Biomedical subjects
Publications and source records attributed to S Deb.
The profiles of plasma and ovarian cholesterol altered similarly as a result of seasonal influence. Fish pituitary extract and LH significantly depleted plasma and ovarian free cholesterol only, esterified cholesterol remaining unaltered. Findings indicated that plasma cholesterol was the primary source of sterol for ovarian steroidogenesis.
Reactive sulfhydryl groups of major hemoglobins from guinea-pig, rat and cat reduced dehydroascorbic acid to ascorbic acid leading to formation of intrachain disulfide bonds. Hybridization experiments indicated that the reduction was carried out by the alpha chain of cat hemoglobin.
In contrast to normal subjects diabetic patients and very low plasma ascorbic acid and significantly high (p less than 0.001) dehydroascorbic acid irrespective of age, sex, duration of the disease, type of treatment, and glycemic control. However, there was no significant difference between the mean leukocyte ascorbate concentrations of the two populations. The in vitro rates of dehydroascorbate reduction in the hemolysate and the erythrocyte reduced glutathione levels and the glucose-6-phosphate dehydrogenase activities, which regulate the dehydroascorbate reduction, were similar in normal and diabetic subjects. The turnover of ascorbic acid was higher in the diabetics than that in the normal volunteers. Experiments with diabetic rats indicated that the increased turnover of ascorbic acid was probably due to increased oxidation of ascorbate to dehydroascorbate in tissue mitochondria. Ascorbic acid supplementation at a dose of 500 mg per day for a brief period of 15 days resulted in an increase in the plasma ascorbate level temporarily, but it did not lower the blood glucose level of the diabetic patients.
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The concept of temporal and spatial relationship between neuronal and vascular changes in the central nervous system following different kinds of anoxia still remains debatable, in that it is uncertain if anoxia-ischaemia primarily produces vascular changes in the brain or it initially damages the cerebral neurons. The present investigation has been undertaken to denote the sequential relationship between neuronal and vascular changes following experimental cerebral ischaemic anoxia. Adult healthy albino rats were subjected to ischaemic anoxia by bilateral clamping of their common carotid arteries for varying intervals of 5, 10 and 15 min. The animals of each group were subsequently sacrificed on days 1, 3, 5, 7 and 10 after the clamping procedure, for light-microscopic study of their brains. Our findings are characterized by initial vascular changes, which appear to have resulted in 'no-reflow' leading subsequently to neuronal damage. The latter, in turn, secondarily caused damage to the microvasculature.
The body balance technique was used to determine the maintenance requirement and the energetic efficiency of 6-week-old male lean and obese Zucker rats. Fifteen lean and 15 obese rats were assigned to three groups of five each and fed three levels of food intake: ad libitum, 75% of ad libitum, and 50% of ad libitum, for a 4-week period. The obese rats consumed more food and gained significantly more weight than the lean rats. Obese rats utilized dietary energy more efficiently than lean rats but the opposite was true for dietary protein. The efficiency with which obese rats utilized metabolizable energy for gain was 36% compared with efficiency of utilization of metabolizable energy above maintenance for obese and lean were 51.4% and 21.4%, respectively. The maintenance requirement on the basis of metabolic body size for the obese and lean was calculated to be 122 and 130.5 kcal ME per day per kg.75 for the 4-week period. These results indicate that the energetic efficiency is higher in obese than in lean Zucker rats and suggest that the higher energetic efficiency is not the result of a significantly lower maintenance requirement.
The effects of exercise and of food restriction on Zucker obese and lean rats were studied. Zucker obese rats pair-fed to lean littermates gained more body fat on the same intake indicating greater efficiency of diet utilization. Exercise significantly reduced the fat pad weights and body fat content of obese rats. Serum insulin levels were higher in the obese rats and were not influenced by exercise. Exercise had no effect on adipose cellularity of the obese rats. Liver tissue in vitro lipogenic capacity and lipogenic enzyme activities were significantly elevated in obese rats. Exercise increased liver tissue hexokinase and in vitro lipogenesis in lean rats. Exercise increased pentose phosphate pathway enzymes in adipose tissue from lean rats only. Although exercise reduced fat content significantly, obese rats were still fatter (27.7% fat) than the lean controls (6.4% fat). The protein content of obese rats was significantly increased by exercise, indicating that physical activity is important in the regulation of protein metabolism.
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Growth characteristics and the expression of trophoblast-associated markers by six cell lines generated from midgestation chorioallantoic placentas of outbred (Holtzman) and inbred (Lewis, PVG.RT Ir8) rats were evaluated. The cells comprising all cell lines were epithelioid (contained cytokeratin-type intermediate filaments), had normal (2n, 4n) DNA content, and synthesized the extracellular matrix glycoprotein laminin. Variability was observed among the lines in all other characteristics: median cell size, rate of growth, serum dependency, responses to transferrin and dibutyryl cyclic adenosine-3',5'-monophosphate, synthesis of some major proteins, alkaline phosphatase activity, and the expression of immunoreactive placental lactogen-II. In general, cell lines with smaller mean cell sizes grew rapidly and required little serum for maintenance in vitro; cell lines with larger mean sizes grew more slowly and preferred higher concentrations of serum. Some associations between mean cell size/rate of growth and other characteristics were observed. No major differences were apparent between cell lines generated from outbred and inbred rat placentas. Trophoblast cell lines expressing distinct phenotypes provide a valuable new approach for studying a wide range of trophoblast cell activities.
In this report, we describe the generation of specific antibodies to rat alkaline phosphatase and the temporal and regional characteristics of alkaline phosphatase expression during maturation of the rat chorioallantoic placenta. An antipeptide antiserum was generated to the amino terminal 15 amino acids of rat alkaline phosphatase. The antiserum specifically recognized alkaline phosphatase. Alkaline phosphatase expression was monitored in the junctional and labyrinth zones of the chorioallantoic placenta by Western and Northern blot analyses. Alkaline phosphatase protein and mRNA were present in both the junctional and labyrinth zones on day 13 of gestation. As gestation advanced, alkaline phosphatase mRNA and protein expression decreased below the limits of detection in the junctional zone, while alkaline phosphatase expression increased in the labyrinth zone. Labyrinthine alkaline phosphatase migrated predominantly as a 95-kDa species, whereas rat kidney expressed exclusively the 75-kDa species. Enzymatic deglycosylation of the 75- and 95-kDa alkaline phosphatase species resulted in the generation of a 55-kDa species. In summary, alkaline phosphatase expression is a useful indicator of trophoblast differentiation.
The controversy regarding the exact nature of the relationship between psychopathology and epilepsy continues. We studied the rate of mental disorder in 150 adults with mental retardation and epilepsy among the residents of a health district of the United Kingdom who lived either in institutions or in the community, and compared them with an age-, sex-, and IQ-matched nonepileptic adult mentally retarded population from the same institution and community. Mental disorder was assessed under three headings, namely severe maladaptive behavior, psychiatric illness according to ICD-9 criteria, and personality disorder. Sixty-five percent of the whole cohort had a diagnosis of mental disorder, and 55% showed severe maladaptive behavior. No significant difference in the rate of mental disorder emerged between the epileptic and nonepileptic groups, although the institutionalized subjects as opposed to the community-based subjects and severely mentally retarded adults compared with the mild to moderately mentally retarded adults showed a significantly higher rate of mental disorder in general and severe maladaptive behavior in particular. We hypothesized that underlying brain damage rather than epilepsy per se is a stronger determinant of psychopathology in the studied patient group.
We report a case of a 64-year-old lady who developed clinical features of Wernicke-Korsakoff syndrome following a laparotomy for small bowel obstruction. Following the operation she developed paralytic ileus and required total parenteral nutrition for one month. A suspected history of average 40 units of weekly alcohol consumption prior to the operation could not be confirmed and the patient did not show any sign of alcohol dependence. Within a few months of treatment with a daily oral dose of thiamine 200 mgs supplemented by multivitamins the patient showed subjective evidence of improvement in confusion, confabulation, and anterograde amnesia, although objective tests showed residual deficits in many areas of cognitive functioning, including immediate and delayed recall of verbal and non-verbal materials, planning and switching of attention.
In neurodegenerative disease or after brain injury, parenchymal cells in the central nervous system are activated to produce inflammatory mediators, mainly consisting of cytokine-induced factors, in a manner similar to, but clearly different from a peripheral inflammatory response. The upregulated expression of several extracellular matrix proteins in astrocytes located surrounding a neuritic plaque in Alzheimer's disease is a good example of such a response. A family of mediators which is cytokine-induced during an inflammatory response in the periphery are the matrix metalloproteinases. Matrix metalloproteinases are calcium-requiring, zinc-containing endopeptidases that constitute a major component of the enzyme cascade responsible for degradation of extracellular matrix proteins such as collagen, proteoglycan and laminin. Little is known about the cellular source or the function of matrix metalloproteinases in the central nervous system or how their expression is regulated in brain. Thus, it was of interest to determine which factors of the so-called 'brain inflammatory response' regulate the expression of these proteases in the nervous system. To this end, we measured the expression of matrix metalloproteinases in cultured rat astrocytes and microglia after treatment with various cytokines. Interleukin-1 beta, tumor necrosis factor-alpha and lipopolysaccharide were potent stimulators of matrix metalloproteinase-2 (gelatinase A) and matrix metalloproteinase-9 (gelatinase B) in cultured rat astrocytes; the effect of each secretagogue was inhibited in the presence of glucocorticoid. Interleukin-1 beta and lipopolysaccharide also stimulated the production of matrix metalloproteinase-3 (stromelysin-1) in astrocytes. In addition, activated microglia release matrix metalloproteinase-9. The 'coactivator' of monocytic phagocytes, interferon-gamma, rather than augmenting the response to lipopolysaccharide, inhibited it. Thus, cytokines appear to be potent regulators of matrix metalloproteinase production in astrocytes and microglia. The presence of these enzymes in 'inflamed' central nervous system may suggest their involvement in the pathogenesis or progression of neurodegenerative diseases which are associated with an inflammatory component. Much remains to be learned about the potential substrates for these enzymes and the mechanism of their activation in the central nervous system.
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