Trans-cultural aspects of social anxiety disorder and related conditions: a Brazilian case series and a review of international clinical studies

Cross-cultural studies have much to teach clinicians and researchers alike about psychopathology in general and about social anxiety disorder (SAD) in particular. Unfortunately, little is known about the degree and the mechanisms through which cultural environment may influence clinical manifestations of SAD. OBJECTIVE: Our objective was to identify culture-related clinical patterns in SAD and related disorders. METHODS: We described socio-demographic and clinical characteristics of a sample of 62 adult outpatients with SAD seen at a university clinic for anxiety and depressive disorders in Rio de Janeiro, Brazil, and compared them with those reported in clinical samples from North America, Europe, Asia and Oceania identified through a systematic review in Medline, PsychINFO, and LILACS. RESULTS: Our comparison of trans-cultural features of SAD lends partial support to Heimberg's (1997) contention that the majority of socio-demographic features and symptoms of this disorder are relatively independent of geographic and cultural differences. CONCLUSION: Patients with SAD were almost universally characterized by: 1) a predominance of males in clinical samples; 2) early onset of the disorder; 3) high educational attainment; and 4) great frequency of comorbidities.

New genes for focal epilepsies with speech and language disorders.

The last 2 years have seen exciting advances in the genetics of Landau-Kleffner syndrome and related disorders, encompassed within the epilepsy-aphasia spectrum (EAS). The striking finding of mutations in the N-methyl-D-aspartate (NMDA) receptor subunit gene GRIN2A as the first monogenic cause in up to 20 % of patients with EAS suggests that excitatory glutamate receptors play a key role in these disorders. Patients with GRIN2A mutations have a recognizable speech and language phenotype that may assist with diagnosis. Other molecules involved in RNA binding and cell adhesion have been implicated in EAS; copy number variations are also found. The emerging picture highlights the overlap between the genetic determinants of EAS with speech and language disorders, intellectual disability, autism spectrum disorders and more complex developmental phenotypes.

Chimeric anti-angiogenin antibody cAb 26–2F inhibits the formation of human breast cancer xenografts in athymic mice

Angiogenin (Ang), an inducer of neovascularization, is secreted by several types of human tumor cells and appears critical for their growth. The murine anti-Ang monoclonal antibody (mAb) 26–2F neutralizes the activities of Ang and dramatically prevents the establishment and metastatic dissemination of human tumor cell xenografts in athymic mice. However, for use clinically, the well-documented problem of the human anti-globulin antibody response known to occur with murine antibodies requires resolution. As a result, chimeric as well as totally humanized antibodies are currently being evaluated as therapeutic agents for the treatment of several pathological conditions, including malignancy. Therefore, we have constructed a chimeric mouse/human antibody based on the structure of mAb 26–2F. Complementary DNAs from the light and heavy chain variable regions of mAb 26–2F were cloned, sequenced, and genetically engineered by PCR for subcloning into expression vectors that contain human constant region sequences. Transfection of these vectors into nonproducing mouse myeloma cells resulted in the secretion of fully assembled tetrameric molecules. The chimeric antibody (cAb 26–2F) binds to Ang and inhibits its ribonucleolytic and angiogenic activities as potently as mAb 26–2F. Furthermore, the capacities of cAb 26–2F and its murine counterpart to suppress the formation of human breast cancer tumors in athymic mice are indistinguishable. Thus cAb 26–2F, with its retained neutralization capability and likely decreased immunogenicity, may be of use clinically for the treatment of human cancer and related disorders where pathological angiogenesis is a component.