Comparison of Rectal and Esophageal Sensitivity in Women With Functional Heartburn.

This study tested the primary hypothesis that there is a correlation of maximum pain threshold (MPT) in the esophagus and rectum in persons with functional heartburn. Secondary aims evaluated correlations with initial perception threshold (IPT) and pain threshold (PT). This study explored objective sensory endpoints of IPT, PT, and MPT in the esophagus and rectum of 14 females with functional heartburn to determine whether visceral hypersensitivity is generalized or organ-specific. Data on volume and pressure measurements at IPT, PT, and MPT with esophageal and rectal barostat distention were collected. The relationship of sensation and pain to volume, pressure, and compliance was analyzed. Esophageal and rectal IPT balloon volume scores were highly and significantly correlated (r = .61, p = .02). Esophageal and rectal PT balloon volume scores were highly and significantly correlated (r = .6, p = .02). Esophageal and rectal MPT balloon volume scores were not correlated (r = .35, p = .26). The correlation of visceral sensitivity in the esophagus and rectum in persons with functional heartburn supports the hypothesis that visceral sensory changes in functional gastrointestinal disorders are not organ specific.

Improving Personal Characterization of Meaningful Activity in Adults with Chronic Conditions Living in a Low-Income Housing Community.

PURPOSE: To understand how adults living in a low-income, public housing community characterize meaningful activity (activity that gives life purpose) and if through short-term intervention, could overcome identified individual and environmental barriers to activity engagement. METHODS: We used a mixed methods design where Phase 1 (qualitative) informed the development of Phase 2 (quantitative). Focus groups were conducted with residents of two low-income, public housing communities to understand their characterization of meaningful activity and health. From these results, we developed a theory-based group intervention for overcoming barriers to engagement in meaningful activity. Finally, we examined change in self-report scores from the Meaningful Activity Participation Assessment (MAPA) and the Engagement in Meaningful Activity Survey (EMAS). RESULTS: Health literacy appeared to impact understanding of the questions in Phase 1. Activity availability, transportation, income and functional limitations were reported as barriers to meaningful activity. Phase 2 within group analysis revealed a significant difference in MAPA pre-post scores (p =0.007), but not EMAS (p =0.33). DISCUSSION: Health literacy should be assessed and addressed in this population prior to intervention. After a group intervention, participants had a change in characterization of what is considered healthy, meaningful activity but reported fewer changes to how their activities aligned with their values.

Update on research-based interventions for anxiety in patients with cancer.

Anxiety may begin at the moment a person is diagnosed with cancer and may fluctuate throughout the cancer trajectory as physical illness improves or declines. The purpose of this article is to present current evidence for nurses to implement interventions to reduce anxiety in patients who have cancer. The PubMed and CINAHL® databases were searched to identify relevant citations addressing interventions that treat or prevent anxiety symptoms in patients with cancer. Based on available evidence, the interventions addressed herein are categorized according to the Putting Evidence Into Practice (PEP®) rating schema. Interventions include pharmacologic and nonpharmacologic approaches to care, and meet criteria for three PEP categories: likely to be effective, effectiveness not established (the largest category of results), or effectiveness unlikely.

Putting evidence into practice: evidence-based interventions for depression.

Depression is a distressing emotion that occurs during various times of the cancer trajectory. Depression often goes unrecognized and untreated, which can significantly affect cost, quality of life, and treatment adherence. The Oncology Nursing Society's Putting Evidence Into Practice depression project team reviewed current literature to identify evidence-based interventions to reduce depression in people with cancer. Pharmacologic and nonpharmacologic interventions were evaluated, and opportunities for nurses to integrate recommendations into practice are offered in this article.

Resilience and stigma influence older African Americans seeking care.

BACKGROUND: Stigma affects older adults' willingness to describe depressive symptoms to health care personnel and others. Specific aims targeted associations among depressive symptoms, resilience, stigma and willingness, predictors of willingness, and estimated causal effects. METHODS: A cross-sectional, correlational design was used; 158 participants from community agencies and churches participated. Multivariate analyses of variance and multiple regression data analyses were used. Principal components analysis was conducted to determine patterns among the items within specified scales. RESULTS: Internal consistency reliability for each scale was 0.84 or above. Significant correlations between depressive symptoms and stigma (p < 0.05), between resilience and willingness (p < 0.0001), and single items were examined. Influences on willingness to seek mental health care for depressive symptoms unrelated to depressive symptom scores were revealed. CONCLUSIONS: Resilience influenced older African American's willingness to seek care for depressive symptoms. Exploration of early interventions to reduce depressive symptom escalation in older adults is warranted.

Mouse cytomegalovirus M33 is necessary and sufficient in virus-induced vascular smooth muscle cell migration.

Mouse cytomegalovirus (MCMV) encodes two potential seven-transmembrane-spanning proteins with homologies to cellular chemokine receptors, M33 and M78. While these virus-encoded chemokine receptors are necessary for the in vivo pathogenesis of MCMV, the function of these proteins is unknown. Since vascular smooth muscle cell (SMC) migration is of critical importance for the development of atherosclerosis and other vascular diseases, the ability of M33 to promote SMC motility was assessed. Similar to human CMV, MCMV induced the migration of mouse aortic SMCs but not mouse fibroblasts. To demonstrate whether M33 was required for MCMV-induced SMC migration, we employed interfering-RNA technology to specifically knock down M33 expression in the context of viral infection. The knockdown of M33 resulted in the specific reduction of M33 protein expression and ablation of MCMV-mediated SMC migration but failed to reduce viral growth in cultured cells. Adenovirus vector expression of M33 was sufficient to promote SMC migration, which was enhanced in the presence of recombinant mouse RANTES (mRANTES). In addition, M33 promoted the activation of Rac1 and extracellular signal-related kinase 1/2 upon stimulation with mRANTES. These findings demonstrate that mRANTES is a ligand for this chemokine receptor and that the activation of M33 occurs in a ligand-dependent manner. Thus, M33 is a functional homologue of US28 that is required for MCMV-induced vascular SMC migration.

Phosphorylation of human cytomegalovirus glycoprotein B (gB) at the acidic cluster casein kinase 2 site (Ser900) is required for localization of gB to the trans-Golgi network and efficient virus replication.

Human cytomegalovirus (HCMV) glycoprotein B (gB), encoded by the UL55 open reading frame, is an essential envelope glycoprotein involved in cell attachment and entry. Previously, we identified residue serine 900 (Ser900) as a unique site of reversible casein kinase 2 phosphorylation in the cytoplasmic domain of HCMV gB. We have also recently shown that gB is localized to the trans-Golgi network (TGN) in HCMV-permissive cells, thereby identifying the TGN as a possible site of virus envelopment. The aim of the current study was to determine the role of Ser900 phosphorylation in transport of gB to the TGN and in HCMV biogenesis. Recombinant HCMV strains were constructed that expressed gB molecules containing either an aspartic acid (gBAsp900) or alanine residue (gBAla900) substitution at Ser900 to mimic the phosphorylated or nonphosphorylated form, respectively. Immunofluorescence analysis of the trafficking of gB mutant molecules in fibroblasts infected with the HCMV recombinants revealed that gBAsp900 was localized to the TGN. In contrast, gBAla900 was partially mislocalized from the TGN, indicating that phosphorylation of gB at Ser900 was necessary for TGN localization. The increased TGN localization of gBAsp900 was due to a decreased transport of the molecule to post-TGN compartments. Remarkably, the substitution of an aspartic acid residue for Ser900 also resulted in an increase in levels of progeny virus production during HCMV infection of fibroblasts. Together, these results demonstrate that phosphorylation of gB at Ser900 is necessary for gB localization to the TGN, as well as for efficient viral replication, and further support the TGN as a site of HCMV envelopment.

Human cytomegalovirus chemokine receptor US28-induced smooth muscle cell migration is mediated by focal adhesion kinase and Src.

The human cytomegalovirus-encoded chemokine receptor US28 induces arterial smooth muscle cell (SMC) migration; however, the underlying mechanisms involved in this process are unclear. We have previously shown that US28-mediated SMC migration occurs by a ligand-dependent process that is sensitive to protein-tyrosine kinase inhibitors. We demonstrate here that US28 signals through the non-receptor protein-tyrosine kinases Src and focal adhesion kinase (FAK) and that this activity is necessary for US28-mediated SMC migration. In the presence of RANTES (regulated on activation normal T cell expressed and secreted), US28 stimulates the production of a FAK.Src kinase complex. Interestingly, Src co-immunoprecipitates with US28 in a ligand-dependent manner. This association occurs earlier than the formation of the FAK.Src kinase complex, suggesting that US28 activates Src before FAK. US28 binding to RANTES also promotes the formation of a Grb2.FAK complex, which is sensitive to treatment with the Src inhibitor PP2, further highlighting the critical role of Src in US28 activation of FAK. Human cytomegalovirus US28-mediated SMC migration is inhibited by treatment with PP2 and through the expression of either of two dominant negative inhibitors of FAK (F397Y and NH2-terminal amino acids 1-401). These findings demonstrate that activation of FAK and Src plays a critical role in US28-mediated signaling and SMC migration.