We studied three groups of patients without previous renal impairment, undergoing elective coronary artery bypass surgery. Group H (n = 7) underwent open heart surgery using moderate hypothermia (28 degrees C); Groups N and M (n = 8, each) were managed at normothermia. The extracorporeal circuit was primed with Hartmann's solution 2.5 L with the addition of mannitol 0.5 g/kg in Group M. Serum concentrations of sodium and creatinine, and the urinary concentrations of microalbumin and N-acetyl-beta-D-glucosaminidase (NAG) were measured in each patient at six different time intervals: T0, 6 h prior to surgery; T1, between sternotomy and 45 min into cardiopulmonary bypass (CPB); T2, in the interval from 45 min into, to prior to weaning off CPB; T3, from coming off CPB to skin closure; T4, in the first 6 h in the intensive care unit; and T5, at 6 days postoperatively. Creatinine clearance (CCR) and fractional sodium excretion (FENA) were calculated at each time point. Urine output during CPB at Interval T2 was significantly higher in Group H compared to Group N (P = 0.03) but not Group M. We found no significant differences in CCR, FENA, microalbuminuria, and urinary NAG among the three groups at any time. However, there were overall significant changes in measured variables over time compared to baseline. We conclude that CPB is associated with a significant alteration in renal function as shown by increased FENA, microalbuminuria, and urinary NAG. The use of hypothermic or normothermic CPB and the use of prophylactic mannitol did not produce any significant modification of these changes.

A model of self-regulation that explains the health behavior of type II diabetic patients was tested by examining the use of symptoms as indicators of perceived blood glucose levels in 38 outpatients. Results of the study supported the self-regulation model by demonstrating that patients use symptoms to monitor blood glucose levels and to guide diabetes-related actions. Implications of the model for planning interventions with type II diabetes are discussed.

Several families of peptides composed of alternating L-alanine (Ala) and alpha-aminoisobutyric acid (Aib) residues with an appended N,N-dimethylanilino and/or 2-naphthalenyl group exist in MeOH and CDCl(3) as alpha-helices. Steady state and time-resolved fluorescence measurements show that the distance and dihedral angle between the appended donor and acceptor and the alignment of the vectors for intramolecular charge transfer interaction (from donor to acceptor) with or against that of the helical dipole moment significantly influence the efficiency of photoinduced electronic coupling and, hence, of intramolecular fluorescence quenching.

Heterozygous loss of X-linked genes like CASK and MeCP2 (Rett syndrome) causes neurodevelopmental disorders (NDD) in girls, while in boys such loss leads to profound encephalopathy. The cellular basis for these disorders remains unknown. CASK is presumed to work through the Tbr1-reelin pathway in neuronal migration during brain development. Here we report our clinical and histopathological analysis of a deceased 2-month-old boy with a CASK-null mutation. We demonstrate that although smaller in size, the CASK-null human brain exhibits normal lamination without defective neuronal differentiation, migration, or axonal guidance, excluding the role of reelin in CASK-linked pathology. The disproportionately hypoplastic cerebellum in humans without CASK expression is associated with cerebellar astrogliosis, a marker for neuronal loss. Cerebellum-specific deletion in mouse confirms a post-developmental degeneration of cerebellar granular neurons that results in a small cerebellum. Mechanistically, cerebellar hypoplasia in CASK mutation thus results from neurodegeneration rather that developmental defects. Zygosity-pathology correlation suggests that NDDs like CASK mutation and Rett syndrome are pathologically neurodegenerative; however, random X-chromosome inactivation in the typical heterozygous mutant girls results in 50% of cells expressing the functional gene, resulting in a non-progressive pathology, whereas complete loss of the only allele in boys leads to unconstrained degeneration and encephalopathy.