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Biomedical subjects

M S Caplan

Publications and source records attributed to M S Caplan.

41 records · Page 3Linked to original sources
PubMed1980

Comparative biochemistry of murine arylsulfatase B.

Arylsulfatase B was purified 4500-fold from liver and kidney of C57BL/6J mice. Hepatic and renal arysulfatase B are apparently determined by a single structural locus; however, posttranslational modification introduces inter- and intratissue microheterogeneity. Partially purified enzyme from C57BL/6J, A/J, C3H/HeJ, and SWR/J mice has similar catalytic properties. The 4500-fold-purified arylsulfatase B from SWR/J and C3H/HeJ mice was more thermostable than that from C57BL/6J and A/J mice, strongly suggesting that the thermostability difference reflects an alteration of the primary structure of the enzyme. Thermal stability of arylsulfatase B was pH dependent and markedly influenced by buffer anion. Variation of thermostability did not appear accountable for the observed activity variation among these strains; however, this possibility cannot be rigorously excluded by presently available data. Thirty-five murine strains were found to possess the As-1a allele (thermostable enzyme), while As-1b was largely restricted to A and C57 strains.

Animals↗
PubMedDate not supplied

Endothelin-1-induced placental and fetal growth restriction in the rat.

The objective of this study was to evaluate the effect of increased circulating endothelin on fetal and placental growth in the rat. Indwelling arterial and venous catheters were placed on day 14 of a 22-day gestation in timed-pregnant Sprague-Dawley rats. Saline, 0.2 nmol/kg/h endothelin, or 0.5 nmol/kg/h endothelin was continuously infused from day 15 through 21 in randomly assigned animals (n = 12 in each group). Maternal arterial blood pressure and serum endothelin levels were evaluated on days 15, 18, and 21 of gestation. On day 21, pregnancy outcome data including fetal and placental weights, litter size, and the occurrence of stillbirths were ascertained, and fetal blood was obtained for serum endothelin levels. All data were compared among the three groups, and statistical significance was determined by analysis of variance. Endothelin infusion resulted in a dose-dependent decrease in fetal and placental weights when compared to saline-treated pregnancies. A significant increase in maternal arterial blood pressure was noted only in the 0.5 nmol/kg/h endothelin group. Fetal and placental growth restriction occurred in the absence of maternal hypertension in the 0.2 nmol/kg/h group. These results demonstrate that endothelin infusion causes restriction of fetal and placental growth, even in the absence of maternal hypertension.

Analysis of Variance↗
PubMedDate not supplied

Necrotizing enterocolitis: a review of pathogenetic mechanisms and implications for prevention.

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature neonates that accounts for 3000 to 4000 deaths each year in the United States. The pathogenesis is not well understood, however theories suggest that prematurity, enteral feeding, bacterial colonization, and intestinal ischemia contribute to the intestinal injury. Furthermore, recent studies have shown that platelet activating factor and perhaps other inflammatory mediators mediate bowel necrosis in animals and possibly in humans. Although no specific intervention for NEC treatment exists, preventive therapy using either enteral IgA supplementation, breast milk feeding, antibiotic prophylaxis, or exogenous steroid administration have reduced the incidence of this overwhelming disease in small randomized trials. These modalities and perhaps PAF antagonists or other inflammatory mediator inhibitors may reduce the incidence or severity of NEC in the next several years.

Enterocolitis, Pseudomembranous↗
PubMedDate not supplied

Role of asphyxia and feeding in a neonatal rat model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a common gastrointestinal disorder affecting premature infants. To investigate critically the importance of the purported risk factors of NEC (formula feeding, asphyxia, bacteria, and prematurity), we developed a neonatal rat model that closely mimics the human disease. Full-term and premature newborn rats were stressed with formula feeding, asphyxia, and/or exogenous bacterial colonization and subsequently evaluated grossly and histologically for the development of intestinal injury. We found that most animals treated with asphyxia, formula feeding, and bacteria developed NEC (77%) and died (86%) by 96 h. All maternally fed animals treated with asphyxia and bacterial colonization survived and had normal intestinal histology. Furthermore, asphyxia was a critical instigating factor, because formula and bacterial exposure without asphyxia resulted in normal intestine and minimal mortality (12%). Enteral bacterial colonization was not a significant determinant of NEC in this model. We conclude that the neonatal rat model is an excellent test system for the study of NEC. As in the human disease, asphyxia and formula feeding play an important role in the pathophysiology of experimental NEC.

Animal Nutritional Physiological Phenomena↗