Subacute dermal toxicity study of bensulfuron-methyl in Sprague-Dawley rats.

Background: Bensulfuron-methyl has recently attracted attention given its widespread use as an herbicide in crops, especially its transdermal safety. However, no dermal toxicity study of this pesticide to mammals has been reported. The present study aims to investigate subacute dermal toxicity of bensulfuron-methyl following repeated doses exposure.Methods: Forty-eight Sprague-Dawley rats were randomly divided into four groups: a normal control group and bensulfuron-methyl groups of different concentrations (250, 500, 1000 mg/kg.bw/day). The rats were topically applied with the substance dermally for 6 h per day for 28 days. At the end of the experiment, all rats were monitored for any changes in their hematological, biochemical parameters, and pathological and histological sections.Results: There were no statistically significant differences (P ≥ 0.05) in the hematological parameters and biochemical parameters. The pathological histological results of rats in the control and the highest concentration group showed no significant abnormalities. The NOAEL of subacute dermal toxicity study was found to be 1000 mg/kg.bw/day in both female and male rats.Conclusion: The result indicated that bensulfuron-methyl is probably safe for humans as a pesticide.

G6PD-NF-κB-HGF Signal in Gastric Cancer-Associated Mesenchymal Stem Cells Promotes the Proliferation and Metastasis of Gastric Cancer Cells by Upregulating the Expression of HK2.

Background: Tumor-associated stromal cells have been widely recognized for their tumor-promoting capability involving paracrine signaling. However, the underlying mechanism and the effects of the molecules in the glycolysis pathway in gastric cancer-associated mesenchymal stem cells (GCMSCs) and gastric cancer cells on tumor progression remain unclear. Methods: The expression of hepatocyte growth factor (HGF) in GCMSCs and bone marrow mesenchymal stem cells (BMMSCs) was detected by enzyme-linked immunosorbent assay (ELISA). The effect of HGF derived from GCMSCs on the proliferation, metastasis, and HK2 expression of gastric cancer cells was evaluated in vitro and in vivo. The effects of G6PD on the production of HGF in mesenchymal stem cells (MSCs) were analyzed by immunoblotting. Results: HGF derived from GCMSCs promoted glycolysis, proliferation, and metastasis of gastric cancer by upregulating c-Myc-HK2 signal. The progression of the disease induced by GCMSCs decelerated in the absence of HK2. The expression of G6PD activated NF-κB signaling and stimulated the production of HGF in GCMSCs. Blocking HGF derived from GCMSCs decreased proliferation, metastasis, and angiogenesis of gastric cancer cells in vivo. Conclusions: GCMSCs highly expressed G6PD and facilitated the progression of gastric cancer through the G6PD-NF-κB-HGF axis coordinates. Blocking HGF derived from GCMSCs is a potential new therapeutic target for the treatment of gastric cancer.

Thermal Evaporation of Large-Area SnS2 Thin Films with a UV-to-NIR Photoelectric Response for Flexible Photodetector Applications.

In addition to device flexibility, the retentivity performance of photoelectric materials after an extreme reverse-bending process is intrinsically important and desirable for next-generation advanced flexible optoelectronics. In this work, we designed and fabricated large-area flexible SnS2 thin films with a novel nanosheet/amorphous blended structure to achieve an outstanding flexible photoelectric performance via a facile evaporation and post-thermal annealing route. Crystal structure analysis showed that the obtained SnS2 thin films were constructed with nanosheets oriented parallel to the substrate which were surrounded and connected by the amorphous component with a smooth surface. This nanosheet/amorphous blended structure allowed extreme bending because of the adhesive and strain-accommodation effect that arises from the amorphous components. The assembled SnS2 flexible photodetectors can bear a small bending radius as low as 1 mm for over 3000 bending-flatting cycles without a drastic performance decay. In particular, over 90% of the initial photoelectric responsivity (40.8 mA/W) was maintained even after 1000 bending-flatting cycles. Moreover, the SnS2 thin film can convert photons to photocurrent over a wide spectral range from ultraviolet to near infrared. These unique characteristics indicate that the strategy used in this work is attractive for the development of future wearable photoelectric and artificial intelligence applications.

Reducing the Schottky Barrier by SnS2 Underlayer Modification to Enhance Photoelectric Performance: The Case of Ag2S/FTO.

The transfer and recombination of photoinduced charge carriers play the crucial roles in a photoelectric conversion system. In this work, the Ag2S/fluorine-doped tinoxide (FTO) was used as the platform to understand the photoinduced charge carrier transfer and recombination at the light absorber and electrode interface. SnS2 was evaporated onto the FTO surface to cooperate the Fermi level with Ag2S, which reduced the Schottky barrier at the Ag2S/FTO interface. Kelvin probe force microscopy measurements reveal that the Fermi level of FTO can be tuned from -4.93 to -4.75 eV by various SnS2 with different evaporation amounts. Transient surface photovoltage tests confirm that the recombination of the photogenerated charge carrier can be drastically suppressed. The photoelectric conversion efficiency of the resulting solar cell devices has been significantly improved.

Hypoxia-inducible factor 1-α-AA-modified bone marrow stem cells protect PC12 cells from hypoxia-induced apoptosis, partially through VEGF/PI3K/Akt/FoxO1 pathway.

Bone marrow stem cells (BMSCs) have been shown to improve neurological function recovery in cerebral ischemia. Hypoxia-inducible factor-1 (HIF-1) α-AA is a more stable mutant form of HIF-1α, which is a crucial oxygen-sensitive regulator. To investigate the protective effects of HIF-1α-AA-modified BMSCs on neuron survival in cerebral ischemia models, we co-cultured HIF-1α-AA-modified BMSCs with neuron-like cells (PC12 cells) and observed a significant increase in the release of vascular endothelial growth factor (VEGF) from BMSCs, the decreased PC12 cell apoptosis, and the upregulation of Survivin expression reduced by hypoxia in PC12 cells compared to enhanced green fluorescent protein (EGFP) BMSCs. In addition, to explore whether VEGF secreted by HIF-1α-AA-modified BMSCs plays an important role in preventing hypoxia-induced apoptosis and the possible mechanism involved, exogenous VEGF were applied and the similar protective effects on PC12 cells were observed in vitro. Furthermore, hypoxia reduced the expression of phosphorylated Akt and phosphorylated FoxO1, whereas the administration of VEGF reversed these changes. Transfection of FoxO1 H215R, a DNA-binding mutant, abrogated the inhibitory ability on Survivin promoter activity, whereas FoxO1 AAA, the active form of FoxO1, presented further repression on Survivin promoter, indicating that FoxO1 directly binds on Survivin promoter as a transcriptional repressor and that phosphorylation status of FoxO1 affects its inhibition on the Survivin promoter. Transplantation of HIF-1α-AA-modified BMSCs after cerebral ischemia in vivo sufficiently reduced neurons apoptosis, decreased cerebral infarction volume, and induced a significant improvement on the modified neurological severity score compared to the EGFP BMSCs group. In conclusion, HIF-1α-AA-modified MSCs showed an obvious protective effect on neuron-like cells or neuron after ischemia in vitro and in vivo, at least in part, through the VEGF/PI3K/Akt/FoxO1 pathway.