BackgroundEquity is one of the major goals of China’s recent health system reform. This study aimed to evaluate the equality of the distribution of health resources and health services between hospitals and primary care institutions.MethodsData of this study were drawn from the China Health Statistical Year Books. We calculated Gini coefficients based on population size and geographic size, respectively, for the indicators: number of institutions, number of health workers and number of beds; and the concentration index (CI) for the indicators: per capita outpatient visits and annual hospitalization rates.ResultsThe Gini coefficients against population size ranged between 0.17 and 0.44 in the hospital sector, indicating a relatively good equality. The primary care sector showed a slightly higher level of Gini coefficients (around 0.45) in the number of health workers. However, inequality was evident in the geographic distribution of health resources. The Gini coefficients exceeded 0.7 in the geographic distribution of institutions, health workers and beds in both the hospital and the primary care sectors, indicating high levels of inequality. The CI values of hospital inpatient care and outpatient visits to primary care institutions were small (ranging from -0.02 to 0.02), indicating good wealth-related equality. The CI values of outpatient visits to hospitals ranged from 0.16 to 0.21, indicating a concentration of services towards the richer populations. By contrast, the CI values of inpatient care in primary care institutions ranged from -0.24 to -0.22, indicating a concentration of services towards the poorer populations. The eastern developed region also had a high internal inequality compared with the other less developed regions.ConclusionSignificant inequality in the geographic distribution of health resources is evident, despite a more equitable per capita distribution of resources. Richer people are more likely to use well-resourced hospitals for outpatient care. By contrast, poorer people are more likely to use poorly-resourced primary care institutions for inpatient care. There is a risk of the emergence of a two-tiered health care delivery system.

No abstract

Glaucoma is the second leading cause of blindness worldwide and elevated intraocular pressure (IOP) is the most important risk factor. High IOP usually occurs as a result of an increase in aqueous humor outflow resistance at the trabecular meshwork (TM). An abnormal TM contributes to the development of glaucoma. Oxidative stress and vascular damage are considered two major cellular factors that lead to alterations in the TM. In this review, we discuss the findings related to oxidative damage to the TM, including the sources of oxidative stress in the TM such as the mitochondria, peroxisomes, endoplasmic reticulum, membrane, cytosol and exogenous factors. We also discuss antioxidants and clinical studies related to protection against oxidative stress in the TM. Although many questions remain unanswered, it is becoming increasingly clear that oxidative stress-induced damage to the TM is related to glaucoma. This may inspire new studies to find better and more stable antioxidants, and better models with which to elucidate the mechanisms involved, and to determine whether in vitro findings translate into in vivo observations. The regulation of the oxidative/redox balance may be the ultimate target for protecting the TM from oxidative stress and preventing glaucoma.

No abstract

Cancer invasion and metastasis depend on accurate and rapid modulation of both chemical and mechanical activities. The S-nitrosylation (SNO) of membrane cytoskeletal cross-linker protein ezrin may regulate the malignant process in a tension-dependent manner. Methods : The level of nitrosylated ezrin in non-small cell lung cancer (NSCLC) tissues and A549 cell line were evaluated by biotin-switch assay. A few cysteine mutated plasmids of ezrin were used to identify active site for SNO. Newly designed ezrin or mutated-ezrin tension probes based on Förster resonance energy transfer (FRET) theory were applied to visually observe real-time tension changes. Cytoskeleton depolymerizing and motor molecular inhibiting experiments were performed to reveal the alternation of the mechanical property of ezrin after SNO. Transwell assays and xenograft mouse model were used to assess aggressiveness of A549 cells in different groups. Fluorescent staining was also applied to examine cellular location and structures. Results : High inducible nitric oxide synthase (iNOS) levels were observed to induce ezrin-SNO, and then promote malignant behaviors of NSCLC cells both in vitro and in vivo. Cys 117 was identified as the only active site for ezrin-SNO. Meanwhile, an increased level of ezrin tension was observed after iNOS-induced SNO. Enhanced ezrin tension was positively correlated with aggressiveness of NSCLC. Moreover, Microfilament (MF) forces instead of microtubule (MT) forces played dominant roles in modulating ezrin tension, especially after ezrin nitrosylation. Conclusion : This study revealed a SNO-associated mechanism underlying the mechanical tension of ezrin. Ezrin-SNO promotes NSCLC cells invasion and metastasis through facilitating mechanical transduction from the cytoskeleton to the membrane. These studies implicate the therapeutic potential by targeting ezrin in the inhibition NSCLC invasion and metastasis.

Background and Aim Incidental pancreatic cystic lesions (PCLs) are being diagnosed more frequently. However, little is known about the prevalence of PCLs in the Chinese population. The aim of the study was to assess the crude prevalence of PCLs in individuals who underwent magnetic resonance imaging (MRI). Methods Data from consecutive patients who underwent MRI without pancreatic indications were included. MRI images were reviewed for the presence of pancreatic cysts. The prevalence of PCLs and high‐risk PCLs in different gender and age groups was calculated. To assess the crude prevalence, the prevalence and demographic data were standardized on the basis of Chinese national population data in 2017. Results A total of 10 987 individuals were included (7344 men). Incidental PCLs were identified in 212 individual (128 men). The prevalence of PCLs was 1.93%, and PCLs were more often discovered in women (1.74% vs 2.31%, P = 0.043). Prevalence increased with age (r = 0.804, P < 0.001). The prevalence of high‐risk PCLs was 0.12% (n = 13). Gender predominance and age distribution showed no difference between high‐risk PCLs and low‐risk PCLs (P = 0.234 and P = 0.855), but cysts located in the pancreatic head were more likely to develop into high‐risk PCLs (P = 0.001). After data standardization, the crude prevalence of PCLs was 1.31%, and PCLs were more often discovered in women (1.11% vs 1.5%, P < 0.001). The crude prevalence of high‐risk PCLs was 0.07%. Conclusion Pancreatic cystic lesions in the Chinese population are not rare. The prevalence of PCLs increased with age and is higher in the female population. The prevalence of high‐risk PCLs should not be ignored.

In healthy myopic subjects, 88.4% and 37% of eyes did not comply with the ISNT rule on RNFL thickness and rim area, respectively. Due to significant low compliance in healthy eyes, the ISNT rule and its variants have limited potential utility in diagnosing glaucoma in myopic subjects.

Recent evidence suggests that chloride channels are critical for cell proliferation, migration, and differentiation. We examined the effects of transforming growth factor (TGF)-β1 on chloride channel expression and associations with human conjunctival fibroblast (HConF) biology. To investigate the potential role of chloride channel (CLC)-2 in migration, transition to myofibroblasts and extracellular matrix (ECM) synthesis of HconF, a small interfering RNA (siRNA) approach was applied. TGF-β1-induced migration and transition of fibroblasts to myofibroblasts characterized by α-smooth muscle actin (α-SMA) expression, supported by increased endogenous expression of CLC-2 protein and mRNA transcripts. ECM (collagen I and fibronectin) synthesis in HConF was enhanced by TGF-β1. CLC-2 siRNA treatment reduced TGF-β1-induced cell migration, transition of fibroblasts to myofibroblasts, and ECM synthesis of HConF. CLC-2 siRNA treatment in the presence of TGF-β1 inhibited phosphorylation of PI3K and Akt in HConF. These findings demonstrate that CLC-2 chloride channels are important for TGF-β1-induced migration, differentiation, and ECM synthesis via PI3K/Akt signaling in HConF.