The paper summarized the compound medical insurance payment system under a ceiling control with Shenzhen characteristics.This practice features ceiling control,prepaid at year beginning,multiple payment methods,monthly payment,year-end closing,and reward for surplus.The following measures have been implemented,namely controlling the total amount,compound payment mode,setting up the scientific and reasonable payment standards and establishing a perfect supervision system.This reform has achieved such outcomes as accessibility of the insured people to primary medical insurance,balance for the medical insurance fund,curbing of rapid rise of medical expenses,progress in the policy of first contact in the community health organization,promoting the development of the health system and raising satisfaction among the insured people year by year.

In order to set up a medical security system suitable for laborers and solve for them the problem of inadequate and expensive medical services,the city of Shenzhen started on March 1,2005(apilot) cooperative medical care for laborers in the four neighborhoods of Buji,Longgang,Longhua and Shajing on the basis of an earlier model.The new model,which stipulated that each person paying 12 yuan each month,with the employer paying 8 yuan and the individual laborer paying 4 yuan,was entitled to both outpatient and inpatient medical services,was popular with both businesses and laborers.At present the number of people participating in the new model of cooperative medical care for laborers exceeded 1 million,the number of designated medical institutions was gradually increasing,and medical expenses were put under control.

Glycolytic metabolism enzymes have been implicated in the immunometabolism field through changes in metabolic status. PGK1 is a catalytic enzyme in the glycolytic pathway. Here, we set up a high-throughput screen platform to identify PGK1 inhibitors. DC-PGKI is an ATP-competitive inhibitor of PGK1 with an affinity of K _d = 99.08 nmol/L. DC-PGKI stabilizes PGK1 in vitro and in vivo, and suppresses both glycolytic activity and the kinase function of PGK1. In addition, DC-PGKI unveils that PGK1 regulates production of IL-1β and IL-6 in LPS-stimulated macrophages. Mechanistically, inhibition of PGK1 with DC-PGKI results in NRF2 (nuclear factor-erythroid factor 2-related factor 2, NFE2L2) accumulation, then NRF2 translocates to the nucleus and binds to the proximity region of Il-1β and Il-6 genes, and inhibits LPS-induced expression of these genes. DC-PGKI ameliorates colitis in the dextran sulfate sodium (DSS)-induced colitis mouse model. These data support PGK1 as a regulator of macrophages and suggest potential utility of PGK1 inhibitors in the treatment of inflammatory bowel disease.

The global COVID-19 coronavirus pandemic has infected over 109 million people, leading to over 2 million deaths up to date and still lacking of effective drugs for patient treatment. Here, we screened about 1.8 million small molecules against the main protease (M^pro) and papain like protease (PL^pro), two major proteases in severe acute respiratory syndrome-coronavirus 2 genome, and identified 1851M^pro inhibitors and 205 PL^pro inhibitors with low nmol/l activity of the best hits. Among these inhibitors, eight small molecules showed dual inhibition effects on both M^pro and PL^pro, exhibiting potential as better candidates for COVID-19 treatment. The best inhibitors of each protease were tested in antiviral assay, with over 40% of M^pro inhibitors and over 20% of PL^pro inhibitors showing high potency in viral inhibition with low cytotoxicity. The X-ray crystal structure of SARS-CoV-2 M^pro in complex with its potent inhibitor 4a was determined at 1.8 Å resolution. Together with docking assays, our results provide a comprehensive resource for future research on anti-SARS-CoV-2 drug development.
Humans ; Antiviral Agents/chemistry* ; COVID-19 ; COVID-19 Drug Treatment ; High-Throughput Screening Assays ; Molecular Docking Simulation ; Protease Inhibitors/chemistry* ; SARS-CoV-2/enzymology* ; Viral Nonstructural Proteins