Molecular characterization of Legionella pneumophila-induced interleukin-8 expression in T cells

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Retraction: NF-κB activation by Helicobacter pylori requires Akt-mediated phosphorylation of p65

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Soluble epoxide hydrolase maintains steady-state lipid turnover linked with autocrine signaling in peritoneal macrophages

Summary: Soluble epoxide hydrolase is a widely distributed bifunctional enzyme that contains N-terminal phosphatase (N-phos) and C-terminal epoxide hydrolase (C-EH) domains. C-EH hydrolyzes anti-inflammatory epoxy-fatty acids to corresponding diols and contributes to various inflammatory conditions. However, N-phos has been poorly examined. In peritoneal macrophages, the N-phos inhibitor amino-hydroxybenzoic acid (AHBA) seemed to primarily interrupt the dephosphorylation of lysophosphatidates and broadly attenuated inflammation-related functions. AHBA activated intrinsic lysophosphatidate and thromboxane A2 receptors by altering lipid-metabolite distribution; downstream the signaling, phospholipase C was facilitated to dampen intracellular Ca2+ stores and AKT kinase (protein kinase B) was activated to presumably inhibit inflammatory gene expression. Our data suggest that N-phos maintains steady-state phospholipid turnover connecting autocrine signaling and is a prospective target for controlling inflammatory responses in macrophages

sj-pdf-2-cep-10.1177_03331024231156925 - Supplemental material for Developing an artificial intelligence-based headache diagnostic model and its utility for non-specialists’ diagnostic accuracy

Supplemental material, sj-pdf-2-cep-10.1177_03331024231156925 for Developing an artificial intelligence-based headache diagnostic model and its utility for non-specialists’ diagnostic accuracy by Masahito Katsuki, Tomokazu Shimazu, Shoji Kikui, Daisuke Danno, Junichi Miyahara, Ryusaku Takeshima, Eriko Takeshima, Yuki Shimazu, Takahiro Nakashima, Mitsuhiro Matsuo and Takao Takeshima in Cephalalgia</p

sj-pdf-1-cep-10.1177_03331024231156925 - Supplemental material for Developing an artificial intelligence-based headache diagnostic model and its utility for non-specialists’ diagnostic accuracy

Supplemental material, sj-pdf-1-cep-10.1177_03331024231156925 for Developing an artificial intelligence-based headache diagnostic model and its utility for non-specialists’ diagnostic accuracy by Masahito Katsuki, Tomokazu Shimazu, Shoji Kikui, Daisuke Danno, Junichi Miyahara, Ryusaku Takeshima, Eriko Takeshima, Yuki Shimazu, Takahiro Nakashima, Mitsuhiro Matsuo and Takao Takeshima in Cephalalgia</p

sj-xlsx-3-cep-10.1177_03331024231156925 - Supplemental material for Developing an artificial intelligence-based headache diagnostic model and its utility for non-specialists’ diagnostic accuracy

Supplemental material, sj-xlsx-3-cep-10.1177_03331024231156925 for Developing an artificial intelligence-based headache diagnostic model and its utility for non-specialists’ diagnostic accuracy by Masahito Katsuki, Tomokazu Shimazu, Shoji Kikui, Daisuke Danno, Junichi Miyahara, Ryusaku Takeshima, Eriko Takeshima, Yuki Shimazu, Takahiro Nakashima, Mitsuhiro Matsuo and Takao Takeshima in Cephalalgia</p

Helicobacter pylori-Induced Interleukin-12 p40 Expression▿

Interleukin-12 (IL-12) is a heterodimeric cytokine produced by antigen-presenting cells that promotes the development of T-helper lymphocyte 1 (Th1). Chronic gastritis induced by Helicobacter pylori is considered a Th1-mediated process. IL-12 levels in gastric biopsy samples of H. pylori-infected patients are higher than in those of uninfected individuals, but the cellular source of IL-12 remains elusive. IL-12 staining was detected in mucosal epithelial cells, lymphocytes, and macrophages in specimens of patients with H. pylori-positive gastritis. Therefore, we investigated IL-12 p40 mRNA induction by H. pylori in gastric epithelial cells and T cells. Although cag pathogenicity island (PAI)-positive H. pylori induced IL-12 p40 mRNA expression, an isogenic mutant of the cag PAI failed to induce it in both cell types. Supernatants from H. pylori cultures and H. pylori VacA induced IL-12 p40 mRNA expression in T cells but not in epithelial cells. The activation of the IL-12 p40 promoter by H. pylori was mediated through NF-κB. The transfection of IκB kinase and NF-κB-inducing kinase dominant-negative mutants inhibited H. pylori-induced IL-12 p40 activation. Inhibitors of NF-κB, phosphatidylinositol 3-kinase, p38 mitogen-activated protein kinase, and Hsp90 suppressed H. pylori- and VacA-induced IL-12 p40 mRNA expression. The results indicate that H. pylori induces IL-12 p40 expression by the activation of NF-κB, phosphatidylinositol 3-kinase, and p38 mitogen-activated protein kinase. Hsp90 is also a crucial regulator of H. pylori-induced IL-12 p40 expression. In addition to the cag PAI, VacA might be relevant in the induction of IL-12 expression and a Th1-polarized response only in T cells

Effects of preoperative cinacalcet hydrochloride treatment on the operative course of parathyroidectomy and pathological changes in resected parathyroid glands

Abstract Background Secondary hyperparathyroidism (SHPT) is associated with higher cardiovascular risk and mortality in patients undergoing dialysis. Cinacalcet hydrochloride (CH), which has been clinically available in Japan since 2008, could effectively reduce parathyroid hormone (PTH) levels even in patients with severe SHPT. However, parathyroidectomy (PTx) is performed in patients with severe SHPT refractory to CH. This study investigated the effects of preoperative CH treatment on the operative course and pathological findings of resected parathyroid glands (PTGs) in patients undergoing PTx. Methods We retrospectively analyzed 194 PTx cases for SHPT in long-term hemodialysis patients at Showa University Northern Yokohama Hospital from April 2002 to March 2014. Results A total of 45 patients were administered CH before PTx (CH group), and 149 patients never received CH (non-CH group). No significant difference was seen in intact PTH levels, the number of resected PTGs, or operative time between the two groups. However, the total volume of all PTGs and the volume of the largest PTG were significantly lower in the CH than in the non-CH group. Patients with PTG adhesion to surrounding tissues were significantly more prevalent in the CH than in the non-CH group. In addition, cystic changes or hemorrhagic necrosis in the resected PTGs was observed more frequently in the CH group than in the non-CH group. Conclusions The results of the present study suggest that preoperative CH treatment might introduce pathological changes in resected PTGs in PTx for severe SHPT, but it does not affect the operative time