Isolation and Characterization of Pseudomonas aeruginosa Phages with a Broad Host Spectrum from Hospital Sewage Systems and Their Therapeutic Effect in a Mouse Model.

This study aimed to isolate and characterize phages as an alternative treatment of multidrug- or pan-drug-resistant Pseudomonas aeruginosa. Phage titers and bacterial densities correlated, with the phages disappearing after bacteria were eliminated. We isolated phages in filtered sewage water by a double-layered agar spot test.

Epidemic, risk factors of carbapenem-resistant infection and its effect on the early prognosis of liver transplantation.

Background: Carbapenem-resistant (CRKP) infection remains a major cause of morbidity and mortality in early-stage post-liver transplantation (LT).

Methods: We retrospectively analyzed the demographic and clinical infections characteristics of all LT recipients in our hospital between January 2019 and December 2021.

Results: Among the 272 LT recipients who received LT between January 2019 and December 2021, sixty-two patients had at least one infection within 3-months post-LT, with a prevalence of 22.

The interplay between TGF-β/SMAD and BMP/SMAD signaling pathways in the epithelial mesenchymal transition of A549 cells induced by silica.

The epithelial-mesenchymal transition (EMT) is a phenotype transdifferentiation of epithelial into mesenchymal cells and contributes to pulmonary fibrotic disease. SMAD-dependent pathway has been reported to play a key role in the multiple fibrotic diseases. We hypothesized that TGF-β/SMAD signaling could cross-interact with BMP/SMAD signaling pathways in silica-induced EMT in A549 cells.

Sodium tanshinone IIA sulfonate suppresses pulmonary fibroblast proliferation and activation induced by silica: role of the Nrf2/Trx pathway.

Alveolar macrophages are believed to induce oxidative stress reactive oxygen species (ROS) when silica particles are inhaled. This process can contribute to the pathogenesis of silicosis, but the mechanism is unclear. A traditional Chinese herbal derivative, sodium tanshinone IIA sulfonate (STS), displays significant antioxidant effects.

BMP-7 attenuated silica-induced pulmonary fibrosis through modulation of the balance between TGF-β/Smad and BMP-7/Smad signaling pathway.

Objective: To investigate the anti-fibrotic effects and possible mechanisms of bone morphogenetic protein-7 (BMP-7) on silica induced fibrosis in RLE-6TN cells, and compare the preventive treatment of experimental silicosis with BMP-7 with therapeutic treatment of silicosis in vitro models.

Methods: RLE-6TN cells were incubated with the supernatant of RAW264.7, treated by 50 μg/mL silica in either presence or absence of BMP-7 in different phases.

AEG-1 Promotes Metastasis Through Downstream AKR1C2 and NF1 in Liver Cancer.

Liver cancer is one of the most lethal cancers, but our knowledge of the molecular mechanism underlying this process remains insufficient. Through deep sequencing and expression regulation analysis in liver cancer cells, we identified two novel factors, AKR1C2 (positive factor) and NF1 (negative factor), as the AEG-1 downstream players in the process of metastasis in liver cancer. They were experimentally validated to have the capacities of regulating cell migration, cell invasion, cell proliferation, and EMT.

High-Content Functional Screening of AEG-1 and AKR1C2 for the Promotion of Metastasis in Liver Cancer.

Liver cancer is one of the most lethal cancer types in humans, but our understanding of the molecular mechanisms underlying this process remains insufficient. Here, we conducted high-content screening of the potential genes involved in liver cancer metastasis, which we selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database, based on the SAMcell method and RNA interference technology. We identified two powerful genes in the liver cancer metastasis process, AEG-1 and AKR1C2, both of which proved to be positive regulators in promoting metastasis in liver cancer.

A Huaier polysaccharide reduced metastasis of human hepatocellular carcinoma SMMC-7721 cells via modulating AUF-1 signaling pathway.

TP-1 is a polysaccharide from one famous fungus Huaier. Treatment with TP-1 significantly inhibited the cell growth, adhesion, migration, and motility of SMMC-7721 cells in a dose-dependent manner. Real-time quantitative RT-PCR revealed a dose-dependent decrease in RNA-binding factor 1 (AUF-1) and astrocyte elevated gene-1 (AEG-1) messenger RNA (mRNA) levels in TP-1-treated SMMC-7721 cells, which is consistent with their protein expression detected by Western blotting.

Effect of bone morphogenic protein-7 on the expression of epithelial-mesenchymal transition markers in silicosis model.

This study presented the effect of bone morphogenic protein-7 (BMP-7) inhibiting epithelial-mesenchymal transition (EMT) in silicosis model. In vivo, Wistar rats were exposed to silica by intratracheal instillation. Seven days later rats were treated with BMP-7.

A Huaier polysaccharide restrains hepatocellular carcinoma growth and metastasis by suppression angiogenesis.

Hepatocellular carcinoma (HCC) is a highly metastatic cancer. Huaier polysaccharide (TP-1) is a naturally occurring bioactive macromolecule, found in Huaier fungus and has been shown to exert in vitro antitumor and antimetastasis for HCC, but no study has addressed in vivo efficacy and mechanisms of action. Presently, we found that TP-1 at doses of 0.

A Huaier polysaccharide inhibits hepatocellular carcinoma growth and metastasis.

This study was carried out to evaluate the effects of a Huaier polysaccharide (TP-1) on the tumor growth and immune function in hepatocellular carcinoma (HCC) H22-based mouse in vivo. Results showed that TP-1 was capable of repressing transplanted H22 solid hepatic tumor cell growth in vivo, prolonging the live time of mice bearing ascetic H22 tumors, and repressing the pulmonary metastasis of H22-bearing mice. Moreover, the relative weight of immune organ (spleen and thymus) and lymphocyte proliferation were improved after TP-1 treatment.

Long non-coding RNA NR_045623 and NR_028291 involved in benzene hematotoxicity in occupationally benzene-exposed workers.

Benzene is an established human hematotoxicant and leukemogen. New insights into the pathogenesis of benzene hematotoxicity are urgently needed. Long non-coding RNA (lncRNA) widely participate in various physiological and pathological processes.

Differential gene expression profiling analysis in workers occupationally exposed to benzene.

Unlabelled: Benzene is an important industrial chemical and an environmental contaminant, but the pathogenesis of hematotoxicity induced by chronic occupational benzene exposure remains to be elucidated. To gain an insight into the molecular mechanisms and new biomarkers, microarray analysis was used to identify the differentially expressed mRNA critical for benzene hematotoxicity. RNA was extracted from four chronic benzene poisoning patients occupationally exposed to benzene, three benzene-exposed workers without clinical symptoms and three health controls without benzene exposure and mRNA expression profiling was performed using Gene Chip Human Gene 2.

Suppression of thioredoxin system contributes to silica-induced oxidative stress and pulmonary fibrogenesis in rats.

Silicosis is one of the most prevalent occupational lung diseases worldwide. This study aimed to investigate the possible mechanism that silica affected thioredoxin (Trx) system during the development of silicosis in vivo. Male Wistar rats were randomly divided into saline group and silica group in which rats were intratracheally instilled with a single dose of silica suspension (50mg in 1ml saline/rat).

Bone morphogenetic protein-7 inhibits silica-induced pulmonary fibrosis in rats.

Bone morphogenetic protein-7 (BMP-7) has been shown to inhibit liver and renal fibrosis in in vivo and vitro studies. There is no study to investigate BMP-7's role in the development of pulmonary fibrosis induced by silica. In the current study, we used the rat model to explore the potential antifibrotic role of BMP-7 and its underlying mechanism in silica-induced pulmonary fibrosis.