The results of our study support the association between benign breast diseases and thyroid diseases. An important implication of this finding may be demonstration of the necessity of scanning for potential breast pathology in women with nodular or autoimmune thyroid disease in clinical practice.

The results of the study show that although there was a decrease in the levels of disulfide, native thiol, and total thiol, the balance of thiol/disulfide was maintained. This is the first study to research the homeostasis of dynamic thiol/disulfide from the perspective of the new method that was used. We hope that this study will encourage and facilitate further studies in this area.

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The aim of this study was to examine the theory that oxidative stress might have an important mediating effect on the deleterious results of vitamin B12 metabolism deficiency seen throughout the body.Materials and methods: Forty patients with vitamin B12 deficiency and 40 healthy controls were included in the study. Venous blood samples were collected from all participants to evaluate serum vitamin B12, homocysteine, methylmalonic acid, total antioxidant status (TAS), and total oxidant status (TOS) levels in the pre-and posttreatment periods.Results: There were no significant differences in TAS, TOS, or oxidative stress index (OSI) levels between the pretreatment patient and control groups, and there were no significant differences in TAS or TOS levels between the posttreatment and control groups. In addition, there were no significant differences between the pre-and posttreatment TAS, TOS, and OSI levels of the patients. Conclusion:These findings are remarkable in that cyanocobalamin treatment had no direct effect on oxidant and antioxidant status in patients with vitamin B12 deficiency. The fact that there were no differences in oxidant and antioxidant status between the patients and the controls might suggest that oxidative stress does not play a role in the systemic negative effects of vitamin B12 deficiency.

Background: Chronic myeloproliferative diseases are clonal stem cell diseases which occur as a result of uncontrollable growth and reproduction of hematopoietic stem cells, which are the myeloid series source in bone marrow. Recent studies have suggested that chronic inflammation can be a triggering factor in the clonal change in chronic myeloproliferative neoplasia (CMPN). In our study, we evaluated the existence of a chronic inflammation process in our Philadelphia negative (Ph-)CMPN patients using inflammation parameters in combination with demographic, laboratory and clinical characteristics of the patients. Materials and Methods: Demographic characteristics, clinical and laboratorial data, and thrombosis histories of 99 Ph-CMPN patients, who were diagnosed at our outpatient clinic of hematology in accordance with WHO 2008 criteria, were analyzed retrospectively,with 80 healthy individuals of matching gender and age included as controls. Complete blood counts, sedimentation, C reactive protein (CRP), JAK V617F gene mutations, abdomen ultrasound images and previous thrombosis histories of these patients were retrospectively analyzed. Results: Ph-CMPN and healthy control groups included 99 and 80 cases, respectively. PV, ET and MF diagnoses of patients were 43 (%43.4), 44 (44.4%) and 12 (12.1%), respectively. JAK V617F gene mutation was found to be positive in 64 (71.1%) of all cases and in 27(65.8%), 32 (82%), 5 (50%) of the cases in PV, ET and PMF groups, respectively. Thrombosis was determined as 12 (12%) in the entire group, 12.5% in the JAK V617F negative and 15.3% in the positive patients, with no statistical significance (p=0.758). No significant difference was observed between patients with and without previous thrombosis history in respect to hemogram parameters, sedimentation and CRP (p>0.05), neutrophil to lymphocyte ratio (NLR), erythrocyte distribution width (RDW), mean platelet volume (MPV) and sedimentation levels of the patient.