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Biomedical subjects

V K Vijayan

Publications and source records attributed to V K Vijayan.

At least 73 records · Page 4Linked to original sources

Morphometric effects of preweaning lead exposure on the hippocampal formation of adult rats.

We previously observed that lead exposure beginning at parturition reduced or retarded neuropil development and synaptogenesis in specific regions of the hippocampal formation in 15-day-old rats. To determine if morphologic effects of perinatal lead exposure persist into adulthood, the hippocampus of rats exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate was analyzed by light and electron microscopy at 90-97 days of age. Preweaning lead exposure did not cause obvious hippocampal cytotoxicity, edema, damaged vasculature or altered numerical density (number per unit area) of dentate granule or hippocampal pyramidal neurons. However, lead exposure increased the area of the hilar portion of stratum pyramidale, increased the number of blood vessels per section in the dentate stratum granulosum and tended to increase the number of glial cells per section in the non-hilar CA3 stratum pyramidale. Effects of early postnatal lead exposure on synaptic profiles in the suprapyramidal mossy fiber zone (MFZ) were limited to the proximal (close to the dentate gyrus) region of the extrahilar zone. Both numerical density and areal density (proportion of neuropil covered) of complex invaginated (Ci) profiles, typical of mature mossy fiber boutons, were increased by lead exposure in the deep (close to stratum pyramidale) subfield of the proximal portion of the suprapyramidal MFZ. Lead exposure tended to increase the mean cross-sectional area of Cl profiles in the superficial (distant from stratum pyramidale) subfield of the proximal portion, and reduced the cross-sectional area of complex noninvaginated (CN) synaptic profiles in some subfields. Although lead exposure reduced or delayed neuropil development in selected late developing hippocampal regions examined at 15 days of age, it appeared to allow normal growth or to induce compensatory hypertrophy in these same regions in the adult.

Animals↗

Passive avoidance performance of mice fed marginally or severely zinc deficient diets during post-embryonic brain development.

Swiss-Webster outbred mice were fed marginally or severely zinc deficient diets (9 or 2 ppm zinc) from day 16 gestation to day 15 postnatal. Control mice were fed a 100 ppm diet either ad lib or in amounts equal to the diet intake of deprived mice (pair fed controls). Male and female offspring were tested at 70 days of age in a one-trial passive avoidance task with a 30 min train-test interval. Both marginally and severely zinc deprived offspring (but not pair fed controls) had shorter avoidance latencies than offspring of ad lib fed zinc replete controls. Zinc deprived offspring did not differ from control mice when either baseline or "stressed" (exposure to novel environment) plasma corticosterone levels were quantitated. Further, zinc staining patterns of the hippocampus (Timm-sulfide stain) were not altered in the nutritionally deprived offspring. Thus marginal dietary zinc deficiency during development can lead to impaired passive avoidance performance in adult mice. This behavioral effect is not associated with altered pituitary-adrenocortical activity or with a permanent reduction in hippocampal zinc staining. This result has significant implications for the influence of zinc deprivation in utero and in the neonatal animal on adult behavior characteristics.

Animals↗

Lysosomal enzyme changes in young and aged control and entorhinal-lesioned rats.

In the hippocampus of young and aged rats, lysosomal acid phosphatase and beta-glucuronidase were localized by enzyme histochemistry to the pyramidal and granule cells and to the mossy fiber zone (acid phosphatase only). Following a unilateral entorhinal lesion, enhancement in enzyme staining was observed within GFA (glial fibrillary acidic) protein-positive astrocytes and in cells resembling microglia and oligodendroglia in the ipsilateral dentate outer molecular layer and the hippocampal stratum lacunosum-moleculare. In young animals, these changes, first detected on day 2 post-lesion, were maximum on days 4 and 10 post-lesion and declined subsequently. The aged animals exhibited a delayed time-course of enzyme changes with minimal increases on days 2 and 4 post-lesion and greater increases on days 10 and 30 and gradual diminution thereafter. The delayed lysosomal response in the aged animal paralleled a reduction in the induction of glial cells following the lesion. Our findings suggest that the previously reported impairment in the clearing of degeneration debris in the aged animal is mediated by reduced glial induction and delayed glial lysosomal activation.

Acid Phosphatase↗

Morphometric effects of postnatal lead exposure on hippocampal development of the 15-day-old rat.

Neurotoxic sequelae of developmental lead exposure suggest that the hippocampus may be affected. Therefore, rats received low-level exposure via the milk of dams drinking 0.2% lead acetate beginning at parturition, and mid-dorsal sections of the hippocampus and dentate gyrus (DG) from 15-day-old pups were examined by light and electron microscopy. Lead exposure did not reduce body weight nor produce obviously abnormal vascularity or signs of cytotoxicity in the hippocampal formation, and total numbers per section of dentate granule cells or CA3 pyramidal cells were not reduced. On the other hand, lead exposure reduced neuropil development as evidenced both by reduced areas of the dentate hilus and dentate infrapyramidal stratum moleculare and by increased number of hilar CA3 pyramidal cells per unit area. Also, lead exposure reduced numbers of several types of synaptic profiles per unit area in the suprapyramidal mossy fiber zone. Complex invaginated (CI) profiles, assumed to be mature mossy fiber boutons, were characterized by multiple membrane densities and deep invaginations around dendritic spines of pyramidal cells. Complex noninvaginated (CN) boutons exhibited bag-like profiles with multiple membrane densities. Smaller, less numerous, simple (S) profiles contacted either dendritic trunks (ST) or spines (SS). Lead exposure reduced the numerical density of any of the profiles in the deep (close to stratum pyramidale) part of the proximal (close to DG) region of the suprapyramidal mossy fiber zone, but did not alter the numerical density of any of the profiles in the superficial (distal to stratum pyramidale) parts of either proximal or distal (close to CA1) regions. Average size of CN profiles in the distal region was increased by lead exposure. The pattern of effects suggests that low-level lead exposure during development preferentially affects later developing structures within the hippocampal formation, rather than affecting mature structures.

Animals↗

Postnatal development of cholinergic neurotransmitter enzymes in the mouse cerebellum. Biochemical, light microscopic and electron microscopic cytochemical investigations.

The activity and distribution of the cholinergic neurotransmitter enzymes acetylcholinesterase (AChE) and choline acetyltransferase (ChAc) in the developing cerebellum of the mouse were investigated using biochemical assays and light microscopic histochemistry for AChE and ChAc, and electron microscopic histochemistry for AChE. Postnatal alterations in the levels of AChE and ChAc in the cerebellum of the mouse are characterized by a divergent pattern. During the first two postnatal weeks, AChE activity increases progressively, whereas ChAc activity remains low. Beyond day 14, when AChE activity is steady or gradually decreasing, ChAc increases sharply to reach a peak on day 32. Histochemically, AChE activity is associated with the glomeruli and the Golgi cells of the internal granular layer, the medullary layer, and the deep cerebellar nuclei. Purkinje cells exhibit transient staining between days 2 and 9. At the structural level, AChE staining is first demonstrated on day 6 within the Golgi cell soma, on day 9 at the mossy fiber-granule cell synapse, and on day 11 at the Golgi terminal-granule cell synapse. The staining intensity of these structures reaches that of the adult on day 19. The histochemical reaction for ChAc is localized to moderate number of presumed Bergmann glial cells, a few large cells of the deep cerebellar nuclei, small numbers of Golgi cells, and all immature Purkinje cells. The molecular distribution of ChAc sharply contrasts with the localization established by other methods previously and is interpreted in the light of the drawbacks of the histochemical procedure. The biochemical fluctuations in AChE activity, correlated with the histochemical and cytochemical data, suggest that the postnatal increases in the enzyme are related to the ingrowth of the mossy fibers and to the maturation of the AChE-positive Golgi cells. Histochemical evidence for the correlation between the ontogenetic increases in cerebellar ChAc activity and progressive mossy fiber innervation must await the application of the immunohistochemical method to the developing cerebellum.

Acetylcholinesterase↗

Acetylcholinesterase activity and menstrual remissions in myasthenia gravis.

Menstrually related temporary remissions of myasthenic symptoms are reported to occur in 25 to 50% of female patients. Even though this has been attributed to hormonal changes associated with the menstrual cycle the underlying mechanism of this hormonal influence has remained elusive. The present study demonstrated a cyclical variation in the activity of red cell acetylcholinesterase (EC 3.1.1.7) enzyme (AChE) with a marked reduction at the time of menstrual remission of symptoms of myasthenia. These cyclical changes were abolished by thymectomy. It appears, therefore, that menstrual remission in myasthenia is at least partly due to hormone-induced changes in AChE activity. This process seems to be under the control of the thymus gland.

Acetylcholinesterase↗

Acetylcholinesterase activity in the cerebellum of the lurcher (Lc) mutant mouse.

The activity and distribution of the enzyme acetylcholinesterase in the cerebellum of adult lurcher (Lc) mutant mice and of their normal littermates was investigated using biochemical assay and light microscopic histochemistry. The biochemical assay demonstrated an approximate two-fold increase of enzyme activity in the lurcher cerebellum compared to the values obtained for the normal controls. Acetylcholinesterase activity in the cerebellum of the normal adult mouse was predominantly evident in the granular layer, corresponding to the location of the glomeruli. In contrast, the lurcher cerebellum exhibited enzyme activity in both molecular and granular layers. In the molecular layer the staining appeared to be associated with ectopic granule cells. In both normal and lurcher mice, the Golgi cells, subcortical white matter and deep nuclei also showed varying degrees of staining for acetylcholinesterase.

Acetylcholinesterase↗

Increase in glial fibrillary acidic protein following neural trauma.

Immunohistochemical staining and quantitative evaluation of glial fibrillary acidic protein (GFAP) were carried out in a stab wound model of neural trauma in the rat. Increased GFAP staining was detected in reactive cortical astrocytes in the vicinity of the wound at 3, 7, and 30 d following injury. Western blots immunostained for GFAP also demonstrated an increase in GFAP in homogenates from the lesioned cortex, compared to the contralateral control side, on days 3, 7, and 30. Specific activity of GFAP expressed as a ratio of lesion/control values showed a fivefold increase from day 0 to day 7, with no further change on day 30. We conclude that neural trauma elicits a quantitative increase in GFAP in the rat cortex during the first week following injury. This increase correlates with both astrocyte hyperthrophy and proliferation. Thus, specific activity of GFAP is a reliable indicator of the onset and progression of astrogliosis in neural trauma.

Animals↗

Short course chemotherapy for tuberculous lymphadenitis in children.

OBJECTIVE: To assess the efficacy of a short course chemotherapy regimen for treating tuberculosis of the lymph nodes in children. DESIGN: Open, collaborative, outpatient clinical trial. SETTING: Outpatient department of the Tuberculosis Research Centre, paediatric surgery departments of the Institute of Child Health and Hospital for Children and the Government Stanley Hospital, Madras, South India. PATIENTS: Children aged 1-12 years with extensive, multiple site, superficial tuberculous lymphadenitis confirmed by biopsy (histopathology or culture). INTERVENTIONS: Patients were treated with a fully supervised intermittent chemotherapy regimen consisting of streptomycin, rifampicin, isoniazid, and pyrazinamide three times a week for two months followed by streptomycin and isoniazid twice a week for four months on an outpatient basis. Surgery was limited to biopsy of nodes for diagnosis and assessment. MAIN OUTCOME MEASURES: Response to chemotherapy was assessed by regression of lymph nodes and healing of sinuses and abscesses during treatment and follow up. Compliance with treatment and frequency of adverse reactions were also estimated. RESULTS: 197 Patients were admitted to the study and 168 into the analysis. The regimen was well tolerated and compliance was good with 101 (60%) patients receiving the prescribed chemotherapy within 15 days of the stipulated period of six months. Those whose chemotherapy extended beyond that period received the same total number of doses. Clinical response was favourable in most patients at the end of treatment. Sinuses and abscesses healed rapidly. Residual lymphadenopathy (exceeding 10 mm diameter) was present in 50 (30%) patients at the end of treatment; these nodes were biopsied. Fresh nodes, increase in size of nodes, and sinuses and abscesses occurred both during treatment and follow up. After 36 months of follow up after treatment only 5 (3%) patients required retreatment for tuberculosis. CONCLUSION: Tuberculous lymphadenitis in children can be successfully treated with a short course chemotherapy regimen of six months.

Antitubercular Agents↗

Pre-operative short-term pulmonary rehabilitation for patients of chronic obstructive pulmonary disease undergoing coronary artery bypass graft surgery.

The role of pre-operative short-term pulmonary rehabilitation in patients with chronic obstructive pulmonary disease who undergo coronary artery bypass graft surgery has been assessed for the first time prospectively. Forty-five patients posted for coronary artery bypass graft surgery were randomised to receive either short-term pulmonary rehabilitation (group I) or no such programme (group II). Patients of both the groups were evenly matched with respect to age, sex, body surface area, duration and severity of chronic obstructive pulmonary disease and coronary artery disease. Normal individuals who evenly matched with the study group were assessed for normal respiratory function parameters. Pre-operative and post-operative peak expiratory flow rate, inspiratory capacity, post-operative ventilation time, post-operative pulmonary complication and hospital stay were determined in both the groups. Peak expiratory flow rate (220.0 +/- 12.9 and 324.3 +/- 84.3 in group I, 218.0 +/- 16.4 and 260.5 +/- 35.2 in group II) and inspiratory capacity (844.0 +/- 147.4 and 1100.0 +/- 158.1 in group I, 830.0 +/- 117.4 and 1090 +/- 137 in group II) were significantly lower before and after surgery respectively in both groups compared to normal values. Even though both groups showed a significant rise in post-operative peak expiratory flow rate and inspiratory capacity after surgery, the post-operative peak expiratory flow rate and inspiratory capacity in group I was significantly higher than in group II. In group I, the post-operative ventilation time (24.5 +/- 6.00 hours), post-operative complications (n = 4) and hospital stay (12.4 +/- 3.6 days) were significantly lower than in group II (35.2 +/- 22.3 hours, n = 11, 18.8 +/- 6.6 days respectively). These data suggest that short-term pulmonary rehabilitation is feasible and effective in improving pulmonary functions before and after surgery and in reducing surgical morbidity and cost of medical care significantly.

Breathing Exercises↗

Pulmonary function in normal south Indian children aged 7 to 19 years.

There are only a few studies that have established reference standards for pulmonary function of Indian children. Reference standards for pulmonary function that are reported for Indian children are mainly from northern and western parts of the country and there is a paucity of data on pulmonary function in normal South Indian children. Therefore, pulmonary function tests (spirometry and maximal expiratory flow rates) were carried out in 469 South Indian healthy children (246 boys and 223 girls) between 7-19 years of age to derive regression equations to predict pulmonary function. The correlations of forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) were, in general highest with height followed by weight and age. Peak expiratory flow rate (PEFR), forced mid-expiratory flow (FMF) and forced expiratory flow rates at 25%, 50% and 75% of FVC (FEF25% FVC, FEF50%FVC and FEF75%FVC) were also significantly correlated with physical characteristics (age, height and weight). With a view to find out regression equations to predict spirometric functions based on physical characteristics (age, height and/or weight), the functions were regressed over all possible combinations of regressor variables, i.e. age, height and weight separately for boys and girls. The height influences the prediction equation in males to a great extent, whereas age and weight had greater influence in girls. Regression equations were derived for boys and girls for predicting normal pulmonary functions for children in South India. The pulmonary function measurements in South Indian children were similar to those reported for subjects from Western India and lower than those reported for Caucasians.

Adolescent↗