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Em bryonic kidneys (EK) induced the form ation of branching tubular structures in both m IM CD and M DCK cells after 48 hours of incubation at 37oC buy cafergot 100 mg with amex pain treatment for lupus. EKs produce a num ber of growth factors purchase 100 mg cafergot visa coccyx pain treatment physiotherapy, including hepatocyte growth factor, transform ing growth factor-alpha, insulin-like growth factor, and transform ing growth factor– , which have been shown to effect tubulo- A B genic activity [86–93]. Interestingly, m any of these sam e growth factors have been FIGURE 16-19 shown to be effective in the recovery of An exam ple of the branching tubulogenesis of renal epithelial cells cultured in three- renal function after acute ischem ic insult dim ensional extracellular m atrix gels. Flow chart of the establishm ent of ureteric bud and m etanephric m es- enchym al cell lines from day 11. Although the results obtained from the analysis of kidney epithelial cells— Pregnant SV40–transgenic mouse M adin-Darby canine kidney (M DCK) or m urine inner m edullary collecting duct (m IM CD) seeded in three-dim ensional extracellular m atrix gels has been invaluable in furthering our understanding of Isolate embryos the m echanism s of epithelial cell branching tubulogenesis, ques- tions can be raised about the applicability to em bryonic develop- Dissect out embryonic kidney m ent of results using cells derived from term inally differentiated adult kidney epithelial cells. Therefore, kidney epithelial cell lines have been established that appear to be derived from the Isolate metanephric mesenchyme Isolate ureteric bud ureteric bud and m etanephric m esenchym e of the developing em bryonic kidney of SV-40 transgenic m ice [94, 95]. These m ice have been used to establish a variety of “im m ortal” cell lines. A, UB cells grown for 1 week in the presence of condi- ureteric bud (UB) and m etanephric m esenchym e from day 11. B, After three-dim ensional extracellular m atrix gels. C, Interestingly, “conditioned” m edia collected from the culture of m etanephric after 2 weeks of culture in a three-dim ensional gel com posed m esenchym al cells. During norm al kidney m orphogenesis, these entirely of growth factor–reduced M atrigel, ureteric bud cells have two em bryonic cell types undergo a m utually inductive process not form ed cords or tubules, only m ulticellular cysts. Thus, chang- that ultim ately leads to the form ation of functional nephrons ing the m atrix com position can alter the m orphology from tubules [74–76]. This m odel system illustrates this process, ureteric bud to cysts, indicating that this m odel m ight also be relevant to renal cells being induced by factors secreted from m etanephric m es- cystic disease, m uch of which is of developm ental origin. Thus, this system could represent the sim plest in Sakurai et al. Proposed m odel for the gener- FIGURE 16-22 alized response of epithelial cells to growth factors, which the Signalling pathway of hepatocyte growth factor action. Epithelial cells constantly m onitor the proposed intracellular signaling pathway involved in hepatocyte their surrounding environm ent via extracellular receptors (ie, inte- growth factor (HGF)–mediated tubulogenesis. Although HGF is per- grin receptors) and respond accordingly to growth factor stim ula- haps the best-characterized of the growth factors involved in epithe- tion. If the cells are in the appropriate environm ent, growth factor lial cell-branching tubulogenesis, very little of its mechanism of binding induces cellular responses necessary for branching tubulo- action is understood. However, recent evidence has shown that the genesis. There are increases in the levels of extracellular proteinases HGF receptor (c-M et) is associated with Gab-1, a docking protein and of structural and functional changes in the cytoarchitecture believed to be involved in signal transduction. Thus, on binding that enable the cells to form branching tubule structures. Ultimately, these alter- ations lead to epithelial cell–branching tubulogenesis. Acute Renal Failure: Cellular Features of Injury and Repair 16. This table tubulogenesis or to affect recovery of kidney tubules after ischem ic describes the roles of different growth factors in renal injury or in or other injury. Interestingly, growth factors that facilitate branch- branching tubulogenesis. A large variety of growth factors have ing tubulogenesis in vitro also enhance the recovery of injured been tested for their ability either to m ediate ureteric branching renal tubules. Nigam SK, Denisenko N, Rodriguez-Boulan E, Citi S: The role of phos- kidney to ischem ia: Assessm ent of adenine nucleotide and catabolite phorylation in development of tight junctions in cultured renal epithelial profiles. N igam SK, Rodriguez-Boulan E, Silver RB: Changes in intracellular 304:93–108. Toback FG: Regeneration after acute tubular necrosis.

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Intermediate outcomes of interest are restoration of sinus rhythm 100mg cafergot mastercard treatment for shingles pain and itching, maintenance of sinus rhythm safe 100 mg cafergot pain medication for osteosarcoma in dogs, recurrence of AF at 12 months, ventricular rate control, and development of cardiomyopathy. Final outcomes of interest are mortality (all-cause and cardiovascular), myocardial infarction, cardiovascular hospitalizations (including AF hospitalizations), heart failure symptoms, control of AF symptoms (e. Also of interest are the following adverse events associated with pharmacological treatment: hypotension, hypo/hyperthyroidism, arrhythmias, allergic reactions, hepatotoxicity, neurotoxicity, pulmonary toxicity, ophthalmological toxicity, and dermatological toxicity. Procedural complications of interest include pulmonary vein stenosis, left atrial esophageal fistula, phrenic nerve palsy, cardiac tamponade, and other complications (such as infection, bleeding, and thromboembolic events). For all six KQs, we will attempt to determine whether the comparative safety and effectiveness of the various therapies investigated differ among specific patient subgroups of interest. Patient characteristics to be assessed here include age, comorbidities, type of AF, previous pharmacological therapy failure, sex, enlarged left atrium, and high risk for stroke and bleeding events. The main sections in this chapter reflect the elements of the protocol established for the CER; certain methods map to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 23 (PRISMA) checklist. Topic Refinement and Review Protocol During the topic refinement stage, we solicited input from Key Informants representing medical professional societies/clinicians in the areas of general internal medicine, geriatrics, cardiology, electrophysiology, and primary care; patients; scientific experts; Federal agencies; and payers to help define the Key Questions (KQs). The KQs were then posted for public comment for 4 weeks from September 27 to October 25, 2011, and the comments received were considered in the development of the research protocol. We next convened a Technical Expert Panel (TEP) comprising clinical, content, and methodological experts to provide input to the draft protocol in defining populations, interventions, comparisons, and outcomes, and in 24 identifying particular studies or databases to search. Before involvement in the CER process, the Key Informants and members of the TEP were required to disclose any financial conflicts of interest greater than $10,000 and any other relevant business or professional conflicts. Any potential conflicts of interest were balanced or mitigated. Neither Key Informants nor members of the TEP performed analysis of any kind, nor did any of them contribute to the writing of this report. Literature Search Strategy Search Strategy ® ® To identify relevant published literature, we searched PubMed , Embase , and the Cochrane Database of Systematic Reviews (CDSR), limiting the search to studies published from January 1, 2000, to August 1, 2012. We believe that the evidence published from 2000 on represents the current standard of care for patients with atrial fibrillation (AF) and relevant comorbidities. In addition, a 2001 AHRQ report on the management of new onset AF summarized the evidence 25-27 prior to 2000. Where possible, we used existing validated search filters (such as the Clinical Queries Filters in PubMed). An experienced search librarian guided all searches. We supplemented the electronic searches with a manual 16,19,25-135 search of citations from a set of key primary and systematic review articles. We also considered studies identified through suggestions from external peer and public reviewers. Final updating of all database searches was performed during the review period. All citations were ® imported into an electronic database (EndNote X4; Thomson Reuters, Philadelphia, PA). We used several approaches to identify relevant grey literature including requests to drug and device manufacturers for scientific information packets and searches of study registries and conference abstracts for relevant articles from completed studies. Grey literature databases searched included ClinicalTrials. Search terms used for all of the above sources are provided in Appendix A. Inclusion and Exclusion Criteria The PICOTS (Populations, Interventions, Comparators, Outcomes, Timings, and Settings of interest) criteria used to screen articles for inclusion/exclusion at both the title-and-abstract and full-text screening stages are detailed in Table 1. Inclusion and exclusion criteria PICOTS Element Inclusion Criteria Exclusion Criteria Populations • Humans • Patients who have known • Adults (age ≥ 18 years of age) reversible causes of AF (including • Patients with AF (includes atrial flutter) but not limited to postoperative, o Paroxysmal AF (recurrent episodes that self- postmyocardial infarction, terminate in less than 7 days) hyperthyroidism) o Persistent AF (recurrent episodes that last more • All subjects are <18 years of age, than 7 days) or some subjects are under <18 o Permanent AF (an ongoing, long-term episode) years of age but results are not • Subgroups of potential interest include: broken down by age o Patients stratified by age (≤ 40, 41–64, 65–74, 75–84, 85+) o Patients with different types of AF (paroxysmal, persistent, permanent) o Patients with specific comorbidities (heart failure, coronary artery disease, kidney disease, hypertrophic cardiomyopathy, thyroid disease, pulmonary disease) o Patients for whom a prior rate- (KQ 3) or rhythm- control (KQ 5) pharmacological strategy was ineffective o Women o Patients with an enlarged left atrium o Patients at high risk for stroke and bleeding events (patients with diabetes, heart failure, and hypertension) 8 Table 1. Inclusion and exclusion criteria (continued) PICOTS Element Inclusion Criteria Exclusion Criteria Interventions • Pharmacological agents for rate control (KQ 1, KQ 2, • Studies comparing different KQ 3, KQ 6): imaging or mapping techniques o Beta blockers (e.

Acute ethanol administration to animals or Magnetic Resonance Imaging discount 100mg cafergot fast delivery pain treatment center kingston ny, ethanol perfusion of cultured pituitary or hypothalamic tis- Postmortem) sue increased (183) or had no effect on (184) tissue content or release of -endorphin generic 100mg cafergot visa pain disorder treatment plan. Ethanol also raised enkephalin Preclinical studies describe alcoholism-related neurotoxic- and dynorphin levels in some brain regions in some studies ity. These toxic effects appear to reflect a combination of (183,185). Chronic ethanol administration to rodents de- the neurotoxic effects of ethanol, the interaction of ethanol creased pituitary -endorphin processing and reduced hy- with nutritional deficiencies, and the neurotoxic conse- pothalamic mRNA levels of the peptide precursors proopio- quences of ethanol withdrawal (205). In rats, extended con- melanocortin (POMC) and prodynorphin (186,187). However, ethanol withdrawal was associated with tor binding. Ethanol concentrations, in the range of 10 to reductions in dendritic arborization and neuronal loss 25 mM, produce a small, but significant, increases in the (206). Under physiologic conditions, the receptor may cortical and limbic regions (207). With respect to brain be more sensitive to ethanol-induced inhibition than the volume, postmortem research suggests that white matter receptor (189). Chronic ethanol administration reduces the loss appears to be more prominent than gray matter loss Chapter 100: Ethanol Abuse, Dependence, and Withdrawal 1433 (208). Neuronal loss appears to be primarily loss of pyrami- Structural neuroimaging studies are consistent with the dal neurons, with relative sparing of interneurons (208). Cortical and limbic volu- Another study was unable to replicate neuronal loss using metric losses in ethanol-dependent patients have been de- uniform sampling and unbiased neuron counting methods scribed using computed axial tomography (CAT) and mag- (209). However, even when neurons are extant, they may netic resonance imaging (MRI) (212,213). Gray and white exhibit structural deficits consistent with neurotoxicity matter volumetric losses are progressive with heavy drinking (210). Generally, cortical and limbic brain shrinkage and and are most prominent in frontal and temporal cortex neuronal loss may be more prominent in individuals whose (213–215). Reductions in the volume of the Korsakoff syndrome has been associated with abnormalities corpus callosum has also been described (217). Brain atro- in frontal cortex, as well as in several subcortical structures phy documented in structural neuroimaging studies is most including the thalamus, hippocampus, mamillary bodies, more prominent with advancing age in adults (Fig. This age-related effect may reflect an age-related vul- FIGURE 100. The top two panels illustrate the relationship between drinking severity and duration with gray and white matter volume loss in ethanol-dependent patients. The bottom two panels illustrate the interaction between alcoholism and volume loss with age. Top figures: The relationship between corticalgray matter rate of change and theamount of alcohol consumed during the follow-up period (left) (Spearman rho 0. One alcoholic patient who reported 950 kg of alcohol consumption is omitted from the left panel so as not to distort scaling. The darker circle represents two patients with overlapping values. A controlled study of cortical gray matter and ventricular changes in alcoholic men over a 5-year interval. Data from individual ethanol-dependent pa- tients are expressed as age-corrected Z-scores plotted as a function of age. Brain gray and white matter volume loss accelerates with aging in chronic alcoholics: a quantitative MRI study. Alcohol Clin Exp Res 1992;16:1078–1089, with permission. There is a limited understanding of the extent populations. Thus, atrophy may not be detectable in young to which these studies also reflect genetic or alcohol-related healthy ethanol-dependent populations (220). Studies of ethanol intoxication ethanol-dependent adolescents show hippocampal volumet- suggest that it reduces cortical metabolism in humans (233). The study in adolescents raises the possibility that or following medications for detoxification, predominately adolescents show disruptive effects on brain development or describe reductions in regional cerebral perfusion or glucose an increased sensitivity to the neurotoxic effects of ethanol. More Over the initial years of sobriety, there is recovery in the pronounced deficits were observed in patients with evidence volumes of gray and white matter and reductions in sulcal of cortical atrophy based on structural neuroimaging (236), and ventricular volume (222).

In contrast buy 100mg cafergot with mastercard homeopathic pain treatment for dogs, ASO-RAD is cheap cafergot 100mg overnight delivery achilles heel pain treatment exercises, technically, much less amenable to PTRA (particularly Ischemic atrophy common Ischemic atrophy rare ostial lesions), and surgical intervention or Surgical intervention or angioplasty: Surgical intervention or angioplasty: PTRA produce mediocre-to-poor cure rates Mediocre cure rates of the hypertension Good cure rates of the hypertension of the hypertension. ASO-RAD and medial Less amenable to PTRA More amenable to PTRA fibroplasia m ay cause hypertension and when the hypertension is cured or markedly improved following intervention, the patient m ay be viewed as having “renovascular FIGURE 3-8 hypertension. The m ost far m ore likely to occur in patients with com m on types of renal artery disease (atherosclerotic renal artery disease [ASO -RAD] and m edial fibroplasia than in patients with m edial fibroplasia) are com pared here. In general, ASO -RAD is observed in m en and ASO-RAD. ASO-RAD and medial fibroplasia wom en older than 50 to 55 years of age, whereas m edial fibroplasia is observed prim arily involve both main renal arteries in approxi- in younger white wom en. Total occlusion of the renal artery and, hence, atrophy of the mately 30% to 40% of patients. In the Stenotic presence of hem odynam ically sufficient unilateral renal artery kidney stenosis, the kidney distal to the stenosis is rendered ischem ic, activating the renin angiotensin system , and producing high levels of angiotensin II, causing a “vasoconstrictor” type of hypertension. N um erous studies have established the causal relationship between angiotensin II–m ediated vasoconstriction Contralateral Ischemia and hypertension in the early phase of this experim ental m odel. This sec- • Pressure natriuresis Angiotensin II ondary aldosteronism also produces hypokalem ia. The degree of renal artery stenosis necessary to produce hem odynam ically Vasoconstriction Aldosterone significant reductions in perfusion, triggering renal ischem ia and activation of the renin angiotensin system , generally does • Intrarenal hemodynamics not occur until a reduction of 80% or m ore in both lum en diam eter • Sodium retention and cross-sectional area of the renal artery takes place. Lesser degrees of renal artery constriction do not initiate this sequence of events. This m odel of 2K,1C Goldblatt hypertension im plies that FIGURE 3-9 the contralateral (nonaffected) kidney is present, and that its Schematic representation of renovascular hypertension. Renovascular renal artery is not hem odynam ically significantly narrowed. In addition, the high Clip III levels of angiotensin II stim ulate thirst, which further augm ents Blood pressure expansion of the extracellular fluid volum e. The expanded extra- cellular fluid volume results in a progressive suppression of peripheral renin activity. During this transition phase, the hypertension is still Renin responsive to rem oval of the unilateral renal artery stenosis, to angiotensin II blockade, or unilateral nephrectom y, although these Change in blood pressure m aneuvers do not norm alize the blood pressure as prom ptly and on removing clip consistently as in the acute phase. After several weeks, a chronic phase (phase III) ensues wherein unclipping the renal artery of the experimental animal does not lower the blood pressure. This failure of “unclipping” to lower the blood pressure in this chronic phase (III) of 2K,1C hypertension is due to FIGURE 3-10 widespread arteriolar damage to the “contralateral kidney,” conse- Sequential phases in two-kidney, one-clip (2K,1C) experimental reno- quent to prolonged exposure to high blood pressure and high levels vascular hypertension. The schematic representation of renovascular of angiotensin II. In this chronic phase of 2K,1C renovascular hyper- hypertension depicted in Figure 3-9 is an oversim plification. In tension, extracellular fluid volum e expansion and system ic vasocon- fact, the course of experimental 2K,1C hypertension may be divided striction are the m ain pathophysiologic abnorm alities. In phase I, renal ischemia and activation natriuresis of the “contralateral kidney” blunts the extracellular of the renin angiotensin system are of fundam ental im portance, fluid volum e expansion caused by the “stenotic kidney;” but as the and in this early phase of experim ental hypertension, the blood contralateral kidney suffers vascular damage from extended exposure pressure elevation is renin- or angiotensin II–dependent. Acute to elevated arterial pressure, its excretory function diminishes and adm inistration of angiotensin II antagonists, adm inistration of extracellular fluid volume expansion persists. In this third phase of angiotensin-converting enzym e (ACE) inhibitors, rem oval of the experim ental 2K,1C hypertension, acute blockade of the renin renal artery stenosis (ie, rem oval of the clip in the experim ental angiotensin system fails to lower blood pressure. Sodium depletion anim al or rem oval of the “stenotic kidney”) prom ptly norm alizes m ay am eliorate the hypertension but does not norm alize it. Several days after renal artery clamping, renin levels clinical surrogate of phase III experimental 2K,1C hypertension is fall, but blood pressure rem ains elevated. W idespread clinical experience indicates experim ental 2K,1C hypertension m ay be viewed as a pathophysio- that major improvements in blood pressure control or cure of the logic transition phase that, depending on the experim ental m odel hypertension following renal revascularization or even removal of and species, m ay last from a few days to several weeks. During this the kidney ipsilateral to the renal artery stenosis are rarely observed transition phase (phase II), salt and water retention are observed as in patients with a long duration (ie, >5 years) of hypertension. The discussion so far of the pathophysiology of renovascular hypertension has focused on the two-kidney, one-clip m odel of renovascular hypertension (“two-kidney hypertension”), wherein the artery to the “contralateral kidney” is patent and the “contralateral” nonaffected kidney is present. Elevated peripheral renin activity, norm al plasm a volum e, and hypokalem ia are typically associated with the elevated arterial pressure. There is another type of “reno- Blood Renin Volume Blood Renin Volume vascular hypertension” known as “one-kidney” hypertension, pressure pressure wherein in the experim ental m odel, one renal artery is constricted High Normal Normal High and the contralateral kidney is removed.

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