Effect Of PC Research Articles

다층 구조방정식 모형 평가를 위한 수준 특수적 평가 방법의 적용

While a level-specific approach has been proposed for the valid evaluation of multilevel structural
 equation modeling (MSEM), the traditional simultaneous approach remains predominant among
 researchers. In fact, research on level-specific approaches is limited, and some studies have focused on
 multilevel confirmatory factor analysis models. This study conducted a Monte Carlo study to explore
 the performance of a LS approach for MSEM with a direct path between variables under five design
 factors: intraclass correlation (ICC), the number of groups (NG), group size (GS), the size of path
 coefficient (PCS), and misspecification type (MT). The results showed that the LS approach performed
 better than the SI approach even in MSEM at between-group level. This study identified three key
 findings. First, the performance of RMSEA was found to improve with an increase of ICC or GS.
 Second, the performance of LS fit indices (RMSEA, CFI, and TLI) was more promising for detecting
 the misspecified between-level model with a decrease of PCS. Third, the effect of PCS on CFI or TLI
 was strong when ICC was small. The study concludes with a summary and implications of the results.

The uremic toxin p-cresyl sulfate induces proliferation and migration of clear cell renal cell carcinoma via microRNA-21/ HIF-1\u03b1 axis signals

p-Cresyl sulfate (pCS), a uremic toxin, can cause renal damage and dysfunction. Studies suggest that renal dysfunction increases the prevalence of renal cancer. However, the effect of pCS on the proliferation and migration of renal cancer is unclear. Clear cell renal cell carcinoma (ccRCC) expresses mutant von Hippel-Lindau gene and is difficult to treat. Hypoxia-inducible factor-1α and 2-α (HIF-1α and HIF-2α) as well as microRNA-21 (miR-21) can regulate the proliferation and migration of ccRCC cells. However, the association between HIF-α and miR-21 in ccRCC remains unclear. Therefore, the effects of pCS on ccRCC cells were investigated for HIF-α and miR-21 signals. Our results showed that pCS induced overexpression of HIF-1α and promoted the proliferation and regulated epithelial-mesenchymal transition-related proteins, including E-cadherin, fibronectin, twist and vimentin in ccRCC cells. pCS treatment increased miR-21 expression. Specifically, inhibition of miR-21 blocked pCS-induced proliferation and migration. Taken together, the present results demonstrate that pCS directly induced the proliferation and migration of ccRCC cells through mechanisms involving miR-21/HIF-1α signaling pathways.

Ground-based Mid-infrared Study of the Compton-thick AGN in M51 at 10–100 pc Scale*

Abstract We performed near-diffraction-limited ( FWHM) N-band imaging of one of the nearest active galactic nuclei (AGNs) in M51 with the 8.2 m Subaru Telescope to study the nuclear structure and spectral energy distribution (SED) at 8–13 μm. We found that the nucleus is composed of an unresolved core (at pc resolution, orintrinsic size corrected for the instrumental effect of pc) and an extended halo (at a few tens of parsec scale), and each of their SEDs is almost flat. We examined the SED by comparing with the archival Spitzer IRS spectrum processed to mimic our chopping observation of the nucleus and the published radiative transfer model SEDs of the AGN clumpy dusty torus. The halo SED is likely due to circumnuclear star formation showing deficient polycyclic aromatic hydrocarbon emission due to the AGN. The core SED is likely dominated by the AGN because of the following two reasons. First, the clumpy torus model SEDs can reproduce the red mid-infrared continuum with apparently moderate silicate 9.7 μm absorption. Second, the core 12 μm luminosity and the absorption-corrected X-ray luminosity at 2–10 keV in the literature follow the mid-infrared–X-ray luminosity correlation known for the nearby AGNs, including the Compton-thick ones.

P-Cresyl sulfate suppresses lipopolysaccharide-induced anti-bacterial immune responses in murine macrophages in vitro.

p-Cresyl sulfate (pCS) is a known uremic toxin that is metabolized from p-cresol produced by intestinal bacteria. Abnormal accumulation of pCS in the blood is a characteristic of chronic kidney disease (CKD). pCS is suggested to cause immune dysfunction and increase the risk of infectious diseases in CKD patients. In this study, we focused on the effects of pCS on macrophage functions related to host defense. We evaluated the effects of pCS on cytokine production, nitric oxide (NO) production, arginase activity, expression of cell-surface molecules, and phagocytosis in the macrophage-like cell line, RAW264.7. pCS significantly decreased interleukin (IL)-12 p40 production and increased IL-10 production. pCS also decreased NO production, but did not influence arginase activity. pCS suppressed lipopolysaccharide-induced CD40 expression on the cell surface, but did not influence phagocytosis. We further assessed whether the effects of pCS observed in the macrophage-like cell line were consistent in primary macrophages. Similar to RAW264.7 cells, pCS decreased IL-12 p40 and p70 production and increased IL-10 production in primary peritoneal macrophages. These data indicate that pCS suppresses certain macrophage functions that contribute to host defense, and may play a role in CKD-related immune dysfunction.

P ‐Cresyl Sulfate Aggravates Cardiac Dysfunction Associated With Chronic Kidney Disease by Enhancing Apoptosis of Cardiomyocytes

BackgroundCardiovascular disease is the leading cause of death in patients with chronic kidney disease. A body of evidence suggests that p-cresyl sulfate (PCS), a uremic toxin, is associated with the cardiovascular mortality rate of patients with chronic kidney disease; however, the molecular mechanisms underlying this feature have not yet been fully elucidated.Methods and ResultsWe aimed to determine whether PCS accumulation could adversely affect cardiac dysfunction via direct cytotoxicity to cardiomyocytes. In mice that underwent 5/6 nephrectomy, PCS promoted cardiac apoptosis and affected the ratio of left ventricular transmitral early peak flow velocity to left ventricular transmitral late peak flow velocity (the E/A ratio) observed by echocardiography (n=8 in each group). Apocynin, an inhibitor of NADPH oxidase activity, attenuates this alteration of the E/A ratio (n=6 in each group). PCS also exhibited proapoptotic properties in H9c2 cells by upregulating the expression of p22phox and p47phox, NADPH oxidase subunits, and the production of reactive oxygen species. Apocynin and N-acetylcysteine were both able to suppress the effect of PCS, underscoring the importance of NADPH oxidase activation for the mechanism of action.ConclusionsThis study demonstrated that the cardiac toxicity of PCS is at least partially attributed to induced NADPH oxidase activity and reactive oxygen species production facilitating cardiac apoptosis and resulting in diastolic dysfunction.