6 research outputs found

    The association between 3020INSC mutation in NOD2 gene and arterial stiffness in hypertensives

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    Background The innate immune system elicits an inflammatory process which is believed to be involved in the development of vascular damage in hypertension. The NOD2 gene (CARD15) is involved in the control of the innate immune system. The aim of this study was to assess the occurrence of the 3020insC mutation in the NOD2 gene in relation to vascular damage in hypertensives. Materials and methods In 466 hypertensives, genotyping for 3020insC mutation, cholesterol, serum creatinine, and echocardiography were carried out. Systolic (SBP) and diastolic (DBP) blood pressure and pulse pressure (PP) were taken at 2-3 month intervals for one year and treated according to ESC/ESH guidelines. Results The 3020insC mutation was found in 7.08% of hypertensives and was associated with earlier onset of hypertension 48.2 &#177; 12.1 v. 42.8 &#177; 10.9, p < 0.01 (age of pts). After one year of treatment, patients with the mutation had significantly higher SBP (138.48 &#177; 18.35 v. 131.74 &#177; 14.97, p < 0.04) and PP (57.27 &#177; 14.04 v. 52.70 &#177; 12.96, p < 0.04) than patients without the mutation, whereas the number of drugs was the same in both groups. Conclusions The results suggest that the 3020insC mutation is associated with earlier onset of hypertension and increased arterial stiffness

    The association between 3020INSC mutation in NOD2 gene and arterial stiffness in hypertensives.

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    The innate immune system elicits an inflammatory process which is believed to be involved in the development of vascular damage in hypertension. The NOD2 gene (CARD15) is involved in the control of the innate immune system. The aim of this study was to assess the occurrence of the 3020insC mutation in the NOD2 gene in relation to vascular damage in hypertensives

    The outline of immunopathogenesis of Crohn's disease with special consideration of NOD2/CARD15 gene polymorphism.

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    Crohn sdisease is achronic inflammatory disease affecting different parts of digestive tract. Despite the extensive research, t here is still no exact explanation of its pathogenesis. In the paper we present modern views on the origin of the disorder, concerning the influence o f infectious, immu- nological, neuroendocrine and molecular factors on the disease development. We pay special attention to the role of NOD2/CARD15 gene in the pathogenesis of inflammatory bowel disease.Choroba Le niowskiego-Crohna jest przewlek┬│┬╣ chorob┬╣ zapaln┬╣ przewodu pokarmowego atakuj┬╣c┬╣ r├│┬┐ne jego odcinki. Mimo intensywny ch ba- da├▒, jak dot┬╣d nie uda┬│o si├¬ ustali├Ž dok┬│adnie jej patogenezy. Wpracy przedstawiono najnowsze pogl┬╣dy na temat mechanizm├│w pows tawania tej choroby obejmuj┬╣ce wp┬│yw czynnik├│w inf ekcyjnych, neuroendokrynnych, immunologiczn ych iinnych. Szczeg├│lny nacisk po┬│o┬┐ono na znacze- nie uwarunkowa├▒ genetycznych. Om├│wiono r├│wnie┬┐ biologiczne funkcje oraz kluczow┬╣ rol├¬ genu NOD2/CARD15 wprocesie powstawania prze- wlek┬│ych chor├│b zapalnych przewodu pokarmoweg

    Harnessing Epigenetics for Breast Cancer Therapy: The Role of DNA Methylation, Histone Modifications, and MicroRNA

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    Breast cancer exhibits various epigenetic abnormalities that regulate gene expression and contribute to tumor characteristics. Epigenetic alterations play a significant role in cancer development and progression, and epigenetic-targeting drugs such as DNA methyltransferase inhibitors, histone-modifying enzymes, and mRNA regulators (such as miRNA mimics and antagomiRs) can reverse these alterations. Therefore, these epigenetic-targeting drugs are promising candidates for cancer treatment. However, there is currently no effective epi-drug monotherapy for breast cancer. Combining epigenetic drugs with conventional therapies has yielded positive outcomes and may be a promising strategy for breast cancer therapy. DNA methyltransferase inhibitors, such as azacitidine, and histone deacetylase inhibitors, such as vorinostat, have been used in combination with chemotherapy to treat breast cancer. miRNA regulators, such as miRNA mimics and antagomiRs, can alter the expression of specific genes involved in cancer development. miRNA mimics, such as miR-34, have been used to inhibit tumor growth, while antagomiRs, such as anti-miR-10b, have been used to inhibit metastasis. The development of epi-drugs that target specific epigenetic changes may lead to more effective monotherapy options in the future
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