This article defines the concept of \"multidimensional health poverty,\" considering both the monetary aspects and multidimensional health deprivation of health poverty. Moreover, we set up the multidimensional health poverty index (MHPI) to measure health poverty in China by revising the traditional A-F MPI method, specifically we use the Catastrophic Health Expenditure (CHE) as a sufficient condition and income poverty as a necessary condition, and take physical, mental, and social health into account. The measurement result evidences that physical health, monetary dimensions (CHE and income poverty), and mental health contribute most to health poverty in China. In addition, the MHPI is significantly higher in rural areas than urban because of higher out-of-pocket medical payments and health deprivation in more dimensions. Compared with the traditional method, the MHPI is more accurate, stable, and comprehensive, making it more suitable for measuring health poverty.

China has built a social medical insurance system that covers the entire population so as to reduce the impact of diseases on individuals and families. Although the decline in the incidence of catastrophic health expenditures (CHEs) in China is encouraging, this issue remains important. On the basis of considering selectivity bias and heterogeneity, we applied propensity score matching (PSM) to analyze the 2018 data from the China Family Panel Studies. We assigned CHE households and non-CHE households to the treatment group and the control group, respectively, and used non-random data to simulate a randomized trial to investigate the impact of CHE on household consumption in China. The results of this study indicate that, when the threshold is set at 40%, the consumption of households experiencing CHEs (CHE household) is significantly lower than that of households not experiencing CHEs (non-CHE households) and that CHEs have a significant negative impact on other household consumption and a significant impact on the household property and debt. This effect still exists when the threshold is set lower, with household essential consumption most affected. The occurrence of CHEs leads to a reduction in household consumption and a significantly worsening financial situation for the CHE households, impacting the basic quality of life of the families. Therefore, it is necessary to further reform the medical and health system to reduce the high medical expenses.

Cholinesterases are key enzymes in central and peripheral cholinergic nerve system functioning on nerve impulse transmission in animals. Though cholinesterases have been identified in most vertebrates, the knowledge about the variable numbers and multiple functions of the genes is still quite meagre in invertebrates, especially in scallops. In this study, the complete cholinesterase (ChE) family members have been systematically characterized in Yesso scallop (Patinopecten yessoensis) via whole-genome scanning through in silico analysis. Ten ChE family members in the genome of Yesso scallop (designated PyChEs) were identified and potentially acted to be the largest number of ChE in the reported species to date. Phylogenetic and protein structural analyses were performed to determine the identities and evolutionary relationships of these genes. The expression profiles of PyChEs were determined in all developmental stages, in healthy adult tissues, and in mantles under low pH stress (pH 6.5 and 7.5). Spatiotemporal expression suggested the ubiquitous functional roles of PyChEs in all stages of development, as well as general and tissue-specific functions in scallop tissues. Regulation expressions revealed diverse up- and down-regulated expression patterns at most time points, suggesting different functional specialization of gene superfamily members in response to ocean acidification (OA). Evidences in gene number, phylogenetic relationships and expression patterns of PyChEs revealed that functional innovations and differentiations after gene duplication may result in altered functional constraints among PyChEs gene clusters. Collectively, our results provide the potential clues that the selection pressures coming from the environment were the potential inducement leading to function allocation of ChE family members in scallop.

To evaluate the trend of catastrophic health expenses (CHE) for inpatient care in relation to the commencement of the New Cooperative Medical Scheme (NCMS) in rural China from 2003 to 2013, and the roles of NCMS in protecting affected households from CHE.
We assessed the 10-year trend of the incidence and severity of CHE in rural households with hospitalised members using data from the Chinese National Health Services Survey. Generalised estimating equations were used to estimate the OR and 95% CI of the association between incidence rates of CHE ([Formula: see text]) and NCMS reimbursement.
The incidence and severity of CHE after NCMS reimbursement both decreased and their changes increased rapidly from 2003 to 2013. After adjustment of the covariates, [Formula: see text] before reimbursement was significantly higher than that after reimbursement, and the OR (95% CI) was 1.50 (1.24 to 1.81), 1.79 (1.69 to 1.90) and 2.94 (2.77 to 3.11) in 2003, 2008 and 2013, respectively.
The incidence and severity of CHE both reduced after NCMS reimbursements in each year. Excluding some confounding factors, [Formula: see text] was significantly associated with NCMS reimbursement. NCMS partly protected the rural households with hospitalised members from CHE. However, the inequalities between different income groups still existed. [Formula: see text] in rural households with hospitalised members was still rather high in 2003, 2008 and 2013 even though they were covered by NCMS. This study will provide suggestions for further reforms in China and guidance for other low-income/middle-income countries.

The quaternary benzo[c]phenanthridine alkaloid, chelerythrine (CHE), is of great practical and research interest because of its pronounced, widespread physiological effects, primarily antimicrobial and anti-inflammatory, arising from its ability to interact with proteins and DNA. Although CHE was originally shown to possess anti-inflammatory properties, its effects on acute gastric ulcer have not been previously explored. The aim of the present study is to evaluate the protective effect of CHE on ethanol induced gastric ulcer in mice. Administration of CHE at doses of 1, 5 and 10mg/kg bodyweight prior to ethanol ingestion dose-dependently inhibited gastric ulcer. The gastric mucosal lesion was assessed by ulcer area, gastric juice acidity, myeloperoxidase (MPO) activities, macroscopic and histopathological examinations. CHE significantly reduced the gastric ulcer index, myeloperoxidase activities, macroscopic and histological score in a dose-dependent manner. In addition, CHE also significantly inhibited nitric oxide (NO) concentration, pro-inflammatory interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) level in serum and gastric mucosal in the mice exposed to ethanol induced ulceration in a dose-dependent manner. In addition, immunohistochemical analysis revealed that CHE markedly attenuated the overexpression of nuclear factor-κB in gastric mucosa of mice. It was concluded that CHE represents a potential therapeutic option to reduce the risk of gastric ulceration. In addition, acute toxicity study revealed no abnormal sign to the mice treated with CHE (15mg/kg). These findings suggest that the gastroprotective activity of CHE might contribute in adjusting the inflammatory cytokine by regulating the NF-κB signalling pathway.

The extensive neuroprotective effects of estrogen against Alzheimer\'s disease (AD) have been proven in numerous laboratory studies. However, in clinical studies, the exact role of estrogen in AD is still ambiguous. Some evidences even suggested the high levels of estrogen or estrogen replacement treatment increased the risk of AD. Thus, there must be other factors affecting the neuroprotective effects of estrogen. Multiple enzymes and receptor proteins are involved in the biosynthesis, metabolism and signaling pathways of estrogen, and mediate the beneficial effects of estrogen on AD. Previous studies have suggested some polymorphisms of genes encoding these enzymes and proteins are associated with the risk of AD. In addition to the genes associated with estrogen biosynthesis and metabolism and the genes encoding estrogen receptor proteins, some other genes also modulate the effects of estrogen on AD, or interact with other estrogen-associated genes on the progress of AD. The gene-hormone and gene-gene interactions may be key to unraveling the conflicting results regarding the effect of estrogen on AD. In this paper, we will review and discuss the associations between polymorphisms of these genes and their interactions and the susceptibility to AD. A better understanding of these estrogen-associated genes is significant to explore the pathogenesis of AD.