Some abnormal effects of stimulating nerve trunks through the skin.
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Biomedical subjects
Publications and source records attributed to A Angel.
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1. Experiments have been performed on animals anaesthetized with various anaesthetics to determine the responsiveness of the cortex to the second of a pair of identical stimuli applied at three sites along the sensory pathway, i.e. to the periphery, the medial lemniscus and to thalamocortical fibres.2. It has been found that in deeply anaesthetized animals the mass response recorded from the cerebral cortex to the second of a pair of peripheral or lemniscal stimuli became reduced in size if the interval between the stimuli was 30-500 msec. If the interval was less than 30 msec for peripheral stimuli or between 10 and 30 msec for lemniscal stimuli responses were not obtained to the second stimulus. This was found to be a basic pattern which could be modified in animals less deeply anaesthetized. In these animals, periods of relatively increased responsiveness were seen after peripheral stimulation.3. The post-synaptic responses recorded from the ventrobasal thalamus showed the same behaviour to the second of a pair of peripheral stimuli as did the cortex both as regards size and latency of the responses.4. The post-synaptic responses recorded from the cuneate nucleus rarely showed any reduction in size unless the separation between the stimuli was 10 msec or less; even at intervals as low as 3 msec there was no increase in the latency of the response.5. When a pair of stimuli were applied to thalamocortical fibres, a different pattern of cortical responsiveness was found. At the time the cortical response to stimulation at pre-thalamic sites was reduced or abolished, the response to stimulation at post-thalamic sites was unaltered or increased in size.6. Finally an attempt was made to correlate the mass response recorded from the cortical surface and the activity of single cortical cells. Two types of cell could be distinguished in the rat. Those lying from 0.35 to 1.2 mm deep in the cortex showed a response pattern, to paired stimuli, closely resembling that of the cortical mass response. Others situated deeper in the cortex were found which had a very long absolute unresponsive time, from 50 to 80 msec and a very long relative unresponsive time of 1 sec.
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High density lipoprotein (HDL) binding proteins were identified in nonreduced detergent extracts of plasma membranes or crude membrane fractions of rat adipocytes by ligand blotting. Using 125I-labelled human apolipoprotein-E-free HDL ([125I]HDL3), two binding proteins in adipocyte membranes were detected with apparent molecular masses of 122 and 88 kilodaltons (kDa), respectively. The binding of HDL3 to both binding proteins was abolished by pronase treatment and was inhibited by excess unlabelled HDL3. Excessive unlabelled low density lipoprotein reduced the binding of [125I]HDL3 to the 122-kDa binding protein relatively less than that to the 88-kDa binding protein. Polyclonal antisera against purified rat apolipoprotein A-I (apoA-I) effectively inhibited the binding of HDL3 to adipocyte membranes. Affinity-purified antibodies against rat apoA-I also revealed two HDL-binding proteins in rat adipocyte and liver plasma membranes preincubated with rat HDL. The sizes of the HDL-binding proteins in adipocyte plasma membranes detected by anti-apoA-I were similar to those detected by radiolabelled ligand blotting and their counterparts in rat liver plasma membranes. The study demonstrates two HDL-binding proteins, distinguishable by apparent molecular masses and ligand binding affinity, in plasma membrane proteins of mature rat adipocytes using radiolabelled ligand and immunoligand blotting techniques. The results suggest that apoA-I is involved in the interactions between HDL and both variants of HDL-binding proteins.
The present study investigated transcellular signalling mechanism involved in thrombin-induced production of plasminogen activator inhibitor-1 (PAI-1) in cultured vascular baboon aortic smooth muscle cells (BASMC). Treatments with thrombin dose-dependently increased the steady state levels of PAI-1 mRNA and the generation of PAI-1 antigen from BASMC. Thrombin receptor-activating peptide mimicked the effect of thrombin on the generation of PAI-1. Sodium fluoride (1 mM) stimulated PAI-1 generation from BASMC. Pertussis toxin dose-dependently suppressed thrombin-induced increase of PAI-1 generation. Treatment with 5 mM neomycin, 10 microM U73122 or 1 microM calphostin C blocked thrombin-induced PAI-1 generation. Phorbol myristate acetate at 10 nM for 3 h strongly stimulated the generation of PAI-1 from BASMC. Forskolin (100 microM) or 8-bromo-cAMP (100 microM) suppressed thrombin-induced PAI-1 generation. The responses of quiescent BASMC to thrombin or the inhibitors on PAI-1 generation were comparable to that of growing cells. The results of the present study suggest that pertussis toxin-sensitive G proteins and a phospholipase C are involved in thrombin-induced generation of PAI-1 in BASMC, which may transmit signals from occupied thrombin receptor to protein kinase C and thereby increase the generation of PAI-1. Elevated levels of intracellular cAMP may negatively regulate the generation of PAI-1 from vascular SMC.
In normal dogs fed diets containing 1% cholesterol and 30% saturated fat, cholesterol concentration increased in plasma, cardiac lymph, and peripheral lymph. The increase in cardiac lymph cholesterol always exceeded that of peripheral lymph. At plateau, LDL cholesterol increased in plasma and peripheral lymph but not in cardiac lymph; HDL2 cholesterol increased in all compartments and HDLc appeared in plasma (86.6 +/- 22.2 mg cholesterol/dl) with cholesterol feeding. In cardiac and peripheral lymph, a lipoprotein fraction with ultracentrifugal and pevikon electrophoretic characteristics of plasma HDLc (designated HDL 1.063) was isolated and contained 9.4 +/- 1.3 and 11.9 +/- 6.8 mg cholesterol/dl respectively. The lymph/plasma (L/P) ratios of lipoproteins were generally higher in cardiac lymph compared to peripheral lymph. In cholesterol-fed dogs, the L/P ratios of LDL were reduced compared to control dogs while HDL2 was unaffected, indicating selective interstitial distribution of lipoproteins. On agarose electrophoresis, lymph lipoproteins migrated faster than plasma lipoproteins, suggesting subtle changes in the structure and/or composition, findings consistent with the suggestion that lipoproteins undergo modification in the interstitial space. Thus, each interstitial space, as reflected by lymph, has a characteristic mixture of lipoproteins that can be altered by a high cholesterol diet in a manner that is unique to each particular tissue compartment.
BACKGROUND/AIMS: We present the results obtained from 100 new cases of clinical esophagitis caused by gastroesophageal reflux at the Hospital of Caldas and at the Service of Gastroenterology of VIME (Endoscopical Video Medicine) in Manizales, Caldas, Colombia; between the months of June and November of 1996, evaluated by digestive endoscopy and classified based on the New Savary-Miller 5-Grade Classification. METHODOLOGY: The patients were selected based on the presence of symptomatology suggestive of esophagitis caused by gastroesophageal reflux; an endoscopy was performed followed by 24-hour esophageal pH monitoring. The patients were grouped according to their grade of esophagitis in the New Savary-Miller Classification. The central analysis was focused on determining the existing relationship between the observed esophagitis and the results obtained by the 24-hour esophageal pH monitoring. RESULTS: Findings show that 51% and 48% of patients with esophagitis grades 1 and 2 had a normal DeMeester's score (< 14.7) in channel 1. In channel 2 we found normal scores in 86% and 82% of esophagitis grades 1 and 2, respectively. CONCLUSIONS: We ask whether the average level of pathological reflux of 14.7 can be extrapolated to our population; also whether endoscopical overdiagnosis of esophagitis caused by gastroesophageal reflux exists, or if non-recognized causes of esophagitis exist. Another question is if it is justified to order 24-hour esophageal pH monitoring in patients with grades 1 and 2 esophagitis.
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