Objective:To detect A20 mutation and to investigate its relationship with clinicopathologic features, prognosis, and re-sistance to therapy of diffuse large B cell lymphoma (DLBCL). Methods:A total of 104 cases with DLBCL and their clinical data were collected;follow-up was performed on a few of DLBCL patients. The expression of P-gP and Ki-67 protein was detected with immuno-histochemical staining. The A20 gene mutation in exons 3, 6, and 7 were examined by polymerase chain reaction and DNA sequencing. Finally, the correlation of genetic abnormality of A20 with clinicopathologic features was analyzed. Results:Missense mutation in ex-on 3 of A20 gene was identified in 18 of 104 patients (17.3%). The A20 gene mutation at site 73 of exon 3 was greater in the cases with activated B cell-like-DLBCL than with germinal center B-cell-like-DLBCL (18.5%vs. 2.5%, P=0.010). In contrast to the advanced clin-ical stage and high International Prognostic Index (IPI) cases, the rate of A20 mutation was superior to the opposite (P<0.05). The ex-pression for P-gP was higher in the cases with mutation than that of those with wild-type A20 gene (16/18 vs. 52/86, P=0.021). The dif-ference in A20 mutation between the groups of low and high positive expression for Ki-67 (1/17 vs. 26/60, P=0.030) was significant. DLBCL with A20 mutation had an increasing recurrence tendency (P=0.06) and a worse survival (P=0.016) compared with those with wild-type A20 gene. Conclusion:The A20 mutation has a certain influence on the clinicopathologic characteristics and survival condi-tions of BLBCL patients. Probably, A20 mutation is a factor associated with a poor prognosis of DLBCL.

Objective To evaluate the feasibility and efficacy of endoscopic push?radial dissection (EPRD)for benign esophageal stricture(BES). Methods Clinical data of 24 patients diagnosed as having BES who received EPRD were analyzed. The procedure and efficacy were evaluated. Results All 24 patients underwent EPRD successfully with mean operation time being 32 min(15?45 min).The mean esophageal stric?ture incision length was 3?? 2 cm (1?? 0?8?? 0 cm).No severe complications related to EPRD occurred, or trans?ferred for surgery. Patients were followed up for 1?5 months (mean 2?? 8 months). Dysphagia was relieved signif?icantly during the follow?up in 23 patients where endoscopy could go through smoothly. But dysphagia re?oc?curred in one patient 2 weeks after the operation, who underwent a second EPRD and stent implantation, then dysphagia was relieved. Conclusion EPRD is safe, feasible and effective for benign esophageal stricture.

Death domain-associated protein (DAXX) as a multifunctional nuclear protein widely resides in nucleolus, nucleoplasm, chromatin, promyelocytic leukaemia nuclear bodies (PML-NBs) and cytoplasm. It plays significant roles in transcriptional regulation, apoptosis, cell cycle and other biological activities. Small ubiquitin-like modifier (SUMO) is required for SUMOylation which is a highly conserved post-translational modification in a wide variety of cellular processes. Numerous studies demonstrated that SUMOylation has a great effect on the subcellular localization and functional regulation of DAXX. This review will provide a summary for SUMOylation of DAXX.
Adaptor Proteins, Signal Transducing ; physiology ; Gene Expression Regulation ; Humans ; Nuclear Proteins ; physiology ; Sumoylation

Based on the principle of the pathway engineering, a novel pathway of producing glycerol was built in E. coli. The gpd1 gene encoding glycerol 3-phosphate dehydrogenase and the hor2 gene encoding glycerol 3-phosphatase were cloned from Saccharomyces cerevisiae, respectively. The two genes were inserted into expression vector pSE380 together. A recombinant plasmid pSE-gpd1-hor2 containing polycistron was constructed under the control of the strong trc promoter. Then it was transformed into E. coli BL21. The result showed the recombinant microorganism GxB-gh could convert glucose to glycerol directly. And the recombinant microorganism GxB-gh was incubated to produce glycerol from D-glucose in the fermentor. The maximal concentration of glycerol was 46.67g/L at 26h. Conversion rate of glucose was 42.87%. The study is about "green" producing glycerol by recombinant microorganism and is also useful for further working in recombining microorganism of producing 1,3-propanediol.
Cloning, Molecular ; Escherichia coli ; genetics ; metabolism ; Fermentation ; Fungal Proteins ; biosynthesis ; genetics ; Genetic Engineering ; Glycerol ; metabolism ; Glycerolphosphate Dehydrogenase ; biosynthesis ; genetics ; Phosphoric Monoester Hydrolases ; biosynthesis ; genetics ; Saccharomyces cerevisiae ; enzymology ; genetics

Objective: To explore the intrinsic mechanism of emotional intelligence and trait anger in the association between childhood psychological abuse and aggressive behavior among middle school students,and to provide a theoretical basis for intervention of aggressive behaviors. Methods: By using the multi-stage stratified random sampling method, 2 458 middle school students in Guizhou Province were selected, and group tests were carried out using psychological abuse scale, attack behavior scale,emotional intelligence scale and characteristic anger scale. Results: Agressive behavior, trait anger and emotional intelligence differed significantly by gender(t=2.19，5.12，-2.34，P<0.05), and there were significant differences in aggressive behavior, psychological abuse, emotional intelligence and trait anger among middle school students of different student origins by residence(t=-18.77，-6.04，9.10，-9.94，P<0.05). Childhood psychological abuse (r=0.41), temperamental trait anger (r=0.52) and reactive trait anger (r=0.49) were significantly positively correlated with aggressive behavior（P<0.05）. Emotional intelligence was significantly negatively correlated with aggressive behavior (r=-0.33, P<0.05). The test of multiple mediation effects showed that emotional intelligence, temperamental trait anger and reactive trait anger played multiple mediation roles between psychological abuse and aggressive behavior in childhood. Conclusion Childhood psychological abuse could not only directly affect the aggressive behavior of middle school students, but also further affect the aggressive behavior through emotional intelligence and trait anger. Emotional intelligence and idiosyncratic anger are important internal mechanisms by which childhood psychological abuse affects aggressive behavior.

OBJECTIVETo provide a quantitative summary in estimating the association between polymorphisms of 3 loci in NRAMP1 gene and susceptibility to tuberculosis in East-Asia population by means of meta-analysis.

METHODSWe searched databases (MEDLINE, OVID and CBM disc) from January 1995 to May 2005 using "NRAMP1" or "SLC11A1", in combination with "tuberculosis", also performed a manual search of citations from relevant original studies and literature. For each study involved, information was collected concerning the characteristics of the subjects, such as mean age of cases and the size of study. These characteristics were used to evaluate the sources of variation. Summary ORs and corresponding 95% CI were estimated by fixed effects (Mantel-Haenszel) or random effects (DerSimonian and Laird) model. To check for publication bias,a funnel plot, using Egger's linear regression method, was constructed. Cumulative meta-analysis was performed to evaluate whether the summary OR for studies with the polymorphisms of the 3 loci in the NRAMP1 gene was changing along with the accumulation of more data. Chi-square goodness of fit was used to test deviation from Hardy-Weinberg equilibrium.

RESULTSEight publications, with the number of cases and controls of 1067 and 1084 respectively, were identified and all genotype frequencies were consistent with Hardy-Weinberg equilibrium. The summary ORs for studies with polymorphisms of 3' UTR, D543N and INT4 loci of the NRAMPI gene among the East-Asia population were 1.68(95% CI: 1.31-2.16, P< 0.001), 1.78(95% CI: 1.38-2.30, P< 0.001), 1.56 (95% CI: 0.72- 3.35, P = 0.26), respectively when compared with their corresponding common homozygotes. Publication bias was not found in the studies with the three loci, except for INT4 locus, by Egger linear regression method. The cumulative summary effects ORs were 1.85 (P = 0.02) in 2000, 1.35 (P = 0.12) in 2002,1.64 (P= 0.001) in 2003, and 1.68 (P<0.001) in 2004 for 3'UTR locus, 1.88 (P = 0.001) in 2000,1.65(P = 0.001) in 2002,1.70(P<0.001) in 2003,1.76(P<0.001) in 2004, and 1.78(P<0.001) in 2005 for D543N locus, and 0.88(P = 0:70) in 2002, 2.50(P = 0.41) in 2003, 1.52(P = 0.42) in 2004 and 1.56(P = 0.26) in 2005 for INT4 loucs.

CONCLUSIONPolymorphisms at 3' UTR and D543N loci had statistically significant association between the NRAMP1 variants and susceptibility to tuberculosis in the East-Asia descendants, and variant in the INT4 locus failed to show statistically significant association in the East-Asia population.

Asian Continental Ancestry Group ; genetics ; Cation Transport Proteins ; genetics ; Far East ; Genetic Predisposition to Disease ; Humans ; Odds Ratio ; Polymorphism, Genetic ; Tuberculosis ; genetics

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

OBJECTIVE: To investigate the relationship between acute myeloid leukemia (AML) patients ASXL2, ZBTB7A gene mutations and the prognosis. METHODS: 42 AML Patients treated in our hospital from January 2014 to January 2016 were selected and ASXL2 and ZBTB7A genes of their bone marrow samples were sequenced, the genetic characteristics and prognosis of core-binding factor-AML(CBF-AML) patients with ASXL2 and ZBTB7A mutations were analyzed. RESULTS: ASXL2 (33.3%) and ZBTB7A (9.5%) mutations were found in t (8; 21) AML patients. Compared with wild-type, patients with ASXL2 mutations showed significantly higher white blood cell count at diagnosis ［(9.49±1.85)×10 CONCLUSION ASXL2 and ZBTB7A mutations are frequently found in t (8; 21) AML patients. The mutation of ASXL2 and ZBTB7A genes shows no significant effect on the prognosis of AML patients.
Cell Line, Tumor ; DNA-Binding Proteins/genetics* ; Humans ; Leukemia, Myeloid, Acute/genetics* ; Mutation ; Oncogene Proteins, Fusion/genetics* ; Prognosis ; Repressor Proteins/genetics* ; Transcription Factors/genetics*