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Background: Our previous research reported a novel deeper intubation technique (DIT) of the ileus tube for acute bowel obstruction patients. The present study was designed to evaluate the effect of this novel technique on the clinical outcomes of patients with obstruction using a large cohort. Methods: The detailed clinical data were analyzed retrospectively from 496 obstruction patients who underwent intubation technique from 2014 to 2019 in five hospitals. The patients were divided into either the DIT group or the traditional intubation technique (TIT) group. The groups were matched in a 1:1 ratio using propensity scores, and the primary outcome was the short-term clinical outcomes for patients. Results: The baseline characteristics were similar between the DIT group and the TIT group after matching. Compared with the TIT group, the DIT group had a significantly deeper intubation depth, with shorter hospital days, shorter time to first flatus and defecation, lower pain score, increased drainage volume, and lower emergency surgery rate. Importantly, the inflammatory factors such as white blood cell, C-reactive protein, and procalcitonin levels were significantly lower in the DIT group. In addition, the DIT treatment was significantly useful for adhesive obstruction patients. Conclusion: The DIT procedure led to better short-term clinical outcomes compared with the TIT procedure, indicating that DIT is a safe and feasible technique for the treatment of intestinal obstruction that is worthy of further popularization and clinical application.
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BACKGROUND: Histone modification plays essential roles in hepatocellular carcinoma (HCC) pathogenesis, but the regulatory mechanisms remain poorly understood. In this study, we aimed to analyze the roles of Megakaryoblastic leukemia 1 (MKL1) and its regulation of COMPASS (complex of proteins associated with Set1) in HCC cells. METHODS: MKL1 expression in clinical tissues and cell lines were detected by bioinformatics, qRT-PCR and western blot. MKL1 expression in HCC cells were silenced with siRNA, followed by cell proliferation evaluation via Edu staining and colony formation, migration and invasion using the Transwell system, and apoptosis by Hoechst staining. HCC cell tumorigenesis was assessed by cancer cell line-based xenograft model, combined with H&E staining and IHC assays. RESULTS: MKL1 expression was elevated in HCC cells and clinical tissues which was correlated with poor prognosis. MKL1 silencing significantly repressed proliferation, migration, invasion and colony formation but enhanced apoptosis in HepG2 and Huh-7 cells. MKL1 silencing also inhibited COMPASS components and p65 protein expression in HepG2 and Huh-7 cells. HepG2 cell tumorigenesis in nude mice was severely impaired by MKL1 knockdown, resulted into suppressed Ki67 expression and cell proliferation. CONCLUSION: MKL1 promotes HCC pathogenesis by regulating hepatic cell proliferation, migration and apoptosis via the COMPASS complex and NF-κB signaling.
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Carcinoma Hepatocelular/metabolismo , N-Metiltransferasa de Histona-Lisina/metabolismo , Neoplasias Hepáticas/metabolismo , FN-kappa B/metabolismo , Transactivadores/metabolismo , Factor de Transcripción ReIA/metabolismo , Animales , Apoptosis/genética , Carcinoma Hepatocelular/etiología , Carcinoma Hepatocelular/patología , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Femenino , Silenciador del Gen , Células Hep G2 , Xenoinjertos , Código de Histonas , Humanos , Neoplasias Hepáticas/etiología , Neoplasias Hepáticas/patología , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Invasividad Neoplásica , Proteínas de Neoplasias/metabolismo , Trasplante de Neoplasias , Pronóstico , ARN Interferente Pequeño , Transactivadores/genética , Ensayo de Tumor de Célula MadreRESUMEN
BACKGROUND: This study aims to determine whether palliative bypass surgery (choledochojejunostomy and gastrojejunostomy), which has a lower incidence of complications and mortality, remains an option for elderly patients with resectable periampullary carcinoma. METHODS: The clinical data of elderly patients with resectable periampullary carcinoma who had been admitted to Qilu Hospital and had undergone palliative bypass surgery in recent years was collected. Factors concerning these patients, including surgical duration, intraoperative haemorrhage, the incidence of complications, mortality, and survival rate, were compared to those in patients who had received radical surgery. RESULTS: Surgical duration, intraoperative haemorrhage, the incidence of complications, pancreatic fistula, abdominal infections, pneumonia, and postoperative hospital stay were found to be more apparent in patients in the radical surgery group than in patients in the palliative bypass surgery group and the difference was statistically significant (P<0.05). However, regarding blood transfusions, deaths, biliary fistula, postoperative haemorrhage, wound infection, delayed gastric emptying, and heart disease, the difference was not statistically significant (P≥0.05). CONCLUSIONS: For elderly patients with periampullary carcinoma, palliative bypass surgery offers safety, low risks, a quick recovery, a shorter surgery duration, less intraoperative haemorrhage, and a lower incidence of complications compared to radical surgery. Although it has a lower long-term survival rate compared to radical surgery, palliative surgery remains an option for elderly patients who prefer not to undergo the invasive procedure of radical surgery.
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Nephrotic syndrome is one of the most common kidney diseases in children, most of which were caused by minimal change disease, which could be typically reversible with the use of corticosteroid therapy in steroid-sensitive nephrotic syndrome. At the same time, there still exist some side effects caused by drugs and steroid-resistant nephrotic syndrome. It's urgent to investigate more accurate treatment to improve the situation. In this study, we chose mice model by adriamycin to observe the effect of IL-18BP intervention. It was shown that (1) weak general conditions appeared after adriamycin administration; (2) Proteinuria showed up after adriamycin-administration and then decreased with IL-18 binding protein intervention; (3) the level of triglyceride, cholesterol, IL-18, IFN-γ, and TNF-α in the IL-18 binding protein intervening group were significantly lower than those in the adriamycin-minimal change disease MCD group (all P < 0.01), and the levels of serum total protein, albumin, and IL-4 were significantly higher than those in the adriamycin-minimal change disease MCD group (P < 0.05, P < 0.01, P < 0.05); (4) ultramicrostructural examination demonstrated wide fusion of foot processes of glomerular epithelial cells in adriamycin-minimal change disease MCD mice, while only focal fusion occurred in IL-18 binding protein intervening mice. In conclusion, IL-18BP repaired the proteinurine, histopathological injury of kidney, and the induction of serum cytokines in mice models of minimal change disease induced by adriamycin.
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Despite evidence that MRTF-A/B, co-activators of serum response factor (SRF), promotes tumor cell invasion and metastasis in cancer, there are no studies describing MRTF-A/B in pancreatic cancer. To clarify involvement of MRTF-A/B expression in pancreatic cancer, we used quantitative reverse transcription-polymerase chain reaction and western blot analysis to detect MRTF-A/B in pancreatic cancer, intraductal papillary mucinous neoplasm (IPMN) and non-neoplastic pancreata. MRTF-A/B expression differs significantly between cancer and non-neoplastic tissues as well as between non-neoplastic tissues and IPMN bulk tissues. Next, we studied the roles of MRTF-A/B in vitro. Overexpression of MRTF-A/B promoted epithelial-mesenchymal transition (EMT) and generated stem cell-like cells in normal pancreatic cells. We performed quantitative reverse transcription-polymerase chain reaction to detect the level of MRTF-A/B in 19 pancreatic cancer cell lines. We found that their expression was associated with gemcitabine resistance. Like in normal pancreatic cells, MRTF-A/B also promoted EMT and promoted formation of stem cell-like cells in pancreatic cancer and they could regulate microRNA expression associated with EMT and CICs. Finally, to further demonstrate the roles of MRTF-A/B in vivo, we performed nude mouse model of s.c. xenograft and found that overexpression of MRTF-A and MRTF-B promoted pancreatic cancer growth. Elucidating the roles of MRTF-A/B will help us to further understand molecular basis of the disease and offer new gene targets for effective therapies.
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Regulación Neoplásica de la Expresión Génica , Neoplasias Pancreáticas/genética , Transactivadores/genética , Factores de Transcripción/genética , Animales , Línea Celular Tumoral , Desoxicitidina/análogos & derivados , Desoxicitidina/farmacología , Resistencia a Antineoplásicos , Transición Epitelial-Mesenquimal , Humanos , Ratones , Trasplante de Neoplasias , Células Madre Neoplásicas/metabolismo , Células Madre Neoplásicas/patología , Neoplasias Pancreáticas/metabolismo , Neoplasias Pancreáticas/patología , Transactivadores/metabolismo , Factores de Transcripción/metabolismo , GemcitabinaRESUMEN
AIMS: Our study aimed to investigate the association of cytotoxic T-lymphocyte antigen-4 (CTLA-4) rs231775 polymorphism with hepatocellular carcinoma (HCC) susceptibility. METHODS: Genotypes distribution of the control was tested by Hardy-Weinberg Equilibrium (HWE). CTLA-4 rs231775 polymorphism was analyzed in 80 patients with HCC and 78 healthy controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, and the expression level of CTLA-4 in the serum of all subjects was detected using enzyme linked immunosorbent assay (ELISA) kit. Odd ratio (OR) with 95% confidence interval (CI) were calculated by chi-squared test to determine the correlation of CTLA-4 rs231775 polymorphism and the risk of HCC. RESULTS: The genotypes frequencies of the control group were in accordance with HWE. The frequencies of genotype AA and allele A in CTLA-4 rs231775 polymorphism were significantly higher in cases than the control group (AA vs. GG: OR=2.81, P=0.043; A vs. G: OR=1.63, P=0.022). Meanwhile, the expression level of CTLA-4 was remarkably higher in cases compared with the controls. The association analysis indicated that AA genotype carriers exhibited highest level of CTLA-4 (P<0.01). CONCLUSIONS: The genotype AA and allele A of CTLA-4 rs231775 polymorphism may have negative effects on HCC by modifying the expression and functions of CTLA-4.
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Carcinoma Hepatocelular/genética , Predisposición Genética a la Enfermedad/genética , Neoplasias Hepáticas/genética , Proteínas de Transporte de Membrana/genética , Polimorfismo de Nucleótido Simple , Adulto , Anciano , Estudios de Casos y Controles , Ensayo de Inmunoadsorción Enzimática , Femenino , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo de Longitud del Fragmento de RestricciónRESUMEN
BACKGROUND: Both transcriptional factor Ets-1 and integrin αvß6 play an important role in the development and progression of cancer. The aim of our study was to investigate the expression of Integrin αvß6 and Ets-1, two proteins' correlation and their clinical significance in colorectal cancerous tissues. RESULTS: The specimens were arranged into microarray using the immunohistochemistry method to investigate the expression of integrin αvß6 and transcriptional factor Ets-1 in these tissues. Among the 158 tissue specimens, 36.07% were positive for αvß6 expression, and 57.59% were positive for Ets-1 expression. There were obvious statistical differences existed regarding differentiation, N stage, M stage and TNM stage between αvß6 and Ets-1 positively and negatively expressing tumors. The correlation analysis confirmed the expression of αvß6 and Ets-1 were positively correlated in colorectal cancer. The Kaplan-Meier survival analysis showed that patients who were both αvß6 and Ets-1 positive relapsed earlier than those who were both αvß6 and Ets-1 negative; and the former group had much shorter survival time than the latter. And Cox model indicated that αvß6 and Ets-1 were the independent prognostic factors (RR = 2.175, P = 0.012 and RR = 3.903, P < 0.001). CONCLUSIONS: The expression of αvß6 and Ets-1 were positively correlated, and their expression degrees were associated with the differentiation, N stage, M stage and TNM stage of the tumors. Hence, the combination of αvß6 and Ets-1 can be used as a prognostic marker in colorectal cancer, especially for the early stage.