19 research outputs found

    CDK4 IVS4-nt40 AA genotype and obesity-associated tumors/cancer in Italians – a case-control study

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    <p>Abstract</p> <p>Background</p> <p>Cell cycle checkpoint regulation is crucial for prevention of tumor in mammalian cells. Cyclin-dependant kinase 4 (CDK4) is important in cell cycle regulation, as it controls the G1-S phase of the cell cycle. CDK4 has potential mitogenic properties through phosphorylation of target proteins. We aimed at identifying a role of <it>CDK4 </it>IVS4-nt40 G→A gene variant in benign and/or malignant tumors and in obesity-associated benign and/or malignant tumors in an Italian adult subject dataset.</p> <p>Methods</p> <p>We recruited 263 unrelated Italian subjects: 106 subjects had at least one benign tumor and 46 subjects had at least one malignant tumor, while 116 subjects had at least two tumors and/or cancers. We collected BMI data for 90% of them: 186 subjects had a BMI≥30 Kg/m<sup>2 </sup>and 52 subjects had a BMI ≥ 30 Kg/m<sup>2</sup>. We performed statistical power calculations in our datasets. DNA samples were directly sequenced with specific primers for the <it>CDK4 </it>IVS4-nt40 G→A variant. Genotype association tests with disease were performed.</p> <p>Results</p> <p>In our study, no significant association of the <it>CDK4 </it>IVS4-nt40 AA genotype with cancer and/or tumors/cancer are/is detected. However, the <it>CDK4 </it>IVS4-nt40 AA genotype is significantly associated with cancer and tumors/cancer in obese patients.</p> <p>Conclusion</p> <p>This finding is interesting since obesity is a risk factor for tumors and cancer. This study should prompt further work aiming at establishing the role of <it>CDK4 </it>in contributing to tumor/cancer genetic risk predisposition, as well as its role as a potentially effective therapeutic target gene for obesity-associated tumor/cancer management.</p

    Lipid and lipoprotein profiles among middle aged male smokers: a study from southern India

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    <p>Abstract</p> <p>Objectives</p> <p>The objectives were to investigate into the relationship between lipid profile including Apolipoprotein-A1 (Apo-A1) and Apolipoprotein-B (Apo-B) and smokers and to relate them with smoking pack years.</p> <p>Materials and Methods</p> <p>A total of 274 active male smokers without any other illnesses and age matched male healthy control subjects (78) with similar socio-cultural background were assessed for clinical details, dietary habits, physical activities, smoking and alcohol consumption. Standard methods were adopted to check the lipid levels. The data were analyzed statistically.</p> <p>Results</p> <p>Their ages ranged from 40 to 59 years, systolic BP from 110 to 130 mmHg, and diastolic BP from 76 to 88 mmHg. All of them had similar pattern of diet (vegetarianism with occasional meat). None was on any medication influences lipid level. Their physical activity was moderate. Number of pack years varied from 10 to 14 (mild), 15 to 19 (moderate) and 20 and above (heavy) among 69, 90 and 115 cases, whose mean ages were 43, 44 and 49 respectively. The mean (+SD) values in mg/dl of total cholesterol (TC), Triglyceride (TGL), Apo-B, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol and Apo-A1 in mg/dl among mild/ moderate/ heavy smokers and control subjects were 198 (30.6)/ 224 (27.2)/ 240 (24.3) and 160 (20.4); 164(42.6)/ 199 (39.5)/ 223(41.7) and 124 (31.6); 119 (24.9)/ 121 (27)/ 127 (28.3) and 116 (21.4); 94 (19.7)/ 104 (21.8)/ 120 (20.5) and 82 (17.6); 42 (5.9)/ 39 (3.1)/ 35(4.4) and 48 (5.3); and 120 (17)/ 119 (21)/ 115 (25) and 126 (19), respectively. In smokers, there was a rise in TC, TGL, LDL, Apo-B and fall in HDL and Apo-A; these changes were significant (P < 0.05).</p> <p>Conclusion</p> <p>Number of pack years was directly proportional to abnormal lipid profile. It is also concluded that changes in Apo-A1 and Apo-B were more significant when compared to HDL and LDL cholesterol among smokers. In the view of double risk for smokers (smoking and altered lipid profile) efforts may be made to introduce smoking cessation program.</p

    CHOP 5'UTR-c.279T>C and +nt30C>T variants are not associated with overweight condition or with tumors/cancer in Italians – a case-control study

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    <p>Abstract</p> <p>Background</p> <p>Type 2 diabetes (T2D) is associated with obesity and has been shown recently to be associated with tumors/cancer. <it>HNF1-beta </it>and <it>JAZF1 </it>genes are associated with T2D and prostate cancer. We have previously shown that <it>CHOP </it>5'UTR-c.279T>C and +nt30C>T haplotype variants contribute to T2D. CHOP deficiency causes obesity in mice, thus <it>CHOP </it>gene variants may contribute to human obesity. Furthermore, <it>CHOP </it>mediates apoptosis and is implicated in cancer pathogenesis. Hence, we aimed at identifying any potential association of <it>CHOP </it>5'UTR-c.279T>C and +nt30C>T genotypes and corresponding haplotypes with overweight condition/pre-obesity and tumors/cancer in an Italian dataset.</p> <p>Methods</p> <p>We recruited from Italy 45 overweight subjects (body mass index (BMI) ≥ 25) and 44 control subjects (BMI < 25) as well as 54 cases with at least one cancer or at least one tumor and 43 control subjects without tumors/cancer from the general population. We excluded allelic departure from Hardy-Weinberg equilibrium in cases and control subjects, separately.</p> <p>Results</p> <p>We assessed the power to detect risk odds ratios by association tests in our datasets. We tested the hypothesis of association of CHOP 5'UTR-c.279T>C and +nt30C>T genotypes and haplotypes with tumors/cancer and, separately, with overweight condition. Both associations were not significant.</p> <p>Conclusion</p> <p>From our study, we may conclude that <it>CHOP </it>5'UTR-c.279T>C and +nt30C>T genotypes and corresponding haplotypes are not associated with tumors/cancer and pre-obesity. However, more studies are warranted to establish the role of <it>CHOP </it>variants in tumor/cancer predisposition and in overweight condition.</p

    Risk factors for myocardial infarction among low socioeconomic status South Indian population

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    <p>Abstract</p> <p>Background</p> <p>As longevity increases, cases of myocardial infarction (MI) are likely to be more. Cardiovascular disease (CVD) is a major global health problem reaching epidemic proportions in the Indian subcontinent, also among low socio-economic status (SES) and thin individuals.</p> <p>Objectives</p> <p>The present study was undertaken to elicit risk factors for MI among low SES Southern Indians and to find out its association with body mass index (BMI).</p> <p>Materials and methods</p> <p>A case-control study of patients with MI matched against healthy control subjects was carried out in a tertiary care teaching hospital. Standard methods were followed to elicit risk factors and BMI. Chi-square and Fishers exact test for categorical versus categorical, to show relationship with risk factors were analyzed.</p> <p>Results</p> <p>A total of 949 patients (male (M) = 692 and post menopausal female (F) = 257) and 611 age and sex matched healthy controls were included. In our study, BMI was below 23 in 48.2% of patients and below 21 in 22.5%. The risk of developing MI was significantly more in males (odds ratio (OR) = 3.3, 95% confidence interval (C.I.) = 2.69-4.13), among females with post-menopausal duration (PMD) of more than or equal to 3 years (OR = 9.27, 95% C.I. = 6.36-13.50) and in those with BMI less than 23 with one or other risk factors (P = 0.002, OR = 1.38, 95% C.I. = 1.13-1.70).</p> <p>Conclusion</p> <p>BMI cannot be considered as a lone independent risk factor, as the study population had low BMI but had one or more modifiable risk factors. It would be advisable to keep BMI at least 21 kg/m<sup>2 </sup>for screening program. Health education on life style modification and programs to diagnose and control diabetes and hypertension have to be initiated at community level in order to reduce the occurrence.</p

    Hypothesis of snake and insect venoms against Human Immunodeficiency Virus: a review

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    Abstract Background Snake and insect venoms have been demonstrated to have beneficial effects in the treatment of certain diseases including drug resistant human immunodeficiency virus (HIV) infection. We evaluated and hypothesized the probable mechanisms of venoms against HIV. Methods Previous literatures published over a period of 30 years (1979-2009) were searched using the key words snake venom, insect venom, mechanisms and HIV. Mechanisms were identified and discussed. Results & Conclusion With reference to mechanisms of action, properties and components of snake venom such as sequence homology and enzymes (protease or L- amino acid oxidase) may have an effect on membrane protein and/or act against HIV at multiple levels or cells carrying HIV virus resulting in enhanced effect of anti-retroviral therapy (ART). This may cause a decrease in viral load and improvement in clinical as well as immunological status. Insect venom and human Phospholipase A2 (PLA2) have potential anti-viral activity through inhibition of virion entry into the cells. However, all these require further evaluation in order to establish its role against HIV as an independent one or as a supplement.</p
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