scholarly journals Polymorphisms in Glutathione S-Transferase M1, T1, and P1 in Patients with Chronic Periodontitis: A Pilot Study

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Victor Raul Camargo Ortega ◽  
Leliette Deyanira Bravo López ◽  
Angel Visoso Salgado ◽  
Fernando Mejia Sanchez ◽  
Julieta Castillo Cadena
Keyword(s):  
Risk Factor ◽  
Chronic Periodontitis ◽  
Fragment Length Polymorphism ◽  
Genetic Material ◽  
Glutathione S Transferase ◽  
Gstm1 Gene ◽  
Gst Polymorphisms ◽  
Genetic And Environmental Factors ◽  
Severity Of The Disease ◽  
Gstp1 Genes

Background. Although the direct cause of chronic periodontitis is bacterial infection, the progression of this disease depends on genetic and environmental factors, and smoking is a known risk factor in the development and severity of the disease. An individual’s susceptibility may be influenced by polymorphisms in the glutathione S-transferase genes. These genes encode enzymes that metabolize xenobiotic compounds. The aim of this study was to determine the frequency of GSTM1, GSTT1, and GSTP1 polymorphisms in Mexicans with chronic periodontitis. Methods. 60 Mexicans with chronic periodontitis (30 smokers and 30 nonsmokers) were studied. A peripheral blood sample was taken for subsequent DNA extraction. The genetic material was PCR-amplified followed by restriction fragment length polymorphism with the aim of identifying GST polymorphisms. Results. Polymorphisms in the GSTT1 and GSTP1 genes were not significantly different between the smokers and nonsmokers. However, there were significant differences (P=0.05) between groups in polymorphisms in the GSTM1 gene. The patients with chronic periodontitis have a higher frequency of null and mutant polymorphisms in GSTM1, GSTT1, and GSTP1 compared with historical data from a healthy Mexican population. Conclusions. The presence of these polymorphisms may be a risk factor for the development of chronic periodontitis.

scholarly journals Is ventricular arrhythmias the end for all conditions ?

2021 ◽  
Author(s):  
Ahmet Goktug Ertem ◽  
Mehmet Akif Erdol ◽  
Koray Demirtas ◽  
Sefa Unal ◽  
Mustafa Karanfil ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Risk Factor ◽  
Antiretroviral Therapy ◽  
Ventricular Arrhythmias ◽  
Combination Antiretroviral Therapy ◽  
T Wave ◽  
Medical Status ◽  
Immunodeficiency Virus ◽  
Duration Of Disease ◽  
Severity Of The Disease

Dear Editor, We read the article entitled “Abnormal Dispersion of Ventricular Repolarization as a Risk Factor in Patients with Human Immunodeficiency Virus: Tp-e Interval, Tp-e/QTc Ratio” by Unal Evren et al. with interest[1]. The authors evaluated the changes in Tp-e interval, Tp-e/QT and Tp-e/corrected QT (QTc) ratios, and traditional electrocardiographic features of electrical dispersion in adults infected with Human Immunodeficiency Virus (HIV) and their study revealed that the cTp-e interval, Tp-e/QT and Tp-e/QTc ratios were prolonged and correlated to the severity of the disease in HIV-infected patients. Previous studies have revealed that the Tp–e interval, the Tpeak-Tend interval (Tpe), the interval from the T-wave peak to the end of the T wave, has been related to arrhythmogenesis, is specified as an index of totaldispersion of repolarization[2]. Prolonged Tp–e interval is predictable for ventricular arrhythmias and mortality [3]. Unal et al. showed that HIV-infected patients receiving combination antiretroviral therapy (cART) were associated withlonger Tp–e interval and Tp–e/QTc ratio and correlated positively with the duration of disease and the electrophysiologicalabnormalities, and negatively with CD4 count[4]. There were no informations about medical status of patients with HIV, duration of the disease and why hsCRP is higher in patients’ group. The patients were in active phases of infection. We think that these are important datas for results of the study. We thank the authors for adding this article to the literature

scholarly journals Association Between Glutathione S-Transferase (GST) Polymorphisms and Schizophrenia in a Chinese Han Population

2020 ◽  
Vol Volume 16 ◽  
pp. 479-487
Author(s):  
Ci Yan ◽  
Li Duan ◽  
Chunfeng Fu ◽  
Chunsheng Tian ◽  
Bihui Zhang ◽  
...  
Keyword(s):  
Chinese Han Population ◽  
Glutathione S Transferase ◽  
Chinese Han ◽  
Han Population ◽  
Gst Polymorphisms

Gene-Gene and Gene-Environment Interactions Determine Risk of Thrombosis in Families With Inherited Antithrombin Deficiency

Blood ◽  
1999 ◽  
Vol 94 (8) ◽  
pp. 2590-2594 ◽  
Author(s):  
H.H. van Boven ◽  
J.P. Vandenbroucke ◽  
E. Briët ◽  
F.R. Rosendaal
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Genetic Risk ◽  
Factor V Leiden ◽  
Genetic Defects ◽  
Factor V ◽  
Antithrombin Deficiency ◽  
Gene Environment ◽  
Genetic And Environmental Factors

To analyze inherited antithrombin deficiency as a risk factor for venous thromboembolism in various conditions with regard to the presence or absence of additional genetic or acquired risk factors, we compared 48 antithrombin-deficient individuals with 44 nondeficient individuals of 14 selected families with inherited antithrombin deficiency. The incidence of venous thromboembolism for antithrombin deficient individuals was 20 times higher than among nondeficient individuals (1.1% v 0.05% per year). At the age of 50 years, greater than 50% of antithrombin-deficient individuals had experienced thrombosis compared with 5% of nondeficient individuals. Additional genetic risk factors, Factor V Leiden and PT20210A, were found in more than half of these selected families. The effect of exposure to 2 genetic defects was a 5-fold increased incidence (4.6% per year; 95% confidence interval [CI], 1.9% to 11.1%). Acquired risk factors were often present, determining the onset of thrombosis. The incidence among those with exposure to antithrombin deficiency and an acquired risk factor was increased 20-fold (20.3% per year; 95% CI, 12.0% to 34.3%). In conclusion, in these thrombophilia families, the genetic and environmental factors interact to bring about venous thrombosis. Inherited antithrombin deficiency proves to be a prominent risk factor for venous thromboembolism. The increased risks among those with exposure to acquired risk factors should be considered and adequate prophylactic anticoagulant therapy in high-risk situations seems indicated in selected families with inherited antithrombin deficiency.

The Interaction between KCNJ11 Gene Polymorphism and Refined Carbohydrates Intake on Obesity in Indonesian Adolescents

2020 ◽  
Vol 16 (2) ◽  
pp. 185-189
Author(s):  
Emy Huriyati ◽  
Harry Freitag Luglio ◽  
Ahmad H. Sadewa ◽  
Mohammad Juffrie
Keyword(s):  
Gene Polymorphism ◽  
Pancreatic Beta Cells ◽  
Fragment Length Polymorphism ◽  
Female Adolescents ◽  
High Intake ◽  
Kcnj11 Gene ◽  
Pcr Rflp ◽  
Polymerase Chain ◽  
Genetic And Environmental Factors ◽  
Refined Carbohydrates

Background: Obesity has been associated with genetic and environmental factors. Although carbohydrate intake was previously shown to be associated with a high risk of obesity and insulin resistance, some studies reported that genetic factors also have a role in this association. KCNJ11 is a gene involved in protein K-ATP channels of pancreatic beta cells and previously associated with obesity. Objective: The objective of this study was to determine the interaction between KCNJ11 polymorphism with a high intake of refined carbohydrates in relation to the incidence of obesity in adolescents. Method: This was an observational study with a case-control design. The subjects of this study were male and female adolescents from 10 high schools in Yogyakarta. Dietary intake, body weight, and height were collected. KCNJ11 gene polymorphism was detected by polymerase Chain Reaction- Restriction Fragment Length Polymorphism (PCR-RFLP) method. Result: There is a significant association between KCNJ11 polymorphism with a high intake of refined carbohydrates in the incidence of obesity in adolescents (OR = 2.35, p =0.036). Conclusion: There is a significant association between the KCNJ11 polymorphism with a high intake of refined carbohydrates in adolescent obesity.

The clinical course of chronic periodontitis. IV. Gingival inflammation as a risk factor in tooth mortality

2004 ◽  
Vol 31 (12) ◽  
pp. 1122-1127 ◽  
Author(s):  
Marc Schatzle ◽  
Harald Loe ◽  
Niklaus P. Lang ◽  
Walter Burgin ◽  
Age Anerud ◽  
...  
Keyword(s):  
Risk Factor ◽  
Chronic Periodontitis ◽  
Clinical Course ◽  
Gingival Inflammation

scholarly journals Association between Inflammatory Marker, Environmental Lead Exposure, and Glutathione S-Transferase Gene

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Jintana Sirivarasai ◽  
Winai Wananukul ◽  
Sming Kaojarern ◽  
Suwannee Chanprasertyothin ◽  
Nisakron Thongmung ◽  
...  
Keyword(s):  
Lead Exposure ◽  
Inflammatory Marker ◽  
Blood Lead ◽  
Genetic Determinants ◽  
Glutathione S Transferase ◽  
Environmental Lead ◽  
Gst Polymorphisms ◽  
Gst Polymorphism ◽  
Hs Crp ◽  
Environmental Lead Exposure

A number of studies suggested that lead is related to the induction of oxidative stress, and alteration of immune response. In addition, modifying these toxic effects varied partly by GST polymorphism. The objectives of this study were to assess the association between the lead-induced alteration in serum hs-CRP, with GSTM1, GSTT1, and GSTP1 Val105Ile genetic variations and the health consequence from environmental lead exposure. The 924 blood samples were analyzed for blood lead, CRP, and genotyping of three genes with real-time PCR. Means of blood lead and serum hs-CRP were 5.45 μg/dL and 2.07 mg/L. Both CRP and systolic blood pressure levels were significantly higher for individuals with blood lead in quartile 4 (6.48–24.63 μg/dL) compared with those in quartile 1 (1.23–3.47 μg/dL,P<0.01). In particular, in men with blood lead >6.47 μg/dL the adjusted odds ratio (OR) of CRP levels for individuals with GSTP1 variants allele, GSTM1 null, GSTT1 null, double-null GSTM1, and GSTT1 compared with wild-type allele was 1.46 (95% CI; 1.05–2.20), 1.32 (95% CI; 1.03–1.69), 1.65 (95% CI; 1.17–2.35), and 1.98 (95% CI; 1.47–2.55), respectively. Our findings suggested that lead exposure is associated with adverse changes in inflammatory marker and SBP. GST polymorphisms are among the genetic determinants related to lead-induced inflammatory response.

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