Biomedical subjects
Publications and source records attributed to A Shukla.
A diet containing 18-20 mg iron/kg to young weaned rats for 8 weeks altered the metabolism of gamma-aminobutyric acid and glutamate in the central nervous system without affecting blood hemoglobin. Subsequent rehabilitation with 390 mg iron/kg diet for 2 weeks normalized these changes.
Seven different metals (iron, copper, zinc, calcium, manganese, lead, and cadmium) were studied in eight different brain regions (cerebral cortex, cerebellum, corpus striatum, hypothalamus, hippocampus, midbrain, medulla oblongata, and pons) of weaned rats (21-d-old) maintained on an iron-deficient (18-20 mg iron/kg) diet for 8 wk. Iron was found to decrease in all the brain regions, except medulla oblongata and pons, in comparison to their respective levels in control rats, receiving an iron-sufficient (390 mg iron/kg) diet. Brain regions showed different susceptibility toward iron deficiency-induced alterations in the levels of various metals, such as zinc, was found to increase in hippocampus (19%, p less than 0.05) and midbrain (16%, p less than 0.05), copper in cerebral cortex (18%, p less than 0.05) and corpus striatum (16% p less than 0.05), calcium in corpus striatum (22%, p less than 0.01) and hypothalamus (17%, p less than 0.02), and manganese in hypothalamus (18%, p less than 0.05) only. Toxic metals lead and cadmium also increased in cerebellum (19%, p less than 0.05) and hippocampus (17%, p less than 0.05) regions, respectively. Apart from these changes, liver (64%, p less than 0.001) and brain (19%, p less than 0.01) nonheme iron contents were found to decrease significantly, but body, liver, and brain weights, packed cell volume, and hemoglobin content remained unaltered in these experimental rats. Rehabilitation of iron-deficient rats with an iron-sufficient diet for 2 wk recovered the values of zinc in both the hippocampus and mid-brain regions and calcium in the hypothalamus region only. Liver nonheme iron improved significantly; however, no remarkable effect was noticed in brain nonheme iron following rehabilitation. It may be concluded that latent iron deficiency produced alterations in various metal levels in different brain regions, and corpus striatum was found to be the most vulnerable region for such changes. It is also evident that brain regions were resistant for any recovery in their altered metallic levels in response to rehabilitation for 2 wk.
Eight weeks of latent iron deficiency in weaned rats maintained on an experimental low iron content diet (18-20 mg/kg) did not significantly alter the packed cell volume and hemoglobin concentration; however, the hepatic and brain nonheme iron contents decreased by 66% and 21% (p less than 0.001), respectively. The tryptophan concentration decreased by 31% and 34% in liver and brain, respectively, in rats on experimental diet (p less than 0.01). The brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid contents were reduced by 21% and 23% (p less than 0.01 and p less than 0.02), respectively. However, in the brain, weight, protein, DNA, and the activities of monoamine oxidase, aldehyde dehydrogenase, and liver tryptophan oxygenase were found to remain unaltered. When rehabilitated with a diet containing 390 mg/kg iron, rats previously maintained on the experimental diet for 2 weeks showed partial recovery in tryptophan levels both in liver and brain. However, brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels remained unaltered. The hepatic iron content improved without any change in brain iron content. The latent iron deficiency produced significant alterations in the metabolism of 5-hydroxytryptamine and brain iron content that could not be recovered 2 weeks after the iron rehabilitation.
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Colloid osmotic pressure (COP) was measured serially in 81 critically ill neonates with hyaline membrane disease (HMD) during the first five days of life, and these changes were correlated with the birth weight, gestational age, serum protein level, clinical status, and outcome. Colloid osmotic pressure correlated better with the total protein level (n = 81; r = 0.54) than with birth weight (r = 0.23) and gestational age (r = 0.31; n = 81). Seventy-one of 81 neonates survived. Among the survivors, COP increased significantly by day 5, whereas changes in the total protein level were not significant during the same period. Colloid osmotic pressure decreased significantly in nine of ten nonsurvivors (mean +/- SE, 11 +/- 0.5 to 8 +/- 0.55 mm Hg), whereas the total protein level did not show a similar change. Thus, COP cannot be accurately predicted by measuring serum protein during acute illness. Serial measurement of COP was a better prognostic indicator than the total protein level in infants with HMD.
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Clinical usefulness and factors affecting transcutaneous CO2 (PtcCO2) monitoring were studied in 22 critically ill neonates. In 10 of 22 infants, both tissue pH (pHt) and PtcCO2 were monitored simultaneously using Roche pHt and CO2 electrodes. Arterial blood gases were obtained from umbilical artery catheter. The effect of variations in blood pressure, oxygenation, arterial pH (pHa) pHt, and medications on PtcCO2 were studied. There was a linear correlation between pHt and pHa (n = 108, r = 0.85, slope 1.08), PtcCo2 and PaCO2 (n = 188, r = 0.85, slope 1.49). The pHt changes correlated better with PtcCO2 than with arterial CO2 (r = 0.78, slope 1.35). The major factors affecting the PtcCO2 relationship were (a) hypoxia and (b) acidosis. When PaO2 less than 40 torr, PtcCO2 correlated poorly to PaCO2 (n = 23, r = 0.48, slope 0.72) whereas, during normoxia (PaO2 greater than 40 torr), it correlated well, r = 0.85, slope 1.51 similarly. When pHt was greater than 7.30, PtcCO2 correlated better with PaCO2 (r = 0.88, slope 1.37) than during tissue acidosis (r = 0.71, slope 1.51). Mean blood pressure down to 30 mm Hg and administration of dopamine and tolazoline did not affect the PtcCO2 to PaCO2 relationship (n = 69, r = 0.86, slope 1.6). Clinically, both continuous pHt and PtcCO2 were found to be very useful in the management of critically ill neonates.
A survey of feeding patterns and nutrient intake in relation to the growth of 300 normal infants up to 1 year of age in Dudley, Worcestershire, highlights a problem of overnutrition in the group; 50 (16.7%) were found to be suffering from infantile obesity and a further 83 (27.7%) were overweight.During the first three months of life the daily energy intakes of 136 cal/kg body weight for boys and 149 for girls were markedly greater than the level of 120/kg recommended by the Department of Health and Social Security. This coincided with the early addition of solid foods to a full milk intake. 119 babies (39.7%) were offered solids before they were 4 weeks old and 280 (93.3%) before 13 weeks of age. Some babies had solids from the first week after birth. Protein intake was persistently high throughout the first year, and the mean intake of 32.7 g/day was much greater than the intake of 20 g for infants aged up to 1 year recommended by the Department of Health. Standards for fat and carbohydrate intake are not available but in comparison with the levels reported in breast-fed babies intake of fat and carbohydrate was high in the first three months and came closer to the desired level for the former and remained slightly high for the latter in the subsequent age quarters.The relation of childhood and subsequent adult obesity to infant feeding patterns is not yet clear, but there is a high correlation between obese parents and obese and overweight babies; had these babies not been overfed the condition might have been prevented.
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Fibrosis is a consequence of injury which is characterized by accumulation of excess collagen and other extracellular matrix components, resulting in the destruction of normal tissue architecture and function. Transforming growth factor-beta, a potent wound healing agent, has also been shown to be an agent that can produce fibrosis because it is a potent stimulator of collagen synthesis. Both glucocorticoids and bleomycin have recently been shown to affect collagen synthesis in opposite directions, by utilizing a common pathway of involving transforming growth factor-beta activator protein binding to the transforming growth factor-beta element. This article presents a mechanistic overview of collagen synthesis regulation by glucocorticoids and bleomycin through the transforming growth factor-beta pathway.
A new, sensitive, and selective method is described for the spectrophotometric determination of Ta(V). The method is based on the extraction of the Ta(V)-F-CV+ complex (CV+ = crystal violet cation) with a benzene solution of imidoyl derivatives (ID), i.e., N,N'-diphenylbenzamidine (DPBA), N-hydroxy-N,N'-diphenylbenzamidine, and N-(2,5-dimethyl)phenyl-p-tolylimidoylphenylhydrazine, from sulfuric acid solution; DPBA was selected for detailed study. The molar absorptivities of the Ta(V)-F-CV+-ID complexes in the benzene solution were in the range of (1.00-1.65) x 10(5) L/mol x cm at 600 nm. The limit of detection was 7 ng Ta/mL (which had an absorbance greater than that of the blank + 3 standard deviations). The optimization of the analytical variables, the composition of the complex, and the effect of diverse ions in the determination of Ta are discussed. The present method was applied to the determination of Ta in environmental samples, i.e., soil, sediment, minerals, and alloys.
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