Primary Open Angle Glaucoma (POAG) is a chronic, irreversible optic neuropathy leading to the progressive death of retinal ganglion cells, clinically observed as silent visual field loss along with a decrease in colour and contrast sensitivity. Multiple pathogenic theories have been issued and some of them have proven their involvement in disease development: mechanical damage due to increased intraocular pressure, variable susceptibility of the optic nerve, mutation in specific nuclear genes, increased glutamate levels, alteration in nitric oxide (NO) metabolism, changes in the mitochondrial genome, vascular disturbances, and toxic effects and oxidative damage caused by reactive oxygen species [1].The aim of this article is to highlight the pathogenic role of vascular disturbances and reactive oxygen species in POAG with the further possibilities for prevention and gene therapy.

DNA repair plays an important role in maintaining the integrity of the genome by repairing DNA damage induced by carcinogens. Certain genetic polymorphisms that occur in DNA-repair genes may affect the ability to repair DNA defects, and may represent a risk factor in carcinogenesis. The gene XRCC1 is involved in DNA repair. The purpose of our study was to investigate the association between XRCC1 Arg194Trp and Arg399Gln polymorphisms and the risk of lung cancer in a Romanian population. We recruited 222 healthy controls and 102 patients with lung cancer. Genotypes were determined by multiplex polymerase chain-reaction restriction fragment-length polymorphism. Statistical analysis (odds ratio, recessive model) revealed an increased risk for lung cancer for the homozygous 194Trp genotype (χ2=0.186, odds ratio 10.667, 95% confidence interval 1.309–86.933; P=0.007). Also, we found an association between the 194Trp allele and women with lung adenocarcinoma. In conclusion, the results of the study place the XRCC1 Arg194Trp polymorphism among independent risk factors for developing lung cancer.

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Aim. The present study aims to analyze the potential role of VEGF +936 C/T polymorphism in cervical intraepithelial neoplasia. Material and Method. One hundred and eighty-six patients were included in the study: 75 cases (patients diagnosed with CIN) and 111 controls (negative for both HPV testing and cytology). For each patient a single visit was scheduled when colposcopy was performed. From cervical specimen, cytology and HPV testing were performed and from peripheral blood VEGF +936 genotyping was determined. For statistical analysis purposes OR and chi-square were used at a level of significance of <0.05. Results. No link has been found in the detection of CT genotype in cases versus controls, OR = 0.8295, [0.42, 1.62]. An inverse correlation has been found between T allele and HSIL, OR = 0.2121, [0.0473, 0.9517], p = 0.0866. Conclusion. No link has been found between VEGF +936 C/T and cervical intraepithelial neoplasia.

Introduction: Stroke is one of the leading causes of death in Romania. Evidence in supporting the role of the pro-infl ammatory cytokine TNFalpha in ischemic pathogenesis is now well established. The aim of the present study is to evaluate the relationship between TNF -308G>A polymorphism and ischemic stroke in a Northern Romanian population group and to determine whether it has an infl uence on the risk of cerebral events. This is a cross-sectional, randomized, case-control study for the evaluation of TNF -308G>A polymorphism alleles frequency among patients with ischemic stroke. Material and method: The study included 108 patients diagnosed with ischemic stroke (neurological and CT scan examination), and 118 healthy unrelated controls. TNF -308G>A genotyping was carried out using PCR-RFLP technique. The amplifi cation of the relevant gene fragment was subjected to restriction enzyme digestion, followed by gel electrophoresis. Results: Molecular analysis did not reveal an increased frequency of GA mutant genotype in the study group compared to the control group (p = 0.879, OR = 0.928, CI = 0.512-1.682). Conclusions:We found no signifi cant differences in distribution of the TNF -308G>A polymorphism between ischemic stroke patients and controls.