ABSTRACT
BACKGROUND: Pancreatoduodenectomy (PD) is the most effective surgical procedure to remove a pancreatic tumor, but the prevalent postoperative complications, including postoperative pancreatic fistula (POPF), can be life-threatening. Thus far, there is no consensus about the prevention of POPF. AIM: To determine possible prognostic factors and investigate the clinical effects of modified duct-to-mucosa pancreaticojejunostomy (PJ) on POPF development. METHODS: We retrospectively collected and analyzed the data of 215 patients who underwent PD between January 2017 and February 2022 in our surgery center. The risk factors for POPF were analyzed by univariate analysis and multivariate logistic regression analysis. Then, we stratified patients by anastomotic technique (end-to-side invagination PJ vs modified duct-to-mucosa PJ) to conduct a comparative study. RESULTS: A total of 108 patients received traditional end-to-side invagination PJ, and 107 received modified duct-to-mucosa PJ. Overall, 58.6% of patients had various complications, and 0.9% of patients died after PD. Univariate and multivariate logistic regression analyses showed that anastomotic approaches, main pancreatic duct (MPD) diameter and pancreatic texture were significantly associated with the incidence of POPF. Additionally, the POPF incidence and operation time in patients receiving modified duct-to-mucosa PJ were 11.2% and 283.4 min, respectively, which were significantly lower than those in patients receiving traditional end-to-side invagination PJ (27.8% and 333.2 minutes). CONCLUSION: Anastomotic approach, MPD diameter and pancreatic texture are major risk factors for POPF development. Compared with traditional end-to-side invagination PJ, modified duct-to-mucosa PJ is a simpler and more efficient technique that results in a lower incidence of POPF. Further studies are needed to validate our findings and explore the clinical applicability of our technique for laparoscopic and robotic PD.
ABSTRACT
BACKGROUND: Most colorectal cancer (CRC) patients are diagnosed at an advanced or metastatic stage with poor prognosis. Ubiquitin-specific protease 6 N-terminal-like protein (USP6NL) with high expression in CRC tissues regulates CRC cell proliferation via Wnt/ß-catenin pathway. We hypothesized that USP6NL impacts CRC growth and inhibition of USP6NL may be a novel treatment strategy to improve CRC therapy. METHODS: USP6NL level in human CRC tissues and its association with tumor growth and metastasis were examined. Its roles and potential mechanisms in regulating tumor growth were studied by genetic and pharmacological manipulation of CRC cells in vitro and in vivo. RESULTS: Herein, we found that USP6NL was up-regulated in tumorous tissues of CRC patients. Our data suggested that knockdown of USP6NL in human CRC cell lines (HCT116 and LOVO cells) inhibited cell proliferation, induced G0/G1 cell cycle arrest, and prevented the tumorigenicity of HCT116 cells in nude mice, and which was associated with the prevention of Wnt/ß-catenin pathway. On the contrary, USP6NL overexpression in human CRC cells (SW480) showed the opposite result. Our data suggested that the promoted cell proliferation, G1/S cell cycle progression, and the enhanced expression of ß-catenin Cyclin D1 and C-myc while reduced P27 induced by the overexpression of USP6NL were significantly reversed by additional treatment of XAV939, indicating that activating Wnt/ß-catenin pathway was the mechanism, by which USP6NL exerted carcinogenesis in CRC in vitro. Besides, our data suggested that knockdown of USP6NL increased the ubiquitination of ß-catenin, indicating that USP6NL may serve as a deubiquitinase that regulated ß-catenin accumulation in this process. Furthermore, 10058-F4 down-regulated USP6NL, inhibited CRC cell proliferation and induced cell cycle arrest. The result demonstrated a possible feedback loop between USP6NL, ß-catenin and C-myc in regulating CRC cell growth. CONCLUSION: USP6NL was an oncogene in CRC, and it may be a potential target for the treatment of CRC.
ABSTRACT
The risk factors of high trait anger of juvenile offenders were explored through questionnaire study in a youth correctional facility of Hubei province, China. A total of 1090 juvenile offenders in Hubei province were investigated by self-compiled social-demographic questionnaire, Childhood Trauma Questionnaire (CTQ), and State-Trait Anger Expression Inventory-II (STAXI-II). The risk factors were analyzed by chi-square tests, correlation analysis, and binary logistic regression analysis with SPSS 19.0. A total of 1082 copies of valid questionnaires were collected. High trait anger group (n=316) was defined as those who scored in the upper 27th percentile of STAXI-II trait anger scale (TAS), and the rest were defined as low trait anger group (n=766). The risk factors associated with high level of trait anger included: childhood emotional abuse, childhood sexual abuse, step family, frequent drug abuse, and frequent internet using (P<0.05 or P<0.01). Birth sequence, number of sibling, ranking in the family, identity of the main care-taker, the education level of care-taker, educational style of care-taker, family income, relationship between parents, social atmosphere of local area, frequent drinking, and frequent smoking did not predict to high level of trait anger (P>0.05). It was suggested that traumatic experience in childhood and unhealthy life style may significantly increase the level of trait anger in adulthood. The risk factors of high trait anger and their effects should be taken into consideration seriously.
Subject(s)
Adult Survivors of Child Abuse/psychology , Anger , Criminals/psychology , Adolescent , Adult , China , Female , Humans , Life Style , Logistic Models , Male , Psychiatric Status Rating Scales , Risk Factors , Surveys and Questionnaires , Young AdultABSTRACT
The risk factors of high trait anger of juvenile offenders were explored through question naire study in a youth correctional facility of Hubei province,China.A total of 1090 juvenile offenders in Hubei province were investigated by self-compiled social-demographic questionnaire,Childhood Trauma Questionnaire (CTQ),and State-Trait Anger Expression Inventory-Ⅱ (STAXI-Ⅱ).The risk factors were analyzed by chi-square tests,correlation analysis,and binary logistic regression analysis with SPSS 19.0.A total of 1082 copies of valid questionnaires were collected.High trait anger group (n=316) was defined as those who scored in the upper 27th percentile of STAXI-Ⅱ trait anger scale (TAS),and the rest were defined as low trait anger group (n=766).The risk factors associated with high level of trait anger included:childhood emotional abuse,childhood sexual abuse,step family,frequent drug abuse,and frequent internet using (P＜0.05 or P＜0.01).Birth sequence,number of sibling,ranking in the family,identity of the main care-taker,the education level of care-taker,educational style of care-taker,family income,relationship between parents,social atmosphere of local area,frequent drinking,and frequent smoking did not predict to high level of trait anger (P＞0.05).It was suggested that traumatic experience in childhood and unhealthy life style may significantly increase the level of trait anger in adulthood.The risk factors of high trait anger and their effects should be taken into consideration seriously.
