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Background: Vision impairment (VI) and depression are highly prevalent among adults. However, few nationally representative studies from China on the self-reported VI and its association with depression symptoms. Aims: This study re-estimated the relationship between self-reported VI and depression symptoms. Methods: In this analysis, 62,525 respondents from the China Health and Retirement Longitudinal Study 2011–2018 were included. Based on self-reports, respondents with VI were allocated to distance VI (DVI), near VI (NVI), both distance and near VI (DNVI), or a blindness group. Multivariable pooled logistic regression models were used to evaluate the groups' odds ratios (ORs) for depression symptoms and self-reported VI. Results: Overall, 35.9% of the respondents were self-reported VI. DVI (OR: 1.51, 95% confidence interval [95% CI]: 1.28–1.79) and DNVI (OR: 1.51, 95% CI: 1.21–1.88) showed the highest ORs for depression symptoms, followed by NVI (OR: 1.31, 95% CI: 1.11–1.54). Depression symptoms were associated with a significantly increased risk of DVI (OR: 1.49, 95% CI: 1.26–1.76), DNVI (OR: 1.49, 95% CI: 1.20–1.86), and NVI (OR: 1.29, 95% CI: 1.10–1.52), respectively. However, these associations between self-reported blindness and depression symptoms were not significant. All models provided similar results by excluding respondents aged 45–59 years. Conclusion: Self-reported DVI, NVI, and DNVI are associated with depression symptoms. A strong reverse association was found between depression and self-reported DVI, NVI, and DNVI, but not for blindness. Our findings emphasize the urgent need for depression screening for self-reported VI among Chinese adults.

Background Tumor markers CYFRA21-1, CEA, NSE, CA125, pro-GRP and SCC are routinely used for lung cancer. However, there has been no systematic evaluation of these markers in the same cohort. The aim of this study was to evaluate the diagnostic and therapeutic monitoring value of these markers.Methods The levels of 6 serum tumor markers were measured in 392 patients, including 308 patients with non-small cell lung cancer (NSCLC) and 84 with small cell lung cancer (SCLC), and 116 patients with benign lung diseases and 144 healthy controls. 34 patients were followed up after operation and chemotherapy. Multiple logistic models and receiver operating characteristic (ROC) curves were used to evaluate their diagnostic value.Results CEA, NSE, CA125 and pro-GRP in SCLC, and CYFRA21-1 as well as CEA in NSCLC, were higher than those in control groups. The level of CEA and CA125 were related to the clinical stages of NSCLC. Pro-GRP was significantly increased in extensive disease (ED) compared with limited disease (LD) in SCLC. CYFRA21-1 was reduced after the third and fifth treatment cycle respectively in patients who undergoing operation and without operation. NSE and pro-GRP were reduced significantly after the second and third treatment cycles, respectively.Conclusions CEA, NSE, CA125 and pro-GRP could serve as biomarkers for SCLC, and CEA and CYFRA21-1 could serve as biomarkers for NSCLC. Pro-GRP, CA125 and CEA were related to the clinical stages of lung cancer. CYFRA21-1, NSE and pro-GRP could be used for monitoring the effect of chemotherapy.

Quantitative agreement has been found between observed and calculated charge mobilities through organic conductors, despite the use of many assumptions in the calculations, including: the relative strength of the intermolecular electronic coupling to the reorganization energy driving charge localization, the treatment of site variability in the material, the involvement of tunneling processes during charge hopping between sites, the use of weak-coupling-based perturbation theory to determine hopping rates, the residence times for charges on sites, the effect of the large field strengths used in experimental studies, the general appropriateness of simple one-dimensional diffusion modeling approaches, and the involvement of molecular excited states of the ions. We investigate the impact of these assumptions, concluding that allmay be very significant. In some cases, methodological options are considered, and optimum procedures are determined, showing that (i) the use of Koopmans' theorem to estimate intermolecular couplings in solids is problematic and (ii) the correct expression for the residence lifetime of a charge on a crystal site. These conclusions are drawn from simulations of anisotropic charge mobilities through the β phase of mer-tris(8-hydroxyquinolinato)aluminum(III) (Alq3) crystal, a material commonly used in OLED applications. Calculations are compared that determine mobilities at finite applied field from drift velocities through either semianalytical solutions of the master equation or else kinetic Monte Carlo simulations, as well as those that determine mobilities from multidimensional diffusion coefficients at zero field by Monte Carlo and those that analytically solve simplified one-dimensional diffusion models. For crystalline Alq3 itself, the calculations predict electron mobilities that are 4–6 orders of magnitude larger than those predicted by similar methods for amorphous Alq3, in agreement with experimental findings. This work vindicates recent theories describing the poor mobilities of the amorphous material, forming a complete basic picture for Alq3 conductivity.

Tissue inhibitor of metalloproteinase-3 (TIMP-3) is one of a family of proteins inhibiting matrix metalloproteinases, which has also been identified as a mediator for checking inflammation. Meanwhile, it is well known that inflammation causes the activation of the immune response. However, it is not clear whether TIMP-3 plays a role in the immune system. In the present study, we demonstrated a novel function of TIMP-3 in Th1/Th2 polarization through its influence on the antigen-presenting cells. First, TIMP-3 was found strikingly up-regulated by IL-4 during the differentiation of human dendritic cells via the p38MAPK pathway. Second, the expression of costimulatory molecule-CD86 was repressed by TIMP-3. Besides, the induction of IL-12 in matured dendritic cells was significantly inhibited in a PI3K-dependent manner. Furthermore, dendritic cells matured in the presence of TIMP-3 could stimulate allogeneic naive T helper (Th) cells to display a prominent Th2 polarization. Importantly, in an autoimmune disorder–primary immune thrombocytopenia, TIMP-3 showed a statistically positive correlation with IL-4 and platelet count, but a negative correlation with IFN-γ in patient blood samples. Collectively, these in vitro and in vivo data clearly suggested a novel role of TIMP-3 in Th1/Th2 balance in humans.

Tissue inhibitor of metalloproteinase-3 (TIMP-3) is one of a family of proteins inhibiting matrix metalloproteinases, which has also been identified as a mediator for checking inflammation. Meanwhile, it is well known that inflammation causes the activation of the immune response. However, it is not clear whether TIMP-3 plays a role in the immune system. In the present study, we demonstrated a novel function of TIMP-3 in Th1/Th2 polarization through its influence on the antigen-presenting cells. First, TIMP-3 was found strikingly up-regulated by IL-4 during the differentiation of human dendritic cells via the p38MAPK pathway. Second, the expression of costimulatory molecule-CD86 was repressed by TIMP-3. Besides, the induction of IL-12 in matured dendritic cells was significantly inhibited in a PI3K-dependent manner. Furthermore, dendritic cells matured in the presence of TIMP-3 could stimulate allogeneic naive T helper (Th) cells to display a prominent Th2 polarization. Importantly, in an autoimmune disorder–primary immune thrombocytopenia, TIMP-3 showed a statistically positive correlation with IL-4 and platelet count, but a negative correlation with IFN-γ in patient blood samples. Collectively, these in vitro and in vivo data clearly suggested a novel role of TIMP-3 in Th1/Th2 balance in humans.

Hypoxia is a major characteristic of the tumor microenvironment, and its effects on immune cells are proposed to be important factors for the process of tumor immune escape. It has been reported that hypoxia affects the function of dendritic cells and the antitumor function of T cells. Here we discuss the effects of hypoxia on T-cell survival. Our results showed that hypoxia induced apoptosis of T cells. Adenosine and adenosine receptors (AR) are important to the hypoxia-related signaling pathway. Using AR agonists and antagonists, we demonstrated that hypoxia-induced apoptosis of T cells was mediated by A2a and A2breceptors. Furthermore, we are the first, to our knowledge, to report that hypoxia significantly inhibited the expression of chemokine C receptor 7 (CCR7) of T cells via the A2R signal pathway, perhaps representing a mechanism of hypoxia-induced apoptosis of T cells. Collectively, our research demonstrated that hypoxia induces T-cell apoptosis by the A2R signaling pathway partly by suppressing CCR7. Blocking the A2R signaling pathway and/or activation of CCR7 can increase the anti-apoptosis function of T cells and may become a new strategy to improve antitumor potential.