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Biomedical subjects

C A Thompson

Publications and source records attributed to C A Thompson.

At least 91 records · Page 5Linked to original sources
PubMed1994

Cytoskeletal reorganization underlying growth cone motility.

Recent studies have implicated cytoskeletal dynamics as an important component in directing neuronal outgrowth. By using modern imaging techniques to observe the kinetics of individual cytoskeletal elements in living cells, these results have converged upon a common theme: functional coupling between the intracellular cytoskeleton and extracellular substrates, and regulation thereof, appears to be crucial in controlling neuronal migration.

Actins↗
PubMed1993

Delayed lactogenesis in women with insulin-dependent diabetes mellitus.

Breast milk lactose, total nitrogen, conductivity, osmolality, and intake by infants of 33 women with insulin-dependent diabetes mellitus (IDDM), 33 control women without diabetes, and 11 reference women were determined in a 3-mo study of lactation. Milk of women with IDDM had significantly lower lactose and higher total nitrogen (2-3 d postpartum), and their infants had significantly less milk intake (7-14 d postpartum) than did control or reference women. Total nitrogen was negatively correlated with milk lactose for women with IDDM at all times and for control women through day 14 postpartum. The data indicate delayed lactogenesis for women with IDDM, which was more likely to occur with poor metabolic control. Differences in milk composition of women with IDDM do not preclude them from breast-feeding their infants.

Diabetes Mellitus, Type 1↗
PubMed1992

Regulation of pH by the M2 protein of influenza A viruses.

Inhibition of the function of the M2 protein by amantadine can cause a conformational change in the haemagglutinin (HA) of H7 influenza A viruses and the consequent expression of the low pH form of the glycoprotein on the surface of virus-infected cells. Immunofluorescence studies showed that this conversion occurs shortly after HA exists from the Golgi complex apparently during its transport through the trans Golgi network and using the pH probe, DAMP/anti-DNP, that it is the direct result of reduced vesicular pH. The lowest pHs encountered were estimated using mutant HAs differing in pH stability to be approximately 5.2 and 5.6 in virus-infected CEF or MDCK cells, respectively, in the absence of functional M2. Depending on the particular M2, this protein was responsible for increases in vesicular pH of up to 0.8 units. The influence of mutations in both HA and M2 on the maturation of native HA illustrates the important relationship between the structural and functional properties of these two proteins. Using the fluorescent probe SNARF-1 the M2 protein was also shown to be largely responsible for the 0.3-0.4 unit reduction in intracellular pH of virus-infected cells. The data thus provide further evidence for the pH regulatory function of M2 and its importance for the maturation of the HA glycoprotein.

Amantadine↗
PubMed1991

Impairment of carotid-cardiac vagal baroreflex in wheelchair-dependent quadriplegics.

The incidence of orthostatic hypotension can increase after prolonged exposure to chair rest and bedrest and is associated with post-bed rest impairment of the carotid-cardiac baroreflex response. We therefore hypothesized that the hypotension observed in humans confined to wheelchairs may be manifested by a reduced baroreflex sensitivity. We compared baroreflex responses of 16 wheelchair-dependent (WCD) quadriplegics with those of 15 able-bodied subjects (ABS) matched for age, height, and weight. Beat-to-beat R-R intervals were measured during application of graded pressures from 40 to -65 mmHg using a neck chamber for noninvasive stimulation of the carotid baroreceptors. Changes of R-R intervals were plotted against carotid distending pressures. The maximum slope of the stimulus-response relationship was greater (P less than 0.0001) in ABS (6.1 +/- 0.6 ms/mmHg) than in WCD (2.6 +/- 0.4 ms/mmHg). The range of the R-R interval response, i.e., the capacity to buffer blood pressure changes, was only 138 +/- 19 ms in WCD compared with 253 +/- 19 ms in ABS (P less than 0.001). Mean sitting systolic-to-diastolic blood pressures in WCD (92/60 mmHg) were less (P less than 0.0001) than in ABS (120/77 mmHg), although there were no significant differences between groups in supine resting blood pressures. Chronic loss of stimulation to carotid baroreceptors by routine standing posture is associated with attenuated sensitivity and reduced buffer capacity of the arterial baroreflex and hypotension during sitting in WCD patients.

Adult↗
PubMed1991

Carotid baroreceptor influence on forearm vascular resistance during low level lower body negative pressure.

The degree of forearm vasoconstriction induced by low levels of lower body negative pressure (LBNP) provides a measure of the responsiveness of the cardiopulmonary baroreflex. The validity of this measurement is based on the assumption that this vasoconstriction response is not influenced by unloading of carotid baroreceptors. To test the hypothesis that arterial baroreceptor unloading does not alter the degree of forearm vascular resistance during low levels of LBNP, we exposed 12 subjects to -15 and -20 mm Hg LBNP with and without additional artificial (+10 mm Hg neck pressure) unloading of the carotid baroreceptors. There was no measurable influence of carotid unloading on forearm vascular resistance at either level of LBNP. We conclude that forearm vascular resistance measured during cardiopulmonary baroreceptor unloading is unaffected by carotid baroreceptor unloading within the magnitude encountered during low levels of LBNP.

Adult↗
PubMed1991

Diminished baroreflex control of forearm vascular resistance following training.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR units in mm Hg.min.100 ml.ml-1) were studied in 14 volunteers before and after 10 wk of endurance training. We assessed the relationship between reflex stimulus (changes in central venous pressure, CVP) and response (FVR) during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP, 0 to -20 mm Hg). Changes in CVP during LBNP were estimated from pressure changes in a large peripheral vein in the dependent arm of the subject in the right lateral decubitus position. Maximal oxygen uptake (VO2max) and total blood volume increased with endurance training from 37.8 +/- 1.4 ml.min-1.kg-1 and 63.6 +/- 2.1 ml.kg-1 to 45.3 +/- 1.4 ml.min-1.kg-1 and 69.3 +/- 2.8 ml.kg-1, respectively (P less than 0.05). Reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP, and the absolute change in FVR per unit of CVP was reduced from -5.96 +/- 0.79 to -4.06 +/- 0.52 units.mm Hg-1 (P less than 0.05) following exercise training but was unchanged from -6.10 to 0.57 to -6.22 +/- 0.94 units.mm Hg-1 for the time control group (N = 7). Resting values for FVR were similar before and after exercise training; however, resting estimated CVP was elevated from 9.5 +/- 0.5 mm Hg before training to 11.3 +/- 0.6 mm Hg after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

In vitro correlation of ultrastructural morphology and creatine phosphokinase release in L6 skeletal muscle cells after exposure to parenteral antibiotics.

Morphologic changes in a rat skeletal muscle cell line (L6) exposed for 1 h to the parenteral antibiotics amphotericin B (AMP), tetracycline-HCl (TET), erythromycin lactobionate (ERY), and cephaloridine (CEP) were characterized by transmission and scanning electron microscopy and compared to cellular release of creatine phosphokinase (CPK). AMP (0.05, 0.1, 0.5 mg/ml) caused a concentration-related swelling of nuclei, endoplasmic reticulum, and mitochondria. Loss of membrane integrity associated with AMP exposure was evident at the middle concentration and extensive at the high concentration, which correlated well with the 43 and 90% depletion of CPK from the muscle cells, respectively. TET (0.25, 1.0, 2.5 mg/ml) caused dilation of endoplasmic reticulum and cytoplasmic blebbing at the low concentration but had no effect on the cytoplasmic membrane or CPK. Cells exposed to the high concentration of TET had extensive damage to the cytoplasmic membrane, and CPK was completely depleted. ERY (2.5, 5.0, 25 mg/ml) caused a pattern of morphologic changes and CPK depletion similar to TET. CEP (4.0, 20, 50 mg/ml) had no effect on membrane integrity or CPK; however, membranous whorls were prominent in the cytoplasm. A good correlation between CPK release and cytoplasmic membrane integrity was evident and the ability of these agents to release CPK from muscle cells in culture correlated with the known irritancy potential of these parenteral antibiotics. Furthermore, CPK depletion seems to be a reliable indicator of muscle cell damage after cytoplasmic membrane perturbation and is therefore an appropriate index of toxicity in this in vitro muscle irritation model.

Amphotericin B↗
PubMed1990

Haemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans.

Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 degrees head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (BP less than 0.05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P less than 0.05). PV was increased by 6.3% (P less than 0.05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 +/- 5 ml pre-HDT to 105 +/- 4 ml during HDT and returned to 88 +/- 5 ml in seated recovery. Plasma ADH was reduced by 28% (P less than 0.05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P less than 0.05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.

Adult↗