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Objective: To investigate the effects of systemically given propolis on the expanded premaxillary suture in a rat study model. Materials and Methods: The 24 rats were randomly divided into three groups-only expansion (OE), expansion plus propolis (PRO), and nonexpansion (control) groups. After the 5-day expansion period was completed, the OE and PRO groups underwent 12 days of mechanical retention. At the end of this period, the animals were euthanatized and their pre-maxillae were dissected and fixed. Histomorphometric examination was performed to determine the number of osteoclasts, osteoblasts, and capillaries as well as the intensity of inflammatory cells and amount of new bone formation. Results: Statistical analysis showed that the intensities of inflammatory cells, number of osteoblasts, and amount of new bone formation were greater in the PRO group than in the other groups. The PRO group also had more osteoclasts and new capillaries. Conclusion: Systemic use of propolis may hasten new bone formation at the expanded suture in rats. (Angle Orthod. 2013;83:286-291.)

Cancer stem cells (CSC) isolated from multiple tumor types differentiate in vivo and in vitro when cultured in serum; however, the factors responsible for their differentiation have not yet been identified. The first aim of the present study was to identify CD133high/CD44high DU145 prostate CSCs and compare their profiles with non-CSCs as bulk counterparts of the population. Subsequently, the two populations continued to be three-dimensional multicellular spheroids. Differentiation was then investigated with stem cell-related genomic characteristics. Polymerase chain reaction array analyses of cell cycle regulation, embryonic and mesenchymal cell lineage-related markers, and telomerase reverse transcriptase (TERT) and Notch signaling were performed. Immunohistochemistry of CD117, Notch1, Jagged1, Delta1, Sox2, c-Myc, Oct4, KLF4, CD90 and SSEA1 were determined in CSC and non-CSC monolayer and spheroid subcultures. Significant gene alterations were observed in the CD133high/CD44high population when cultured as a monolayer and continued as spheroid. In this group, marked gene upregulation was determined in collagen type 9 α1, Islet1 and cyclin D2. Jagged1, Delta-like 3 and Notch1 were respectively upregulated genes in the Notch signaling pathway. According to immunoreactivity, the staining density of Jagged1, Sox2, Oct4 and Klf-4 increased significantly in CSC spheroids. Isolated CSCs alter their cellular characterization over the course of time and exhibit a differentiation profile while maintaining their former surface antigens at a level of transcription or translation. The current study suggested that this differentiation process may be a mechanism responsible for the malignant process and tumor growth.

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Idiopathic hypercalciuria (IH) has been speculated to have a predisposing role in the development of urinary tract infection (UTI), due to the uroepithelial cell damage it leads to. In this study, we aimed to investigate the effects of hypercalciuria on the bladder, ureters, and kidneys in rats with experimentally induced hypercalciuria.Normocalcemic hypercalciuria was induced by furosemide (60 mg/100 mL of drinking water) administration to 16-week-old male Wistar Albino rats for 14 days. Calciuria (calcium/creatinine ratio, mg/mg, Ca/Cr) increased from 0.07+/-0.01 at the beginning of administration to 0.41+/-0.1 on day 14 (p=0.000). The Ca/Cr ratio was 0.14+/-0.06 at the beginning of the study and 0.25+/-0.06 on day 14 in the control group rats (p=0.002 vs. the hypercalciuric group rats on day 14). Bladder, ureter, and kidney specimens of the rats, dissected on the 14th day, were fixed in 10% formalin and 2.5% gluteraldehyde solutions for light and electron microscopic examination, respectively. Histopathological and ultrastructural examination of the hypercalciuric rats revealed proliferation and apical cytoplasmic vacuole formation in transitional epithelial cells, mitotic activity in the intermediate cell line, vasodilatation, edema, and separation of collagen fibers in the bladder and ureter specimens. Light microscopic examination of the kidney specimens revealed a lot of erythrocyte in the glomerular capillary lumen, while electron microscopy revealed vacuolization of proximal and distal tubules, tubular degeneration, interstitial edema, and vasodilatation.In this study, hypercalciuria was observed to have adverse effects on the cell architecture of the uroepithelium and disruption of the epithelial barrier of the bladder and ureters and all kidney structures, especially on the proximal epithelial cells.

Our goal in this study was to investigate the presence of angiogenesis-related factors in endometriomas by evaluating their vascular surface densities. Thirty ovarian samples were included in the study. Of these, ten were histologically confirmed endometriomas, ten were ovarian specimens in the follicular phase and ten were ovarian specimens in the luteal phase, serving as controls. Histological specimens were immunostained for von Willebrand factor (vWF: factor VIII-related antigen) and CD34. The area with the highest microvessel density in endometriosis and in the normal ovary was evaluated by using an intercept grid. All microvessels in a specific field (x 100 magnification) were counted and vascular surface density was measured, as 164.01 +/- 21.26 vs. 125.15 +/- 11.28 and 117.44 +/- 9.27 by using vWF, and as 172.97 +/- 25.64 vs. 138.65 +/- 32.21 and 120.34 +/- 18.40 by using CD34 in endometriotic, follicular and luteal ovarian samples, respectively (p < 0.001). The mean vascular surface density was significantly higher in endometriosis than in the ovarian samples of the follicular phase or the luteal phase. No significant difference was seen between normal ovarian samples. Endometriosis was associated with angiogenic properties. Having demonstrated elevated angiogenic factors in endometriotic samples, we concluded that activation of angiogenesis might be a key factor in the pathogenesis of endometriosis.

These findings confirm the important trophic and protective role of GH in the homeostasis of the small intestine. The trophic effect is mediated by an increase in IGF-I synthesis in the small intestine, but the protective effect is not related to IGF-I.