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The state of Maharashtra and the city of Mumbai have been referred to as the epidemic epicentre of India since the time of the plague of 1896 and influenza epidemic of 1918. During the COVID-19 pandemic too, the state experienced the highest cases with maximum fatalities. Against the structural backdrop of India's underfinanced public health infrastructure, this paper engages with the subnational state's capacity, legitimacy, and authority in managing the pandemic. The paper highlights the socio-economic and spatial-demographic context to explain the reasons behind the severity of the pandemic in Maharashtra. Through an analysis of regulatory information at different levels during crucial phases of the pandemic, and statistics about tests, caseloads, medical resources (such as hospital beds, essential drugs, and oxygen), migrants' welfare, excess deaths, vaccines, etc., the paper explores how knowledge about the unfolding crisis and the capacity to respond kept changing as the pandemic progressed. The emphasis is on demonstrating how the state improved its response, from a situation of confusion to an augmentation of infrastructure and a coordinated response. Despite fiscal constraints and centre-state tensions, the reliance on rational bureaucracy, scientific knowledge, and the decentralization of the response helped to develop several models and good practices that were widely acknowledged. The paper emphasizes that the case of Maharashtra underscores the importance of decentralized planning and recognizes the value of collaborative federalism.

Supplemental material, sj-docx-1-jop-10.1177_0269881120985147 for Role of nitric oxide signaling in the antidepressant mechanism of action of ketamine: A randomized controlled trial by Laura Bevilacqua, Alex Charney, Charlotte R Pierce, Samantha M Richards, Manish K Jha, Andrew Glasgow, Jess Brallier, Katherine Kirkwood, Emilia Bagiella, Dennis S Charney and James W Murrough in Journal of Psychopharmacology

Supplemental material, sj-docx-2-jop-10.1177_0269881120985147 for Role of nitric oxide signaling in the antidepressant mechanism of action of ketamine: A randomized controlled trial by Laura Bevilacqua, Alex Charney, Charlotte R Pierce, Samantha M Richards, Manish K Jha, Andrew Glasgow, Jess Brallier, Katherine Kirkwood, Emilia Bagiella, Dennis S Charney and James W Murrough in Journal of Psychopharmacology

Supplemental material, sj-docx-2-jop-10.1177_0269881120985147 for Role of nitric oxide signaling in the antidepressant mechanism of action of ketamine: A randomized controlled trial by Laura Bevilacqua, Alex Charney, Charlotte R Pierce, Samantha M Richards, Manish K Jha, Andrew Glasgow, Jess Brallier, Katherine Kirkwood, Emilia Bagiella, Dennis S Charney and James W Murrough in Journal of Psychopharmacology

Supplemental material, sj-docx-1-jop-10.1177_0269881120985147 for Role of nitric oxide signaling in the antidepressant mechanism of action of ketamine: A randomized controlled trial by Laura Bevilacqua, Alex Charney, Charlotte R Pierce, Samantha M Richards, Manish K Jha, Andrew Glasgow, Jess Brallier, Katherine Kirkwood, Emilia Bagiella, Dennis S Charney and James W Murrough in Journal of Psychopharmacology

The efficacy of antidepressant treatment for depression is controversial due to the only modest superiority demonstrated over placebo. However, neurobiological heterogeneity within depression may limit overall antidepressant efficacy. We sought to identify a neurobiological phenotype responsive to antidepressant treatment by testing pretreatment brain activation during response to, and regulation of, emotional conflict as a moderator of the clinical benefit of the antidepressant sertraline versus placebo. Using neuroimaging data from a large randomized controlled trial, we found widespread moderation of clinical benefits by brain activity during regulation of emotional conflict, in which greater downregulation of conflict-responsive regions predicted better sertraline outcomes. Treatment-predictive machine learning using brain metrics outperformed a model trained on clinical and demographic variables. Our findings demonstrate that antidepressant response is predicted by brain activity underlying a key self-regulatory emotional capacity. Leveraging brain-based measures in psychiatry will forge a path toward better treatment personalization, refined mechanistic insights and improved outcomes.

Animal and human studies suggest an association between depression and aberrant immune response. Further, common inflammatory markers may change during the course of antidepressant treatment in patients. The objective of this study was to evaluate changes in inflammatory markers and clinical outcomes from subjects enrolled in the Combination of Medications to Enhance Depression Outcome (CO-MED) trial. At baseline and week 12 (treatment completion), plasma samples of 102 participants were analyzed via a multiplex assay comprised of inflammatory markers using a 27-plex standard assay panel plus a 4-plex human acute phase xMAP technology based platform. We carried out analyses in two steps. First, t-tests were used to identify inflammatory marker levels that changed between baseline and week 12. For markers that were altered, logistic regression models were then conducted to look for associated changes in remission at week 12. Among the 31 inflammatory markers analyzed, several cytokines (IL-5, IFN-γ, IL-13), two chemokines (Eotaxin-1/CCL11, RANTES) and an acute-phase reactant (serum amyloid P component) showed change from baseline to week 12. However, only two indicated differential remission responses. Interestingly, increased levels of Eotaxin-1/CCL11 correlated with remission at week 12, whereas decreased levels of IFN-γ correlated with non-remission at week 12. Results suggest that these inflammatory proteins may serve as predictors of treatment response.

Functional impairments often remain despite symptomatic improvement with antidepressant treatment, supporting the need for novel treatment approaches. The present study examined the extent to which exercise augmentation improved several domains of psychosocial functioning and quality of life (QoL) among depressed participants.Data were collected from 122 partial responders to antidepressant medication. Participants were randomized to either high- (16 kcal/kg of weight/week [KKW]) or low-dose (4-KKW) exercise. Participants completed a combination of supervised and home-based exercise for 12 weeks. The Short-Form Health Survey, Work and Social Adjustment Scale, Social Adjustment Scale, Quality of Life Enjoyment and Satisfaction Questionnaire, and Satisfaction with Life Scale were collected at 6 and 12 weeks. Participants with data for at least one of the two follow-up time points (n = 106) were analyzed using a linear mixed model to assess change from baseline within groups and the difference between groups for each psychosocial outcome measure. All analyses controlled for covariates, including baseline depressive symptomatology.Participants experienced significant improvements in functioning across tested domains, and generally fell within a healthy range of functioning on all measures at Weeks 6 and 12. Although no differences were found between exercise groups, improvements were observed across a variety of psychosocial and QoL domains, even in the low-dose exercise group.These findings support exercise augmentation of antidepressant treatment as a viable intervention for treatment-resistant depression to improve function in addition to symptoms.