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Because GLSRV showed additive predictive value to age and LV function, it can be the strongest parameter of RV systolic function evaluating the prognosis after PCI for acute inferior STEMI particularly in patients with preserved LV function.

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BackgroundEpicardial fat is a visceral thoracic fat and known to be related with presence of dyslipidemia and coronary arterial stenosis. We evaluated the effects and differences of statins on epicardial fat thickness (EFT) in patients underwent successful percutaneous coronary intervention (PCI).MethodsIn this retrospective cohort study, we enrolled consecutive patients underwent successful PCI and scheduled six to eight-months follow-up coronary angiography from March 2007 to June 2009. EFT was measured by echocardiography twice at the time of PCI and the follow-up coronary angiography. We included 145 patients (58 females; mean, 63.5 ± 9.5 years).ResultsOf the 145 patients, 82 received 20 mg of atorvastatin (atorvastatin group) and 63 medicated with 10 mg of simvastatin with 10 mg of ezetimibe (simvastatin/ezetimibe group). With statin treatments, total cholesterol concentration (189.1 ± 36.1 to 143.3 ± 36.5 mg/dL, p < 0.001), triglycerides (143.5 ± 65.5 to 124.9 ± 63.1 mg/dL, p = 0.005), low density lipoprotein-cholesterol (117.4 ± 32.5 to 76.8 ± 30.9 mg/dL, p < 0.001) and EFT (4.08 ± 1.37 to 3.76 ± 1.29 mm, p < 0.001) were significantly decreased. Atorvastatin and simvastatin/ezetimibe showed similar improvements in the cholesterol profiles. However, atorvastatin decreased EFT more significantly than simvastatin/ezetimibe (EFT change 0.47 ± 0.65 in the atorvastatin vs. 0.12 ± 0.52 mm in the simvastatin/ezetimibe group; p = 0.001).ConclusionIn this study, the atorvastatin group showed significant reduction in EFT than in the simvastatin/ezetimibe group. This might be originated from the statin difference. More large, randomized study will be needed to evaluate this statin difference.

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The LAMMER kinase in eukaryotes is a well-conserved dual-specificity kinase. Aspergillus species cause a wide spectrum of diseases called aspergillosis in humans, depending on the underlying immune status of the host, such as allergy, aspergilloma, and invasive aspergillosis. Aspergillus fumigatus is the most common opportunistic fungal pathogen that causes invasive aspergillosis. Although LAMMER kinase has various functions in morphology, development, and cell cycle regulation in yeast and filamentous fungi, its function in A. fumigatus is not known. We performed molecular studies on the function of the A. fumigatus LAMMER kinase, AfLkhA, and reported its involvement in multiple cellular processes, including development and virulence. Deletion of AflkhA resulted in defects in colonial growth, production of conidia, and sexual development. Transcription and genetic analyses indicated that AfLkhA modulates the expression of key developmental regulatory genes. The AflkhA-deletion strain showed increased production of gliotoxins and protease activity. When conidia were challenged with alveolar macrophages, enodocytosis of conidia by macrophages was increased in the AflkhA-deletion strain, resulting from changes in expression of the cell wall genes and thus content of cell wall pathogen-associated molecular patterns, including β-1,3-glucan and GM. While T cell-deficient zebrafish larvae were significantly susceptible to wild-type A. fumigatus infection, AflkhA-deletion conidia infection reduced host mortality. A. fumigatus AfLkhA is required for the establishment of virulence factors, including conidial production, mycotoxin synthesis, protease activity, and interaction with macrophages, which ultimately affect pathogenicity at the organismal level.

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