Biomedical subjects

S Barve

Publications and source records attributed to S Barve.

21 records · Page 2Linked to original sources

PubMed1996

Neurologic sequelae in high risk infants--a three year follow up.

OBJECTIVE: To determine the neurologic sequelae in high risk infants. DESIGN: A three year longitudinal follow up. SETTING: Inborn and outborn infants discharged from the Neonatal Special Care Unit (NSCU) of a referral hospital. METHODS: High risk infants were identified for follow up using predetermined risk criteria. A detailed neurodevelopmental examination was done 3 monthly in the first year and 6 monthly subsequently. The Amiel-Tison Method, Bayley Scales of Infant Development and Raval's Scale for social maturity were used. EEG was done in children with seizures. Hearing and ophthalmic assessments were done at 6 months. RESULTS: Three hundred and thirty six high risk infants and 70 normal control infants came for regular follow up. Out of these, 16 (4.8%) had cerebral palsy and 11 had associated mental retardation. Six other children had mental retardation without motor problems. None of the children in the control group had any neurological problems. Sensorineural hearing loss was present in 5 (1.5%) children while 1 subject had corfical blindness. Three children with cerebral palsy had infantile myoclonus, nine had generalized seizures and one child had a focal seizure. The incidence of seizure disorders was 3.9%. CONCLUSIONS: The incidence of major handicap in our study was low. Many of the risk factors which caused adverse outcome, could have been prevented by good antenatal and perinatal care.

Child Development↗

PubMed1996

T10B9 (MEDI-500) mediated immunosuppression: studies on the mechanism of action.

The murine IgM anti-human CD3/TCR mAb T10B9 is an effective agent for the reversal of acute cellular renal allograft rejection which offers several advantages over conventional OKT3 therapy. These include reduced morbidity and a more rapid decrease in serum creatinine levels. In the studies presented here comparing T10B9 and OKT3, soluble T10B9 is shown to be a nonactivating anti-T cell mAb. Evidence for its lack of activating potential includes in vitro failure to stimulate PBMC proliferation either alone or in the presence of nonmitogenic doses of phorbol ester, failure to induce the expression of early and late activation antigens and failure to induce IFN-gamma, TNF-alpha, IL-6 or IL-2 release. Analysis of acute renal allograft rejection patient plasma cytokine levels 2 h after the first dose support the hypothesis that T10B9 has reduced immunoactivation activity in vivo. Both TNF alpha and IFN gamma patient plasma levels are significantly reduced in T10B9 as compared to OKT3 therapy. However, T10B9 is capable of cellular signaling as demonstrated by its ability to induce apoptosis and IL-2 release in the human T cell line Sup-T13. Thus T10B9 retains the potent immunosuppressive activity of OKT3 with reduced immunoactivation.

Antibodies, Monoclonal↗

PubMedDate not supplied

Acetaminophen hepatotoxicity: An update.

Acetaminophen is a widely used nonprescription analgesic and antipyretic agent. It is also a dose-related hepatotoxin that can cause fulminant liver failure when taken in massive overdoses or, much less commonly, at therapeutic doses in susceptible individuals. Persons who regularly consume alcohol or persons who have been fasting may be more susceptible to this hepatotoxicity. This liver injury is due not to the drug itself but to the formation of the toxic metabolite N-acetyl-p-benzoquinine imine generated through the cytochrome P-450 drug-metabolizing system. Normally, hepatic stores of glutathione combine with the toxic metabolite and prevent liver cell injury. When glutathione stores are depleted by overproduction of this metabolite, however, the reactive metabolite binds to liver cell proteins and causes hepatic necrosis. P-450 2E1 is induced by alcohol consumption and possibly starvation, and glutathione depletion can occur due to the inadequate nutrition occurring in chronic alcohol use or in starvation. Recent studies have shown that activated Kupffer cells and their secreted toxic agents such as cytokines may also play a role in this liver injury. This liver injury is characterized by extremely high levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (> 1000), and bad prognostic signs include severe prolongation of the prothrombin time, renal dysfunction, and, most importantly, acidosis. N-acetylcysteine is a highly effective antidote when given early (within 15 hours) of overdose. Some patients may develop such fulminant liver injury that they require transplantation. Unfortunately, many such patients have a course so rapid that a donor liver may not become available in time. Thus, both the medical community and the general public require a heightened understanding of this clinical problem in order to initiate prevention measures and to implement early therapeutic measures if an overdose situation occurs.

Acetaminophen↗