A mitochondrion-targeted cyanine agent for NIR-II fluorescence-guided surgery combined with intraoperative photothermal therapy to reduce prostate cancer recurrence.

Poorly identified tumor boundaries and nontargeted therapies lead to the high recurrence rates and poor quality of life of prostate cancer patients. Near-infrared-II (NIR-II) fluorescence imaging provides certain advantages, including high resolution and the sensitive detection of tumor boundaries. Herein, a cyanine agent (CY7-4) with significantly greater tumor affinity and blood circulation time than indocyanine green was screened. By binding albumin, the absorbance of CY7-4 in an aqueous solution showed no effects from aggregation, with a peak absorbance at 830 nm and a strong fluorescence emission tail beyond 1000 nm. Due to its extended circulation time (half-life of 2.5 h) and high affinity for tumor cells, this fluorophore was used for primary and metastatic tumor diagnosis and continuous monitoring. Moreover, a high tumor signal-to-noise ratio (up to ~ 10) and excellent preferential mitochondrial accumulation ensured the efficacy of this molecule for photothermal therapy. Therefore, we integrated NIR-II fluorescence-guided surgery and intraoperative photothermal therapy to overcome the shortcomings of a single treatment modality. A significant reduction in recurrence and an improved survival rate were observed, indicating that the concept of intraoperative combination therapy has potential for the precise clinical treatment of prostate cancer.

Single-dye NIR-II chemiluminescence system for H2O2 imaging.

An efficient single-dye NIR-II CL system was proposed for the first time with the longest emission peak around 1000 nm. Biocompatible CL nanoparticles were developed and a surprising CL intensity enhancement was found in the presence of the BASZn nanoenzyme by about three orders of magnitude. Such an NIR-II CL system was demonstrated for glucose sensing, tumor therapy and in vivo H2O2 imaging. Via theoretical and experimental analyses, a novel electron transfer model was established for such a chemiluminescence system rather than the generally considered HOMODye-LUMODOD model. These findings provide useful guidelines for designing efficient single-dye NIR-II CL systems.

Simulating the Structure of Carbon Dots via Crystalline π-Aggregated Organic Nanodots Prepared by Kinetically Trapped Self-Assembly.

This work reports the successful preparation of a new type of crystalline luminescent organic nanodot (<3.5 nm) by kinetically trapped self-assembly, which is then used as a simplified π-packing model to simulate the structure of CDs. The precise structure and J-aggregation-induced photoluminescence (PL) of the nanodots are revealed by investigating the structural relationship between the nanodots and the corresponding single crystals and their properties. Compared with the single crystals, crystalline organic nanodots show longer PL lifetime, higher PL quantum yield, and narrower PL peak, indicating that they are potential organic quantum nanodots. In addition, the efficient π-stacking environment in the corresponding single crystals can promote π-aggregation-induced PL anisotropy. This work indicates crystalline organic nanodots with precise structures to be potentially useful for understanding the structures of CDs and to be attractive potential luminescent materials.

Increased plasma level of apelin with NYHA grade II and III but not IV.

The change in plasma apelin level in heart failure (HF) patients is controversial. We investigated the change in plasma apelin level in HF patients versus control and non-HF patients. The plasma level of apelin was measured by ELISA and plasma level of B-type natriuretic peptide (BNP) by fluorescence immunoassay. We included 101 patients with HF, 32 patients without HF and 20 controls. The three groups did not differ in general and clinical characteristics. Plasma levels of apelin and BNP were both higher in HF patients than non-HF patients and controls. Plasma levels of apelin and BNP were not correlated. Plasma level of BNP was increased with increasing New York Heart Association grade and apelin level was decreased. Apelin level was lower in HF patients with NYHA grade IV than in controls and non-HF patients. Apelin level had 75% diagnostic value for HF, and BNP level had 96.8% diagnostic value. At a cutoff of 6.44 ng/mL apelin level, sensitivity was 69.3%, and specificity 97.1%. However, the diagnostic of apelin for NYHA II patients was higher than that of BNP (99.6% vs. 96.1%). These results suggested that apelin might be particularly useful in association with BNP in mild HF patients.

[Interaction of polymorphisms of PPAR-γ2 gene -C34G and NADPH oxidase subunit p22phox gene -C242T with Helicobacter pylori infection in esophageal squamous cell carcinoma].

OBJECTIVE: To investigate the interaction of polymorphisms of PPAR-γ2 gene -C34G and NADPH oxidase subunit p22phox gene -C242T with helicobacter pylori (H. pylori) infection in esophageal squamous cell carcinoma (ESCC) . METHODS: A total of 200 cases of LSCC of Broder grade I, 200 of Broder grade II and of grade III were enrolled in this study with 200 healthy individuals as the control group. The genetic polymorphisms of PPAR-γ2 gene -C34G and NADPH oxidase subunit p22phox gene -C242T were analyzed using PCR-RFLP in peripheral blood leukocytes. 14C-urea breath test (14C-UBT) was used to test 14C disntegration per minute (DPM) for evaluating the infection status of H. pylori. An unconditional logistic regression model was used to analyze the interaction of nucleotide polymorphisms and H. pylori infection. RESULTS: The risk of ESCC significantly increased in subjects with -C34G (CG), -C34G(GG), -C242T (CT), and -C242T (TT) genotypes. Combined analysis of the polymorphisms showed that the subjects carrying -C34G (GG)/ -C242T (TT) had a high risk of ESCC, and a positive interaction was found between -C34G (GG) and -C242T (TT) in increasing the risk of ESCC. Positive interactions in the pathogenesis of ESCC were also found between -C34G (CG) and -C242T (TT), between -C34G (CG) and -C242T (CT), and between -C34G (GG) and -C242T (CT) (γ>1). The risk of ESCC significantly increased in subjects with H. pylori infection, which showed positive interactions with -C34G (CG), -C34G (GG), -C242T (CT) and -C242T (TT) in increasing the risk of ESCC (γ>1). CONCLUSION: Individuals carrying -C34G(CG), -C34G(GG), -C242T (CT) and -C242T (TT) genotypes have a high risk of developing ESCC, and these genotypes interact with H. pylori infection in the pathogenesis of LSCC, suggesting the importance of eradicating H. pylori for prevention of ESCC.

Correlation between Helicobacter pylori infection and polymorphism of adiponectin gene promoter-11391G/A, superoxide dismutase gene innonalcoholic fatty liver disease.

OBJECTIVE: To investigate the correlation between Helicobacter pylori (H. Pylori) infection and polymorphism of adiponectin gene promoter -11391G/A, extracellular superoxide dismutase (EC-SOD) gene in nonalcoholic fatty liver disease (NAFLD).
 METHODS: From June, 2010 to July, 2014, a hospital-based 1:1 matched case-control study was carried out, with 600 cases of NAFLD and 600 healthy people in the First Affiliated Hospital of Xinxiang Medical University. The genetic polymorphisms of adiponectin gene promoter -11391G/A and EC-SOD were analyzed by polymorphism-polymerase chain reaction (PCR) technique in peripheral blood leukocytes of the subjects. 14C-urea breath test (14C-UBT) was used to test 14C disntegration per minute (DPM) for evaluating the infections status of H. Pylori. The synergistic effect between the two mutants and the gene-environment interaction of the genotypes with H. Pylori infection were analyzed.
 RESULTS: The frequencies of -11391G/A (AA) and EC-SOD (CG+GG) were 50.67% and 50.33% in NAFLD cases, 23.83% and 24.17% in healthy controls, respectively. Statistical tests showed significantly higher frequencies of -11391G/A (AA) and EC-SOD (CG+GG) in the NAFLD group (-11391G/A: P=0.0051; EC-SOD: P=0.0057). The risk of NAFLD with -11391G/A (AA) was significantly higher than those with -11391G/A(GG+GA) (OR=3.2822, 95% CI 1.9170 to 5.2039). The individuals who carried EC-SOD (CG+GG) had a high risk of NAFLD (OR=3.1800, 95% CI 1.7974 to 5.2391). Combined analysis of the polymorphisms showed that percentage of -11391G/A (AA)/EC-SOD (CG+GG) in the NAFLD group was significantly higher than that in the control groups (25.50% vs 5.83%, P=0.0039). The people who carried with -11391G/A (AA)/EC-SOD (CG+GG) had a high risk of NAFLD (OR=10.3190, 95% CI 8.1869 to 20.5102). The H. Pylori infection rate in the NAFLD group was significantly higher than that in the control group (OR=3.1667, 95% CI 1.9139 to 5.7443, P=0.0062), and statistical analysis suggested a positive correlation between H. Pylori infection and NAFLD with -11391G/A (AA) and EC-SOD (CG+GG) (-11391G/A: γ=1.8532; EC-SOD: γ=1.7899).
 CONCLUSION: These carriers of -11391G/A(AA) and EC-SOD (CG+GG) genotypes may have a high risk of NAFLD, and the gene genotypes can interact with H. Pylori infection in the pathogenesis of NAFLD. Therefore, effective prevention measures for NAFLD should consider eradicating H. Pylori or regulating gene expression.

[Interaction between polymorphisms of TLR4 gene G11367C in 3' untranslated region and IκB-α Hae III in acute pancreatitis and the degree of severity].

OBJECTIVE: To investigate the interaction between polymorphism of Toll-like receptor 4 (TLR4) gene G11367C in 3' untranslated region (UTR) and inhibitor of nuclear factor kappaB (IκB)-α Hae III in acute pancreatitis (AP) and the degree of severity.
 METHODS: A total of 450 patients with confirmed AP (AP group), who came from the First Affiliated Hospital of Xinxiang Medical College from May 2013 to June 2015, were divided into a mild AP subgroup (MAP subgroup), a moderately severe AP (MSAP subgroup), and a severe acute AP (SAP subgroup) (n=150 in each group). One hundred fifty healthy persons were served as a control group. There was no significant difference in age, gender, ethnicity and birthplace among all groups. The genetic polymorphisms of TLR4 gene G11367C in 3' untranslated region and IκB-α Hae III were analyzed by polymerase chain reaction (PCR). Eligible participants were personally interviewed by a questionnaire. Unconditional logistic regression model and single factor analysis were performed to calculate the adjusted odds ratios (OR) and 95% confidence intervals (95% CI) of G11367C and IκB-α Hae III polymorphisms, respectively. The interaction of nucleotide polymorphisms was analyzed.
 RESULTS: The frequencies of G11367C (GC), IκB-α Hae III (AG) and IκB-α Hae III (GG) were 69.56%, 33.78% and 36.22% in the AP group; 49.33%, 24.67% and 26.00% in the MAP subgroup; 70.67%, 34.67% and 36.67% in the MSAP subgroup; 88.67%, 42.00% and 46.00% in the SAP subgroup and 26.67%, 14.00% and 14.67% in the control group, respectively. There was significant difference in the frequencies betweenc the AP group and the control group, or among each AP subgroup (all P<0.01). The risk of AP was significantly increased in the subjects with G11367C (GC) genotype (ORAP=6.2828, ORMAP=2.6776, ORMSAP=6.6250, ORSAP=21.5147), which was also increased in those with IκB-α Hae III (AG) genotype (ORAP=5.7369, ORMAP=2.5277, ORMSAP=6.1824, ORSAP=17.8572) and in those with IκB-α Hae III (GG) genotype (ORAP=5.8724, ORMAP=2.5902, ORMSAP=6.4027, ORSAP=18.9022). The combined analysis of the polymorphisms showed that the percentage of G11367C (GC)/ IκB-α Hae III (GG) in the AP group, the MAP subgroup, the MSAP subgroup, the SAP subgroup and the control groups was 26.44%, 12.67%, 26.00%, 40.67% and 4.00%, respectively, with significant difference in the frequency among all groups (all P<0.01). The people who carried with Pro12Ala (AA)/Pro198Leu (LL) had a high risk of AP (ORAP=30.1314, ORMAP=6.7612, ORMSAP=39.5000, ORSAP=401.5833), and the statistical analysis suggested a positive interaction between Pro12Ala (AA) and Pro198Leu (LL) in increasing the risk of AP (All γ>1). Similarly, there were also positive interactions in the pathogenesis of AP between G11367C (GC) and IκB-α Hae III (AG) (All γ>1). 
 CONCLUSION: These carriers of G11367C(GC), IκB-α Hae III(AG) and IκB-α Hae III (GG) genotypes may have a high risk of AP occurency, and there are significant interactions between genetic polymorphisms of G11367C and IκB-α Hae III, which increaes the risk of the occurrence and development of AP.

[Interaction of MIF gene -173G/C polymorphism and GPX1 gene 594C/T polymorphism with high-fat diet in ulcerative colitis].

OBJECTIVE: To investigate the interaction of single nucleotide polymorphisms of macrophage migration inhibitory factor (MIF) gene -173G/C and glutathione peroxidase 1(GPX1) gene 594C/T polymorphisms and high-fat diet in ulcerative colitis (UC). METHODS: The genetic polymorphisms of MIF -173G/C and GPX1 594C/T were determined with a polymorphism-polymerase chain reaction (PCR)-endonuclease method in peripheral blood leukocytes derived from 1500 UC cases and 1500 healthy controls. RESULTS: The frequencies of MIF -173CC and GPX1 594TT were 55.60% and 55.73% in the UC cases and 16.67% and 16.47% in the healthy controls, respectively. Statistical tests also showed a significant difference in the frequencies between the two groups (P<0.01; P<0.01, respectively). Individuals carrying MIF -173CC also had a significantly higher risk of UC compared with those with MIF -173GG (OR=6.8662, 95%CI: 4.5384-9.6158). Individuals carrying GPX1 594TT had a high risk of UC (OR=7.0854, 95%CI: 4.4702-10.5283). Combined analysis showed that the percentages of MIF -173CC/GPX1 594TT in the UC and control groups were 31.00% and 2.73%, respectively (P<0.01). Individuals carrying MIF -173CC/GPX1 594TT had a high risk of UC (OR=49.0113, 95%CI: 31.7364-61.8205). The high-fat diet rate of the case group was significantly higher than that of the control group (OR=3.3248, 95%CI: 1.9461-5.0193, P<0.01), and statistic analysis suggested an interaction between high-fat diet and MIF -173CC and GPX1 594TT which increase risk of UC (γ =6.9293; γ =6.9942). CONCLUSION: MIF -173CC and GPX1 594TT and high-fat diet are the risk factors for UC, and the significant interactions between genetic polymorphisms of MIF -173G/C, GPX1 594C/T and high-fat diet may increase the risk for UC.

Association of polymorphisms of adiponectin gene promoter-11377C/G, glutathione peroxidase-1 gene C594T, and cigarette smoking in nonalcoholic fatty liver disease.

BACKGROUND: The number of studies on adiponectin, GPx-1 gene polymorphisms, and nonalcoholic fatty liver disease (NAFLD) susceptibility is increasing, but none have investigated the effect of cigarette smoking in combination with the gene polymorphisms on the susceptibility to NAFLD. In order to understand the distribution of adiponectin and GPx-1 in the local population, to explore the possible association of cigarette smoking with adiponectin and GPx-1 gene polymorphisms in the pathogenesis of NAFLD, we conducted this research, examining the distribution of polymorphisms of adiponectin and GPx-1 in NAFLD patients and healthy controls, analyzing the association between these polymorphisms and cigarette smoking. METHODS: Two hundred nonalcoholic simple fatty liver (NAFL), 200 nonalcoholic steatohepatitis (NASH), and 200 nonalcoholic fatty hepatic cirrhosis (NAFHC) cases from the First Affiliated Hospital of Xinxiang Medical College in China from February 2011 to November 2014 were selected for this study, and 200 healthy individuals as a control group. No significant difference among the four groups in age, sex, ethnicity, and birthplace was observed. The genetic polymorphisms of adiponectin gene promoter-11377C/G and GPx-1 gene C594T were analyzed using polymerase chain reaction-restriction fragment length polymorphisms in peripheral blood leukocytes of the above-mentioned cases. The interaction between the two mutants and the gene-environment association of the genotypes with cigarette smoking were analyzed. RESULTS: The frequencies of adiponectin gene promoter-11377C/G(CG), -11377C/G (GG), GPx-1 gene C594T (CT) and C594T (TT) were 24.50%, 26.00%, 24.00%, and 25.50% in the NAFL group, 34.50%, 37.00%, 35.00%, and 36.00% in the NASH group, 42.00%, 46.00%, 43.50%, and 45.50% in the NAFHC group, and 14.00%, 14.50%, 13.00%, and 14.00% in the control group, respectively. Statistical tests showed a significant difference in the frequencies among each group (p < 0.01). The risk of NAFLD significantly increased in patients with adiponectin gene promoter-11377C/G (CG) genotype [odds ratio (OR)NAFL = 2.5278; ORNASH = 6.1823; ORNAFHC = 17.8570), in those with -11377C/G (GG) genotype (ORNAFL = 2.5900; ORNASH = 6.4017; ORNAFHC = 18.9023), in those with GPx-1 gene C594T (CT) genotype (ORNAFL = 2.6687; ORNASH = 6.7772; ORNAFHC = 22.2063), and in those with C594T (TT) genotype (ORNAFL = 2.6330; ORNASH = 6.4729; ORNAFHC = 21.5682). Combined analysis of the polymorphisms showed that percentages of adiponectin gene promoter -11377C/G (GG)/GPx-1 gene C594T (TT) in the NAFL, the NASH, NAFHC, and control groups was 7.00%, 13.50%, 21.00%, and 2.00%, respectively (p < 0.01). The people who carried the adiponectin gene promoter -11377C/G (GG)/GPx-1 gene C594T (TT) had a high risk of NAFLD (ORNAFL = 7.2800; ORNASH = 41.2941; ORNAFHC = 363.9724), and statistical analysis suggested a positive association between -11377C/G (GG) and C594T (TT) in increasing the risk of NAFLD (γ2NAFL = 2.2071, γ4 NAFL = 2.0773; γ2 NASH = 2.1084; γ4NASH = 2.0543; γ2 NAFHC = 2.1387; γ4NAFHC = 2.0004). Likewise, there were also positive association in the pathogenesis of NAFLD between -11377C/G (CG) and C594T (TT), -11377C/G (CG) and C594T (CT), -11377C/G (GG), and C594T (TT) (CT).The frequencies of smoking index (SI) ≤ 400 and SI > 400 were 22.50% and 26.50% in the NAFL group, 29.00% and 40.50% in the NASH group, 34.00% and 51.50% in the NAFHC group, and 15.50% and 12.00% in the control group, respectively. Statistical tests showed a significant difference in the frequencies among each group (all p < 0.01). The risk of NAFLD significantly increased in patients with SI ≤ 400 (ORNAFL = 2.0636; ORNASH = 4.4474; ORNAFH C = 10.9677) and in those with SI > 400 (ORNAFL = 3.1393; ORNASH = 8.0225; ORNAFHC = 21.4583), and statistical analysis suggested a positive association between cigarette smoking and -11377C/G (CG), -11377C/G (GG), C594T (CT), and C594T (TT) in increasing the risk of NAFLD (all γ > 1). CONCLUSION: Adiponectin gene promoter -11377C/G (CG), -11377C/G (GG), GPx-1 gene C594T (CT), C594T (TT), and cigarette smoking are risk factors in NAFLD, and the significant association between genetic polymorphisms of -11377C/G, C594T, and cigarette smoking amplify the risk of NAFLD.

[Interaction of polymorphisms of monocyte chemoattractant protein-1 receptor CCR2 gene 190A/G, nicotinamide adenine dinucleotide phosphate oxidase subunit p22phox gene C242T and cigarette smoking increases the risk of nonalcoholic fatty liver disease].

OBJECTIVE: To investigate the interaction of polymorphisms of monocyte chemoattractant protein-I (MCP-1) receptor CCR2 gene 190A/G, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p22phox gene C242T and cigarette smoking in nonalcoholic fatty liver disease (NAFLD ). METHODS: The genetic polymorphisms of MCP-1 receptor CCR2 gene 190A/G and NADPH oxidase subunit p22phox gene C242T were analyzed by the technique of polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) in peripheral blood leukocytes of 600 NAFLD cases and 600 healthy persons. RESULTS: The frequencies of 190A/G (GG) and C242T (TT) were 50. 17% and 50. 00% in NAFLD cases and 23. 83% and 24. 17% in healthy controls, respectively. There were significant differences in the frequencies between the two groups (χ2 = 88. 8462, P = 0. 0031, χ2 = 85. 8100, P = 0. 0039). The risk of NAFLD with 190A/G (GG) was significantly higher than those with 190A/G (AA + AG) (OR = 3. 2171, 95% CI 1. 9351 - 5. 2184). The individuals who carried with C242T (TT) had a high risk of NAFLD (OR = 3. 1379, 95% CI 1. 7973 - 5. 2362). Combined analysis of the polymorphisms showed that percentage of 190A/G (GG)/C242T (TT) in NAFLD and control groups was 39. 67% and 13. 00%, respectively (χ2 = 118. 3021, P =0. 0017). The people who carried with 190A/G (GG)/C242T (TT) had a high risk of NAFLD (OR =5. 0211, 95% CI 3. 1853 -7. 7926). The cigarette smoking rate of the case group was significantly higher than that in the control group (χ2 = 92. 2234, P = 0. 0025), smokers have a higher risk of lung cancer than non-smokers (OR = 3. 3032, 95% CI 1. 9147 -5. 7413 ), and statistic analysis suggested an interaction between cigarette smoking and 190A/G (GG) and C242T (TT) which increase risk of NAFLD (r = 3. 9983, r = 3. 8553 ). CONCLUSION: 190A/G (GG), C242T (TT) and cigarette smoking are the risk factors in NAFLD, and the significant interactions between genetic polymorphisms of 190A/G (GG), C242T (TT) and cigarette smoking added the risk of NAFLD.

Interaction of Polymorphisms of Resistin Gene Promoter -420C/G, Glutathione Peroxidase -1 Gene Pro198Leu and Cigarette Smoking in Nonalcoholic Fatty Liver Disease.

BACKGROUND: Many studies have suggested that cigarette smoking and polymorphisms of resistin and glutathione peroxidase-1 (GPx-1) genes are closely correlated with the pathogenesis of nonalcoholic fatty liver disease (NAFLD). However, few reports have investigated these associations with respect to NAFLD susceptibility. We, therefore, examined the distribution of polymorphisms in GPx-1 and resistin genes in NAFLD patients and healthy controls and analyzed the relationship between these polymorphisms and smoking status. METHODS: Nine hundred NAFLD patients and 900 healthy controls were selected, and the genetic polymorphisms of resistin gene promoter-420C/G and GPx-1 gene Pro198Leu were analyzed by polymorphism-polymerase chain reaction (PCR) in DNA extracted from peripheral blood leukocytes. Interactions between the two mutants and the gene-environment interaction with cigarette smoking were also analyzed. RESULTS: Genotype frequencies of -420C/G (GG) and Pro198Leu (LL) were significantly higher in NAFLD cases (49.56% and 50.11%, respectively) compared with healthy controls (23.67% and 24.22%, respectively) (P = 0.0069; P = 0.0072). Moreover, the risk of NAFLD with -420C/G (GG) was significantly higher than in controls (odds ratio [OR] =3.1685, 95% confidence interval (CI) =1.9366-5.2073). Individuals carrying Pro198Leu (LL) had a high risk of NAFLD (OR = 3.1424, 95% CI = 1.7951-5.2367). Combined analysis of the polymorphisms showed that the -420C/G (GG)/Pro198Leu (LL) genotype was significantly more common in the NAFLD group than in the control group (39.44% vs. 12.78%, respectively, P = 0.0054), while individuals with -420C/G (GG)/Pro198Leu (LL) had a high risk of NAFLD (OR = 5.0357, 95% CI = 3.1852-7.8106). Moreover, the cigarette smoking rate in the NAFLD group was significantly higher than in the control group (OR = 1.8990, P = 0.0083 in the smoking index (SI) ≤400 subgroup; OR = 5.0937, P = 0.0051 in the SI >400 subgroup), and statistical analysis suggested a positive interaction between cigarette smoking and -420C/G (GG) (γ = 5.6018 in the SI ≤400 subgroup; γ = 4.4770 in the SI >400 subgroup) and Pro198Leu (LL) (γ = 5.7715 in the SI ≤400 subgroup; γ = 4.5985 in the SI >400 subgroup) in increasing the risk of NAFLD. CONCLUSION: NAFLD risk factors include -420C/G (GG), Pro198Leu (LL) and cigarette smoking, and these three factors have a significant additive effect on NAFLD risk.

Dalitong granule combined with electroacupuncture in the treatment of functional dyspepsia: A randomized controlled trial.

OBJECTIVE: To explore clinical short and long-term effect of combining dalitong granule (DG) and electroacupuncture group (EA) in the treatment of functional dyspepsia. METHODS: Totally 640 patients with confirmed functional dyspepsia were randomly divided into 4 groups using a randomized digital table: the DG group, the EA group, the combined group and the control group, 160 cases in each group. The DG group was treated with 6 g DG 3 times daily; the EA group was treated with puncture of points Zusanli (ST36), Zhongwan (CV12), Neiguan (PC6), Taichong (LR3) and Gongsun (SP4) twice daily; the combined group with above-mentioned DG and EA; and the control group with 5 mg mosapride 3 times, 20 mg pantoprazole and 25 mg amitriptylines twice daily. The treatment course was 4 weeks for all groups. The symptom score, quality of life score by Short Form 36 Health Survey Questionnaires (SF-36), plasma motilin by radioimmunoassay, electrogastrographic frequencies by electrogastrogram (EGG) and gastric emptying by B-sonography were examined, and adverse reactions were observed before, at the end of treatment and 60 weeks post-treatment. RESULTS: In the DG group 1 case dropped out for not taking medicine strictly and 1 case was lost to follow-up, while 1 case in the EA group and 2 cases in the combined therapy group were lost to follow-up. Compared with pre-treatment, quality of life score, plasma motilin, electrogastrographic frequencies and gastric emptying were all increased significantly, while symptom score was decreased significantly at the end of treatment in each group (P<0.01); in the combined group quality of life score, plasma motilin, electrogastrographic frequencies and gastric emptying were all significantly higher than those in the other groups, while symptom score was significantly lower than in the other groups (P<0.05). Compared with at the end of treatment, these indices changed insignificantly in the combined group and the EA group 60 weeks post-treatment (P>0.05), but the 4 increased indices were all decreased significantly, and symptom score was increased significantly in the DG and the control groups (P>0.05). The short and long-term total effective rates in the combined group were all significantly higher than those in the other treatment groups (P<0.05 or P<0.01). No serious adverse reaction occurred in the four groups. CONCLUSION: Combined treatment of DG and EA could increase both plasma motilin and electrogastrographic frequencies, promote gastric emptying, alleviate the symptom of dyspepsia so as to increase quality of life, with better safety and long-term effect.

Interaction between the polymorphisms of cyclooxygenase-2-1195G/A,MnSOD9Ala/val genes and the high-fat diets and its correlation with ulcerative colitis.

OBJECTIVE: To investigate the interaction of the polymorphisms of cyclooxygenase-2-1195G/A (COX-2-1195G/A) and manganese superoxide dismutase 9Ala/Val (MnSOD9Ala/Val) genes and the high-fat diets and its potential correlation with ulcerative colitis (UC). METHODS: The genetic polymorphisms of COX-2-1195G/A and MnSOD9Ala/Val were analyzed by polymorphism-polymerase chain reaction (PCR) in peripheral blood leukocytes obtained from 750 UC patients (UC group) and 750 healthy subjects (control group). RESULTS: The frequencies of COX-2-1195G/A(A/A) and MnSOD9Ala/Val(V/V) were 49.07% and 50.13% in UC group and 21.20% and 22.40% in control group, respectively (P<0.01). The risk of UC significantly increased in subjects with COX-2-1195G/A(A/A) genotype (OR=3.5808,95%CI=1.8062-5.3478) and in those with MnSOD9Ala/Val(V/V) genotype(OR=3.4828,95%CI=1.9137-5.5496). Pooled analysis of the polymorphisms showed that distribution frequency of COX-2-1195G/A(A/A)/MnSOD9Ala/Val (V/V) was 40.67% in UC group and 8.40% in control group (P<0.01). Subjects with COX-2-1195G/A(A/A)/MnSOD9Ala/Val(V/V) had a significantly higher risk of UC (OR=7.5655,95% CI=4.1849-11.2037). The rate of high-fat diets was significantly higher in the UC group than in the control group(49.73 vs.20.13%,P<0.01),and statistic analysis suggested an interaction between high-fat diet and COX-2-1195G/A(A/A)(Γ=11.81821)and MnSOD9Ala/Val (V/V)(Γ=9.0107), which increase risk of UC. CONCLUSIONS: COX-2-1195G/A(A/A),MnSOD9Ala/Val (V/V), and high-fat diet are the risk factors of UC. The interaction between the genetic polymorphisms of COX-2-1195G/A and MnSOD9Ala/Val and the high-fat diet increases the risk of UC.

[Interaction of polymorphisms of Leptin receptor gene Gln223Arg, MnSOD9Ala/Val genes and smoking in nonalcoholic fatty liver disease].

OBJECTIVE: To investigate the interaction of polymorphisms of leptin receptor (LR) gene Gln223Arg, manganese superoxide dismutase9Ala/Val (MnSOD9Ala/Val) genes and smoking in nonalcoholic fatty liver disease. METHODS: The genetic polymorphisms of LEPR gene Gln223 Arg and MnSOD9Ala/Val were analyzed bypolymorphism-polymerase chain reaction (PCR) technique in peripheral blood leukocytes of 600 NAFLD cases and 600 healthy persons. RESULTS: The frequencies of LR gene Gln223Arg (G/G) and MnSOD9Ala/Val (V/V) were 48. 67% and 50.17% in NAFLD cases and 21. 17% and 21. 50% in healthy controls respectively. Statistical tests showed significant difference in the frequencies between the two groups (P <0.01). The risk of NAFLD with Gln223Arg (G/G) was significantly higher than those of controls (OR = 3. 5309, 95% CI =21. 8165 -5.0724). The individuals who carried with MnSOD9Ala/Val (V/V) had a high risk of NAFLD (OR = 3. 6756, 95% CI = 1. 9137 - 5.5496). Combined analysis of the polymorphisms showed that percentage of Gln223Arg (G/G)/ MnSOD9Ala/Val (V/V) in NAFLD and control groups was40.33% % and 7.50% Respectively (P <0.01). The people who carried with Gln223 Arg (G/G)/ MnSOD9Ala/ Val (V/V) had a high risk of NAFLD (OR = 8. 4014,95% CI= 4. 2926 - 12. 4238). The smoking rate of the case group was significantly higher than which in the control group (OR = 3. 6754, 95% CI = 1. 4193 - 4. 9581, P <0. 01 ), and statistic analysis suggested an interaction between smoking and Gln223Arg ( G/G)/ MnSOD9Ala/Val (V/V) which increase risk of NAFLD ( OR = 9. 8665; OR = 8. 5476). CONCLUSION: Gln223Arg (G/G), MnSOD9Ala/Val (V/V) and smoking are the risk factors in NAFLD, and the significant interactions between geneticpolymorphisms of Gln223Arg,MnSOD9Ala/Val and smoking added the risk of NAFLD.

[Correlation of polymorphisms of adiponectin receptor 2 gene +33371Gln/Arg, cytochrome P4502E1 gene Rsa I and smoking with nonalcoholic fatty liver disease].

OBJECTIVE: To investigate the correlation of the polymorphisms of adiponectin receptor 2 (AdipoR2) gene +33371Gln/;Arg and cytochromes P4502E1 gene Rsa I (CYP2E1-Rsa I) as well as smoking with nonalcoholic fatty liver disease (NAFLD). METHODS: The polymorphisms of AdipoR2 gene +33371Gln/Arg and CYP2E1-Rsa I were analyzed with PCR technique in peripheral blood leukocytes from 750 NAFLD cases and 750 healthy subjects. RESULTS: The frequencies of AdipoR2 gene +33371Gln/Arg (A/A) and CYP2E1-Rsa I (c2/c2 ) were 39.20% and 71.73% in NAFLD cases, respectively, significantly higher than those in healthy subjects (21.07% and 43.07%, respectively, P<0.01). The risk of NAFLD increased significantly in subjects carrying +33371Gln/Arg (A/A) (OR=2.4156, 95% CI=1.8164-4.0725) and CYP2E1-Rsa I (c2/c2) (OR=3.3547, 95% CI=1.9182-4.5057). Combined analysis of the polymorphisms showed that the percentage of +33371Gln/Arg (A/A)/CYP2E1-Rsa I (c2/c2) was 32. 67% in NAFLD cases, significantly higher than that in the healthy subjects (6.40%, P<0.01), and subjects carrying both +33371Gln/Arg (A/A) and CYP2E1-Rsa I (c2/c2) had a high risk of NAFLD (OR=9.9264, 95% CI=4.2928-12.4241). The smoking rate was significantly higher in the case group than in the control group (OR=2.5919, 95% CI=1.4194-4. 9527, P<0.01), and statistical analysis suggested an interaction between smoking and +33371Gln/Arg (A/A)/CYP2E1-Rsa I (c2/c2) to increase the risk of NAFLD (OR=34.6764, 95% CI=18.9076-61.5825). CONCLUSION: +33371Gln/Arg (A/A), CYP2E1-Rsa I (c2/c2 ) and smoking are risk factors for NAFLD and coordinately contribute to the occurrence of NAFLD.

Correlations between polymorphisms of extracellular superoxide dismutase, aldehyde dehydrogenase-2 genes, as well as drinking behavior and pancreatic cancer.

OBJECTIVE: To investigate the correlation between drinking behavior combined with polymorphisms of extracellular superoxide dismutase (EC-SOD) and aldehyde dehydrogenase-2 (ALDH2) genes and pancreatic cancer. METHODS: The genetic polymorphisms of EC-SOD and ALDH2 were analyzed by polymerase chain reaction restriction fragment length polymorphism in the peripheral blood leukocytes obtained from 680 pancreatic cancer cases and 680 non-cancer controls. Subsequently the frequency of genotype was compared between the pancreatic cancer patients and the healthy controls.The relationship of drinking with pancreatic cancer was analyzed. RESULTS: The frequencies of EC-SOD (C/G) and ALDH2 variant genotypes were 37.35% and 68.82% respectively in the pancreatic cancer cases, and were significantly higher than those in the healthy controls (21.03% and 44.56%, all P<0.01). People who carried EC-SOD (C/G) (OR=2.24, 95% CI= 1.81-4.03, P<0.01) or ALDH2 variant genotypes (OR=2.75, 95% CI=1.92-4.47, P<0.01) had a high risk to develop pancreatic cancer. Those who carried EC-SOD (C/G) genotype combined with ALDH2 variant genotype had a high risk for pancreatic cancer (29.56% vs. 6.76%, OR=7.69, 95% CI=3.58-10.51, P<0.01). The drinking rate of the pancreatic cancer group (64.12%) was significantly higher than that of the control group (40.15%; OR=2.66, 95% CI=1.30-4.42, P<0.01). An interaction between drinking and EC-SOD (C/G)/ALDH2 variant genotypes increased the risk of occurrence of pancreatic cancer (OR=25.00, 95% CI= 11.87-35.64, P<0.01). CONCLUSION: EC-SOD (C/G), ALDH2 variant genotypes and drinking might be the risk factors of pancreatic cancer.

[Correlation between drinking behavior and polymorphisms of extracellular superoxide dismutase, aldehyde dehydrogenase 2 genes, and oral squamous cell carcinoma].

OBJECTIVE: To investigate the correlation between drinking behavior and polymorphism combination of extracellular superoxide dismutase (EC-SOD) and aldehyde dehydrogenase 2 (ALDH2) genes and oral squamous cell carcinoma. METHODS: The genetic polymorphisms of EC-SOD and ALDH2 were analyzed by polymorphism-polymerase chain reaction technique in peripheral blood leukocytes of 750 oral squamous cell carcinoma cases and 750 non-cancer controls. RESULTS: The frequencies of EC-SOD (C/G) and ALDH2 variant genotypes were 38.27% and 69.47% in oral squamous cell carcinoma cases and 21.07% and 44.40% in healthy controls, respectively. Statistical tests showed significant difference in the frequencies between the two groups (P < 0.01). The risk of oral squamous cell carcinoma with EC-SOD (C/G) was significantly higher than that of controls (OR = 2.32). Individuals carrying ALDH2 variant genotypes had high risk of oral squamous cell carcinoma (OR = 2.85). Combined analysis of the polymorphisms showed that percentages of EC-SOD (C/G)/ALDH2 variant genotypes in oral squamous cell carcinoma and control groups were 30.67% and 6.80%, respectively (P < 0.01). Individuals carrying EC-SOD (C/G)/ALDH2 variant genotypes had high risk of oral squamous cell carcinoma (OR = 8.13). The drinking rate of the case group was significantly higher than that in the control group (OR = 2.70). Statistical analysis suggested an interaction between drinking and EC-SOD (C/G) and ALDH2 variant genotypes, which increase risk of oral squamous cell carcinoma (OR = 25.00). CONCLUSION: EC-SOD (C/G) and ALDH2 variant genotypes and drinking are the risk factors in oral squamous cell carcinoma, which could carry out a coordinated attack of oral squamous cell carcinoma.

Short and long-term efficacy of combining Fuzhengliqi mixture with acupuncture in treatment of functional constipation.

OBJECTIVE: To explore the short and long-term efficacy of combining Fuzhengliqi mixture (FLM) with acupuncture in treating functional constipation (FC). METHODS: The 560 patients with confirmed diagnosis of FC were randomly assigned to four groups: FLM group, acupuncture group, combined therapy group, and control group. There were 140 cases in each group. The FLM group was administered FLM 60 mL twice a day, while the acupuncture group was treated with acupuncture at acupoints Tianshu (ST 25), Shangjuxu (ST 37), Zusanli (ST 36), Dachangshu (BL 25), and Zhigou (TE 6) twice a day, the combined therapy group with FLM and acupuncture, and the control group was administered mosapride (5 mg thrice a day) and Macrogol 4000 (10 g twice a day). The treatment lasted 6 weeks. The defecation interval, stool property, constipation symptoms, and accompanying symptoms were recorded, graded, and scored. The gastrointestinal transit time (GITT) and motilin (MTL) level in serum and life quality score were detected at three time points (pre-treatment, at the end of treatment, and 60 weeks post-treatment). Moreover, the adverse reactions were also observed. RESULTS: In the FLM group 2 cases were eliminated for not taking medication strictly according to the research plan and 1 case was lost to follow-up, while 2 cases in the acupuncture group and 2 cases in the combined therapy group were lost to follow-up. Compared with those detected pre-treatment, the defecation interval, stool property, constipation symptom grade, accompanying symptom grade, and GITT were all decreased markedly at the end of treatment in every group, while the MTL levels in serum and life quality score were increased markedly (P < 0.01), the above-mentioned detecting indices were better in the combined therapy group than those in other groups (P < 0.05). Compared with the end of treatment, above-mentioned detecting indices all recurred significantly in the FLM group and control group 60 weeks post-treatment (P > 0.05), but these indices recurred insignificantly in the acupuncture and combined therapy groups (P > 0.05). The short and long-term total effective rates in the combined therapy group were significantly different from those in other groups (P < 0.05 or P < 0.01). No serious adverse reactions were found in four groups. CONCLUSION: Both FLM and acupuncture can significantly shorten the defecation interval and GITT, increase MTL levels in serum, decrease the scores of stool property, constipation symptoms, and accompanying symptoms in patients with FC to increase their life quality. The combined therapy is much better in long-term efficacy and the safety is also good, worth spreading in clinical practice.

[Correlation of the polymorphism of EC-SOD and GSTM1 and smoking with oral cancer risk].

OBJECTIVE: To investigate the correlation of the polymorphisms of EC-SOD and GSTM1, as well as smoking, with oral cancer risk. METHODS: A case-control study and polymerase chain reaction (PCR) technique was used to identify the genotype of EC-SOD and GSTM1 in 600 oral cancer cases and 600 controls. Logistic regression was conducted to evaluate the odds ratio of relative gene and the interaction between the genes and smoking with oral cancer. RESULTS: The frequencies of EC-SOD genotype in cases and controls were 61. 17% and 78.50% for C/C, and 38.33% and 21.50% for C/G respectively (P < 0.01). EC-SOD (C/G) correlated with susceptible to oral cancer (OR = 2.27, 95% CI 1.73 - 4.02). The frequency distribution of GSTM1 ( - ) was significantly different in patients (69.17%) and controls (44.17%) (P < 0.01). GSTM1 ( -) increased the risk of developing oral cancer (OR = 2.84, 95% CI 1.95 - 4.47). Combined polymorphism analysis showed that the percentage of EC-SOD (C/G)/GSTM1 (-) for oral cancer and control groups was 30.50% and 6.67% respectively) (P < 0.01). The risk of developing oral cancer in those with EC-SOD(C/G)/GSTM1 (-) genotype was significantly higher than that with EC-SOD (C/C)/GSTM1 (+) genotype (OR = 8.16, 95% CI 3.73 - 12.91). There were significant differences in smoking rate between the two groups (P < 0.01), smoking correlated with susceptible to oral cancer (OR = 2.66, 95% CI 1.45-4.36), and statistical analysis suggested an interaction between smoking and EC-SOD(C/G)/GSTM1(-) genotype, which increase the risk of oral cancer (OR = 25.11, 95% CI 12.37 - 36.62). CONCLUSION: EC-SOD (C/G) and GSTM1 (-) are risk factors in oral cancer. Smoking is also related to the susceptibility to oral cancer. There may be a synergetic interaction among EC-SOD (C/G), GSTM1 (-) and smoking on the elevated susceptibility of oral cancer.

Association of genetic polymorphisms of aldehyde dehydrogenase-2 and cytochrome P450 2E1-RsaI and alcohol consumption with oral squamous cell carcinoma.

OBJECTIVE: To investigate the association of the polymorphisms of aldehyde dehydrogenase-2(ALDH2) and CYP2E1-RsaI genes and alcohol consumption with oral squamous cell carcinoma (OSCC). METHODS: The genetic polymorphisms of ALDH2 and CYP2E1-RsaI were determined by polymorphism-polymerase chain reaction (PCR) technique in the peripheral blood leukocytes of 320 OSCC patients and 320 non-cancer controls. RESULTS: The frequencies of ALDH2 variant genotypes and CYP2E1-RsaI (c2/c2) were 70.94% and 39.06% in the OSCC group and 43.44% and 20.62% in the control group (both P<0.01). The risk of OSCC with ALDH2 variant genotypes was significantly higher than that in control group (OR=3.178, 95% CI=1.917-4.749), whereas the subjects carried with CYP2E1-RsaI (c2/c2) also had a high risk of OSCC (OR=2.467, 95%CI=1.783-4.045). Combined analysis of the polymorphisms showed that percentage of ALDH2 variant genotypes/CYP2E1-RsaI (c2/c2) in OSCC group and control group was 32.19% and 6.25%, respectively (P<0.01). Carriers of ALDH2 variant genotypes/CYP2E1-RsaI (c2/c2) had a high risk of OSCC (OR=9.792, 95%CI=3.583-12.472). The percentage of alcohol consumption was significantly higher in OSCC group than in the control group (OR=2.861, 95% CI=1.541-4.781, P<0.01), and ALDH2 variant genotypes and CYP2E1-RsaI (c2/c2) showed synergic effects with alcohol consumption for the increased risk of OSCC (OR=41.152, 95%CI=19.903-67.551). CONCLUSION: The polymorphisms of ALDH2 and CYP2E1-RsaI genes and alcohol consumption, independently and synergically, increase the risk of OSCC.