Objective To investigate the influence of transforming growth factor-?1(TGF-?1) on macrophage scavenger receptor (ScR) class A and B(ScR-B,CD36) in order to provide theoretical foundation for expounding the formation and therapy of atherosclerosis(AS).Methods THP-1 derived macrophages were divided into control group and experimental group,the cells in experimental group were treated with 3.0 mg?L-1Anti TGF-?1 Ab,the cells in control group were treated with 3.0 mg?L-1 IgG. The 125I-acetylated low density lipoprotein (125I-Ac-LDL for ScR-A) and 125I-oxidized low density lipoprotein (125I-Ox-LDL for CD36) uptaking (including 4℃ binding,37℃ association and degradation) were measured respectively.Influence of anti TGF-?1 antibody (Anti TGF-?1 Ab) on the ScR-A and CD36 mRNA expressions in THP-1 derived macrophages was measured meanwhile,respectively.Results Compared with control group ( binding: 8.23 ?g?g-1 ?1.24 ?g?g-1 protein,association:45.69 ?g?g-1 ?6.92 ?g?g-1 protein,and degradation: 112.18 ?g?g-1 ?20.15 ?g?g-1 protein),Anti TGF-?1 Ab increased 125I-Ac-LDL binding(48.67 ?g?g-1 ?6.52 ?g?g-1 protein),association (412.30 ?g?g-1?12.21 ?g?g-1 protein),and degradation (896.48 ?g?g-1 ?32.74 ?g?g-1 protein) significantly (P

The paper described the periodic progress of public hospitals reform in Anhui province,and analyzed the difficulties encountered,proposing measures and recommendations.These include reasonable adjustment of medicine prices for betterment of public hospital compensation mechanism; toplevel design in supportive measures of county-level public hospital reform; breakthrough of existing personnel system to ease shortage of medical staff in primary institutions; encouragement of diversified investment in medical sector to invite private resources into public hospital reform.

Objective:To investigate the mechanism of benzyl isothiocyanate(BITC) in the treatment of anaplastic thyroid cancer(ATC).Methods:Using network pharmacological analysis, key targets of BITC and ATC were screened, followed by GO and KEGG enrichment analysis. In order to validate the findings, AutoDock software was used to dock BITC and ATC key targets. BITC was applied to two ATC cell lines(8505C and CAL-62). Flow cytometry was used to analyze cell apoptosis. Autophagy inhibitors hydroxychloroquine sulfate(HCQ) and 3-methyladenine(3MA) were used in combination with BITC. Real-time quantitative PCR was conducted to detect the gene level of LC3B, while Western blotting was utilized to examine the expression of NF-κB, LC3B Ⅱ, Beclin-1, and Bcl-2. In animal experiments, a mouse tumor model was constructed using CAL-62 cells, treated with intraperitoneal injections of BITC(100 mg/kg) and normal saline respectively, administered every other day for a total of 21 days. Immunoblotting of tumor tissue was performed to detect the expression of LC3B Ⅱ, Bcl-2, Beclin-1, and NF-κB.Results:A total of 10 key targets with binding energies≤-4.0 kcal/mol were identified. KEGG analysis showed that these genes are mainly involved in NF-κB signaling pathway and apoptosis. BITC inhibited ATC cells with IC50 values of 27.56 μmol/L for 8505C and 28.30 μmol/L for CAL-62. The expression levels of NF-κB, Beclin-1, and Bcl-2 decreased, while LC3B Ⅱ and LC3B gene expression increased. Combining 3MA with BITC enhanced cell inhibition LC3B Ⅱ expression. HCQ increased LC3B Ⅱ expression without enhancing cell and viability inhibition. In the mouse tumor model, compared to the control group, the treatment group had higher LC3B Ⅱ and lower Bcl-2, Beclin-1, and NF-κB levels.Conclusion:BITC could inhibit the growth of ATC cells in vitro and in vivo, disrupt the autophagy degradation, and inhibit the NF-κB pathway.

Gastric cancer is the most prevalent gastrointestinal tumor in China， threatening the life and health of patients. Surgery is one of the available therapies， which， however， induces postoperative gastrointestinal dysfunction （PGD） and other common complications. The pathogenesis of PGD is still unclear and no efficient targeted drug is available. In addition， the limited treatment measures fail to effectively improve gastrointestinal function. As a result， patients generally suffer from low quality of life and poor prognosis. In Chinese medicine， PGD belongs to the categories of "vomiting"， "stuffiness and fullness"， "regurgitation"， "abdominal distension"， "intestinal impediment"， and "intestinal accumulation". In recent years， there has been an explosion of research on the PGD of gastric cancer in Chinese medicine， and many research results have been obtained. On this basis， this study introduced PGD in modern medicine， and causes and pathogenesis， syndrome differentiation-based treatment， and clinical studies of PGD. It was found that diverse internal and external treatments are available in Chinese medicine for PGD such as internal use of Chinese medicine， Chinese medicine enema， auricular point seed-embedding， acupuncture， and moxibustion， which feature ease of implementation， small side effects， definite efficacy， and significant effect in combination with other therapies. This paper summarized the ideas and measures for treatment of PGD of gastric cancer by Chinese medicine， the research outcomes， limitations， and research directions， which can serve as a reference for further research on treatment of PGD of gastric cancer by Chinese medicine.

Activation of the heart normally begins in the sinoatrial node (SAN). Electrical impulses spontaneously released by SAN pacemaker cells (SANPCs) trigger the contraction of the heart. However, the cellular nature of SANPCs remains controversial. Here, we report that SANPCs exhibit glutamatergic neuron-like properties. By comparing the single-cell transcriptome of SANPCs with that of cells from primary visual cortex in mouse, we found that SANPCs co-clustered with cortical neurons. Tissue and cellular imaging confirmed that SANPCs contained key elements of glutamatergic neurotransmitter system, expressing genes encoding glutamate synthesis pathway (Gls), ionotropic and metabotropic glutamate receptors (Grina, Gria3, Grm1 and Grm5), and glutamate transporters (Slc17a7). SANPCs highly expressed cell markers of glutamatergic neurons (Snap25 and Slc17a7), whereas Gad1, a marker of GABAergic neurons, was negative. Functional studies revealed that inhibition of glutamate receptors or transporters reduced spontaneous pacing frequency of isolated SAN tissues and spontaneous Ca