BackgroundChina has the world's largest floating (migrant) population, which has characteristics largely different from the rest of the population. Our goal is to study health insurance coverage and its impact on medical cost for this population.MethodsA telephone survey was conducted in 2012. 644 subjects were surveyed. Univariate and multivariate analysis were conducted on insurance coverage and medical cost.Results82.2% of the surveyed subjects were covered by basic insurance at hometowns with hukou or at residences. Subjects' characteristics including age, education, occupation, and presence of chronic diseases were associated with insurance coverage. After controlling for confounders, insurance coverage was not significantly associated with gross or out-of-pocket medical cost.ConclusionFor the floating population, health insurance coverage needs to be improved. Policy interventions are needed so that health insurance can have a more effective protective effect on cost.

In the mammalian neocortex, projection neuron types are sequentially generated by the same pool of neural progenitors. How neuron type specification is related to developmental timing remains unclear. To determine whether temporal gene expression in neural progenitors correlates with neuron type specification, we performed single-cell RNA sequencing (scRNA-Seq) analysis of the developing mouse neocortex. We uncovered neuroepithelial cell enriched genes such as Hmga2 and Ccnd1 when compared to radial glial cells (RGCs). RGCs display dynamic gene expression over time; for instance, early RGCs express higher levels of Hes5, and late RGCs show higher expression of Pou3f2. Interestingly, intermediate progenitor cell marker gene Eomes coexpresses temporally with known neuronal identity genes at different developmental stages, though mostly in postmitotic cells. Our results delineate neural progenitor cell diversity in the developing mouse neocortex and support that neuronal identity genes are transcriptionally evident in Eomes-positive cells.

To assess whether and to what extent the anti-poverty relocation and settlement program (APRSP) in China will be able to resolve the development dilemma of ecosystem conservation and human wellbeing, it is important to study the effects of policy on rural households in terms of the income generation from ecosystem services (ES). We constructed an index of dependence on ecosystem services (IDES) to evaluate the dependence of households’ net income generation on ecosystem services. Using data collected from South Shaanxi Province, we examined the effects of the relocation program on rural households’ IDES. We find that this relocation may benefit the ecosystem by significantly decreasing participants’ IDES. Relocation households have higher net incomes than non-relocation households from total ecosystem services, provisioning services, regulating services, and cultural services as well as socio-economic activities. There are significant differences in IDES between groups with different relocation and resettlement characteristics. The anti-poverty relocation program optimized the rural households’ income structure by increasing the proportion of income from socio-economic activities while reducing the proportion of income from ecosystem services. This study provides new evidence for evaluating eco-conservation and development policies by linking ecosystem services and human well-being at a micro scale. We also address the policy implications of our analysis for anti-poverty relocation programs.

Adducins interconnect spectrin and actin filaments to form polygonal scaffolds beneath the cell membranes and form ring-like structures in neuronal axons. Adducins regulate mouse neural development, but their function in the human brain is unknown. Methods: We used exome sequencing to uncover ADD1 variants associated with intellectual disability (ID) and brain malformations. We studied ADD1 splice isoforms in mouse and human neocortex development with RNA sequencing, super resolution imaging, and immunoblotting. We investigated 4 variant ADD1 proteins and heterozygous ADD1 cells for protein expression and ADD1-ADD2 dimerization. We studied Add1 functions in vivo using Add1 knockout mice. Results: We uncovered loss-of-function ADD1 variants in 4 unrelated individuals affected by ID and/or structural brain defects. Three additional de novo copy number variations covering the ADD1 locus were associated with ID and brain malformations. ADD1 is highly expressed in the neocortex and the corpus callosum, whereas ADD1 splice isoforms are dynamically expressed between cortical progenitors and postmitotic neurons. Human variants impair ADD1 protein expression and/or dimerization with ADD2. Add1 knockout mice recapitulate corpus callosum dysgenesis and ventriculomegaly phenotypes. Conclusion: Our human and mouse genetics results indicate that pathogenic ADD1 variants cause corpus callosum dysgenesis, ventriculomegaly, and/or ID.

No abstract