The structure of feared social situations among race-ethnic minorities and Whites with social anxiety disorder in the United States

We investigated feared social situations in individuals with social anxiety disorder from different racial and ethnic groups in the United States. The sample included 247 African Americans, 158 Latinos, and 533 non-Latino Whites diagnosed with social anxiety disorder within the past 12 months from the integrated Collaborative Psychiatric Epidemiology Studies data set. After randomly splitting the full sample, we conducted an exploratory factor analysis with half of the sample to determine the structure of feared social situations in a more diverse sample than has been used in previous studies. We found evidence for a model consisting of three feared social domains: performance/public speaking, social interaction, and observational. We then conducted a confirmatory factor analysis on the remaining half of the sample to examine whether this factor structure varied significantly between the race-ethnic groups. Analyses revealed an adequate fit of this model across all three race-ethnic groups, suggesting invariance of the factor structure between the study groups. Broader cultural contexts within which these findings are relevant are discussed, along with important implications for comprehensive, culturally sensitive assessment of social anxiety.R01 MH078308 - NIMH NIH HHS; R01 MH081116 - NIMH NIH HHS; MH-081116 - NIMH NIH HHS; K23 MH096029 - NIMH NIH HHS; MH-078308 - NIMH NIH HH

Distinguishing features of cetuximab and panitumumab in colorectal cancer and other solid tumors

Cetuximab and panitumumab are two distinct monoclonal antibodies (mAbs) targeting the epidermal growth factor receptor (EGFR), and both are widely used in combination with chemotherapy or as monotherapy to treat patients with RAS wild-type metastatic colorectal cancer. Although often considered interchangeable, the two antibodies have different molecular structures and can behave differently in clinically relevant ways. More specifically, as an immunoglobulin (Ig) G1 isotype mAb, cetuximab can elicit immune functions such as antibody-dependent cell-mediated cytotoxicity involving natural killer cells, T-cell recruitment to the tumor, and T-cell priming via dendritic cell maturation. Panitumumab, an IgG2 isotype mAb, does not possess these immune functions. Furthermore, the two antibodies have different binding sites on the EGFR, as evidenced by mutations on the extracellular domain that can confer resistance to one of the two therapeutics or to both. We consider a comparison of the properties of these two antibodies to represent a gap in the literature. We therefore compiled a detailed, evidence-based educational review of the known molecular, clinical, and functional differences between the two antibodies and concluded that they are distinct therapeutic agents that should be considered individually during treatment planning. Available data for one agent can only partly be extrapolated to the other. Looking to the future, the known immune activity of cetuximab may provide a rationale for this antibody as a combination partner with investigational chemotherapy plus immunotherapy regimens for colorectal cance

Carbon Nanomaterials Promote M1/M2 Macrophage Activation

Toxic effects of certain carbon nanomaterials (CNM) have been observed in several exposure scenarios both in vivo and in vitro. However, most of the data currently available has been generated in a high-dose/acute exposure setup, limiting the understanding of their immunomodulatory mechanisms. Here, macrophage-like THP-1 cells, exposed to ten different CNM for 48 h in low-cytotoxic concentration of 10 mu g mL(-1), are characterized by secretion of different cytokines and global transcriptional changes. Subsequently, the relationships between cytokine secretion and transcriptional patterns are modeled, highlighting specific pathways related to alternative macrophage activation. Finally, time- and dose-dependent activation of transcription and secretion of M1 marker genes IL-1 beta and tumor necrosis factor, and M2 marker genes IL-10 and CSF1 is confirmed among the three most responsive CNM, with concentrations of 5, 10, and 20 mu g mL(-1) at 24, 48, and 72 h of exposure. These results underline CNM effects on the formation of cell microenvironment and gene expression leading to specific patterns of macrophage polarization. Taken together, these findings imply that, instead of a high and toxic CNM dose, a sub-lethal dose in controlled exposure setup can be utilized to alter the cell microenvironment and program antigen presenting cells, with fascinating implications for novel therapeutic strategies.Peer reviewe

Soluble tumor necrosis factor receptor 1 and 2 predict outcomes in advanced chronic kidney disease : a prospective cohort study

Background : Soluble tumor necrosis factor receptors 1 (sTNFR1) and 2 (sTNFR2) have been associated to progression of renal failure, end stage renal disease and mortality in early stages of chronic kidney disease (CKD), mostly in the context of diabetic nephropathy. The predictive value of these markers in advanced stages of CKD irrespective of the specific causes of kidney disease has not yet been defined. In this study, the relationship between sTNFR1 and sTNFR2 and the risk for adverse cardiovascular events (CVE) and all-cause mortality was investigated in a population with CKD stage 4-5, not yet on dialysis, to minimize the confounding by renal function. Patients and methods : In 131 patients, CKD stage 4-5, sTNFR1, sTNFR2 were analysed for their association to a composite endpoint of all-cause mortality or first non-fatal CVE by univariate and multivariate Cox proportional hazards models. In the multivariate models, age, gender, CRP, eGFR and significant comorbidities were included as covariates. Results : During a median follow-up of 33 months, 40 events (30.5%) occurred of which 29 deaths (22.1%) and 11 (8.4%) first non-fatal CVE. In univariate analysis, the hazard ratios (HR) of sTNFR1 and sTNFR2 for negative outcome were 1.49 (95% confidence interval (CI): 1.28-1.75) and 1.13 (95% CI: 1.06-1.20) respectively. After adjustment for clinical covariables (age, CRP, diabetes and a history of cardiovascular disease) both sTNFRs remained independently associated to outcomes (HR: sTNFR1: 1.51, 95% CI: 1.30-1.77; sTNFR2: 1.13, 95% CI: 1.06-1.20). A subanalysis of the non-diabetic patients in the study population confirmed these findings, especially for sTNFR1. Conclusion : sTNFR1 and sTNFR2 are independently associated to all-cause mortality or an increased risk for cardiovascular events in advanced CKD irrespective of the cause of kidney disease

Associations Between Inflammation and Cognitive Function in African Americans and European Americans

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109795/1/jgs13165.pd

Applying the Cry of Pain model as a predictor of deliberate self-harm in an early-stage adult male prison population

Purpose: Deliberate self-harming behaviour is more prevalent within the prison environment than in community samples, with those in the first weeks of imprisonment at greatest risk. Research in this area has been largely atheoretical and a unifying model may improve the predictability of assessment and the development of intervention approaches. This study applied William and Pollock’s (2001) Cry of Pain model as the theoretical process of deliberate self-harm in the early stages of imprisonment. Method: A prospective study of new arrivals at an adult male prison. Participants (n =181) completed questionnaires and it was hypothesised that the factors derived from the model (perceived stress, defeat, entrapment and absence of rescue factors) would be predictive of future deliberate self-harm. Prisoners with active psychosis and non-English speakers were excluded. All participants were followed up for four months for instances of self-harm. Eighteen participants engaged in self-harm during this period. Results: The Cry of Pain Model was supported in the analysis. Hierarchical binary logistic regression confirmed that all features of the model were supported as predictive of future self-harm in prison, even after controlling for previous self-harm, depression and hopelessness. Conclusion: The Cry of Pain model is supported as a predictive model for deliberate self-harm in prison. Suggestions are offered as to the impact on assessment and intervention directions in prison