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Biomedical subjects

V Handa

Publications and source records attributed to V Handa.

14 recordsLinked to original sources
PubMed2005

Human babesiosis--a case report.

Babesiosis is an emerging, tick-transmitted, zoonotic disease caused by hematotropic parasites of the genus Babesia. Most cases of Babesial infections in humans have been acquired in temperate regions of the United States, Europe, France and England. A few cases of Babesiosis have been described in other parts of the world, including China, Taiwan, Egypt, South Africa, and Mexico.1,2 We report the first case of human Babesiosis, in a normosplenic, previously healthy individual from India.

Animals↗
PubMed2003

Transcription defects induced by repeat expansion: fragile X syndrome, FRAXE mental retardation, progressive myoclonus epilepsy type 1, and Friedreich ataxia.

Fragile X mental retardation syndrome, FRAXE mental retardation, Progressive myoclonus epilepsy Type I, and Friedreich ataxia are members of a larger group of genetic disorders known as the Repeat Expansion Diseases. Unlike other members of this group, these four disorders all result from a primary defect in the initiation or elongation of transcription. In this review, we discuss current models for the relationship between the expanded repeat and the disease symptoms.

Base Sequence↗
PubMed2001

Deficiency of the 50 kDa dystrophin-associated-glycoprotein (adhalin) in an Indian autosomal recessive limb girdle muscular dystrophy patient : immunochemical analysis and clinical aspects.

Abnormalities of dystrophin are a common cause of muscular dystrophy and testing for dystrophin gene or protein has become a part of routine diagnostic evaluation of patients who present with progressive proximal muscle weakness, high serum creatine kinase concentrations, and histopathological evidence of a dystrophic process. Patients who have no dystrophin abnormalities are assumed to have autosomal recessive muscular dystrophy. In a family consisting of 5 sibs, 2 mentally normal brothers presented with abnormal gait and protrusion of chest and hips. Muscle biopsy from one of them showed dystrophic changes and reduced patchy binding of dystrophin. No detectable deletion was observed in the patient's DNA and his brother with cDMD probes. Dystrophin associated proteins, beta-dystroglycan showed discontinuous immunostaining in the sarcolemma and alpha-sarcoglycan (adhalin) was totally absent, while beta-, gamma-, and delta-sarcoglycans were highly reduced. Immunoblot analysis showed dystrophin of normal molecular weight but of decreased quantity, beta-dystroglycan was reduced by about 37% while alpha-sarcoglycan was completely absent. This study is a first attempt for a systematic clinical, genetic and molecular investigation of the autosomal recessive LGMD in India.

Adolescent↗
PubMed1991

Nuclear size and DNA content in rat cardiac myocytes during growth, maturation and aging.

Changes in nuclear volume and DNA content were examined in cardiac myocytes isolated from 21-day-old (weanling, W), 3-month-old (adult, A), and 2-year-old (old, O) rats to document normal parameters for nuclear growth and DNA content. Nuclear volume was calculated from direct measurements of isolated myocyte nuclear profiles and DNA content was measured from DAPI-stained nuclei using an image analysis microdensitometry system. Myocyte volume was measured with a Coulter Channelyzer system. Nuclear volume increased 79% from W to A as a result of an increase in nuclear length. Nuclear width was unchanged. Nuclear volume was not changed from A to O. Approximately 98% of the left ventricular myocytes from all three rat groups contained a diploid DNA content with the remainder of nuclei being tetraploid. The degree of polyploidy increased slightly, but significantly, in right ventricular myocytes from O. Due to the substantially greater increase in myocyte volume relative to nuclear volume, nuclear volume percentage decreased from 3.65 +/- 0.28 to 1.64 +/- 0.13 from W to A but was unchanged from A to O. To summarize: (1) nuclear volume of rat cardiac myocytes increases significantly during normal physiological growth (W to A) but the rate of nuclear growth is less than that of cell volume; (2) the increase in nuclear size from W to A is not due to an increase in DNA content; (3) cardiac myocytes from Sprague-Dawley rats are predominantly diploid; and (4) there is little change in DNA content of cardiac myocytes from rats of this strain during growth, maturation and aging.

Aging↗