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PubMed1989

Limiting dilution analysis of in vivo-activated (IL-2 responsive) peripheral blood lymphocytes in HIV-1-infected subjects.

The progression of infection with human immunodeficiency virus, type 1 (HIV-1), is associated with a loss of helper T cell function, but the mechanism for this loss (e.g., decreased absolute number of helper cells, altered function of helper cells, or both) has not been delineated. Many studies have suggested that T-cell production of and/or responsiveness to the T cell growth factor interleukin-2 (IL-2) declines over the course of HIV-1 infection. Using a highly quantitative 6-day limiting dilution assay (LDA), we investigated whether the number and the proliferative capacity of circulating IL-2 responsive cells in patients with AIDS differ from those in patients in earlier stages of HIV-1 infection (asymptomatic or AIDS-related complex) and healthy seronegative individuals. The frequency of IL-2 responsive cells declined progressively in asymptomatic seropositive subjects, those with ARC, and those with AIDS. In contrast, the proliferative capacity of individual IL-2 responsive cells, as reflected by the magnitude of thymidine uptake per precursor, was reduced only in patients with frank AIDS and was normal in asymptomatic subjects and in those with ARC. These results suggest that the development of AIDS in the setting of HIV-1 infection may reflect a combination of qualitative as well as quantitative changes in lymphocyte function. They also suggest that analysis of lymphocyte responsiveness to IL-2 may provide a useful approach to prediction of the development of AIDS in individuals infected with HIV-1.

Acquired Immunodeficiency Syndrome↗
PubMed2002

The effects of deleting the mouse neurotensin receptor NTR1 on central and peripheral responses to neurotensin.

Mice deficient in the neurotensin (NT)-1 receptor (NTR1) were developed to characterize the NT receptor subtypes that mediate various in vivo responses to NT. F2 generation (C57BL6/Sv129J) NTR1 knockout (-/-) mice were viable, and showed normal growth and overt behavior. The -/- mice lacked detectable NTR1 radioligand binding in brain, whereas NTR2 receptor binding density appeared normal compared with wild-type (+/+) mice. The gene deletion also resulted in the loss of NTR1 expression as determined by reverse transcription-polymerase chain reaction and in situ hybridization. Intracerebroventricular injection of NT (1 microg) to +/+ mice caused a robust hypothermic response (5-6 degrees C) and a significant increase in hot-plate latency. These effects were absent in the -/- mice. Similar results were obtained with i.p. injections of the brain-penetrant NT analog NMe-Arg-Lys-Pro-Trp-Tle-Leu (NT-2, 1 mg/kg i.p.). NT-2 administration also impaired rotarod performance in wild-type mice, but had no effect on motor coordination in knockout mice. In vitro, NT and NT-2 at 30 nM caused predominantly contraction and relaxation in isolated distal colon and proximal ileum, respectively, from +/+ mice, but no responses were observed with tissues from -/- mice. A similar loss of the contractile effects of NT was observed in the isolated stomach fundus from the knockout mice. In vivo, NT-2 administration reduced colonic propulsion substantially in wild-type mice. In contrast, NT-2 had no effect in NTR1 null mice, whereas the hypomotility effect of clonidine was intact. These data indicate that NTR1 mediates several of the central and peripheral effects of NT.

Analgesics↗
PubMed1982

Early peripheral responses to intravenous L-thyroxine in primary hypothyroidism.

The metabolic, cardiovascular, renal, and pulmonary responses of 10 hypothyroid patients were studied during the first week of therapy with intravenous levothyroxine (L-thyroxine), 100 micrograms per day. Mean serum thyroxine, triiodothyronine, and reverse triiodothyronine concentrations were normalized within four days. Significant decreases in serum thyrotropin, creatine phosphokinase, and cholesterol levels, and an increase in the basal metabolic rate, were observed. An early cardiovascular response was demonstrated by serial measurement of the mean pre-ejection period (138 to 134 msec, p less than 0.05), its ratio to left ventricular ejection time (0.49 to 0.46, p less than 0.02), and pulse-wave arrival time (236 to 224 msec, p less than 0.05). The mean renal excretion of a water load (four hours) increased (54 to 77 percent, p less than 0.02) by the fourth day. The blunted ventilatory responses to hypercapnea seen in two patients were improved. We conclude that a physiologic replacement dose of intravenous L-thyroxine for one week produces significant responses in organ systems responsible for the common clinical complications of myxedema.

Adult↗
PubMed1992

Endurance training changes central and peripheral responses to physostigmine.

Whether the pharmacodynamics of physostigmine (Phy) [rate of decarbamylation of cholinesterase (ChE) enzyme] (Kd) is altered due to acute and/or trained exercise in brain and various tissues of rat has been addressed. Acute exercise (AE) + Phy increased, whereas endurance training (ET) + Phy decreased ChE activity in brain, red blood cells (RBC), and various tissues as compared to Phy alone. The Kd of brain ChE was significantly increased (181% of control) by AE + Phy and decreased (66% of control) by ET + Phy as compared to Phy alone. There was a slight increase (114% of control) in Kd of RBC-ChE in AE + Phy as compared to Phy alone. The Kd of heart ChE was significantly decreased (44% of control) by ET + Phy as compared to Phy alone. The Kd of diaphragm ChE was significantly increased (384% of control) in AE + Phy and decreased (80% of control) in ET + Phy as compared to Phy alone. The Kd of muscle ChE significantly decreased (67% of control) by AE + Phy as compared to Phy alone, but ET + Phy did not affect the Kd in muscle. These results suggested that AE and ET have opposite effects on Kd after Phy administration.

Animals↗
PubMed1993

Concurrent acute exercise alters central and peripheral responses to physostigmine.

This study reports the modulatory effects of physostigmine (Phy) and concurrent acute exercise on the time course of cholinesterase (ChE) activity, the rate of decarbamylation (Kd), and half-time of recovery of ChE in red blood cells (RBC) and various tissues of rats. Acute exercise equivalent to 80% VO2-max (maximal oxygen consumption) transiently increased the RBC ChE activity, whereas Phy decreased ChE activity in RBC and various tissues. Physostigmine along with concurrent acute exercise increased the Kd in RBC, brain, and heart by 56.4%, 66.7%, and 139%, respectively, compared to Phy alone. The Kd in diaphragm and muscle decreased to 14.1% and 56.2%, respectively, compared to Phy alone. The variation in Kd might be due to the effect of concurrent acute exercise on the redistribution of Phy in various tissues of rat as a result of changes in blood flow.

Animals↗
PubMed1976

The nature of the training response; peripheral and central adaptations of one-legged exercise.

13 male subjects were studied and placed in 3 groups. Each group exercised one leg with sprint (S), or endurance (E) training and the other leg oppositely or not at all (NT). Oxygen uptake (Vo2), heart rate and blood lactate were measured for each leg separately and for both legs together during submaximal and maximal bicycle work before and after 4 weeks of training with 4-5 sessions per week. Muscle samples were obtained from the quadriceps muscle and assayed for succinate dehydrogenase (SDH) activity, and stained for myofibrillar ATPase. In addition, eight of the subjects performed after the training two-legged exercise at 70% Vo2 max for one hour. The measurements included muscle glycogen and lactate concentrations of the two legs as well as the blood flow and the a-v difference for O2, glucose and lactate.

Adaptation, Physiological↗
PubMed1982

Peripheral response of the retina to polarized light.

The perception of polarized light by the human eye is facilitated with Savart's double-plate polarimeter. This device converts polarized light into interference fringes from which criteria for the polarization sensitivity of the retinal hemisphere may be derived. The rather preliminary tests in this report covered the entire visual field of the eye and led to the discovery of a nonuniform off-axis distribution of the retinal sensitivity to polarized white light. The results are reminiscent of similar effects in geometrical optics, where oblique light rays become slightly polarized upon the penetration of successive layers of translucent optical surfaces. Similar experiments with incident elliptically polarized rays suggest that the retina responds in the same nonuniform manner.

Biophysical Phenomena↗
PubMed1981

Peripheral responses to thyroid hormone before and after L-thyroxine therapy in patients with subclinical hypothyroidism.

Twenty patients with serum levels of T4 and T3 within the normal range but with elevated serum concentrations of TSH were evaluated before and after treatment with L-T4. This therapy increased serum T4 (5.5 +/- 1.1 to 8.8 +/- 1.8 microgram/dl) and T3 (116 +/- 20 to 137 +/- 28 ng/dl) levels. Cardiac systolic time intervals (STI) were significantly (P less than 0.01) reduced by this therapy. The preejection period (123 +/- 18 to 114 +/- 14 msec; n = 12), the change in preejection period (+17 +/- 17 to +6 +/- 15 msec; n = 12), the ratio of preejection period to left ventricular ejection time (0.412 +/- 0.068 to 0.357 +/- 0.063 msec; n = 12), and the interval from the Q wave of the electrocardiogram to the pulse wave arrival time at the brachial artery (224 +/- 10 to 200 +/- 13 msec; n = 10) were consistently reduced. Cardiac STI were significantly correlated with serum TSH and T4 levels, but not with serum T3 levels. Normalization of serum TSH levels was associated with changes in QKd measurements even in those patients with minimal elevations in serum TSH. These studies demonstrate that patients having the combination of elevated TSH but T4 and T3 levels in the normal range have alterations in STI which can be changed significantly by L-T4 in doses which normalize TSH secretion. These data suggest that such patients have a mild form of primary hypothyroidism.

Adult↗
PubMed1998

Different central and peripheral responses to leptin in rhesus monkeys: brain transport may be limited.

The purpose of this experiment was to determine the effect of leptin administration on food intake and energy expenditure in rhesus monkeys. Four adult male rhesus monkeys, cannulated in the left lateral cerebral ventricle, were used for all phases of this experiment. Food intake was measured following intracerebroventricular injections of vehicle or three doses (500 ng, 2 micrograms, and 22 micrograms) leptin. Leptin administration resulted in a dose-dependent decrease in food intake (P < 0.05), with food intake decreased by an average of 54% at 22 micrograms leptin. Energy expenditure was also measured at two intracerebroventricular doses of leptin. Energy expenditure was not different (P > 0.10) between placebo and leptin injections at either dose. Food intake was also measured following i.v. injection of 3 mg leptin. In this case, leptin did not alter (P > 0.10) food intake, despite increasing serum leptin levels by as much as 100-fold. These results suggest that leptin is a potent inhibitor of food intake in rhesus monkeys, but this effect requires elevation of leptin concentrations in the cerebrospinal fluid or critical brain sites. The transport system for movement of leptin across the blood-brain barrier may limit the influence of circulating leptin on food intake in monkeys.

Animals↗
PubMed1983

Altered peripheral responsiveness to beta-adrenergic stimulation in experimental renal hypertension.

Hypertension, induced in male rats by encapsulation of both kidneys with latex envelopes, is associated with a reduction in maximal responsiveness to beta-adrenergic stimulation. Responsiveness was assessed by measurement of both water intake and plasma renin activity following acute subcutaneous administration of graded doses of isoproterenol, a beta-adrenergic agonist. At doses of isoproterenol in excess of 6 micrograms/kg body weight, s.c., the dipsogenic response of rats with renal hypertension was significantly (p less than 0.05) less than that of normotensive controls. Basal, unstimulated plasma renin activities were similar in both the normotensive and renal hypertensive groups. However, following administration of isoproterenol at doses of 5, 10, or 20 micrograms/kg body weight, s.c., plasma renin activity was elevated significantly (p less than 0.01) in the normotensive, but only in the lowest dose in the renal hypertensive group. These results suggest that maximal responsiveness to beta-adrenergic stimulation is reduced in the renal hypertensive rat; however, the mechanism(s) responsible for the reduced beta-adrenergic responsiveness remains speculative.

Animals↗