Browsing by Author "Nikolic, Tatjana (57235024600)"

Background/Aim. Osteoporosis is the most common metabolic bone disorder worldwide characterized by decreased bone strength that predisposes to an increased fracture risk, especially in postmenopausal women. Today, over 25 million people, mainly women, suffer from this metabolic disorder. In addition to genetic predispositions, hormonal disorders, lifestyle, and insufficient Vitamin D levels in the blood are significant risk factors for the occurrence of osteoporosis and low-energy fractures. The aim of our study was to analyze the incidence of osteoporosis and the correlation between Vitamin D deficiency and secondary hyperparathyroidism in women of different ages with low-energy fractures. Methods. This cross-sectional study included 559 women who were not previously treated for osteoporosis. All women were clinically examined and their anamnesis of chronic illnesses, fractures, and therapies was taken. Height and weight were measured, and body mass index (BMI) was calculated. Risk factors for osteoporosis, including the concentration of 25-hydroxyVitamin D [25(OH)D] and parathyroid hormone (PTH), were measured. Vitamin D deficiency was defined as serum level of 25(OH)D less than 30 ng/mL (75 nmol/L). Results. The study included a total of 559 women, of which low-energy fractures were identified in 102 women. Women with fractures were older (63.69 ± 13.88 years) compared to women without fractures (54.39 ± 14.10 years) (p < 0.0005). Furthermore, BMI was also higher (27.75 kg/m2) in women with fractures compared to the other group (26.49 kg/m2) (p < 0.025). Out of 102 women with fractures, 88 were postmenopausal. The most frequent fractures were the humerus and radius fractures, 11.62% (65/559), followed by femoral neck fractures, 7.15% (40/559), and body vertebrae fractures, 3.04% (17/559). A significant decrease of the bone mineral density (BMD) in the spinal and the femoral neck sites was observed in women with femoral neck and body vertebrae fractures, but not in women with humerus and radius fractures. Vitamin D deficiency did not have a significant impact on fracture incidence. The increased concentration of PTH was statistically significant in women with femoral neck and body vertebrae fractures. Conclusion. In women with all three types of low-energy fractures, compared to women without fractures, significant risk factors for osteoporosis were age, BMD, and the strength of mechanical force during fall (estimated through BMI). © 2021 Inst. Sci. inf., Univ. Defence in Belgrade. All rights reserved.

Post-traumatic stress disorder (PTSD) is a highly prevalent and impairing disorder. Oxidative stress is implicated in its pathogenesis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important source of free radicals. The aim of the study was to assess oxidative stress parameters, activities of respiratory chain enzymes, and the expression of NADPH oxidase subunits (gp91phox, p22phox, and p67phox) in the single prolonged stress (SPS) animal model of PTSD. Twenty-four (12 controls; 12 subjected to SPS), 9-week-old, male Wistar rats were used. SPS included physical restraint, forced swimming, and ether exposure. The rats were euthanized seven days later. Cortex, hippocampus, amygdala, and thalamus were dissected. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), Complex I, and cytochrome C oxidase were measured using spectrophotometric methods, while the expression of NADPH oxidase subunits was determined by Western blot. Increased MDA and decreased GSH concentrations were found in the amygdala and hippocampus of the SPS rats. SOD activity was decreased in amygdala and GPx was decreased in hippocampus. Increased expression of the NADPH oxidase subunits was seen in amygdala, while mitochondrial respiratory chain enzyme expression was unchanged both in amygdala and hippocampus. In the cortex concentrations of MDA and GSH were unchanged despite increased Complex I and decreased GPx, while in the thalamus no change of any parameter was noticed. We conclude that oxidative stress is present in hippocampus and amygdala seven days after the SPS procedure. NADPH oxidase seems to be a main source of free radicals in the amygdala. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.

Post-traumatic stress disorder (PTSD) is a highly prevalent and impairing disorder. Oxidative stress is implicated in its pathogenesis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important source of free radicals. The aim of the study was to assess oxidative stress parameters, activities of respiratory chain enzymes, and the expression of NADPH oxidase subunits (gp91phox, p22phox, and p67phox) in the single prolonged stress (SPS) animal model of PTSD. Twenty-four (12 controls; 12 subjected to SPS), 9-week-old, male Wistar rats were used. SPS included physical restraint, forced swimming, and ether exposure. The rats were euthanized seven days later. Cortex, hippocampus, amygdala, and thalamus were dissected. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), Complex I, and cytochrome C oxidase were measured using spectrophotometric methods, while the expression of NADPH oxidase subunits was determined by Western blot. Increased MDA and decreased GSH concentrations were found in the amygdala and hippocampus of the SPS rats. SOD activity was decreased in amygdala and GPx was decreased in hippocampus. Increased expression of the NADPH oxidase subunits was seen in amygdala, while mitochondrial respiratory chain enzyme expression was unchanged both in amygdala and hippocampus. In the cortex concentrations of MDA and GSH were unchanged despite increased Complex I and decreased GPx, while in the thalamus no change of any parameter was noticed. We conclude that oxidative stress is present in hippocampus and amygdala seven days after the SPS procedure. NADPH oxidase seems to be a main source of free radicals in the amygdala. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.

Background: The variations in proinflamatory cytokine levels have been associated with schizophrenia (SCH), duration of illness, psychopathology and treatment. The aim of the study was to investigate serum levels of interleukin-6 (IL-6) and tumor necrosis factoralpha (TNF-a) in schizophrenic patients during exacerbation and remission, and its association with course of illness and therapy. Subjects and methods: We measured serum levels of IL-6 and TNF-a in 43 schizophrenic patients in exacerbation and remission and compared them to 29 healthy controls, matched by sex, age, body mass index (BMI) and smoking habits. The severity of psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS). Results: There was no difference in levels of IL-6 and TNF-a in exacerbation compared to remission in schizophrenic patients. IL-6 was higher and TNF-a was lower in schizophrenic patients in both exacerbation and remission in comparison with healthy controls. TNF-a in exacerbation was in negative correlation with IL-6 in remission. No statistical significance was found between levels of cytokines and sex, age, BMI, smoking habits, antipsychotic medication, duration of treatment and duration of illness. IL-6 levels were in positive correlation with the age of onset and the duration of untreated psychosis. In schizophrenic patients on adjunctive treatment with mood stabilizers, TNF-a levels increased in remission. Conclusion: Our results suggest that the connection between schizophrenia, cytokines and medication is multifaceted, and not necessarily linear. Adjunct mood stabilizers not only ameliorate psychopathology, but might convey immunomodulatory effects as well. Further longitudinal studies could elucidate potential beneficial effect of combined therapy in treatment of SCH. © Medicinska naklada - Zagreb, Croatia. © Medicinska naklada - Zagreb, Croatia.