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                "description": "Are stem cells patentable? What is the patenting process? What rights does a patent provide? Why should I patent?\n\nApplying for and obtaining a patent is a process that can be unpredictable and intimidating, although it does not necessarily need to be. Novice and experienced inventors often have questions regarding patenting and the patenting process. This e-book is provided to answer many questions regarding the patenting process before the United States Patent and Trademark Office (USPTO). It also generally describes the technologies typically patented in connection with regenerative medicine.\n\nThis e-book is provided for informational purposes only and should not replace legal advice, which is necessary to anticipate and address the nuances of the patenting process. In addition, there are issues that should be considered and addressed when considering patenting isolated stem cells and associated technologiessuch as the process for obtaining patent rights outside the United States, post-grant procedures for challenging patents, non-patent protection of intellectual property, and enforcement of patents through litigationwhich are beyond the scope of this chapter.",
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                "description": "Stroke is a major global health problem because of its large contribution to mortality, morbidity, and disability. The most common form of stroke is ischemic stroke which accounts for approximately 80% of all strokes. During the past decade, our knowledge of the molecular and cellular processes that contribute to stroke pathophysiology has increased substantially and offers many targets for future therapeutic strategies. This book provides an overview of the current knowledge of stroke pathophysiology and the mechanisms that interfere with recovery and regeneration. Moreover, this book reviews the latest advances in the development of future therapeutic strategies.",
                "author": "Christoph Kleinschnitz, Christiane Albert-Weissenberger, Antje Schmidt, Jens Minnerup",
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                "description": "The clinical syndrome of chronic heart failure (CHF) is the hallmark of progressive cardiac decompensation, one of the most common chronic medical conditions that affect around 2% of the adult population worldwide irrespective of ethnic and geographic origin (Anonymous). Apart from ischemic heart disease, hypertension, infection, and inflammation, several other etiologic factors account for irreparable and irreversible myocardial damage leading to heart failure (HF). Genetic and genomic factors are now increasingly identified as one of the leading underlying factors (Arab and Liu 2005). These factors may be related to pathogenic alterations (mutation or polymorphism) within specific cardiac genes, mutations in genes incorporating single or multiple molecular pathways (protein families) relevant to cardiac structure and/or function, genetic or genomic polymorphisms of uncertain significance (gene variants, single-nucleotide polymorphisms (SNPs), and copy number variations (CNVs)), and epigenetic or epigenomic changes that influence cardiac gene functions scattered across the human genome. Recent genetic and genomic studies in both systolic and diastolic ventricular dysfunction, the hallmark of CHF, have revealed a number of mutations in genes belonging to specific cardiac protein families. For example, around 200 mutations are now known to exist in around 15 genes coding for several different types of sarcomere proteins (Liew and Dzau 2004). The sarcomere protein family, alone, accounts for the bulk of inherited cardiomyopathies including hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), and left ventricular (LV) non-compaction (LVNC). In addition, there are several other potentially relevant factors involving different genes and genome-level elements. This article presents a systematic account on the available factual information and interpretations based on genetic and genomic studies in CHF (Liew and Dzau 2004). Genomic and molecular approaches have opened the way for a renewed debate for taxonomy of CHF (Ashrafian and Watkins 2007). The review draws attention to the potential diagnostic and therapeutic implications of genomic and transcriptional profiling in HF and translational genomics research that is likely to permit greater personalization of prevention and treatment strategies to address the complexities of managing clinical HF (Creemers, Wilde et al. 2011).",
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                "description": "The major purpose of this book is to review the evidence supporting the concept that intrinsic cell survival programs can be activated by a variety of mildly noxious stimuli or pharmacologic agents to confer protection against the deleterious effects of ischemia/reperfusion (I/R). We begin with a discussion of the concept of hormesis (a term used most extensively in the toxicologic literature which refers to biphasic cellular responses that depend on concentration or intensity of a stimulus), review the seminal studies that led to the discovery of the cardioprotective effects of ischemic preconditioning, and outline its therapeutic potential (Chapter 1). This is followed by a summary of our current understanding of the mechanisms of I/R injury (Chapter 2), as this provides several points of intervention in limiting postischemic tissue injury that may be targeted by the adaptive programs invoked by conditioning stimuli. Chapters 3 and 4 focus on the mechanisms underlying ischemic pre-, post-, and remote conditioning, which establishes the mechanistic rationale for development of pharmacologic conditioning strategies that may mimic the remarkably powerful effects of ischemic conditioning (and are covered in Chapter 5). Lifestyle interventions, including exercise, caloric restriction, and consumption of alcoholic beverages and/or phytochemicals, that may induce hormetic responses will also be reviewed in this chapter. While the promise for conditioning as a therapeutic approach is enormous, there are obstacles to its practical application in patients, which are covered in Chapter 6. The final chapter (Chapter 7) examines the extension of our mechanistic understanding of the signaling pathways invoked by conditioning stimuli into the realm of gene therapy and to the preservation of stem cell viability in the harsh ischemic environment as natural translational outgrowths of preconditioning into therapeutics.",
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                "description": "Epilepsy affects approximately 3% of the population, and is usually defined as a tendency to experience recurrent seizures arising from periodic neuronal hyperexcitability of unknown causes. Different genetic factors, through various mechanisms, can cause this abnormal neuronal behavior. The etiology of epilepsy is a major determinant of clinical course and prognosis. Many of the genes that have been implicated in idiopathic epilepsies code for ion channels, whereas a wide spectrum of syndromes where epilepsy is a main clinical feature are caused by mutated genes that are involved in functions as diverse as cortical development, brain malformations, mitochondrial function, and cell metabolism. Similarly, different conditions as hypoxia, trauma, infections, or metabolic unbalances can develop epileptic syndromes where upregulation of several genes could be related to the epileptogenic mechanisms. The most common human genetic epilepsies display a complex pattern of inheritance, and the susceptible genes are largely unknown. However, major advances have recently been made in our understanding of the genetic basis of monogenic inherited epilepsies. As we continue to unravel the molecular genetic basis for epilepsies, it will increasingly influence their classification and diagnosis. A majority of epileptic patients may control their crisis with anticonvulsant drugs, however 30%40% became refractory to pharmacological therapies and require surgical treatment. The challenge of the molecular revolution will be the design of the best treatment protocols based on genetic profiles that include both the specific mechanistic etiology of the epilepsies, as well as their potential refractory behavior to current medications. This includes also the design of new therapeutic agents and targets, so as to reduce the number of cases with refractory epilepsy and epileptogenesis, and perhaps avoid the current surgical treatment (a procedure that was first described more than 4000 years ago) except as a last option.",
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