SUMMARY OBJECTIVE: Stroke is a chronic health problem that affects all areas of life. The presence of thyroid autoantibodies can augment the severity of stroke. The aim of this work is to investigate whether there is a relationship between the site of stroke involvement and the anti-thyroid peroxidase antibody (anti-TPO) or not. This is the first study in the English-language literature. METHODS: A total of 39 patients with a diagnosis of acute ischemic stroke were included, and the cases under 18 years of age with an infection and the ones with autoimmune diseases other than Hashimoto's thyroiditis were excluded from the study design. The patients’ age, gender, smoking status, comorbid conditions, and stroke localization in brain imaging were recorded. The region involving the anterior circulation area originating from the internal carotid artery was evaluated as anterior, and the region possessing the vertebrobasilar circulation area from the vertebral arteries was considered posterior involvement. Thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), C-reactive protein (CRP), sedimentation, and anti-TPO were retrospectively analyzed. RESULTS: As a consequence, gender distribution, smoking, comorbid conditions, TSH, T3, T4, triglyceride, HDL, LDL, CRP, and sedimentation did not differ significantly, while the age of the posterior-located stroke was lower than that of the cases with the anterior. The anti-TPO value was significantly lower in posterior-located strokes than in the anterior system. CONCLUSION: In summary, the anti-TPO value was recognized as higher in the anterior stroke localization. Thyroiditis and accompanying anti-TPO autoantibody positivity are conditions that should not be ignored by thyroidologists and thyroid-health providers. OBJECTIVE life antithyroid anti antiTPO TPO (anti-TPO Englishlanguage English language literature METHODS 3 included 1 Hashimotos Hashimoto s design status recorded Thyroidstimulating Thyroid stimulating TSH , (TSH) T3 T (T3) T4 (T4) triglyceride highdensity high density HDL (HDL) lowdensity low LDL (LDL) Creactive C reactive CRP (CRP) analyzed RESULTS consequence distribution posteriorlocated located system CONCLUSION summary thyroidhealth providers (TSH (T3 (T4 (HDL (LDL (CRP (T

Abstract Objective: The present study purposed to determine characteristics of ovarian carcinoma and to analyze predictors of survival in patients with ovarian carcinoma. Method: A retrospective cohort study was conducted including the patients with diagnosed ovarian carcinoma treated at the Clinic for Operative Oncology, Oncology Institute of Vojvodina in the period from January 2012 to December 2016. Seventy-two women with ovarian carcinoma were included in the analysis. The data about the histological type of tumor, disease stage, treatment, lymphatic infiltration, and surgical procedure were collected retrospectively, using the database of the institution where the research was conducted (BirPis 21 SRC Infonet DOO – Information System Oncology Institute of Vojvodina). Descriptive statistics and multivariate analysis using Cox proportional hazards model were performed. Results: The univariate Cox regression analysis identified histology, tumor grade, FIGO (International Federation of Gynecology and Obstetrics) stage, NACT (Neoadjuvant Chemotherapy), number of therapy cycles, type of surgery, and chemotherapy response as independent predictors of mortality. Finally, the type of tumor and chemotherapy response had an increased hazard ratio for mortality in the multivariate Cox regression model. Herewith, the percentage of high-grade, advanced-stage ovarian cancer patients with complete response to chemotherapy, absence of recurrent disease, and lymphovascular space invasion were significant predictors of survival in patients with ovarian carcinoma. Conclusions: Herein, emerging data regarding precision medicine and molecular-based personalized treatments are promising and will likely modify the way the authors provide multiple lines of treatments in the near future. Objective Method 201 2016 Seventytwo Seventy two stage treatment infiltration retrospectively BirPis 2 Vojvodina. . Vojvodina) performed Results histology grade International Obstetrics Neoadjuvant Chemotherapy, Chemotherapy , Chemotherapy) cycles surgery Finally Herewith highgrade, highgrade high high-grade advancedstage advanced Conclusions Herein molecularbased molecular based future 20

Abstract Programmed Cell Death-1 (PCD-1) is a key immune checkpoint receptor, which mainly expresses on activated T, B, Dendritic (DC), Natural Killer (NK), and Treg cells. On the surface of activated T-cells, PCD-1 expression is upregulated after the recognition of peripherals antigens by T cells; subsequently, the elevated binding of PD-1 to Programmed Death Ligand-1 (PD-L1) and Programmed Death Ligand-2 (PD-L2) becomes a key step for downstream inhibitory signaling. Although the role of PD-L1 has been evaluated more thoroughly by clinical research, and PD-L1 has also been used more widely in the clinical setting, PD-L2 also plays an important role in the negative regulation of T-cells, one of the necessary conditions that lead to immune tolerance. Expression of PD-L1 either in tumors or in infiltrating immune cells has been verified predominantly by Immunohistochemistry (IHC) in a variety of tumors, suggesting a role for the PD-1/PD-L1 axis as a prognostic trait and therapeutic target across multiple histotypes. The complex interplay between these factors plays a major role in the diffusion and clinical application of PD-L1 IHC assays as predictive biomarkers of response to PD-1/PD-L1 inhibitors. Checkpoint blockades are registered for the treatment of various cancers, including gynecological malignancies. Death1 1 Death- PCD1 PCD (PCD-1 receptor B DC, DC , (DC) NK, NK (NK) Tcells, Tcells cells, T-cells PCD- subsequently PD1 PD PD- Ligand1 Ligand Ligand- PDL1 PDL L1 L (PD-L1 Ligand2 2 PDL2 L2 (PD-L2 signaling PD-L research setting tolerance (IHC PD1/PDL1 PD1PDL1 PDPDL 1/PD PD-1/PD-L histotypes inhibitors cancers malignancies (PCD- (DC (NK (PD-L PD1/PDL PD1PDL 1PD (PCD

Abstract PCOS is an endocrine disorder characterized by chronic anovulation, hyperandrogenism, and polycystic ovaries. Its etiology is uncertain. It is debated whether BPA would be a component of the environmental factor in the etiology of PCOS. Contamination by BPA can occur from food packaging (exposure during the diet) and through skin absorption and/or inhalation. It can be transferred to the fetus via the placenta or to the infant via breast milk, and it can be found in follicular fluid, fetal serum, and amniotic fluid. The phenolic structure of BPA allows it to interact with Estrogen Receptors (ERs) through genomic signaling, in which BPA binds to nuclear ERα or Erβ, or through nongenomic signaling by binding to membrane ERs, prompting a rapid and intense response. With daily and constant exposure, BPA's tendency to bioaccumulate and its ability to activate nongenomic signaling pathways can alter women's metabolic and reproductive function, leading to hyperandrogenism, insulin resistance, obesity, atherogenic dyslipidemia, chronic inflammatory state, and anovulation and favoring PCOS. The harmful changes caused by BPA can be passed on to future generations without the need for additional exposure because of epigenetic modifications. Not only high BPA levels can produce harmful effects, but at low levels, BPA may be harmful when exposure occurs during the most vulnerable periods, such as the fetal and neonatal periods, as well as during the prepubertal age causing an early accumulation of BPA in the body. Learning how BPA participates in the pathogenesis of PCOS poses a challenge and further studies should be conducted. hyperandrogenism ovaries uncertain diet andor inhalation milk fluid serum ERs (ERs Erβ response BPAs s womens women function resistance obesity dyslipidemia state modifications effects periods body conducted

SUMMARY OBJECTIVE: The aim of this study was to examine the changes on the Purkinje cells in the cerebella of male rat pups born to pregnant dams that were exposed to an electromagnetic field in the prenatal period. METHODS: The first stage of the study involved 12 Sprague-Dawley rats, 6 male and 6 female, weighing between 180 and 250 g. The female rats in the experimental group were exposed to a 900-MHz electromagnetic field for 1 h at the same time every day, and no procedure was performed on the control group. Following pregnancy, six male pups from each group were divided into experimental and control groups without any procedure on the pups. After 2 months, they were sacrificed and their cerebella were removed. Histopathologically, following routine processing and fixation procedures, the cerebella were embedded in the tissue blocks. The sections taken from these blocks were stained with cresyl violet. The Purkinje cells in the cerebella were then counted on sections using the optical dissector method on an image analysis system. RESULTS: The estimation of number of the Purkinje cells in the groups revealed more cells in rats in the control group than in the experimental group. Histopathologically, Purkinje cells exhibited a normal morphological structure in the control group, while the cells in the experimental group showed damage. CONCLUSIONS: It might be asserted that the exposure of mothers to an electromagnetic field in the prenatal period may affect the development of Purkinje cells in the pup cerebella. OBJECTIVE METHODS SpragueDawley Sprague Dawley 18 25 g 900MHz MHz 900 day pregnancy months removed Histopathologically procedures violet system RESULTS damage CONCLUSIONS 90 9