Objective To study the association of TCF7L2 gene rs11196218,rs290487 polymorphisms with metabolic syndrome in type 2 diabetes mellitus population.Methods According to the diagnostic criteria of international diabetes federation (IDF),680 cases of type 2 diabetes patients were divided into metabolic syndrome (MS) group and non metabolic syndrome (control) group.DNA was extracted from peripheral mononuclear cells,and then PCR was performed to specifically amplify TCF7L2 gene fragments.Gene polymorphisms were determined by connected enzyme detection reaction.After population representative was checked by Hardy-Weinberg equilibrium,statistical analysis was completed by software SPSS 13.0.Results The population was accorded with Hardy-Weinberg equilibrium and possessed the population representative.Frequency distributions of genotypes (GG,AG and AA) in TCF7L2 gene rs11196218 in MS and control groups were 55.6％(233/419),35.8％(150/419),8.6％ (36/419) and 54.8％ (126/230),39.1％ (90/230),6.1％ (14/230),respectively.Frequency distributions of alleles(G and A) in TCF7L2 gene rs11196218 in MS and control groups were 73.5％(616/838),26.5％(222/838)and 74.3％(342/460),25.7％(118/460),respectively.Frequency distributions of genotypes (GG,AG and AA) in TCF7L2 gene rs290487 in MS and control groups were 14.8％(62/418),42.3％(177/418),42.9％(179/418) and 15.0％(34/226),48.2％(109/226),36.8％(83/226),respectively.Frequency distributions of alleles(G and A) in TCF7L2 gene rs11196218 in MS and control groups were 36.0％ (301/836),64.0％ (535/836) and 39.1％ (177/452),60.9％ (275/452),respectively.Frequency distribution of allele and genotype in TCF7L2 genes rsl 1196218 and rs290487 between the two groups were not associated with metabolic syndrome in type 2 diabetes population (P ＞ 0.05).Conclusions TCF7L2 gene rs11196218,rs290487 polymorphisms has not association with metabolic syndrome of type 2 diabetes.

Objective To investigate the correlation between microembolic signal (MES) and immune inflammation in patients with acute ischemic stroke. Methods The consecutive patients with acute ischemic stroke were enroled. According to the results of MES, they were divided into either a positive group or a negative group. The Immune inflammatory indexes, demographics, and baseline clinical data in both groups were compared. Multivariate logistic regression analysis was used to analyze the independent influencing factors of MES in acute ischemic stroke. Results A total of 237 patients were enroled, including 52 in the MES positive group and 185 in the MES negative group. There were significant differences in the levels of triglyceride (2. 130 ± 0. 933 mmol/L vs. 1. 811 ± 0. 962 mmol/L; t = 2. 126, P = 0. 035), plasma fibrinogen (2. 946 ± 0. 255 g/L vs. 2. 833 ± 0. 322 g/L; t = 2. 332, P = 0. 021 ), Lp-PLA2 level ( 288. 265 ± 27. 855 μg/L vs. 261. 652 ± 29. 961 μg/L; t = 2. 897, P = 0. 004 ), as wel as the proportions of CD4 + CD25high Treg (8. 695% ± 1. 461% vs. 9. 445% ± 1. 397% ; t = 3. 386, P = 0. 001), artery stenosis ≥70% (21. 15% vs. 5. 41% ; χ2 = 10. 592, P = 0. 001 ) and smal arterial occlusive stroke (9. 62% vs. 23. 24% ; χ2 = 4.667, P = 0. 031) between the MES positive group and the MES negative group. Multivariate logistic regression analysis showed that the increased plasma fibrinogen level (odds ratio [OR] 3. 257, 95%confidence interval [CI] 1. 124 - 9. 438; P = 0. 030), artery stenosis ≥ 70% (OR 3. 585, 95% CI 1. 394 -9. 219; P = 0. 008), and the decreased ratio of Treg (OR 3. 801, 95% CI 1. 190 - 12. 148; P = 0. 024) were the independent risk factors for positive MES, and smal arterial occlusive stroke was its independent protective factor (OR 0. 244, 95% CI 0. 072 - 0. 829; P = 0. 024). Conclusions MES may be associated with immune inflammation. The relationship between stroke and immune inflammation should be taken seriously.

Adult ; Aged ; Aged, 80 and over ; Carcinoma, Non-Small-Cell Lung ; genetics ; Female ; Genes, erbB-1 ; genetics ; Humans ; Lung Neoplasms ; genetics ; Male ; Middle Aged ; Mutation ; Nucleic Acid Amplification Techniques ; methods ; Receptor, Epidermal Growth Factor ; genetics

OBJECTIVETo evaluate the oxidative stress in patients with colorectal cancer and to investigate the relationship between oxidative stress and colorectal cancer.

METHODSSeventy-six subjects were divided into two groups (36 colorectal cancer patients as the study group and 40 normal healthy individuals as the control group). Their protein oxidation, DNA damage, lipid peroxidation and antioxidants, vitamin C, vitamin E, glutathione (GSH), and antioxidative enzymes in serum were detected.

RESULTSThe levels of protein carbonyl and advanced oxidation protein products (AOPP) were significantly higher in the study group than in the control group (P<0.01). Serum 8-OHdG was significantly increased in the study group compared to the control group (P<0.01). However, the mean serum level of MDA and conjugated diene was lower in the study group than in the control group (P<0.01). The activity of antioxidative enzymes was significantly decreased in the study group compared to the control group (P<0.01). Serum vitamins C and E concentrations were significantly reduced in the study group compared to the control group (P<0.01).

CONCLUSIONColorectal cancer is associated with oxidative stress, and assessment of oxidative stress and given antioxidants is important for the treatment and prevention of colorectal cancer.

Adult ; Aged ; Aged, 80 and over ; Colorectal Neoplasms ; metabolism ; DNA Damage ; Female ; Humans ; Lipid Peroxidation ; Male ; Middle Aged ; Oxidative Stress

OBJECTIVETo study the impact of total flavones from Artemisia anomala (TFAS) on activation of macrophages, cell oxidative stress, auto-nitration of CuZn-SOD, platelet aggregation and isolated vascular tension.

METHODLPS and IFN-gamma induced activation of macrophages and oxidative stress in rats; H2O2 and nitrite induced auto-nitration of CuZn-SOD; ADP, AA and collagen induced platelet aggregation in vitro in mice; PE stimulates isolated vascular tension; nitrite content of macrophages was measured by Griess assay; MTT assay and FRAP assay was applied for cell viability and total cell antioxidant capacity; auto-nitration of CuZn-SOD was measured by Western blot and colorimetric methods; platelet aggregation was detected by turbidimetry; and aorta ring relaxation was recorded by isolated vascular function experience devices for rats.

RESULTTFAS demonstrated dose dependence (25, 50, 100, 200 mg x L(-1)) on inhibiting induced macrophages NO production from generating, while increasing cell viability and total anti-oxidant capacity. Auto-nitration of CuZn-SOD was suppressed by TFAS in dose dependence (0.5, 5, 50 mg x L(-1)). TFAS showed an inhibitory effect on collagen-induced platelet aggregation at 50 mg x L(-1) and an endothelium-dependent relaxation effect on PE-induced vasoconstriction at 1 g x L(-1).

CONCLUSIONTFAS shows effect on anti-inflammation, anti-oxidation, anti-nitration, anti-platelet aggregation and vasodilatation in experiment in vitro, which may inhibit vascular inflammatory by regulating multiple target points. It is among material bases for promoting blood circulation and removing blood stasis.

Animals ; Anti-Inflammatory Agents ; pharmacology ; Aorta ; drug effects ; immunology ; physiology ; Artemisia ; chemistry ; Drugs, Chinese Herbal ; pharmacology ; Flavones ; administration & dosage ; Humans ; Macrophages ; drug effects ; immunology ; Mice ; Oxidative Stress ; drug effects ; Rats ; Vasodilation ; drug effects

Currently, individualized exercise prescription plays a vital role in the cardiac rehabilitation of patients with chronic cardiovascular diseases. Many cardiopulmonary exercise tests proved that individualized exercise prescription can lower blood pressure and glucose of patients with cardiovascular diseases, improve cardiopulmonary function, and improve exercise endurance and quality of life. At the same time, this paper also summarized that the individualized exercise prescription should be formulated in compliance with the principle (individuality, effectiveness, safety, professionalization, comprehensiveness and permanence), exercise intensity evaluation method (from previous heart rate, fatigue grading methods into cardiopulmonary exercise test) and the contents of the individualized exercise prescription (with a focus on the exercise intensity formulation).

Objective To evaluate the operative outcomes of a triple procedure including simultaneous penetration keratoplasty (PKP),extracapsular cataract extraction (ECCE) and intraocular lens (IOL) implantation,and to investigate the relationship between postoperative corneal refractive power and preoperative lens diopter.Methods This retrospective analysis study involved 15 patients who had undergone a triple procedure surgery in Beijing You'an hospital from April to October 2016.Outcomes including the best corrected visual acuity (BCVA),intraocular pressure (IOP),corneal refractive power,axial length,postoperative complications,corneal endothelial cell counts and the survival of corneal graft were determined one year after surgery.Results All corneal grafts were transparent and corneal endothelium were (1974.20 ±472.82) cell · mm-2.The mean postoperative LogMAR visual acuity (0.80 ±0.27) had a significant improvement compared with the mean preoperative LogMAR visual acuity (2.63 ±0.62) (t =13.042,P ＜0.001).There were no statistically significant differences in preoperative IOP (15.27 ± 2.37) mmHg (1 kPa =7.5 mmHg) and postoperative data (14.53 ± 3.04) mmHg (t =0.685,P =0.505),preoperative axial length (23.69 ±2.01) mm and postoperative data (23.62 ±2.12)mm (t =-0.138,P=0.893)and preoperative keratometry (45.01 ± 1.66) D of the control eye and postoperative data (42.56 ± 5.48) D (t =1.202,P =0.260).The postoperative spherical equivalent refractive was (0.40 ±4.65) D,and the target refraction was (0.58 ±0.25)D.Conclusion The triple procedures are safe and effective for the treatment of patients with coexisting corneal pathologies and cataracts.Selection of emmetropia lens diopter may result in the satisfactory postoperative visual acuity.However,unpredictable postoperative corneal curvature changes will still affect the final refractive state.

OBJECTIVETo investigate the anti-tumor activity of combined gemcitabine with dihydroartemisinin, and the mechanism of the anti-tumor effect of gemcitabine enhanced by dihydroartemisinin on pancreatic cancer.

METHODSFor cultured cells, cell growth was determined by the MTT assay and apoptosis was evaluated by flow cytometry analysis and confocal laser scanning microscope stained with Annexin V-FITC/PI. The nuclear extract for determining NF-kappaB DNA-binding activity was analyzed by EMSA, while nuclear P65 and its downstream gene expression was determined by Western blot assay. BxPC-3 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors and the tumor volume was monitored after exposure to agents. TUNEL assay was used to assess tumor cell apoptosis in tumor tissue.

RESULTSAfter combination of gemcitabine and dihydroartemisinin treatment, the proliferative inhibition rates of pancreatic cancer cells BxPC-3 and Panc-1 reached up to (81.1 +/- 3.9)% and (76.5 +/- 3.3)%, and the apoptosis rates were up to (53.6 +/- 3.8)% and (48.3 +/- 4.3)%, the differences were significantly (P < 0.01) compared with gemcitabine [(24.8 +/- 2.9)% and (21.8 +/- 3.5)%]. All the treatment groups inhibited the growth of pancreatic xenograft tumors in nude mice. The tumor volume and apoptosis index were (262 +/- 37) mm(3) and (50 +/- 4)% respectively in the combined treatment, compared to those of [(384 +/- 56) mm(3) and (25 +/- 3)%] in gemcitabine, the differences were significantly (P < 0.05). EMSA showed that gemcitabine alone obviously enhanced its DNA-binding activity compared to control. However, dihydroartemisinin significantly reduced its DNA-binding activity, so that abrogated the inducing effect of gemcitabine on NF-kappaB activation. Western blot assay indicated that dihydroartemisinin downregulated expression of nuclear P65, and combined treatment not only downregulated the expression of Cyclin D1, Bcl-xL and Bcl-2 while upregulated Bax, thus reduced the Bcl-2/Bax ratio, but also increased the caspase-3 activation, all of which increased apoptosis in both BxPC-3 and Panc-1 cells.

CONCLUSIONDihydroartemisinin significantly abrogated the inducing effect of gemcitabine on NF-kappaB activation and downregulated the expression of NF-kappaB targeted gene products, which may be one possible mechanism by which dihydroartemisinin augments the anti-tumor effect of gemcitabine on pancreatic cancer.

Animals ; Antimetabolites, Antineoplastic ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Apoptosis ; drug effects ; Artemisinins ; therapeutic use ; Cell Line, Tumor ; Deoxycytidine ; analogs & derivatives ; therapeutic use ; Humans ; Male ; Mice ; Mice, Nude ; NF-kappa B ; metabolism ; Pancreatic Neoplasms ; drug therapy ; metabolism ; pathology ; Xenograft Model Antitumor Assays

OBJECTIVEThis paper aims to assess the interaction between common variations in catalase (CAT) polymorphic gene and environmental factors for antioxidant defense enzyme in modulating individual susceptibility to colorectal cancer (CRC).

METHODSA case-control study with 880 colorectal cancer cases and 848 controls was conducted to investigate whether variations in the catalase (CAT) gene, one of the genes involved in scavenging oxidative stress, influenced susceptibility to CRC.

RESULTSThe interaction between life style and genotypes as well as with their effects on colorectal cancer was deduced from the present study. Significant difference (P = 0.01) was identified in the distribution of CAT genotype between the colorectal cancer cases and the controls. The CRC cases had significantly lower mean activity than the controls (P < 0.01). Correlation analyses revealed statistically significant correlations between CAT activity and CAT genotype (P < 0.01).

CONCLUSIONThe risk of CRC was associated with smoking, low vegetable consumption, high pork and poultry consumptions, and low or high BMI. This is the first study reporting an association of polymorphism CAT-21A > T with colorectal cancer. Low CAT activity was associated with an increased risk of CRC; however, no evidence was found to support an association between CAT-21A > T polymorphism and CRC risk.

Adult ; Aged ; Case-Control Studies ; Catalase ; genetics ; Colorectal Neoplasms ; enzymology ; epidemiology ; metabolism ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Polymerase Chain Reaction

OBJECTIVETo investigate the effect and mechanism of NF-kappaB P65 gene silencing by small interference RNA on the apoptosis of human pancreatic cancer cells induced by gemcitabine in vitro and in vivo.

METHODSHuman pancreatic cancer cells (BxPC-3 and PANC-1) were cultured and respectively divided into five groups: blank control group, negative control siRNA group, gemcitabine group, NF-kappaB P65 siRNA group and gemcitabine + P65 siRNA group. The ability of cell proliferation was analyzed by MTT; the expression of NF-kappaB P65 and the apoptosis related proteins were examined by Western blot assay; the apoptosis was evaluated by the flow cytometry and laser scanning confocal microscopy analysis stained with Annexin V-FITC/PI; the DNA binding activity of NF-kappaB was examined by electrophoretic mobility shift assay. BxPC-3 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors. The tumor volume was monitored and TUNEL assay was used to assess the apoptosis index in tumor tissue after treatment.

RESULTSAt 72 h after transfection, the combination with gemcitabine and p65 siRNA significantly decreased the cell viability index (P < 0.05), and down-regulated the expression of Bcl-2 and procaspase-3 and up-regulated the expression of Bax compared with other groups. The combined treatment significantly increased the rate of apoptosis compared with other groups (P < 0.05). EMSA assay indicated that the DNA binding activity of NF-kappaB significantly decreased in NF-kappaB P65 siRNA group and gemcitabine+P65 siRNA group compared with Control group. The combined therapy inhibited the growth of pancreatic xenograft tumors by apoptosis induction in nude mice (P < 0.01).

CONCLUSIONSThe effect of gemcitabine inducing cell apoptosis may be potentiated through inhibiting the DNA binding activity of NF-kappaB and regulating the expression of apoptosis related proteins by NF-kappaB P65 siRNA, which can activate the mitochondria apoptosis pathway in pancreatic cancer in vitro and in vivo.

Animals ; Apoptosis ; drug effects ; genetics ; Cell Line, Tumor ; Deoxycytidine ; analogs & derivatives ; pharmacology ; Humans ; Mice ; Mice, Inbred BALB C ; Pancreatic Neoplasms ; drug therapy ; metabolism ; pathology ; RNA, Small Interfering ; genetics ; Transcription Factor RelA ; genetics ; metabolism ; Transfection ; Xenograft Model Antitumor Assays