Can Hounsfield unit values of the cortex and papillae determined by computed tomography demonstrate the possibility of kidney stone formation?

Baran, Smet | Voyvoda, Nuray | Tokgoz, Ozlem | Tokgoz, Husnu

Article | 2012 | EUROPEAN JOURNAL OF RADIOLOGY81 ( 7 ) , pp.1446 - 1449

Purpose: This study is aimed at measuring HU values of the renal cortex and papillae in patients with nephrolithiasis and demonstrating renal changes associated with nephrolithiasis. Materials and methods: Measurements were performed with regard to HU values of the cortex and papillae of 82 patients with unilateral nephrolithiasis and 81 patients in the control group at the level of the upper pole, middle region and lower pole of both kidneys. Results: When the HU values obtained from the upper pole, middle region and lower pole of the kidney with calculi and unaffected kidney in patients with nephrolithiasis were compared with thos . . .e for the control group, the difference among the groups were found to be significant (p < 0.001). A comparison of the cortex and papillae densities of the affected and unaffected kidneys in patients with unilateral nephrolithiasis were compared with regard to the upper pole and middle region, no statistically significant difference was observed with regard to both the cortex and papillae densities of the upper pole, middle region. However, in those patients with calculi in the lower pole, the region with calculi has a higher papillae density as compared to the unaffected region. Conclusion: Both kidneys in patients with calculi have a comparatively high renal cortex and papillae densities. In the future, this information may be useful in predicting which patients may develop nephrolithiasis. (C) 2011 Elsevier Ireland Ltd. All rights reserved Daha fazlası Daha az

Pathogenesis of Crimean–Congo Hemorrhagic Fever From an Immunological Perspective

Arasli M.

Review | 2016 | Current Tropical Medicine Reports3 ( 1 ) , pp.14 - 19

Crimean–Congo hemorrhagic fever (CCHF) is a severe viral infection disease. Infection is a battle between the virus and host immune system. The CCHF virus can enter to the organism by way of skin, mucosa, or inhalation and encounters innate immune system cells like monocytes, macrophages, and dendritic cells. These cells cannot successfully eliminate viruses. Thus, the viruses are able to disseminate to regional lymph nodes and to whole body. Different viral pathogen-associated molecular patterns (PAMPs) stimulate the intracellular Toll-like receptors, RIG-like Helicase receptors, and NOD-like receptors. So, different inflammatory c . . .ytokines, chemokines, and adhesion molecules are induced. The virus has both direct cytopathic effects on parenchymal cells especially on the liver, spleen, and endothelial cells and non-cytopathic indirect effects depending upon releasing factors from innate immune cells. In severe fatal cases, infection causes coagulation by stimulating both intrinsic and extrinsic coagulation pathways and disseminated intravascular coagulopathy occurs. The prognosis of the disease is dependent on the balance between the viral load and host’s immune system. While high values of IL-12/IL-10, IL-15/IL-10, IL-18/IL-10, and IFN-?/IL-10 ratios show strong TH1 immune status, low values show suppressed immune system. These ratios together with viral load can indicate the patients’ clinical prognosis from an immunological perspective. © 2016, Springer International Publishing AG Daha fazlası Daha az

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