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Links to related articles. Darryl Strawberry is not even making that much money. Color-coded reconstruction of three pyramidal neurons in the mouse brain. The sports network already offers scores, games and news to a number of wireless providers but the new deal with Sprint will give ESPN total control and subscribers the ability to customize their phones to receive pop up news and stats on their favorite teams as well as video clips and ring tones. James who was killed in a plane crash in November, had a trail named after him at The Telluride Ski Resort in Colorado. Infectious disease is often untreatable, even when caused by a pathogen that is not resistant to antibiotics.

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Ben Affleck's Strip Show. Lo's Grammy Gown Raises Eyebrows. Edit Personal Details Other Works: Edit Did You Know? This is a proposal to establish a new paradigm for the study of cellular signal transduction that combines biosensor design and live cell imaging to produce a transformative approach to studying cellular signal transduction and decision processes.

These advances promise a breakthrough in our ability to probe complex, spatially and temporally organized signaling processes in cell models of normal and diseased physiology. A fundamental property of the brain is that our experiences cause modifications in the number and strength of the connections among neurons. These changes, which are thought to underlie memory and cognition, require the precise control of the synthesis of specific proteins at the sites of these connections.

The mechanisms governing this local synthesis of synaptic proteins are poorly understood, although it is known that disruption of this process has severe consequences. This defect is thought to be responsible for Fragile-X syndrome, the most common inherited form of mental retardation.

This proposal describes a method that can provide individual reporters of the regulation of protein synthesis for each gene in the genome, and can identify the regulatory mechanisms controlling each one. The work will be conducted in Drosophila although the high degree of conservation of gene regulatory mechanisms and function, is it likely that much of what we learn will be transferable to humans. The success of artemisinin-based combination therapies in combating Plasmodium falciparum malaria has inspired calls for the eradication of this devastating parasitic disease.

However, new reports of emerging artemisinin resistance, and the absence of alternative first-line drugs, highlight an urgent need for new control methods. Exploiting the dependency of fatty acid synthesis by liver stage parasites, they will develop fatty acid synthesis-deficient, genetically-attenuated parasite vaccines that arrest in the liver, causing a host immune response that protects against infectious challenge.

In addition, they will target parasite synthesis as well as salvage of host fatty acids, as a means to develop novel prophylactic and curative medicines that can prevent and control this widespread and devastating disease. A tremendous gap exists between available culture and animal models and methods that can extract detailed information on cell-cell communication networks governing system responses to perturbations, such as an inflammatory cue.

Networks inherently operate in a complex, interlinked fashion, and often exhibit non-intuitive outcomes from intervention at a particular point in the network, as evidenced by failure of many targeted therapeutics to operate in the clinical setting after promising results in currently- available preclinical trials.

The goal of this project is transform our ability to probe cell-cell communication networks in human cell systems via linking systems biology with tissue engineering.

Development of new methods that do not rely on genetic manipulation of the cell populations will generate valuable information about systems operation. A central paradigm of medical genetics is that the phenotype of a deletion syndrome results from the disruption of the deleted genes themselves.

In direct contradiction to this dogma is the idea that genetic diseases can be caused or modified by changes in physical, long-range interactions that normally occur between loci that are now deleted and genes that are far from the deleted region when plotted on a linear genetic map. In some cancers and genetic diseases, long range associations between genes are lost because a part of a chromosome becomes deleted.

By examining the network of long range interactions among genes, we will learn how diseases are caused by the change in the expression of many genes which become abnormally regulated when the interactions are lost.

This project seeks to address the mechanisms underlying the integrity of tissues, networks of interacting cells and matrices.

The project will determine how cells come together to form tissues, and test the hypothesis that tissue integrity results from the integration of information that arises from the dynamic interactions between the different cell types and the matrices that bind these cells together. Using the filtration barrier of the kidney cortex as a model system, the researchers will apply a combination of mathematical models and engineering approaches to develop a 3-D tissue assembly to study this phenomenon.

These studies will identify general design principles for assembling functional tissues that can aid in understanding disease processes and for screening for new drugs. The detection of proteins is fundamental to essentially all biomedical research.

Current strategies to detect proteins include techniques such as Western blotting and enzyme-linked immunosorbent assays. Currently, there are no techniques that permit the levels of endogenously expressed proteins to be monitored in real time in living cells.

The sensors will be used to monitor protein expression in cells in real time. The experiments will result in powerful new tools for protein detection that will markedly enhance and expand biomedical research.

More than 30 million Americans suffer from unrelieved chronic pain, such as nerve injury-induced neuropathic pain. Although a considerable amount is known about how chronic pain is induced, little is known about how acute pain naturally resolves. Current management of chronic pain mainly focuses on two types of drugs, ones that treat pain symptoms by blocking neurotransmission and those that modify disease progression by suppressing neuroinflammation.

This project employs a novel approach for chronic pain therapy using newly uncovered endogenous pro-resolving lipid mediators. The project will investigate whether and how these mediators can prevent and reverse neuropathic pain after nerve injury. The results from the proposed studies are likely to transform and positively impact on the entire pain community, from acute postoperative pain to chronic inflammatory and neuropathic pain.

Protein-capture reagents are indispensable for delineating the molecular mechanisms of diseases, to detect and characterize cellular abnormalities, and to characterize biological effects of drugs. However, the current paucity of high-quality protein-capture reagents presents a major bottleneck in virtually all areas of biomedical sciences.

This project will establish a totally new approach to facile generation of detection reagents that are high performance, easy to produce and easily made available to the research community.

This innovative and powerful technology will fill a major void in the currently available molecular tools and will have a major impact on virtually all areas of molecular biomedical sciences, diagnosis and drug development.

The adult human intestine performs essential roles in physiologic homeostasis including digestion, nutrient absorption, secretion of hormones, and immune functions. Diseases of the intestine, such as inflammatory bowel diseases, infection, malabsorptive states and neoplasia, are a considerable source of human morbidity and mortality.

Human primary intestinal culture is essentially not utilized as an experimental tool because primary tissue types lack appropriate in vitro culture methods. To meet this need, this project proposes to employ an innovative approach to enable the primary culture of three-dimensional 3-D human intestinal tissue, which is currently not possible.

The ability to reproducibly culture 3-D tissues outside of the body will enable scientists to test new hypotheses and models of physiology and disease, to develop high-throughput screens of pharmaceutical targets, and to enable the expansion of cells for regenerative medicine therapies.

Hepatocyte transplantation has been reported as a possible therapeutic approach for liver disease; however, transplantation has been directed at the liver itself, limiting efficacy in patients with end-stage liver diseases, when cirrhosis and fibrosis are common.

This proposal will demonstrate that the generation of an ectopic liver within lymph nodes is an efficient method to restore hepatic function, highlighting the novel use of this organ as a site for hepatocyte transplantation. The project addresses some of the hurdles confronting the development of complex 3-D tissue models, and provides a new paradigm for tissue modeling, by using lymph nodes as in vivo bioreactors to grow tissue or organ substitutes.

Nitric Oxide NO is an essential signaling molecule for diverse physiological and disease processes. While the regulation of NO flux has focused primarily on the study of the three NO synthases NOS , their respective genetic deficiencies exhibit relatively modest phenotypes, which has led to difficulties in dissecting the specific cellular contributions to NO in different disease processes.

This project will study a new way that NO production may be regulated in the body by the chemical argininosuccinate lyase ASL which may control the production of arginine needed for NO production. The investigators will determine whether inhibiting ASL is the most effective way for controlling NO production in diseases affecting the brain, heart, and pancreas. The Hydroxylprolylproteome Grant ID: Posttranslational modifications of proteins play important roles in many signal transduction pathways, although the full extent to which these modifications impact cell function is not known.

Recent studies have highlighted a key role for a distinctive modification, prolyl hydroxylation, in the hypoxic response. This project seeks to develop novel capture reagents for a posttranslational modification, prolyl hydroxylation, that plays a central role in the oxygen- regulated turnover of Hypoxia Inducible Factor. The long term goal will be to employ these reagents to determine the extent to which prolyl hydroxylation regulates the cellular hypoxic response, and to characterize changes in the hydroxylprolylproteome in response to differing oxygen concentrations.

These studies will have implications for understanding diseases such as heart attacks, stroke, and cancer that are characterized by hypoxia. Infectious disease is often untreatable, even when caused by a pathogen that is not resistant to antibiotics. This paradox could be explained by the fact that microbial populations produce persisters, dormant cells that are not mutants, but phenotypic variants of the wild type that are tolerant to antibiotics.

The project will test the hypothesis that the agent responsible for untreatable infections is a super-persister cell which carries a high-persister mutation and has induced stress responses.

Mutants of the pathogens are able to enter into a state of dormancy highly tolerant to existing antibiotics. The findings are likely to change the way we view infectious diseases and provide rational approaches for discovering drugs that completely eradicate the infection. Until recently, small RNAs have been thought to function mainly as the mediators of an evolutionally conserved gene silencing mechanism known as RNAi.

This application will establish a new paradigm of gene regulation mediated by small RNA that targets gene promoter sequence to induce potent and prolonged gene activation at the transcriptional level and in a sequence-specific manner, a phenomenon termed RNAa. Despite the enormous potential for reprogramming gene expression in living cells, the molecular mechanism of RNAa is largely unknown and the rules for target selection are still quite obscure.

Understanding the mechanism of RNAa will provide new insight to many physiological and diseases processes, may provide a tool to interrogate gene function and study their involvement in diseases, and may be a promising surrogate for traditional gene therapy for many diseases especially cancer.

Novel protein capture and detection reagents are required to understand comprehensively the interplay of the proteome in basic biological processes and in human health and disease.

These reagents need to have high affinity and specificity for particular protein targets, and they need to be easily created and produced, and be amenable to modification and immobilization for high throughput analysis of proteins.

This project seeks to transform an existing technology to facilitate and streamline identification of novel capture reagents for human proteins and to incorporate these new reagents in assays that can accommodate simultaneous analysis of many proteins. This project will not only develop new technology and assays that enable analysis of human proteins critical in human health and disease, but also generate the novel reagents that can be used for therapy.

Many diseases strike humans without obvious cause and, despite intense research, their etiology remains idiopathic. For example, it is likely that some idiopathic or autoimmune conditions or even cancers may be attributable to infectious agents even if conventional research avenues favor other mechanisms. The proposal will test the hypothesis that viral pathogens constitute the inciting events in aplastic anemia or other immune-mediated cytopenias, challenging the traditional understanding of autoimmunity in these specific conditions.

Contesting current theories of pathogenesis for such conditions may result in unexpected progress and new lines of scientific inquiry. If infectious agents, likely viruses, can be identified, such a discovery would change the paradigm not only for these diseases but also for many other autoimmune diseases, and open avenues to prevention, diagnostics and effective treatments.

Chronic illness kills too many and costs too much. The current chronic illness system needs to be changed in order to deliver better care.

This project will join patients and physicians together in a collaborative innovation network to design, prototype and optimize, and evaluate a system for improving the chronic illness care system. If successful, this project will lead to improved care and self- management, better outcomes for people with chronic illness, and lower costs of care.

This project will test the hypothesis that endogenous retroviruses, such as modern HERV-K HML-2 , can still replicate in modern humans using cutting-edge and complementary techniques. Proving this hypothesis will be contrary to the entrenched dogma and have substantial implications for human genetics, cancer biology, and the safety of the human blood supply.

One third of all individuals who develop colon cancer will die of metastatic spread of this disease. The classic genetic model for colon cancer development holds that colon cancer progression is due to accumulation of multiple gene mutations in the cancer cell. This proposal advances the novel paradigm that cancer metastasis, the ultimate cause of death from this dread disease, is not due to new "metastasis-causing" gene mutations in the cancers, but rather is crucially depend on inborn genetic susceptibility factors.

The import of this new paradigm for cancer metastasis will be felt in the identification of entirely new biological pathways that will be key to cancer management, to cancer prognosis, and to developing new and more effective anti-cancer therapies.

The ability of cells to form defined shapes, and to dynamically regenerate their cytoskeletal and membrane structures following damage, is one of the current mysteries of cell biology. Most studies of regenerative medicine have focused on developing methods to use stem cells to replace damaged cells. This proposal adopts an alternative approach using a classical model system, the giant ciliate Stentor, to study how injured cells repair themselves.

In addition to being a fundamental cell biological problem, understanding development and regeneration of cellular morphology would be a starting point for developing a whole new approach to regenerative medicine, in which rather than attempting to replace damaged cells with stem cell derived substitutes, one would induce the damaged cells to regenerate in situ.

Brain function is dictated by its circuitry, yet we know little about its wiring architecture: The study of mouse models of neuropsychiatric disorders provides hope for the development of therapies for these burdensome illnesses, but progress has been slow due to the lack of knowledge about how the mouse brain is wired. This project aims to close this gap by generating the first brain-wide wiring diagram of mouse, using automating techniques that are known to work but are labor-intensive.

If successful, the project has the potential to fundamentally transform our understanding of brain function and brain disorders. Mitochondrial number is very tightly regulated within the cell. Dysregulation of mitochondrial metabolism leads to decreased energy production, increased reactive oxygen species ROS , and altered apoptosis. These three factors play a role in a multitude of diseases, including heart disease, diabetes, cancer, obesity, and neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.

The project will investigate the way in which cells regulate the amount of mitochondria within a cell, with an eye towards their evolutionary origins.

The proposed research challenges the assumption that a traditional straightforward recitation of the facts is the optimal way to convey health-related information and empirically tests whether utilizing a narrative format might produce a greater and longer lasting impact on knowledge, attitudes and prevention behavior.

It also involves examination of the effect of communication modality i. Although the proposed research will focus on breast and cervical cancer, the results have clear implications for virtually all health care communication and could radically change how health messages are conveyed across different ethnic groups, generations and modalities.

Insulin Regulation of Monoamine Signaling: Pathway to Obesity Grant ID: Obesity and other dopamine-related pathologies such as schizophrenia, bipolar disorder, and attention-deficit disorder are a tremendous public health burden. Despite knowing better, we consume too many calories, too much fat, and too much sugar. This proposal promises to transform our approach to this problem of obesity by analyzing how parallel changes in insulin and dopamine signaling, induced by high-fat feeding, cement changes in feeding behavior that lead to obesity and related co-morbidities.

The finding may allow the development of new therapeutic interventions. There has been a 4-fold increase in obesity U. The dramatic rise in overweight and obesity over the last 40 years coincides with equally dramatic decreases in childhood infections.

Infections of childhood are disappearing due to changes in family size, improvements in hygiene, the addition of new vaccines, and other preventive health measures. This proposal seeks to determine whether the inverse trends of rising obesity and declining infection are coincidently related or causal. This study intends to establish methods and collect preliminary data to determine whether decreases in childhood infection are linked to development of obesity. This project will test whether water plays a primary role in a number of representative biological systems, including osmosis and diffusion, surface tension and oxygen exchange, self-assembly, light-induced effects, vascular effects, and global health applications.

If the newly discovered features prove to be centrally relevant as hypothesized, then their relevance might extend more generally. If so, then this water-based approach may crack open the door to a new realm of biological understanding. The human liver serves as the reservoir for several important human pathogens, including hepatitis B HBV and C viruses HCV and Plasmodium species, all of which represent serious global health concerns.

A vaccine for HCV has not yet been developed, and, while HCV-specific protease and polymerase inhibitors are showing promise in early clinical development, rapid emergence of resistance indicates that additional targets and combinations of antivirals will be needed for effective control. The scarcity of in vitro and in vivo systems that faithfully mimic liver biology and susceptibility to human hepatotropic pathogens has severely hampered drug and vaccine development.

This project uses an interdisciplinary approach that combines tissue engineering with molecular virology and humanized mouse technology to create platforms that will facilitate studies of basic virus-host and virus-virus interactions, promote understanding of the mechanisms of liver disease progression, and provide predictive systems to test drug and vaccine efficacy and toxicity.

They will develop and apply this powerful new technology toward creating a comprehensive reagent set aimed at the Hepatitis C virus HCV proteome.

Applying high- throughput approaches to create new protein capture reagents has the potential to speed the pace of proteomics research. The basic functions of many cell types are sensitive to physiological levels of mechanical forces acting on them and this phenomenon is always studied in the laboratory using monotonous mechanical stimuli. However, cells in the body are exposed to irregularly varying stimuli and this variability may fundamentally alter all essential cell functions including secretion, growth and death.

Uncovering how cells deal with such physiological variability may help understand how cells work in real living tissues as well as the pathogenesis of several major diseases including atherosclerosis, neuro-degenerative diseases, metabolic disorders, aging or cancer.

RNA as a Hormone: The conventional paradigm of the endocrine system does not include RNA molecules as a class of hormones. This proposal seeks to establish the new scientific paradigm that RNA molecules can function as hormones, traveling via the bloodstream to target organs where they are taken up and influence the activity of specific recipient cells.

To establish this new paradigm, the researchers will focus on microRNAs secreted into the blood by cancer cells and use mouse models to determine whether the microRNAs are taken up by and influence distant organs and tissues. Establishing this new paradigm will have a major impact not only on basic understanding of human physiology but could also open up new ways of diagnosing and treating disease based on RNA hormones in the blood.

Whether fleeting or stable, normal or aberrant, protein interactions and their sites of contact form the basis for discovery of biological pathways, disease mechanisms, and opportunities for therapeutic intervention. Like the teeth of a key that perfectly fit into a lock, complementary protein shape is critical to the execution of biological interactions.

The goal of this proposal is to intertwine chemistry, biology, and medicine to create a transformative high- throughput technology that precisely identifies protein targets and their explicit sites of interaction. This new technology will address the current formidable challenge of identifying, distinguishing, and drugging the broad array of human protein targets.

Not surprisingly, small-RNA therapeutics and biologic tools based on single gene interference are often plagued by "off-target" effects, resulting in poor therapeutic indices. The approach holds promise for identifying and optimizing shRNA sequences for studies of stem-cell induction and cell differentiation, and for developing small RNAs to be used as therapeutics or biologic tools.

Before human embryonic stem hES cell-based therapies for conditions such as neuronal disease, cardiovascular disease, diabetes, Parkinson's, and others can be translated to the clinic, new strategies are needed to overcome the immunological barrier to usage. To address this critical bottleneck, this interdisciplinary team of investigators will develop novel and effective strategies to induce immunological tolerance for hES cell therapy.

If successful, the project will represent a major scientific advancement in hES cell immunology and a significant step toward their eventual clinical translation. Imaging the Invisible with No Labels: Small molecules such as metabolites and drugs are crucial to the biochemistry of living organisms but are difficult to study because they cannot be visualized easily in a living cell or organism.

Label-free optical imaging based on Raman scattering is a highly desirable approach to use, but is limited by low sensitivity and long acquisition times. This project team recently developed stimulated Raman scattering SRS microscopy which offers an unprecedented combination of high sensitivity, rapid image acquisition, chemical specificity and noninvasiveness.

Studies of lipid metabolism and drug distributions in tissue are already underway in their laboratory. In this TR01 project, they will continue to probe lipid metabolism, including lipogenesis, lipolysis and insulin resistance.

The ability to visualize small molecules such as metabolites and drugs in living cells and organisms without labels will revolutionize biomedical research, particularly lipid metabolism, pharmacokinetics and cancer diagnosis.

More Americans suffer from chronic pain than heart disease, diabetes and cancer combined. Unfortunately, existing analgesics are not completely effective for all pain conditions and have serious side effects. A critical challenge for modern biomedical research is the need to provide pain relief without serious side effects.

This project addresses this need by harnessing enzymes, called ectonucleotidases, that are found in nociceptive pain-sensing circuits in nervous system dorsal root ganglia DRG and in the spinal cord.

Ectonucleotidases degrade purine nucleotides like ATP and ADP that cause pain into adenosine-a compound that has analgesic properties in rodents and humans. These studies are important in developing new proteins and small molecules that target ectonucleotidases for the treatment of acute and chronic pain, and have the potential to transform how we treat pain in millions of patients with fewer side effects.

Science News Multimedia Outreach Activities. Massachusetts Institute of Technology Project Title: University of Washington Project Title: The Rockefeller University Project Title: John M Leong, M. California Institute of Technology Project Title: Keith Andrew Maggert, Ph.

University of Alabama Project Title: Broad Institute Project Title: Northwestern University Project Title: Harvard Medical School Project Title: Dartmouth College Project Title: University of California, Davis Project Title: Georgia Institute of Technology Project Title: University of North Carolina Project Title: Columbia University Project Title: The Broad Institute Project Title: University of Southern California Project Title: Johns Hopkins University Project Title: Stanford University Project Title: Cornell University Project Title: Augusto C Ochoa, M.

David Arnold Relman, M. Alice Y Ting, Ph. University of Minnesota, Minneapolis Project Title: Harvard University Project Title: RNS 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. RAG 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.

RNS 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. RAR 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.

RGM In the United States, more than , patients receive general anesthesia daily to safely undergo most surgical and many non-surgical procedures.

While Golic says they're fine, he said the two weren't really friends off the air, even noting that Greenberg once said he thought it was best if the two didn't hang out outside work. On the new morning show he'll be joined by Michelle Beadle and Jalen Rose.

While Greenberg's show is still a few months away, Golic's new radio show alongside Trey Wingo begins Nov. Golic told the Coloradoan he was in Colorado for a stem cell procedure, the Fort Collins newspaper reported his show with Wingo will be more like a "radio show on TV morning show with fun bits, entertainment and sports.

Only time will tell if ESPN's gamble was worth the risk. The Daily News Flash Newsletter. You are now following this newsletter.

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