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Biomedical subjects

R Linder

Publications and source records attributed to R Linder.

At least 55 records · Page 3Linked to original sources
PubMed1990

Late graft pancreatitis.

Among 40 type I diabetic patients who received a segmental pancreatic allograft with enteric exocrine diversion and had normal endocrine graft function for more than one year, 12 patients have had occasional episodes of "graft pain" associated with short-term hyperamylasemia. The symptoms usually resolved after 1-4 days. To determine possible precipitating factors, 80 such episodes were analyzed by interviewing all the patients and reviewing their files. To study the impact on endocrine graft function, the results of the serial intravenous glucose tolerance tests were plotted versus time. Episodes of late graft pancreatitis occurred at any given time between 6 and 51 months after transplantation. The frequency of bouts ranged between 1 and 31 per patient. The symptoms and clinical course were clearly different from late rejection episodes. Except for one severe case which resulted in graft loss, endocrine graft function did not deteriorate. Four conditions were found to correlate with the attacks: mental stress, alcohol and food intake, infections, and direct mechanical pressure to the pancreatic graft. We conclude that late graft pancreatitis can be distinguished from late rejection episodes and that the pancreatic graft may be more prone to acute pancreatitis than the native pancreas. The endocrine capacity of the pancreatic graft is usually not affected even by repeated attacks.

Alcohol Drinking↗
PubMed1989

Fibromuscular dysplasia in donor kidneys--experience with three cases.

In 1987, three patients received kidney grafts bearing medial fibroplasia at our hospital. Two of the grafts were from a cadaveric donor and one was from a living related donor kidney. The vascular affection was known before transplantation. Only one of the recipients developed stenosis and hypertension. With balloon catheter dilatation, the progressive stenosis of the renal graft artery could, however, be successfully corrected.

Adult↗
PubMed1989

A dose-response analysis of methoxychlor-induced alterations of reproductive development and function in the rat.

In the present study rats were dosed from weaning, through puberty and gestation, to Day 15 of lactation with methoxychlor at 25, 50, 100, or 200 mg/kg/day. Morphological landmarks of puberty were measured, including the ages at vaginal opening, first estrus, and first estrous cycle in females and at preputial separation in males. In the female, estrous cyclicity, fertility, litter size, number of implantation sites, organ weights, and ovarian and uterine histology were also measured. The viability of the offspring (F1) and their fertility were evaluated using a continuous breeding protocol. Males were necropsied after breeding, the reproductive organs were weighed, and the cauda epididymal sperm counts were determined. One testis was used for histopathology, while the other was used to quantify interstitial fluid (IF) content, IF testosterone concentration, and testicular sperm production. Testosterone and androgen-binding protein were measured in the caput epididymis, and sperm motility and morphology were evaluated from a caudal sample. The serum and pituitary were saved for hormonal determinations. Methoxychlor accelerated the age at vaginal opening and first estrus, and the vaginal smears were cornified. Growth was retarded at 100 and 200 mg/kg/day and fertility was reduced when the females were bred with untreated or similarly treated males. In the highest-dose group, the mated females went from constant estrus into pseudopregnancy following mating, but they had no implants. In males, methoxychlor treatment markedly reduced growth, seminal vesicle weight, cauda epididymal weight, caudal sperm content, and pituitary weight. Puberty was delayed in the two highest-dosage groups. Testicular sperm measures were much less affected than caudal measures. Testis weight and histology were slightly affected, and testicular sperm production, sperm morphology, and motility were unaffected. Endocrine function of the testes and pituitary was altered by methoxychlor administration. Leydig cell testosterone production, in response to human chorionic gonadotropin challenge, was reduced and pituitary levels of prolactin, thyroid-stimulating hormone (TSH), and follicle-stimulating hormone (FSH) were altered. In contrast, serum levels of prolactin, FSH, and luteinizing hormone were unaffected. Serum TSH was reduced by 50% of control at 100 and 200 mg/kg/day, while pituitary levels were increased. Gonadotropin-releasing hormone concentration in the mediobasal hypothalamus was also elevated. In spite of the many reproductive alterations, the fertility of treated males was not reduced when they were mated with untreated females.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Cytotoxicity of cholesterol oxidase to cells of hypercholesterolemic guinea pigs.

1. A high cholesterol diet caused guinea pig erythrocytes to become sensitive to lysis by cholesterol oxidase (CO), a protein not hemolytic to normal cells. 2. Lysis was associated with conversion of membrane cholesterol to its oxidation product (delta-4-cholesten-3-one). 3. Intravenous injection of CO to hypercholesterolemic guinea pigs produced a reduction in serum cholesterol, but was not lethal as it was in rabbits. 4. Homogenized spleen, liver and kidney from the hyperlipidemic animals were sensitive to in vitro cholesterol oxidation while tissues from non-lipemic animals were resistant to modification.

3-Hydroxysteroid Dehydrogenases↗
PubMed1989

Correlation of sperm and endocrine measures with reproductive success in rodents.

This paper compares the statistical precision and biological sensitivity of multiple indices of reproductive function to infertility in the male rodent. The studies discussed include those that examined reproductive function in the male following perinatal exposure to reproductive toxicants and others in which the compounds were administered to young-adult males, often with very diverse results. For example, some chemicals that alter sex differentiation reduce fertility by affecting breeding performance alone (polychlorinated biphenyls (PCBs), fenarimol, or losulazine), without altering sperm and testicular measures. Others also markedly alter sex differentiation of the genitalia, the accessory glands and the testis in addition to their effects on central nervous system (CNS) sex differentiation and mating behavior (testosterone, flutamide, cyproterone acetate, tamoxifen, estradiol and diethylstilbestrol (DES)). In contrast, prenatal exposure to compounds that alter primary germ cell survival (busulphan, congo red) induce partial gonadal/germ cell agenesis without altering sex differentiation. These chemicals dramatically reduce testicular sperm production in the male offspring, and the most severely affected males are infertile. In a series of studies conducted in our laboratory, young male rats were exposed to known reproductive toxicants in a dose related manner from puberty, through young adulthood and breeding. We have found that the profile of effects varies considerably depending upon the chemical's mechanism of toxicity. When a compound produced infertility through direct effects of testicular function (Carbendazim (MBC) and dibutyl phthalate (DBP)), then testis weight, testicular histology, and testicular sperm head counts provided sensitive indicators of toxicity. In general, dramatic reductions in sperm production are required to induce infertility and these changes were accompanied by elevated serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and changes in human chorionic gonadotropin (hCG)-stimulated testosterone synthesis. Chemicals that have hormonal activity, alter the internal endocrine environment, or directly effect CNS function induce a completely different profile of effects. For example, estrogen administration alters the function of the seminal vesicle and the endocrine system, and reduces epididymal sperm reserves; while testicular measures are relatively unaffected. Since very different spectrums of effects are produced by different compounds, no single endpoint will consistently be the most sensitive indicator of reproductive toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Cutaneous spider nevi in liver cirrhosis: capillary microscopical and hormonal investigations.

Nailfold capillary microscopical and hormonal investigations were carried out in 25 patients with cirrhosis of the liver and in 20 age- and sex-matched controls. Several structural and functional capillary microscopical parameters were significantly different between the group of cirrhotics as a whole and the controls; no capillaroscopic feature helped to distinguish cirrhotics with spiders from those without. Serum estradiol and total testosterone were comparable in cirrhotics and controls; free serum testosterone was reduced in male cirrhotics, particularly in cirrhotics with spider nevi. The estradiol/free testosterone ratio was highest in male cirrhotics with spiders. Cirrhosis, thus, leads to both structural and functional effects on the cutaneous capillary system whether or not spider nevi are present. The presence of spider nevi is accompanied by an increased serum estradiol/free testosterone ratio in male cirrhotics. It remains to be determined whether the hormonal alterations described do indeed play a role in spider nevi formation.

Adult↗
PubMed1988

The development of a protocol to assess reproductive effects of toxicants in the rat.

The determination that a chemical poses a reproductive risk to man typically relies upon fertility studies using rodents. However, fertility in rodents is often difficult to disrupt and more sensitive indicators of reproductive function should be included in the risk assessment process. The present discussion compares the sensitivity of fertility to other endpoints following exposure to known reproductive toxicants. In our studies rats were dosed from weaning through puberty , gestation, and lactation. The reproductive function of the male, the female, and the offspring was assessed. The effects of methoxychlor, carbendazim (MBC), dibutyl phthalate (DBP), and lindane are discussed and compared to fertility. For each compound a ratio (SR = sensitivity ratio) of the lowest effect level (LEL) for infertility or reduced fecundity to the LEL for the most sensitive physiologic endpoint was calculated. The SR should be large when a compound produces effects over a wide range of doses, but should equal unity when the dose-response curve is very steep. For methoxychlor, which blocked implantation, pubertal landmarks and estrous cyclicity provided rapid and sensitive indicators of the subsequent reproductive failure. The SR = 8 (100/12) for methoxychlor using data from females. In contrast, DBP and MBC directly altered testicular function, and for these compounds, sperm and testicular measures provided sensitive indicators of toxicity. The SR for MBC was 2 (100/50), while DBP had a SR of 1 (500/500). In the lindane study, fertility was not reduced but most of the pups (F1) died shortly after birth. The SR for lindane is equal to 0.5 (10/20). At 20 mg/kg the treated females were larger and their estrous cycles were erratic.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Toxicity of enzymically-oxidized low-density lipoprotein.

Intravenous injection of cholesterol oxidase into hyperlipidemic rabbits in which aortic atheromatous lesions have been induced by dietary means is lethal within hours, whereas injection of the same enzyme into normal rabbits has no visible adverse effect. The lethal effect of the enzyme is explicable by the finding that injection of cholesterol-oxidase treated low-density lipoprotein kills normal rabbits, in contrast to untreated low-density lipoprotein which does not. Enzymically oxidized low-density lipoprotein was also found to be cytotoxic for two human cell lines and for cultured bovine aortic endothelial cells. We suggest that in vivo enzymic conversion of low-density lipoprotein cholesterol to low-density lipoprotein cholestenone may possibly play a role in the initiation of atheromatous lesions in humans.

3-Hydroxysteroid Dehydrogenases↗
PubMed1987

Isolation and characterization of a phospholipase B from venom of Collett's snake, Pseudechis colletti.

Phospholipase B in the venom of the Australian elapid snake, Pseudechis colletti, was purified to near homogeneity. By means of gel filtration it had an Mr of about 35,000, and by SDS-polyacrylamide gel electrophoresis an Mr of about 16,500. These presumably are dimeric and monomeric forms of the enzyme. It was isoelectric at pH 6.2 as compared to 7.8 for phospholipase A2 from which it was readily separated. It was relatively thermostable. As determined by release of water-soluble phosphorous, it degraded phosphatidylcholine and phosphatidylethanolamine, but did not degrade other phospholipids tested. The purified enzyme was strongly hemolytic in vitro for rabbit and human erythrocytes, but not for bovine or ovine erythrocytes. Hemolysis of rabbit erythrocytes gave rise to membranes showing ultrastructural changes that may be unique for this enzyme. The protein was highly active in producing turbidity in dilute solutions of egg yolk. It was cytotoxic for cultured rhabdomyosarcoma cells and was lethal for mice in which death was preceded by massive myoglobinuria.

Animals↗