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| Sep 30, 2007 | Molecular profiling of lung carcinoma: identifying clinically useful tumor markers for diagnosis and prognosis. | |||||||||||||||||
| The overall survival of patients with lung cancer is dismal despite extensive effort in improvement of diagnosis and treatment. A better understanding of the multistep genetic and epigenetic alterations in lung cancer pathogenesis and progression is necessary for development of improved diagnostic approaches and new targeted therapies. Identification of molecular alterations in the early lung carcinogenesis, together with advanced molecular techniques, may facilitate development of rapid and effective methods for early diagnosis and prognosis of lung carcinoma. In this review, we discuss current understanding of lung carcinogenesis and prospective molecular markers in lung cancer diagnosis. Although the impact of translating new technologies into clinical practice on survival has not been completely determined, they offer a new avenue of exciting novel approaches to early diagnosis of this deadly disease. | ||||||||||||||||||
| Sep 29, 2007 | Clinicians’ Guide to New Tools and Features of PubMed | |||||||||||||||||
| Practicing clinicians need to have the skills required to obtain up- to-date medical information to address both the expansion of scientific knowledge and patients' increasing use of the Internet. PubMed (www.pubmed.gov) allows clinicians free access to the largest biomedical resource available. This article is the third in a Mayo Clinic Proceedings series designed specifically to help clinicians unlock the tools and information available through this valuable resource. | ||||||||||||||||||
| Sep 28, 2007 | Embryonic stem cell proteomics | |||||||||||||||||
| Human embryonic stem cells potentially represent an unlimited source of cells and tissues for regenerative medicine. Understanding signaling events that drive proliferation and specialization of these cells into various differentiated derivatives is of utmost importance for controlling their behavior in vitro. Major progress has been made in unraveling these signaling events with large-scale studies at the transcriptional level, but analysis of protein expression, interaction and modification has been more limited, since it requires different strategies. Recent advances in mass spectrometry-based proteomics indicate that proteome characterization can contribute significantly to our understanding of embryonic stem cell biology. In this article, we review mass spectrometry-based studies of human and mouse embryonic stem cells and their differentiated progeny, as well as studies of conditioned media that have been reported to support self-renewal of the undifferentiated cells in the absence of the more commonly used feeder cells. In addition, we make concise comparisons with related transcriptome profiling reports. | ||||||||||||||||||
| Sep 27, 2007 | New Transcription Factors in Diagnostic Hematopathology | |||||||||||||||||
| The transcription factors (TFs) that controls the intricate machinery of multistep differentiation and activation programs of the lymphoid system, represent a complex array of proteins, whose identification and function has only in part been completed. TFs are usually expressed during specific differentiation or activation cellular programs, making them interesting tools in diagnostic immunohistochemistry. In fact, the specificity of some of these TFs for lineage or activation/differentiation passages or their abnormal expression in specific disease entity, represents a feature that has been exploited in diagnostic/prognostic immunohistochemistry. Bcl-6 was the prototype of this class of markers. Currently, the expanding knowledge of the TFs involved in the differentiation programs and in the activation processes of T-lymphocyte and B-lymphocyte in normal and neoplastic conditions and the availability of antibodies able to efficiently recognize these TFs in histologic material, represent a powerful tool in diagnostic hematopathology. In this review we will consider the basic biologic aspects and the applications in hematopathology of some of the lymphocyte-related TFs, including Pax5/BSAB, MUM1/IRF4, BOB1, Oct-2, T-bet, and FOXP3. This field is rapidly evolving, as witnessed by the ongoing growing number of novel TFs with possible diagnostic applications appearing in the literature. | ||||||||||||||||||
| Sep 26, 2007 | Chemokine:Receptor Structure, Interactions, and Antagonism | |||||||||||||||||
| Chemokines are critical mediators of cell migration during routine immune surveillance, inflammation, and development. Chemokines bind to G protein-coupled receptors and cause conformational changes that trigger intracellular signaling pathways involved in cell movement and activation. Although chemokines evolved to benefit the host, inappropriate regulation or utilization of these proteins can contribute to or cause many diseases. Specific chemokine receptors provide the portals for HIV to get into cells, and others contribute to inflammatory diseases and cancer. Thus, there is significant interest in developing receptor antagonists. To this end, the structures of ligands coupled with mutagenesis studies have revealed mechanisms for antagonism based on modified proteins. Although little direct structural information is available on the receptors, binding of small molecules to mutant receptors has allowed the identification of key residues involved in the receptor-binding pockets. In this review, we discuss the current knowledge of chemokine:receptor structure and function, and its contribution to drug discovery. | ||||||||||||||||||
| Sep 25, 2007 | Cardiac regeneration by resident stem and progenitor cells in the adult heart | |||||||||||||||||
| Two main pieces of data have created a new field in cardiac research. First, the traditional view on the heart as a postmitotic organ has been challenged by the finding of small dividing cells in the heart expressing cardiac contractile proteins with stem cell properties and, second, cellular therapy of the diseased heart using a variety of different cells has shown encouraging effects on cardiac function. These findings immediately raise questions like "what is the identity and origin of the cardiac progenitor cells?","which molecular factors are involved in their mobilization and differentiation?", and "can these cells repair the damaged heart?" This review will address the state of current answers to these questions. Emerging evidence suggests that several subpopulations of cardiac stem or progenitor cells (CPCs) reside within the adult heart. CPCs with the ability to differentiate into all the constituent cells in the adult heart including cardiac myocytes, vascular smooth muscle and endothelial cells have been identified. Valuable knowledge has been obtained from the large number of animal studies and a number of small clinical trials that have utilized a variety of adult stem cells for regenerating infarcted hearts. However, contradictory reports on the regenerative potential of the CPCs exist, and the mechanisms behind the reported hemodynamic effects are intensely debated. Besides directly replenishing cardiac tissue, CPCs could also function by stimulating angiogenesis and improving survival of existing cells by secretion of paracrine factors. With this review we suggest that a better understanding of CPC biology will be pivotal for progressing therapeutic cardiac regeneration. This includes an extended knowledge of the molecular mechanisms behind their mobilization, differentiation, survival and integration in the myocardium. | ||||||||||||||||||
| Sep 24, 2007 | Circulating nucleic acids (CNAs) and cancer—A survey | |||||||||||||||||
| It has been known for decades that it is possible to detect small amounts of extracellular nucleic acids in plasma and serum of healthy and diseased human beings. The unequivocal proof that part of these circulating nucleic acids (CNAs) is of tumor origin, initiated a surge of studies which confirmed and extended the original observations. In the past few years many experiments showed that tumor-associated alterations can be detected at the DNA and RNA level. At the DNA level the detection of point mutations, microsatellite alterations, chromosomal alterations, i.e. inversion and deletion, and hypermethylation of promoter sequences were demonstrated. At the RNA level the overexpression of tumor-associated genes was shown. These observations laid the foundation for the development of assays for an early detection of cancer as well as for other clinical means. | ||||||||||||||||||
| Sep 23, 2007 | Bioinformatics approaches in the study of cancer. | |||||||||||||||||
| A revolution is underway in the approach to studying the genetic basis of cancer. Massive amounts of data are now being generated via high-throughput techniques such as DNA microarray technology and new computational algorithms have been developed to aid in analysis. At the same time, standards-based repositories, including the Stanford Microarray Database and the Gene Expression Omnibus have been developed to store and disseminate the results of microarray experiments. Bioinformatics, the convergence of biology, information science, and computation, has played a key role in these developments. Recently developed techniques include Module Maps, SLAMS (Stepwise Linkage Analysis of Microarray Signatures), and COPA (Cancer Outlier Profile Analysis). What these techniques have in common is the application of novel algorithms to find high-level gene expression patterns across heterogeneous microarray experiments. Large-scale initiatives are underway as well. The Cancer Genome Atlas (TCGA) project is a logical extension of the Human Genome Project and is meant to produce a comprehensive atlas of genetic changes associated with cancer. The Cancer Biomedical Informatics Grid (caBIG), led by the NCI, also represents a colossal initiative involving virtually all aspects of cancer research and may help to transform the way cancer research is conducted and data are shared. | ||||||||||||||||||
| Sep 22, 2007 | Ratcheting mRNA out of the Nucleus | |||||||||||||||||
| Export of mature mRNA to the cytoplasm is the culmination of the nuclear portion of eukaryotic gene expression. After transport-competent mature mRNP export complexes are formed in the nucleus, their passage through nuclear pore complexes (NPCs) is facilitated by the Mex67:Mtr2 heterodimer. At the NPC cytoplasmic face, mRNP remodeling prevents its return to the nucleus and so functions as a molecular ratchet imposing directionality on transport. In budding yeast, recent work suggests that the DEAD-box helicase Dbp5 remodels mRNPs at the NPC cytoplasmic face by removing Mex67 and that the Dbp5 ATPase is activated by Gle1 and inositol hexaphosphate (IP(6)). | ||||||||||||||||||
| Sep 21, 2007 | Systemic hypertension | |||||||||||||||||
| Hypertension is a growing public health problem worldwide. Only 37% of American hypertensives currently have their blood pressures controlled. Hypertension is traditionally diagnosed in the medical office, but both home and ambulatory blood pressure monitoring can help. Lifestyle modifications are recommended for everyone who has higher than "normal" blood pressure (<120/80 mm Hg). Voluminous clinical trial data support beginning drug therapy with low-dose chlorthalidone, unless the patient has a specific indication for a different drug. Additional drugs (typically in the sequence, angiotensin converting-enzyme inhibitor or angiotensin receptor blocker, calcium antagonist, beta-blocker, alpha-blocker, aldosterone antagonist, direct vasodilator, and centrally acting alpha(2)-agonist) can be added to achieve the blood pressure goal (usually <140/90 mm Hg, but <130/80 mm Hg for diabetics and those with chronic kidney disease). Special circumstances exist for treatment of hypertension in pregnancy, in childhood, in the elderly, and in both extremes of blood pressure (pre-hypertension or hypertensive emergencies). | ||||||||||||||||||
| Sep 20, 2007 | Filling out the Hippo pathway | |||||||||||||||||
| How cell numbers are controlled during organ development is a problem that is still in need of answers. Recent studies in Drosophila melanogaster have delineated a novel signalling pathway, the Hippo pathway, which has an important role in restraining cell proliferation and promoting apoptosis in differentiating epithelial cells. Much like cancer cells, cells that contain mutations for components of the Hippo pathway proliferate inappropriately and have a competitive edge in genetically mosaic tissues. Although poorly characterized in mammals, several components of the Hippo pathway seem to be tumour suppressors in humans. | ||||||||||||||||||
| Sep 19, 2007 | Self-eating and self-killing: crosstalk between autophagy and apoptosis | |||||||||||||||||
| The functional relationship between apoptosis ('self-killing') and autophagy ('self-eating') is complex in the sense that, under certain circumstances, autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis), whereas in other cellular settings, it constitutes an alternative cell-death pathway. Autophagy and apoptosis may be triggered by common upstream signals, and sometimes this results in combined autophagy and apoptosis; in other instances, the cell switches between the two responses in a mutually exclusive manner. On a molecular level, this means that the apoptotic and autophagic response machineries share common pathways that either link or polarize the cellular responses. | ||||||||||||||||||
| Sep 18, 2007 | Targeting the glycans of glycoproteins: a novel paradigm for antiviral therapy | |||||||||||||||||
| Several chronic viral infections (such as HIV and hepatitis C virus) are highly prevalent and are a serious health risk. The adaptation of animal viruses to the human host, as recently exemplified by influenza viruses and the severe acute respiratory syndrome coronavirus, is also a continuous threat. There is a high demand, therefore, for new antiviral lead compounds and novel therapeutic concepts. In this Review, an original therapeutic concept for suppressing enveloped viruses is presented that is based on a specific interaction of carbohydrate-binding agents (CBAs) with the glycans present on viral-envelope glycoproteins. This approach may also be extended to other pathogens, including parasites, bacteria and fungi. | ||||||||||||||||||
| Sep 17, 2007 | Engineering targeted viral vectors for gene therapy | |||||||||||||||||
| To achieve therapeutic success, transfer vehicles for gene therapy must be capable of transducing target cells while avoiding impact on non-target cells. Despite the high transduction efficiency of viral vectors, their tropism frequently does not match the therapeutic need. In the past, this lack of appropriate targeting allowed only partial exploitation of the great potential of gene therapy. Substantial progress in modifying viral vectors using diverse techniques now allows targeting to many cell types in vitro. Although important challenges remain for in vivo applications, the first clinical trials with targeted vectors have already begun to take place. | ||||||||||||||||||
| Sep 16, 2007 | Modelling of the blood–brain barrier in drug discovery and development | |||||||||||||||||
| The market for neuropharmaceuticals is potentially one of the largest sectors of the global pharmaceutical market owing to the increase in average life expectancy and the fact that many neurological disorders have been largely refractory to pharmacotherapy. The brain is a delicate organ that can efficiently protect itself from harmful compounds and precisely regulate its microenvironment. Unfortunately, the same mechanisms can also prove to be formidable hurdles in drug development. An improved understanding of the regulatory interfaces that exist between blood and brain may provide novel and more effective strategies to treat neurological disorders. | ||||||||||||||||||
| Sep 15, 2007 | Maximizing mouse cancer models | |||||||||||||||||
| Over the past 15 years it has become clear that mutations in genes that regulate endocrine signalling pathways can prolong lifespan. Lifespan can be increased by altered endocrine signalling in a group of cells or a single tissue, which indicates that crosstalk between tissues functions to coordinate ageing of the organism. These endocrine pathways might serve as targets for the manipulation of the ageing process and prevention of age-related diseases. | ||||||||||||||||||
| Sep 14, 2007 | Maximizing mouse cancer models | |||||||||||||||||
| Animal models of cancer provide an alternative means to determine the causes of and treatments for malignancy, thus representing a resource of immense potential for cancer medicine. The sophistication of modelling cancer in mice has increased to the extent that investigators can both observe and manipulate a complex disease process in a manner impossible to perform in patients. However, owing to limitations in model design and technology development, and the surprising underuse of existing models, only now are we realising the full potential of mouse models of cancer and what new approaches are needed to derive the maximum value for cancer patients from this investment. | ||||||||||||||||||
| Sep 13, 2007 | Getting to the site of inflammation: the leukocyte adhesion cascade updated | |||||||||||||||||
| Neutrophil recruitment, lymphocyte recirculation and monocyte trafficking all require adhesion and transmigration through blood-vessel walls. The traditional three steps of rolling, activation and firm adhesion have recently been augmented and refined. Slow rolling, adhesion strengthening, intraluminal crawling and paracellular and transcellular migration are now recognized as separate, additional steps. In neutrophils, a second activation pathway has been discovered that does not require signalling through G-protein-coupled receptors and the signalling steps leading to integrin activation are beginning to emerge. This Review focuses on new aspects of one of the central paradigms of inflammation and immunity - the leukocyte adhesion cascade. | ||||||||||||||||||
| Sep 12, 2007 | Small-molecule therapies for cardiac hypertrophy: moving beneath the cell surface | |||||||||||||||||
| Pathological stress from cardiovascular disease stimulates hypertrophy of heart cells, which increases the risk of cardiac morbidity and mortality. Recent evidence has indicated that inhibiting such hypertrophy could be beneficial, encouraging drug discovery and development efforts for agents that could achieve this goal. Most existing therapies that have antihypertrophic effects target outside-in signalling in cardiac cells, but their effectiveness seems limited, and so attention has recently turned to the potential of targeting intracellular signalling pathways. Here, we focus on new developments with small-molecule inhibitors of cardiac hypertrophy, summarizing both agents that have been in or are poised for clinical testing, and pathways that offer further promising potential therapeutic targets. | ||||||||||||||||||
| Sep 11, 2007 | Translation matters: protein synthesis defects in inherited disease | |||||||||||||||||
| The list of genetic diseases caused by mutations that affect mRNA translation is rapidly growing. Although protein synthesis is a fundamental process in all cells, the disease phenotypes show a surprising degree of heterogeneity. Studies of some of these diseases have provided intriguing new insights into the functions of proteins involved in the process of translation; for example, evidence suggests that several have other functions in addition to their roles in translation. Given the numerous proteins involved in mRNA translation, it is likely that further inherited diseases will turn out to be caused by mutations in genes that are involved in this complex process. | ||||||||||||||||||
| Sep 10, 2007 | Initiation to end point: the multiple roles of fibroblast growth factors in neural development | |||||||||||||||||
| From a wealth of experimental findings, derived from both in vitro and in vivo experiments, it is becoming clear that fibroblast growth factors regulate processes that are central to all aspects of nervous system development. Some of these functions are well known, whereas others, such as the roles of these proteins in axon guidance and synaptogenesis, have been established only recently. The emergent picture is one of remarkable economy, in which this family of ligands is deployed and redeployed at successive developmental stages to sculpt the nervous system. | ||||||||||||||||||
| Sep 9, 2007 | Beyond toothpicks: new methods for isolating mutant bacteria | |||||||||||||||||
| Over the past 50 years genetic analysis in microbiology has relied predominantly on selections and plate assays using chromogenic enzyme substrates - for example, X-gal assays for the detection of beta-galactosidase activity. Recent advances in fluorescent assays and high throughput screening technologies have paved the way for the rapid isolation of mutants that confer complex phenotypes and for the quantitative analysis of the evolution of new traits in bacterial populations. This Review highlights the power of novel single-cell screening technologies and their applications to genetics, evolution and the biotechnological uses of bacteria. | ||||||||||||||||||
| Sep 8, 2007 | RNA-binding proteins: modular design for efficient function | |||||||||||||||||
| Many RNA-binding proteins have modular structures and are composed of multiple repeats of just a few basic domains that are arranged in various ways to satisfy their diverse functional requirements. Recent studies have investigated how different modules cooperate in regulating the RNA-binding specificity and the biological activity of these proteins. They have also investigated how multiple modules cooperate with enzymatic domains to regulate the catalytic activity of enzymes that act on RNA. These studies have shown how, for many RNA-binding proteins, multiple modules define the fundamental structural unit that is responsible for biological function. | ||||||||||||||||||
| Sep 7, 2007 | Treatment of obesity | |||||||||||||||||
| For primary care physicians, obesity is one of the most challenging problems confronted in office practice. The disorder is Increasing in prevalence despite the efforts of both patients and physicians. Treatment requires a multimodality approach that addresses diet, physical activity, and behavioral issues. Medication and surgical approaches may be appropriate as well. This review outlines the evidence for each approach, suggests how primary care physicians can best help obese patients, and provides practical tips for weight loss. | ||||||||||||||||||
| Sep 6, 2007 | Cross-species microarray hybridizations: a developing tool for studying species diversity | |||||||||||||||||
| The use of cross-species hybridization (CSH) to DNA microarrays, in which the target RNA and microarray probe are from different species, has increased in the past few years. CSH is used in comparative, evolutionary and ecological studies of closely related species, and for gene-expression profiling of many species that lack a representative microarray platform. However, unlike species-specific hybridization, CSH is still considered a non-standard use of microarrays. Here, we present the recent developments in the field of CSH for cDNA and oligomer microarray platforms. We discuss issues that influence the quality of CSH results, including platform choice, experiment design and data analysis, and suggest strategies that can lead to improvement of CSH studies to investigate species diversity. | ||||||||||||||||||
| Sep 5, 2007 | A review of the genetics of essential hypertension | |||||||||||||||||
| Essential hypertension affects more than 20% of the adult population, and has a multifactorial origin arising from an interaction between susceptibility genes and environmental factors. Several strategies have been used to identify hypertension susceptibility genes. This review highlights recent efforts in genetic dissection of essential hypertension. Recently, further chromosomal regions harboring blood pressure loci have emerged in genome-wide linkage studies. Findings from a new systematic two-dimensional genome scan are presented, as well as sex-specific loci linked to hypertension in inbred rodent models. Many case-control association studies have been carried out, but results so far have been equivocal. This review discusses some interesting studies combining linkage and association strategies using gene-gene interactions, and studies the use of haplotypes instead of SNPs. | ||||||||||||||||||
| Sep 4, 2007 | Therapeutic RNA interference for neurodegenerative diseases: From promise to progress | |||||||||||||||||
| RNA interference (RNAi) has emerged as a powerful tool to manipulate gene expression in the laboratory. Due to its remarkable discriminating properties, individual genes, or even alleles can be targeted with exquisite specificity in cultured cells or living animals. Among its many potential biomedical applications, silencing of disease-linked genes stands out as a promising therapeutic strategy for many incurable disorders. Neurodegenerative diseases represent one of the more attractive targets for the development of therapeutic RNAi. In this group of diseases, the progressive loss of neurons leads to the gradual appearance of disabling neurological symptoms and premature death. | ||||||||||||||||||
| Sep 3, 2007 | How a Single T Cell Receptor Recognizes Both Self and Foreign MHC | |||||||||||||||||
| alphabeta T cell receptors (TCRs) can crossreact with both self- and foreign- major histocompatibility complex (MHC) proteins in an enigmatic phenomenon termed alloreactivity. Here we present the 2.35 A structure of the 2C TCR complexed with its foreign ligand H-2L(d)-QL9. Surprisingly, we find that this TCR utilizes a different strategy to engage the foreign pMHC in comparison to the manner in which it recognizes a self ligand H-2K(b)-dEV8. 2C engages both shared and polymorphic residues on L(d) and K(b), as well as the unrelated QL9 and dEV8 peptide antigens, in unique pair-wise contacts, resulting in greater structural complementarity with the L(d)-QL9 complex. In the structure of an engineered, high-affinity 2C TCR variant bound to H-2L(d)-QL9, the "wild-type" TCR-MHC binding orientation persists despite modified TCR-CDR3alpha interactions with peptide. Thus, a single TCR recognizes two globally similar, but distinct ligands by divergent mechanisms, indicating that receptor-ligand crossreactivity can occur in the absence of molecular mimicry. | ||||||||||||||||||
| Sep 2, 2007 | Reviews of Translational Medicine and Genomics in Cardiovascular Disease: New Disease Taxonomy and Therapeutic Implications | |||||||||||||||||
| The enduring subdivision of cardiomyopathies into hypertrophic (HCM), dilated (DCM), and restrictive (RCM) categories reflects the emphasis of traditional classifications on morphology. Rapid advances in the genetic interrogation of these disorders have redefined their taxonomy and revealed potential conflicts between the old and new classifications. Hypertrophic cardiomyopathy has been redefined as a disease of perturbed sarcomere function. Dilated cardiomyopathy is a disease that results from more varied perturbations, including, but not limited to, defects of the cytoskeleton. Positional cloning and candidate gene approaches have been successful in identifying >40 disease loci, many of which have led to disease genes in HCM, DCM, RCM, and arrhythmogenic right ventricular cardiomyopathy. These findings provide mechanistic insights, permit genetic screening, and to a limited extent, facilitate prognostication. Although single gene analyses rapidly focus down to the underlying mechanistic pathways, they do not take account of all relevant variation in the human genome. Correspondingly, advances in genomics, through microarrays, have facilitated characterization of these broader downstream elements. As well as refining the taxonomic reclassification of cardiomyopathies, these genomic approaches, coupled with functional studies, have identified novel potential therapeutic targets, such as cardiac energetics, calcium handling, and apoptosis. We review the successes and pitfalls of genetic and genomic approaches to cardiomyopathy and their impact on current and future clinical care. | ||||||||||||||||||
| Sep 1, 2007 | Modulation of mRNA stability as a novel therapeutic approach | |||||||||||||||||
| During the last decade evidence has accumulated that modulation of mRNA stability plays a central role in cellular homeostasis, including cell differentiation, proliferation and adaptation to external stimuli. The functional relevance of posttranscriptional gene regulation is highlighted by many pathologies, wherein occurrence tightly correlates with a dysregulation in mRNA stability, including chronic inflammation, cardiovascular diseases and cancer. Most commonly, the cis-regulatory elements of mRNA decay are represented by the adenylate- and uridylate (AU)-rich elements (ARE) which are specifically bound by trans-acting RNA binding proteins, which finally determine whether mRNA decay is delayed or facilitated. Regulation of mRNA decay by RNA stabilizing and RNA destabilizing factors is furthermore controlled by different intrinsic and environmental stimuli. The modulation of mRNA binding proteins, therefore, illuminates a promising approach for the pharmacotherapy of those key pathologies mentioned above and characterized by a posttranscriptional dysregulation. Most promisingly, intracellular trafficking of many of the mRNA stability regulating factors is, in turn, regulated by some major signaling pathways, including the mitogen-activated protein kinase (MAPK) cascade, the AMP-activated kinase (AMPK) and the protein kinase (PK) C (PKC) family. In this review, we present timely examples of genes regulated by mRNA stability with a special focus on signaling pathways involved in the ARE-dependent mRNA decay. A better understanding of these processes may form the basis for the development of novel therapeutics to treat major human diseases. |
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