Optic nerve involvement in tuberculous meningitis.
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Biomedical subjects
Publications and source records attributed to V Kalra.
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The binding of [3H]phencyclidine (PCP) to receptors in rat brain cortex has been studied. Two receptors have been detected, a high affinity receptor site with a KD of 23.5 +/- 7.4 nM and a low affinity site with a KD of 7.6 +/- 1.8 microM. The binding of [3H]PCP to its receptors was pH and temperature dependent and was destroyed by heat-denaturation. The binding of [3H]PCP was inhibited by compounds which produce PCP-like behavioral effects including dexoxadrol, etoxadrol and ketamine as well as a novel series of benz(f)isoquinolines. The low affinity site was blocked by PCP, etoxadrol and (+)-SKF-10,047 but not morphine or leu-enkephalin, suggesting that it also represents a specific PCP site. Stereoselective displacement of PCP at the high affinity receptor was observed with the isomers of cyclazocine, cyclorphan, SKF-10,047 and dioxadrol (dexoxadrol and levoxadrol). Naloxone, 4,5,6,7-tetrahydroisoxazolo(S,4-C)pyridin-3-ol (THIP) hydrate and haloperidol inhibited binding poorly (Ki greater than 1 microM), suggesting that these compounds do not interact significantly with the high affinity PCP receptor in vivo. The affinity of ligands for the phencyclidine receptor was highly correlated (r = 0.714, P less than 0.01) with their potency to produce catalepsy in pigeons.
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Pedigree charts of 20 families with an index case of Indian childhood cirrhosis, and 70 families of age-matched controls are analysed. Only 177 families were informative for segregation analysis. A single ascertainment model was used for analysis. The hypotheses of autosomal-recessive, partial sex-linkage, and doubly recessive inheritance were found untenable. Multifactorial inheritance was found more plausible. The estimates of heritability of liability were 0.904 for propositi sib and 1.587 for propositi cousins, which indicates a strong role of heredity in the etiology of the disease.
Considerable immunological dysfunction has been reported in Indian childhood cirrhosis (Chandra, 1970; Chawla et al., 1973). These observations suggest that the progressive tissue damage observed in this disease may have an immunological basis. To further test this hypothesis, sera from 18 patients with Indian childhood cirrhosis (ICC) and nine age-matched siblings were examined for the presence of soluble immune complexes and activation of complement. The presence of circulating immune complexes (CIC) in ICC is reported for the first time. Immune complexes were measured by the liquid phase 125I-Clq binding (Clq BA) and 125I-conglutinin binding (KBA) assays, and observed in 13/18 (72%) and 10/18 (56%) patients respectively. A significant correlation was found between the two tests. In contrast, only two out of nine siblings had elevated levels of immune complexes, and these were positive in both tests. Evidence was also obtained for in vivo activation of complement via the classical pathway. Total haemolytic complement (CH50) values were depressed in 13/18 (72%) patients, while C4 and C3 values were low in 5/16 (31%) and 4/18 (22%) patients respectively. C3 degradation products were found in substantial amounts in six patients. Complement levels in siblings were uniformly normal. These observations suggest that the immune complexes demonstrated may be of phlogistic significance and merit further characterization.
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Liver biopsies from 29 siblings of patients with Indian childhood cirrhosis (ICC) and from two age-matched controls were examined by routine light and transmission electron microscopy. Histochemical stainings for copper and copper-binding protein were also carried out. The mild and non-specific structural alterations that were observed did not differ from those seen in control livers, even though a slight to moderate excess of copper and copper-binding protein was demonstrated in the majority. Aggregates of microtubules seen in some siblings, as well as in control livers, may indicate the preconditions for development of Mallory hyaline. It is possible that these features suggest a susceptibility for the development of ICC but not early disease.
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The sera of 20 atopic patients, 10 with hypersensitivity symptoms upon ingestion of milk and 10 without such symptoms, were tested by a radioimmunoassay for the detection of IgE antibodies to whole bovine milk, betalactoglobulin (BL), enzymatic digests of BL and fractions thereof. While only 4/10 patients had IgE antibodies to undigested BL all 10 patients had IgE antibodies to BL digests. All controls gave negative results. These findings suggest that enzymatic digestion of BL may yield antigenic fractions which elicit IgE antibodies and that these antibodies would be missed if the undigested food protein were to be used solely in testing.
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