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Biomedical subjects

R Kumar

Publications and source records attributed to R Kumar.

At least 1,333 records · Page 74Linked to original sources
PubMed1983

Erythrocyte membrane phosphorylation in untreated and in etretinate-treated psoriatic patients.

Levels of phosphorylation were decreased in bands 2 to 2.1, 2.9 to 3 and 4.5 to 4.8 of erythrocyte membranes from psoriatic patients compared with control values. In addition, higher than control levels of 32P were incorporated into a new polypeptide band (mol.wt. 18-20,000 daltons) of red cell membranes from patients. Uptake of 32P by these bands returned towards normal after the patients received oral etretinate treatment. These results suggest there is a generalized plasma membrane defect in psoriasis and that etretinate may affect the metabolism of red cell membrane proteins.

Adenosine Triphosphate↗
PubMed1983

The effects of nicotine on locomotor activity in non-tolerant and tolerant rats.

1--Rats were tested for locomotor activity in photocell cages, for 80 min starting immediately after subcutaneous injection of (-)-nicotine bitartrate or 0.9% w/v NaCl solution (saline). In non-tolerant subjects, nicotine (0.1 to 0.4 mg/kg base) depressed activity and induced ataxia in the first 20 min, but increased activity later in the session; these actions were dose-dependent. 2--Tolerance was studied by comparing rats given nicotine (0.4 mg/kg s.c.) every day with control rats given saline instead. Each week, every subject was tested once with nicotine (0.4 mg/kg) and once with saline. With daily or even weekly injections of nicotine, the initial depressant action of the drug was replaced by a dose-dependent stimulant action which occurred throughout the session. In these tolerant animals, little ataxia was seen except when a larger dose of 0.8 mg/kg was given. Tolerance to the depressant action of nicotine persisted for at least 3 weeks. 3--In non-tolerant subjects, mecamylamine (0.5, 1.0 mg/kg s.c.) prevented the initial depressant action of nicotine (0.4 mg/kg). In tolerant rats, the locomotor stimulant action of nicotine (0.4 mg/kg) was prevented by mecamylamine (0.1, 0.32, 1.0 mg/kg s.c.) in a dose-related way; the quaternary ganglion blocker, hexamethonium (0.2, 1.0, 5.0 mg/kg s.c.) had little or no such effect. Neither mecamylamine nor hexamethonium altered activity when given alone. 4--It is suggested that a few treatments with nicotine can unmask a stimulant action of the drug, probably of central origin, which possibly reflects a stimulation of nicotine receptors.

Animals↗
PubMed1983

Characteristics of conditioned taste aversion produced by nicotine in rats.

1 Nicotine produced conditioned taste aversions in rats which were directly related to the dose of nicotine and to the number of conditioning trials. 2 The tobacco alkaloid (-)-nicotine was four to five times as potent as its stereoisomer, (+)-nicotine. 3 Mecamylamine but not hexamethonium blocked the development of taste aversions produced by nicotine. 4 Mecamylamine did not block the development of taste aversions produced by apomorphine. 5 Prolonged treatment with mecamylamine prior to conditioning did not produce supersensitivity to nicotine.

Amphetamine↗
PubMed1983

Characterization of the locomotor stimulant action of nicotine in tolerant rats.

Tests of locomotor activity (photocell cages) were used to investigate the development of tolerance to nicotine in rats. Repeated exposure to the apparatus did not influence the rate at which tolerance was acquired. Comparisons of (+)-nicotine (0.4-1.6 mg kg-1, s.c.) and (-)-nicotine (0.1-0.4 mg kg-1, s.c.) in tolerant rats showed that the (-)-isomer was at least ten times more potent in stimulating motor activity. Subcutaneous pretreatment with mecamylamine (1.0 mg kg-1) completely prevented the locomotor stimulant action of nicotine in tolerant rats, whereas chlorisondamine (0.01 or 0.1 mg kg-1 s.c.) only partially reduced it. When mecamylamine was given after an injection of nicotine, the locomotor stimulant action of nicotine was blocked, and nicotine actually reduced activity. A single intraventricular dose of chlorisondamine (2 micrograms) blocked the stimulant actions of nicotine for the duration of the experiment (23-24 days).

Animals↗
PubMed1983

Time estimation and time production in depressive patients.

Twenty-three depressive inpatients and matched controls were studied three times at 2-week intervals. Both patients and controls initially overestimated, and subsequently approximated to, the "short" time spans (5-240 sec) whilst both correctly estimated the "long" ones (15 and 30 min) over the three occasions (Time Estimation Test, TET). There were no differences in the TET scores among the patients themselves, or between the patients and controls with the exception of one time span which the patients overestimated more than the controls. Among the depressive symptoms, only retardation was correlated with the TET scores. Similarly in the production of 30 sec (Time Production Test, TPT) there were no differences among the patients or between patients and controls. Again, only retardation was negatively correlated with the TPT score. Since the TET scores of the "short" time spans were negatively correlated with the TPT scores, it was speculated that both results derived from a single faculty, which was clinically manifested as retardation.

Adult↗
PubMed1983

Alkaline phosphatase secretion-negative mutant of Bacillus licheniformis 749/C.

An alkaline phosphatase secretion-blocked mutant of Bacillus licheniformis 749/C was isolated. This mutant had defects in the phoP and phoR regions of the chromosome. The selection procedure was based on the rationale that N-methyl-N'-nitro-N-nitrosoguanidine can induce mutations of closely linked multiple genes. The malate gene and the phoP and phoR genes are located at the 260-min position in the Bacillus subtilis chromosome; hence, the malate gene could be used as a marker for the mutation of the phoP and phoR regions of the chromosome. In a two-step selection procedure, strains defective in malate utilization were first selected with the cephalosporin C procedure. Second, these malate-defective strains were further screened in a dye medium to select strains with defects in alkaline phosphatase secretion. One stable mutant (B. licheniformis 749/cNM 105) had a total secretion block for alkaline phosphatase and had the following additional characteristics: (i) the amount of alkaline phosphatase synthesized was comparable to that in the wild type; (ii) the alkaline phosphatase was membrane bound; (iii) the mutant strain alkaline phosphatase, in contrast to that of the wild type, could not be extracted with MgCl2, although the amounts of protein extracted from each strain were comparable; (iv) the sodium dodecyl sulfate-polyacrylamide gel pattern of MgCl2-extracted proteins from the mutant strain was different from that of the wild-type proteins; (v) the mutant, unlike the wild type, could not use malate as a sole source of carbon; and (vi) the outside surface of the wall of the mutant cells contained an additional electron-dense layer that was not present on the wild-type cell wall surface.

Alkaline Phosphatase↗
PubMed1983

Blink rate in psychiatric illness.

Twenty-three patients diagnosed as depressed and a matched group of normal subjects were interviewed on three occasions using standardised procedures. Their behaviour was quantified from video recordings. The results indicate that blink rate is increased in depression and falls to normal levels during treatment. The effect on blink rate was found to be independent of medication, but was related to the degree of improvement in the patients' condition. By contrast a sample of schizophrenic patients seen on one occasion showed a reduced blink rate which was probably a result of neuroleptic administration.

Blinking↗
PubMed1983

Specific neurotoxin lesions of median raphe serotonergic neurons disrupt maternal behavior in the lactating rat.

Impairments in lactation after electrolytic lesions of the median raphe (MR) nucleus have been corrected by treatment with PRL. Specific serotonin neurotoxin lesions were used in the present study to determine whether decrements in litter growth after electrolytic lesions could be attributed to serotonergic neuron damage at the MR locus, and whether MR lesions (MRL) disrupted suckling-induced PRL release. Intracerebral microinjection of 5,7-dihydroxytryptamine (5,7-DHT) into the MR nucleus produced dose-related decrements in litter growth after either 4 micrograms (sham, 1.35 +/- 0.05; MRL, 1.04 +/- 0.05 g/pup X day; P less than 0.001) or 8 micrograms 5,7-DHT (sham, 1.35 +/- 0.06; MRL, 0.87 +/- 0.11 g/pup X day; P less than 0.001). Despite hypothalamic serotonin depletions of 15% and 55%, respectively, for the two doses of 5,7-DHT, there was no difference between sham and MRL animals in either basal or suckling-induced PRL release. When lesions were placed on day 1 of lactation (L) so that killing on day 7-L corresponded to the early maximal neurotoxin effect, MRL mothers still showed litter growth decrements (0.37 +/- 0.07; sham, 0.98 +/- 0.08 g/pup X day; P less than 0.001) and normal PRL values. When maternal behavior was examined, MRL animals exhibited a higher incidence of abnormal behaviors (failure to retrieve pups, cannibalism, and failure to initiate suckling during a 1-h test period; Fisher's exact P, Sham vs. MRL, less than 0.01, less than 0.05, and 0.15, respectively) than sham animals or animals with 5,7-DHT lesions in the dorsal raphe nucleus or superior colliculus. In addition, suckling behavior scores, determined from daily suckling behavior observations, were lowest in the MRL group and correlated with litter growth only in this group (r = 0.789; P less than 0.01). These data suggest that serotonergic elements in the MR nucleus play an obligatory role in maintaining normal maternal behavior during lactation, but they are not involved in suckling induced PRL release.

5,7-Dihydroxytryptamine↗
PubMed1983

Hyperphosphatemic tumoral calcinosis: effects of phosphate depletion on vitamin D metabolism, and of acute hypocalcemia on parathyroid hormone secretion and action.

In hyperphosphatemic tumoral calcinosis, plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels are inappropriately elevated, suggesting an abnormality in vitamin D metabolism. To define this abnormality further, we measured vitamin D metabolites in two patients and four controls before and after phosphate depletion. The patients showed elevated plasma levels of 1,25(OH)2D in the basal state. Phosphate depletion reduced serum phosphate in patients from a mean of 6.1 to 2.6 mg/dl; this was accompanied by a rise in plasma 25-hydroxyvitamin D from 33.6 to 41.9 ng/dl, and in 1,25(OH)2D from 67.7 to 93.2 pg/ml. The absolute rise in 1,25(OH)2D was similar to that of controls. EDTA infusion produced a normal increase of serum immunoreactive PTH levels and urinary cAMP excretion. In this form of tumoral calcinosis, 1,25(OH)2D levels are elevated despite hyperphosphatemia, normal immunoreactive PTH, and normal serum calcium concentrations, suggesting an abnormality in the regulation of 1,25(OH)2D synthesis or metabolism, or alternatively, another undefined stimulus for 1,25(OH)2D synthesis. These patients appear to have concurrent abnormalities of renal tubular phosphate transport and vitamin D metabolism.

Calcinosis↗
PubMed1983

Enhancement of reactivity of HLA-Cw antisera by extending the incubation time.

HLA-Cw antisera showing weak cytotoxic activity when tested at 1 1/2 hours in the conventional HLA-A,B, Cw testing procedure, were found to react better in the test using an extended incubation period of 3 hours. Of the 71 sera which were tested, 15 (21%) sera demonstrated an increase in anti-HLA-Cw reactivity against cells from donors possessing the corresponding Cw antigen. In addition, the use of B cells in the testing procedure appeared to be more favorable than T cells in the enhancement of reactivity of weak HLA-Cw antisera.

B-Lymphocytes↗
PubMed1983

Continuous ambulatory peritoneal dialysis. Three years' experience at the Mayo Clinic.

From January 1979 through January 1982, 69 patients with end-stage renal failure of various causes were treated by continuous ambulatory peritoneal dialysis. The dialysis was adequate and stable in all except four patients; two of these four became irreversibly uremic, and the other two had inadequate ultrafiltration. Hemoglobin levels increased initially and remained stable in all but two patients. In our experience, metabolic problems included control of secondary hyperparathyroidism, adequate protein nutrition, progressive neuropathy, abnormal lipoprotein profiles, and excessive weight gain. Technical problems included recurrent peritonitis, maintenance of adequate peritoneal access, and development of abdominal hernias. In general, all but two patients remained enthusiastic about this type of therapy despite inherent problems. The long-term potential of continuous ambulatory peritoneal dialysis remains uncertain at this point, but for most patients, adequate short-term treatment by this method is a reasonable alternative to hemodialysis.

Adult↗