Unveiling adcyap1 as a protective factor linking pain and nerve regeneration through single-cell RNA sequencing of rat dorsal root ganglion neurons.

Background: Severe peripheral nerve injury (PNI) often leads to significant movement disorders and intractable pain. Therefore, promoting nerve regeneration while avoiding neuropathic pain is crucial for the clinical treatment of PNI patients. However, established animal models for peripheral neuropathy fail to accurately recapitulate the clinical features of PNI.

CDYL knockdown reduces glioma development through an antitumor immune response in the tumor microenvironment.

Gliomas are highly prevalent and aggressive brain tumors. Growing evidence shows that epigenetic changes are closely related to cancer development. Here we report the roles of Chromodomain Y-like (CDYL), an important epigenetic transcriptional corepressor in the central nervous system in glioma progression.

A novel anti-inflammatory mechanism of high density lipoprotein through up-regulating annexin A1 in vascular endothelial cells.

High density lipoprotein (HDL) as well as annexin A1 have been reported to be associated with cardiovascular protection. However, the correlation between HDL and annexin A1 was still unknown. In this study, HDL increased endothelial annexin A1 and prevented the decrease of annexin A1 in TNF-α-activated endothelial cells in vitro and in vivo, and above effects were attenuated after knockdown of annexin A1.

Sorafenib suppresses the epithelial-mesenchymal transition of hepatocellular carcinoma cells after insufficient radiofrequency ablation.

Background: Epithelial-mesenchymal transition (EMT) played an important role in the progression of hepatocellular carcinoma (HCC) after insufficient radiofrequency ablation (RFA). However, whether sorafenib could be used to suppress the EMT of HCC after insufficient RFA and further prevent the progression of residual HCC remains poorly unknown.

Methods: Insufficient RFA was simulated using a water bath (47 °C 5, 10, 15, 20 and 25 min gradually).

Association of endothelial microparticle with NO, eNOS, ET-1, and fractional flow reserve in patients with coronary intermediate lesions.

Endothelial microparticle (EMP) is a biomarker for endothelial dysfunction. The aim of this study is to investigate the utility of EMP in evaluating coronary intermediate lesions. Participants included 49 patients with coronary intermediate lesions and 24 subjects with normal coronary arteries.

Low Concentration of Caffeine Inhibits the Progression of the Hepatocellular Carcinoma via Akt Signaling Pathway.

Accumulating evidences have reported that caffeine has anticancer effects at high blood concentrations. However, whether caffeine has anticancer effects on human hepatocellular carcinoma (HCC) cells at low concentration, especially at physiologically applicable concentration (< 412 μM) is still not well understood. In this study, HCC cell lines HepG2 and Huh7 were used.

Correlations of platelet-derived microparticles with thromboxane B2, platelet-activating factor, endothelin-1, and neutrophil to lymphocyte ratio in patients with coronary intermediate lesions.

This study was to investigate the utility of platelet-derived microparticles (PMPs) to detect coronary intermediate lesions. Fifty-two patients with coronary intermediate lesions and 24 subjects with normal coronary arteries were enrolled. In the former group, 31 patients accepted both intravenous ultrasound (IVUS) and fractional flow reserve (FFR).

Insufficient radiofrequency ablation promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells through Akt and ERK signaling pathways.

Background: Residual tumor progression after insufficient radiofrequency ablation (RFA) has been recently reported. However, whether epithelial-mesenchymal transition (EMT), which is a key process that drives cancer metastasis, is involved in the tumor progression after insufficient RFA is not well understood.

Methods: Human hepatocellular carcinoma (HCC) cell lines SMMC7721 and Huh7 were used.

High-density lipoprotein nitration and chlorination catalyzed by myeloperoxidase impair its effect of promoting endothelial repair.

High-density lipoprotein (HDL) plays a key role in protecting against atherosclerosis. In cardiovascular disease, HDL can be nitrated and chlorinated by myeloperoxidase (MPO). In this study, we discovered that MPO-oxidized HDL is dysfunctional in promoting endothelial repair compared to normal HDL.

After insufficient radiofrequency ablation, tumor-associated endothelial cells exhibit enhanced angiogenesis and promote invasiveness of residual hepatocellular carcinoma.

Background: The mechanism regarding rapid progression of residual hepatocellular carcinoma (HCC) after insufficient radiofrequency ablation (RFA) has been preliminarily discussed. However, most studies have mainly focused on RFA-induced changes in the tumor cells. The present study was designed to determine whether tumor-associated endothelial cells (TAECs) could contribute to the invasiveness of HCC after insufficient RFA.

Insufficient radiofrequency ablation promotes angiogenesis of residual hepatocellular carcinoma via HIF-1α/VEGFA.

Background: The mechanism of rapid growth of the residual tumor after radiofrequency (RF) ablation is poorly understood. In this study, we investigated the effect of hyperthermia on HepG2 cells and generated a subline with enhanced viability and dys-regulated angiogenesis in vivo, which was used as a model to further determine the molecular mechanism of the rapid growth of residual HCC after RF ablation.

Methodology/principal Findings: Heat treatment was used to establish sublines of HepG2 cells.

Hypochlorite-induced oxidative stress elevates the capability of HDL in promoting breast cancer metastasis.

Background: Previous studies suggest that oxidative stress plays an important role in the development of breast cancer. There is a significant inverse relationship between HDL and the risk and mortality of breast cancer. However, it is well known that under conditions of oxidative stress, such as breast cancer, HDL can be oxidatively modifiedand these modifications may have an effect on the functions of HDL.