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There is increasing attention to the impacts of stigma and discrimination related to mental health on quality of life and access to and quality of healthcare. Effective strategies for stigma reduction exist, but most evidence comes from high-income settings. Recent reviews of stigma research have identified gaps in the field, including limited cultural and contextual adaptation of interventions, a lack of contextual psychometric information on evaluation tools, and, most notably, a lack of multi-level strategies for stigma reduction. The Indigo Partnership research programme will address these knowledge gaps through a multi-country, multi-site collaboration for anti-stigma interventions in low- and middle-income countries (LMICs) (China, Ethiopia, India, Nepal, and Tunisia). The Indigo Partnership aims to: (1) carry out research to strengthen the understanding of mechanisms of stigma processes and reduce stigma and discrimination against people with mental health conditions in LMICs; and (2) establish a strong collaborative research consortium through the conduct of this programme. Specifically, the Indigo Partnership involves developing and pilot testing anti-stigma interventions at the community, primary care, and mental health specialist care levels, with a systematic approach to cultural and contextual adaptation across the sites. This work also involves transcultural translation and adaptation of stigma and discrimination measurement tools. The Indigo Partnership operates with the key principle of partnering with people with lived experience of mental health conditions for the development and implementation of the pilot interventions, as well as capacity building and cross-site learning to actively develop a more globally representative and equitable mental health research community. This work is envisioned to have a long-lasting impact, both in terms of the capacity building provided to participating institutions and researchers, and the foundation it provides for future research to extend the evidence base of what works to reduce and ultimately end stigma and discrimination in mental health.

Objective To study the effect of Lichong decoction (LD) on expression of matrix metalloproteinase-2 (MMP-2) and metalloproteinase-2 (TIMP-2) in a rat model of uterine leiomyoma (UL). Methods UL was induced in rats using exogenous estrogen and progesterone. LD was administered (p.o.) for 4 weeks, and mifepristone (RU-486) used as a control. To observe the effect of LD on the uterine coefficient and uterine transverse diameter, a radioimmunoassay method was used to detect serum levels of sex hormones. Light microscopic analyses of pathologic changes in the tissues of UL rats were evaluated. Expression of the proteins of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in uterine tissues was assessed by immunohistochemical staining and western blotting. Results A UL model in rats was established successfully. LD reduced uterine weight, uterine coefficient, and uterine transverse diameter compared with untreated controls. LD reduced levels of estradiol, progesterone, follicle-stimulating hormone, and luteinizing hormone in our UL models. LD improved the pathologic condition of uterine muscle. Expression of MMP-2 protein decreased to varying extents in LD-treated groups, but TIMP-2 levels were enhanced. LD appears to reduce MMP-2 expression and increase TIMP-2 expression in UL tissue. Conclusion These data suggest that the mechanism of action of LD on ULs may involve reduction of MMP-2 expression and increase in TIMP-2 expression in rats.

Mounting evidence suggest that astrocytes might be involved in the pathogenesis of schizophrenia. Of particular interest is S100B, a protein produced primarily by astrocytes that plays a critical role in the maintenance of functional neuronal and astroglial activation. Abnormalities in S100B levels have been associated with schizophrenia. In this study, we examined serum S100B protein levels and the relationship between S100B levels and psychopathological symptoms in first-episode, drug-naïve patients with schizophrenia (SCZ). Sixty-four patients with schizophrenia were compared with 66 age- and sex-matched healthy controls (HC). Psychopathology in the SCZ group was assessed by the Positive and Negative Syndrome Scale (PANSS). Serum S100B protein levels were measured by sandwich enzyme-linked immunosorbent assay (ELISA). The results showed that S100B protein-like immunoreactivity was significantly higher in the SCZ group than the HC group. S100B-like immunoreactivity was correlated with age, duration of illness, and PANSS subscale scores for negative and general psychopathology and total scores. In the SCZ group, serum S100B levels in residual-subtypes were significantly higher than in the paranoid- and disorganized-subtypes. Our findings suggest an upregulation of a marker for astrocyte activity, i.e., S100B, in first-episode medication-free patients with schizophrenia, and thus support the involvement of astrocytes in the pathogenesis of schizophrenia.