The estrous cycle of the squirrel monkey (Saimiri sciureus).
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Biomedical subjects
Publications and source records attributed to C M Lang.
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Salt intake is restricted under clinical conditions for which thiazide diuretics are customarily used. Dietary iodide intake offsets any effect of thiazide on iodide loss. However, our correlation coefficients relating Na+ to Cl- to I- excretion indicate that as thiazide administration or sodium chloride intake increases renal Na+ and Cl- excretion, I- reabsorption by the nephron coordinately decreases. Increased sodium chloride and water intake by the dog doubled I-excretion rates. Hydrochlorothiazide increased the sodium chloride and water enhanced I-excretion rate as much as eight-fold. Without added NaCl, hydrochlorothiazide increased the excretion rate of 131I by three- to eightfold, acutely. Within five to seven days after 131I oral administration, hydrochlorothiazide (1 or 2 mg/kg twice daily) doubled the rate of 131I disappearance from plasma, reduced the fecal output of 131I, and increased its rate of renal excretion. When hydrochlorothiazide was administered, as much 131I was excreted in the first 24 hours as occurred in 48 hours when sodium chloride and water were given without hydrochlorothiazide. Thiazide administration in customary clinical dosage twice a day with substantial sodium chloride and water for the first two days after exposure to 131I, should therefore facilitate the safe excretion of 131I. This accelerated removal of 131I might be enhanced even more if thyroid uptake of 131I is blocked by administration of potassium iodide, as judged by the greater 131I recovery from thyroidectomized dogs.
Specific guidelines for the optimal collection of blood from calves maintained as donors do not exist. This investigation was conducted to document erythrocytic changes in calves subjected to controlled blood loss. Two groups of Holstein calves ranging in age from 2 to 5 months were compared. Six animals were designated controls and six were subjected to a series of three blood collections over an 8 day period. Each collection was roughly 50% of the total circulating blood volume (30 ml/kg of body weight). Hematologic values were compared for 18 days. All calves survived the study. There was no significant difference in circulating cortisol levels or growth rate between groups. Packed cell volumes (PCVs) for the phlebotomized group did not return to original levels during the monitoring period (initial 36%, final 26%), but were within normal limits at 30 days. All phlebotomized calves had a high reticulocyte count (0% control, 11% phlebotomized). Reticulocytes were not observed until the PCV fell below 20. HbF to HbA ratios were a sensitive and acute indicator of accelerated erythropoiesis. Variant ratios stabilized within 18 days. Other parameters compared were red cell indices, total erythrocyte count, total leukocyte count, total plasma protein, total hemoglobin values, and neutrophil to lymphocyte ratios.
The influence of the time of injury on subsequent epidermal regeneration is unknown. Epidermal cell proliferation of tail skin in C57BL/6J mice in response to tape stripping was followed for 7 days by radiolabelled thymidine incorporation and autoradiography. The homeostatic labelling index (LI) of the basal epidermis of unmanipulated, unwounded (control) animals was 7.6% and did not vary depending on the time of day. Tape stripping increased the LI of epidermal basal cells 110% above control values 24 h after injury. Labelling indexes of epidermal basal cells in the skin adjacent to the wounded area were 7.0%. Basal cell DNA synthesis stimulated by wounding exhibited a distinct temporal variation at 24 h postinjury, with tail skin wounded at 12.00 h found to be 275% greater than control values and elevated 78% from LIs recorded at any other time point. This temporal spike was due to the time of day at which wounding occurred rather than the time point when the LI was determined. Mice wounded at 12.00 h and terminated 27 h later (15.00 h) had LIs that were 52% greater than wounds created at 09.00 h and examined at 12.00 h the following day. Higher levels of DNA synthesis in tail skin injured at 12.00 h compared to wounding at 09.00 h was detected 12-48 h after injury. Furthermore, DNA synthesis in wounds created at 12.00 h returned to baseline levels 1-2 days earlier than tail skin wounded at 09.00 h. Investigation of other strains of mice detected differences in radiolabelling of epidermal basal cells 24 h after tape stripping at 12.00 h or 09.00 h in CD-1 and BALB/cJ mice, but not in the C3H/HeJ strain. These results indicate: (a) there is no diurnal variation in the LI of mouse tail skin under normal homeostatic conditions (b) tape stripping is a potent stimulator of basal cell turnover in the epidermis (c) the time of wounding determines the magnitude of the increase in the LI of basal cells following injury, and (d) the proliferative response to wounding of the tail is dependent on the strain of mouse.
1. The purpose of this study was to determine whether hepatic mitochondria of guinea-pigs with spontaneous diabetes mellitus differ from those of non-diabetic guinea-pigs in the oxidation of fatty acids, the activity of beta-hydroxybutyrate dehydrogenase, or respiration-linked oxidative phosphorylation. During the course of the study, a third group of animals (referred to as the unclassified group) was discovered which, on the basis of the clinical chemistry and histological changes in the pancreas, appeared to be in a pre-diabetic or post-diabetic state. 2. No differences in the respiratory control ratios were found between any of the three groups. Fatty-acid oxidation in hepatic mitochondria was greater in both the unclassified and diabetic groups than in the non-diabetic group. Beta-Hydroxybutyrate dehydrogenase activity, however, was increased only in the diabetic group. These findings suggest that increased fatty acid oxidation is probably an intermediate change in the development of or the recovery from diabetes mellitus, whereas the activity of beta-hydroxybutyrate dehydrogenase is affected only in more advanced stages.
BACKGROUND: Chronically implanted catheters often become covered with a thin, white adherent covering of tissue that has been referred to as a fibrin sheath. This tissue often interferes with catheter function. METHODS: To chronicle the development of this sheath, rats were implanted with silicone rubber central venous catheters. Five rats were euthanized at 3,7, and 60 days postimplantation so that gross necropsy and histology could be performed on the catheterized vessels. RESULTS: The coating that developed around the external portion of the catheter started as a dark red thrombus containing fibrin and progressed into vascularized, fibrous connective tissue. CONCLUSIONS: The translucent to white sheath that forms around chronically implanted catheters is not composed of fibrin and is therefore not likely to be dissolved by fibrinolytic agents such as urokinase, streptokinase, or tissue plasminogen activator.