PUBLIC POLICY ISSUES IN RURAL DEVELOPMENT

Community/Rural/Urban Development,

RURAL POLICY AFTER THE RENAISSANCE: WESTERN EUROPEAN AND AMERICAN PERSPECTIVES

Agricultural and Food Policy,

How Does Brief Cognitive Behavioral Therapy Work? Potential Mechanisms of Action for Veterans with Physical and Psychological Comorbidities

Depression and anxiety are commonly comorbid among patients with chronic medical conditions. These comorbidities are associated with negative outcomes including poorer quality of life and worse physical functioning. Evidence that traditional cognitive behavioral therapy (CBT) is less effective for these populations has led to the development of brief CBT protocols that incorporate physical health self-management skills and are delivered in primary care. To continue refining treatment packages, it is important to understand how brief CBT works. The present study used the transactional model of stress and coping as a framework for investigating potential mechanisms of action of brief CBT. Veterans with chronic obstructive pulmonary disease and/or heart failure and elevated symptoms of depression and/or anxiety were randomized to receive brief CBT (n =180) or enhanced usual care (EUC; n = 122). At 4-month follow-up, depression and anxiety symptoms were significantly lower in veterans who received brief CBT, compared to EUC. Multiple mediation analyses revealed that brief CBT was associated with higher self-efficacy and less avoidant coping at 4-month follow-up, which were in turn associated with less depression and anxiety symptoms. Illness intrusiveness was also a significant mediator of the relationship between brief CBT and anxiety symptoms, but not depression symptoms. In contrast, increases in active coping attributable to brief CBT were not associated with improvements in depression or anxiety symptoms. These results demonstrate the utility of the transactional model of stress and coping as a framework for understanding mechanisms of action of brief CBT in patients with comorbid physical and psychological conditions

Peritoneal inflammation – A microenvironment for Epithelial Ovarian Cancer (EOC)

Epithelial ovarian cancer (EOC) is a significant cause of cancer related morbidity and mortality in women. Preferential involvement of peritoneal structures contributes to the overall poor outcome in EOC patients. Advances in biotechnology, such as cDNA microarray, are a product of the Human Genome Project and are beginning to provide fresh opportunities to understand the biology of EOC. In particular, it is now possible to examine in depth, at the molecular level, the complex relationship between the tumor itself and its surrounding microenvironment. This review focuses on the anatomy, physiology, and current immunobiologic research of peritoneal structures, and addresses certain potentially useful animal models. Changes in both the inflammatory and non-inflammatory cell compartments, as well as alterations to the extracellular matrix, appear to be signal events that contribute to the remodeling effects of the peritoneal stroma and surface epithelial cells on tumor growth and spread. These alterations may involve a number of proteins, including cytokines, chemokines, growth factors, either membrane or non-membrane bound, and integrins. Interactions between these molecules and molecular structures within the extracellular matrix, such as collagens and the proteoglycans, may contribute to a peritoneal mesothelial surface and stromal environment that is conducive to tumor cell proliferation and invasion. These alterations need to be examined and defined as possible prosnosticators and as therapeutic or diagnostic targets

Subperiostial recurrence of chondroblastoma

AbstractWe present a case of subperiosteal recurrence of chondroblastoma adjacent to the greater trochanter that was initially thought to represent septic arthritis of the hip in a 10-year-old girl. Soft-tissue recurrence of chondroblastoma is very rare, with fewer than ten cases reported in the literature. We demonstrate the recurrence on both CT and MRI. The MRI clearly demonstrates the soft-tissue recurrence and the associated inflammatory changes, with signal characteristics not unlike the primary tumor

Monocyte/macrophage and T-cell infiltrates in peritoneum of patients with ovarian cancer or benign pelvic disease

BACKGROUND: We previously showed that tumor-free peritoneum of patients with epithelial ovarian cancer (EOC) exhibited enhanced expression of several inflammatory response genes compared to peritoneum of benign disease. Here, we examined peritoneal inflammatory cell patterns to determine their concordance with selected enhanced genes. METHODS: Expression patterns of selected inflammatory genes were mined from our previously published data base. Bilateral pelvic peritoneal and subjacent stromal specimens were obtained from 20 women with EOC and 7 women with benign pelvic conditions. Sections were first stained by indirect immunoperoxidase and numbers of monocytes/macrophages (MO/MA), T cells, B cells, and NK cells counted. Proportions of CD68+ cells and CD3+ cells that coexpressed MO/MA differentiation factors (CD163, CCR1, CXCR8, VCAM1, and phosphorylated cytosolic phospholipase A(2 )[pcPLA(2)]), which had demonstrated expression in EOC peritoneal samples, were determined by multicolor immunofluorescence. RESULTS: MO/MA were present on both sides of the pelvic peritoneum in EOC patients, with infiltration of the subjacent stroma and mesothelium. CD68+ MO/MA, the most commonly represented population, and CD3+ T cells were present more often in EOC than in benign pelvic tumors. NK cells, B cells, and granulocytes were rare. CXCL8 (IL-8) and the chemokine receptor CCR1 were coexpressed more frequently on MO/MA than on CD3+ cells contrasting with CD68+/CD163+ cells that coexpressed CXCL8 less often. An important activated enzyme in the eicosanoid pathway, pcPLA(2), was highly expressed on both CD68+ and CD163+ cells. The adherence molecule Vascular Cell Adhesion Molecule-1 (VCAM1) was expressed on CD31+ endothelial cells and on a proportion of CD68+ MO/MA but rarely on CD3+ cells. CONCLUSION: The pelvic peritoneum in EOC exhibits a general pattern of chronic inflammation, represented primarily by differentiated MO/MA, and distinct from that in benign conditions concordant with previous profiling results

Written language skills in children with specific language impairment

Background. Young children are often required to carry out writing tasks in an educational context. However, little is known about the patterns of writing skills that children with Specific Language Impairment (CwSLI) have relative to their typically developing peers

Paraneoplastic thrombocytosis in ovarian cancer

<p>Background: The mechanisms of paraneoplastic thrombocytosis in ovarian cancer and the role that platelets play in abetting cancer growth are unclear.</p> <p>Methods: We analyzed clinical data on 619 patients with epithelial ovarian cancer to test associations between platelet counts and disease outcome. Human samples and mouse models of epithelial ovarian cancer were used to explore the underlying mechanisms of paraneoplastic thrombocytosis. The effects of platelets on tumor growth and angiogenesis were ascertained.</p> <p>Results: Thrombocytosis was significantly associated with advanced disease and shortened survival. Plasma levels of thrombopoietin and interleukin-6 were significantly elevated in patients who had thrombocytosis as compared with those who did not. In mouse models, increased hepatic thrombopoietin synthesis in response to tumor-derived interleukin-6 was an underlying mechanism of paraneoplastic thrombocytosis. Tumorderived interleukin-6 and hepatic thrombopoietin were also linked to thrombocytosis in patients. Silencing thrombopoietin and interleukin-6 abrogated thrombocytosis in tumor-bearing mice. Anti–interleukin-6 antibody treatment significantly reduced platelet counts in tumor-bearing mice and in patients with epithelial ovarian cancer. In addition, neutralizing interleukin-6 significantly enhanced the therapeutic efficacy of paclitaxel in mouse models of epithelial ovarian cancer. The use of an antiplatelet antibody to halve platelet counts in tumor-bearing mice significantly reduced tumor growth and angiogenesis.</p> <p>Conclusions: These findings support the existence of a paracrine circuit wherein increased production of thrombopoietic cytokines in tumor and host tissue leads to paraneoplastic thrombocytosis, which fuels tumor growth. We speculate that countering paraneoplastic thrombocytosis either directly or indirectly by targeting these cytokines may have therapeutic potential. </p&gt

Socially Disorganized Rural Communities

The article talks about the social disorganization of rural communities in the U.S. It is stated that family farming has been on the decline for decades, with the numbers of farmers dropping by 16 million since 1950 and farms decreasing by over 4 million during the past century. It is inferred that a part of a community\u27s history and way of life are being forfeited when local business are closing. According to the author, the theory of social disorganization emphasizes social integration and stability as necessary conditions for community. It offers some of the disadvantages of disorganized communities, such as the lack of collective efficacy

Src activation by β-adrenoreceptors is a key switch for tumor metastasis

Norepinephrine (NE) can modulate multiple cellular functions important for cancer progression; however, how this single extracellular signal regulates such a broad array of cellular processes is unknown. Here, we identify Src as a key regulator of phosphoproteomic signaling networks activated in response to beta-adrenergic signaling in cancer cells. These results also identify a new mechanism of Src phosphorylation that mediates beta-adrenergic/PKA regulation of downstream networks, thereby enhancing tumor cell migration, invasion and growth. In human ovarian cancer samples, high tumoral NE levels were correlated with high pSrcY419 levels. Moreover, among cancer patients, the use of beta blockers was significantly associated with reduced cancer-related mortality. Collectively, these data provide a pivotal molecular target for disrupting neural signaling in the tumor microenvironment