Stigma, social anxiety, and illness severity in bipolar disorder: Implications for treatment.

BACKGROUND: Studies indicate that comorbid anxiety disorders predict a more severe course of illness in bipolar disorder (BD). The relatively high prevalence of social anxiety in BD points to the potential role that socio-cultural factors, such as stigma, play in exacerbating the progression of this disorder. Stigma creates social anxiety in affected individuals because it essentially forces them into a vulnerable social status that is marked by public disgrace. Although the etiology of debilitating social anxiety in BD may involve multiple factors, stigma deserves particular clinical attention because research in this area indicates that it is common and its internalization is associated with poor outcome. METHODS: We conducted a literature review using search terms related to stigma, social anxiety, bipolar disorder, illness severity, and outcomes. The electronic databases searched included PsychINFO, PubMed, JSTOR, and EBSCOhost Academic Search Complete with limits set to include articles published in English. RESULTS: The literature indicates that internalized stigma often triggers the core psychological experiences of social anxiety and is highly correlated with clinical and functional outcome in BD. On a psychological level, internalized stigma and social anxiety can create distress that triggers symptoms of BD. From a biological perspective, stigma constitutes a chronic psychosocial stressor that may interact with the pathophysiology of BD in inflammatory ways. CONCLUSIONS: The connection between stigma and social anxiety, and their combined effects on people with BD, carries important implications for psychiatric care. To obtain an accurate clinical formulation, initial evaluations may seek to examine stigma-related experiences and determine their relationship to anxiety symptoms and psychosocial functioning. In addition, direct interventions for reducing the ill effects of stigma in BD deserve clinical attention, because they may carry the potential to enhance outcomes.

Fluctuations in gene regulatory networks as Gaussian colored noise.

The study of fluctuations in gene regulatory networks is extended to the case of Gaussian colored noise. First, the solution of the corresponding Langevin equation with colored noise is expressed in terms of an Ito integral. Then, two important lemmas concerning the variance of an Ito integral and the covariance of two Ito integrals are shown. Based on the lemmas, we give the general formulas for the variances and covariance of molecular concentrations for a regulatory network near a stable equilibrium explicitly. Two examples, the gene autoregulatory network and the toggle switch, are presented in details. In general, it is found that the finite correlation time of noise reduces the fluctuations and enhances the correlation between the fluctuations of the molecular components.

The B-cell transcription factors BSAP, Oct-2, and BOB.1 and the pan-B-cell markers CD20, CD22, and CD79a are useful in the differential diagnosis of classic Hodgkin lymphoma.

Even with routine immunohistochemical evaluation, distinguishing classic Hodgkin lymphoma (CHL) from diffuse large B-cell lymphoma (DLBCL) or anaplastic large cell lymphoma (ALCL) can be difficult. In these cases, the transcription factors (B cell-specific activator protein [BSAP], octamer-binding transcription factor 2 [Oct-2], and B-cell Oct-binding protein 1 [BOB.1]) and the pan-B-cell markers (CD20, CD22, and CD79a) may aid in clarifying the diagnosis. In 57 cases of CHL, 5 cases of nodular lymphocyte predominant Hodgkin lymphoma (NLPHL), and 33 cases of non-Hodgkin lymphoma (25 DLBCL and 8 ALCL) we found the transcription factor phenotype BSAP+ and either Oct-2- or BOB.1- to be predictive of CHL; BSAP+/Oct-2+/BOB.1+ was predictive of NLPHL or DLBCL, while BSAP- was predictive of ALCL. Expression of all 3 pan-B-cell markers was seen only in NLPHL and DLBCL; positivity for a single B-cell marker was present only in CHL. Thus, together, the transcription factors and pan-B-cell markers might be useful in the differential diagnosis of CHL.