Objective To evaluate the effect and safety of pseudomonas aeruginosa injection (PA-MSHA) combined with ulinastatin (UTI) injection in the treatment of patients with malignant pleural effusion and/or ascites.Methods 52 patients were randomly divided into PA-MSHA group and PA-MSHA combined with UTI group,each group including 26 patients.All patients were given ultrasonic testing before treatment.The single drug group was given PA-MSHA 10 ml intrapleural and/or intraperitoneal injection.The two-drug combination group was given PA-MSHA 10ml and UTI 300 000 U,twice per week.Evaluation of the efficacy and adverse reaction was performed after 4 times.Results The effective rate of single PA-MSHA group was 34.6 ％ (CR 1 case,PR 8 cases),while the effective rate of PA-MSHA combined with UTI group was 61.5 ％ (CR 2 cases,PR 14 cases).The effective rate of PA-MSHA combined with UTI group was statistically higher than that of single PA-MSHA group (P ＜ 0.05).8 cases got fever in single PA-MSHA group,3 cases in PA-MSHA combined with UTI group got fever,side effect had no statistical significance (P ＞ 0.05).Conclusion PA-MSHA combined with UTI has better effect in the treatment of patients with malignant pleural effusion and/or ascites compared with single PA-MSHA,and both treatments have low side effects.

Aim To study the regulatory of Jiaweisini-san on expression of hippocampal BDNF, NR1 and dental gyrus ( DG ) neurogenesis in rats with chronic stressed-depression and its possible mechamisms. Methods Chronic unpredictable mild stress was used to establish the rat model of stressed depression. The expression of BrdU, NeuN, brain -derived neurotro-phic factor ( BDNF ) and N-methyl-D-aspartate recep-tor1 ( NR1 ) in hippocampal dental gyrus were detected by fluorescently labeled immunohistochemical method. In addition, BDNFmRNA was detected by in situ hy-bridization. Results Chronic stress could inhibit the proliferation of neural precursors in hippocampal DG ( P<0. 01 );the expression of BDNF decreased signifi-cantly in DG in model rats ( P <0. 01 ) , while the ex-pression of NR1 increased significantly ( P <0. 01 ) . JWSNS and Fluoxetine hydrochloride significantly en-hanced the amount of new proliferating cells and the number of neurons in unit area of DG ( P<0. 01 ) , in-creased the expression of BDNF ( P <0. 01 ) and de-creased the expression of NR1 in DG(P<0. 01). Con-clusion JWSNS could promote the neuronal prolifera-tion in hippocampal DG of rat with chronic stressed-de-pression,and may exert an effect of promoting the pro-liferation of neurons in hippocampal DG by enhancing the expression of BDNF and decreasing the expression of NR1 .

Objective To observe the effects of melatonin (MT) on the expression of heme oxygenase-1 (HO-1),phosphorylated adenine dinucleotide quinone oxidoreductase-1 (NQO-1) and nuclear factor erythroid-2-related factor 2 (Nrf2),so as to explore the mechanism of MT's action in the Nrf2-ARE signaling pathway.Methods A total of 72 Sprague-Dawley rats were randomly divided into a control group,an injury group and a melatonin group,each of 24.T11-T12 acute SCI was induced in the injury and melatonin groups using the modified Allen's method.Ten minutes after the injury,equal amounts of absolute ethyl alcohol and melatonin were intraperitoneally injected into the rats in the injury and melatonin groups.For the control group,the vertebral plate was cut to expose the T11-T12 spinal cord without any injury of the nerves.Six rats from each group were randomly selected for sacrifice at 6,12 and 24 hours after the operation,and T11-T12 spinal cord specimens were collected.The spinal cord injury and inflammatory response were observed using haematoxylin eosin staining.The expression of HO-1,NQO-1 and Nrf2 was examined using immunofluorescence,while the expression of HO-1,NQO-1 and Nrf2 protein and mRNA were detected using RT-PCRs.Results The neuronal cells in the spinal cords of the control rats were of normal shape,without edema,necrosis or obvious hemorrhagic foci.Hemorrhagic foci,significantly more inflammatory cells and some spinal cord neurons with edema and necrosis were observed in the injury group.However,significantly fewer hemorrhagic spots and cells with edema were found in the melatonin group compared with the injury group.The average expression of HO-1,NQO-1 and Nrf2 protein and mRNA was significantly higher in the melatonin group than in the other two groups.The levels in the injury group were also significantly higher than in the control group 12 and 24 hours after the experiments.Immunofluorescence showed that the greatest number of cells with HO-1,NQO-1 and Nrf2 was found in the melatonin group,followed by the injury group and then the control group,with significant differences among all 3 groups.Conclusion Melatonin can promote the expression of HO-1,NQO-1 and Nrf2 in rats with acute spinal cord injury,which might be related with its activating the Nrf2-ARE signaling pathway.

【Objective】 To investigate the incidence and possible risk factors of FMH among pregnant women in Changsha. 【Methods】 A total of pregnant women (6~42 weeks of gestation) who underwent prenatal examinations in our hospital from June 2019 to December 2020 were enrolled as subjects. In this study, the modified Kleihauer-Betke (K-B) test was used for preliminary screening and flow cytometry was applied to confirme initially positive samples to evaluate the incidence of FMH and estimate fetal blood loss. The logistic regression analysis was used to study the risk factors of FMH. 【Results】 The incidence of FMH in pregnant women was 10.45% (183/1 752), the average volume of fetal blood loss was (2.50±3.87)mL, and 0.11% (2/1 752) of the fetal losed blood > 30 mL. Univariate analysis showed that age, twin pregnancy, pregnancy complicated with uterine fibroids, in vitro fertilization, fetal growth restriction, preeclampsia, and number of pregnancies may be risk factors for FMH. Multivariate analysis showed that twin pregnancy (OR 2.274, 95%CI: 1.135-4.458, P<0.05) and preeclampsia (OR 2.341, 95%CI: 1.082-4.837, P<0.05) were independent risk factors for FMH. 【Conclusion】 Maternal age and various physiological and pathological factors during pregnancy may be associated with the risk of FMH, especially twin pregnancy and pre-eclampsia are independent risk factors for FMH.

BACKGROUND: The switch/sucrose nonfermentable chromatin-remodeling (SWI/SNF) complex is a pivotal chromatin remodeling complex, and the genomic alterations (GAs) of the SWI/SNF complex are observed in several cancer types, correlating with multiple biological features of tumor cells. However, their role in liver metastasis of non-small cell lung cancer (NSCLC) remains unclear. Our study aims to investigate the role and potential mechanisms underlying NSCLC liver metastasis induced by the GAs of SWI/SNF complex. METHODS: The GAs of SWI/SNF complex in NSCLC cell lines (H1299, H23 and H460) were identified by whole-exome sequencing (WES). ARID1A knockout H1299 cell was constructed with the CRISPR/Cas9 technology. The mouse model of liver metastasis from NSCLC was established to simulate lung cancer liver metastasis and observe the metastasis rate under different gene mutation conditions. RNA sequencing and Western blot were conducted for differential gene expression analysis. Immunohistochemistry (IHC) analysis was used to assess protein expression levels of SWI/SNF-regulated target molecules in mouse liver metastases. RESULTS: WES analysis revealed intracellular gene mutations. The animal experiments demonstrated a correlation between the GAs of SWI/SNF complex and a higher liver metastasis rate in immunodeficient mice. Transcriptome sequencing and Western blot analysis showed upregulated expression of ALDH1A1 and APOBEC3B in SWI/SNF-mut cells, particularly in ARID1A-deficient H460 and H1299 sgARID1A cells. IHC staining of mouse liver metastases further demonstrated elevated expression of ALDH1A1 in the H460 and H1299 sgARID1A group. CONCLUSIONS This study underscores the critical role of the GAs of SWI/SNF complex, such as ARID1A and SMARCA4, in promoting liver metastasis of lung cancer cells. The GAs of SWI/SNF complex may promote liver-specific metastasis by upregulating ALDH1A1 and APOBEC3B expression, providing novel insights into the molecular mechanisms underlying lung cancer liver metastasis.
Animals ; Mice ; Carcinoma, Non-Small-Cell Lung/genetics* ; Lung Neoplasms/genetics* ; Mutation ; Liver Neoplasms/genetics*

Humans ; Asthma/drug therapy* ; Biological Therapy