Nephrotoxic effects of tetanus toxin: An ultrastructural study

Generalized nephrotoxicity was observed in the rat as early as 6 hr after intramuscular injection of 1000 of tetanus toxin. The most striking morphological changes, including swelling and rupture of the mitochondria, sloughing of the microvilli, and dissolution of cells, were found exclusively in the renal proximal tubule. Acute tubular necrosis with degeneration of the organelles and disruption of the cell membrane were also encountered throughout the entire nephron.Since these observations parallel those reported in patients with complicated acute tubular necrosis secondary to nephrotic syndrome and chemical toxicity, perhaps the kidney is one of the major targets in tetanus intoxication. It is possible that injury to the nephron results in electrolyte imbalance that can contribute to the neuromuscular manifestation accompanying tetanus toxicity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/21937/1/0000344.pd

Intracellular sodium in macula densa cells and renin release

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24023/1/0000272.pd

Ultrastructural characteristics of experimental arterial medial fibroplasia induced by Vasa vasorum occlusion,

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/22644/1/0000195.pd

Comparative evaluation of vein graft preparation media: Electron and light microscopic studies,

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/22114/1/0000541.pd

Analysis of arterial intimal hyperplasia: review and hypothesis

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology? Hypothesis: I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign " intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates earl

Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial: Health-related quality of life outcomes, resource utilization, and cost-effectiveness analysis

BackgroundThe Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial showed that survival in patients with severe lower limb ischemia (rest pain, tissue loss) who survived postintervention for >2 years after initial randomization to bypass surgery (BSX) vs balloon angioplasty (BAP) was associated with an improvement in subsequent amputation-free and overall survival of about 6 and 7 months, respectively. We now compare the effect on hospital costs and health-related quality of life (HRQOL) of the BSX-first and BAP-first revascularization strategies using a within-trial cost-effectiveness analysis.MethodsWe measured HRQOL using the Vascular Quality of Life Questionnaire (VascuQol), the Short Form 36 (SF-36), and the EuroQol (EQ-5D) health outcome measure up to 3 years from randomization. Hospital use was measured and valued using United Kingdom National Health Service hospital costs over 3 years. Analysis was by intention-to-treat. Incremental cost-effectiveness ratios were estimated for cost per quality-adjusted life-year (QALY) gained. Uncertainty was assessed using nonparametric bootstrapping of incremental costs and incremental effects.ResultsNo significant differences in HRQOL emerged when the two treatment strategies were compared. During the first year from randomization, the mean cost of inpatient hospital treatment in patients allocated to BSX ($34,378) was estimated to be about$8469 (95% confidence interval, $2,417-$14,522) greater than that of patients allocated to BAP ($25,909). Owing to increased costs subsequently incurred by the BAP patients, this difference decreased at the end of follow-up to$5521 ($45,322 for BSX vs$39,801 for BAP) and was no longer significant. The incremental cost-effectiveness ratio of a BSX-first strategy was $184,492 per QALY gained. The probability that BSX was more cost-effective than BAP was relatively low given the similar distributions in HRQOL, survival, and hospital costs.ConclusionsAdopting a BSX-first strategy for patients with severe limb ischemia does result in a modest increase in hospital costs, with a small positive but insignificant gain in disease-specific and generic HRQOL. However, the real-world choice between BSX-first and BAP-first revascularization strategies for severe limb ischemia due to infrainguinal disease cannot depend on costs alone and will require a more comprehensive consideration of individual patient preferences conditioned by expectations of survival and other health outcomes