ABSTRACT
Extracorporeal membrane oxygenation (ECMO) is a technique in which breathing and circulation are supported extracorporeally. Severe trauma may induce cardiopulmonary failure, for which ECMO can play an adjunctive role in the salvage treatment of circulatory and respiratory failure when conventional treatments are ineffective. Bypass with ECMO can rapidly improve the state such as circulatory failure and hypoxemia in critically ill patients in short term and can partially or fully replace their cardiopulmonary function in long term, winning valuable time for normal recovery of cardiopulmonary function. Because of the physical state of severe trauma patients and the ECMO equipment, there are still various complications clinically. Trauma patients show high risk of bleeding, vulnerability to wound infection and probability of combined organ injury and dysfunction, so more comprehensive measures for the prevention and treatment of complications during the use of ECMO therapy are required. The authors review the research progress in complications and corresponding prevention and treatment strategies during ECMO support for severe trauma, aiming to provide a reference to prevent and treat these complications.
ABSTRACT
Objective To investigate the dynamic changes of gene expressions in mouse jejunum after lethal dose abdomen irradiation (ABI).Methods RNA was extracted from mouse jejunum at 0 and 6 h,3.5 and 5 d after 14 Gy 137Cs γ-ray ABI and then subjected to RNA-sequence analysis.Gene with expressions changed more than 2-fold of control were identified as differentially expressed ones.The selected genes were subsequently analyzed using IPA,Funrich,GO and KEGG software.Results Gene analysis of mouse jejunum samples showed that radiation activated p53 pathway at 6 h and 3.5 d after ABI.Interaction network analysis of genes suggested that Lck,Cdkl and Fyn,genes could play an important role in jejunum damage at 3.5 d after ABI.The gene expression profiles demonstrated that ABI up-regulated DNA damage repair pathways and down-regulated cell adhesion molecules,focal adhesion and IgA production pathways.Conclusions The p53 signaling pathway and some key genes such as Lck,Cdkl,and Fyn may contribute to the radiation-induced intestinal injury.
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Objective To investigate the correlation between the level of apoptosis protein 1 (c-IAP1) and the radiosensitivity of lung cancer cells.Method The survival rate and proliferation of the lung cancer cells lines (A549,H460,H1299,H358,HCC827,H1650) from six human were detected by thiazolyl blue tetrazolium bromide (MTT) and cell colony formation assay.The DNA damage effects of radiation on lung cancer cells were detected by comet assay.The expressions of c-IAP1 protein and its mRNA were determined by Western blot and real-time quantitative PCR.Results The results of MTT and colony formation showed that the radiosensitivity of different lung cancer cells was also different,among which H358 and H460 cells had the highest radiosensitivity than that of H1650 and HCC827 cells,and H1299 and A549 cells had the weakest radiosensitivity.The results of comet assay showed that six kinds of lung cancer cells were suffered by DNA damage after radiation,and the DNA damage of H358 cells was most serious.The results of Western blot and real-time quantitative PCR showed that the c-IAP1 protein level was negatively correlated with the radiosensitivity of lung cancer cells.The higher the c-IAP1 protein level,the weaker the radiosensitivity of cells.The radiosensitivity was also affected by Smac protein levels.Conclusions c-IAP1 may be a selective target gene in mediating the radiosensitivity of lung cancer cells and this paper may contribute to the study of radioresistance and radiosensitization of cancer cell.
ABSTRACT
Objective To investigate the correlation between the level of apoptosis protein 1 (c-IAP1) and the radiosensitivity of lung cancer cells.Method The survival rate and proliferation of the lung cancer cells lines (A549,H460,H1299,H358,HCC827,H1650) from six human were detected by thiazolyl blue tetrazolium bromide (MTT) and cell colony formation assay.The DNA damage effects of radiation on lung cancer cells were detected by comet assay.The expressions of c-IAP1 protein and its mRNA were determined by Western blot and real-time quantitative PCR.Results The results of MTT and colony formation showed that the radiosensitivity of different lung cancer cells was also different,among which H358 and H460 cells had the highest radiosensitivity than that of H1650 and HCC827 cells,and H1299 and A549 cells had the weakest radiosensitivity.The results of comet assay showed that six kinds of lung cancer cells were suffered by DNA damage after radiation,and the DNA damage of H358 cells was most serious.The results of Western blot and real-time quantitative PCR showed that the c-IAP1 protein level was negatively correlated with the radiosensitivity of lung cancer cells.The higher the c-IAP1 protein level,the weaker the radiosensitivity of cells.The radiosensitivity was also affected by Smac protein levels.Conclusions c-IAP1 may be a selective target gene in mediating the radiosensitivity of lung cancer cells and this paper may contribute to the study of radioresistance and radiosensitization of cancer cell.
ABSTRACT
The cGAS-STING pathway plays a significant role in host defense against viral and bacterial infection.In the process,the cytoplasmic free DNA,considered as a danger signal,is recognized by nucleotidyl transferase cGAS.cGAS is activated by double-stranded DNA (dsDNA) and catalyzes the synthesis of a noncanonical cyclic dinucleotide 2'5'-cGAMP from adenosine triphosphate (ATP) and guanosine triphosphate (GTP).cGAMP serve as an endogenous second messenger to stimulate the induction of type Ⅰ interferons via STING.In addition to the exogenous bacterial or viral DNA,abnormal deposition of host DNA in cytosol also activates the cGAS-STING signaling pathway cascade,resulting in inflammation and autoimmune diseases.Subsequent studies found that this pathway also plays an important role in tumor's responsiveness to radio-therapy and chemo-therapy.Activation of cGAS-STING pathway produces or enhances the therapeutic efficacy.These findings suggest that specifically interfering with cGAS-STING activation may hold therapeutic value for the treatment of cancer,infection and inflammatory diseases.In this paper,the activation mechanism of cGAS-STING pathway and its relationship with the treatment of diseases were summarized,and the regulation of cGAS-STING pathway was introduced in detail.