Cloud optical thickness and effective particle radius derived from transmitted solar radiation measurements : Comparison with cloud radar observations

A method is presented for determining the optical thickness and effective particle radius of stratiform clouds containing liquid water drops in the absence of drizzle from transmitted solar radiation measurements. The procedure compares measurements of the cloud transmittance from the ground at water-absorbing and nonabsorbing wavelengths with lookup tables of the transmittance precomputed for plane-parallel, vertically homogeneous clouds. The optical thickness derived from the cloud transmittance may be used to retrieve vertical profiles of cloud microphysics in combination with the radar reflectivity factor. To do this, we also present an algorithm for solving the radar equation with a constraint of the optical thickness at the visible wavelength. Observations of clouds were made in August and September 2003 at Koganei, Tokyo, Japan, using a PREDE i-skyradiometer and a 95-GHz cloud radar Super Polarimetric Ice Crystal Detection and Explication Radar (SPIDER). The optical thickness and effective radius of water clouds were derived from the i-skyradiometer. Then, the vertical profile of the effective radius was retrieved from SPIDER, using the optical thickness determined from the i-skyradiometer. We found that the effective radii derived by using these two instruments were in good agreement

Comparative Analysis of Cellular and Growth Factor Composition in Bone Marrow Aspirate Concentrate and Platelet-Rich Plasma

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The Peroxisome Proliferator-Activated Receptor α (PPARα) Agonist Pemafibrate Protects against Diet-Induced Obesity in Mice

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A Novel Unidirectional Porous β-tricalcium Phosphate Bone Substitute in Orthopedic Surgery : A Technical Note and Case Illustrations

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Sexual Function Is an Indicator of Central Arterial Stiffness and Arterial Stiffness Gradient in Japanese Adult Men

BackgroundAs arterial stiffness increases in the absence of subjective symptoms, a personal indicator that reflects increased risk of cardiovascular disease is necessary. Penile erection is regulated by vascular function, and atherosclerosis affects the penile artery earlier than it affects the coronary and carotid arteries. Therefore, we hypothesized that deterioration of erectile function could be a marker of increased risk for cardiovascular disease. To test our hypothesis, we assessed erectile function and arterial stiffness in a cross‐sectional study.Methods and ResultsCarotid‐femoral pulse wave velocity (PWV), brachial‐ankle PWV, femoral‐ankle PWV, and arterial stiffness gradient (PWV ratio: carotid‐femoral PWV/femoral‐ankle PWV) were measured as indexes of central, systemic, and peripheral arterial stiffness and peripheral organ damage, respectively, in 317 adult men. In addition, erectile function was assessed by using the questionnaire International Index of Erectile Function 5 (a descending score indicates worsening of erectile function). The scores of male sexual function were inversely correlated with carotid‐femoral PWV (rs=−0.41), brachial‐ankle PWV (rs=−0.35), femoral‐ankle PWV (rs=−0.19), and PWV ratio (rs=−0.33). Furthermore, multivariate linear regression analyses revealed that International Index of Erectile Function 5 scores were significantly associated with carotid‐femoral PWV (β=−0.22) and PWV ratio (β=−0.25), but not with brachial‐ankle PWV and femoral‐ankle PWV.ConclusionsOur results indicated that erectile function is independently associated with central arterial stiffness and peripheral organ damage. These findings suggest that male sexual function could be an easily identifiable and independent marker of increased central arterial stiffness and peripheral organ damage

IL-10 Inhibits Transforming Growth Factor-ß-Induction of Type I Collagen mRNA Expression via Both JNK and p38 Pathways in Human Lung Fibroblasts

Transforming growth factor-ß (TGF-ß) is a key factor for understanding the pathogenesis of fibrotic disorders such as idiopathic pulmonary fibrosis (IPF). We have demonstrated that interleukin-10 (IL-10) suppresses TGF-ß-induced expression of type I collagen (COL1) mRNA in a human lung fibroblast cell line (WI-38). However, the inhibitory mechanism has not yet been clearly elucidated. Thus, in the current study, we investigate the effects of IL-10 blockade of TGF-ß signaling which regulates COL1 mRNA expression. In WI-38 cells, IL-10 inhibits TGF-ß-mediated phosphorylation of both, c-Jun HN2-terminal kinase (JNK) and p38, but does not suppress TGF-ß- mediated phosphorylation of Smad2 or affect TGF-ß-upregulation of Smad7 mRNA expression. In addition, SP600125 and SB203580, specific inhibitors of JNK and p38, respectively, attenuate TGF-ß-induced COL1 mRNA expression in WI-38 cells. These results suggest that IL-10 inhibits TGF-ß-induced COL1 mRNA expression via both JNK and p38 pathways but not Smad pathways in WI-38 cells. This inhibitory mechanism may provide a novel insight into therapeutic strategies for fibrotic disorders such as IPF

Cysteinyl-tRNA synthetase governs cysteine polysulfidation and mitochondrial bioenergetics

Cysteine hydropersulfide (CysSSH) occurs in abundant quantities in various organisms, yet little is known about its biosynthesis and physiological functions. Extensive persulfide formation is apparent in cysteine-containing proteins in Escherichia coli and mammalian cells and is believed to result from post-translational processes involving hydrogen sulfide-related chemistry. Here we demonstrate effective CysSSH synthesis from the substrate l-cysteine, a reaction catalyzed by prokaryotic and mammalian cysteinyl-tRNA synthetases (CARSs). Targeted disruption of the genes encoding mitochondrial CARSs in mice and human cells shows that CARSs have a crucial role in endogenous CysSSH production and suggests that these enzymes serve as the principal cysteine persulfide synthases in vivo. CARSs also catalyze co-translational cysteine polysulfidation and are involved in the regulation of mitochondrial biogenesis and bioenergetics. Investigating CARS-dependent persulfide production may thus clarify aberrant redox signaling in physiological and pathophysiological conditions, and suggest therapeutic targets based on oxidative stress and mitochondrial dysfunction