Prevalence and causes of vision loss in China from 1990 to 2019: findings from the Global Burden of Disease Study 2019.

Background: Vision loss is an important public health issue in China, but a detailed understanding of national and regional trends in its prevalence and causes, which could inform health policy, has not been available. This study aimed to assess the prevalence, causes, and regional distribution of vision impairment and blindness in China in 1990 and 2019.

Methods: Data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 were used to estimate the prevalence of moderate and severe vision impairment and blindness in China and compare with other Group of 20 (G20) countries.

Burden of Neurological Disorders Across the US From 1990-2017: A Global Burden of Disease Study.

Importance: Accurate and up-to-date estimates on incidence, prevalence, mortality, and disability-adjusted life-years (burden) of neurological disorders are the backbone of evidence-based health care planning and resource allocation for these disorders. It appears that no such estimates have been reported at the state level for the US.

Objective: To present burden estimates of major neurological disorders in the US states by age and sex from 1990 to 2017.

Systematic review of interventions for reducing stigma experienced by children with disabilities and their families in low- and middle-income countries: state of the evidence.

Objectives: To identify and assess the evidence for interventions to reduce stigma experienced by children with disabilities and their families in low- and middle-income settings.

Methods: Systematic review of seven databases (MEDLINE, EMBASE, Global Health, PsycINFO, Social Policy and Practice, CINAHL, IBSS) for studies of interventions that aimed to reduce stigma for children with disabilities published from January 2000 to April 2018. Data were extracted on study population, study design, intervention level(s) and target group, and type(s) of stigma addressed.

Assessing the social determinants of health care costs for Medicaid-enrolled adolescents in Washington State using administrative data.

Objective: The study used administrative data to identify the social determinants that have the greatest impact on Medicaid expenditures in adolescence.

Data Sources: Data were compiled using the Washington State Department of Social and Health Services Integrated Client Databases, which link data from state systems including Medicaid claims and social services receipt.

Study Design: Medical system and behavioral health service costs of over 180 000 Medicaid-enrolled adolescents aged 12-17 were measured using integrated administrative data from Washington State.

Preferential Targeting of Lateral Entorhinal Inputs onto Newly Integrated Granule Cells.

Mature dentate granule cells in the hippocampus receive input from the entorhinal cortex via the perforant path in precisely arranged lamina, with medial entorhinal axons innervating the middle molecular layer and lateral entorhinal cortex axons innervating the outer molecular layer. Although vastly outnumbered by mature granule cells, adult-generated newborn granule cells play a unique role in hippocampal function, which has largely been attributed to their enhanced excitability and plasticity (Schmidt-Hieber et al., 2004; Ge et al.

Blocking PirB up-regulates spines and functional synapses to unlock visual cortical plasticity and facilitate recovery from amblyopia.

During critical periods of development, the brain easily changes in response to environmental stimuli, but this neural plasticity declines by adulthood. By acutely disrupting paired immunoglobulin-like receptor B (PirB) function at specific ages, we show that PirB actively represses neural plasticity throughout life. We disrupted PirB function either by genetically introducing a conditional PirB allele into mice or by minipump infusion of a soluble PirB ectodomain (sPirB) into mouse visual cortex.

Developmental Sculpting of Intracortical Circuits by MHC Class I H2-Db and H2-Kb.

Synapse pruning is an activity-regulated process needed for proper circuit sculpting in the developing brain. Major histocompatibility class I (MHCI) molecules are regulated by activity, but little is known about their role in the development of connectivity in cortex. Here we show that protein for 2 MHCI molecules H2-Kb and H2-Db is associated with synapses in the visual cortex.

Synapse elimination and learning rules co-regulated by MHC class I H2-Db.

The formation of precise connections between retina and lateral geniculate nucleus (LGN) involves the activity-dependent elimination of some synapses, with strengthening and retention of others. Here we show that the major histocompatibility complex (MHC) class I molecule H2-D(b) is necessary and sufficient for synapse elimination in the retinogeniculate system. In mice lacking both H2-K(b) and H2-D(b) (K(b)D(b)(-/-)), despite intact retinal activity and basal synaptic transmission, the developmentally regulated decrease in functional convergence of retinal ganglion cell synaptic inputs to LGN neurons fails and eye-specific layers do not form.

Neuroprotection from stroke in the absence of MHCI or PirB.

Recovery from stroke engages mechanisms of neural plasticity. Here we examine a role for MHC class I (MHCI) H2-Kb and H2-Db, as well as PirB receptor. These molecules restrict synaptic plasticity and motor learning in the healthy brain.

CD8+ T cells directed against a viral peptide contribute to loss of motor function by disrupting axonal transport in a viral model of fulminant demyelination.

Demyelination, a pathological hallmark of multiple sclerosis, may be a necessary but not a sufficient condition for motor dysfunction associated with this disease. We favor a neurodegenerative model of multiple sclerosis and suggest that demyelination creates a permissive environment wherein the denuded axon becomes susceptible to immune-mediated injury. Unfortunately, the cellular effectors responsible for eliciting such axonal injury are currently unknown.

Short days increase hypothalamic-pituitary-adrenal axis responsiveness.

Individuals dramatically alter physiology and behavior to adapt to seasonal changes in their environment. To cope with winter stressors such as reduced food availability and low temperatures, central stress responses are presumably modulated at the level of the hypothalamic-pituitary-adrenal (HPA) axis, but the details remain unspecified. We examined the effects of long or short photoperiods (day lengths) on corticosterone responses to restraint, HPA negative feedback sensitivity, glucocorticoid receptor gene expression in the hippocampus, the role of corticosterone in spatial learning, and corticosterone responses to stressors associated with the spatial water maze task in adult male white-footed mice (Peromyscus leucopus).

Absence of perforin expression confers axonal protection despite demyelination.

Current evidence suggests that demyelination may be a necessary but not a sufficient condition for neurologic deficits associated with multiple sclerosis. Axon injury that occurs within the permissive environment of the demyelinated lesion is better correlated with functional deficits, but the mechanisms and cellular effectors of this injury are largely unknown. In an effort to identify potential axon injury mediators, we examined demyelination, motor function, and the number of spinal axons in perforin-deficient mice.