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Medical Instructor, University of Wisconsin School of Medicine and Public Health
It has been hypothesized that biomechanical regulation of renal tubular Na1 and K1 transport in the distal nephron may have evolved as a response to defend against sudden increases in extracellular K1 concentration that occur in response to ingestion of K1-rich diets typical of early vertebrates (22) medicine 1900 order secnidazole 500 mg fast delivery. These events would enhance K1 secretion treatment naive buy discount secnidazole 500 mg on-line, thus providing a buffer to guard against development of hyperkalemia treatment ingrown hair generic secnidazole 500mg with mastercard. The nature of the adaptive process is thought to be similar to the adaptive process that occurs in response to high dietary K1 intake in normal subjects (35) kerafill keratin treatment buy secnidazole 1 gr with amex. Chronic K1 loading in animals augments the secretory capacity of the distal nephron, and, therefore, renal K1 excretion is significantly increased for any given plasma K1 level. Increased K1 secretion under these conditions occurs in association with structural changes characterized by cellular hypertrophy, increased mitochondrial density, and proliferation of the basolateral membrane in cells in the distal nephron and principal cells of the collecting duct. Aldosterone Paradox Under conditions of volume depletion, activation of the renin-angiotensin system leads to increased aldosterone release. The increase in circulating aldosterone stimulates renal Na1 retention, contributing to the restoration of extracellular fluid volume, but occurs without a demonstrable effect on renal K 1 secretion. Under condition of hyperkalemia, aldosterone release is mediated by a direct effect of K1 on cells in the zona glomerulosa. The subsequent increase in circulating aldosterone stimulates renal K1 secretion, restoring the serum K1 concentration to normal, but does so without concomitant renal Na1 retention. In part, this ability can be explained by the reciprocal relationship between urinary flow rates and distal Na1 delivery with circulating aldosterone levels. Under conditions of volume depletion, proximal salt and water absorption increase, resulting in decreased distal delivery of Na1 and water. Although aldosterone levels are increased, renal K1 excretion remains fairly constant, because the stimulatory effect of increased aldosterone is counterbalanced by the decreased delivery of filtrate to the distal nephron. Under condition of an expanded extracellular fluid volume, distal delivery of filtrate is increased as a result of decreased proximal tubular fluid reabsorption. Once again, renal K1 excretion remains relatively constant in this setting, because circulating aldosterone levels are suppressed. It is only under pathophysiologic conditions that increased distal Na1 and water delivery are coupled to increased aldosterone levels. Renal K1 secretion also remains stable during changes in flow rate resulting from variations in circulating vasopressin. In this regard, vasopressin has a stimulatory effect on renal K1 secretion (38,39). This kaliuretic property may serve to oppose a tendency to K1 retention under conditions of antidiuresis when a low-flow rate-dependent fall in distal tubular K1 secretion might otherwise occur. In contrast, suppressed endogenous vasopressin leads to decreased activity of the distal K1-secretory mechanism, thus limiting excessive K losses under conditions of full hydration and water diuresis. This disorder is inherited in an autosomal dominant fashion and is characterized by hypertension and hyperkalemia (42). Thiazide diuretics are particularly effective in treating both the hypertension and hyperkalemia (43). The net effect is increased NaCl reabsorption combined with decreased K1 secretion. In addition to increasing Na1 retention, this change in permeability further impairs K1 secretion, because the lumennegative voltage, which normally serves as a driving force for K1 secretion, is dissipated. For this reason, renal K1 excretion is kept independent of changes in extracellular fluid volume. Hypokalemia caused by renal K1 wasting can be explained by pathophysiologic changes that lead to coupling of increased distal Na1 delivery and aldosterone or aldosterone-like effects. When approaching the hypokalemia caused by renal K1 wasting, one must determine whether the primary disorder is an increase in mineralocorticoid activity or an increase in distal Na1 delivery. Hyperkalemia, or an increase in dietary K1 intake, can increase renal K1 secretion independent of change in mineralocorticoid activity and without causing volume retention. This effect was shown in Wistar rats fed a diet very low in NaCl and K1 for several days and given a pharmacologic dose of deoxycorticosterone to ensure a constant and nonvariable effect of mineralocorticoids (54,55). In the first 2 hours, there was a large increase in the rate of renal K1 excretion that was largely caused by an increase in the K1 concentration in the cortical collecting duct.
Kuriyama S medications an 627 proven 1 gr secnidazole, Tomonari H treatment quality assurance unit cheap secnidazole 1 gr without prescription, Tokudome G treatment models order secnidazole 500mg without prescription, Horiguchi M treatment ind cheap 500mg secnidazole visa, Hayashi H, Kobayashi H, Ishikawa M, Hosoya T: Antiproteinuric effects of combined antihypertensive therapies in patients with overt type 2 diabetic nephropathy. Rosario R, Epstein M: Relationship between erythropoietin administration and alterations of renin-angiotensin-aldosterone. Yamauchi Y, Abe K, Mantani A, Hitoshi Y, Suzuki M, Osuzu F, Kuratani S, Yamamura K: A novel transgenic technique that allows specific marking of the neural crest cell lineage in mice. Karger C, Kurtz F, Steppan D, Schwarzensteiner I, Machura K, Angel P, Banas B, Risteli J, Kurtz A: Procollagen I-expressing renin cell precursors. Analysis of correlations in endocapillary (acute) glomerulonephritis and in moderately severe mesangioproliferative glomerulonephritis. Renal Physiology Handling of Drugs, Metabolites, and Uremic Toxins by Kidney Proximal Tubule Drug Transporters Sanjay K. The analysis of murine knockouts has revealed a key role for these transporters in the renal handling not only of drugs and toxins but also of gut microbiome products, as well as liverderived phase 1 and phase 2 metabolites, including putative uremic toxins (among other molecules of metabolic and clinical importance). Functional activity of these transporters (and polymorphisms affecting it) plays a key role in drug handling and nephrotoxicity. Apart from excreting unmodified small molecule drugs, the kidney handles many conjugated metabolites, most of which are produced by phase 1 and phase 2 metabolism in the liver. Genes for phase 1 and 2 reactions are also expressed in the kidney and are likely to be very important in metabolic functions of the proximal tubule cells of kidney as well (9), although this area of research is underexplored. This scenario thus includes a host of drugs, metabolites, and molecules that are handled by proximal tubule transporters, which orchestrate their clearance from the blood and their elimination into the urine. The variables that affect serum, tissue, and body fluid levels of a single drug, toxin, or metabolite excreted by the transporters that handle small molecules is quite complicated; much more so if one simultaneously considers several small molecules. Nevertheless, a great deal of progress has been made in the past few decades on the basic biology of drug, toxin, and metabolite handling, including those functioning in the kidney proximal tubule. With these details at hand, integration of this information and application to clinical settings, such as the scenario presented in the preceding paragraph, should eventually be feasible. Many of the small molecules of clinical interest are charged: organic anions, organic cations, or molecules that have a zwitterionic character (both positive and negative charges). Molecules that are too large or albumin bound have limited glomerular filtration, and excretion instead depends largely on tubular secretion. For the most part, these molecules are secreted unchanged into the tubular lumen by a set of transporters at the apical (luminal or urine) surface of the proximal tubule cell. There appear to be more than two dozen types of transporters involved in the net transport of organic anion, organic cation, or organic zwitterions by the proximal tubule. Classification of Organic Ion Transporters Organic ion transporters in the proximal tubule are frequently collectively called multispecific drug transporters because of their multispecific nature and their crucial role in drug handling. But depending on the discipline (physiology, biochemistry, or pharmacology), or for historical reasons, a single transporter can sometimes be described by multiple different names in the literature (Table 1) (1). Furthermore, while much of the data from in vitro transport assays and mouse knockout studies seems relevant to humans, caution must be exercised in extrapolating to human physiology. By convention, transporters are displayed as all uppercase letters when referring to proteins or human genes. Basic Organic Ion Transporter Physiology Excretion of organic cations begins with transport on the basolateral surface of the proximal tubular cell (Figure 1A). Several carriers on the apical surface subsequently transport organic cations across the apical membrane through electroneutral transport by exchange with proton (H1), which capitalizes on the electrochemical gradient that favors movement of H1 into the cells. These transporters are organic anion/ dicarboxylate exchangers, which use a tertiary active transport system on the basolateral side of the proximal tubule cell.
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Our goal is to provide coastal and ocean managers with scientific understanding and tools to help protect healthy coral reef ecosystems and restore degraded ones medications ending in lol cheap 500mg secnidazole amex. The commitment to share information symptoms synonym order 1gr secnidazole overnight delivery, ideas symptoms joint pain fatigue order secnidazole 1gr fast delivery, and common goals led to the development of a national research plan treatment of pneumonia order 500 mg secnidazole fast delivery, Coral Disease and Health: A National Research Plan (Woodley et al. Recent reviews have documented an explosion in the incidence of disease, particularly in the Caribbean. The first disease report occurred in 1965 related to skeletal anomalies (Squires 1965), with the next report coming 8 years later by Antonius (1973), from these reports through the early 1990s, only four diseases had been recognized: skeletal anomalies, Black band, White plague Type I, and Shutdown reaction (Sutherland et al. Since the early 1990s, monitoring programs in the Florida Keys have documented a sharp increase in the number and prevalence (the ratio, for a given time period of the number of occurrences of a disease or event to the number of units at risk in the population) of coral diseases. Reports from the Indo-Pacific suggest an emerging crisis in coral disease as monitoring efforts are able to explore new areas. The picture of coral disease has expanded from the simple perception of an infectious disease agent to a plethora of possible interactions with a variety of possible agents attacking not just the coral animal, but an intricate group of organisms consisting of plant, animal and microbial associates. The complexity of this growing disease problem made it 84 more difficult to design management regimes and increased significantly the need for cross-disciplinary tools to combat the problem (see diagram below). Realizing these were complex and complicated issues, we recognized that our lack of understanding of the underlying mechanisms of coral pathologies was inhibiting our ability to manage the growing number of coral health problems. Also, to improve our ability to identify the factors responsible for coral health decline and increased disease incidence would require embracing a new paradigm of scientific investigation that incorporates new methods and new technologies able to help elucidate mechanisms that link cause and effect relationships so the field could move from just descriptive science into mechanistic science. There was an obvious need to unify the coral disease community, build scientific skills and capacity, and provide standardization in investigative nomenclature, methodologies and technologies in order to competently communicate and interact with other main stream disease fields. This document provided an integrated roadmap that began tying these ideas together. This document outlined gaps in our knowledge and recommended research directions needed to support this new paradigm. Four major themes with accompanying strategic objectives were identified: Biology (6), Disease Identification and Disease Investigation (4), Disease Diagnostics (5) and Environmental Factors Affecting Susceptibility and Infectivity (11). The 26 recommendations encompassed 9 topic areas: Nomenclature, Model System(s), Field Assessment of Coral Reef Condition, Microbiology, Toxicology, Histopathology, Molecular, Bioinformatics, and Advanced Education and Outreach. Research Information is limited on the physiological parameters that define healthy coral and even less on coral pathology. Our challenge is to apply advanced technologies in functional genomics, proteomics, toxicology, and systems biology to expand our knowledge to understand and recognize coral health and elucidate disease dynamics. The knowledge gained from this research approach is positioning us to move aggressively toward characterizing the processes that control ecological connectivity among reefs and discover critical control points for management strategies. The first step is to establish and make available tools that can support discovery and applied research. There are also over 28,000 ribosomal gene sequences cloned from coral-associated bacteria available to assist in microbial diversity 85 and pathogen research efforts. This type of information is vital and basic to developing an understanding for how an organism responds to its environment, is key to developing diagnostic tools to assess coral health and lays the foundation for identifying critical control points and viable management options. Diagnostic Resources There is limited application of medical/veterinary knowledge or protocols to the study of coral health and disease, resulting in ambiguous and often misleading communication of findings. Compounded by inadequate diagnostic tools and insufficient application of diagnostic procedures, the challenge is to develop standardized procedures based on medical principles that clearly define terminology, pathology and diagnostic criteria. Education Experts in coral biology, pathology and veterinary science are developing resources and web-enabled tools for use in recognizing gross signs of disease and in clinical diagnostic pathology as well as developing case definitions for selected coral syndromes. Diagnostic Tools Consortium members have achieved significant advances in diagnostic assay development that assist researchers in identifying coral stressors. The overarching goal for us is to "Promote the effective detection, identification and management of coral reef diseases". We have convened this meeting to: x Synthesize the state of knowledge of Pacific coral diseases x Develop a strategic plan to: x Identify research needs to help understand etiologies, epidemiology and ecology of coral diseases x Identify innovative strategies for disease management on coral reefs x Identify novel strategies to engage public and political sectors in partnering with us to combat the spread of coral disease Disease "any impairment that interferes with or modifies the performance of normal functions, including responses to environmental factors such as nutrition, toxicants, and climate; infectious agents; inherent or congenital defects, or combinations of these factors" Wobeser 1981. Within that time frame approximately 30 new syndromes and diseases have been identified. To date, only few diseases or syndromes have been characterized in terms of causality and even fewer have been characterized in terms of the physiological effect on the coral. The coral holobiont may be considered a "super-organism" composed of the coral host, its algal symbionts, and accompanying microorganisms.
This can get in the way of bargaining 4 medications list at walmart buy secnidazole 500mg low price, increase transaction costs symptoms gastritis order 1 gr secnidazole with amex, and the like-but it also spurs the development of "alternative" means of deal-making in treatment 1-3 order 1gr secnidazole, monitoring medicine queen mary secnidazole 1gr visa, and enforcement. These alternatives often involve mass violence-though, to be clear, from the point of view of those participating in these markets, such incidents of violence are undesirable because they increase the cost of doing business. Its success does not result in the long-term production of public goods, both because the deviant entrepreneurs are (for reasons of selection bias if nothing else) not public-minded sorts and because the profits from deviant industries are rarely if ever taxed by the state, the classic provider of public goods-but what the state loses, local communities and organizations partly gain in the form of jobs and capital. While all entrepreneurs are risk-takers, deviant entrepreneurs, virtually by definition, have a heightened willingness to flout social norms and conventions. Their success in turn degrades respect for other social norms and conventions, which may be otherwise unrelated to the market in question, leading to generalized decay of the dominant social order. At the same time, this is no subversively heroic Robin Hood morality 8 Deviant Globalization tale. Rather, they are opportunists whose public personae and brands are built around unbridled capitalist spirits-living fast, dying hard, and letting the rest of the world go to hell. The form of development they are enacting, ironically, is in many respects an ultra-libertarian one-one that tacitly rejects what liberal political economy defines as "the public good," and denies the need for any sort of state. The second major reason why deviant globalization matters follows directly from the insight that this phenomenon is really the truest manifestation of libertarianism: deviant globalization degrades state power, erodes state capacity, corrodes state legitimacy, and, ultimately, undermines the foundations of mainstream globalization in ways that are only now being fully recognized. More specifically, deviant globalization is creating a new type of nonstate political actor, what John Robb calls a "global guerrilla,"10 the sort of super-empowered individuals whose geopolitical importance is only likely to grow in the coming decade. As we have seen, deviant entrepreneurs control huge, growing swathes of the global economy, operating most prominently in places where the state is hollowed or hollowing out. Third, and most controversially, deviant entrepreneurs in some cases are emerging as private providers of security, health care, and infrastructure-that is, precisely the kind of goods that functional states are supposed to provide to their citizens. What makes these political actors unusual is that, rather that seeking to build or capture institutionalized state power, they thrive in (and indeed prefer) weak-state environments, and their activities reinforce the conditions of this weakness. Deviant entrepreneurs generally do not start out as political actors in the sense of actors who wish to control or usurp the state. In the first iteration, deviant globalization represents an entrepreneurial response to the failure of mainstream development: an effort by bootstrapping individuals to get ahead in a world where the state is no longer leading the way. Once these deviant industries take off, however, they begin to take on a political life of their own. They siphon off money, loyalty, and sometimes territory; they increase corruption; and they undermine the rule of law. They also force well-functioning states in the global system to spend an inordinate 9 Gilman, Goldhammer, and Weber amount of time, energy, and attention trying to control what comes in and out of their borders. Although deviant globalization may initially have flowered as a result of state hollowing, as it develops, it becomes a positive feedback loop in much the same way that many successful animal and plant species, as they invade a natural ecosystem, reshape their ecosystem in ways that improve their ability to exclude competitors. Deviant entrepreneurs have developed market niches in which extractable returns are more profitable, and frankly easier, than anything they could get by "owning" enough of the state functions to extract rents from those instead. Organizations such as the First Command of the Capital in Brazil, the `Ndrangheta in Italy, or the drug cartels in Mexico have no interest in taking over the states in which they operate. This would only mean that they would be expected to provide a much broader and less selective menu of services to everyone, including ungrateful and low-profit clients, those so-called citizens. None of these organizations plan to declare sovereign independence and file for membership in the United Nations. What they want, simply, is to carve out autonomous spaces where they can do their business without state intervention. This underscores a crucial point about deviant globalization: it does not thrive in truly "failed" states-that is, in places where the state has completely disappeared-but rather in weak but well-connected states, in which the deviant entrepreneur can establish a zone of autonomy while continuing to rely on the state for some of the vestigial services it continues to furnish. On the one hand, the more deviant industries grow, the more damage they do to the political legitimacy of the states within which the deviant entrepreneurs operate, thus undermining the capacity of the state to provide the infrastructure and services that the deviant entrepreneurs want to catch a free ride on. On the other hand, the people living in the semi-autonomous zones controlled by deviant entrepreneurs increasingly recognize those entrepreneurs rather than the hollowed out state as the real source of local power and authority-if for no other reason than the recognition that if you cannot beat them, you should join them. Of course, just because these deviant providers of alternative governance functions end up seeming "legitimate" in the eyes of local stakeholders (if only because of the economic "development" benefits they provide), this type of governance is usually poorly institutionalized and nontransparent about both ends and means. Nonetheless, as these groups take over functions that would have been expected of the state, their stakeholders increasingly lose interest in the hollowed-out formal state institutions. Something like this took place in Colombia in the 1980s, in Zaire/Congo since the 1990s, and may be taking place in Mexico today. Think Regulatory Harmonization, Not Eradication So where does the concept of deviant globalization leave us from a policy perspective
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