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Biomedical subjects

S L Watkins

Publications and source records attributed to S L Watkins.

52 records · Page 3Linked to original sources
PubMed1996

Does renal osteodystrophy develop and/or progress during the course of rhGH treatment?

Recent expansion of the use of recombinant growth hormone (GH) to non-GH-deficient patients demands close attention to possible complications in these patients, including the effects on bone. Recent studies on the use of GH in children with chronic renal failure (CRF) provide some early data. In several studies of GH in CRF no significant differences in radiographic osteodystrophy scores, serum calcium, phosphorus or parathyroid hormone (PTH) levels between treated and untreated groups have been found. Alkaline phosphatase increases transiently. The effect of ROD on growth response has not yet been reported. Children with CRF treated with GH should be serially monitored for ROD with serial radiographs and for serum calcium, phosphorus, alkaline phosphatase and PTH levels.

Child↗
PubMed1994

Escherichia coli O 157:H7-associated hemolytic-uremic syndrome after ingestion of contaminated hamburgers.

We conducted a retrospective analysis of 37 children with Escherichia coli O157:H7-associated hemolytic-uremic syndrome. The infection was traced to contaminated hamburgers at a fast-food restaurant chain. Within 5 days of the first confirmed case, the Washington State Department of Health identified the source and interrupted transmission of infection. Ninety-five percent of the children initially had severe hemorrhagic colitis. Nineteen patients (51%) had significant extrarenal abnormalities, including pancreatitis, colonic necrosis, glucose intolerance, coma, stroke, seizures, myocardial dysfunction, pericardial effusions, adult respiratory disease syndrome, and pleural effusions. Three deaths occurred, each in children with severe multisystem disease. At follow-up two children have significant impairment of renal function (glomerular filtration rate < 80 ml/min/per 1.73 Hm2); both of these children have a normal serum creatinine concentration. Hemolytic-uremic syndrome is the most common cause of acute renal failure in children, and this experience emphasizes the systemic nature of this disease. Clinicians should anticipate that multisystem involvement may occur in these patients, necessitating acute intervention or chronic follow-up. This outbreak of Hemolytic-uremic syndrome also highlights the microbiologic hazards of inadequately prepared food and emphasizes the importance of public health intervention in controlling Hemolytic-uremic syndrome.

Adolescent↗
PubMed1994

Peritoneal equilibration test curves and adequacy of dialysis in children on automated peritoneal dialysis.

Peritoneal equilibration tests (PETs) and adequacy studies have been performed to guide dialysis prescriptions in adult continuous ambulatory peritoneal dialysis patients, although few studies have been reported in pediatric patients on nightly cycling peritoneal dialysis. We performed 49 PETs in 28 children on automated peritoneal dialysis (mean age, 8.9 years; age range, 0.2 to 19.8 years; mean time on dialysis, 14.1 months) using Dianeal 2.5% dialysate (Baxter Healthcare Corp, McGaw Park, IL) inflow volumes of 1,200 mL/m2 (approximately 40 mL/kg), and standard technique. Mean 4-hour dialysate/plasma creatinine was 0.73 +/- 0.12 (range, 0.45 to 1.03). Mean 4-hour dialysate glucose/initial dialysate glucose was 0.28 +/- 0.10 (range, 0.06 to 0.50). Eighty percent of these PETs fell into the high average/high solute transport categories proposed by Twardowski, based on adult PETs. Twenty-four-hour dialysate collections were analyzed in 28 patients for protein loss and glucose absorption, as well as for calculation of weekly Kt/V. Mean weekly Kt/V was 1.94 +/- 0.94 (range, 0.63 to 5.10). Mean dialytic creatinine clearance calculated from the 4-hour dwell was 5.6 +/- 1.0 mL/min/1.73 m2 (56 L/wk/1.73 m2). Mean daily protein loss was 0.20 +/- 0.13 g/kg/d (range, 0.2 to 9.1 g/d) and glucose absorption was 3.49 +/- 2.24 g/kg/d (range, 17 to 196 g/d). Our results show higher solute diffusion rates in children compared with the published adult PET results (P = 0.0013 and P < 0.0001 for 4-hour creatinine and glucose results, respectively), with trends toward more rapid solute transport in younger compared with older children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

A unique costimulatory pathway defined with T cell hybridomas specific for myelin basic protein: third party costimulators restrict antigenic responses in time and space.

Costimulatory signals regulate T cell responses to myelin basic protein (MBP) during induction of EAE in Lewis rats. However, the physiology of these costimulatory pathways has yet to be resolved. In this study, costimulatory pathways were defined by comparing MBP-stimulated IL-2 production by two types of T cell hybridoma (designated THYB-1 and THYB-2). THYB-1 hybrids required presentation of MBP/Ia complexes to stimulate IL-2 production, whereas THYB-2 hybrids also required the additional presence of costimulatory signals from radiosensitive (RS), nonadherent (NAdh) splenocytes (SPL). This study shows that allogeneic SPL, syngeneic B cells, or syngeneic T cells provided costimulatory signals to THYB-2 hybrids, although only syngeneic B cells were able to provide APC activity. Transduction of costimulatory signals did not occur across a microporous membrane but rather required close proximity of T cell hybrids with RS accessory cells. Simultaneous presence of costimulatory signals together with MHC-restricted antigen were required to initiate and maintain IL-2 production by THYB-2 hybrids. These findings support a model in which costimulatory molecules expressed by effector cells serve to restrict lymphokine production by T-helper cells. That is, THYB-2-like T-helper cells may mediate a paracrine pathway of IL-2 production that provides "help" to antigen-activated effector cell types that coexpress IL-2 receptors with appropriate costimulatory molecules.

Animals↗
PubMed1993

Emergence of a radioresistant population of co-stimulatory splenocytes during remission of experimental autoimmune encephalomyelitis in Lewis rats.

T-cell hybridomas specific for myelin basic protein (MBP) were used to assess regulation of co-stimulatory signals during remission of experimental autoimmune encephalomyelitis (EAE) in Lewis rats. Both THYB-1 and THYB-2 subsets of T-cell hybridomas recognize class II major histocompatibility complex-restricted determinants in the 72-86 encephalitogenic region of MBP. However, THYB-2 hybrids uniquely express additional requirements for co-stimulatory signals from radiosensitive splenocytes (SPL) to support the response of MBP-stimulated IL-2 production. Hence, this subset provides a means to study regulation of THYB-2 specific co-stimulatory signals during the course of EAE. This study revealed that sensitization of Lewis rats with MBP in complete Freund's adjuvant induced a radioresistant subpopulation of co-stimulatory SPL that emerged during the remission phase of EAE. These radioresistant SPL provided specific accessory cell activities that fulfilled the co-stimulatory requirements of THYB-2 hybrids. These findings support the hypothesis that in vivo activation events elicit radioresistance in an emergent clonally expanding population of antigen-specific lymphocytes. A central prediction of this hypothesis is that cellular activation should confer radioresistance to co-stimulatory lymphocytes. This prediction was verified by the observation that in vitro activation of naive SPL with different B- and T-cell mitogens conferred radioresistance to co-stimulatory SPL. Mitogenic activation not only induced radioresistance but also dramatically augmented co-stimulatory activity of purified B cells. In summary, the results of this study support the hypothesis that in vivo activation of co-stimulatory lymphocytes may regulate activities of encephalitogenic T-helper cells during progression and remission of EAE.

Animals↗
PubMed1992

Dialysis-associated seizures in children and adolescents.

A retrospective medical chart review was conducted to document seizure occurrence in 180 children and adolescents (newborn to 22 years of age) receiving hemodialysis (HD) and/or peritoneal dialysis (PD) from January 1974 through June 1988 at Children's Hospital and Medical Center in Seattle, Washington. The purpose of the review was to identify risk factors associated with seizure activity during or up to 24 h following dialysis treatment. Seventy-eight patients received only HD, 79 received only PD and 23 received both HD and PD. Dialysis-associated seizures (DAS) were seen in 7.2% (13/180) of all dialyzed patients; 12 occurred during HD and 1 occurred during PD. Patients receiving only HD were more likely to experience DAS (7/78, 9%), than patients receiving only PD (0/79, 0%) (chi-squared = 5.5, 1 df, P = 0.02). Among the 101 patients who received HD, the risk of HD-associated seizures among those with a prior history of seizure (6/21, 29%) was significantly higher than among those with no history of seizure (6/80, 8%) (chi-squared = 5.2, 1 df, P = 0.02). Prior history of seizure did not influence the risk of seizures among patients receiving PD. These data suggest that patients receiving HD, and especially those with a prior history of seizure, should be monitored closely during dialysis and measures taken to reduce the risk of seizures.

Acute Kidney Injury↗
PubMed1992

Treatment of bladder dysfunction in children with end-stage renal disease.

The appropriate management of the urinary bladder in patients requiring a renal transplant is significantly different in children than in adults. The etiology of end-stage renal disease (ESRD) in 13 of 50 children (26%) transplanted since 1985 was obstructive uropathy/dysplasia. Five of these children had small-capacity, poorly compliant bladders. Our current approach is to restore bladder compliance, improve emptying, and transplant into the restored bladder rather than divert. Pretransplant gastrocystoplasty was performed in three children and the donor ureter was implanted into the augmented bladder. One child awaits transplantation following his bladder augmentation. Bladder function is followed postoperatively by voiding cystourethrography (VCUG) and urodynamics. All of the children who have received transplants into augmented bladders are infection-free, voiding per urethra, and have functioning allografts. We recommend: (1) an initial VCUG in all children; (2) complete urodynamics, if appropriate; (3) urological reconstruction to include augmentation prior to transplantation; (4) transplantation into the reconstructed bladder; and (5) comprehensive follow-up including regular urodynamic assessment.

Adolescent↗
PubMed1990

Escherichia coli O157:H7 and the hemolytic uremic syndrome: importance of early cultures in establishing the etiology.

Fifty-two patients were studied prospectively to determine the etiology of postdiarrheal hemolytic uremic syndrome (HUS). Escherichia coli O157:H7 was isolated from 33 patients (63.4%). If stool obtained within 2 days of the onset of diarrhea was cultured for E. coli O157:H7, the recovery rate was 100%. This rate decreased to 91.7% and 33.3% if stool was cultured for this pathogen 3-6 or greater than or equal to 7 days, respectively, after diarrhea began. The culture-positive group was more likely to have had bloody diarrhea and fecal leukocytes and to have received transfusions than the culture-negative group but was otherwise similar in clinical characteristics. E. coli O157:H7 is the predominant pathogen associated with HUS in western Washington. Recovery of this pathogen is highly dependent on obtaining stool cultures within 6 days of onset of diarrhea.

Adolescent↗
PubMed1989

The increasing incidence of the hemolytic-uremic syndrome in King County, Washington: lack of evidence for ascertainment bias.

The annual incidence of the hemolytic-uremic syndrome was determined for the well-defined population of King County, Washington, between 1971 and 1986, inclusive, to ascertain temporal trends in the epidemiology of this disease. The average annual incidence rose from 0.69 cases per 100,000 children under age 15 years between 1971 and 1975 to 1.77 cases between 1976 and 1980 and 1.74 cases between 1981 and 1986. The mean hematocrits, platelet counts, and blood urea nitrogen and creatinine concentrations on admission were similar in all periods, as were the mean length of hospital stay and the proportions of patients requiring erythrocyte and/or platelet transfusions and dialysis. These results indicate that the increased incidence of hemolytic-uremic syndrome in childhood has been sustained in King County, Washington, and that this increase is not due to ascertainment bias caused by the diagnosis of less severely ill cases. Further investigations are needed to determine whether this increased incidence is being experienced in other populations and to assess strategies for the prevention of microangiopathic sequelae to hemorrhagic colitis.

Adolescent↗
PubMedDate not supplied

Low levels of glucose-6-phosphate hydrolysis in the sarcoplasmic reticulum of skeletal muscle: involvement of glucose-6-phosphatase.

Glucose-6-phosphate hydrolysis was measured in a fraction obtained from rabbit fast-twitch skeletal muscle and corresponding to total sarcoplasmic reticulum, as well as in three subfractions containing longitudinal tubules, terminal cisternae or both structures. In all cases the levels of hydrolysis measured both in native and disrupted membranes were approximately 60-100 times lower than the microsomal glucose-6-phosphatase activity of the corresponding livers. In contrast to liver microsomes, most (up to 80%) of the glucose-6-phosphate hydrolysing activity in muscle sarcoplasmic reticulum membranes was not inactivated by pH 5.0 pre-incubation indicating that it was not catalysed by the specific glucose-6-phosphatase enzyme. Osmotically induced changes in light-scattering intensity of sarcoplasmic reticulum vesicles revealed that, in contrast to liver microsomes, sarcoplasmic reticulum vesicles were not selectively permeable to glucose-6-phosphate as mannose-6-phosphate was also permeable and in addition they were poorly permeable to glucose. Immunoblot experiments using antibodies raised against the glucose-6-phosphatase enzyme, and liver endoplasmic reticulum glucose and Pi translocases, failed to detect the presence of these protein components in sarcoplasmic reticulum membranes. Southern blot analysis of reverse transcriptase-polymerase chain reaction products from rat muscle revealed that glucose-6-phosphatase mRNA is present in muscle. Quantification of Northern blot analysis of liver and muscle mRNA indicated that muscle contains less than 2% of the amount of glucose-6-phosphate mRNA found in corresponding livers. We conclude that very low levels of specific glucose-6-phosphatase (e.g. as in liver; E.C. 3.1.3.9) are present in muscle sarcoplasmic reticulum and that the muscle and liver glucose-6-phosphatase systems have several different properties.

Animals↗