Density-dependent changes in effective area occupied for sea-bottom-associated marine fishes

The spatial distribution of marine fishes can change for many reasons including density-dependent distributional shifts. Previous studies show mixed support for either the proportional-density model, PDM (no relationship between abundance and area occupied, supported by ideal-free distribution theory) or the basin model, BM (positive abundance–area relationship, supported by density-dependent habitat selection theory). The BM implies that fishes move towards preferred habitat as the population declines. We estimate the average relationship using bottom trawl data for 92 fish species from six marine regions, to determine whether the BM or PDM provides a better description for sea-bottom-associated fishes. We fit a spatio-temporal model and estimate changes in effective area occupied and abundance, and combine results to estimate the average abundance–area relationship as well as variability among taxa and regions. The average relationship is weak but significant (0.6% increase in area for a 10% increase in abundance), whereas only a small proportion of species–region combinations show a negative relationship (i.e. shrinking area when abundance increases). Approximately one-third of combinations (34.6%) are predicted to increase in area more than 1% for every 10% increase in abundance. We therefore infer that population density generally changes faster than effective area occupied during abundance changes. Gadiforms have the strongest estimated relationship (average 1.0% area increase for every 10% abundance increase) followed by Pleuronectiformes and Scorpaeniformes, and the Eastern Bering Sea shows a strong relationship between abundance and area occupied relative to other regions. We conclude that the BM explains a small but important portion of spatial dynamics for sea-bottom-associated fishes, and that many individual populations merit cautious management during population declines, because a compressed range may increase the efficiency of harvest

The economic impact of chronic fatigue syndrome in Georgia: direct and indirect costs

<p>Abstract</p> <p>Background</p> <p>Chronic fatigue syndrome (CFS) is a debilitating chronic illness affecting at least 4 million people in the United States. Understanding its cost improves decisions regarding resource allocation that may be directed towards treatment and cure, and guides the evaluation of clinical and community interventions designed to reduce the burden of disease.</p> <p>Methods</p> <p>This research estimated direct and indirect costs of CFS and the impact on educational attainment using a population-based, case-control study between September 2004 and July 2005, Georgia, USA. Participants completed a clinical evaluation to confirm CFS, identify other illnesses, and report on socioeconomic factors. We estimated the effect of CFS on direct medical costs (inpatient hospitalizations, provider visits, prescription medication spending, other medical supplies and services) and loss in productivity (employment and earnings) with a stratified sample (n = 500) from metropolitan, urban, and rural Georgia. We adjusted medical costs and earnings for confounders (age, sex, race/ethnicity, education, and geographic strata) using econometric models and weighted estimates to reflect response-rate adjusted sampling rates.</p> <p>Results</p> <p>Individuals with CFS had mean annual direct medical costs of $5,683. After adjusting for confounding factors, CFS accounted for$3,286 of these costs (p < 0.01), which were driven by increased provider visits and prescription medication use. Nearly one-quarter of these expenses were paid directly out-of pocket by those with CFS. Individuals with CFS reported mean annual household income of $23,076. After adjustment, CFS accounted for$8,554 annually in lost household earnings (p < 0.01). Lower educational attainment accounted for 19% of the reduction in earnings associated with CFS.</p> <p>Conclusions</p> <p>Study results indicate that chronic fatigue syndrome may lead to substantial increases in healthcare costs and decreases in individual earnings. Studies have estimated up to 2.5% of non-elderly adults may suffer from CFS. In Georgia, a state with roughly 5.5 million people age 18-59, illness could account for $452 million in total healthcare expenditures and$1.2 billion of lost productivity.</p

The CCL2 chemokine is a negative regulator of autophagy and necrosis in liminal B breast cancer cells

Luminal A and B breast cancers are the most prevalent forms of breast cancer diagnosed in women. Compared to luminal A breast cancer patients, patients with luminal B breast cancers experience increased disease recurrence and lower overall survival. The mechanisms that regulate the luminal B subtype remain poorly understood. The chemokine CCL2 is overexpressed in breast cancer, correlating with poor patient prognosis. The purpose of this study was to determine the role of CCL2 expression in luminal B breast cancer cells. Breast tissues, MMTV-PyVmT and MMTV-Neu transgenic mammary tumors forming luminal B-like lesions, were immunostained for CCL2 expression. To determine the role of CCL2 in breast cancer cells, CCL2 gene expression was silenced in mammary tumor tissues and cells using TAT cell-penetrating peptides non-covalently cross linked to siRNAs (Ca-TAT/siRNA). CCL2 expression was examined by ELISA and flow cytometry. Cell growth and survival were analyzed by flow cytometry, immunocytochemistry, and fluorescence microscopy. CCL2 expression was significantly increased in luminal B breast tumors, MMTV-PyVmT and MMTV-Neu mammary tumors, compared or normal breast tissue or luminal A breast tumors. Ca-TAT delivery of CCL2 siRNAs significantly reduced CCL2 expression in PyVmT mammary tumors, and decreased cell proliferation and survival. CCL2 gene silencing in PyVmT carcinoma cells or BT474 luminal B breast cancer cells decreased cell growth and viability associated with increased necrosis and autophagy. CCL2 expression is overexpressed in luminal B breast cancer cells and is important for regulating cell growth and survival by inhibiting necrosis and autophagy

Analysis of CARD14 Polymorphisms in Pityriasis Rubra Pilaris: Activation of NF-κB.

Pityriasis rubra pilaris (PRP) is a rare inflammatory papulo-squamous disorder manifesting with palmoplantar keratoderma and follicular hyperkeratotic papules which tend to coalesce into large, scaly, erythematous plaques often progressing to exfoliative erythroderma (Klein et al., 2010; Petrof et al., 2013). PRP is often misdiagnosed as psoriasis, a more common papulo-squamous inflammatory disorder. Nevertheless, the two conditions, in their classic presentations, are clearly distinct, and can be distinguished by clinical findings and histopathologic features (Magro and Crowson, 1997). Clinically, PRP manifests with characteristic “sparing islands ” of apparently normal skin, palmoplantar keratoderma and follicular papules. The disease is frequently self-limiting within a few years ’ timeframe. Histopathology of PRP is characterized by alternating ortho- and parakeratosis rete ridges oriented in vertical and horizontal arrays (“checkerboard pattern”), acanthosis with broadened bases, follicular plugging, perivascular lymphocytic infiltrate in the dermis, and lack of neutrophils in the epidermis. Currently, there is no specific or uniformly effective treatment for PRP. Most cases of PRP are sporadic and without family history, but a familial form with an autosomal dominant inheritance with partial penetrance represents &lt;6 % of al

Role of CCR7 in Facilitating Direct Allosensitization and Regulatory T-Cell Function in High-Risk Corneal Transplantation

Purpose. Chemokine receptor 7 (CCR7) is a key homing molecule for immune cell trafficking, including corneal antigen-presenting cell (APC) migration from the inflamed cornea to draining lymph nodes (LNs). Here, the authors investigated the effect of CCR7-facilitated donor APC trafficking on allosensitization, regulatory T-cell (Treg) function, and graft survival in corneal transplantation. Methods. CCR7−/− or wild-type (WT) allogeneic corneal grafts were transplanted onto the neovascularized high-risk recipient beds. Two weeks later, the frequency of directly alloprimed host T cells was measured by the IFN-γ ELISPOT assay. Treg function was tested by a coculture suppression assay and an IFN-γ ELISPOT assay. Kaplan-Meier analysis was performed to evaluate graft survival. Results. The recipients of CCR7−/− grafts had fewer migrated donor APCs and lower frequency of IFN-γ–producing T cells in the draining LNs. However, there was no statistically significant difference in transplant survival between recipients of CCR7−/− and those of WT grafts. Tregs from the CCR7−/− graft recipient group showed reduced regulatory potential for the suppression of proliferation of naive T cells and direct alloprimed T cells and expressed lower Foxp3 levels. In vitro studies confirmed that mature CCR7+ major histocompatibility complex class II+ CD86+ graft-derived dendritic cells were critical for Treg function. Conclusions. Not only is CCR7-mediated donor-derived APC trafficking to the draining LNs important in the initiation of host T-cell priming, it is crucial for Treg-mediated tolerance

A.Actinomycetemcomitans‐Induced Periodontal Disease Promotes Systemic and Local Responses in Rat Periodontium

Aim To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. Material & Methods Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF‐α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. Results An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p \u3c 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p \u3c 0.05). TNF‐α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF‐α expression in the connective tissue (p \u3c 0.05). PMN recruitment significantly increased after Aa infection (p \u3c 0.05). Aa also increased the number of CD8+ T cells (p \u3c 0.05), but not CD4+ T cells or regulatory T cells (Tregs) (p \u3e 0.05). Conclusion Aa infection stimulated a local response that increased numbers of PMNs and TNF‐α expression in the junctional epithelium and loss of attachment. Both TNF‐α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF‐α in the connective tissue, osteoclast numbers and CD8+ T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction