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Biomedical subjects

A Verma

Publications and source records attributed to A Verma.

At least 145 records · Page 8Linked to original sources
PubMed1994

Development of a 23S rRNA-based PCR assay for the detection of mycobacteria.

The partial nucleotide sequence of a recombinant plasmid containing the 23S rRNA gene of Mycobacterium tuberculosis was determined and an assay was developed for amplifying 23S rRNA gene sequences of mycobacteria. The PCR-based non-radioactive test enabled us to distinguish Mycobacterium from other closely related genera and was sensitive enough to detect 2 bacterial genome equivalents. The assay was extended to the detection of mycobacterial DNA in uncultured clinical specimens; 23S rRNA sequences were detected in thirty four of forty eight (70.8%) sputum and cerebrospinal fluid (CSF) specimens by the PCR assay, whereas direct smear examination and culture methods demonstrated a positivity rate of 29.2% and 16.7% respectively for the same specimens. A RNA-based PCR assay with a detection limit of 1 genome equivalent was also developed. These PCR assays should prove useful for the early and rapid detection of mycobacterial infection in uncultured clinical specimens.

Base Sequence↗
PubMed1993

Mitochondrial voltage-dependent anion channel. Immunochemical and immunohistochemical characterization in rat brain.

The purified mitochondrial benzodiazepine receptor (mBzR) is a complex comprising the voltage-dependent anion channel (VDAC), adenine nucleotide carrier, and an 18-kDa protein that binds isoquinoline carboxamide ligands (McEnery, M. W., Snowman, A. M., Trifiletti, R. R., and Snyder, S. H. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 3170-3174). An antiserum raised against the mBzR complex reacts selectively with VDAC and is used, along with purification, electrophysiological and immunohistochemical techniques, to characterize the properties and distribution of rat brain VDAC. Although purified VDAC displays biochemical and electrical conductance properties similar to VDAC from other sources, the immunohistochemical distribution of VDAC in rat brain is heterogeneous with pronounced regional variations; the pontine nuclei, the supraoptic nucleus, Purkinje cells of the cerebellum, and the caudate putamen evidence the highest density. The distribution of VDAC is inclusive of the more discretely localized 18-kDa mBzR protein, suggesting that only a portion of the total VDAC participates in the mBzR. The histochemical localizations of the mitochondrial marker enzymes glutamate dehydrogenase and cytochrome c oxidase also indicate marked regional variability in both mitochondrial content and composition. The discrete expression of VDAC reflects a striking heterogeneity of rat brain mitochondria and underlying differences in the utilization of mitochondrial outer membrane ion channels.

Animals↗
PubMed1993

Carbon monoxide: a putative neural messenger.

Carbon monoxide, an activator of guanylyl cyclase, is formed by the action of the enzyme heme oxygenase. By in situ hybridization in brain slices, discrete neuronal localization of messenger RNA for the constitutive form of heme oxygenase throughout the brain has been demonstrated. This localization is essentially the same as that for soluble guanylyl cyclase messenger RNA. In primary cultures of olfactory neurons, zinc protoporphyrin-9, a potent selective inhibitor of heme oxygenase, depletes endogenous guanosine 3',5'-monophosphate (cGMP). Thus, carbon monoxide, like nitric oxide, may be a physiologic regulator of cGMP. These findings, together with the neuronal localizations of heme oxygenase, suggest that carbon monoxide may function as a neurotransmitter.

5-Aminolevulinate Synthetase↗
PubMed1993

Time of first stool in extremely low birth weight (< or = 1000 grams) infants.

The time of first stool was studied in 144 infants with a birth weight of 1000 gm or less. Median age at passage of the first stool was 3 days, and 90% of the infants passed stool by 12 days after birth. There was no relationship between the time of passage of the first stool and either birth weight or gestational age. Of the 114 infants, 88 (77%) passed stool before the initiation of any enteral feeding. The passage of the first stool was delayed in male compared with female infants (p = 0.03).

Birth Weight↗
PubMed1993

Effect of D1- and D2-dopamine agonists on neocortical and hippocampal EEG activity of rat brain: modulation of rimcazole effect.

The effect of selective D1- and D2-dopamine (DA) receptor stimulation on neocortical and hippocampal electroencephalographic (EEG) activity of rat brain was studied. The modulation of the effect of rimcazole, a sigma receptor antagonist, by D1- and D2-DA receptor agonists was also investigated. B-HT 920 (0.5 mg/kg), a D2 DA agonist, produced significant inhibition of EEG activity in neocortex and hippocampus. The lower doses of B-HT 920 (0.1 and 0.25 mg/kg) either enhanced the frequency and amplitude of cortical and hippocampal firing or lacked any significant effect. The inhibitory effect of B-HT 920 was blocked by haloperidol (0.5 mg/kg), a D2-receptor antagonist and enhanced by idazoxan (1.0 mg/kg), an alpha 2-adrenoceptor antagonist. SKF 38393 (5.0 mg/kg), a D1-DA receptor agonist and dopamine (10 mcg/rat) or apomorphine (0.5 mg/kg), a mixed D1-/D2-agonist, also inhibited the frequency and amplitude of cortical and hippocampal EEG. A significantly higher inhibition of electrical activity was observed following concomitant administration of B-HT 920 (0.1 mg/kg) and SKF 38393 (5.0 mg/kg) in comparison with the effect of each drug alone. Rimcazole (6.0 mg/kg) increased the frequency of cortical and hippocampal firing. Amplitude of cortical firing was enhanced but not of hippocampal EEG following administration of rimcazole. Rimcazole blocked the effect of SKF 38393 (5.0 mg/kg) and apomorphine (0.5 mg/kg) but not of B-HT 920 (0.5 mg/kg) on cortical and hippocampal EEG, respectively. The above data suggests a modulatory effect of D1-receptor activation on the inhibitory effect of D2-receptor stimulation in cortex as well as hippocampus and the blockade by rimcazole of the effect of D1-DA receptor agonist in these areas.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Protective effect of BR-16A (Mentat), a herbal preparation on alcohol abstinence-induced anxiety and convulsions.

Chronic administration of ethanol (2-5 g/kg, po) on days 1 to 6 and its withdrawal produced anxiogenic reaction in mice and rats as assessed on the elevated plus-maze. Daily administration of BR-16A (100 mg/kg) prior to ethanol intoxication for 6 days prevented withdrawal induced anxiety in both rats and mice. However, acute administration of a single dose of BR-16A, to animals withdrawn from ethanol, i.e. on the 7th day, showed significant anxiogenic response. Ethanol withdrawal also sensitized the convulsogenic reaction to pentylenetetrazole (PTZ). A non-convulsive dose (40 or 60 mg/kg) of PTZ produced full blown convulsions and increased mortality in ethanol withdrawn rats and mice, respectively. Both acute and chronic administration of BR-16A (100 mg/kg) exhibited significant protection against ethanol withdrawal-induced reduction in PTZ threshold in rats and mice. The results suggest the usefulness of this safe herbal psychotropic preparation in the management of ethanol withdrawal reactions.

Animals↗
PubMed1992

Modulation of MK-801 response by dopaminergic agents in mice.

Various doses of the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists, MK-801 (0.1-0.5 mg/kg) and ketamine (2.5-10 mg/kg), produced a dose-dependent increase in stereotypic behaviour in naive mice. MK-801 (0.1 mg/kg) and ketamine (2.5 mg/kg) potentiated the stereotypic response of apomorphine (0.1-0.5 mg/kg) in mice pretreated with reserpine (5 mg/kg, 24 h prior) and alpha-methyl-p-tyrosine (150 mg/kg, 1 h prior) but not in naive mice. SKF 38393, a D1 dopamine agonist, enhanced whereas B-HT 920, a D2 dopamine agonist, reduced the stereotypic response of MK-801 in naive mice. The response of MK-801 was blocked by pretreatment with haloperidol (0.5 mg/kg), molindone (2.5 mg/kg), clozapine (7.5 mg/kg) and SCH 23390 (0.1 mg/kg). The present data suggest involvement of endogenous DA transmission in the stimulant action of non-competitive NMDA antagonists in mice. Dopamine D1 and D2 receptor stimulation, respectively, exert opposing effects on the behavioral expression of MK-801 in mice.

Animals↗
PubMed1992

D1/D2 dopamine and N-methyl-D-aspartate (NMDA) receptor participation in experimental catalepsy in rats.

Mixed D1/D2 dopamine (DA) antagonists, perphenazine (5 mg/kg) and haloperidol (2 mg/kg) induced catalepsy in rats. SCH 23390 (1 mg/kg), a D1 DA antagonist, also produced catalepsy. Co-administration of perphenazine (0.5 mg/kg) and SCH 23390 (0.1 mg/kg), at low doses, produced a marked increase in cataleptic response. B-HT 920, a D2 agonist, reversed the cataleptogenic effects of perphenazine, haloperidol and SCH 23390. SKF 38893 (5 mg/kg) reduced the cataleptogenic effect of SCH 23390 but failed to reverse haloperidol- or perphenazine-induced catalepsy. SKF 38393 (10 mg/kg), however, protected the animals against perphenazine- induced catalepsy. Combined administration of B-HT 920 (0.1 mg/kg) and SKF 38393 (5 mg/kg) enhanced the protective effect of B-HT 920 in SCH 23390-treated animals but not in animals treated with haloperidol or perphenazine. MK-801 (0.025-0.5 mg/kg), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, reduced the cataleptogenic effects of perphenazine, haloperidol as well as SCH 23390. The anticataleptic action of MK-801 was enhanced by scopolamine (0.1 mg/kg) but not by bromocriptine (1 mg/kg) or clonidine (0.05 mg/kg) in perphenazine-treated rats. Unlike B-HT 920 (0.1 mg/kg), SKF 38393 (5 mg/kg) potentiated the anticataleptic effect of MK-801 (0.01 mg/kg) against SCH 23390-induced catalepsy. The above data suggests D1/D2 interdependence in catalepsy and a modulatory role of D1 and D2 DA receptor stimulation on the anticataleptic effect of MK-801.

Animals↗
PubMed1992

Quantitative morphometric study of muscle in inclusion body myositis.

Clinical and electromyographic findings do not clearly distinguish inclusion body myositis (IBM) from chronic polymyositis (PM). The rimmed vacuoles and filamentous nuclear and cytoplasmic inclusions that characterize IBM are often sparse and may be overlooked; conversely, these features may occasionally be seen in other diseases. Preliminary studies suggested that muscle fiber hypertrophy occurred more frequently in IBM than in PM. To investigate whether fiber hypertrophy can be used to improve the ability to separate IBM from PM, we report a morphometric analysis of 28 IBM cases, 22 PM and 22 dermatomyositis (DM) cases. The analysis, using a computer automated system, included proportion of hypertrophied fibers and also fiber type proportions, average fiber diameter, proportion of atrophic and angulated fibers, and the co-dispersion index (CDI). The proportion of hypertrophied fibers was greater in IBM than the other two conditions (IBM (mean +/- SEM) 31.0 +/- 4.7% and 12.2 +/- 2.4% for type 1 and type 2 fibers, respectively, compared to 9.8 +/- 3.0% and 3.3 +/- 1.7% in PM, and 7.7 +/- 2.7% and 3.9 +/- 1.9% in DM). These differences were statistically significant (P < 0.05) in both sexes for type 1 fibers and in women for type 2 fibers. Also, the average fiber size and hypertrophy factors for type 1 and type 2 fibers were increased in IBM compared to PM and DM. This study confirms that the presence of muscle fiber hypertrophy in biopsies from IBM patients may help differentiate them from other clinically similar inflammatory myopathies.

Dermatomyositis↗
PubMed1992

Calcium pools mobilized by calcium or inositol 1,4,5-trisphosphate are differentially localized in rat heart and brain.

Calcium-induced calcium release (CICR) pools have been demonstrated in brain and heart microsomes biochemically and autoradiographically by the sensitivity of 45Ca2+ accumulation to Mg2+, ATP, ruthenium red, caffeine, and tetracaine. The CICR pool colocalizes with [3H]ryanodine binding sites, supporting the notion that [3H]ryanodine labels CICR pools. Sites of CICR pools in the brain contrast with those of inositol 1,4,5-trisphosphate (IP3)-sensitive Ca2+ pools with reciprocal localizations between the two Ca2+ pools in several structures. Thus, in the hippocampus CA-1 is enriched in IP3-sensitive Ca2+ pools, whereas CICR pools are highest in CA-3 and the dentate gyrus. The corpus striatum and cerebellum are enriched in IP3 pools, whereas the medial septum and olfactory bulb have high CICR densities. In cardiac tissue, CICR is localized to atrial and ventricular muscle, whereas IP3 pools are concentrated in coronary vessels and cardiac conduction fibers. The reciprocal enrichment of IP3 and CICR Ca2+ pools implies differential regulation of Ca2+ hemostasis in these tissues.

Adenosine Triphosphate↗
PubMed1992

Attenuated late positivity in the visual evoked potential in aphasia induced by lesions in anterior speech area.

Seven anterior aphasics, 7 nonbrain-damaged subjects and 7 normal controls were tested for their visual evoked potentials. Aphasics showed an attenuation of the long latency positivity related to interest in the stimulus. The attenuation may indicate the subject's failure to signal communicative intention. Thus the attenuated positivity may be a physiological correlate of a behavioral state (aphasia) induced by brain lesions.

Adult↗
PubMed1992

Prevention of development of tolerance and dependence to opiate in mice by BR-16A (Mentat), a herbal psychotropic preparation.

Chronic treatment with BR-16A (20-500 mg/kg) followed by saline on days 1 to 9 failed to produce any significant change in tail-flick latency from the saline-pretreated group in mice. Repeated administration of BR-16A(20-500 mg/kg) for 9 days however, attenuated the development of tolerance to the analgesic effect of morphine (10 mg/kg). BR-16A (20-500 mg/kg) also suppressed, in a dose-dependent manner, the development of morphine dependence as assessed by naloxone (2 mg/kg)-precipitated withdrawal on day 10 of testing.

Analysis of Variance↗
PubMed1992

Dystrophin test in differential diagnosis of childhood muscular dystrophies.

Two cases of childhood muscular dystrophy are described. One of them had clinical features suggestive of Emery-Dreifuss muscular dystrophy and the other with some features of Prader-Willi syndrome, besides proximal muscle weakness. Muscle biopsy from both cases revealed a clear abnormality of dystrophin, and were diagnosed as having Duchenne muscular dystrophy (DMD) by immunofluorescence examination; that is, absent dystrophin at the membrane of the muscle fibers. The clinical spectrum of DMD-related myopathies and the importance of dystrophin testing in childhood muscular dystrophies is discussed.

Biopsy↗