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1
Muise, Brandon. Examining caspase mediated apoptotic pathways through RNAi as a means of procaspase downregulation. Sudbury, Ont: Laurentian University, 2006.
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2
Porges, Stephen W. Vagal Pathways. Edited by Emma M. Seppälä, Emiliana Simon-Thomas, Stephanie L. Brown, Monica C. Worline, C. Daryl Cameron, and James R. Doty. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190464684.013.15.
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In this chapter, contemplative practices are conceptualized as methods that function as neural exercises enhancing vagal regulation of the autonomic nervous system. The model presented proposes that specific voluntary behaviors (e.g., breath, vocalizations, and posture), which characterize ancient rituals and form the core of contemplative practices, can trigger a physiological state mediated by vagal pathways that fosters health and optimizes subjective experiences. The model emphasizes that, in order for the positive benefits of contemplative practices to be experienced, the rituals associated with contemplative practices (e.g., chants, prayers, meditation, and dance) must be performed in a context defined by physical features that are calming and soothing and promote feelings of safety.
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Sukhai, Mahadeo A. Cytokine-mediated pathways of mdr1 gene regulation in cultured rat hepatocytes. 2001.
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Cozza, Cynthia L. A model for the prediction of biologically mediated reductive dechlorination pathways. 1990.
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Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.
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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.
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Lee, David WK. Dopamine-induced Gbetagamma-mediated inhibitory pathways in vesicle release in an identified respiratory Lymnaea neuron. 2007.
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Herman, James P. Limbic Pathways to Stress Control. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0008.
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Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.
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Blunt, MO, A. Stannard, E. Pauliac-Vaujour, CP Martin, Ioan Vancea, Milovan Suvakov, Uwe Thiele, Bosiljka Tadic, and P. Moriarty. Patterns and pathways in nanoparticle self-organization. Edited by A. V. Narlikar and Y. Y. Fu. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199533046.013.8.
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This article reviews relatively recent forms of self-assembly and self-organization that have demonstrated particular potential for the assembly of nanostructured matter, namely biorecognition and solvent-mediated dynamics. It first considers the key features of self-assembled and self-organized nanoparticle arrays, focusing on the self-assembly of nanoparticle superlattices, the use of biorecognition for nanoparticle assembly, and self-organizing nanoparticles. It then describes the mechanisms and pathways for charge transport in nanoparticle assemblies, with particular emphasis on the relationship between the current–voltage characteristics and the topology of the lattice. It also discusses single-electron conduction in nanoparticle films as well as pattern formation and self-organization in dewetting nanofluids.
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Huang, Ruili, and Menghang Xia, eds. Tox21 Challenge to Build Predictive Models of Nuclear Receptor and Stress Response Pathways as Mediated by Exposure to Environmental Toxicants and Drugs. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-197-5.
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Dupuy, Béatrice, and Muriel Grosbois, eds. Language learning and professionalization in higher education: pathways to preparing learners and teachers in/for the 21st century. Research-publishing.net, 2020. http://dx.doi.org/10.14705/rpnet.2020.44.9782490057757.
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In this volume, language learning and professionalization are explored by addressing the existing gap between pressing needs for enhanced soft skills in work environments wherein technology-mediated, multilingual communication is increasingly the norm, and current foreign language teaching and learning offerings in higher education. Considering theoretical, methodological, and pedagogical perspectives for preparing language learners and teachers in/for the 21st century, this volume’s eight chapters underscore that research findings should inform the design of learning experiences so that people’s communication needs in fast-changing work environments are met and the link between language education and professionalization, within a lifelong learning perspective, is sustained.
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Heeringa, Peter, and Coen A. Stegeman. The patient with vasculitis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0158.
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Vasculitis is an inflammatory destructive process affecting blood vessels resulting in fibrinoid necrosis of the vessel wall that eventually can lead to occlusion of the vascular lumen and organ failure. Vasculitis may be the primary manifestation of a disease, or be a secondary manifestation of another underlying disease.The pathogenesis of vasculitis is complex, involving innate and adaptive immune effector mechanisms that range from cell-mediated inflammation, immune-complex-mediated inflammation, and inflammation triggered by autoantibodies. Here it is discussed with respect to general pathogenic patterns and more disease-specific pathogenic pathways related to primary and secondary vasculitic syndromes.
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Gonzalez-Albarrán, Olga, and Luis M. Ruilope. The kidney and control of blood pressure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0210.
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The kidneys can be at the root of the development of arterial hypertension or they can participate in the maintenance of hypertension and its sequels. Renal alterations interfering with the regulation of sodium homeostasis or facilitating the generation of vasoconstrictors, particularly angiotensin II, are involved in the dysregulation of arterial blood pressure that underlies the development of arterial hypertension. The biology of angiotensin is described in detail.The kidneys are also the mediator of hypertension in such examples as renal ischaemia and hyperaldosteronism. The role of renal nerves, and renal depressor substances, are also described.Transplantation experiments in animals and observations in human transplantation, as well as some primary gene defects, show the importance of renal mechanisms in hypertension. Once kidneys have been damaged, they often contribute to an increase in arterial pressure. Salt sensitivity is probably a major part of the mechanism, but it is mediated by multiple pathways.
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Patisaul, Heather B., and Scott M. Belcher. The Neuroendocrine System and General Mechanisms of Endocrine Disruption. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0004.
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The neuroendocrine system is the interface between the endocrine and nervous systems. This chapter presents an overview of the neuroendocrine system and endogenous hormones, with a primary focus on the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid axis (HPT). The importance of impacts of exogenous compounds, both natural and man-made, on the neuroendocrine system is discussed, with a focus on endocrine-disruptive actions of plant-derived phytoestrogens and the role of the aryl hydrocarbon receptor as an environmental sensor. The impacts of EDCs on feed-forward and negative feedback regulation of neuroendocrine functions, including those mediated by estrogen, androgen, and thyroid pathways, as well as other less studied pathways of hormonal signaling that involve disruption of neurosteroids, peptide hormones, and adrenal hormone signaling are also presented.
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Colombetti, Giovanna, and Neil Harrison. From physiology to experience: Enriching existing conceptions of “arousal” in affective science. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198811930.003.0013.
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This chapter examines the notion of “arousal”, an influential notion in affective science referring to the degree of an individual’s “activation” or “excitement” during an emotional state. It considers this notion specifically in relation to interoception, defined broadly as “sensitivity to stimuli arising inside the organism.” “Physiological arousal” is distinguished from “experienced arousal” and it is argued that both need to be characterized more broadly than commonly done. Physiological arousal cannot be reduced to sympathetic activation, as it involves complex interactions between multiple functionally distinct pathways within sympathetic and parasympathetic divisions of the autonomic nervous system, as well as endocrine and immune systems, and even the gut microbiota. Relatedly, experienced arousal does not reduce to the perception of changes in the body sensed by visceral afferents in response to autonomic nervous system activity but also includes humorally mediated interoceptive pathways, somatic sensations of various kinds, and “background” bodily feelings.
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Félétou, Michel. Endothelium, Part II: EDHF-Mediated Responses the Classical Pathway. Morgan & Claypool Life Science Publishers, 2011.
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Chassin, Laurie, Moira Haller, Matthew Lee, Elizabeth Handley, Kaitlin Bountress, and Iris Beltran. Familial Factors Influencing Offspring Substance Use and Dependence. Edited by Kenneth J. Sher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199381678.013.008.
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This chapter reviews evidence concerning familial influences on the development of offspring substance use disorders (SUDs). Familial influences are diverse and operate on multiple levels, including heritable individual differences, parent–child relationships, parenting practices (both general and substance use-specific), sibling influences, and the effects of the broader family environment. Moreover, familial factors both influence and interact with other social contextual influences on offspring substance use outcomes, including peer groups, schools, and neighborhoods. Thus, familial influences operate across development, on multiple levels, and within complex, multivariate, mediated, and moderated pathways to influence offspring substance use outcomes from initial substance use onset to the remediation of clinical SUDs.
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Gunawardana, Geeth. Inhibition of intrinsic and extrinsic pathway-mediated apoptosis by cadmium. 2004.
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Feletou, Michel. Endothelium, the Part 2 : Edhf: -Mediated Responses the Classical Pathway. Morgan & Claypool Life Science Publishers, 2011.
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19
Baudouin, Simon, and Steve Ball. Normal physiology of the endocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0249.
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The endocrine system describes an array of chemical signals (hormones). Working in concert with the nervous system, the endocrine system forms a complex neurohumoral network, communicating changes in the environment to facilitate adaptive responses and serving to integrate those responses in a coherent, coordinated manner. The endocrine system has inherent rhythmicity, which has important implications for the integration and coordination of metabolism, and how we measure endocrine signals in clinical settings. At a cellular level, hormone action is mediated through a series of discrete, but interacting signal transduction pathways. This chapter outlines a functional design approach to endocrinology; providing a framework covering the principles of hormone regulation and hormone action—critical for understanding the role of the endocrine system in physiology and pathophysiology.
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Dalbeth, Nicola. Pathophysiology of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0039.
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The clinical features of gout occur in response to monosodium urate (MSU) crystals. Gout should be considered a chronic disease of MSU crystal deposition. A number of pathophysiological checkpoints are required for development of gout. First, elevated urate concentrations are required: urate overproduction and underexcretion contribute to total urate balance. Overproduction occurs due to alterations in the purine synthesis and degradation pathways. Renal underexcretion is an important cause of elevated serum urate concentrations (hyperuricaemia), and occurs through alterations in the urate transporters within the renal tubule (collectively known as the urate transportasome). Gut underexcretion (extrarenal urate underexcretion) also contributes to development of hyperuricaemia. The next checkpoint is MSU crystal formation. In some individuals with evidence of MSU crystal deposition, symptomatic gout develops. The acute inflammatory response to MSU crystals represents a self-limiting sterile acute auto-inflammatory response which is mediated by the innate immune system activation. Interleukin 1 beta is the key cytokine that contributes to the acute inflammatory response to MSU crystals. In some patients, advanced gout may occur with structural joint damage. Joint damage in gout is mediated both by direct effects of MSU crystals on joint tissue and by indirect effects of joint inflammation. In addition to their central role in pathogenesis of gout, MSU crystals have a physiological role, particularly as an adjuvant or ‘danger signal’ in immune surveillance.
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Patisaul, Heather B., and Scott M. Belcher. Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0005.
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In this chapter, the current understanding of the mechanisms of endocrine disruption on the brain and nervous system are presented. Because the overwhelming majority of mechanistic studies on EDCs have focused on the actions mediated by nuclear hormone receptors, this mechanisms is described in detail. The chapter also discusses the classic transcriptional mechanisms of steroid action and the impact of EDCs on rapid signaling (non-genomic) mechanisms. It presents an overview of the enzymes and pathways involved in the biosynthesis of steroid hormones, which are critical to proper functioning of the HPA and HPG axis, and the neuroactive steroids synthesized and active in the mammalian brain. The potential for EDCs to alter metabolic enzymes, with a focus on possible targets in the metabolic blood-brain barrier, is presented as a potential, though largely unexplored, mode of EDC action in the brain.
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Mease, Philip. Biologic treatments for psoriatic arthritis apart from TNF inhibition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0030.
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Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressive structural damage of joints. However, not all patients responded to these agents and many patients displayed initial response which waned over time, partly due to immunogenicity (development of antibodies which blocked full therapeutic effect of the biologic protein), or because of tolerability and side effect issues. Thus, it has been important to develop new medicines which target other key cytokines and immunologic pathways. Several medicines with a different mechanism of action have been approved or are in development for the treatment of PsA. Ustekinumab inhibits both IL12 and IL23 and thus is felt to work in both the TH1 and TH7 pathways of inflammation. The oral medicine apremilast inhibits phosphodiesterase 4, thus modulating the cyclic AMP pathway in immunologic cells, yielding an anti-inflammatory effect. Both of these medicines have been approved for the treatment of PsA as well as psoriasis. An emerging group of therapies, the IL17 inhibitors, has demonstrated significant effectiveness in psoriasis and PsA and one of these, Secukinumab, has been approved for psoriasis, PsA, and AS. Other medicines in development include the co-stimulatory blockade agent, abatacept, oral Janus Kinase (JAK) inhibitors, and an emerging group of therapies which inhibit IL23. As modulators of immune cell function, these agents have the potential to increase risk for infection, as well as other side effects. These must be discussed with the patient and considered when determining overall risk benefit analysis regarding their use. The emergence of medicines with a different mechanism of action than TNF inhibition has broadened and strengthened our ability to effectively treat PsA.
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Herrero, Rolando, and Raul Murillo. Cervical Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0048.
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Cervical cancer is the fourth most common cancer in women worldwide, with more than 500,000 cases and 250,000 deaths per year. The disease is characterized by marked regional differences, with more than 80% of the cases and deaths occurring in developing countries. The etiology and natural history of the disease are very well studied, with persistent infection with one of thirteen human papillomavirus (HPV) types now considered to be a necessary cause. The molecular mechanisms have also been elucidated and are mediated mainly by the expression of viral oncogenes that interfere with cellular pathways. The two most common HPV types, namely HPV-16 and HPV-18, are associated with about 70% of all cases around the world. Immunologic (e.g., HIV infection), hormonal (e.g., high parity), environmental (e.g., smoking), and genetic (e.g., HLA type) cofactors determine the risk of persistence and cancer among women harboring HPV infection.
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Medjeral-Thomas, Nicholas, Anna Richards, and Matthew C. Pickering. Molecular basis of complement-mediated renal disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0333.
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Abnormal regulation of complement is intimately associated with C3 glomerulopathy and atypical haemolytic uraemic syndrome. Atypical haemolytic uraemic syndrome is characterized by renal thrombotic microangiopathy due to an inability to regulate complement activation along the renal endothelium. The development of thrombosis is critically dependent on the ability to activate C5. Eculizumab, a monoclonal anti-C5 antibody, is an effective therapy for this condition. C3 glomerulopathy refers to glomerular lesions characterized by accumulation of C3 in the absence of immunoglobulin. The prototypic example is dense deposit disease. This condition is associated with impaired regulation of the alternative pathway in plasma. In other subtypes of C3 glomerulopathy, familial studies have identified mutations within the complement factor H-related protein family. Polymorphic variation within this protein family also influences susceptibility to IgA nephropathy. The mechanism underlying these associations remains unknown and is the subject of ongoing research efforts.
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Hyysalo, Sampsa, and Jouni K. Juntunen. User Innovation and Peer Assistance in Small-Scale Renewable Energy Technologies. Edited by Debra J. Davidson and Matthias Gross. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190633851.013.22.
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There have been many attempts to include citizens as more active players in the proliferation of renewable energy technologies. However, the roles that citizen users play in renewables proliferation are not limited to adoption, but include technological domestication, innovation, and market creation. This chapter first reviews innovation by citizen users in the early phases of small-scale renewable energy technologies (S-RET) technology development in wind turbines, solar collectors, and low-energy housing. It then examines user innovation and peer assistance in the later phases of diffusion in air-source and ground-source heat pumps, pellet-burning systems, and solar collectors. It reviews research user motivations, diffusion pathways, and peer intermediation, and pays particular attention to how the forms of innovative citizen energy communities are changing from locality-based community energy initiatives to distributed and Internet-mediated energy communities. The chapter concludes by drawing policy implications regarding user innovation and peer assistance in the transformation of energy systems.
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Levi, Marcel, and Marcus J. Schultz. Disseminated intravascular coagulation in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0270.
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Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. In patients with DIC, a variety of altered coagulation parameters may be detectable, such as thrombocytopenia, prolonged global coagulation times, reduced levels of coagulation inhibitors, or high levels of fibrin split products. There is not a single test, however, that is sufficiently accurate to establish or reject a diagnosis of DIC. Nevertheless, a combination of widely available tests may be helpful in making the diagnosis of DIC and can also be helpful in guiding the selection of DIC patients that require specific, often expensive, interventions in the coagulation system. Recent knowledge on important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with DIC. Strategies aimed at the inhibition of coagulation activation may theoretically be justified and have been found beneficial in experimental and clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation or restoration of physiological anticoagulant pathways.
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Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.
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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.
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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.
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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα) and in patients who have failed TNFα inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Z.Y. Luo, Q. Song, X.P. Xiong, M. Abdulai, H.H. Liu, L. Li, H.Y. Xu, S.Q. Hu, and C.C. Han*. The PI3K/Akt/mTOR signaling pathway regulates lipid metabolism mediated by endoplasmic reticulum stress in goose primary hepatocytes. Verlag Eugen Ulmer, 2021. http://dx.doi.org/10.1399/eps.2021.325.
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Bianchi, Elisabetta, Lars Rogge, and Matteo Vecellio, eds. Role of the IL-23/IL-17 Pathway in Chronic Immune-Mediated Inflammatory Diseases: Mechanisms and Targeted Therapies. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-621-0.
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Bhole, Malini. Complement deficiencies. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0299.
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The complement system comprises a group of heat-labile proteins which form part of the innate immune system. The main physiological functions of the complement system include defence against pyogenic bacterial infections, clearance of immune complexes and products of inflammatory damage, and acting as a bridge between the innate and adaptive immune system. The complement system is regulated by various complement inhibitors (regulatory proteins) that are present in both the classical pathway and the alternate pathway and which regulate and prevent spontaneous activation of the complement system, thereby preventing complement-mediated damage to tissues under normal circumstances. This chapter addresses the clinical features, diagnosis, and management of inherited and acquired deficiencies of complement proteins or inhibitors.
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Frenkel, Joost, and Hans R. Waterham. Mevalonate Kinase Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0039.
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Mevalonate kinase deficiency (MKD) is an autosomal recessive inborn error of isoprenoid biosynthesis, a pathway yielding sterols and nonsterol isoprenoids.In patients, the enzyme activity of mevalonate kinase is severely reduced due to mutations in the encoding gene, MVK. The substrate, mevalonate, accumulates and is elevated in blood and urine. Shortage of certain downstream products of the pathway, nonsterol isoprenoids, leads to dysregulation of the innate immune system, activation of inflammasomes, and interleukin (IL)-1 mediated inflammation.Symptoms start in early childhood with recurrent attacks of fever, vomiting, diarrhea, headache, sore throat, abdominal pain, arthralgias, painful lymphadenopathy, hepatosplenomegaly, skin rash, and mucosal ulcers. Severely affected patients have additional symptoms, such as intellectual impairment, progressive cerebellar ataxia, and tapetoretinal degeneration. Complications include intestinal obstruction, AA-amyloidosis, hemophagocytosis, and severe infection.Management of MKD is directed at controlling inflammation.
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Levinthal, Daniel A. Evolutionary Processes and Organizational Adaptation. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780199684946.001.0001.
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Strategists are encouraged to identify sustained competitive advantages. This volume takes a different tact and provides a perspective on how organizations adapt over time to changing circumstances. This process is characterized as not driven by the inspired wisdom of a grand strategist, but by an ecology of initiatives within the organization. A central role of the organization is to mediate between the market forces in which it operates and the culling and amplification of these initiatives within the organization. In this spirit, a useful touchstone is that of Mendel, who sits intermediate between the blind watchmaker of a purely Darwinian process and a “chess master” strategist as suggested by stylized rational choice approaches. The “Mendelian executive” operates with intentionality, but this intentionality is with respect to the design of the experimental process rather than the identification of specific pathways forward. The two core conceptual pillars of the work are that of path-dependence, what are the adjacent “spaces” to which an organization might move, and “artificial selection,” how the organization mediates aggregate immediate outcomes and the allocation of resources and rewards to the various initiatives and actors within the organization. Entities that have a sustained lifespan are not static, but engage in processes of renewal, whether cells in the human body or lines of business within a firm. A conceptual framework is provided to illuminate some of the fundamental mechanisms underlying this process.
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Sada, Nagisa, and Tsuyoshi Inoue. Lactate Dehydrogenase. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0029.
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Glucose is transported into neurons and used as an energy source. It is also transported into astrocytes, a type of glial cell, and converted to lactate, which is then released to neurons and used as another energy source. The latter is called the astrocyte-neuron lactate shuttle. Although the lactate shuttle is a metabolic pathway, it also plays important roles in neuronal activities and brain functions. We recently reported that this metabolic pathway is involved in the antiepileptic effects of the ketogenic diet. Lactate dehydrogenase (LDH) is a metabolic enzyme that mediates the lactate shuttle, and its inhibition hyperpolarizes neurons and suppresses seizures. This enzyme is also a molecular target of stiripentol, a clinically used antiepileptic drug for Dravet syndrome. This review provides an overview of electrical regulation by the astrocyte-neuron lactate shuttle, and then introduces LDH as a metabolic target against epilepsy.
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Studies on the mechanism of action of "New Pressor protein": Participation of a systemic bradykinin-mediated pathway stimulating the sympatho-adrenal system and potentiated by ace inhibition. Ottawa: National Library of Canada, 2002.
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Callaghan, Helen. Conclusion. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198815020.003.0006.
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The final chapter highlights the theoretical significance of the findings, reflects on their generalizability, and outlines supplementary explanations. By identifying systematic differences in the policy feedback processes triggered by market-enabling and market-restraining rules, the book bridges a gap between abstract theories of institutional change and more specific theories on the dynamics of capitalist development. Apart from self-reinforcing and self-undermining feedback effects, several other features of economic governance in advanced industrialized democracies also shape pathways to marketization. These features include eventfulness and periodicity, economic interdependence, multilevel governance, the influence of ideas on the content and intensity of public debates, and institutional structures that mediate interests and ideas, including electoral systems, legal systems, and the division of regulatory competences between levels of government as well as between elected and unelected rule-makers.
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Loewenstein, David A., Rosie E. Curiel, and Arlene Raffo. PTSD and Neurodegenerative Disorders. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0006.
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This chapter examines the potential effects of post-traumatic stress disorder (PTSD) on cognitive function, evaluates mechanisms that may mediate this relationship, determines the potential effects of PTSD on neurobiological systems such as the hypothalamic–pituitary–adrenal axis and different limbic and frontal lobe pathways, and discusses how this might be related to an increased risk for neurodegeneration. The chapter propose that associations and increased odds ratios associated with PTSD and dementia, while worthy of study, do not firmly establish a causative relationship between PTSD and dementia. The barriers to studying the associations between PTSD and dementia as they relate to causal mechanisms are also examined. Further research is needed, with more precise definitions, diagnostic rigor, and a focus on examining actual brain–behavior mechanisms that may shed light on potential causation.
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Cooper, M. Lynne, Emmanuel Kuntsche, Ash Levitt, Lindsay L. Barber, and Scott Wolf. Motivational Models of Substance Use. Edited by Kenneth J. Sher. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199381678.013.017.
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This chapter uses Cox and Klinger’s motivational model of alcohol use as a framework for reviewing research on motives for using alcohol, marijuana, and tobacco. Results of this review provide strong support for key premises underpinning this model in the alcohol literature, including that people drink alcohol to manage internal feeling states and to obtain valued social outcomes. Importantly, these motives may provide a final common pathway to alcohol use through which the influences of more distal variables are mediated. The research literature on motives for marijuana use revealed important similarities in the nature of motives underlying use and in the unique patterns of use and use-related consequences associated with specific motives. Research on tobacco use motives showed few similarities, with tobacco use being more habitual, automatic, and largely motivated by withdrawal cues, at least among more experienced and dependent users.
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Elewaut, Dirk, Heleen Cypers, Matthew L. Stoll, and Charles O. Elson. Extra-articular manifestations: inflammatory bowel disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0017.
Full textAbstract:
A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.
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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.
Full textAbstract:
Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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Nestler, Eric J. The Biological Basis of Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0001.
Full textAbstract:
Most major advances in biomedical research have relied on the use of animal and cell models of disease. This is a particularly difficult challenge in psychiatry, because many core symptoms of mental illnesses are inherently inaccessible in animals. Moreover, because still today there are no bona fide molecular-cellular abnormalities that are pathogenomic for these illnesses, cell models are even more far afield. This chapter reviews efforts to overcome these obstacles and use animal and cell studies to better understand the biological basis of depression and to develop improved treatments. An important distinction is made between acute vs. chronic stress models as well as differentiating the changes that stress induces in brain that mediate deleterious maladaptations as opposed to homeostatic adaptations that help the individual cope with the stress. Studies along these lines are making major strides in identifying candidate molecular pathways that should be mined for new antidepressant treatments. However, a major gap in the field is the great difficulty in testing novel mechanisms in humans; closing this gap is one of the highest priorities for the field.