Background Jiangsu was one of the first four pilot provinces to engage in comprehensive health care reform in China, which has been on-going for the past 5 years. This study aims to evaluate the equity, efficiency and productivity of health care resource allocation in Jiangsu Province using the most recent data, analyse the causes of deficiencies, and discuss measures to solve these problems. Methods Data were extracted from the Jiangsu Health/Family Planning Statistical Yearbook (2015–2019) and Jiangsu Statistical Yearbook (2015–2019). The Gini coefficient (G), Theil index (T) and health resource density index (HRDI) were chosen to study the fairness of health resource allocation in Jiangsu Province. Data envelopment analysis (DEA) and the Malmquist productivity index (MPI) were used to analyse the efficiency and productivity of this allocation. Results From 2014 to 2018, the total amount of health resources in Jiangsu Province increased. The G of primary resource allocation by population remained below 0.15, and that by geographical area was between 0.14 and 0.28; additionally, the G of health financial resources was below 0.26, and that by geographical area was above 0.39. T was consistent with the results for G and Lorenz curves. The HRDI shows that the allocated amounts of health care resources were the highest in southern Jiangsu, except for the number of health institutions. The average value of TE was above 0.93, and the DEA results were invalid for only two cities. From 2014 to 2018, the mean TFPC in Jiangsu was less than 1, and the values exceeded 1 for only five cities. Conclusion The equity of basic medical resources was better than that of financial resources, and the equity of geographical allocation was better than that of population allocation. The overall efficiency of health care resource allocation was high; however, the total factor productivity of the whole province has declined due to technological regression. Jiangsu Province needs to further optimize the allocation and increase the utilization efficiency of health care resources.

The tumor microenvironment (tumor cells are located in the internal and external environment) is vital for the occurrence, growth and metastasis of tumors. An increasing number of studies have shown that exosomes are closely related to the tumor microenvironment. The mechanisms involved, however, are unclear. The focus of this review is on the exosome-related tumor microenvironment and other relevant factors, such as hypoxia, inflammation and angiogenesis. Many studies have suggested that exosomes are important mediators of metastasis, angiogenesis, and immune modulation in the tumor microenvironment. Additionally, exosomes can be isolated from bodily fluids of cancer patients, including urine, blood, saliva, milk, tumor effusion, cerebrospinal fluid, amniotic fluid and so on. Consequently, exosomes are potential biomarkers for clinical predictions and are also good drug carriers because they can cross the biofilm without triggering an immune response. Collectively, these findings illustrate that exosomes are crucial for developing potential targets for a new generation of pharmaceutical therapies that would improve the tumor microenvironment.

Vascular smooth muscle cell (VSMC) proliferation and migration triggered by inflammatory stimuli contributes importantly to the pathogenesis of atherosclerosis and restenosis. On the other hand, genipin, an aglycon of geniposide, exhibits diverse pharmacological functions such as antitumor and anti-inflammatory effects. The protective effects of genipin on the cardiovascular system have also been reported. However, the molecular mechanism involved remains unknown. This study aimed to elucidate the precise function of genipin in VSMCs, focusing particularly on the role of heme oxygenase-1 (HO-1), a potent anti-inflammatory enzyme. We found that pretreatment of genipin induced HO-1 mRNA and protein levels, as well as its activity in VSMCs. Genipin inhibited TNF-α-induced VSMC proliferation and migration in a dose-dependent manner. At the molecular level, genipin prevented ERK/MAPK and Akt phosphorylation while left p38 MAPK and JNK unchanged. Genipin also blocked the increase of ROS generation induced by TNF-α. More importantly, the specific HO-1 siRNA partially abolished the beneficial effects of genipin on VSMCs. These results suggest that genipin may serve as a novel drug in the treatment of these pathologies by inducing HO-1 expression/activity and subsequently decreasing VSMC proliferation and migration.

Background As most lung cancer patients present with invasive, metastatic disease, it is vital to investigate anti-metastatic treatments for non-small cell lung cancer (NSCLC). Houttuynia cordata is commonly used as a Chinese anticancer medicine in the clinic, and sodium new houttuyfonate (SNH), a main compound of this herb, has long been found to have antibiotic effects, although its anticancer effects have not been investigated. Here, we tried to address this lack of research from the perspective of the competing endogenous RNA (ceRNA) theory. Methods The effects of SNH on NSCLC cells were analysed with Cell Counting Kit-8 assays and colony formation assays. In addition, transwell assays and wound healing assays were used to determine the effects of SNH on migration and invasion in NSCLC cells. The levels of key genes and proteins were examined by quantitative real-time PCR, western blotting, immunofluorescence staining and IHC staining. Through transcriptome screening and digital gene expression profiling, Linc00668 was identified to be regulated by SNH. Dual-luciferase reporter assays and RNA immunoprecipitation assays verified the binding efficiency between miR-147a and Linc00668 or Slug. Results In the present study, SNH regulated NSCLC cells in multiple ways, the most prominent of which was suppressing the expression of Linc00668, which was indicated to promote migration and invasion in NSCLC cells. Functional studies demonstrated that Linc00668 acted as a ceRNA by sponging miR-147a to further regulate Slug mRNA levels, thereby influencing the progression of the epithelial-mesenchymal transition. Consistently, the results of in vivo animal models showed that SNH depressed Linc00668 and suppressed the metastasis of NSCLC. Conclusions SNH suppressed metastasis of NSCLC cells and the mechanism may involve with the Linc00668/miR-147a/Slug axis. Electronic supplementary material The online version of this article (10.1186/s13046-019-1152-9) contains supplementary material, which is available to authorized users.

Pyroptosis is a distinct form of programmed cell death in eukaryotic cells that has garnered increasing attention in cancer-related research. Moreover, although miR-21 has been reported as abnormally expressed in colorectal cancer, due to a lack of in-depth research on the transcriptional regulation mechanisms of miR-21, its clinical usage remains limited. Our study is the first, to our knowledge, to compare the clinical manifestations and laboratory phenotypes associated with miR-21-3p and miR-21-5p. Morphologically, the transfection of miR-21-3p or miR-21-5p inhibitors, as well as miR-21-5p mimics into HCT-116 and HT-29 cell lines, induced cell death. Surprisingly, overexpression of miR-21-5p induced cell death more strongly than its knockdown. Mechanistic studies of miR-21-5p overexpression revealed that various inflammatory factors including IL-1β and IL-18 were released, while pyroptosis-associated mRNAs were upregulated and proteins were activated. Moreover, miR-21-5p was found to act as a downstream factor to significantly and directly regulate transforming growth factor beta-induced (TGFB1). Specifically, miR-21-5p overexpression caused downregulation of TGFBI, which may have led to pyroptosis. Collectively, we revealed that miR-21-5p induces pyroptosis in colorectal cancer via TGFBI regulation, thereby providing important mechanistic insights into its antitumor effects and expanding its potential for clinical applications.