HIV, hepatitis C virus and risk of new-onset left ventricular dysfunction in women.

Background: HIV and HCV have each been linked with cardiac dysfunction. Studies of HIV have often lacked appropriate controls and primarily involved men, whereas data for HCV are sparse.

Methods: We performed repeat echocardiography over a median interval of 12 years in participants from the Women's Interagency HIV Study in order to evaluate the relationships of HIV and HCV with incident left ventricular (LV) dysfunction (systolic or diastolic).

A Phase 3 Trial of 2 Years of Androgen Suppression and Radiation Therapy With or Without Adjuvant Chemotherapy for High-Risk Prostate Cancer: Final Results of Radiation Therapy Oncology Group Phase 3 Randomized Trial NRG Oncology RTOG 9902.

Purpose: Long-term (LT) androgen suppression (AS) with radiation therapy (RT) is a standard treatment of high-risk, localized prostate cancer (PCa). Radiation Therapy Oncology Group 9902 was a randomized trial testing the hypothesis that adjuvant combination chemotherapy (CT) with paclitaxel, estramustine, and oral etoposide plus LT AS plus RT would improve overall survival (OS).

Methods And Materials: Patients with high-risk PCa (prostate-specific antigen 20-100 ng/mL and Gleason score [GS] ≥ 7 or clinical stage ≥ T2 and GS ≥ 8) were randomized to RT and AS (AS + RT) alone or with adjuvant CT (AS + RT + CT).

JAK/STAT signaling is associated with cardiac dysfunction during ischemia and reperfusion.

Background: Activation of the heart renin-angiotensin system (RAS) under pathophysiological conditions has been correlated with the development of ischemic injury. The binding of angiotensin II to its receptors triggers induction of several, perhaps multifunctional, intracellular signaling pathways, notable among them the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. In this study, we investigated whether the JAK/STAT signaling is involved in the ischemia/reperfusion injury in adult rat myocardium.

Community, service, and policy strategies to improve health care access in the changing urban environment.

Urban communities continue to face formidable historic challenges to improving public health. However, reinvestment initiatives, changing demographics, and growth in urban areas are creating changes that offer new opportunities for improving health while requiring that health systems be adapted to residents' health needs. This commentary suggests that health care improvement in metropolitan areas will require setting local, state, and national agendas around 3 priorities.

Transcobalamin II and the membrane receptor for the transcobalamin II-cobalamin complex.

Transcobalamin II is a plasma protein that binds vitamin B12 (cobalamin) as it is absorbed in the terminal ileum and distributes it to tissues. The circulating transcobalamin II-cobalamin complex binds to receptors on the plasma membrane of tissue cells and is then internalized by receptor-mediated endocytosis. A number of genetic abnormalities are characterized either by a failure to express transcobalamin II or by synthesis of an abnormal protein.

Iron protoporphyrin IX (hemin) but not tin or zinc protoporphyrin IX can stimulate gene expression in K562 cells from enhancer elements containing binding sites for NF-E2.

Many genes whose transcription is erythroid-specific contain enhancer or promoter elements that bind the transcription factor NF-E2. Hemin induction increases the expression of globin genes in the human erythroleukemia cell line K562, and increases the expression of reporters gene regulated by an enhancer elements containing binding sites for NF-E2. The failure of metalloporphyrins other than hemin to stimulate the transient expression of a CAT reporter gene linked to an enhancer element containing a binding site for NF-E2 was correlated with their failure to induce benzidine-positive K562 cells and increase the steady-state level of gamma-globin mRNA.

Familial subungual keratoacanthoma in association with ectodermal dysplasia.

Described is the first report of familial SUKA, occurring in two of three sisters with ectodermal dysplasia, a rare, hereditary disorder involving ectodermally derived organ systems. Although rare, SUKA should be considered when assessing rapidly growing nailbed lesions. Differentiation from subungual squamous cell carcinoma is essential.

Ethanol-induced alterations in electroencephalographic activity in adult males.

The present investigation examined the effects of placebo (P), low-dose (LD), and high-dose (HD) ethanol on electroencephalographic (EEG) activity in 21 healthy, adult males (X = 22.7 years). Only one condition (P, LD, or HD) was presented per day and the condition order was randomized.

Assessment of quality of life before and after surgery for severe obesity.

Quality of life is poor in obese people because of poor physical health and mental well-being and impaired psychosocial functioning. Obese people perceive discrimination and prejudice against them as their heaviest burden. Reports of absence of psychopathology in obese people reflect adaptation to chronic disease or failure of assessment instruments to detect disturbances.

Endothelial cells are required for inhibition of contractile responses induced by reduction in extracellular magnesium and sodium ions in rat aortic smooth muscle [corrected].

The possible importance of facilitation of sodium-calcium (Na(+)-Ca2+) exchange by removal of extracellular magnesium ions ([Mg2+]o) in expression of endothelium-dependent relaxation was investigated in aortic rings isolated from female rats. Simultaneous [Mg2+]o withdrawal (0 mM Mg2+) and reduction in extracellular Na+ (Total [Na+]o = 84 mM), by replacement of NaCl with isosmolar amounts of sucrose in normal Krebs-Ringer bicarbonate (NKRB), induced significant increases of basal tone of denuded rat aortic rings, but not in tissues with intact endothelium. These vascular effects were not affected by indomethacin, phentolamine or atropine in any of the tissues tested.

A single point mutation of Ala-25 to Asp in the 14,000-Mr envelope protein of vaccinia virus induces a size change that leads to the small plaque size phenotype of the virus.

The molecular defect responsible for a structural and functional abnormality of the 14,000-molecular-weight (14K) envelope protein of vaccinia virus has been identified. Through DNA sequence analysis of the entire 14K gene from wild-type vaccinia virus and three vaccinia virus mutants, a single base change of C to A was found that resulted in the substitution of Asp for Ala-25. This mutation is responsible for protein size abnormality, as documented by cell-free translation in a rabbit reticulocyte lysate of in vitro mRNA transcripts.