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Biomedical subjects

S Roy

Publications and source records attributed to S Roy.

At least 649 records · Page 36Linked to original sources
PubMed1988

Acute renal failure at onset of therapy for advanced stage Burkitt lymphoma and B cell acute lymphoblastic lymphoma.

Aggressive therapeutic maneuvers to reduce the risk for acute renal failure are routine in the management of children receiving therapy for advanced stage Burkitt lymphoma and B cell acute lymphoblastic leukemia. The case histories of 40 children entered into a prospective treatment protocol for high-risk disease revealed that ten of 40 patients (25%) had acute renal failure, two at the time of hospital admission and eight in whom renal insufficiency developed 12 to 132 hours following initiation of cytotoxic chemotherapy. Admission values for serum lactic dehydrogenase and serum uric acid were not statistically different between patients with and without subsequent renal failure. Urine output in the 12 hours prior to antineoplastic therapy was 2.9 +/- 0.8 mL/kg/h in the eight children in whom renal failure developed and 5.3 +/- 0.4 mL/kg/h in the patients who did not (P less than .01). The urinary flow rate in the 24 hours following initiation of chemotherapy was significantly lower in children in whom renal impairment developed (1.0 +/- 0.2 mL/kg/h, mean +/- SE) compared with those who did not (3.7 +/- 0.3 mL/kg/h, P less than .001). Renal failure could not be attributed to hyperuricemia or hyperphosphatemia in the majority of patients with renal failure. One to four hemodialysis treatments (2.5 +/- 0.3) were required for the ten patients. Serum creatinine concentrations returned to normal in the nine survivors. Response to initial antineoplastic therapy was not affected by the presence of renal failure. Renal failure continues to be a major clinical problem in children with Burkitt lymphoma and B cell lymphoblastic leukemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1988

Infection of human monocytes/macrophages by HIV-1: effect on secretion of IL-1 activity.

We have infected peripheral blood-derived monocyte/macrophage cultures with HIV-1 in order to determine the effect of such infection on cellular immunoregulatory function. We have confirmed that monocytes/macrophages are susceptible to infection by HIV-1, as determined by in situ hybridization using a HIV-1-specific RNA probe and by the presence of reverse transcriptase activity in culture supernatants. The cells employed efficiently supported viral replication in the absence of significant cytopathic effect, and secreted as little as 20% of the amount of IL-1 activity of uninfected controls in response to stimulation with either latex beads or lipopolysaccharide. This effect was not observed when UV-inactivated HIV-1 was used to infect the cells.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Immunoregulatory studies in patients with IgA nephropathy.

Numerous studies have evaluated T cell subsets and in vitro IgA synthesis in patients with IgA nephropathy. These reports have resulted in the hypothesis that defective regulation of IgA synthesis is important in the pathogenesis of IgA nephropathy. Baseline immunologic measurements were performed in a clinically well characterized group of 19 pediatric and 13 adult (greater than or equal to 18 years) patients with no macrohematuria or intercurrent infection at the time of study. Mean percentages of OKT3 and OKT4 subsets were significantly decreased for the patients as compared to healthy adult controls. Mean T4:T8 ratios were similar for control and patient groups although 7 patients had T4:T8 ratios greater than 2 SD above the control mean. Unstimulated and pokeweed mitogen stimulated in vitro IgA synthesis was similar for patients and controls. During six episodes of macrohematuria in five patients no significant changes occurred for T cell subset percentages, while mean T4:T8 ratios decreased from baseline. Mean serum concentration of IgA increased during these episodes, although in vitro IgA synthesis remained normal. Our data fail to demonstrate a consistent immunoregulatory abnormality for patients with IgA nephropathy.

Adolescent↗
PubMed1988

Efficacy and safety of single-dose ceftizoxime vs. multiple-dose cefoxitin in preventing infection after vaginal hysterectomy.

The efficacy, safety and effect of a single, 1-g dose of ceftizoxime on the return of vaginal flora were compared to those of the standard regimen of three 2-g doses of cefoxitin for prophylaxis in 99 randomized women undergoing vaginal hysterectomy. Thirty-four were studied in Dallas and 65 in Los Angeles. Surgical procedures were comparable for all the antibiotic groups, although proportionately more simple hysterectomies were performed in Dallas. The patients received a povidone-iodine vaginal preparation immediately before surgery; vaginal packs, when used, contained no antimicrobial agents. Primary prophylactic failure (operative site infection) occurred in 1 of 52 (1.9%) and 4 of 47 (8.5%) of the ceftizoxime- and cefoxitin-treated patients, respectively, for a nonsignificant difference. All five primary prophylactic failures occurred in the Los Angeles patients. One patient in each antibiotic group developed a urinary tract infection and was classified as a secondary prophylactic failure. Febrile morbidity, length of hospital stay and incidence of adverse effects did not differ by antibiotic. The enterococcus was commonly found in the postoperative vaginal flora and was of no value in predicting operative-site infection. Enterobacter species and Pseudomonas aeruginosa were isolated more commonly in patients who received cefoxitin. Diphtheroids, Staphylococcus epidermidis and Peptostreptococcus species were isolated more commonly in patients treated with ceftizoxime.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Focal segmental glomerulosclerosis in children: comparison of nonedematous and edematous patients.

Persistent proteinuria without edema, associated with focal segmental glomerulosclerosis (FSGS), has been increasingly observed in our pediatric population. The clinical and pathological features and long-term outcome of these patients are poorly understood and less frequently reported. Ten nonedematous children (10.3 +/- 1.4 years) with proteinuria and FSGS are compared with 16 children (9.0 +/- 0.4 years) with FSGS and nephrotic syndrome (NS). Urinary protein excretion and serum cholesterol were statistically higher and serum albumin statistically lower in the children with FSGS-NS. The percentage of glomeruli with sclerosis was similar in the two groups. Mesangial proliferation was observed more frequently in the nephrotic children and focal or diffuse tubular atrophy more often in the nonedematous children with FSGS. Followup serum creatinines are more than 1 SD above the mean for age in 3 of 10 nonedematous patients with FSGS and 9 of 16 patients with FSGS-NS. Of 10 nonedematous patients with FSGS, 1 progressed to renal failure 20 months after diagnosis, while 3 of 16 patients with FSGS-NS progressed to renal failure. We conclude from these data that NS is a poor prognostic sign in FSGS in children and that neither the percentage of glomeruli with sclerosis nor the presence of tubular atrophy is predictive of NS in our patients.

Adolescent↗
PubMed1987

Cranio-cerebral erosion (growing fracture of the skull in children). Part I. Pathology.

Seventeen cases of cranio-cerebral erosion were subjected to detailed histopathological study in order to get a better insight into the pathogenesis of this lesion. It was found that the bone and brain at the site and edge of the defect show not only evidence of damage at the time of initial injury, but also of "active" progressive damage months and years later. The possible causes for continuing damage to the brain and bone are discussed.

Brain↗
PubMed1987

The azobenzenearsonate conjugate of poly-glutamic-lysine-tyrosine will induce tyrosine-azobenzenearsonate-specific T-cell responses and clones in nonresponder mice.

Mice of the H-2b haplotype are low responders to ABA-tyr. However, when they were immunized with ABA coupled to poly-GLT15 for which they are nonresponders, they developed strong proliferative responses to ABA-tyr in draining lymph node cells. Clones derived from these cells were highly reactive to ABA-tyr although the original mice were not. No evidence was found to indicate that suppression played a role in the failure to respond to ABA-tyr. Characterization of two clones showed an absolute specificity for the arsonic acid group and the Azo linkage. Alterations in the terminal amino acid residues produced varying changes in reactivity which could not be ascribed unequivocally to an effect on epitope or agretope.

Animals↗
PubMed1987

Biological activity of mu opioid receptor.

The purification of the mu-opioid receptor has proved to be more difficult than most other receptors for at least two reasons. First, they are easily inactivated by most detergents and the second problem is the heterogeneous existence of the opioid receptor. Despite these problems, this laboratory, and several others, have recently reported purification of the mu-opioid receptor. The 58,000 molecular weight of the purified mu-opioid receptor agrees closely with the value reported by other investigators. In addition, it was found that this purified mu-opioid receptor was associated with a phosphatase activity. While the relevance of this phosphatase activity to opioid receptor action remains to be determined, it is interesting to note that this activity was stimulated by Mn++ and Mg+ ions, both of which also increase opioid binding.

Animals↗
PubMed1987

Renal and pancreatic calcification in rheumatoid arthritis with Sjögren's syndrome.

We describe a female patient who developed seropositive rheumatoid arthritis (RA) at the age of 12 years. After 10 years her disease was complicated by Sjögren's syndrome (SS) and distal (type 1) renal tubular acidosis (RTA). Seven years later she was noted to have nephrocalcinosis. At the age of 32, investigation of a short history of weight loss and abdominal pain revealed a benign gastric ulcer and chronic calcific pancreatitis. We believe she is the first patient with RA and SS in whom complicating renal and pancreatic calcification have been reported. Her case emphasizes the good prognosis of type 1 RTA in SS and suggests that pancreatic involvement may be more common than clinically apparent.

Arthritis, Rheumatoid↗
PubMed1987

Cardiomegaly following extensive burns.

One of our patients had been recovering from prolonged illness for about eight months following extensive deep burns of the lower limbs, along with other complications, when he had a sudden attack of acute dyspnea with orthopnea. The cause of this condition was diagnosed as secondary hypodynamic cardiomyopathy. We found no previous report of such a complication following burns in the available literature.

Adolescent↗
PubMed1987

Severe chloride deficiency in the neonate: the canine puppy as an animal model.

Studies were designed to develop an animal model for the syndrome of hypochloremic, hypokalemic metabolic alkalosis (HMA), and failure to thrive in infants due to intake of chloride-deficient formula. Littermate canine puppies, 2 wk old, were fed soy formula containing normal chloride, 20 mEq/liter (NC, n = 5), or low chloride, 1 mEq/liter (LC, n = 5) for 4 wk, first by gavage and ad libitum thereafter. After 1 wk of LC formula, HMA developed in LC puppies although both NC and LC puppies had similar fluid and caloric intake and gain in weight and forelimb length. Two wk of LC formula also resulted in a higher serum creatinine and calcium but lower phosphate level in LC than NC puppies. After 4 wk of LC, weight and forelimb length were much less in LC than NC puppies. Plasma renin activity decreased with age in NC but remained elevated in LC. In a separate group of puppies (n = 6) with HMA, chloride supplementation of LC formula as NaCl to NC levels corrected HMA despite continued citrate intake. We conclude that the canine puppy is an appropriate model to study HMA due to decreased chloride intake. Low chloride intake independent of citrate caused the HMA.

Alkalosis↗