No abstract

No abstract

In oxygenic photosynthesis, PSII carries out the oxidation of water and reduction of plastoquinone. The product of water oxidation is molecular oxygen. The water splitting complex is located on the lumenal side of the PSII reaction center and contains manganese, calcium, and chloride. Four sequential photooxidation reactions are required to generate oxygen from water; the five sequentially oxidized forms of the water splitting complex are known as the Sn states, where n refers to the number of oxidizing equivalents stored. Calcium plays a role in water oxidation; removal of calcium is associated with an inhibition of the S state cycle. Although calcium can be replaced by other cations in vitro, only strontium maintains activity, and the steady-state rate of oxygen evolution is decreased in strontium-reconstituted PSII. In this article, we study the role of calcium in PSII that is limited in water content. We report that strontium substitution or 18OH2 exchange causes conformational changes in the calcium ligation shell. The conformational change is detected because of a perturbation to calcium ligation during the S1 to S2 and S2 to S3 transition under water-limited conditions.

One hundred eighty-eight patients with acute myocardial infarction were studied prospectively from August 1980 to September 1982. One hundred thirty-six of these patients were entered into a intracoronary streptokinase study after informed consent was obtained. The remaining 52 patients, who either met exclusion criteria for the study or refused to participate, served as a control group and were treated as those in the study group except that they did not undergo emergency cardiac catheterization. Left ventricular function was determined in both groups by gated radionuclide ejection fraction (EF) on admission to the hospital, at discharge, and 6 months after discharge. With successful reperfusion up to 18 hr after onset of chest pain, mean left ventricular function in the study group improved (EF 39 + 13% on admission and 46 + 12% at discharge; p < .001). Mean EF in control patients and those not achieving reperfusion did not change from admission to discharge. Mean EF at 6 month follow-up was not significantly different than at discharge in the study group or the control group. Total cardiac mortality in the control group was 19% compared with 10% in the study group (p = .06, NS). When patients admitted in pulmonary edema or shock (Killip class III or IV) were excluded from both groups, total cardiac mortality in the study group was significantly lower (4%) compared with in the control group (12.5%, p < .05). The administration of intracoronary streptokinase during evolving myocardial infarction up to 18 hr after onset of chest pain may result in decreased mortality and sustained improvement in left ventricular function. Circulation 68, No. 1, 131-138, 1983. STANDARD CURRENT THERAPY for acute myocardial infarction entails prevention or treatment of complications secondary to evolving myocardial necrosis. Mortality during the first 30 days after acute myocardial infarction has been reported to be between 16% and 30% in large series and no definite decrease in this rate was noted between 1960 and 1975.14 Although there is no universally accepted method for reducing myocardial damage, emergency aortocoronary bypass surgery has been reported to decrease mortalityl'6 in certain patients. Intracoronary streptokinase From the University of Texas Medical School at Houston.

No abstract