Objective To investigate the relationships between the severity of non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS).Methods One hundred and twenty-seven cases of NAFLD patients were selected from March 2011 to August 2012 in the First Hospital Affiliated to Fujian Medical University,of them,61 patients with mild NAFLD,45 patients with moderate and 21 patients with severe.And 21 cases without NAFLD were selected as control group during the same hospitalized period.All objects received the measures of height,body weight,waist circumference (WC),blood pressure; Liver ultrasonic examination,the examination of fasting plasma glucose,blood fat and hepatic function detections were also handed by special people.Results The proportion of overweight in the control group and the three NAFLD subgroups were 57.1％ (12/21),88.5％ (54/61),95.6％ (43/45) and 100％ (21/21) respectively (x2 =18.376,P ＜0.001) ;The proportion of the obesity in control group and the three NAFLD subgroups were 19.0％ (4/21),44.3％ (27/61),64.4％ (29/45) and 71.4％ (15/21) respectively(x2 =16.440,P =0.001).The proportion of the metabolic syndrome of the control group and the three NAFLD subgroups were 14.3％ (3/21),45.9％(28/61),71.1％ (32/45) and 71.4％ (15/21) respectively (x2 =22.637,P ＜ 0.05).All three subgroups of NAFLD were higher than the control group (x2 =6.641,P ＜ 0.05 ; x2 =18.562,P ＜ 0.05 ; x2 =14.000,P ＜0.05,respectively).The severity of NAFLD was positively correlated with BMI,WC,TG,FBG,SBP,and DBP (r =0.467,0.503,0.386,0.369,0.279,0.295,P ＜ 0.01),and negatively correlated with HDL-C (r =-0.209,P ＜0.05).Conclusion The severity of NAFLD had significant correlations with metabolic syndrome's components.

Objective To study the clinical curative effect of the recombinant human granulocyte-macro-phage colony-stimulating factor ( rhGM -CSF) joint R-CHOP regimen in the treatment of diffuse large B cell lymphoma (DLBCL).Methods 72 hospitalized patients with DLBCL were chosen from January 2014 to January 2015.The patients were randomly divided into joint CHOP rituxan group ( R-CHOP group,36 cases) and the joint treatment group (36 cases) .The R-CHOP group was treated by R-CHOP regimen,the joint group was given rhGM-CSF on the basis of R-CHOP treatment.Before chemotherapy and 15 days,1 month,3 months after chemotherapy, the peripheral blood was collected,and the monocytes were separated,flow cytometry was used to count HLA-DR, CD197 marked M1 cells and CD68,CDl63 marked M2 cells.4 months after chemotherapy,the curative effect was evaluated.Results 4 months after treatment,the ORR of joint group (91.67%) was significantly higher than that of R-CHOP group (75.00%),and the difference was statistically significant (χ2 =4.372,P<0.05).After treatment, the adverse reactions of joint group,the liver function injuryⅠ-Ⅱlevel 8.33%,Ⅲ-Ⅳlevel 0.00%;White blood cells reduceⅠ-Ⅱlevel 25.00%,Ⅲ-Ⅳ level 5.56%;Thrombocytopenia Ⅰ-Ⅱ level 19.44%,Ⅲ-Ⅳ level;8.33%;Nausea and vomitingⅠ-Ⅱ level 8.33%,Ⅲ-Ⅳ level 0.00%.The adverse reactions after treatment of R-CHOP group,the liver function injury Ⅰ-Ⅱ level 13.89%,grade Ⅲ-Ⅳ2.78%;White blood cells reduceⅠ-Ⅱlevel 36.11%,Ⅲ-Ⅳlevel 11.11%;ThrombocytopeniaⅠ-Ⅱlevel 33.33%,Ⅲ-Ⅳlevel 2.78%;Nau-sea and vomitingⅠ-Ⅱ level 13.89%,Ⅲ-Ⅳ level 0.00%.The increased ratio of TAM quantity in combined treatment group (63.89%) was significantly more than R-CHOP group (38.89%),the difference was statistically significant (χ2 =7.938,P <0.05).In joint group,the positive expression rates of CD68 (46.11%),IL -6 (44.44%),IL-8 (58.33%) were significantly higher than those of R-CHOP group[CD68 (13.89%),IL-6 (19.44%),IL-8 (38.89%)],the differences were statistically significant (χ2 =3.278,3.278,4.489,all P<0.05).Conclusion R-CHOP joint rhGM -CSF has better curative effect than R-CHOP plan and less adverse reaction,and under the induction of rhGM -CSF,mononuclear cells can develop into M1 macrophages,in DLBCL microenvironment,to induce TAM to M1 M2 type in reverse polarization,improve the microenvironment of DLBCL and provide chance for cure of DLBCL.

Risk factors of hyperamylasemia in 152 diabetic ketoacidosis(DKA)patients who had no acute pancreatitis were examined.Serum levels of hemodiastase,natrium,kalium,chlorine,calcium,phosphonium,creatinine,carbon dioxide combining power,osmotic pressure,blood glucose,blood lipids and uric acid were measured.With hemodiastase and other 14 factors as independent variables,the multiple linear regression analysis was performed and the partial regression coefficient was estimated.Blood glucose,serum natrium,osmotic pressure and triglyceride entered the regression equation,and their partial coefficients were 10.26,10.35,2.21 and 8.00,respectively.The constant quantitv was -2162.06.Compared with amylase-normal group,hyperamylasemia group showed statistically significant difference in blood glucose,serum natrium,osmotic pressure and triglyceride levels.Higher blood glucose and triglyceride might be the primary causes of hyperamylasemia.

ObjectiveTo investigate the risk factors and insulin resistance (IR) of nonalcoholic fatty liver disease (NAFLD) with a normal visceral adipose tissue (VAT) area. MethodsA total of 45 NAFLD persons with a normal VAT area who were admitted to Quanzhou First Hospital Affiliated to Fujian Medical University from June 2017 to May 2018 were enrolled as observation group, and 27 non-NAFLD patients with a normal VAT area were enrolled as control group. VAT area, waist circumference, fasting blood glucose (FBG), and fasting insulin (FINS) were measured for both groups, homeostasis model assessment of insulin resistance (HOMA-IR) was calculated, and the correlation of IR with the indices including waist circumference was analyzed. The independent samples t-test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups; the chi-square test was used for comparison of categorical data between groups. Pearson correlation analysis and Spearman correlation analysis were used to investigate the correlation of normally and non-normally distributed continuous data. A forward logistic regression analysis was used to identify related risk factors. ResultsThe NAFLD group had a significantly higher level of IR than the control group, and there was a significant difference in HOMA-IR between the two groups (2.66(1.59-4.06) vs 1.84(125-2.47), Z=364.000, P=0005). IR was positively correlated with FBG (r=0.412, P=0.005), FINS (r=0.789, P＜0001), and TG (r=0.306, P=0041). IR was negatively correlated with HDL(r=-9398,P=0007). The multivariate regression analysis showed that waist circumference was an independent risk factor for NAFLD with a normal VAT area (regression coefficient = 0.181, odds ratio = 1.198, 95% confidence interval: 1.099-1.306, P＜0.001). ConclusionThere is a certain degree of IR in NAFLD patients with a normal VAT, and waist circumference is an independent risk for NAFLD with a normal VAT.

The root cause of tumor recurrence or metastasis is a small part of the tumor with unlimited proliferation of tumor stem cells,which can exist for a long time and continue to self-renewal causing rapid tumor proliferation and invasion, metastasis capacity, drug sensitivity, eventually resulting in the problem of weakened clinical treatment. Therefore,it is of great importance to in-depth understanding of tumor stem cells and then to seek strategies to suppress tumor stem cells in clinical targeted tumor therapy. In this paper,the discovery process of tumor stem cells,biological characteristics,identification and culture methods were described to summary a va-riety of methods to inhibit tumor stem cells according to their characteristics so as to treat tumor. Moreover,it focu-ses on the research progress on antibiotic treatment of cancer stem cells.

Using tree shrew as an animal model, our previous studies have demonstrated synergistic effects of aflatoxin B-1 (AFB(1)) and human hepatitis B virus (HHBV) in the induction of hepatocellular carcinoma (HCC). In the present study, we have examined expression of p53 gene in HCCs induced by AFB(1) with or without HHBV infection in tree shrews. Avidin-biotin-peroxidase complex immunohistochemical method with human p53-CM1 polyclonal antibody has been used to detect p53 expression in serial sections of paraffin-embedded liver and HCC tissues. Five out of 9 animals with HCCs (55.6%) induced by AFB(1) with HHBV infection and 2/3 animals with HCCs (66.7%) induced by AFB(1) alone expressed the p53 protein. Out of 18 HCCs examined, expression of p53 protein was observed in 9/10 moderately and poorly differentiated HCCs (0/8). None of the well differentiated HCCs (0/8) expressed p53 (0%). Similarly, no p53 expression was observed in either non-tumorous or hyperplastic liver tissues or nodules. These results suggest that p53 expression associated with p53 mutation is a late event occurring probably during tumor progression in AFB(1) and HHBV induced hepatocarcinogenesis in the tree shrew. This report is the first example of an experimental animal model where combination of human HBV and AFB(1)-induced HCCs demonstrate p53 expression.
Aflatoxin B1* ; Aflatoxins* ; Animals ; Carcinoma, Hepatocellular* ; Genes, p53* ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis* ; Humans* ; Liver ; Models, Animal ; Tupaiidae*

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lycium barbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl4). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl4 solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl4-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase Ⅱ detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I?V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl₄). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl₄ solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl₄-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.
Animals ; Dogs ; Antioxidants/metabolism* ; Carbon Tetrachloride ; Chemical and Drug Induced Liver Injury/drug therapy* ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Liver ; Metabolic Networks and Pathways ; Mitochondria/metabolism* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Polysaccharides/pharmacology* ; Lycium/chemistry*