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K Kumar

Publications and source records attributed to K Kumar.

At least 109 records · Page 6Linked to original sources

Comparison of alpha-tubulin mRNA and heat shock protein-70 mRNA in gerbil brain following 10 min of ischemia.

In situ hybridization and Northern blot analysis were used to characterize the mRNA expression of alpha-tubulin, a neuroprotein crucial for neuronal structural and functional restoration, in comparison to that of the stress inducible heat shock protein-70 (HSP-70), in the same gerbil brain following 10 min of forebrain ischemia. The HSP-70 expression was noted in the dentate granule layer 1 h postischemia (PI) and became prominent in all pyramidal cell fields of the hippocampus in addition to the dentate layer at 6 h PI. The induction of HSP-70 persisted in CA1 and CA2 regions and partly in dentate gyrus for up to the 1 day PI period examined. There was no significant HSP-70 expression in any of the regions of the nonischemic or 15 min PI brain. alpha-Tubulin, on the other hand, was expressed in all pyramidal fields of the hippocampus as well as dentate gyrus in nonischemic controls. A decline was noted in the CA1 region 1 h PI onward and was maximal at 6 h PI. Its expression, however, increased at 24 h PI (significant only in comparison to 15 min and 6 h PI but not to control) when it became rather strong in the dentate gyrus. Thus, the temporal pattern of expression of alpha-tubulin sharply contrasted with that of HSP-70 in the PI brain as it declined in the vulnerable CA1 region during the 1st 24 h PI, i.e., the period when HSP-70 was induced and its expression was lowest in the 6 h group when HSP-70 peaked. It was maximum in the dentate gyrus at 24 h PI when HSP-70 was marginally detectable in that region. These studies indicate that in early recirculation period following prolonged ischemia, HSP-70 mRNA is expressed in both vulnerable regions as well as in regions of the brain that are destined to survive while alpha-tubulin is diminished in vulnerable regions. These data suggest a positive correlation between the loss of alpha-tubulin mRNA and delayed neuronal necrosis that follows in the vulnerable CA1 region.

Animals↗

Dose-dependent biodistribution of [153Gd]Gd(acetate)n in mice.

[153Gd]Gd(acetate)n was administered i.v. to mice to study the effect of dose on the distribution of free Gd. Distribution from blood was slow with the majority of the Gd distributing in the liver. Gd saturated in bone. Heart, lungs, kidneys, brain and skeletal muscle exhibited time-dependent decreases in Gd concentration. Gd that washed out of heart, lungs, kidneys and/or muscle redistributed in liver, spleen and femur. These results indicate a complex dose- and time-dependent tissue distribution for Gd and emphasize the importance of eliminating unchelated free Gd as a contaminant in Gd-chelates before testing in biodistribution experiments. The long-term residual accumulation of Gd suggests the need to minimize Gd-chelate dissociation in vivo.

Acetates↗

Expression of protein kinase C isozymes in rat glial cell line.

To study the presence and distribution of various isozymes of PKC in glial cells, immunofluorescent studies were performed on a cortical glial cell line cultured derived from rat cerebral cortex and analyzed by a highly sensitive automated laser cytometric device, ACAS-570 (Adherent Cell Analysis and Sorting). The antibodies tested were against alpha, beta, gamma and epsilon isozymes of PKC, and the catalytic domain (cd), i.e. antibody against the cd to all isozymes of PKC. The data indicate that rat cortical glial cell line expresses at least three isozymes of PKC, epsilon, beta, and alpha, the degree of intensity of immunofluorescence being epsilon > beta > alpha. The immunofluorescence for PKC-cd was the most intense.

Animals↗

Danazol in Indian haemophiliacs.

Danazol, 10 mg/kg/day (maximum 600 mg/day) was given in two divided doses for 14 days in 30 patients with haemophilia-A. Rise in factor-VIII level was observed in all the patients after one week of danazol therapy, irrespective of initial factor-VIII Levels. In haemophiliacs with less than 1% factor VIII level, rise was maximum (3-6 folds); mean factor-VIII level at 7th and 14th day of danazol therapy was 2.3 +/- 0.6% and 4.8 +/- 1.1%, respectively. Only marginal increase in factor-VIII was noted in haemophiliacs with initial factor-VII levels more than 3%. The raised level of factor-VIII persisted after stopping the therapy during the observation period of 2 more weeks, irrespective of initial levels. No adverse effect was observed during or after.

Adolescent↗

Fixation of fractures by twisted plates. A new concept of osteosynthesis.

A new twisted plate has been designed for biplane fixation of diaphyseal fractures of long bones. Comparative mechanical testing of the new twisted plate and conventional flat plates showed that the twisted plate was 40% stronger when a bending moment was applied and 132% stronger to a twisting moment. The overall improvement in strength was 90.5%. Clinical trials have been carried out and this paper describes the use of the new plate.

Bone Plates↗

The penetration of drugs into the lesions of spinal tuberculosis.

The concentration of antituberculous drugs in blood and pus from tuberculous spinal lesions was measured initially, and again after 3 to 5 months of treatment in 4 cases. The pre- and post-chemotherapy drug concentrations were almost the same. This indicated that healing does not interfere with the penetration of the drugs into the lesion.

Adolescent↗

Expression of protein kinase C in postischemic brain: an in situ hybridization study.

Cerebral ischemia leads to a number of biochemical and molecular changes which include increase in intracellular calcium, arachidonic acid, and diacylglycerol, all of which are capable of activating protein kinase C (PKC). To investigate how the expression of PKC is affected in postischemic brain, ischemia was produced in gerbils by bilateral common carotid artery occlusion for 10 min followed by reperfusion for 15 min, 6 h, and 24 h. The brains of postischemic and normal control animals were removed, forebrains dissected, fresh frozen, and processed for in situ hybridization. The mRNA expression of PKC was analyzed by using oligonucleotide probes based on the sequences of PKC alpha and epsilon isozymes in this preliminary study. There was no change observed in the expression of PKC alpha in any region of the brain in any of the postischemic groups examined. There was, however, a qualitative increase in the transcription for PKC epsilon in two out of three brains of 15 min postischemic group which continued through 24 h of reperfusion. Since the protein itself was not examined, it can not be said how these observations regarding transcription relate to the synthesis of the protein and whether there are any changes in the subcellular distribution of PKC following ischemia. However, since there was no decrease in transcription demonstrated in our study, it appears that the reported decrease in PKC activity following ischemia is not due to decreased mRNA expression.

Animals↗

Dissociation of gadolinium chelates in mice: relationship to chemical characteristics.

Tissue distributions of seven 153Gd-labeled Gd chelates were determined at five residence intervals (5 min to 14 days) following intravenous administration of 0.4 mmol/kg to mice. Relationships were sought among physicochemical parameters: thermodynamic and conditional (pH 7.4) equilibrium stability constants (log K and log K'), acid dissociation rate constants (k(obs)), lipophilicity (log P), overall charge, and size (molecular weight). Size and lipophilicity did not correlate with tissue distributions. There were possible correlations between anionic charge and rapid, early renal excretion and between stability constants and long-term residual Gd deposition. Strong correlations (r greater than 0.99) were found between acid dissociation rates and long-term deposition of Gd in the whole body, liver, and femur. This is attributed to dissociation of Gd from the chelates in vivo. Acid dissociation rates may be useful in predicting dissociation of Gd from chelates in vivo.

Animals↗

Quantitative dependence of MR signal intensity on tissue concentration of Gd(HP-DO3A) in the nephrectomized rat.

Cardiac-gated SE 20/224 +/- 20 MR images were obtained from nephrectomized rats before and after intravenously administering 153Gd-Gd(HP-DO3A). The concentration of Gd, [Gd], was linear in dose in myocardium, skeletal muscle, and blood. Under steady-state conditions, where d[Gd]/dt = 0, image intensities (IIN) in regions of interest were compared with the measured [Gd]. IIN was linear in myocardium at less than or equal to 0.61 mumol/g-myocardium (less than or equal to 0.5 mmol/kg dose) and in skeletal muscle at less than or equal to 0.63 mumol/g-muscle (less than or equal to 0.75 mmol/kg). Above 0.6 mumol Gd/g-tissue, IIN did not increase further. The in vivo data were consistent with measured ex vivo and in vivo relaxivities. A 29% greater slope for IIN versus [Gd] in myocardium [14,439 +/- 4350 IIN (mumol/g)] than in muscle [10,258 +/- 5,296 IIN/(mumol/g)] was attributed to a significant difference in blood content: 25% versus 2% weight blood in myocardium and skeletal muscle, respectively. Two components were apparent from plots of ex vivo 1/T1 versus [Gd] in myocardium and muscle, and only one for blood.

Animals↗

Post kala-azar dermal leishmaniasis: a neglected aspect of kala-azar control programmes.

Post kala-azar dermal leishmaniasis (PKDL) was studied in relation to the kala-azar epidemic in Bihar, India. Between 1970 and 1989, 530 individuals, 302 males and 228 females, were admitted to the hospital of Patna Medical College with PKDL, the number of cases steadily rising from two in 1970 to 59 in 1989. The age of the patients varied from four to 70 years, with 33% aged 11-20 years and 16% 0-10 years. The prevalence of kala-azar in India also increased in the same period, mostly as the result of an epidemic of the disease in Bihar. There were no cases of this disease admitted to Patna Medical College from 1958-1970, it having become rare in India in the 1950s, possibly as a result of the DDT sprayed during the National Malaria Eradication Programme. In the period 1977-1990, however, there were 301,076 cases of kala-azar reported in Bihar alone, with a mortality rate over 2% (compared with 31,074 cases and a mortality rate below 0.4% for the rest of India). It seems possible that, once DDT spraying stopped, the re-establishment of large sandfly population and infection of these vectors, largely as a result of them feeding on cases of PKDL, provoked the resurgence of kala-azar. The study emphasizes the need to search for cases of PKDL, even in young children, and to monitor and effectively treat them as part of kala-azar control programmes. All patients could be cured if treated with the right dosage for the right period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

A correlative study of serum zinc and in vivo cell mediated immune status in rheumatic heart disease.

This study was conducted to determine the zinc status and assess relationship between serum zinc and in vivo cell mediated immunity (CMI) in patients with rheumatic heart disease (RHD). The study comprised 22 patients with active rheumatic heart disease (ARHD), 15 patients with chronic rheumatic heart disease without activity (CRHD) (selection based on Jone's Criteria--Revised), and 15 age and sex matched healthy control. Zinc estimation was done by atomic absorption spectrophotometer. To assess CMI in vivo, phytohaemagglutinin skin test and skin window test were done. Serum zinc and in vivo CMI in patients with ARHD and CRHD compared with controls. Mean serum zinc was significantly decreased in patients with ARHD and CRHD, more pronounced in the former (P less than 0.001); and mean 24 h urinary zinc was significantly increased in patients with ARHD (P less than 0.001) as compared to controls. A significant depression in CMI in vivo was observed in patients with ARHD and CRHD (P less than 0.001). A significant positive correlation was seen among serum zinc and markers of in vivo CMI (P less than 0.001). In conclusion, depletion of zinc, observed in RHD, probably causes immune alterations and suggest role of zinc in immunopathogenesis of RHD. Zinc supplementation may alter the course of rheumatic fever and RHD.

Adolescent↗