Acute acalculous cholecystitis in a young child.
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Biomedical subjects
Publications and source records attributed to A Bansal.
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NADP+-specific glutamate dehydrogenase from Salmonella typhimurium, cloned and expressed in Escherichia coli, has been purified to homogeneity. The nucleotide sequence of S. typhimurium gdhA was determined and the amino acid sequence derived. The nucleotide analogue 2-[(4-bromo-2,3-dioxobutyl)thio]-1,N6-ethenoadenosine 2',5'-bisphosphate (2-BDB-T epsilon A-2',5'-DP) reacts irreversibly with the enzyme to yield a partially inactive enzyme. After about 60% loss of activity, no further inactivation is observed. The rate of inactivation exhibits a nonlinear dependence on 2-BDB-T epsilon A-2',5'-DP concentration with kmax = 0.160 min-1 and KI = 300 microM. Reaction of 200 microM 2-BDB-T epsilon A-2',5'-DP with glutamate dehydrogenase for 120 min results in the incorporation of 0.94 mol of reagent/mol of enzyme subunit. The coenzymes, NADPH and NADP+, completely protect the enzyme against inactivation by the reagent and decrease the reagent incorporation from 0.94 to 0.5 mol of reagent/mol enzyme subunit, while the substrate alpha-ketoglutarate offers only partial protection. These results indicate that 2-BDB-T epsilon A-2',5'-DP functions as an affinity label of the coenzyme binding site and that specific reaction occurs at only about 0.5 sites/enzyme subunit or 3 sites/hexamer. Glutamate dehydrogenase modified with 200 microM 2-BDB-T epsilon A-2',5'-DP in the absence and presence of coenzyme was reduced with NaB3H4, carboxymethylated, and digested with trypsin. Labeled peptides were purified by high performance liquid chromatography and characterized by gas phase sequencing. Two peptides modified by the reagent were isolated and identified as follows: Phe-Cys(CM)-Gln-Ala-Leu-Met-Thr-Glu-Leu-Tyr-Arg and Leu-Cys(CM)-Glu-Ile-Lys. These two peptides were located within the derived amino acid sequence as residues 146-156 and 282-286. In the presence of NADPH, which completely prevents inactivation, only peptide 146-156 was labeled. This result indicates that modification of the pentapeptide causes loss of activity. Glutamate 284 in this peptide is the probable reaction target and is located within the coenzyme binding site.
This study was undertaken with the aim of providing adequate calories for optimal growth in low birth weight (LBW) by fortifying human milk with medium chain triglycerides and sugar. Twenty-one LBW babies with birth weight between 1.0 and 1.75 kg and gestational age 28-36 weeks constituted the study material. They were administered expressed human milk, initially with gavage and then by spoon. Coconut oil and sugar were added to increase the caloric density to (0.8 cal/ml). The aim was to achieve a caloric intake of 200 cal/kg. This was achieved between 6 and 11 days of birth. Additionally, vitamin C (50 mg) and vitamin E (25 IU/kg/day) were administered. Weight was recorded daily to the nearest 50 g. Head circumference was measured weekly using a non-stretch tape measure. Blood urea nitrogen was measured once the neonate started taking high calorie feeds. Stools were examined daily for the presence of fat globules and reducing substances and for the pH. All but one neonate tolerated the feeds well and there were no complications, such as vomiting, diarrhoea, abdominal distension, or necrotizing enterocolitis. The weight gain recorded was 17.29 +/- 5.30 g/day or 13.95 +/- 5.52 g/kg/day. The study demonstrates that optimal growth can be achieved within the metabolic tolerance of low birth weight infants by administering fortified high calorie breast milk.
Seventy-five infants and children presenting during the period December 1984 to December, 1987 with the clinical features of vomiting, failure to thrive, chronic cough, recurrent pneumonia and atypical asthma were evaluated for gastroesophageal reflux by standard barium esophagram. Fifty six cases (74.7%) and as many as 80% of the infants studied had gastroesophageal reflux; Grade II reflux was seen in 12 cases, Grade III in 30 and Grade IV in 14 cases. The patients with gastroesophageal reflux were put on medical treatment. All the patients had subjective improvement after 6 weeks to 6 months of conservative treatment and none of them developed further complications of gastroesophageal reflux during a follow-up period varying from two months to fifteen months. Anti-reflux surgery was not considered owing to the subjective improvement in all the patients on conservative treatment. We conclude that gastroesophageal reflux is very common in infants and children and urge the need to evaluate the patients presenting with the symptoms suggesting gastroesophageal reflux by barium esophagram; conservative treatment is the mainstay in the management of these children.
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The circadian patterns of serum and urinary urate were studied in 25 healthy Indians and 25 renal stone formers. A marked circadian variation in uric acid concentration was recorded in both the groups with acrophases at 1441 and 1347 hr, respectively (cosinor analysis). Similarly, cosinor rhythmometry confirmed a significant circadian rhythm in urinary uric acid levels during different hours of the 24-hr day-night period in healthy Indians (acrophase at 1229 hr) and renal stone formers (acrophase at 1121 hr). Serum uric acid was found to be elevated at all time points during the 24-hr period in the stone formers compared to healthy subjects. The excretory pattern, however, did not exhibit any significant difference in uric acid levels between the two groups although the excretion was a little higher in the stone formers compared to the healthy controls. Maximum urate excretion at 1121 hr (around midday) might be the peak hour for maximum crystallization of stones containing an admixture of urate in stone formers; if such is true, it could prove to be of clinical significance when trying to inhibit crystallization of renal stones and to minimize the risk of crystal growth (urate admixture) in renal tubules.
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A case of salmonella meningitis with accompanying septicaemia and pericarditis is reported in an adult following an episode of enteritis.
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107 patients with neonatal tetanus were studied and the value of intrathecal antitetanus serum with steroid was noted. The mortality rate in a control group (68%) was significantly higher than that of the test group (37%). Furthermore, a delay in antitetanus serum administration was found to have a strong positive linear correlation with the mortality rate. In fact, the mortality rate for neonates who were given antitetanus serum 24 hours after the onset of convulsions was found to be as high as for the control group. This suggests that intrathecal antitetanus serum is ineffective unless it is administered within 24 hours of the onset of convulsions. There was no significant difference in mortality rate whether a dose of 100 units or one of 50 units antitetanus serum was given intrathecally. The mean duration in hospital for survivals of the test group (7.4 days) was significantly shorter than that for survivals of the control group (10.4 days). No complication of intrathecal antitetanus serum was observed during the study.
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