OBJECTIVEThe discrepancy of diabetes incidence and care between socioeconomic statuses has seldom been studied concurrently in nations with universal health coverage. We aimed to delineate whether income disparity is associated with diabetes incidence and inequality of care under a national health insurance (NHI) program in Asia.RESEARCH DESIGN AND METHODSFrom the Taiwan NHI database in 2000, a representative cohort aged ≥20 years and free of diabetes (n = 600,662) were followed up until 2005. We regarded individuals exempt from paying the NHI premium as being poor. Adjusted hazard ratios (HRs) were used to discover any excess risk of diabetes in the poor population. The indicators used to evaluate quality of diabetes care included the proportion of diabetic patients identified through hospitalization, visits to diabetes clinics, and completion of recommended diabetes tests.RESULTSThe incidence of type 2 diabetes in the poor population was 20.4 per 1,000 person-years (HR, 1.5; 95% CI, 1.3–1.7). Compared with their middle-income counterparts, the adjusted odds ratio (OR) for the poor population incidentally identified as having diabetes through hospitalization was 2.2 (P < 0.001). Poor persons with diabetes were less likely to visit any diabetes clinic (OR, 0.4; P < 0.001). The ORs for the poor population with diabetes to receive tests for glycated hemoglobin, low-density lipoprotein cholesterol, triglycerides, and retinopathy were 0.6 (0.4–0.9), 0.4 (0.2–0.7), 0.5 (0.4–0.8), and 0.4 (0.2–0.9), respectively.CONCLUSIONSPoverty is associated not only with higher diabetes incidence but also with inequality of diabetes care in a northeast Asian population, despite universal health coverage.

Objective. The expression of autoimmunity in mice deficient in programmed death 1 (PD-1) suggests that PD-1 is a candidate gene involved in the development of human autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). We therefore tested the potential association between PD-1 and the development of SLE and RA by conducting case-control genetic-association studies.Methods. Ninety-eight SLE patients, 84 RA patients, and sex-matched control subjects for each disease group were recruited and genotyped for a singlenucleotide polymorphism, C؉872T, in the human PD-1 gene. The significance of the association of the PD-1 gene with SLE or with RA was analyzed by statistical tests for the difference in genotype distribution between disease and control groups.Results. The human PD-1 gene was found to be significantly associated with disease development in RA patients, but not SLE patients. The risk of RA development appeared to be significantly increased by carriage of the T allele (odds ratio 3.32, P < 0.0001) or the C/T genotype (odds ratio 3.52, P < 0.00005).Conclusion. The PD-1 gene is significantly associated with RA susceptibility, suggesting the possibility that PD-1 may contribute to the pathogenesis of RA.Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are two human autoimmune diseases that are mediated by damaging immune overreactivity to self antigens. Although the pathogenesis of SLE and RA remains unclear, it is possible that dysregulated lymphocyte activation initiates the breakdown of tolerance and predisposes the patient to the development of these autoimmune diseases, because lymphocyte activation appears to be governed by immunostimulatory and immunoinhibitory signals that are delivered through lymphocyte surface receptors. More solid evidence to support this hypothesis comes from the fact that autoimmune diseases can develop in mice that have either an overexpression of a stimulatory receptor or a deficiency of an inhibitory receptor. However, further efforts toward establishing a correlation between each immunoregulatory receptor and human autoimmune diseases are still needed in order to gain more insight into the disease pathogenesis and to develop better therapeutic strategies.Programmed death 1 (PD-1), which was originally identified in a T cell line undergoing activationinduced cell death, is a CD28 family member that contains a cytoplasmic immunoreceptor tyrosine-based inhibitory motif and is expressed on the surface of activated T cells and B cells (1-5). As an immunoinhibitory receptor, PD-1 has been shown to inhibit lymphocyte activation and cytokine production after interacting with its ligands PDL-1 (B7-H1) and PDL-2 (B7-DC) (6-10). The immunoinhibitory function of PD-1 was further supported by the observation that mice deficient in PD-1 expression developed autoimmune diseases, despite having distinct phenotypes on different genetic backgrounds. C57BL/6 mice with PD-1 deficiency had an increased incidence of progressive glomerulonephrit...

Evidence is limited regarding the effect of diagnosis-to-treatment interval (DTI) on the survival of colorectal cancer (CRC) patients. In addition, previous studies on treatment delay and CRC survival have largely grouped patients from all stages (I-IV) into one cohort. Our study provides analysis on each stage individually. We conducted a retrospective cohort study with 39,000 newly diagnosed CRC patients obtained from the Taiwan Cancer Registry Database from 2004–2010 to examine the effect of DTIs on overall survival. DTIs were divided into 3 groups: ≤ 30 days (36,115 patients, 90.5% of study patients), 31–150 days (2,533, 6.4%), and ≥ 151 days (1,252, 3.15%). Risk of death was increased for DTI 31–150 days (hazard ratio 1.51; 95% confidence interval 1.43–1.59) and DTI ≥ 151 days (1.64; 1.54–1.76) compared to DTI ≤ 30. This risk was consistent across all cancer stages. Additional factors that increased risk of death include male gender, age >75, Charlson Comorbidity Index ≥7, other catastrophic illnesses, lack of multidisciplinary team involvement, and treatment in a low volume center. From these results, we advise that the DTI for all CRC patients, regardless of cancer staging, should be 30 days or less.

Apart from clinical features, nutritional factors also had a significant influence on the survival of patients with oral cancer. Therefore, good nutritional status is crucial for patients with oral cancer in improving their survival.