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Background: Making a definite diagnosis of infectious uveitis is a challenging task because many other infectious, and non-infectious uveitis, may have similar non-specific symptoms and overlapping clinical appearances. Co-infections in immunocompetent patients are not frequently proved with traditional serologic-diagnostic tools., Methods: Descriptive transversal study, in a Uveitis Service of an Ophthalmology Reference Center, in Bogotá, Colombia, from July 2014 to February 2016. Aqueous humor (AH) and/or vitreous fluid, blood and serum samples were collected from consecutive patients suspected of having infectious uveitis. The diagnosis of ocular toxoplasmosis (OT) was confirmed by the Goldmann-Witmer coefficient (GWC) and by polymerase chain reaction (PCR). Differential diagnosis by PCR in AH was done for viral origin such as Cytomegalovirus (CMV), Herpes simplex virus type 1 (HSV1), Herpes simplex virus type 2 (HSV2), Varicella zoster virus (VZV), Epstein-Barr virus (EBV) and Mycobacterium tuberculosis., Results: In 66 Colombian patients with uveitis of presumed infectious origin: 22 (33.3%) were confirmed as OT, 16 (24.2%) as undetermined OT, five (7.5%) as co-infections and 23 (34.8%) as other uveitis. Toxoplasma coinfection with M. tuberculosis was identified in one case by PCR and in four cases with HSV by GWC. The initial clinical diagnosis changed, after laboratory examination, in 21 cases (31.8%)., Conclusions: Clinical diagnosis can be changed by laboratory examination in a significant proportion of cases of uveitis. Diagnosis of OT should combine the use of PCR and GWC to reach the maximum of confirmation of cases. The use of multiple laboratory methods is necessary to identify co-infections and viral infections that can mimic OT in immunocompetent patients.

Background: The aetiological boundary between obsessive-compulsive related disorders (OCRDs) including obsessive-compulsive disorder (OCD) and anxiety disorders is unclear and continues to generate debate., Aims: To determine the genetic overlap and the pattern of causal relationships among OCRDs and anxiety disorders., Method: Multivariate twin modelling methods and a new regression analysis to infer causation were used, involving 2495 male and female twins., Results: The amount of common genetic liability observed for OCD symptoms was higher when considering anxiety disorders and OCRDs in the model v. modelling OCRD symptoms alone. OCD symptoms emerged as risk factors for the presence of generalised anxiety, panic and hoarding symptoms, whereas social phobia appeared as a risk factor for OCD symptoms., Conclusions: OCD represents a complex phenotype that includes important shared features with anxiety disorders and OCRDs. The novel patterns of risk identified between OCD and anxiety disorder may help to explain their frequent co-occurrence., (© The Royal College of Psychiatrists 2016.)

Objective: To characterize the pathways induced by transforming growth factor beta1 (TGFbeta1) that lead to the expression of endothelin 1 (ET-1) in human dermal fibroblasts, and to study the effects of TGFbeta1 and ET-1 on the acquisition of a profibrotic phenotype and assess the contribution of the TGFbeta1/ET-1 axis to skin wound healing and fibrosis in vivo., Methods: The mechanism of induction of ET-1 expression by TGFbeta1 and its effect on the expression of alpha-smooth muscle actin and type I collagen were studied in human dermal fibroblasts, in experiments involving the TGFbeta receptor inhibitor GW788388 and the ET receptor antagonist bosentan, by real-time reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay, immunofluorescence, Western blotting, and promoter/reporter transient transfection analyses. Experiments assessing dermal wound healing in mice were performed with adenovirus-driven overexpression of active TGFbeta1 and ET-1, with or without treatment with bosentan. The contributions of TGFbeta1 and ET-1 to the fibrotic response were also assessed in a mouse model of bleomycin-induced skin fibrosis, by histologic, immunohistochemical, RT-PCR, and protein analyses., Results: TGFbeta1 induced ET-1 expression in human dermal fibroblasts through Smad- and activator protein 1/JNK-dependent signaling. The ability of TGFbeta1 to induce the expression of profibrotic genes was dependent on ET-1. Adenovirus-mediated overexpression of TGFbeta1 and ET-1 in mouse skin was associated with accelerated wound closure, increased fibrogenesis, and excessive scarring. Treatment with bosentan prevented the effects of TGFbeta1. In the bleomycin-induced fibrosis model, treatment with GW788388 and bosentan prevented the fibrotic response., Conclusion: Our results strongly support the notion that the TGFbeta1/ET-1 axis has a role in wound repair and skin fibrosis. ET-1 receptor antagonists, such as bosentan, may represent a useful therapeutic tool in the treatment of excessive scarring and fibrosis-related diseases.