Interactions of cyclophosphamide with phenytoin, busulfan with metronidazole, dexamethasone, or clarithromycin were the only detected PDDI between anticancer and non-anticancer medications. Type of HSCT and the numbers of administered medications were significantly associated with major PDDIs. The epidemiology, real clinical consequence, and economic burden of DDIs on patients undergone HSCT particularly around the transplantation period should be assessed

further by prospective, multicenter studies.”
“Objective-Abdominal aortic aneurysms (AAAs), dilations of the infrarenal aorta, are characterized by inflammation and oxidative stress. We previously showed increased levels of peroxiredoxin-1 (PRDX-1) in macrophages cultured from AAA patients. The purpose of the study was to determine which subpopulation of macrophages AG-120 Metabolism inhibitor is present in AAAs and is involved in upregulation of PRDX-1 in aneurysmal disease.\n\nMethods and Results-This study used immunohistochemistry with antibodies against CD68 and mannose receptor (MR) to determine the subtype of macrophages in AAA tissue samples (n=33); laser AZD4547 Angiogenesis inhibitor capture microdissection to isolate each subtype; and quantitative-reverse transcriptase-polymerase chain reaction, Western blot, and ELISA to assess PRDX-1 mRNA and PRDX-1protein levels in both types. Proinflammatory CD68(+)MR(-) macrophages predominated in adventitial tissue, whereas the intraluminal thrombus contained

CD68(+)MR(+) macrophages. The presence of lipids and iron-containing deposits confirmed their phagocytic phenotype. Laser Selleck FHPI capture microdissection-isolated CD68(+)MR(-) and CD68(+)MR(+) macrophages, characterized by quantitative-reverse transcriptase-polymerase chain reaction (TNF, IL1B, MRC1, and CCL18) and Western blot (stabilin and hemoglobin), validated the microdissected subtypes. PRDX-1 expression was colocalized with

CD68(+)MR(-) macrophages. PRDX-1 mRNA and PRDX-1 protein were both more abundant in CD68(+)MR(-) than CD68(+)MR(+) macrophages in AAA.\n\nConclusion-These findings suggest that the proteins or mRNAs expressed by the proinflammatory CD68(+)MR(-) macrophages may contribute to aneurysmal pathology. (Arterioscler Thromb Vasc Biol. 2013;33:431-438.)”
“Purpose of review\n\nRecent genome-wide association studies (GWAS) have revealed that the ATP2B1 gene is associated with hypertension not only in people of European origin, but also in Japanese, Chinese, and Koreans. However, ATP2B1 has never been considered to be a candidate gene for essential hypertension. Thus, this review summarizes the findings obtained in GWAS regarding the role of the ATP2B1 gene in essential hypertension, as well as recent suggestions about the mechanisms responsible for the effects of the ATP2B1 gene on calcium homeostasis. We also review the findings of studies involving spontaneously hypertensive rats and tissue-specific ATP2B1 knockout mice examining the effects of ATP2B1 on hypertension.