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Biomedical subjects

D Banker

Publications and source records attributed to D Banker.

3 recordsLinked to original sources

Emergent balloon mitral valvotomy in patients presenting with cardiac arrest, cardiogenic shock or refractory pulmonary edema.

OBJECTIVES: The present study was performed to determine the outcome of emergent balloon mitral valvotomy (BMV) in patients with cardiac arrest, pulmonary edema or cardiogenic shock. BACKGROUND: In India, many patients with mitral stenosis present in critical condition. They have high mortality despite surgical relief. The role of BMV in such patients is ill-defined. METHODS: Of 558 patients undergoing BMV between January 1993 and December 1994, 40 presented with cardiogenic shock, cardiac arrest or pulmonary edema refractory to medical treatment and underwent emergent BMV (group I). Elective BMV was performed in the remaining 518 patients (group II). RESULTS: Age ([mean +/- SD] 40 +/- 13 vs. 31 +/- 9 years, p < 0.05), incidence of atrial fibrillation (35% vs. 11%, p < 0.05), pulmonary artery systolic pressure (PAsP) (64 +/- 14 vs. 51 +/- 12 mm Hg, p < 0.001) and mitral valve (MV) score (7.4 +/- 1.2 vs. 6.4 +/- 1, p < 0.001) were higher and MV area lower (0.74 +/- 0.17 vs. 0.86 +/- 0.14 cm2, p < 0.001) in group I patients. After emergent BMV in group I, mitral regurgitation occurred in 15%, and the mortality rate was 35%. Stepwise logistic regression analysis identified MV score > or =8 (p = 0.008), PAsP > or =65 mm Hg (p = 0.023) and cardiac output < or =3.151 liters/min (p = 0.001) as significant predictors of a fatal outcome. Follow-up of 1 to 16 months (median 8) was available in 20 of 26 survivors in group I, of whom 15 were asymptomatic. The gain in MV area and the decrease in transmitral gradient and PAsP obtained immediately after BMV persisted during the follow-up period. CONCLUSIONS: Emergent BMV is feasible in critically ill patients. In-hospital survivors have excellent clinical and hemodynamic status at intermediate follow-up.

Catheterization↗

HeLa cell mutants resistant to epidermal growth factor ricin A-chain conjugate.

Epidermal growth factor (EGF) was linked to the toxic A chain of ricin toxin (RTA) to produce an EGF-receptor-specific cytotoxic agent, EGF-RTA. Three EGF-RTA-resistant mutants of the human HeLa cell line were selected. These mutant cell lines are 10-fold to more than 100-fold more resistant to EGF-RTA when compared to HeLa cells. The EGF-RTA-resistant mutants have at least as many EGF receptors as parent cells; the basis for the EGF-RTA-resistant phenotype must be distal to EGF binding. The EGF-RTA-resistant cells are not cross-ressitant to ricin or to diphtheria toxin; their mutant phenotype appears to be EGF specific. The EGF-RTA-resistant mutants are able to internalize and degrade EGF. However, the mutants have altered EGF receptor down-regulation and phorbol 12-tetradecanoate 13-acetate modulation properties. EGF-RTA/ammonium chloride and EGF-RTA/adenovirus co-treatment data suggest that the mutant defect(s) which confers EGF-RTA resistance is either in the endosome or at a step(s) in the intracellular EGF processing pathway between the endosome and the lysosome.

Adenoviridae↗