Comparison of short-term outcomes following coronary artery stenting in men versus women.

This study sought to determine whether women have more adverse in-hospital outcomes after percutaneous transluminal coronary angioplasty (PTCA) and stenting compared with men. There is still controversy regarding whether female gender is an independent predictor of mortality after PTCA. No study has examined gender differences in outcomes following the dissemination of stenting. Data were obtained from the Nationwide Inpatient Sample. In 1997, there were 118,548 angioplasties (36% occurred in women and 59% involved placement of stents). Outcomes included same-admission mortality and coronary artery bypass grafting (CABG). Analyses were performed separately for patients with and without acute myocardial infarction (AMI). In 1997, women had a roughly twofold higher mortality than men in every comparison group, including conventional PTCA alone and stents. Mortality rates after stenting were 4.0% for women and 2.0% for men with AMI (p <0.0001), and 1.1% and 0.5%, respectively, for patients without AMI (p <0.0001). The adjusted odds ratios were 1.47 (95% confidence interval 1.23 to 1.75), and 1.65 (95% confidence interval 1.33 to 2.04), respectively. Similarly, following stenting, women had significantly higher CABG rates than men in both the AMI (1.6% vs 1.2%, p = 0.025) and no AMI groups (1.5% vs 1.0%, p <0.0001). After multivariate adjustment, the results retained significance in the no AMI setting, whereas there was a trend toward significance in the AMI group. This study demonstrates that, despite improved overall outcomes in patients who received stents, women who underwent stenting had higher rates of same-admission mortality and CABG compared with men. Furthermore, it confirms that female gender is an independent predictor of mortality after conventional PTCA.

Eruption disturbances of mandibular permanent incisors.

In this study, we analyzed 7 eruption disturbance cases of mandibular permanent incisors (5 males and 2 females), aged 5y9m to 10y4m. The etiology was divided into 3 categories: traumatic injuries (3 cases), odontomas (2 cases), supernumerary teeth (2 cases). The procedures such as removal of cause (4 cases), surgical exposure (5 cases) and traction (1 case) were done.

Negative regulation of gene expression from the HTLV type II long terminal repeat by Rex: functional and structural dissociation from positive posttranscriptional regulation.

Regulation of human T cell leukemia virus type II (HTLV-II) gene expression by Rex is mediated by cis-acting elements in the 5' viral long terminal repeat (LTR). Rex acts posttranscriptionally to enhance cytoplasmic accumulation of incompletely spliced viral mRNAs encoding structural proteins. We report a distinct negative regulatory function mediated by Rex affecting expression from the viral 5' LTR. Using both LTR-driven CAT reporters and a full-length HTLV-II proviral construct, we demonstrate that Rex decreases total cellular levels of LTR-containing mRNA in a dose-dependent manner. Negative regulation is an independent function as demonstrated by structural and functional dissociation from Rex positive posttranscriptional regulation. This negative regulatory action was dependent on nuclear localization sequences, but did not require the previously defined Rex-responsive element (RxRE). Negative regulation was observed in T cell lines but not in B cell lines, suggesting the involvement of cell type-specific factors distinct from those involved in posttranscriptional regulation. An internal deletion mutant of Rex removing aa 38-80 retained the ability to repress, but did not posttranscriptionally increase expression, while negative regulation requires a previously uncharacterized carboxy-terminal region (aa 154-170). These findings suggest that Rex may serve two simultaneous functions: to decrease overall levels of transcribed viral mRNA, and to facilitate nuclear to cytoplasmic export of mRNAs encoding structural proteins. The negative regulatory function of Rex may play a role in viral latency.

Sustained cytokine production and immunophenotypic changes in human neuroblastoma cell lines transduced with a human gamma interferon vector.

The majority of human neuroblastomas express low to undetectable levels of major histocompatibility complex (MHC) class I and II antigens (MHC-I and -II). We studied the effects of gamma interferon (gamma-IFN) transduction on expression of these antigens in six human neuroblastoma cell lines with and without genomic amplification of the N-myc oncogene. All six were stably transduced with an MoMLV-based gamma-IFN retroviral vector (DAh gamma-IFN). G418-resistant cells were assayed for MHC-I, MHC-II, B7-1, and neuroblastoma-associated antigen expression, as well as for gamma-IFN levels in cell culture supernatants. Sustained gamma-IFN production, 2 to > 1000 units/10(6) cells/d, was attained for five of six transduced cell lines and persisted for up to 9 months. This resulted in marked upregulation of MHC-I and MHC-II expression in LA-N-1, LA-N-6, and CHLA-127 cells and moderate upregulation in SK-N-Fi and SK-N-AS cells. One cell line (LA-N-1) had marked induction of MHC-I and MHC-II despite marginal levels of gamma-IFN production. Expression of CD28 ligand B7-1 (as determined by BB1 antibody) remained unchanged in all gamma-IFN-transduced cell lines tested. Expression of several neuroblastoma-associated antigens (NKH1A, 126-4, HSAN 1.2, HNK, 459, and 390) was upregulated in some of the gamma-IFN-transduced cell lines. These results demonstrate that preparation of gamma-IFN expressing neuroblastoma cells for immunotherapeutic purposes is feasible and that gamma-IFN transduction results in phenotypic changes that may improve immunogenicity of human neuroblastoma cells.