Physician-Assisted Suicide: State Legislation Teetering at the Pinnacle of a Slippery Slope

Physician-assisted suicide has become the subject of a hotly contested legal and political debate, both in the United States and abroad. In 1997, the United States Supreme Court rendered two decisions concerning physician-assisted suicide, and two states recently enacted legislation on this issue: Oregon in 1997 and Virginia in 1998. Nevertheless, the legality of physician-assisted suicide remains unclear as doctors, pharmacists, legal commentators, and a growing segment of the general population continue to argue over the line between letting die and killing. This Note analyzes both the constitutional and political aspects of the right-to-die debate, focusing primarily on the political arguments and reasons why the assisted suicide issue should be resolved in the political arena

Pressure ulcers among nursing home residents: United States, 2004

"Data from the National Nursing Home Survey, 2004. In 2004, about 159,000 current U.S. nursing home residents (11%) had pressure ulcers. Stage 2 pressure ulcers were the most common. Residents aged 64 years and under were more likely than older residents to have pressure ulcers. Residents of nursing homes for a year or less were more likely to have pressure ulcers than those with longer stays. One in five nursing home residents with a recent weight loss had pressure ulcers. Thirty-five percent of nursing home residents with stage 2 or higher (more severe) pressure ulcers received special wound care services in 2004. Pressure ulcers, also known as bed sores, pressure sores, or decubitus ulcers, are wounds caused by unrelieved pressure on the skin. They usually develop over bony prominences, such as the elbow, heel, hip, shoulder, back, and back of the head. Pressure ulcers are serious medical conditions and one of the important measures of the quality of clinical care in nursing homes. From about 2% to 28% of nursing home residents have pressure ulcers. The most common system for staging pressure ulcers classifies them based on the depth of soft tissue damage, ranging from the least severe to the most severe. There is persistent redness of skin in stage 1; a loss of partial thickness of skin appearing as an abrasion, blister, or shallow crater in stage 2; a loss of full thickness of skin, presented as a deep crater in stage 3; and a loss of full thickness of skin exposing muscle or bone in stage 4. Clinical practice guidelines for pressure ulcers have been developed and provide specific treatment recommendations for stage 2 or higher pressure ulcers, including proper wound care. This Data Brief presents the most recent national estimates of pressure ulcer prevalence, resident characteristics associated with pressure ulcers, and the use of wound care services in U.S. nursing homes. All material appearing in this report is in the public domain and may be reproduced or copied without permission; citation as to source, however, is appreciated."Eunice Park-Lee and Christine Caffrey.Caption title."February 2009."Includes bibliographical references (p. 7)

USP15 regulates dynamic protein-protein interactions of the spliceosome through deubiquitination of PRP31.

Post-translational modifications contribute to the spliceosome dynamics by facilitating the physical rearrangements of the spliceosome. Here, we report USP15, a deubiquitinating enzyme, as a regulator of protein-protein interactions for the spliceosome dynamics. We show that PRP31, a component of U4 snRNP, is modified with K63-linked ubiquitin chains by the PRP19 complex and deubiquitinated by USP15 and its substrate targeting factor SART3. USP15SART3 makes a complex with USP4 and this ternary complex serves as a platform to deubiquitinate PRP31 and PRP3. The ubiquitination and deubiquitination status of PRP31 regulates its interaction with the U5 snRNP component PRP8, which is required for the efficient splicing of chromosome segregation related genes, probably by stabilizing the U4/U6.U5 tri-snRNP complex. Collectively, our data suggest that USP15 plays a key role in the regulation of dynamic protein-protein interactions of the spliceosome

The effect of a couples intervention to increase breast cancer screening among korean americans.

Purpose/objectivesTo assess the efficacy of Korean Immigrants and Mammography-Culture-Specific Health Intervention (KIM-CHI), an educational program for Korean American (KA) couples designed to improve mammography uptake among KA women.DesignA two-group cluster randomized, longitudinal, controlled design.Setting50 KA religious organizations in the Chicago area.Sample428 married KA women 40 years of age or older who had not had a mammogram in the past year. The women and their husbands were recruited from 50 KA religious organizations.MethodsCouples were randomly assigned to intervention or attention control groups. Those in the KIM-CHI program (n = 211 couples) were compared to an attention control group (n = 217 couples) at baseline, as well as at 6 and 15 months postintervention on mammogram uptake.Main research variablesSociodemographic variables and mammography uptake were measured. Level of acculturation was measured using the Suinn-Lew Asian Self-Identity Acculturation Scale. Researchers asked questions about healthcare resources and use, health insurance status, usual source of care, physical examinations in the past two years, family history of breast cancer, and history of mammography.FindingsThe KIM-CHI group showed statistically significant increases in mammography uptake compared to the attention control group at 6 months and 15 months postintervention.ConclusionsThe culturally targeted KIM-CHI program was effective in increasing mammogram uptake among nonadherent KA women.Implications for nursingNurses and healthcare providers should consider specific health beliefs as well as inclusion of husbands or significant others. They also should target education to be culturally relevant for KA women to effectively improve frequency of breast cancer screening

The effect of a culturally tailored web-based physical activity promotion program on Asian American midlife women’s depressive symptoms

The benefits of physical activities on depressive symptoms have increasingly been reported in the literature, but the effect through which a Web-based physical activity promotion program alleviates depressive symptoms is not clearly known, especially among ethnic minority midlife women. The purpose of this pilot randomized control study is to examine the preliminary efficacy of the Web-based physical activity promotion program in enhancing the depressive symptoms of Asian American midlife women through increasing physical activity. This study adopted a randomized repeated measures pretest/posttest control group design. This study consisted of two groups of research participants: 18 in an intervention group and 15 in a control group. By using multiple instruments, the participants’ background and health status, depressive symptom experience, and physical activity experience were measured at three time points (pre-, post 1-month, and post 3-months). The data were analyzed using a modified intent-to-treat linear mixed-model growth curve analysis. After controlling for covariates, random intercept, and random slope, only discrimination stress showed statistical significances in the group effect (0.18, p = .08 for control) and time effect (-0.04, p = .04), but not in the group × time effect (p = .51). The active living habits scores showed statistical significances in the group effect (0.82, p \u3c 0.01 for control), time effect (0.29, p \u3c 0.01), and group × time effect (-0.31, p = 0.03 for control). Findings support the significant effect of the Web-based physical activity promotion program on the women’s discrimination stress and active living habits

Loss of the Desmosomal Component Perp Impairs Wound Healing In Vivo

Epithelial wound closure is a complex biological process that relies on the concerted action of activated keratinocytes and dermal fibroblasts to resurface and close the exposed wound. Modulation of cell-cell adhesion junctions is thought to facilitate cellular proliferation and migration of keratinocytes across the wound. In particular, desmosomes, adhesion complexes critical for maintaining epithelial integrity, are downregulated at the wound edge. It is unclear, however, how compromised desmosomal adhesion would affect wound reepithelialization, given the need for a delicate balance between downmodulating adhesive strength to permit changes in cellular morphology and maintaining adhesion to allow coordinated migration of keratinocyte sheets. Here, we explore the contribution of desmosomal adhesion to wound healing using mice deficient for the desmosomal component Perp. We find that Perp conditional knockout mice display delayed wound healing relative to controls. Furthermore, we determine that while loss of Perp compromises cell-cell adhesion, it does not impair keratinocyte proliferation and actually enhances keratinocyte migration in in vitro assays. Thus, Perp's role in promoting cell adhesion is essential for wound closure. Together, these studies suggest a role for desmosomal adhesion in efficient wound healing

Clustering of neuronal potassium channels is independent of their interaction with PSD-95

Voltage-dependent potassium channels regulate membrane excitability and cell–cell communication in the mammalian nervous system, and are found highly localized at distinct neuronal subcellular sites. Kv1 (mammalian Shaker family) potassium channels and the neurexin Caspr2, both of which contain COOH-terminal PDZ domain binding peptide motifs, are found colocalized at high density at juxtaparanodes flanking nodes of Ranvier of myelinated axons. The PDZ domain–containing protein PSD-95, which clusters Kv1 potassium channels in heterologous cells, has been proposed to play a major role in potassium channel clustering in mammalian neurons. Here, we show that PSD-95 colocalizes precisely with Kv1 potassium channels and Caspr2 at juxtaparanodes, and that a macromolecular complex of Kv1 channels and PSD-95 can be immunopurified from mammalian brain and spinal cord. Surprisingly, we find that the high density clustering of Kv1 channels and Caspr2 at juxtaparanodes is normal in a mutant mouse lacking juxtaparanodal PSD-95, and that the indirect interaction between Kv1 channels and Caspr2 is maintained in these mutant mice. These data suggest that the primary function of PSD-95 at juxtaparanodes lies outside of its accepted role in mediating the high density clustering of Kv1 potassium channels at these sites

Loss of the p53/p63 Regulated Desmosomal Protein Perp Promotes Tumorigenesis

Dysregulated cell–cell adhesion plays a critical role in epithelial cancer development. Studies of human and mouse cancers have indicated that loss of adhesion complexes known as adherens junctions contributes to tumor progression and metastasis. In contrast, little is known regarding the role of the related cell–cell adhesion junction, the desmosome, during cancer development. Studies analyzing expression of desmosome components during human cancer progression have yielded conflicting results, and therefore genetic studies using knockout mice to examine the functional consequence of desmosome inactivation for tumorigenesis are essential for elucidating the role of desmosomes in cancer development. Here, we investigate the consequences of desmosome loss for carcinogenesis by analyzing conditional knockout mice lacking Perp, a p53/p63 regulated gene that encodes an important component of desmosomes. Analysis of Perp-deficient mice in a UVB-induced squamous cell skin carcinoma model reveals that Perp ablation promotes both tumor initiation and progression. Tumor development is associated with inactivation of both of Perp's known functions, in apoptosis and cell–cell adhesion. Interestingly, Perp-deficient tumors exhibit widespread downregulation of desmosomal constituents while adherens junctions remain intact, suggesting that desmosome loss is a specific event important for tumorigenesis rather than a reflection of a general change in differentiation status. Similarly, human squamous cell carcinomas display loss of PERP expression with retention of adherens junctions components, indicating that this is a relevant stage of human cancer development. Using gene expression profiling, we show further that Perp loss induces a set of inflammation-related genes that could stimulate tumorigenesis. Together, these studies suggest that Perp-deficiency promotes cancer by enhancing cell survival, desmosome loss, and inflammation, and they highlight a fundamental role for Perp and desmosomes in tumor suppression. An understanding of the factors affecting cancer progression is important for ultimately improving the diagnosis, prognostication, and treatment of cancer