The dynamics of triplet energy transfer between the primary donor and the carotenoid were measured on several photosynthetic bacterial reaction center preparations from Rhodobacter sphaeroides: (a) wild-type strain 2.4.1, (b) strain R-26.1, (c) strain R-26.1 exchanged with 13(2)-hydroxy-[Zn]-bacteriochlorophyll at the accessory bacteriochlorophyll (BChl) sites and reconstituted with spheroidene and (d) strain R-26.1 exchanged with [3-vinyl]-13(2)-hydroxy-bacteriochlorophyll at the accessory BChl sites and reconstituted with spheroidene. The rise and decay times of the primary donor and carotenoid triplet-triplet absorption signals were monitored in the visible wavelength region between 538 and 555 nm as a function of temperature from 4 to 300 K. For the samples containing carotenoids, all of the decay times correspond well to the previously observed times for spheroidene (5 +/- 2 microseconds). The rise times of the carotenoid triplets were found in all cases to be biexponential and comprised of a strongly temperature-dependent component and a temperature-independent component. From a comparison of the behavior of the carotenoid-containing samples with that from the reaction center of the carotenoidless mutant Rb. sphaeroides R-26.1, the temperature-independent component has been assigned to the buildup of the primary donor triplet state resulting from charge recombination in the reaction center. Arrhenius plots of the buildup of the carotenoid triplet states were used to determine the activation energies for triplet energy transfer from the primary donor to the carotenoid. A model for the process of triplet energy transfer that is consistent with the data suggests that the activation barrier is strongly dependent on the triplet state energy of the accessory BChl pigment, BChlB.
A 27-year-old woman, G2P1A0, at 35 weeks of gestation with an unremarkable pregnancy, presented with severe acute right flank pain and nausea without any precipitating factors. She denied fever, vomiting, hematuria, urinary symptoms, or lower extremity edema. There was no history of trauma, anticoagulant therapy, or hypertension during this pregnancy. Her previous gestation was complicated by preeclampsia and peripartum cardiomyopathy, although a recent echocardiogram performed earlier during this pregnancy was normal. Examination on admission revealed a patient in severe pain, afebrile, blood pressure of 126/50 mm Hg, and heart rate of 105 beats per minute. Abdominal examination demonstrated marked tenderness in the right flank and across the right costovertebral angle with no guarding or rebound. The cervix was closed and thick. The remainder of the examination was unremarkable. A fetal monitor tracing was unremarkable and an obstetric ultrasonogram showed normal fetal anatomy and growth with no obvious cause for her symptoms. Laboratory tests revealed a hemoglobin of 9.5 g/dL, white blood cell count 10.5ϫ10 9 /L, platelets 200ϫ10 9 /L, normal electrolytes, renal function, and urinalysis. Urine culture showed no growth. The 24-hour proteinuria was 175 mg. Coagulation tests, hepatic function, lipase, peripheral blood smear, and lactic dehydrogenase were normal. An abdominal magnetic resonance imaging (MRI) scan was performed. Coronal and axial T1-and T2-weighted sequences showed a heterogeneous 3.6ϫ2.0-cm mass within the right adrenal gland demonstrating a fluid-fluid level. The T2-weighted sequences disclosed a hyperintense signal in the nondependent portion and T2-isointense material in the dependent portion with no underlying lesions identified within the glands (Figs. 1 and 2). These signal characteristics were consistent with an evolving acute right adrenal gland hemorrhage. Comprehensive tests evaluating inherited and acquired causes of thrombophilia were negative. The flank pain resolved with a low dose of morphine. With conservative treatment, she remained well, with stable hemoglobin, and was kept in the hospital for closer monitoring. However, 2 weeks later she developed acute onset of left flank pain. Another abdominal MRI scan confirmed an acute hemorrhage of the left adrenal gland with a persistent hematoma within the right gland (Fig. 3). The adrenal function was assessed. The morning cortisol level was 13.9 micrograms/dL. A Cortrosyn stimulation test showed minimal increment of cortisol production from a baseline of 10.9 micrograms/dL to 11.4 micrograms/dL 1 hour after 250 micrograms of intravenous Cortrosyn suggesting primary adrenal insufficiency. Hydrocortisone 100 mg three times daily was started. With supportive management, she remained stable and underwent an uncomplicated cesarean delivery a few days later at 38 weeks of gestation. She delivered a healthy male neonate, and her postoperative course was uneventful; she was discharged on the 10th postoperative day with 20 mg prednisone daily a...
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