Incidence of entropion in lambs from two ewe flocks put to the same rams.
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Biomedical subjects
Publications and source records attributed to M Taylor.
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The replicative ability of fibroblasts derived from normal and type II diabetic (non-insulin-dependent) donors and their DNA synthetic capabilities in response to serum and insulin (+/- dexamethasone) have been studied. Comparative replicative life spans of the fibroblasts studied using several lots of serum showed no significant differences between the two donor groups with any lot of serum (p greater than 0.05). Insulin (i.e. 700 nM) and serum (10% v/v) stimulation of DNA synthesis in normal and type II diabetic cultures exhibited no differences in responses. The insulin:control ratios of the normal vs. type II diabetic were 1.61 +/- 0.08 vs. 1.81 +/- 0.11, respectively (p greater than 0.05) while the serum:control ratios were 3.55 +/- 0.58 vs. 4.02 +/- 0.54, respectively (p greater than 0.05). Dexamethasone amplification of the insulin-stimulated DNA synthetic response over a range of insulin concentrations (i.e. 1.6-66.6 nM) expressed no differences between the two donor groups. Additionally, calculation of the insulin concentration necessary for the half-maximal response showed no differences between the normal and diabetic groups (3.47 +/- 0.5 vs. 4.44 +/- 0.8 nM, respectively) (p greater than 0.05). The data suggest that there are no general age-related abnormalities inherent to the type II diabetic cultured cell.
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A histological comparison was made between normal mouse tails and those treated with crude coal tar, and the effect of crude coal tar on the keratin profile of the living cells of treated animals was examined. The prophylactic effect of crude coal tar on the neonatal mouse tail is described. The variation in the anatomical site of prekeratin of the dorsal and tail epidermis of the mouse is reported. These results are discussed with reference to the use of the mouse tail as a model for screening drugs for the treatment of psoriasis.
The hepatic metabolism of [125I]agalactoorosomucoid [( 125I]AGOR) was studied in normal and streptozotocin-induced diabetic rats. The blood clearance, hepatic transport time and rate of catabolism of [125I]AGOR were calculated from data of the blood [125I]AGOR disappearance rates and the appearance in blood of acid-soluble catabolites. In control rats the blood clearance of [125I]AGOR was rapid (8.7 +/- 0.6 ml/min) and the hepatic transport time of the ligand was 12.8 +/- 0.7 min. Insulin prolonged the hepatic transport time (18.1 +/- 1.9 min) and depressed ligand catabolism. Chloroquine had similar effects. Diabetes impaired hepatic [125I]AGOR uptake as judged by the prolonged blood clearance rate and depressed ligand catabolism but did not alter ligand transport time. The measured parameters returned to normal when diabetic animals were rendered acutely normoglycaemic. Diabetic rats, in which implanted osmotic insulin pumps had maintained normoglycaemia for 3 days, cleared [125I]-AGOR from the blood more rapidly than controls. This effect appeared to be due to the lower blood glucose levels in this group. The experiments have shown the complexity of the effects of insulin and diabetes mellitus on the uptake and processing of a glycoprotein by the hepatic mannose receptor.
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Isoquinoline has been identified as a component of coal tar which causes interfollicular regions of parakeratotic stratum corneum in mouse tail epidermis to become orthokeratotic, with concomitant production of a granular layer. In this respect it behaves similarly to coal tar itself, and isoquinoline may contribute to the anti-psoriatic activity of coal tar.
Plasma testosterone, oestradiol, luteinising hormone (LH) growth hormone and prolactin were measured serially in 140 patients with advanced prostatic carcinoma (T3, T4, MI and MO) randomised in a trial of diethylstilboestrol 3 mg/day against estramustine 560 mg/day. Both drugs suppressed plasma testosterone and LH and increased plasma growth hormone and prolactin, though estramustine induced a greater rise in prolactin. Oestradiol levels fell on stilboestrol but were considerably elevated on estramustine. Initial hormone levels reflected neither the extent of disease nor the response to treatment. The data also showed that close attention should be given to plasma LH in identifying patients who are unreliable, since intermittent hormone dosage caused an exaggerated rise even when plasma testosterone remained at castrate levels.
A second recorded case of Waterhouse-Friderichsen syndrome, without purpura, due to Haemophilus influenzae is described. It is suggested that the absence of purpura should not preclude the diagnosis of the Waterhouse-Friderichsen syndrome due to this organism.
Chloride secretion by the in vivo rectal gland of the shark is stimulated by the intravascular infusion of salt solutions of varying osmolar and sodium concentration. In a cross-perfused and denervated rectal gland, the infusion of a small amount of a hypertonic salt solution raises plasma osmolality but does not increase plasma volume in the donor fish. Under these conditions, rectal gland chloride secretion is not stimulated. A subsequent infusion of isotonic shark Ringer solution increases plasma volume 50%, decreases plasma osmolality, and produces a fourfold increase in chloride secretion and a threefold decrease in vascular resistance within the gland. Both the vasodilatory and secretory responses also follow the infusion of a hypotonic shark Ringer solution. The data further support the hypothesis that the rectal gland of the shark is involved in the regulation of intravascular volume rather than in osmoregulation.
The rectal gland of the shark plays a significant role in the homeostasis of extracellular volume. Regulation of rectal gland function is under hormonal control, but the precise identity of the humoral mediator is unknown. Atriopeptin stimulates rectal gland chloride secretion in vivo. This stimulation of epithelial transport is accompanied by systemic and local hemodynamic effects. Atriopeptin also stimulates chloride secretion by the in vitro perfused rectal gland, an effect that is not accompanied by hemodynamic changes. Extracts of shark heart, but not muscle, brain, kidney, or intestine, contain a heat-stable trypsin-sensitive substance capable of in vitro stimulation of rectal gland chloride secretion. Electron micrographic analysis reveals multiple neurosecretory-like granules in atrial cardiocytes that are only rarely seen in ventricular cardiocytes. By using the in vitro perfused gland as a biologic assay, serum obtained after extracellular volume expansion reveals the presence of a rectal gland stimulatory factor that is not present in serum before expansion. These results are consistent with the hypothesis that atriopeptin is present in shark cardiocytes and is released during volume expansion. The atriopeptin stimulates rectal gland chloride secretion, providing a negative feedback mechanism for the regulation of extracellular volume.
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A subset of workers was followed after exposure to polychlorinated biphenyls (PCBs), dioxins, and furans in an occupational medicine clinic setting. Patterns of PCBs found in adipose tissue resembled the pattern seen when soot from the incident or Aroclor 1254 was examined by GC-MS. Adipose tissue also revealed levels of hepta- and octachlorinated furans and dioxins as high as 8400 ppt in one repeatedly exposed worker. Control fat from patients with no known exposure to furans or dioxins was usually in the several hundred parts per trillion range for these isomers, but slightly over 2000 ppt in one sample. Electron microscopic analysis of liver biopsies from three patients who developed mild elevations of hepatic enzymes in their serum revealed morphologic alterations in some ways similar to those seen in animals after feeding experiments with PCBs, dioxins or the Binghamton State Office Building soot. These include pleomorphic mitochondria, giant mitochondria, prominent dense mitochondrial granules, cristae parallel to the long axis of the mitochondria and crystalline structure within same mitochondria as well as lipid droplets in liver cells and slightly dilated smooth endoplasmic reticulum.
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