Objective To explore the effects of cAMP response element binding protein ( CREB) on taxol-induced cell cycle arrest in HeLa cells .Methods MTT assay was used to determine the optimal concentration and treatment time . PCR method was used to construct the recombinant plasmid pCI neo /CREB( PN) and site-directed mutagenesis recombinant plasmid pCI neo/CREB-M(PM).Cell cycle was assayed by flow cytometry .Expressions of pCREB, CREB, cyclins and CDKs were assayed by Western blotting .Results The effective conditions of taxol treatment on HeLa cells were 0.1μmol/L for 24 hours.After cells were treated with 0.1μmol/L taxol, G2/M phase was arrested in a time-dependent manner , accomplished with the decrease of cyclin A , a significant increase of cyclin B1, D1 and phosphorylated CREB (pCREB) protein expression, whereas, no marked changes were observed in cyclin E , CDK1, CDK2, CDK4 and CREB expressions. However, combinantion of PM and taxol treatment significantly reduced taxol-induced G2/M phase arrest, and reversed the effect of taxol-decreased cyclin A, increased cyclin B1 and D1 expression.Conclusion Tanscription factor CREB-mediated specific cyclins play a pivotal role in taxol-induced G 2/M arrest in HeLa cells .

Objective To observe the outcomes of no necrotic cavity lavage after debridement and drainage in patients with infected pancreatic necrosis (IPN).Methods From February 2014 to August 2017,there were 89 patients who were diagnosed as IPN undergoing minimally invasive surgery with no necrotic cavity lavage and large caliber-wide channel drainage in Department of General Surgery,Xuanwu Hospital,Capital Medical University.There were 57 male and 32 female patients aging of (49.5± 14.4)years (ranging from 23 to 84 years).The body mass index of 89 patients was (25.4± 3.8) kg/m2 (ranging from 17.6 to 36.7 kg/m2).Among the 89 patients,37 cases(41.6％) of biliary pancreatitis,10 cases (11.2％) of alcoholic pancreatitis,16 cases (18.0％) of hyperlipidemic pancreatitis,and 26 cases (29.2％) of other reasons.Results Of 89 patients,IPN in 6 patients (6.7％) resolved using only percutaneous catheter drainage;another 83 patients underwent laparoscopic debridement (n =3,3.4％) or video-assisted debridement (n =80,89.9％).No patient was conversed to laparotomy.The average operation frequency and surgery time was (2.3±1.7) times and (56.5±31.7) minutes.The median bleeding volume and total length of stay was 10(0-600) ml and 34(6-172) days separately.The complication rate(Clavien-Dindo grade ≥Ⅲ) was 9.0％ (8/89) which involved mainly abdominal hemorrhage (5/8) and digestive tract fistula formation (3/8).The overall mortality rate was 6.7％ (6/89).Among them,3 cases died of abdominal infection,bacteremia and multiple organ failure,2 cases died of pulmonary infection and bacteremia and 1 case died of fungal infection.Conclusion No necrotic cavity lavage after debridement and drainage operation is considered effective and safe for IPN patients.

Objective To observe the outcomes of no necrotic cavity lavage after debridement and drainage in patients with infected pancreatic necrosis (IPN).Methods From February 2014 to August 2017,there were 89 patients who were diagnosed as IPN undergoing minimally invasive surgery with no necrotic cavity lavage and large caliber-wide channel drainage in Department of General Surgery,Xuanwu Hospital,Capital Medical University.There were 57 male and 32 female patients aging of (49.5± 14.4)years (ranging from 23 to 84 years).The body mass index of 89 patients was (25.4± 3.8) kg/m2 (ranging from 17.6 to 36.7 kg/m2).Among the 89 patients,37 cases(41.6％) of biliary pancreatitis,10 cases (11.2％) of alcoholic pancreatitis,16 cases (18.0％) of hyperlipidemic pancreatitis,and 26 cases (29.2％) of other reasons.Results Of 89 patients,IPN in 6 patients (6.7％) resolved using only percutaneous catheter drainage;another 83 patients underwent laparoscopic debridement (n =3,3.4％) or video-assisted debridement (n =80,89.9％).No patient was conversed to laparotomy.The average operation frequency and surgery time was (2.3±1.7) times and (56.5±31.7) minutes.The median bleeding volume and total length of stay was 10(0-600) ml and 34(6-172) days separately.The complication rate(Clavien-Dindo grade ≥Ⅲ) was 9.0％ (8/89) which involved mainly abdominal hemorrhage (5/8) and digestive tract fistula formation (3/8).The overall mortality rate was 6.7％ (6/89).Among them,3 cases died of abdominal infection,bacteremia and multiple organ failure,2 cases died of pulmonary infection and bacteremia and 1 case died of fungal infection.Conclusion No necrotic cavity lavage after debridement and drainage operation is considered effective and safe for IPN patients.

OBJECTIVE: To summarize the clinical features and spectrum of genetic variants in 12 patients with Loeys-Dietz syndrome (LDS), and to explore the correlation between the type of genetic variants and clinical phenotypes. METHODS: Twelve patients suspected for LDS at Beijing Anzhen Hospital Affiliated to Capital Medical University from January 2015 to January 2022 were selected as the study subjects. Clinical data of the patients were collected. Genomic DNA was extracted from peripheral blood samples and subjected to genetic testing. Pathogenicity of candidate variants was analyzed. RESULTS: The clinical phenotypes of the 12 patients have mainly included cardiovascular, musculoskeletal, craniofacial, skin, ocular and other systemic signs. Four patients (patients 5-1, 5-2, 6, 7) have carried heterozygous missense variants of the TGFBR1 gene, 5 patients (patients 1-1, 1-2, 2, 3, 4) have carried heterozygous variants of the TGFBR2 gene, and 2 patients (patients 8-1, 8-2) had carried heterozygous frameshift variants of the TGFB3 gene. One patient (patient 9) had carried a heterozygous missense variant of the SMAD3 gene. Among these, TGFBR1 c.603T>G (p.1201M) and TGFB3 c.536delA (p.H179FS35) had not been reported previously. CONCLUSION Variants of the TGFBR1, TGFBR2, SMAD3, TGFB2, TGFB3 and SMAD2 genes are mainly associated with LDS. The severity of the disease phenotype caused by the same variant may vary, whilst the clinical phenotype caused by different variant sites may be specific.
Humans ; Loeys-Dietz Syndrome/genetics* ; Receptor, Transforming Growth Factor-beta Type I/genetics* ; Receptor, Transforming Growth Factor-beta Type II/genetics* ; Transforming Growth Factor beta3 ; Face