Megarian Myths: Extrapolating the Narrative Traditions of Megara

This chapter examines the local traditions (through Pausanias and Theognis), discourse environment, and positionality of Megara to establish abstract principles of the Megarian worldview, and then applies those principles to the local traditions in an attempt to present a cohesive account of Megarian myths from the earliest mythistorical times to the beginning of oligarchic government. An important discovery resulting from this is the general avoidance of all things Corinthian in Megarian narrative traditions

An Analysis of Early Renal Transplant Protocol Biopsies - the High Incidence of Subclinical Tubulitis

To investigate the possibility that we have been underestimating the true incidence of acute rejection, we began to perform protocol biopsies after kidney transplantation. This analysis looks at the one-week biopsies. Between March 1 and October 1, 1999, 100 adult patients undergoing cadaveric kidney or kidney/pancreas transplantation, or living donor kidney transplantation, underwent 277 biopsies. We focused on the subset of biopsies in patients without delayed graft function (DGF) and with stable or improving renal function, who underwent a biopsy 8.2 ± 2.6 d (range 3-18 d) after transplantation (n = 28). Six (21%) patients with no DGF and with stable or Improving renal function had borderline histopathology, and 7 (25%) had acute tubulitis on the one-week biopsy. Of the 277 kidney biopsies, there was one (0.4%) serious hemorrhagic complication, in a patient receiving low molecular weight heparin; she ultimately recovered and has normal renal function. Her biopsy showed Banff 1B tubulitis. In patients with stable or improving renal allograft function early after transplantation, subclinical tubulitis may be present in a substantial number of patients. This suggests that the true incidence of rejection may be higher than is clinically appreciated

Relation between renal calcium content and renal impairment in 246 human renal biopsies

Relation between renal calcium content and renal impairment in 246 human renal biopsies. Tissue calcium content from 246 diagnostic human renal biopsies was measured to assess whether elevated tissue calcium concentration could be demonstrated to exist early during the course of human renal disease or was only a manifestation of advanced renal impairment. Renal calcium content correlated significantly with serum creatinine (r = +0.23, P < 0.001, N = 246); serum phosphate (r = +0.27, P < 0.001, N = 169) but not with serum calcium (r = -0.10, P > 0.1, N = 193). Fivefold greater calcium content was measured in biopsied patients with normal renal function than in normal postmortem renal tissue (35.7 ± 5.2 vs. 7.6 ± 0.7 mgCa/100 g wet renal tissue, P < 0.001). Those biopsied patients with significant functional impairment (SCr > 1.5 mg/dl) had a higher mean level of serum phosphorus and serum [Ca] × [P] product than patients with normal renal function (5.19 ± 0.22 vs. 3.92 ± 0.11mg P/dl and 44.8 ± 1.8 vs. 35.7 ± 1.2 mg2/dl2, respectively), and slightly higher renal calcium content (85.3 ± 32.2 vs. 35.7 ± 5.2 Ca/100 g wet renal tissue, P = 0.06), which correlated with histologic calcium deposition (r = +0.52, P < 0.02, N = 20). These findings are consistent with the hypothesis that renal calcium deposition begins early in the course of a variety of renal diseases and hence may play a secondary pathogenetic role that accelerates progression to chronic renal failure. Severity of renal calcium deposition is equally closely related to hyperphosphatemia and to the level of renal impairment

Allografts Surviving for 26 to 29 Years Following Living-Related Kidney Transplantation: Analysis by Light Microscopy, In Situ Hybridization for the Y Chromosome, and Anti-HLA Antibodies

We studied seven patients aged 14 to 40 years who received living-related kidney transplants and had allograft survivals of 26 to 29 years. The blood urea and creatinine were either within normal limits or marginally elevated. Histopathologic examination showed only mild mesangial expansion, interstitial fibrosis, and arteriosclerosis. Immunoperoxidase staining with anti-HLA antibodies or in situ hybridization with a Y chromosome probe showed persistence of donor tubular epithelium and vascular endothelium within the graft. Recipient-derived glomerular cells were seen in one case, and interstitial lymphocytic infiltrates were seen in all cases. A review of the clinicopathologic data available for these cases indicated that both central and peripheral immunologic mechanisms contributed to the maintenance of prolonged graft survival. This extended survival was independent of six antigen matching, downregulation of donor HLA antigen expression, and ingrowth of host epithelium/endothelium into the allograft. © 1994, National Kidney Foundation. All rights reserved. All rights reserved

Mechanisms of lysine-induced acute renal failure in rats

Mechanisms of lysine-induced acute renal failure in rats. We have previously found that lysine produces acute renal failure in rats. To define the acute effects of lysine, rats given lysine at 8.9 mg/kg/min, i.v. for 4.5 hr were compared with control rats receiving equiosmolar dextrose. Systemic blood pressure was stable in both groups. Mean intratubular pressure, inulin clearance (CIn), and renal blood flow were determined at 45-min intervals. Intratubular pressures measured with a servonulling micropressure device were elevated by 90 min in lysine-treated animals, with tubular heterogeneity, while pressures in dextrose-treated rats were normal and homogeneous. By 135 min CIn in lysine-treated rats was 45% of CIn in dextrose rats. Urine output fell in ly sine-treated rats. Renal blood flow determined by flow probe remained normal in ly sine-treated rats through 135 min and did not decline significantly until 180 min. Significant dilatation of surface tubules was documented by intravital microscopy beginning at 90 min in lysine-treated rats. The sequence of elevated intratubular pressure and tubular dilatation, followed by decreased CIn, and then by decreased renal blood flow suggests that lysine produces acute renal failure primarily through tubular obstruction. The tubular obstruction is followed later by an increase in renal vascular resistance

Digital pathology evaluation of complement C4d component deposition in the kidney allograft biopsies is a useful tool to improve reproducibility of the scoring

Complement C4d component deposition in kidney allograft biopsies is an established marker of antibody-mediated rejection. In the Banff 07 classification of renal allograft pathology, semi-quantitative evaluation of the proportion of C4d-positive peritubular capilaries (PTC) is used. We aimed to explore the potential of digital pathology tools to obtain quantitative and reproducible measure of C4d deposition in the renal allograft tissue

Renal Allografts with IF/TA Display Distinct Expression Profiles of Metzincins and Related Genes

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73001/1/j.1600-6143.2008.02512.x.pd

Exile Vol. XVI No. 2

PREFACE 3 ESSAY Observations At The Gap by Paul A. Dimitruk 4 Those Who Choose Words By Keith McWalter 5-6 On Victoria\u27s England by Paul A. Dimitruk 7-8 Facts Are The Enemy of Truth by Nancy Gutierrez FICTION Harmon by Barbara Mackey 22-25 Pilgrimage by Keith McWalter 35-44 ARTWORK by Wandi Solez: 6, 15, 23, 27 by Ken Wernz 10 by Stephen Swift 11 by Laura M. Hyslop 12 by Skip Staudt 19 by W. A. Hoffman 25 by Mary Ann Kowaski 34 by Jo Ann Orgo 40 PHOTOGRAPHY by Roger Block 16 by Tim Heath- all other POETRY My Poems by Susan Hallock 13 Counter-Fugue At Six-Thirty by Sherry Stodola 14-16 Apple Tree Poem by Darby Williams 17 When Snow Falls Into A Pond by Bruce Kidd 17 Woman-Man by Darby Williams 18 Transcendence by Wandi Solez 20 Paris Reflection by Wandi Solez 20 A Sleepless Night In Valencia, Spain by Wandi Solez 21 # 319 by Wandi Solez 21 Strange Lady by John Gillespie 26 Strange Lady II by John Gillespie 26 Where The Hell Is Rembrandt? by John Loveland 26 Years Ago by John Whitt 29 I\u27ve Finished Growing Now by Keith McWalter 29 Charisma by John Whitt 30 I Thought Of Cutting by John Loveland 31 Make Me Eat Peanut Butter by Fred Walton 31 The Cat by John Loveland 32 On The Rim by John Whitt 33 Undercurrent by Keith McWalter 33 Cover: Gail Lutsch Layouts: Keith McWalte

Subclinical toxicity of calcineurin inhibitors in repeated protocol biopsies: an independent risk factor for chronic kidney allograft damage

The purpose of the prospective study was to determine the prevalence of subclinical toxicity of calcineurin inhibitors (CI) in repeated protocol renal allograft biopsies and to assess its impact on the development of chronic graft changes. A total of 424 biopsies were conducted in a cohort of 158 patients; of these biopsies, 158 were in the third week, 142 were in the third month and 124 were in the first year after transplantation. Histological signs of toxicity occurred in the third week in 33 (20.1%) patients, with persistence after CI dose reduction in the third month in 27 (19.0%) and in the first year in 23 (18.5%) patients. Of the toxic changes, 52% were clinically silent. At the end of the one-year follow-up, both subclinical and clinically manifest toxicity resulted in a similar progression of chronic changes quantified by Banff chronicity score and they significantly differed from the control group (P< 0.05). Subclinical toxicity affects a significant percentage of grafts; it occurs independently of dosage, blood level and type of applied CI. It is associated with the progression of chronic changes as early as in the first year after transplantation and represents an independent risk factor for chronic allograft damage. We report here our clinical approach to toxicity