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Introduction. The decrease in serum estrogens concentration at menopause disrupts the metabolic balance and leads to visceral obesity, which causes an increase in serum estradiol levels, through aromatase activity. Also, estrogen deficiency is a reason for the development of osteoporosis. The objective of the study was to investigate the serum estradiol levels and changes in bone alpha estrogen receptor expression in an experimental model of osteoporosis. Materials and methods. The study included 20 female Wistar rats at a reproductive age of two months, divided into two groups: group 1 (G1) – 10 ovariectomized rats, and group 2 (G2) -10 rats sham-operated. SPSS 20 software (SPSS, Inc., Chicago, IL, USA) was used for statistical analysis of the results. For the immunohistochemical study, the nonparametric test – Mann Whitney was used, by comparing the median values. Data were presented as mean ± standard deviation, with p

Introduction. Canonical Wnt signaling pathway regulates stromal stem cells (SSCs) differentiation and controls the balance between adipogenesis and osteogenesis. Estrogen deficiency affects Wnt signaling by altering the expression of sclerostin (SCL) and the peroxisome proliferator-activated receptor-∝ coactivator 1-∝(PGC-1∝) in the bone tissue. The objective of the study was to monitor whether there is a feedback mechanism between SCL and PGC-1∝ and to determine the extent of the immunohistochemical staining of PGC-1∝ and SCL in bone tissue of estrogen deficiency-induced osteoporosis in female Wistar rats. Materials and methods. An experiment was performed on 20 female Wistar rats at reproductive age (2 months), divided into 2 groups: in group 1 (G1) 10 animals were ovariectomized (ovx) and in group 2 (G2) 10 of the remaining were sham-operated (sham). Results. We found that the PGC-1∝ in the bone marrow stromal cells was reduced in the group with osteoporosis (G1 – ovariectomized rats), compared to sham-operated control group G2 (p

Common variable immunodeficiency disease (CVID) is the most common primary immunodeficiency in adults, and multiple organs may be involved. This is a case report of a 49-year-old female patient with granulomatous-lymphocytic interstitial lung disease, liver fibrosis, portal hypertension and rectal cancer. Examinations showed non-necrotic granulomas in her lungs, mediastinal glands and liver, and she was seen in six different specialities. The multifaceted manifestation of CVID calls for multidisciplinary collaboration.

Selenium (Se) is an exogenous antioxidant that performs its function via the expression of selenoproteins. The aim of this study was to explore the effect of varying Se intake on the redox status of the aortic wall in young spontaneously hypertensive rats (SHR). Sixteen male Wistar Kyoto (WKY) rats and nineteen male SHR, 16-week-old, were tested after being given diets with different Se content for eight weeks. They were divided into 4 groups: control groups of WKY NSe and SHR NSe on an adequate Se diet and groups of WKY HSe and SHR HSe that received Se supplementation. The Se nutritional status was assessed by measuring whole blood glutathione peroxidase-1 (GPx-1) activity. Serum concentration of lipid hydroperoxides and serum level of antibodies against advanced glycation end products (anti-AGEs abs) were determined. Expression of GPx-1 and endothelial nitric oxide synthase (eNOS) were examined in aortic wall. Se supplementation significantly increased GPx-1 activity of whole blood and in the aortas of WKY and SHR. Decreased lipid peroxidation level, eNOS-3 expression in the aortic wall, and serum level of anti-AGEs abs were found in SHR HSe compared with SHR NSe. In conclusion, Se supplementation improved the redox status of the aortic wall in young SHR.