements, and medical practices for pharmaceutical products vary from country to country. Skip to main content. Exclusive tools and information to help you set and keep track of weekly healthy goals. Exercise Safely in Winter Weather. Five Workout Motivational Tips. How to Hydrate for Your Active Life.

Easy Exercises to Do Around the House. Walking Your Way to Better Health. Simple Healthy 5-Ingredient Dinner Recipes. Yeast infection of the penis balanitis or balanoposthitis.

Talk to your doctor about what to do if you get symptoms of a yeast infection of the vagina or penis. Talk to your doctor about factors that may increase your risk of bone fracture. Low vitamin B 12 vitamin B 12 deficiency. Using metformin for long periods of time may cause a decrease in the amount of vitamin B 12 in your blood.

Your doctor may do blood tests to check your levels. Tell your doctor if you have any side effect that bothers you or that does not go away. Call your doctor for medical advice about side effects. This site is published by Janssen Pharmaceuticals, Inc. The material on this site is intended only as informational or as an educational aid and it is not intended to be taken as medical advice.

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