Kinetic and dynamic interactions of oral viqualine and ethanol in man

We have studied the interaction of viqualine, a 5-hydroxytryptamine (5-HT) uptake inhibitor, with ethanol in 16 healthy men aged 20 to 34 years. The subjects were randomly assigned to receive ethanol dosed to maintain blood alcohol concentrations of 17-22 mmol.l-1 (n = 8) or orange juice (n = 8) on each of two test days one week apart and preceded, in random order, by 3 days of viqualine 75 mg bd or placebo. Ethanol had no effect on steady-state viqualine concentrations or the inhibition of 5-HT uptake. Viqualine did not affect acetaldehyde concentrations or cause an aversive alcohol-sensitizing reaction. The deleterious effects of ethanol on word recall, manual tracking, body sway, and self-ratings of intoxication, sedation, and performance were not modified by the presence of viqualine. Within each beverage group performances and self-ratings on viqualine and placebo days were not different. The first dose of viqualine was associated with transient nausea. Viqualine and ethanol do not interact kinetically or dynamically on the variables examined in this study.     

THE EPIDEMIOLOGY OF GERMINAL MATRIX HEMORRHAGE DURING THE FIRST HALF-DAY OF LIFE

The personal and maternal characteristics of 27 babies with early-onset germinal matrix hemorrhage (EGMH) were compared with those of 280 babies with normal cranial ultrasonograms, studied in a separate clinical trial. None of the mothers of the babies with EGMH had high blood pressure or pre-eclampsia during pregnancy. Gestational age less than 30 weeks and initial pH less than 7.2 indicated increased risks of EGMH, and maternal receipt of steroids indicated reduced risk of EGMH. Thus prenatal and immediately perinatal factors appear to convey much of the information about the risk of EGMH.     

A conceptual explanation of risk-reduction behavior and intervention development

This study used a new conceptual model of health behavior to examine a specific risk-reduction response. Known to be at risk for fetal abnormalities because of maternal age, 203 women were examined for their acceptance or rejection of an amniocentesis test on the basis of individual characteristics and external significant factors. The multivariate approach to analysis offered a fuller explanation for nonuse of prenatal diagnosis than was previously available. In addition to specific client factors, environmental factors such as financial support for the procedure, multiple information sources, social support, and aspects of the client-provider interaction were determined to be important in explaining client acceptance or rejection of the test. More importantly, the study demonstrated the advantages of using a conceptual model to direct the development of interventions.     

Treatment of antibody-mediated accelerated rejection using plasmapheresis

Accelerated antibody-mediated rejection is believed to be due to an anamnestic response of an allograft recipient to donor antigens. Few reports have demonstrated successful reversal of this type of rejection, and no consensus exists for either diagnosis or treatment. Accelerated antibody-mediated rejection was suspected on the basis of clinical findings and confirmed by cytotoxic and flow crossmatches, and leukocyte antibody screens. Serial crossmatches and antibody screens were performed through post-transplant day 112. Plasmapheresis was performed on post-transplant days 1, 2, 4, 6, 12, 14, 20, and 28. The duration of treatment was determined by the cytotoxic crossmatch results. We present a case of successfully treated accelerated antibody-mediated rejection using plasmapheresis and aggressive immunosuppression. Serial crossmatch and leukocyte antibody screen results are presented that confirm the production of anti-donor antibody and demonstrate the effectiveness of the treatment protocol in eliminating detectable levels of the anti-donor antibody. At 6 months post-transplant, the patient has a serum creatinine of 1.1 and has not had any additional rejection episodes or infectious complications. The protocol suggested in this paper allows for rapid diagnosis, institution of treatment, and monitoring the efficacy of treatment, providing the basis for follow-up clinical trials.     

Designing a leadership development program for nurse managers: an evidence-driven approach

The authors describe an evidence-driven approach used in designing a leadership development program targeted for nurses in middle management positions in an academically affiliated integrated healthcare system. A qualitative study was conducted to investigate leadership development needs and experiences of nurse managers across the health system. Study findings were used to inform educational programs and organizational initiatives responsive to needs of both novice and expert nurse managers across diverse clinical settings.     

LKM-1 autoantibodies recognize a short linear sequence in P450IID6, a cytochrome P-450 monooxygenase.

LKM-1 autoantibodies, which are associated with autoimmune chronic active hepatitis, recognize P450IID6, a cytochrome P-450 monooxygenase. The reactivities of 26 LKM-1 antisera were tested with a panel of deletion mutants of P450IID6 expressed in Escherichia coli. 22 sera recognize a 33-amino acid segment of P450IID6, and 11 of these recognize a shorter segment, DPAQPPRD. PAQPPR is also found in IE175 of herpes simplex virus type 1 (HSV-1). Antibodies for HSV-1 proteins were detected by ELISA in 17 of 20 LKM-1 sera tested. An immobilized, synthetic peptide, DPAQPPRDC, was used to purify LKM-1 antibodies. Affinity purified LKM-1 autoantibodies react on immunoblots with a protein in BHK cells after infection with HSV-1. 11 of 24 LKM-1 sera, including 3 that recognize DPAQPPRD, also exhibit antibodies to the hepatitis C virus (HCV) protein, C100-3. Affinity purified LKM-1 antibodies did not recognize C100-3. However, partial sequence identity was evident between portions of the immunopositive 33-amino acid segment of P450IID6 and other portions of the putative HCV polyprotein. Immune cross-recognition of P450IID6 and HCV or HSV-1 proteins may contribute to the occurrence of LKM-1 autoantibodies.