ABSTRACT
ObjectiveTo explore the effect of external diaphragm pacing therapy combined with abdominal functional electrical stimulation on respiratory function for stroke patients. MethodsFrom October, 2020 to September, 2022, 54 stroke patients were randomly divided into control group (n = 18), external diaphragm pacing group (n = 18) and combined treatment group (n = 18). All the groups received breathing training, while the external diaphragm pacing group received external diaphragm pacing therapy, and the combined treatment group received external diaphragm pacing and abdominal functional electrical stimulation therapy, for two weeks. They were measured forced vital capacity (FVC), forced expiratory volume in first second (FEV1), ratio of forced expiratory volume in first second in forced vital capacity (FEV1/FVC), peak expiratory flow (PEF), maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) with pulmonary function instrument; measured diaphragmatic excursion (DE) and diaphragmatic thickness (DT) with ultrasound, before and after treatment. ResultsThree cases in the control group, two cases in the external diaphragm pacing group and one case in the combined treatment group dropped off. The FVC, FEV1, PEF, MIP, MEP and DE improved in all the groups (|t| > 3.366, P < 0.01) after treatment; and the FVC, FEV1, MIP and DE increased more in the combined treatment group and the external diaphragm pacing group than in the control group (P < 0.05); the FVC and FEV1 increased more in the combined treatment group than in the external diaphragm pacing group (P < 0.05). ConclusionExternal diaphragm pacing therapy may improve ventilation and inspiratory muscle strength, and increase diaphragm movement for stroke patients; while the ventilation improved more after combining with abdominal functional electrical stimulation.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the inhibitory effects of intervention of the tumor necrosis factor-alpha (TNFa)/nuclear factor-kappa B (NF-kappaB) signaling pathway activation on hepatoma cell proliferation and to explore its mechanism.</p><p><b>METHODS</b>A rodent hepatoma model was established by feeding N-2-fluorenylacetamide (2-N-FAA) to male Sprague-Dawley rats. Human subjects with various liver diseases were enrolled in the study, and serum and peripheral blood nuclear cells were collected for analysis. HepG2 cells were cultured in vitro and treated with anti-TNFa (monoclonal antibody, mAb) to down-regulate its expression or transfected with siRNA targeting the p65 subunit of NF-kappaB to inhibit its activation. The liver cell line L02 was used as a control. Changes in protein and gene expression levels of NF-kappaB and TNFa were analyzed by Western blotting or enzyme-linked immunosorbent assay and real-time PCR, respectively. Changes in the cell cycle or apoptosis were evaluated by flow cytometry or Annexin-V/PI double-labeling assay, respectively.</p><p><b>RESULTS</b>TNFa and NF-kappaB expression showed increasing trends during the malignant transformation of rat hepatocytes, and the differential expression patterns showed association with histopathological alterations in the hepatocytes. Following treatment with the TNFa mAb, the HepG2 cells showed a higher percentage of apoptotic cells than the untreated control cells (21.45% +/- 4.07% vs. 5.63% +/- 0.93%, q =10.07, P less than 0.01).There was a significant difference in the rate of cells in the G0/G1 phase in the p65-siRNA transfected cells (66.23% +/- 1.29% vs. untreated control cells: 59.00% +/- 1.02%, q =10.98, P less than 0.01). The decreased expression of TNFa and NF-kappaB in cell culture supernatants was positively correlated with the dose of treatment (r =0.89, P less than 0.01), with the most robust decreases being achieved with the highest concentrations ( P less than 0.01). NF-kappaB expression was significantly higher in the HepG2 cells than in the L02 cells, and transfection of p65-siRNA reduced the mRNA (93%) and protein (62%) levels and increased the cell apoptosis index (to 85%).</p><p><b>CONCLUSION</b>Proliferation of hepatoma cells may be significantly inhibited by intervening in the activation of the TNFa/NF-kappaB signaling pathway, which promotes cell apoptosis and blocks cell cycling.</p>
Subject(s)
Adult , Aged , Animals , Female , Humans , Male , Middle Aged , Rats , Apoptosis , Carcinoma, Hepatocellular , Pathology , Cell Proliferation , Hep G2 Cells , Hepatocytes , Metabolism , Liver Neoplasms , Pathology , NF-kappa B , Metabolism , RNA, Messenger , Genetics , Rats, Sprague-Dawley , Signal Transduction , Transfection , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of Annexin A2 (ANXA2) deficiency on the malignant biological behaviour of hepatoma cells.</p><p><b>METHODS</b>The human hepatocellular carcinoma (HCC) cells lines MHCC97-H, HepG2, SMMC-7721, SMMC-7402 and L02 were evaluated. The expression and distribution of ANXA2 were analysed by western blotting, real-time PCR, immunofluorescence and immunohistochemistry.Cell cycle was assessed by flow cytometry and propidium iodide staining. Effects of ANXA2 silencing on invasion and migration potential were assessed by transwell assay and wound healing assay, respectively. Proliferative potential was assessed by CCK-8 kit in vitro and xenograft tumour-growth assay in vivo. The t-test, chi square test, rank sum test, q-test and F-test were used for statistical analyses.</p><p><b>RESULTS</b>The expression level of ANXA2 was markedly higher in the MHCC97-H cells with high metastasis potential than in the HepG2, SMMC-7721, SMMC-7402 and L02 cells. The efficiency of shRNA-mediated ANXA2 deficiency was more than 80%. Immunofluorescence analysis of the MHCC97-H cells indicated that ANXA2 expression was mainly localized to the cellular membrane and cytoplasm, with some nuclear localization. Down-regulation of ANXA2 led to S-phase arrest of HCC cells (q =8.001, P =0.002) and an inhibition of proliferation (q =17.140, P less than 0.01), migration (q =12.808, P less than 0.01) and invasion potential (q =9.069, P =0.002). Xenograft tumour-growth assay indicated that shRNA targeting of ANXA2 led to lower tumour weight (q =11.968, P < 0.001) and down-regulated ANXA2 expression (Z =2.530, P =0.011).</p><p><b>CONCLUSION</b>Down-regulation of Annexin A2 gene transcription effectively changes the biological behaviours of hepatoma cells, and may represent a potential target of HCC molecular therapies.</p>