Students with disabilities in community colleges : the relationship of select demographic and academic variables to transfer

The original research detailed in this document recognizes that the majority of students with disabilities between 18-69 years of age will attend a community college. The literature also indicates an exponential increase for better job opportunity and earnings relative to individuals with disabilities who attain higher levels of education. This study examined 12 predictors for transfer from the community college to a four-year institution for students with disabilities. Pre-existing data from the California Community College Chancellor’s Office (CCCCO) matched with data from the National Student Clearinghouse, running from the academic year 1995-1996 until 2006-2007, were used. This resulted in a sample of 31,590 students with disabilities. Of the 4741 students with disabilities who transferred to a four-year college during that 12 year time period, the average number of years for a transfer was 5.83. A logistic regression with all 21 predictors significantly predicted transfer, χ² (21, N = 26,751) = 4918.46, _p_ < .001. Variables that were found to have a strong relationship with transfer were also found to be the strongest predictors of transfer: (a) proportion of transfer courses in which enrolled, and (b) proportion of units students completed out of the total number in which students enrolled. Implications for practice and for research are discussed and including the place of self-determination for successful students with disabilities in a postsecondary environment

Reversible acute renal failure from gross haematuria due to glomerulonephritis: not only in IgA nephropathy and not associated with intratubular obstruction

Seven patients with acute renal failure due to gross haematuria caused by glomerulonephritis are described. Gross haematuria lasting 4-40 days led to acute impairment of renal function of variable severity (peak plasma creatinine 1.3-12 mg/dl) and duration. While partial recovery of renal function occurred in all patients within few days, complete remission was observed only some months later. Three patients had IgA nephropathy (2 the primary form and 1 nephritis secondary to Schönlein-Henoch purpura), two patients had acute postinfectious glomerulonephritis, andtwo others had focal necrotizing (pauci-immune) glomerulonephritis. The glomerular changes seen in renal biopsy were not enough to explain per se the renal function impairment. Tubular changes, however, were severe and consisted of tubular necrosis, erythrocyte casts, erythrocyte phagocytosis by tubular cells, accompanied by interstitial damage (oedema, red-cell extravasation, and inflammatory infiltrates). Study of the renal biopsies by immunofluorescence revealed retrodiffusion of Tamm-Horsfall protein into the glomerular Bowman's space, a sign of obstructed tubular flow in any case. It is concluded that acute renal failure due to gross haematuria in glomerulonephritic patients may not occur only in IgA nephropathy, as reported so far, and is not associated with intratubular obstructio

Ureteral endometriosis: a rare and underdiagnosed cause of kidney dysfunction

Little attention has been paid by the renal literature to ureteral endometriosis, a rare and silent disorder that can eventually lead to renal failure. In endometriosis, the ureteral involvement can be limited to a single ureter, more often the left one, or both ureters with consequent urine tract obstruction and ureterohydronephrosis. In most cases, the ureteral obstruction is caused by endometrial tissue surrounding the ureter (extrinsic ureteral endometriosis). In the remaining cases, endometrial cells are located within the ureter (intrinsic ureteral endometriosis). Progressive ureteral obstruction can be insidious in onset and can ultimately lead to renal failure if a correct diagnosis is missed. The true incidence of renal failure caused by endometriosis is completely unknown, although cases have been reported in the literature. The diagnosis of ureteral endometriosis is difficult since the disease may be clinically silent or associated with non-specific symptoms. Only a high index of suspicion and radiological support may help to obtain an early diagnosis. However, while renal imaging is useful in the cases of extrinsic endometriosis, the diagnosis of intrinsic endometriosis often requires ureteroscopy or laparoscopy. The prognosis of ureteral endometriosis depends on the time of diagnosis. In too many cases of bilateral obstruction, the patient is referred to the nephrologist because of an advanced, irreversible renal failure. Although some patients may benefit from progestin or anti-arotamase therapy, in most cases of ureteral endometriosis surgery is needed, laparoscopy surgery being preferred today to laparatomy

Renal Disease in Essential Mixed Cryoglobulinaemia: LONG-TERM FOLLOW-UP OF 44 PATIENTS

The mode of presentation of renal disease in 44 patients with essential mixed cryoglobulinaemia (EMC) was: acute renal failure (two patients), acute nephritic syndrome (six patients), nephrotic syndrome (eight patients), proteinuria and/or haematuria (28 patients). Renal biopsy, performed in 35 patients, showed proliferative lesions in 33, while only minimal glomerular changes were seen in the remaining two. Immunofluorescence studies showed: IgG (85 per cent), IgA (36 per cent), IgM (90 per cent), C3 (90 per cent), Clq (47 per cent), and C4 (33 per cent) deposits, mainly located in subendothelial position. On electron microscopy, crystalloid structure of deposits and monocyte infiltration of capillary loops were the outstanding feature. The survival rate was 75 per cent at 10 years from the onset of clinical symptoms. Thirty-nine patients were followed for three to 146 months (mean 53·8). Twelve patients died, cardiovascular disease and infection being the commonest cause of death. Thirteen patients showed acute renal failure or acute nephritic syndrome: nine recovered completely, whereas the remaining four died during the acute renal episode. Three patients developed chronic renal failure, but only one required chronic dialysis. The ominous significance of renal impairment in EMC should therefore be revaluated. The high prevalence of hypertension (28/44 patients) which was refractory to treatment in six, may be important to the clinical outcom

18F-fluorodeoxyglucose positron emission tomography-positive sarcoidosis after chemoradiotherapy for Hodgkin’s disease: a case report

<p>Abstract</p> <p>Introduction</p> <p>The occurrence of granulomatous disease in the setting of Hodgkin's disease is rare; however, when it occurs it can pose significant clinical and diagnostic challenges for physicians treating these patients.</p> <p>Case presentation</p> <p>We report the case of a 33-year-old Caucasian woman of Mediterranean descent with newly diagnosed ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography (PET)/computed tomography (CT) scan-positive, early-stage Hodgkin's disease involving the cervical nodes who, despite having an excellent clinical response to chemotherapy, had a persistent ¹⁸F-FDG PET scan-positive study, which was suggestive of residual or progressive disease. A subsequent biopsy of her post-chemotherapy PET-positive nodes demonstrated sarcoidosis with no evidence of Hodgkin's disease.</p> <p>Conclusion</p> <p>This case highlights the fact that abnormalities observed on posttherapy PET/CT scans in patients with Hodgkin's disease are not always due to residual or progressive disease. An association between Hodgkin's disease and/or its treatment with an increased incidence of granulomatous disease appears to exist. Certain patterns of ¹⁸F-FDG uptake observed on PET/CT scans may suggest other pathologies, such as granulomatous inflammation, and because of the significant differences in prognosis and management, clinicians should maintain a low threshold of confidence for basing their diagnosis on histopathological evaluations when PET/CT results appear to be incongruent with the patient's clinical response.</p

Cyclosporin in idiopathic glomerular disease associated with the nephrotic syndrome : Workshop recommendations

Management of idiopathic glomerular disease associated with nephrotic syndrome (INS) remains controversial and one of the most complex areas relates to utilization of the drug cyclosporin. This is despite its demonstrated effectiveness in several histologic types of the INS in randomized controlled trials. Cyclosporin is effective in inducing remission of proteinuria in approximately 80% of steroid-sensitive cases of minimal change disease (MCD). Cyclosporin is also effective in both the induction of remission and long-term preservation of renal function in steroid-dependent/-resistant MCD and steroid-resistant focal segmental glomerulosclerosis (FSGS). The overall response rate in FSGS is lower than in MCD, and long-term therapy (>12 months) may be required to both achieve remission and sustain it. Cyclosporin therapy is also of benefit in reducing proteinuria in 70-80% of patients with steroid-resistant membranous nephropathy (MGN). In MGN, the maximum benefit is often delayed compared to MCD (>12 weeks). Cyclosporin is generally well tolerated and safe. The major concern remains the nephrotoxicity, but with careful monitoring of the patient's renal function; minimizing the maintenance dose and utilizing repeat renal biopsy in those receiving long-term therapy, this risk can be minimized. The algorithms have been developed derived from the best evidence in the literature in each of the histologic types to help provide a guide to the integration of cyclosporin into the management of INS for the practicing nephrologist

Phosphorylation-Independent Regulation of Atf1-Promoted Meiotic Recombination by Stress-Activated, p38 Kinase Spc1 of Fission Yeast

BACKGROUND:Stress-activated protein kinases regulate multiple cellular responses to a wide variety of intracellular and extracellular conditions. The conserved, multifunctional, ATF/CREB protein Atf1 (Mts1, Gad7) of fission yeast binds to CRE-like (M26) DNA sites. Atf1 is phosphorylated by the conserved, p38-family kinase Spc1 (Sty1, Phh1) and is required for many Spc1-dependent stress responses, efficient sexual differentiation, and activation of Rec12 (Spo11)-dependent meiotic recombination hotspots like ade6-M26. METHODOLOGY/PRINCIPAL FINDINGS:We sought to define mechanisms by which Spc1 regulates Atf1 function at the ade6-M26 hotspot. The Spc1 kinase was essential for hotspot activity, but dispensable for basal recombination. Unexpectedly, a protein lacking all eleven MAPK phospho-acceptor sites and detectable phosphorylation (Atf1-11M) was fully proficient for hotspot recombination. Furthermore, tethering of Atf1 to ade6 in the chromosome by a heterologous DNA binding domain bypassed the requirement for Spc1 in promoting recombination. CONCLUSIONS/SIGNIFICANCE:The Spc1 protein kinase regulates the pathway of Atf1-promoted recombination at or before the point where Atf1 binds to chromosomes, and this pathway regulation is independent of the phosphorylation status of Atf1. Since basal recombination is Spc1-independent, the principal function of the Spc1 kinase in meiotic recombination is to correctly position Atf1-promoted recombination at hotspots along chromosomes. We also propose new hypotheses on regulatory mechanisms for shared (e.g., DNA binding) and distinct (e.g., osmoregulatory vs. recombinogenic) activities of multifunctional, stress-activated protein Atf1

mTOR Controls Ovarian Follicle Growth by Regulating Granulosa Cell Proliferation

We have shown that inhibition of mTOR in granulosa cells and ovarian follicles results in compromised granulosa proliferation and reduced follicle growth. Further analysis here using spontaneously immortalized rat granulosa cells has revealed that mTOR pathway activity is enhanced during M-phase of the cell cycle. mTOR specific phosphorylation of p70S6 kinase and 4E-BP, and expression of Raptor are all enhanced during M-phase. The predominant effect of mTOR inhibition by the specific inhibitor Rapamycin (RAP) was a dose-responsive arrest in the G1 cell cycle stage. The fraction of granulosa cells that continued to divide in the presence of RAP exhibited a dose-dependent increase in aberrant mitotic figures known as anaphase bridges. Strikingly, estradiol consistently decreased the incidence of aberrant mitotic figures. In mice treated with RAP, the mitotic index was reduced compared to controls, and a similar increase in aberrant mitotic events was noted. RAP injected during a superovulation regime resulted in a dose-dependent reduction in the numbers of eggs ovulated. Implications for the real-time regulation of follicle growth and dominance, including the consequences of increased numbers of aneuploid granulosa cells, are discussed