Objective:To investigate the mechanism of downregulated programmed cell death 10 ( PDCD10) expression mediating glioblastoma multiforme (GBM) resistance to temozolomide (TMZ). Methods:U87, LN229 and T98g cell lines were transfected with PDCD10 small interfering RNA or negative small interfering RNA. TMZ-resistant cell lines were constructed using 300 μmol/L TMZ (transfected T98g cell line) and 150 μmol/L TMZ (transfected U87 and LN229 cell lines), respectively: TMZ-resistant U87 cell line transfected with PDCD10 small interfering RNA (shPDCD10-U87-RG cells), TMZ-resistant U87 cell line transfected with negative small interfering RNA (EV-U87-RG cells), shPDCD10-T98g-RG cells, EV-T98g-RG cells, shPDCD10-LN229-RG cells and EV-LN229-RG cells. Flow cytometry and real-time quantitative polymerase chain reaction (qRT-PCR) were used to detect the transfection efficiency of TMZ-resistant cell lines and PDCD10 expressions; MTT assay and colony formation assay were used to verify the drug-resistant ability of TMZ-resistant cell lines. Bioinformatics analysis was performed to detect the correlations of PDCD10 with key genes ( MSH6 and PMS2) in mismatch repair (MMR) system, and drug resistant mechanism was explored by detecting the cell cycle and neurosphere formation ability of drug-resistant cells. Results:(1) qRT-PCR showed that compared with that in EV-U87-RG cells, the PDCD10 expression in shPDCD10-U87-RG cells was statistically down-regulated by (32.85±1.14)% ( t=2.925, P=0.049); compared with that in EV-T98g-RG cells, the PDCD10 expression in shPDCD10-T98g-RG cells was significantly down-regulated by (57.17±1.81)% ( t=3.179, P=0.043); compared with that in EV-LN229-RG cells, the PDCD10 expression in shPDCD10-LN229-RG cells was significantly down-regulated by (33.68±1.34)% ( t=3.085, P=0.045). (2) MTT assay showed that compared with the EV-U87-RG cells, the shPDCD10-U87-RG cells had significantly increased viability ( P<0.05); compared with the EV-T98g-RG cells, the shPDCD10-T98g-RG cells had significantly increased viability ( P<0.05). Among the same kind of cells, the viability 3 d after wash-out was significantly increased compared with that at 72 h after TMZ treatment ( P<0.05). Colony formation assay showed that cell lines with down-regulated PDCD10 expression had higher tumorigenic ability. (3) Compared with EV-U87-RG cells and EV-T98g-RG cells, cells with down-regulated PDCD10 expression (shPDCD10-U87-RG cells and shPDCD10-T98g-RG cells) escaped from TMZ-induced G2/M arrest, resulting in TMZ resistance. (4) Bioinformatics analysis revealed that the PDCD10 expression was positively correlated with MSH6 and PMS2 expressions ( r=0.262, P<0.001; r=0.327, P<0.001); qRT-PCR indicated that downregulated PDCD10 expression caused decreased MSH6 and PMS2 expressions, which disrupted the MMR system. (5) Compared with that by EV-U87 cells, number of neurospheres formed by shPDCD10-U87 cells was significantly increased ( P<0.05); compared with that by EV-U87-RG cells, number of neurospheres formed by shPDCD10-U87-RG cells was significantly increased ( P<0.05). Conclusion:PDCD10 affects the therapeutic sensitivity of GBM to TMZ by arresting cell cycle, disrupting MMR system, and increasing cell stemness.

Objective To investigate the expression of centromere protein F(CENPF)in pancreatic ductal adenocarcinoma(PDAC)and its relationship with the clinicopathological features and prognosis of patients.Methods Based on Gene Expression Omnibus(GEO)from National Center for Biotechnology Information(NCBI),using GEO2R,Venn diagram,Cytoscape,MCODE and GEPIA software to screen out the suspected differential gene CENPF in PDAC;based on the Cancer Genome Atlas(TCGA)and the Genotype-Tissue Expression(GTEx),using NCBI,GEPIA,Ualcan,Oncomine,TIMER software and Kaplan-Meier on-line survival analysis tool to analyze its possible molecular mechanism from the level of messenger RNA(mRNA).In all,surgical specimens of 121 PDAC cases diagnosed at the pathology department of the First Affiliated Hospital of Fujian Medical Univer-sity were analyzed from the histoprotein level to analyze the relationship between CENPF and clinicopathological features and prognosis of PDAC.Results CENPF gene was abnormally expressed in various human cancers,and there was a difference in expression between pancreatic ductal adenocarcinoma and normal pancreatic tissue(P＜0.05),and it was related to the grading(P＜0.05)and prognosis(P=0.038)of pancreatic ductal adenocarcinoma.Immunohistochemistry showed that the expression of CENPF was correlated with nerve invasion(P=0.036),TNM stage(P=0.041),lymph node metastasis(P=0.023),degree of differentiation(P=0.020)and overall survival of pancreatic ductal adenocarcinoma(Log-rank=18.608,P=0.000016),and CENPF expression(HR=2.654,95％CI=1.373-5.131,P=0.004)was an independent risk factor for the prognosis of PDAC patients.CENPF combined with other key module genes in PDAC was mainly enriched in exosomes,extracellular mechanisms,and was related to serine endopeptidase activity and metalloendopeptidase activity.The action pathway of CENPF single gene in pancreatic ductal adenocarcinoma was mainly related to cell cycle,P53 pathway,ubiquitin-mediated proteolysis,and played a joint role with P53 and MDM2 in PDAC.Immune infiltration studies showed that CENPF expression was negatively correlated with CD4+T lymphocyte infiltration and positively correlated with dendritic cell infiltration(both P＜0.05).Conclusion CEN-PF may be involved in the progression of PDAC,and high expression of CENPF indicates a poorer prognosis.Our research is expected to provide more scientific evidence for the prevention and treatment of PDAC.

Pulmonary blast injury has become the main type of trauma in modern warfare, characterized by externally mild injuries but internally severe injuries, rapid disease progression, and a high rate of early death. The injury is complicated in clinical practice, often with multiple and compound injuries. Currently, there is a lack of effective protective materials, accurate injury detection instrument and portable monitoring and transportation equipment, standardized clinical treatment guidelines in various medical centers, and evidence-based guidelines at home and abroad, resulting in a high mortality in clinlcal practice. Therefore, the Trauma Branch of Chinese Medical Association and the Editorial Committee of Chinese Journal of Trauma organized military and civilian experts in related fields such as thoracic surgery and traumatic surgery to jointly develop the Clinical treatment guideline for pulmonary blast injury ( version 2023) by combining evidence for effectiveness and clinical first-line treatment experience. This guideline provided 16 recommended opinions surrounding definition, characteristics, pre-hospital diagnosis and treatment, and in-hospital treatment of pulmonary blast injury, hoping to provide a basis for the clinical treatment in hospitals at different levels.

Blast injury of the chest injury is the most common wound in modern war trauma and terrorist attacks, and is also the most fatal type of whole body explosion injury. Most patients with severe blast injury of the chest die in the early stage before hospitalization or during transportation, so first aid is critically important. At present, there exist widespread problems such as non-standard treatment and large difference in curative effect, while there lacks clinical treatment standards for blast injury of the chest. According to the principles of scientificity, practicality and advancement, the Trauma Society of Chinese Medical Association has formulated the guidance of classification, pre-hospital first aid, in-hospital treatment and major injury management strategies for blast injury of the chest, aiming to provide reference for clinical diagnosis and treatment.

According to the pathological characteristics of symptomatic chronic thoracic and lumbar osteoporotic vertebral fracture (SCOVF), the different clinical treatment methods are selected, including vertebral augmentation, anterior-posterior fixation and fusion, posterior decompression fixation and fusion, and posterior correction osteotomy. However, there is still a lack of a unified understanding on how to choose appropriate treatment method for SCOVF. In order to reflect the new treatment concept and the evidence-based medicine progress of SCOVF in a timely manner and standardize its treatment, the clinical guideline for surgical treatment of SCOVF is formulated in compliance with the principle of scientificity, practicability and advancement and based on the level of evidence-based medicine.

Objective To explore the effect of Kruppel like factor 4 (KLF4) on epithelial-to-mesenchymal transition and invasion ability of pancreatic cancer.Methods The expression of KLF4 in 70 pancreatic cancer tissues and 10 normal pancreatic tissues was detected by immunohistochemistry,and the correlations between KLF4 expression and pathological characteristics were analyzed.Small hairpin RNA targeting KLF4 (sh-KLF4) and negative control shRNA were constructed.After the transfection of shRNA,qRT-PCR and western blot were used to detect the mRNA and protein expression of KLF4,E-cadherin and vimentin,and cell scratch-wound assay and transwell assay were utilized to determine the ability of invasion and metastasis.Results KLF4 expression (47.1％) was lower in pancreatic cancer tissues compared with normal pancreatic tissues (80.0％),and negatively correlated with cell differentiation,tumor stage and distant metastasis.Down-regulated KLF4 expression in PANC1 cell caused decreased mRNA and protein expression of E-cadherin (F =25.71,P =0.0011) and increased mRNA and protein expression of vimentin (F =24.95,P=0.0012).Knockdown of KLF4 in PANC1 cell promoted the transition from epithelial morphology to mesenchymal morphology,and enhanced the healing ability (F =47.82,P ＜ 0.001),migration (F =53.68,P=0.0001) and invasion (F=27.65,P=0.0009).Conclusions Knockdown of KLF4 can promote EMT and enhance the invasion ability of pancreatic cancer.

Objective To summarize the experience of perioperative management for repair of congenital diaphragmatic hernia (CDH) supported by extracorporeal membrane oxygenation (ECMO). Method Retrospective review was conducted for the clinical data of CDH patients who received surgical repair on ECMO from December 2016 to June 2018 in Guangzhou Women and Children's Medical Center. Result Four fetus with prenatal diagnosis of left-side CDH were transferred to our Center and received standardized perinatal management. Moderate-severe pulmonary hypoplasia was recognized after evaluation by fetal imaging. Four cases were initiated with veno-arterial ECMO at 3, 35, 41, 11 h of life, respectively. Repair of the diaphragmatic defect was performed within two weeks after cannulation of ECMO. Furthermore, activated clotting time goals were adjusted to 180～220 s, activated partial thromboplastin time were stabilized between 50～80 s, platelets count were maintained>100×109/L and hematocrit was kept>30％before the surgery. The surgeries of four patients were completed on the 0.9th, 0.5th, 3.6th, 5.1th day of life on ECMO, respectively. The defect was repaired by parachute patch. The operative time was 85～210 min. According to CDH Staging System defect size (A to D), there were two with defects at grade C and other two at grade D. Postoperative total volume of drainage was 215～1301 ml and ECMO duration was 3.0～39.3 d. Three of them survived during neonatal period, while one died. Conclusion Repair of CDH on ECMO is feasible and help to improve neonatal survival, especially for those with moderate-severe pulmonary hypoplasia.

Objective To studythe cephalocaudal relationship ofabdominal aortic bifurcation relative toumbilicus and iliac crest vertex and their correlations with abdominal adipose tissue thickness and age. Methods The vertical distances,cephalocaudal relationship and other related anatomic parameters of aortic bifurcation relative to umbilicus and iliac crest vertex in 108 patientswere measured by consecutive abdominal CT scanning. The correlations of the acquired data with abdominal adipose tissue thickness and age were analyzed using Pearson correlation coefficient. Results Umbilicus was located at cephalad to aortic bifurcation in 67 patients(62.0%), caudal in 34(31.4%)andthe same level in 7(6.5%),with the vertical distance of(4.53 ± 17.51)mm to the aortic bifurcation. No statistically significant relationship was found between abdominal adipose tissue thickness(P>0.05) or age(P>0.05). Iliac crest vertex relative to aortic bifurcationwas located at cephalad,caudal and the same level in 31,71 and 6 patients,taking up 28.7%,65.7%and 5.6%,respectively. Its vertical distance to the bifurcation was(-6.34 ± 14.49)mm,nonrelated with abdominal adipose tissue thickness(P>0.05),but positively correlated with age(P<0.01). The difference in the cephalocaudal relationship of aortic bifurcation relative to umbilicus and iliac crest vertex was statistically significant(P<0.01). Conclusion Compared with iliac crest vertex,umbilicus is an important landmark of locating abdominal aortic terminal occlusion position in vitro because it mostly lies cephalad to aortic bifurcation in the front of the body,not easy to vary with abdominal adipose tissue thickness and age.

Objective Alprostadil can improve the clinical efficacy of the treatment of hepatitis B cirrhosis, but little literature is available about its effect on serum inflammatory factors in patients with hepatitis B cirrhosis.This study aimed to investigate the effect of alprostadil on serum inflammatory factors and liver function of the patients with hepatitis B cirrhosis and its possible action mechanisms.Methods We equally randomized 162 cases of hepatitis B cirrhosis admitted to our hospital from August 2014 to July 2015 into a control and an observation group, the former treated by conventional antiviral, liver-protecting and supportive therapies, and the latter with alprostadil in addition, both for 4 weeks.Then, we obtained the serum inflammatory factors, the contents of serum interleukin-6 (IL-6), high sensitive C reactive protein (hs-CRP) and tumor necrosis factor alpha (TNF-α) as well as such liver function indexes as glutamic-pyruvic transaminase (ALT), total bilirubin (TBil) and prothrombin activity (PTA), and compared them between the two groups before and after treatment.Results After 4 weeks of treatment, the effectiveness rate was significantly higher in the observation than in the control group (82.72% vs 62.96%, P<0.05).Compared with the baseline, the patients in the observation group showed significant improvement after treatment in serum IL-6 ([275.62±43.39] vs [97.15±19.73] pg/mL, P<0.05), hs-CRP ([425.54±55.58] vs [50.23±6.69] ng/L, P<0.05), TNF-α ([321.74±80.73] vs [85.45±13.61] pg/mL, P<0.05), ALT ([139.54±37.36] vs [96.13±23.62] μmol/L, P<0.05), TBil ([395.39±41.13] vs [271.55±25.12] μmol/L, P<0.05), and PTA ([38.50±4.19] vs [68.36±8.11]%), and the improvement was significantly better than in the control group (P<0.05).Conclusion Alprostadil helps alleviate the inflammatory condition, improve the liver function, and promote clinical efficacy in patients with hepatitis B cirrhosis.

Aim To investigate Jianpi Qinghua Chinese herbal compound( JQCC) on the expressions of the rel-evant proteins of TLR4 and its downstream MyD88-de-pendent pathways, and on the inflammatory factor TNF-α in the animal model of chronic atrophic gastritis ( CAG) in rats, so as to discuss the molecular mecha-nism of JQCC in the treatment of CAG. Methods 53 Wistar rats were randomly divided into the blank con-trol group(n=8) and the CAG model group(n=45), and the animal model of CAG in rats was replicated by the “ammonia + sodium deoxycholic acid + ethanol”method. After the successful modeling was confirmed, the rest of the 40 CAG rats in the CAG model group were divided into the model group, the vitacoenzyme-tablet group, the low dose of JQCC group, the medium dose of JQCC group, the high dose of JQCC group ( each group n =8 ) . The experimental animals of all the groups were given intragastric administration of medication continuously for 30 days. Then the patho-logical histological changes were observed by HE stai-ning. The protein expressions of TLR4, MyD88, NF-КB and COX-2 were tested by Western-blot assay. And the serum TNF-α level was measured by ELISA. Results The protein expressions of TLR4 , MyD88 , NF-КB and COX-2 and the serum TNF-α level in the rats in the model group were increased evidently ( P<0. 01). Compared with the model group, the gastric mucosa lesions were improved in the low dose of JQCC group, the medium dose of JQCC group, the high dose of JQCC group, together with significant decreases of the protein expressions of TLR4 , MyD88 , NF-κB and COX-2 and the serum TNF-α level ( P <0. 05 or P <0. 01 ) . Conclusion JQCC could effectively improve the pathological and histological changes in the gastric mucosa in CAG rats, and the therapeutic mechanism might be related to the expressions of the relevant pro-teins of TLR4-MyD88-dependent pathways and the ex-pressions of anti-inflammatory cytokines.