It is known that histamine suppresses gene expression and synthesis of tumor necrosis factor alpha (TNF-K K) induced by lipopolysaccharide (LPS) in human peripheral blood mononuclear monocytes (HPM) or alveolar macrophages via histamine H2 receptors. We investigated the effect of histamine and differentiation in macrophages on the expression and secretion of TNF-K K, TNF-K K-converting enzyme (TACE), and histamine H1 and H2 receptors by use of a leukemia cell line, U937, and HPM. Differentiation of U937 and HPM cells with 12-Otetradecanoylphorbol-13-acetate (TPA) enhanced the H1 receptor expression and rather suppressed the H2 receptor, resulting in up-regulation of the histamine-induced expression and secretion of TNF-K K, modulated via TACE. Therefore, histamine failed to inhibit up-regulated expression of TNF-K K induced by LPS in macrophages. The switch from H2 to H1 receptors during differentiation in the monocyte/macrophage lineage could participate in the pathogenic processes of atherosclerosis and inflammatory reactions in the arterial wall.z 2000 Federation of European Biochemical Societies.

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We investigated the localization of histidine decarboxylase (HDC), which is the rate-limiting enzyme that generates histamine from histidine, in human aorta/coronary artery. RT-PCR and immunohistochemical staining revealed that the HDC gene was expressed in monocytes/macrophages and T cells in the arterial intima but not in smooth muscle cells in either the arterial intima or the media. A luciferase promoter assay with U937 and Jurkat cells demonstrated that interleukin-4 (IL-4) inhibited the expression of the HDC gene. In contrast, among a scavenger receptor family, IL-4 as well as histamine upregulated U937 cells to express the LOX-1 gene but not the SR-A gene, which genes encode receptors that scavenge oxidized lipids. These findings suggest that histamine synthesized in the arterial wall participates in the initiation and progression of atherosclerosis and that IL-4 can act as an important inhibitory and/or stimulatory factor in the function of monocytes/macrophages modulated by histamine in relation to the process of atherosclerosis. ß

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Treatment with BHT reduced the risk of pneumonia and pneumonia-related mortality in elderly patients with dementia.

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Background A challenging decision exists as whether to abandon or remove noninfectious superfluous leads during lead revisions or cardiac implantable electronic device (CIED) upgrades. There is insufficient data in the Asian population to guide decision making. Methods This study investigated the safety and efficacy of transvenous lead extractions (TLEs) in a high‐volume Japanese center. Among a total of 341 patients who underwent lead revisions or CIED upgrades between 2008 and 2018, 53 patients (16%) who underwent TLEs to remove the superfluous leads were analyzed. Results Indications for TLE were vascular issues (60%), recalled leads (21%), growth of the body size (6%), abandoned leads in young patients (6%), switch to a subcutaneous implanted cardiac defibrillator (4%), need for an MRI conditional CIED (2%), and risks of vascular injury (2%). The population included 29 patients (55%) with nonfunctional leads and 24 (45%) with functional abandoned leads. A total of 74 target leads (mean 1.4 leads/person, median lead age 6.7 years) were extracted with a complete removal achieved in 98%. All coexisting leads, intended for continued use, were not damaged. All new leads (mean 1.4 leads/person) that had been simultaneously implanted during the TLE procedures were successfully implanted. There was one minor complication (2%) involving a pericardial effusion but it did not affect the hemodynamics. Conclusions In this Japanese single center experience, the removal of noninfectious superfluous leads with TLEs seemed to be a safe and effective therapeutic option.

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