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Biomedical subjects

R Lester

Publications and source records attributed to R Lester.

At least 73 records · Page 4Linked to original sources
PubMed1982

Secretory component and serum immunoglobulin A deficiencies with intestinal autoantibody formation and autoimmune disease: a family study.

A teenage boy with both secretory component deficiency and selective serum immunoglobulin A deficiency also developed pernicious anemia, insulin-dependent diabetes mellitus, pancreatic insufficiency, lymphopenia, intestinal candidiasis, and anti-intestinal antibody. The patient's father had pernicious anemia and diabetes mellitus while the paternal grandfather also had pernicious anemia. Because the patient had inherited the paternal grandmother's human leukocyte antigen complex, there was no direct association between pernicious anemia and the genetic markers. The presence of multiple immunologic abnormalities in a single patient supports the concept of an underlying defect in immune regulation as a central factor in the pathogenesis of these disorders.

Adolescent↗
PubMed1982

Glucose absorption by in vitro perfused ileum of the fetal rat.

In vitro intraluminal perfusion of the fetal rat ileum at 19 and 20 days of gestation was employed to measure the rate of glucose absorption and the unidirectional fluxes of 3-O-methylglucose (3-O-MG). Fetal ileum was mounted on pipettes within an oxygenated bath and perfused with a solution containing glucose or 3-O-MG and polyethylene glycol with average molecular weight of 4,000 (PEG) as a marker substance. We verified that the PEG was not transported and did not diffuse across the fetal ileum. Scanning and electron microscopy before and after perfusion demonstrated preservation of mucosal anatomy. The rate of glucose absorption was 200 +/- 17 mumol.h-1.g-1 at 19 days and increased significantly to 378 +/- 12 mumol.h-1.g-1 at 20 days. The absence of sodium abolished this process. The flux of 3-O-MG from lumen to bath was 88 +/- 10 mumol.h-1.g-1 at 19 days and 160 +/- 16 mumol.h-1.g-1 at 20 days. Bath-to-lumen flux was -17 +/- 2 mumol.h-1.g-1 and did not vary with age. Active, rapidly developing transport of glucose and 3-O-MG is demonstrated by in vitro luminal perfusion of the fetal rat ileum at 19 days.

3-O-Methylglucose↗
PubMed1982

Phase I trial of Staphylococcus aureus Cowan I immunoperfusion.

Staphylococcus aureus Cowan I has shown antitumor activity in in vitro and in animal tumor models. It is hypothesized that this antineoplastic effect results from the interaction of protein A on the cell surface of Cowan I strain S. aureus and immunosuppressive circulating immune complexes. Therefore, we treated five patients with ex vivo plasma immuno-perfusion over killed and fixed S. aureus Cowan I. Toxic effects were marked in all patients and appeared to be related to the plasma volume infused and rate of infusion. Toxic reactions occurred in the cardiovascular, respiratory, and hematopoietic systems. No responses even minimal or transient, were observed in this phase I trial. This toxicity may be reduced if the rate of plasma infusion decreases.

Adult↗
PubMed1981

Effects of ethanol and acetaldehyde on the rat adrenal.

A pseudoCushing syndrome, indistinguishable from true Cushing syndrome except that it disappears with abstinence from alcohol, is known to occur in alcoholics. An animal model was used to study this syndrome in vitro, as earlier studies have shown that ethanol administration to animals increases corticosterone secretion. Such secretion appears to be the result of ethanol-induced ACTH secretion. We have examined the effects of ethanol and acetaldehyde on the production of three steroids: corticosterone, progesterone, and androstenedione in the isolated perfused rat adrenal. The adrenal glands and left kidney of rats were perfused with medium and one of the following additions: ethanol, acetaldehyde, ACTH or ACTH with either ethanol or acetaldehyde. The amount of the three steroids in the adrenal and the perfusion effluent was determined and compared to that of nonperfused adrenal glands. We found that perfusion with medium alone increased the production of each steroid (p less than 0.05) in the presence of ethanol or acetaldehyde. Assay of the medium before and after perfusion showed no ACTH, so that the increased steroid production cannot be ascribed to ACTH contamination. Furthermore, the addition of ACTH to perfusion medium which contained ethanol or acetaldehyde did not further enhance the responses.

Acetaldehyde↗
PubMed1981

Gastrointestinal transit: the effect of the menstrual cycle.

Gastrointestinal transit time as well as serum estradiol and progesterone levels were measured in 15 normally menstruating women twice during their menstrual cycle, once in the follicular phase (days 8-10) when progesterone levels are low and once in the luteal phase (days 18-20) when progesterone levels are increased. Each subject had a progesterone rise during the luteal phase and onset of menses at the expected time documenting ovulatory cycles. Gastrointestinal transit time from ingestion of lactulose to the delivery of the disaccharide to the cecum was determined by monitoring breath hydrogen levels at 10-min intervals. Gastrointestinal transit time was significantly (p less than 0.01) prolonged in the luteal phase when progesterone levels were increased compared with the follicular phase. This study demonstrates that the menstrual cycle plays an important role in determining the gastrointestinal transit time in normally menstruating women.

Adult↗
PubMed1980

Alcohol and sexual function.

The pathophysiologic factors which either document or which have been shown to be responsible for not only the hypogonadism and feminization of chronic alcoholic men but also the loss of gonadal function with resultant defeminization of chronic alcoholic women are reviewed. Evidence is presented which suggests that alcohol abuse is associated with the production of a primary form of hypogonadism characterized by loss of endocrine and reproductive function of the gonads. Moreover, evidence is presented which suggests that alcohol abuse is associated with the production of an associated hypothalamic-pituitary defect in gonadotropin secretion which prevents appropriate enhancement of gonadotropin secretion in response to the primary gonadal injury. Finally, the factors which have been found to partially explain the feminization often seen in chronic alcoholic men with advanced liver disease are discussed individually and a composite mechanism incorporating each is presented.

Alcoholism↗
PubMed1979

Intestinal absorption of bile salts: immature development in the neonate.

The intestinal absorption of sodium taurocholate was studied in fetuses, neonates, infants, children, and adults. Absorption rates were measured in vitro in everted rings of jejunum and ileum. Mucosal accumulation of 3H-taurocholate against a concentration gradient was consistently demonstrated in rings of ileum from adults, children, and infants older than 8 months, whereas fetal and neonatal ileal mucosal concentrations were not significantly above those in the incubation medium after exposure of the mucosa to 0.003, 0.03, and 0.3 mM taurocholate. There were no significant differences in mucosal uptake of taurocholate by perinatal jejunal and ileal rings. Incubations of mucosa from older infants, children, and adults in 0.3 mM taurocholate exhibited saturation phenomena. It is concluded that the ileal mechanism for active transport of taurocholate is undeveloped in the fetus and newborn infant. It is probable that the enterohepatic circulation of bile salt during the perinatal period is limited to that fraction of bile salt absorbed passively. The results suggest that losses of bile salt from the immature intestine may contribute to the steatorrhea and so-called diarrhea of newborn infants.

Aged↗
PubMed1979

Synthesis of taurocholate by rat fetal liver in organ culture: effects of cortisol in vitro.

Taurocholate production by fetal hepatic organ cultures was measured by radioimmunoassay. Taurocholate production was maximal on day 1 of in vitro incubation, but was demonstrable in organ cultures maintained for periods up to 15 days. Explants obtained from fetuses of 18 gestational days of age produced only 82 pmol taurocholate per milligram dry weight of tissue during the first 24 h of incubation. Explants obtained from fetuses 21 gestational days of age produced 1,043 pmol taurocholate per milligram dry weight. The presence of cortisol (2.0 X 10(-6) M) in the incubation medium increased synthesis of taurocholate by rat fetal liver in which total taurocholate rose 50-fold above control after 120 h of incubation. In increasing concentrations from 2.0 X 10(-9) M to 2.0 X 10(-7) M, cortisol produced an incremental rise in taurocholate. However, additional increases in cortisol dose failed to provide further stimulation, and taurocholate production was inhibited by cortisol concentrations of 2.0 X 10(-5) M. The results provide further validation for the technique of fetal hepatic organ culture. They demonstrate that taurocholate synthesis is increasing rapidly during the final stages of gestation and show that cortisol augments taurocholate synthesis in a dose-response pattern.

Animals↗
PubMed1979

Taurocholate pool size and distribution in the fetal rat.

Taurocholate concentrations in fetal and neonatal rats were determined by radioimmunoassay. Total body taurocholate pool size varied from 0.0049 +/- 0.0008 to 203 +/- 8 nmol/g body weight from day 5 of gestation to 5 d after birth. A 50-fold increase in taurocholate pool size was observed between days 15 and 19 of gestation. The distribution of taurocholate between liver, intestine, and the remainder of the carcass was determined for rats of gestational age 19 d to 5 d after birth. The major fraction of total body taurocholate was in the liver and intestine, with less than 15% in the remainder of the carcass. The ratio of taurocholate in intestine to taurocholate in liver, which was 1:17 at 19 d of gestation, had altered substantially to a ratio of 6:1 by 5 d after birth. Treatment of pregnant rats with 60 microgram/d of dexamethasone from gestational day 9 until sacrifice increased fetal taurocholate pool size by 80% at 15 d, 40% at 19 d, and 16% at 1 d after birth. Administration of dexamethasone to the mother also changed the ratio of taurocholate in intestine to taurocholate in liver. At 19 d of gestation, dexamethasone-treated mothers had fetuses with approximately equal amounts of taurocholate in intestine and liver. This suggested that adrenocorticosteroids stimulate the early maturation of factors controlling taurocholate pool size and tissue distribution in the rat fetus.

Animals↗