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| 1 | Metabolic syndrome as a risk factor for gallstone disease显示文摘AIM: To establish an association between the presence of metabolic syndrome and the development of gallstone disease.METHOIDS: We carried out a cross-sectional study in a check-up unit in a university hospital in Mexico City. We enrolled 245 subjects, comprising 65 subjects with gallstones (36 women, 29 men) and 180 controls (79women and 101 men without gallstones). Body mass index, waist circumference, blood pressure, plasma insulin, and serum lipids and lipoproteins levels were measured. Insulin resistance was calculated by homeostasis model assessment. Unconditional logistic regressionanalysis (univariate and multivariate) was used to calculate the risk of gallstone disease associated with the presence of at least three of the criteria (Adult Treatment Panel Ⅲ). Analyses were adjusted for age and sex.RESULTS: Among 245 subjects, metabolic syndrome was present in 40% of gallstone disease subjects, compared with 17.2% of the controls, adjusted by age and gender (odds ratio (OR) = 2.79; 95%CI, 1.46-5.33; P = 0.002),a dose-dependent effect was observed with each component of metabolic syndrome (OR = 2.36, 95%CI, 0.72-7.71;P = 0.16 with one component and OR = 5.54, 95%CI,1.35-22.74; P = 0.02 with four components of metabolic syndrome). Homeostasis model assessment was significantly associated with gallstone disease (adjusted OR = 2.25;95%CI, 1.08-4.69; P = 0.03).CONCLUSION: We conclude that as for cardiovascular disease and diabetes mellitus, gallstone disease appears to be strongly associated with metabolic syndrome. | Nahum Méndez-Sánchez Norberto C. Chavez-Tapia Daniel Motola-Kuba Karla Sanchez-Lara Guadalupe Ponciano-Rodríguez Héctor Baptista Martha H. Ramos Misael Uribe | 2005 | World Journal of Gastroenterology2005，11，11： | 32 |
| 2 | Adiponectin as a protective factor in hepatic steatosis显示文摘AIM: Obesityand insulin resistance (IR) are closely related to hepatic steatosis (HS), and adiponectin is a hepatic insulin sensitizer that has important effects in liver function.This study aims at investigating the relationship between serum adiponectin concentration and the presence of HS.METHODS: We carried out a cross-sectional study in a check-up unit of a University Hospital in Mexico City. We enrolled 196 subjects, comprising 98 subjects with HS (27 women, 71 men) and 98 controls (37 women and 61men). Anthropometric, metabolic and biochemical variables were measured in the two groups. Serum adiponectin and leptin concentrations were determined,their association with grade of HS tested, and concentrations,according to quartiles, compared between cases and controls. χ2 analysis for linear trends was used to test for a dose-response relationship and logistic regression analysis was conducted to test for a protective effect of adiponectin.RESULTS: The HS subjects were older and more obese than controls, with a central obesity pattern. In the fourth quartile of adiponectin concentrations, HS was less common and severe. In a multivariate model of the fourth quartile of the adiponectin concentrations, we observed a protective effect (OR = 0.17, 95%CI: 0.04-0.67, P= 0.01).In subjects with more severe HS, we observed higher leptin concentrations, and caloric intakes, total fat and iron consumption were higher than in controls.CONCLUSION: The results of the present study suggest that a high serum concentration of adiponectin is associated with a protective effect against HS. | Nahum Méndez-Sánchez Norberto C.Chávez-Tapia Antonio R.Villa Karla Sánchez-Lara Daniel Zamora-Valdés Martha H.Ramos Misael Uribe | 2005 | World Journal of Gastroenterology2005，11，12： | 12 |
| 3 | Serum leptin levels and insulin resistance are associated with gallstone disease in overweight subjects显示文摘AIM: To establish an association between the serum leptin levels and the development of gallstone disease (GD).METHODS: We carried out a non-matched case-controlled study in a university hospital in Mexico City. Two hundred and eighty-seven subjects were included: 97 cases with gallstones and 190 controls. Body mass index (BMI), fasting plasma leptin, insulin, serum lipid, and lipoprotein levels were measured. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Unconditional logistic regression analysis (univariate and multivariate)stratified by BMI was used to calculate the risk of GD.RESULTS: The multivariate conditional regression analysis revealed a model for those patients with BMI <30. The selected variables in the model were HOMA-IR index with OR = 1.31, P= 0.02 and leptin higher than median with OR = 2.11, P= 0.05. In the stratum of BMI ≥30, we did not find a useful model.CONCLUSION: We concluded that insulin resistance and the development of GD appears to be associated with serum leptin levels in subjects with overweight, but not in obese subjects with similar metabolic profiles. | Nahum Méndez-Sánchez Luisa B Bermejo-Martínez Yolanda Vi(n|~)als Norberto C Chavez-Tapia Irina Vander Graff Guadalupe Ponciano-Rodríguez Martha H Ramos Misael Uribe | 2005 | World Journal of Gastroenterology2005，11，39： | 11 |
| 4 | Prevalence of metabolic syndrome, obesity and diabetes type 2 in cryptogenic cirrhosis显示文摘AIM: To evaluate the prevalence of metabolic syndrome (MS), obesity and type 2 diabetes mellitus (T2DM) in a group of Mexican Mestizo patients with cryptogenic cirrhosis (CC) and to compare this group with patients with cirrhosis secondary to other causes (disease controls). METHODS: Patients with CC, diagnosed between January, 1990 and April, 2005, were included in a retrospective study. Patients with cirrhosis caused by chronic hepatitis C, alcohol abuse or autoimmune hepatitis (AIH) served as disease controls. RESULTS: A total of 134 patients with CC were analyzed. Disease controls consisted of 81 patients with chronic hepatitis C, 33 with alcohol abuse and 20 with AIH. The median age of patients with CC was 57 years (range, 16-87); 83 (61.9%) patients were female; 53 (39.6%) were Child A, 65 (48.5%) Child B, and 16 (11.9%) were Child C cirrhosis. The prevalence of MS (29.1% vs 6%; P < 0.001), obesity (16.4% vs 8.2%; P = 0.04) and T2DM (40% vs 22.4%; P = 0.013) was higher in CC patients than in disease controls. There were no differences in sex, age or liver function tests between the two groups. CONCLUSION: The prevalence of MS, obesityand T2DM were higher in patients with CC than in patients with cirrhosis secondary to others causes. Our findings support the hypothesis that non-alcoholic steatohepatitis (NASH) plays an under-recognized role in CC. | Felix I Tellez-Avila Francisco Sanchez-Avila Mauricio García-Saenz-de-Sicilia Norberto C Chavez-Tapia Ada M Franco-Guzman Gustavo Lopez-Arce Eduardo Cerda-Contreras Misael Uribe | 2008 | World Journal of Gastroenterology2008，14，30： | 6 |
| 5 | Mitochondrial DNA from hepatocytes as a ligand for TLR9: Drivers of nonalcoholic steatohepatitis?显示文摘Nonalcoholic fatty liver disease(NAFLD) is the most common liver disease worldwide, affecting approximately one third of the Western world. It consists of a wide spectrum of liver disorders, ranging from fatty liver to nonalcoholic steatohepatitis(NASH), which consists of steatosis, ballooning injury and inflammation. Despite an alarming growth in the statistics surrounding NAFLD, there are as yet no effective therapies for its treatment. Innate immune signaling has been thought to play a significant role in initiating and augmenting hepatic inflammation, contributing to the transition from nonalcoholic fatty liver to NASH. An immune response is triggered by countless signals called damage-associated molecular patterns(DAMPs) elicited by lipid-laden and damaged hepatocytes, which are recognized by pattern recognition receptors(PRRs) on hepatic immune cells to initiate inflammatory signaling. In this editorial, in addition to summarizing innate immune signaling in NAFLD and discussing potential therapies that target innate immune pathways, we have described a recent study that demonstrated that mitochondrial DNA serves as a DAMP activating a hepatic PRR, TLR9, in mice and in the plasma of NASH patients. In addition to identifying a new ligand for TLR9 during NASH progression, the study shows that blocking TLR9 reverses NASH, paving the way for the development of future NASH therapy. | Priya Handa Akhila Vemulakonda Kris V Kowdley Misael Uribe Nahum Méndez-Sánchez | 2016 | World Journal of Gastroenterology2016，22，31： | 3 |
| 6 | Preparation and hybridization analysis of DNA/RNA from E. coli on microfabricated bioelectronic chips显示文摘 | Cheng Jing Sheldon E L Wu Lei Uribe A Gerrue L O Carrino J Heller M J O'Connell J P | | 0，，： | 2 |
| 7 | Obstetrical hysterectomy, Evolution and change显示文摘 | URIBE ELIAS R ACOSTA ALFARO M A | 1996 | Ginecol Obster Mer1996，64，： | 1 |
| 8 | Closing Small Open Economy Models 显示文摘 | Schmitt-Grohe S Uribe M | 2003 | Journal of International Economics2003，，61： | 1 |
| 9 | Boar spermatozoa eryopreservation in low glycerol/trehalose enriched freezing media improves cellular integrity显示文摘 | Gutierrez P O Juarez M D Uribe C S | 2009 | Cryobiology2009，58，： | 1 |
| 10 | Oxygen-derived free radicals in hepatic ischemia and reperfusion injury in the rat显示文摘 | Nauta KJ Tsimogiannis E Uribe M | 1990 | Surg Gynecol Okstet1990，171，： | 1 |
| 11 | Effect of collection zone height and operating variables on recovery of overload flotation columns 显示文摘 | Garibay R P Gallegos A P M Uribe S A | 2002 | Minerals Engineering2002，15，： | 1 |
| 12 | Resveratrol neuroprotection in a chronic mouse model of multiple sclerosis显示文摘 | Fonseca-Kelly Z Nassrallab M Uribe J | | 0，，： | 1 |
| 13 | Eosinophilic Gastroenteritis: A Review显示文摘 | Nahum Méndez-Sánchez Norberto C. Chávez-Tapia Genaro Vazquez-Elizondo Misael Uribe | 2007 | Digestive Diseases and Sciences2007，，11： | 1 |
| 14 | Role of oxidative stress and molecular changes in liver fibrosis: a review 显示文摘 | Sanchez-Valle V Chavez- Tapia NC Uribe M | 2012 | Curt Med Chem2012，19，28： | 1 |
| 15 | Primary angiitis of the central nervous system: report of five biopsy- confirmed cases from Colombia 显示文摘 | Volcy M Toro ME Uribe CS | 2004 | J Neurol Sci2004，227，： | 1 |
| 16 | Role of oxidative stress and molecular changes in liver fibrosis : a review显示文摘 | SANCHEZ VALLE V CHAVEZ TAPIA N C URIBE M | 2012 | Curt Med Chem2012，19，28： | 1 |
| 17 | Clinical and manmnetric results of endorectal advancement flaps for complex anal fistula 显示文摘 | Uribe N Millan M Minguez M | 2007 | Int J Colorectal Dis2007，22，3： | 1 |
| 18 | Oogenesis and ovarian histology of the american alligator,alligator mississippiensis显示文摘 | URIBE M C A GUILLEEEE JR L J | 2000 | Journal of morphology2000，245，： | 1 |
| 19 | Role of oxi- dative stress and molecular changes in liver fibrosis: a review 显示文摘 | Sanchez-Valle V Chavez-Tapia NC Uribe M | 2012 | Curr Med Chem2012，19，28： | 1 |
| 20 | Posttransplant lymphoproliferative disorder in pediatric liver transplantation 显示文摘 | Uribe M Hunter B Alba A | 2009 | Transplant Proc2009，41，6： | 1 |
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