Objective To evaluate the effects of hyperbaric oxygen (HBO) combined with drug therapy on patients with delayed encephalopathy caused by carbon monoxide poisoning ( COP). Methods Twenty to forty sessions of HBO therapy were used to treat 34 COP patients. Assessment relied on 99mTc-ethyl cysteinate dimer (~(99m)Tc-ECD) single photon emission computed tomography (SPECT) imaging of cerebral perfusion before and after treatment. Results After HBO therapy, cerebral perfusion in the COP patients improved significantly. There was a significant difference of the SPECT images before and after treatment. Conclusions SPECT imaging of cerebral perfusion can play an important role in the diagnosis of delayed encephalopathy caused by carbon monoxide poisoning, and it can be used for the therapeutic surveillance of HBO treatment.

Objective To explore the of miR-10b cordribution in patients with non-small cell lung cancer (NSCLC) and adjacent tissues,and to investigate the effect of miR-10b on the malignant change of lung cancer cell A549 by regulating the expression of Kruppel-like factor 4 (KLF4).Methods Fourty patients with NSCLC were selected with lung cancer and in miR-10b expression adjacent tissues of lung cancer cell A549 transfected miR-10b mimics,changes of CCK-8 assay were used to detect the proliferation of lung cancer cells;real time PCR and Western blot were used to examine the cell KLF4 mRNA and protein levels;soft agar colony formation assay was used to detect the expression of miR-10b on the proliferation of lung cancer cell A549 tumor malignant.Results miR-10b expression in lung cancer A549 cells and lung cancer tissue were higher than that of normal lung epithelial 16HBE cells and cancer adjacent tissues;overexpression of miR-10banalogue in A549 cells,KLF4 protein levels significantly decreased,KLF4 mRNA was not changed significantly;miR-10b expression significantly increased the growth of A549 cells.Conclusions The distribution of miR-10b in different cell types and tissues may be different,which may promote the proliferation and malignancy of lung cancer cells by inhibitingthe expression of KLF4.

Background::Homoharringtonine (HHT) is an effective anti-inflammatory, anti-viral, and anti-tumor protein synthesis inhibitor that has been applied clinically. Here, we explored the therapeutic effects of HHT in a mouse heart transplant model.Methods::Healthy C57BL/6 mice were used to observe the toxicity of HHT in the liver, kidney, and hematology. A mouse heart transplantation model was constructed, and the potential mechanism of HHT prolonging allograft survival was evaluated using Kaplan–Meier analysis, immunostaining, and bulk RNA sequencing analysis. The HHT-T cell crosstalk was modeled ex vivo to further verify the molecular mechanism of HHT-induced regulatory T cells (Tregs) differentiation. Results::HHT inhibited the activation and proliferation of T cells and promoted their apoptosis ex vivo. Treatment of 0.5 mg/kg HHT for 10 days significantly prolonged the mean graft survival time of the allografts from 7 days to 48 days ( P <0.001) without non-immune toxicity. The allografts had long-term survival after continuous HHT treatment for 28 days. HHT significantly reduced lymphocyte infiltration in the graft, and interferon-γ-secreting CD4 + and CD8 + T cells in the spleen ( P <0.01). HHT significantly increased the number of peripheral Tregs (about 20%, P <0.001) and serum interleukin (IL)-10 levels. HHT downregulated the expression of T cell receptor (TCR) signaling pathway-related genes ( CD4, H2-Eb1, TRAT1, and CD74) and upregulated the expression of IL-10 and transforming growth factor (TGF) -β pathway-related genes and Treg signature genes ( CTLA4, Foxp3, CD74, and ICOS). HHT increased CD4 + Foxp3 + cells and Foxp3 expression ex vivo, and it enhanced the inhibitory function of inducible Tregs. Conclusions::HHT promotes Treg cell differentiation and enhances Treg suppressive function by attenuating the TCR signaling pathway and upregulating the expression of Treg signature genes and IL-10 levels, thereby promoting mouse heart allograft acceptance. These findings may have therapeutic implications for organ transplant recipients, particularly those with viral infections and malignancies, which require a more suitable anti-rejection medication.