Towards universal health coverage: achievements and challenges of 10 years of healthcare reform in China.

Universal health coverage (UHC) has been identified as a priority for the global health agenda. In 2009, the Chinese government launched a new round of healthcare reform towards UHC, aiming to provide universal coverage of basic healthcare by the end of 2020. We conducted a secondary data analysis and combined it with a literature review, analysing the overview of UHC in China with regard to financial protection, coverage of health services and the reported coverage of the WHO and the World Bank UHC indicators. The results include the following: out-of-pocket expenditures as a percentage of current health expenditures in China have dropped dramatically from 60.13% in 2000 to 35.91% in 2016; the health insurance coverage of the total population jumped from 22.1% in 2003 to 95.1% in 2013; the average life expectancy increased from 72.0 to 76.4, maternal mortality dropped from 59 to 29 per 100 000 live births, the under-5 mortality rate dropped from 36.8 to 9.3 per 1000 live births, and neonatal mortality dropped from 21.4 to 4.7 per 1000 live births between 2000 and 2017; and so on. Our findings show that while China appears to be well on the path to UHC, there are identifiable gaps in service quality and a requirement for ongoing strengthening of financial protections. Some of the key challenges remain to be faced, such as the fragmented and inequitable health delivery system, and the increasing demand for high-quality and value-based service delivery. Given that China has committed to achieving UHC and 'Healthy China 2030', the evidence from this study can be suggestive of furthering on in the UHC journey and taking the policy steps necessary to secure change

Towards universal health coverage: lessons from 10 years of healthcare reform in China.

Universal health coverage (UHC) is driving the global health agenda. Many countries have embarked on national policy reforms towards this goal, including China. In 2009, the Chinese government launched a new round of healthcare reform towards UHC, aiming to provide universal coverage of basic healthcare by the end of 2020. The year of 2019 marks the 10th anniversary of China's most recent healthcare reform. Sharing China's experience is especially timely for other countries pursuing reforms to achieve UHC. This study describes the social, economic and health context in China, and then reviews the overall progress of healthcare reform (1949 to present), with a focus on the most recent (2009) round of healthcare reform. The study comprehensively analyses key reform initiatives and major achievements according to four aspects: health insurance system, drug supply and security system, medical service system and public health service system. Lessons learnt from China may have important implications for other nations, including continued political support, increased health financing and a strong primary healthcare system as basis

Patterns of Insertion and Deletion in Mammalian Genomes

Nucleotide insertions and deletions (indels) are responsible for gaps in the sequence alignments. Indel is one of the major sources of evolutionary change at the molecular level. We have examined the patterns of insertions and deletions in the 19 mammalian genomes, and found that deletion events are more common than insertions in the mammalian genomes. Both the number of insertions and deletions decrease rapidly when the gap length increases and single nucleotide indel is the most frequent in all indel events. The frequencies of both insertions and deletions can be described well by power law

Effects of sunlight on tundra nitrous oxide and methane fluxes in maritime Antarctica

The relationships of nitrous oxide (N2O) and methane (CH4) emissions to other environmental parameters have been studied extensively in Antarctic terrestrial ecosystems. However, the effects of sunlight on soil N2O and CH4 fluxes are neglected across the Antarctic tundra. Here, fluxes of N2O and CH4 from maritime Antarctic tundra soils were measured in the absence and presence of sunlight during three summers. The N2O fluxes averaged −4.6±1.2 μg·m−2·h−1 in the absence of sunlight and 5.7±1.5 μg·m−2·h−1 in its presence; CH4 fluxes averaged 119.8±24.5 μg·m−2·h−1 (absence) and −40.5±28.3 μg·m−2·h−1 (presence). The correlations between N2O and CH4 fluxes and other environmental variables (e.g., soil moisture, temperature, organic and inorganic material) were not statistically significant (P>0.05) at all sites. On average, sunlight significantly increased N2O emissions and CH4 uptake by 10.3 μg·m−2·h−1 and 160.3 μg·m−2·h−1, respectively. This study indicates that sunlight is critical for accurately estimating N2O and CH4 budgets from maritime Antarctica and necessary for constraining the role of their emissions from tundra soil

Up-regulation of LCN2 in the anterior cingulate cortex contributes to neural injury-induced chronic pain

Chronic pain caused by disease or injury affects more than 30% of the general population. The molecular and cellular mechanisms underpinning the development of chronic pain remain unclear, resulting in scant effective treatments. Here, we combined electrophysiological recording, in vivo two-photon (2P) calcium imaging, fiber photometry, Western blotting, and chemogenetic methods to define a role for the secreted pro-inflammatory factor, Lipocalin-2 (LCN2), in chronic pain development in mice with spared nerve injury (SNI). We found that LCN2 expression was upregulated in the anterior cingulate cortex (ACC) at 14 days after SNI, resulting in hyperactivity of ACC glutamatergic neurons (ACCGlu) and pain sensitization. By contrast, suppressing LCN2 protein levels in the ACC with viral constructs or exogenous application of neutralizing antibodies leads to significant attenuation of chronic pain by preventing ACCGlu neuronal hyperactivity in SNI 2W mice. In addition, administering purified recombinant LCN2 protein in the ACC could induce pain sensitization by inducing ACCGlu neuronal hyperactivity in naïve mice. This study provides a mechanism by which LCN2-mediated hyperactivity of ACCGlu neurons contributes to pain sensitization, and reveals a new potential target for treating chronic pain

Inferring the Individual Psychopathologic Deficits With Structural Connectivity in a Longitudinal Cohort of Schizophrenia.

The prediction of schizophrenia-related psychopathologic deficits is exceedingly important in the fields of psychiatry and clinical practice. However, objective association of the brain structure alterations to the illness clinical symptoms is challenging. Although, schizophrenia has been characterized as a brain dysconnectivity syndrome, evidence accounting for neuroanatomical network alterations remain scarce. Moreover, the absence of generalized connectome biomarkers for the assessment of illness progression further perplexes the prediction of long-term symptom severity. In this paper, a combination of individualized prediction models with quantitative graph theoretical analysis was adopted, providing a comprehensive appreciation of the extent to which the brain network properties are affected over time in schizophrenia. Specifically, Connectome-based Prediction Models were employed on Structural Connectivity (SC) features, efficiently capturing individual network-related differences, while identifying the anatomical connectivity disturbances contributing to the prediction of psychopathological deficits. Our results demonstrated distinctions among widespread cortical circuits responsible for different domains of symptoms, indicating the complex neural mechanisms underlying schizophrenia. Furthermore, the generated models were able to significantly predict changes of symptoms using SC features at follow-up, while the preserved SC features suggested an association with improved positive and overall symptoms. Moreover, cross-sectional significant deficits were observed in network efficiency and a progressive aberration of global integration in patients compared to healthy controls, representing a group-consensus pathological map, while supporting the dysconnectivity hypothesis

CD8(+) T Cells Involved in Metabolic Inflammation in Visceral Adipose Tissue and Liver of Transgenic Pigs

Anti-inflammatory therapies have the potential to become an effective treatment for obesity-related diseases. However, the huge gap of immune system between human and rodent leads to limitations of drug discovery. This work aims at constructing a transgenic pig model with higher risk of metabolic diseases and outlining the immune responses at the early stage of metaflammation by transcriptomic strategy. We used CRISPR/Cas9 techniques to targeted knock-in three humanized disease risk genes, GIPR(dn) , hIAPP and PNPLA3(I148M) . Transgenic effect increased the risk of metabolic disorders. Triple-transgenic pigs with short-term diet intervention showed early symptoms of type 2 diabetes, including glucose intolerance, pancreatic lipid infiltration, islet hypertrophy, hepatic lobular inflammation and adipose tissue inflammation. Molecular pathways related to CD8(+) T cell function were significantly activated in the liver and visceral adipose samples from triple-transgenic pigs, including antigen processing and presentation, T-cell receptor signaling, co-stimulation, cytotoxicity, and cytokine and chemokine secretion. The similar pro-inflammatory signaling in liver and visceral adipose tissue indicated that there might be a potential immune crosstalk between the two tissues. Moreover, genes that functionally related to liver antioxidant activity, mitochondrial function and extracellular matrix showed distinct expression between the two groups, indicating metabolic stress in transgenic pigs' liver samples. We confirmed that triple-transgenic pigs had high coincidence with human metabolic diseases, especially in the scope of inflammatory signaling at early stage metaflammation. Taken together, this study provides a valuable large animal model for the clinical study of metaflammation and metabolic diseases.Peer reviewe