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According to Sharrelle Barber of Drexel University Dornsife School of Public Health (Philadelphia, PA, USA), the pre-existing racial and health inequalities already present in US society are being exacerbated by the pandemic. Spencer Platt/Getty Images 14 US states (mostly in the south and the Plains) have refused to accept the Affordable Care Act Medicaid expansion, leaving millions of the poorest and sickest Americans without access to health care, with the added effect of leaving many regional and local hospitals across the US closed or in danger of closing because of the high cost of medical care and a high proportion of rural uninsured and underinsured people. According to the IHS, there are currently 985 confirmed cases of COVID-19 on tribal reservations, and 536 cases in the Navajo Nation alone (the largest reservation).

Functional imaging studies have reported with remarkable consistency hyperactivity in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and caudate nucleus of patients with obsessive–compulsive disorder (OCD). These findings have often been interpreted as evidence that abnormalities in cortico–basal ganglia–thalamo–cortical loops involving the OFC and ACC are causally related to OCD. This interpretation remains controversial, however, because such hyperactivity may represent either a cause or a consequence of the symptoms. This article analyzes the evidence for a causal role of these loops in producing OCD in children and adults. The article first reviews the strong evidence for anatomical abnormalities in these loops in patients with OCD. These findings are not sufficient to establish causality, however, because anatomical alterations may themselves be a consequence rather than a cause of the symptoms. The article then reviews three lines of evidence that, despite their own limitations, permit stronger causal inferences: the development of OCD following brain injury, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and neurosurgical lesions that attenuate OCD. Converging evidence from these various lines of research supports a causal role for the cortico–basal ganglia–thalamo–cortical loops that involve the OFC and ACC in the pathogenesis of OCD in children and adults.

Rumination, or recursive self-focused thinking, has important implications for understanding the development and maintenance of depressive episodes. Rumination is associated with the worsening of negative mood states, greater affective responding to negative material, and increased access to negative memories. The present study was designed to use fMRI to examine neural aspects of rumination in depressed and healthy control individuals. We used a rumination induction task to assess differences in patterns of neural activation during ruminative self-focus as compared with a concrete distraction condition and with a novel abstract distraction condition in 14 participants who were diagnosed with major depressive disorder and 14 healthy control participants. Depressed participants exhibited increased activation in the orbitofrontal cortex, subgenual anterior cingulate, and dorsolateral prefrontal cortex as compared with healthy controls during rumination versus concrete distraction. Neural activity during rumination versus abstract distraction was greater for depressed than for control participants in the amygdala, rostral anterior cingulate/medial prefrontal cortex, dorsolateral prefrontal cortex, posterior cingulate, and parahippocampus. These findings indicate that ruminative self-focus is associated with enhanced recruitment of limbic and medial and dorsolateral prefrontal regions in depression. Supplemental materials for this article may be downloaded from http://cabn.psychonomic-journals.org/content/supplemental.

Major depressive disorder (MDD) is a recurrent mood disorder. The high rate of recurrence of MDD suggests the presence of stable vulnerability factors that place individuals with a history of major depression at an increased risk for the onset of another episode. Previous research has linked the remitted state, and therefore increased vulnerability for depressive relapse, with difficulties in the use of pleasant autobiographical memories to repair sad mood. In the present study, we examined the neural correlates of these difficulties. Groups of 16 currently euthymic, remitted depressed individuals and 16 healthy (control) women underwent functional magnetic resonance imaging (fMRI) during sad mood induction and during recovery from a sad mood state through recall of mood-incongruent positive autobiographical memories. Sad mood was induced in participants by using film clips; participants then recalled positive autobiographical memories, a procedure previously shown to repair negative affect. During both the sad mood induction and automatic mood regulation, control participants exhibited activation in the left ventrolateral prefrontal cortex (vlPFC) and cuneus; in contrast, remitted participants exhibited a decrease in activation in these regions. Furthermore, exploratory analyses revealed that reduced activation levels during mood regulation predicted a worsening of depressive symptoms at a 20-month follow-up assessment. These findings highlight a dynamic role of the vlPFC and cuneus in the experience and modulation of emotional states and suggest that functional anomalies of these brain regions are associated with a history of, and vulnerability to, depression.

[...]we will model the public health implications of what will happen in the future if present trends in vaccine hesitancy, refusal, and acceptance continue. [...]Commissioners will determine the role of anti-vaccine organisations (and in some cases foreign governments) in suppressing vaccine acceptance through media or political activities. [...]we will make recommendations to shape a new public policy for ensuring high vaccine acceptance in the USA. Texas Children's Center for Vaccine Development, Departments of Pediatrics and Molecular Virology and Microbiology, National School of Tropical Medicine, Baylor College of Medicine, Houston, TX, USA (PJH); Department of Biology, Baylor University, Waco, TX, USA (PJH); Hagler Institute for Advanced Study at Texas A&M University, College Station, TX, USA (PJH); James A Baker III Institute for Public Policy, Rice University, Houston, TX, USA (PJH); Scowcroft Institute of International Affairs, Bush School of Government and Public Service, Texas A&M University, College Station, TX, USA (PJH); The Lancet, New York, NY, USA (REC); Gulf States Health Policy Center, Bayou La Batre, AL, USA (RMB); Department of Health Behavior, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA (NTB); Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA (NTB); Department of Family and Community Health, University of Pennsylvania School of Nursing, and Center for Health Incentives and Behavioral Economics, University of Pennsylvania, Philadelphia, PA, USA (AMB); Department of Health Policy and Management, School of Public Health, Texas A&M University, College Station, TX, USA (TC); New York University Langone School of Medicine, New York University, New York, NY, USA (AC); School of Public Policy, University of California, Riverside, CA, USA (RMC);

Aims/hypothesis Adipose tissue (AT) distribution is a major determinant of mortality and morbidity in obesity. In mice, intra-abdominal transplantation of subcutaneous AT (SAT) protects against glucose intolerance and insulin resistance (IR), but the underlying mechanisms are not well understood. Methods We investigated changes in adipokines, tissue-specific glucose uptake, gene expression and systemic inflammation in male C57BL6/J mice implanted intra-abdominally with either inguinal SAT or epididymal visceral AT (VAT) and fed a high-fat diet (HFD) for up to 17 weeks. Results Glucose tolerance was improved in mice receiving SAT after 6 weeks, and this was not attributable to differences in adiposity, tissue-specific glucose uptake, or plasma leptin or adiponectin concentrations. Instead, SAT transplantation prevented HFD-induced hepatic triacylglycerol accumulation and normalised the expression of hepatic gluconeogenic enzymes. Grafted fat displayed a significant increase in glucose uptake and unexpectedly, an induction of skeletal muscle-specific gene expression. Mice receiving subcutaneous fat also displayed a marked reduction in the plasma concentrations of several proinflammatory cytokines (TNF-α, IL-17, IL-12p70, monocyte chemoattractant protein-1 [MCP-1] and macrophage inflammatory protein-1β [ΜIP-1β]), compared with sham-operated mice. Plasma IL-17 and MIP-1β concentrations were reduced from as early as 4 weeks after transplantation, and differences in plasma TNF-α and IL-17 concentrations predicted glucose tolerance and insulinaemia in the entire cohort of mice ( n  = 40). In contrast, mice receiving visceral fat transplants were glucose intolerant, with increased hepatic triacylglycerol content and elevated plasma IL-6 concentrations. Conclusions/interpretation Intra-abdominal transplantation of subcutaneous fat reverses HFD-induced glucose intolerance, hepatic triacylglycerol accumulation and systemic inflammation in mice.

Glucose-stimulated insulin secretion from beta-cells is a tightly regulated process that requires calcium flux to trigger exocytosis of insulin-containing vesicles. Regulation of calcium handling in beta-cells remains incompletely understood. Gem, a member of the RGK (Rad/Gem/Kir) family regulates calcium channel handling in other cell types, and Gem over-expression inhibits insulin release in insulin-secreting Min6 cells. The aim of this study was to explore the role of Gem in insulin secretion. We hypothesised that Gem may regulate insulin secretion and thus affect glucose tolerance in vivo. Gem-deficient mice were generated and their metabolic phenotype characterised by in vivo testing of glucose tolerance, insulin tolerance and insulin secretion. Calcium flux was measured in isolated islets. Gem-deficient mice were glucose intolerant and had impaired glucose stimulated insulin secretion. Furthermore, the islets of Gem-deficient mice exhibited decreased free calcium responses to glucose and the calcium oscillations seen upon glucose stimulation were smaller in amplitude and had a reduced frequency. These results suggest that Gem plays an important role in normal beta-cell function by regulation of calcium signalling.

Enhancing the social and learning experiences of students with severe disabilities in inclusive classrooms has been a long-standing focus of research, legislative, and advocacy efforts. The authors used a randomized controlled experimental design to examine the efficacy of peer support arrangements to improve academic and social outcomes for 51 students with severe disabilities in high school general education classrooms. Paraprofessionals or special educators recruited, trained, and supported 106 peers to provide individualized academic and social assistance to students with severe disabilities throughout one semester. Compared to students exclusively receiving adult-delivered support (n = 48), students participating in peer support arrangements experienced increased interactions with peers, increased academic engagement, more progress on individualized social goals, increased social participation, and a greater number of new friendships. Moreover, an appreciable proportion of relationships lasted one and two semesters later after the intervention had concluded. These findings challenge prevailing practices for supporting inclusive education and establish the efficacy and social validity of peer support arrangements as a promising alternative to individually assigned paraprofessional support.