Glutathione & Ascorbic acid contents in developing rat brain during undernutrition.
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Biomedical subjects
Publications and source records attributed to R Shankar.
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Na+,K+-ATPase was studied in developing rat brain during undernutrition. The activity of Na+,K+-ATPase was significantly lower in animals that were undernourished from 6 to 17 days after birth than in well-nourished controls. The decreased activity of the enzyme was partially recovered after 4 weeks of rehabilitation. No change in the cation contents of brain following undernutrition was observed. The decrease in Na+,K4-ATPase activity was possibly due to the reduction in cholesterol contents and could be responsible for the observed functional changes associated with malnutrition or undernutrition during development.
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1. Tetrodotoxin, at concentrations at which it abolishes generation of action potentials in the nervous system, enhances by about 300% the rate of anaerobic glycolysis of brain-cortex slices from adult rats, or from adult and infant guinea pigs. This occurs to a greater extent in Ca(2+)-deficient incubation media than in Ca(2+)-rich media. Tetrodotoxin has no accelerative effect on cerebral aerobic glycolysis. 2. Tetrodotoxin does not affect the rate of anaerobic glycolysis of 2-day-old rat brain-cortex slices, nor that of adult rat kidney medulla, nor that of an extract of an acetone-dried powder of brain. 3. Tetrodotoxin does not affect the rate of penetration of glucose into brain slices. 4. Its effect is not apparent if it is added 10min or later after the onset of anoxia. 5. Its effect diminishes as the concentration of K(+) in the incubation medium is increased while that of Na(+) is decreased. 6. Its salient effect, at the onset of anoxia, is to diminish influx of Na(+) into, and efflux of K(+) from, the brain slices. 7. Substances that promote cerebral influx of Na(+), e.g. protoveratrine, sodium l-glutamate, diminish the accelerative action of tetrodotoxin. 8. It is concluded that tetrodotoxin exerts its effect on anaerobic glycolysis by suppressing, at the onset of anoxia, the generation of action potentials and thereby the accompanying influx of Na(+) and efflux of K(+). It is suggested that glycolytic stimulation occurs because a rate-limiting step, e.g. operation of pyruvate kinase, is stimulated by K(+) and depressed by Na(+). 9. Local anaesthetics behave in a manner similar to that of tetrodotoxin in enhancing cerebral anaerobic glycolysis. 10. Sodium Amytal has a marked effect at relatively high concentration. 11. Tetrodotoxin diminishes efflux of amino acids, particularly glutamate and aspartate, at the onset of anoxia.
Serum calcium and phosphorus levels were measured at birth, 6 hours, 24 hours, and on 5th day of life in 35 neonates with birth asphyxia (one-minute Apgar score of 6 or less), and in 37 neonates without asphyxia (one-minute Apgar score of 7 or more). Infants were divided into three groups: FT-AGA (n = 30, asphyxia = 15), FT-IUGR (n = 20, asphyxia = 10) and PT-AGA (n = 22, asphyxia = 10). Asphyxiated infants--FT-AGA as well as FT-IUGR--had significantly lower serum calcium levels than control infants during each of the time period studied. In PT-AGA infants with asphyxia, the serum calcium was significantly low only on 5th day of life. Lack of calcium intake, and hyperphosphatemia were identified as possible risk factors for low serum calcium in asphyxiated infants. No change in serum calcium levels was found in bicarbonate-treated asphyxiated infants in comparison to those who did not receive sodium bicarbonate. In view of the high incidence of low serum calcium in asphyxiated infants, serial monitoring of serum calcium levels is recommended in these infants.
Hematopoietic stem cells represent a long term reservoir of cells to populate blood with multiple formed cells. These hematopoietic stem cells proliferate and mature into lymphoid, erythroid, and myeloid precursor cells, with the balance of these cell populations modulated by major thermal injury, with or without sepsis. Recent studies indicate that thermal injury shifts this balance to favor the monocyte/macrophage lineage at the expense of neutrophil production. The mechanisms for these changes are now being elucidated with the results of clinical importance, because understanding the dynamics of the different precursor pools could be used to identify patients at greater risk for systemic inflammatory sequelae following major thermal injury.
We present the case of an 18-year-old male who 8 months after a living-related donor, one-haplotype-matched renal transplantation developed acute thrombosis of the renal allograft artery, within 10 h of the first dose of OKT3. The antibody therapy had followed five daily doses of intravenous pulse methylprednisolone for a Banff class 1B acute tubulointerstitial rejection, on a ciclosporin-based immunosuppression protocol. We briefly review the literature on the incidence of vascular thrombosis after transplantation and the procoagulant effects of OKT3, pulse methylprednisolone, and ciclosporin therapy.
Treatment of progressive precocious puberty in patients with McCune-Albright syndrome (MAS) has traditionally been with aromatase inhibitors, such as testolactone. However, the use of these agents has been characterized by problems with both efficacy and compliance. We report a case of MAS in which tamoxifen proved to be a successful alternative in the treatment of progressive precocious puberty. An African-American female presented with MAS at 2-5/12 years. Frequent menses, skeletal maturation and growth acceleration prompted initiation of therapy with testolactone at 22 mg/kg/d. Over the next 13 months, the patient's puberty advanced unchecked, despite progressive increases in the dose of testolactone. At age 4 years, medication was discontinued due to treatment failure. At 4-6/12 years, bone age was 10 years, predicted adult height was 137 cm, and monthly bleeding continued. Tamoxifen was then begun on an experimental basis. In response, the patient experienced immediate cessation of menses, and had an abrupt decrease in the rates of pubertal progression and linear growth. This patient has now been maintained on tamoxifen for over three years with no apparent adverse effects. GnRH analogue therapy was begun when the onset of central precocious puberty was noted. Predicted adult height has improved to 154 cm and growth velocity and skeletal maturation remain stable. Our results suggest that tamoxifen may have a valuable role in the treatment of precocious puberty in patients with MAS and may lead to superior results compared with those achieved with aromatase inhibitors.
BACKGROUND: Ultrasonographic measurement of thyroid volume is increasingly being used to assess prevalence of iodine deficiency in a community. OBJECTIVES: To assess thyroid volume by ultrasonography in normal Delhi children, and compare them with the recently adopted WHO reference standards. METHODS: One hundred and three children aged of 6-10 years were enrolled from the paediatric outpatient clinic in a prospective study. Thyroid volume was estimated by ultrasound, and urinary iodine levels were measured for all subjects by spot urine samples. RESULTS: Goitre prevalence was 24.3% on clinical assessment. Urinary iodine levels fell in the range of mild to moderate deficiency in 61% of the children. None of the children met the WHO recommended ultrasonographic criteria for goitre (thyroid volume >97th percentile of the reference standards), when WHO age-specific norms were used for comparison. On applying body surface area (BSA)-specific norms, only two children were classified as having goitre. CONCLUSIONS: The WHO standards for thyroid volume by ultrasonography tended to underestimate goitre prevalence.
Long-term effects of thyroid hormone suppressive therapy on the heart were evaluated in 45 patients by non-invasive techniques. Fifteen patients were athyreotic after surgery for differentiated thyroid cancer and 30 had diffuse or nodular goiter. Mean age of the group was 42 +/- 12 years. Twenty-four age- and sex-matched subjects were taken as controls. Mean daily dose of levothyroxine was 158 +/- 36 micrograms. Plasma thyroid stimulating hormone (TSH) levels were within normal range. Mean serum T4 and free T4 were significantly higher (p < 0.001) whereas mean serum T3 and free T3 did not differ from the control levels. Non-invasive cardiac assessment was done by a standard 12 lead electrocardiogram (ECG), ambulatory electrocardiographic (Holter) monitoring and echocardiographic study. Six patients had left ventricular hypertrophy in ECG. Holter monitoring demonstrated a higher average heart rate in patients compared to controls (86 +/- 10 vs 72 +/- 6 beats/min; p < 0.001). Supraventricular premature beats were more frequent in patients than in the control group (98% vs 60%; p < 0.06). Echocardiogram showed an increased left ventricular (LV) mass index in patient group (98 +/- 28 vs 78 +/- 16 gm/m2; p < 0.02). LV systolic function was increased with higher values of fractional shortening (40 +/- 8% vs 34 +/- 6%; p < 0.05) and rate-adjusted velocity of shortening (1.4 +/- 0.12 vs 1.02 +/- 0.16 circumferences/sec; p < 0.01). It is concluded that long-term levothyroxine suppressive therapy has significant effects on the cardiac functions.