RESUMO
OBJECTIVES: This paper assesses the impact of effective access on out-of-pocket health payments and catastrophic health expenditure. Effective access cannot be attained unless both health services and financial risk protection are accessible, affordable, and acceptable. Therefore, it represents a key determinant in the transition from fragmented health systems to universal coverage that many low- and middle-income countries face. METHODS: We use a definition of effective access as the utilization of health insurance when available. We conducted a cross-sectional analysis using the 2018 Mexican National Health Survey (ENSANUT) at the household level. The analysis is performed in two stages. The first stage is a multinomial analysis that captures the factor associated with choosing effective access against the alternative of paying privately. The second stage consists of an impact analysis regarding the decision of not choosing effective access in terms of out-of-pocket (OOP) health payments and catastrophic health expenditures (CHE). The analysis corrects for both the decision to buy insurance and the decision to pay for health care. RESULTS: We found that, on average, not choosing effective access increases OOP health payments by around 2300 pesos annually. Medicine payments are the most common factor in this increase. Nevertheless, outpatient and medicines health care are the main drivers of the increase in OOP health payments in all insurance beneficiaries. Not having effective access increases the probability of CHE health expenditures by 2.7 p.p. for the case of Social Security Insurance and 4.0 p.p. for Social Government insurance. Household enrolled in Prospera program for the poor are more likely to choose effective access while having household heads with more education and assets value does the opposite. Diabetes illnesses are associated with a higher probability of effective access. CONCLUSION: Improving effective access is a middle step that cannot be disregarded when seeking universal coverage because OOP health payments and catastrophic outcomes are direct consequences. Public insurance in general, has around 50% effective access which remains a challenge in terms of health services utilization and health public policy design, calling for the need of better coordination across insurance types and pooling mechanisms to increase sustainability of needed health services.
Assuntos
Financiamento Pessoal , Cobertura Universal do Seguro de Saúde , Estudos Transversais , Gastos em Saúde , Acessibilidade aos Serviços de Saúde , Humanos , Seguro Saúde , MéxicoRESUMO
Does socioeconomic diversity affect people's perceptions of the income distribution and their preferences for redistribution? I exploit a financial aid reform that drastically raised the share of low-income students at an elite university in Colombia and leverage variation in exposure to low-income peers across cohorts and majors using difference-in-differences. Using original survey data and administrative records, I study how exposure to low-income peers affects high-income students' social networks, perceptions, and preferences. The policy caused high-income students to interact more with low-income students, giving them more accurate perceptions of the income distribution and boosting their support for progressive redistribution.
RESUMO
The mouse 3110001I22Rik gene located in the first intron of Bfar is considered as a Bfar variant coding for the BFARv3 protein. However, it differs from other BFAR isoforms and resembles periphilin 1 (PPHLN1) due to its two (Lge1 and serine-rich) conserved domains. We identified the BFARv3/EGFP-interacting proteins by co-immunoprecipitation coupled to mass spectrometry, which revealed 40S ribosomal proteins (RPS3, RPS14, RPS19, RPS25, RPS27), histones (H1.2, H1.4, H3.3C), proteins involved in RNA processing and splicing (SFPQ, SNRPA1, HNRNPA3, NONO, KHDRBS3), calcium signaling (HPCAL1, PTK2B), as well as HSD17B4, GRB14, POSTN, and MYO10. Co-immunoprecipitation revealed that both Lge1 and Ser-rich domains of BFARv3 were necessary for binding to RNA-interacting factors NONO and SFPQ, known to be components of paraspeckles. Reciprocal co-immunoprecipitation and the proximity ligation assay confirmed that both BFARv3 and PPHLN1 could interact with NONO and SFPQ, suggesting a new function for PPHLN1 as well. BFARv3 and its Lge1 or Ser-rich-deficient mutants preferentially localize in the nucleus. We found an accumulation of BFARv3/EGFP (but not its mutated forms) in the nuclear granules, which was enhanced in response to arsenite treatment and ionizing radiation. Although Bfar v3 is expressed ubiquitously in mouse tissues, its expression is the highest in metaphase II oocytes. The BFARv3 interactome suggests its role in RNA metabolism, which is critical for the transcriptionally silent MII oocyte. Mouse BFARv3 has no ortholog in the human genome, thus it may contribute to the differences between these two species observed in oocyte maturation and early embryonic development.