ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Chemotaxis and adherence to polymorphonuclear neutrophils (PMN) subpopulations from cord blood of 13 healthy neonates and blood of 16 healthy adults as control subjects were determined using the rosetteforming procedure, the modified Boyden method, and51Cr adherence assay. The percentage of rosette-forming neutrophils (RFN) (Fc receptor expression) of cord PMN (35 ± 8%) was significantly lower than that of adult PMN (60 ± 4%, p<0.01). Differences in chemotaxis of PMN subpopulations between cord and adult PMN after stimulation by their own endotoxin-activated plasma were as follows: (i) unfractionated adult PMN (A) (n=10) versus adult RFN (B) (n=5) versus adult nonRFN (C) (n=5); (A)<(B), p<0.01 and (A)>(C), p<0.01; (ii) unfractionated cord PMN (a) (n=5) versus cord RFN (b) (n=5) versus cord non-RFN (c) (n=5); (a)<(b), p<0.01 and (a) versus (c), NS; (iii) (A)>(a), p<0.01; (iv) (B)>(b), p<0.05 and (C) versus (c), NS. Similarly, differences in adherence were as follows: (i) (A) (n=13) versus (B) (n=4), NS and (A)>(C) (n=4), p<0.01; (ii) (a) (n=4) versus (b) («=4), NS and (a)>(c) («=4), p<0.01; (iii) (A)>(a), p<0.05; (iv) (B) versus (b), NS and (C) versus (c), NS. These results suggest that differences in chemotaxis and adherence between cord and adult PMN may relate in part to differences of PMN subpopulations

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The nonprotein amino acid L-allo-isoleucine is formed endogenously in maple syrup urine disease patients from (R)-3-methyl-2-oxo-pentanoic acid. During strict metabolic balance, the plasma L-allo-isoleucine/L-isoleucine ratio correlates inversely with the residual activity of the branched-chain 2-oxoacid dehydrogenase in fibroblasts and thus constitutes a relevantin vivoparameter of the severity of the metabolic defect in MSUD patients.

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The transport of phosphate (PO4) through the placenta is a secondary active phenomenon whose control mechanisms are unknown. In this study, we investigated whether PTH, the main hormone regulating PO4transport in the kidney and gut, has a similar role in the placenta. Incubation of normal term human placenta fragments for 1 min with PTH increased the cAMP content of the tissue by 285%. A dose-response curve of the effect of the hormone showed that the cAMP accumulation reached a maximal level with 3.5 x 10-8M PTH. Incubation of the placenta fragments with 10-4M di-butyryl cAMP resulted in a significant decrease in the PO4uptake by the brush border membranes prepared from these fragments. Increasing concentrations of di-butyryl cAMP from 0 to 10-3M significantly decreased the PO4uptake from 0.29 ± 0.02 to 0.22 ± 0.01 pmol/μg/20 s. Similarly, incubation of the placental tissue with PTH resulted in a comparable decrease in the PO4uptake by the corresponding brush border membrane vesicles. In contrast, direct incubation of brush border membranes with the hormone did not influence PO4uptake. It is concluded that PTH probably regulates the PO4transport through the placenta syncytiotrophoblast cell through cAMP mediation. Because adenylate cyclase is located in the basal plasma membrane, it is likely that only the fetal hormone is implicated in this process

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

L-histidine is an essential amino acid. Its fetal-to-maternal blood concentration ratio is high, suggesting active placental transport. In this study, human placental microvillous membrane vesicles were used to characterize L-histidine transport, heretofore not evaluated in human tissue. L-Histidine uptake by microvillous membrane vesicles was stimulated by an inward sodium gradient, leading to an “overshoot,” followed by apparent equilibration. Linear uptake at 22° C was limited to the 1st min. The initial sodium-dependent uptake rate was proportional to the sodium concentration in the medium. The sodium-dependent uptake was markedly diminished or lost when potassium, cesium, or choline was substituted for sodium but not lithium. Replacement of chloride with sulfate or gluconate had little effect. Sodium-stimulated Lhistidine uptake was further stimulated by an outward potassium gradient (inside-negative) in the presence of valinomycin. Sodium-dependent uptake kinetic constants for L-histidine were: Km=0.44 ± 0.18 mM: Vmax= 536 ± 94 nmol/mg/30 s (mean ± SD). 2-(methylamino) isobutyric acid did not inhibite L-histidine uptake. Conversely, L-histidine noncompetitively inhibited sodium-dependent uptake of 2-(methylamino)isobutyric acid and Lcysteine. L-glutamine competitively inhibited sodium-dependent L-histidine uptake. L-histidine uptake was stimulated by preloading the vesicles with either L-histidine or L-glutamine (transstimulation). L-histidine uptake was not sensitive toN-ethylmaleimide treatment but was strongly inhibited by low pH. These findings suggest that L-histidine is transported in the human placenta by a specific sodium-dependent system similar to the “N” system described in rodent hepatocytes. Furthermore, the ready availability of placental tissue may make it a useful resource for studies of human epithelial transport biology

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

It is assumed that when anticonvulsants arrest seizure, there is rapid return of brain high energy phosphates and brain lactate to control values. To test this hypothesis, diazepam was administered to neonatal dogs during flurothyl-induced seizure. In vivo31P nuclear magnetic resonance spectroscopy disclosed that diazepam quickly arrested electrographic seizure and restored brain phosphocreatine and inorganic phosphate to baseline values. In contrast, in vivo1H nuclear magnetic resonance spectroscopic measurements showed that arrest of seizure with diazepam did not return brain lactate to control values. The sustained increase in cerebral blood flow and prolonged elevation of brain lactate, acetate, valine, and succinate in the postictal period indicate that metabolic recovery of the brain occurs over an extended period of time after the normalization of EEG, phosphocreatine, and brain pH

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Maternal corticosteroid treatments decreased lung protein leaks and increased the compliance responses to exogenous surfactant in 27-day preterm rabbits. We asked if maternal corticosteroid treatments at different gestational ages might alter these responses. Pregnant does were given 0.1 mg/kg betamethasone 48 and 24 h before study of the rabbits at 27, 28, and 29 days of gestational age and term newborns at 31 days of gestational age. Alternate rabbits at each gestation were treated with 50 mg/kg surfactant after delivery. Alveolar saturated phosphatidylcholine pool sizes increased with gestation similarly in control and corticosteroid-treated groups. Corticosteroids improved compliance relative to control values at 29 days of gestational age in animals not treated with surfactant and improved the compliance response to surfactant treatment at 27 and 28 days of gestational age. Corticosteroids decreased the leak of radiolabeled albumin to the lungs and alveolar washes at all preterm gestations with a maximum decrease to 16% of the control value at 29 days of gestation. Surfactant decreased this protein leak more effectively than did corticosteroids at the earlier gestations. There were potentially beneficial effects of corticosteroids either alone or together with surfactant at all preterm gestations studied. No protein leak or compliance effects of either treatment were noted in the term newborns

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

A murine model for short-chain acyl-coenzyme A dehydrogenase (SCAD) deficiency has been identified and characterized in BALB/cByJ mice. These mice have undetectable SCAD activity, severe organic aciduria; excreting ethylmalonic and methylsuccinic acids and Nbutyrylglycine, and develop a fatty liver upon fasting or dietary fat challenge. The mutant mice develop hypoglycemia after an 18-h fast, and have elevated urinary and muscle butyrylcarnitine concentrations. Most of these findings parallel those of human disorders associated with SCAD deficiency and other β-oxidation defects. This mouse model presents important opportunities to investigate the biology of mammalian fatty acid metabolism and the related human diseases

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1989

数据来源: OVID