Association between reduced muscle mass and poor prognosis of biliary sepsis

Abstract Sepsis is a life-threatening disease, contributing to significant morbidity and mortality. This study aimed to investigate the association between low muscle mass and the prognosis of patients with biliary sepsis, focusing on outcomes such as length of hospital stay (LOS), intensive care unit (ICU) admission, and in-hospital mortality. This retrospective, single-center, observational study included adult patients with biliary sepsis who visited the emergency department between January 2016 and December 2021. Low muscle mass was assessed using the psoas muscle index (PMI). Using computed tomography imaging, the area of both sides of the psoas muscle at the L3 level was measured, and the PMI, corrected by the patient’s height was calculated. The primary outcome was in-hospital mortality, and the secondary outcomes were intensive care unit (ICU) admission, LOS, and 14-day mortality. A total of 745 patients were included in this study. Low muscle mass was defined as a PMI < 421 mm2/m2 for males and < 268 mm2/m2 for females with the lower quartile of PMI according to sex. The cohort was classified into sarcopenic (n = 189) and non-sarcopenic (n = 556) groups. There was a significant association between low muscle mass and in-hospital mortality (odds ratio, 3.81; 95% confidence interval, 1.08–13.47; p < 0.001), while there was no significant association between low muscle mass and ICU admission. In addition, the median LOS in the sarcopenic group (10 [7–14] days) was significantly longer than the median (8 [6–11] days) in the non-sarcopenic group. Low muscle mass was significantly associated with clinical outcomes, particularly in-hospital mortality and LOS, in patients with biliary sepsis

Corrosion of Cu in Antifreeze Solutions with Triazine- or Triazole-Type Corrosion Inhibitors for 3 Weeks

The corrosion behavior of Cu in antifreeze solutions containing 2,4,6-Tris(5-carboxypentylamino)1,3,5-triazine, 2,4,6-Tris(11-carboxyundecylamino)1,3,5-triazine, 1-Aminomethyl(N&prime;,N&prime;-di(2-hydroxyethyl)tolutriazole, or 1-Aminomethyl(N&prime;,N&prime;-di(2-hydroxyethyl)benzotriazole as corrosion inhibitors were examined by immersion test for 3 weeks as well as potentiodynamic polarization tests before and after immersion test. The corrosion rate of Cu was as relatively high as 10&minus;5 A/cm2 in antifreeze solution with the inhibitor (2,4,6-Tris(11-carboxyundecylamino)1,3,5-triazine) with a high molecular weight of 713 for a short time duration compared with antifreeze solutions using the other three types of inhibitors. However, the corrosion inhibition effect of this large molecule became prominent after 2 weeks, reducing the corrosion rate by about four orders of magnitude. Corrosion of Cu in the solution with inhibitors of high molecular weight of 440 or higher decreased gradually with time, while that in the solution with small molecules slightly increased over 3 weeks

Hexane-Soluble Fraction of the Common Fig, &lt;i&gt;Ficus carica&lt;/i&gt;, Inhibits Osteoclast Differentiation in Murine Bone Marrow-Derived Macrophages and RAW 264.7 Cells

Osteoclasts, derived from multipotent myeloid progenitor cells, play homeostatic roles in skeletal modeling and remodeling, but may also destroy bone in pathological conditions such as osteoporosis and rheumatoid arthritis. Osteoclast development depends critically on a differentiation factor, the receptor activator of NF-kappa B ligand (RANKL). In this study, we found that the hexane soluble fraction of the common fig Ficus carica (HF6-FC) is a potent inhibitor of osteoclastogenesis in RANKL-stimulated RAW264.7 cells and in bone marrow-derived macrophages (BMMs). HF6-FC exerts its inhibitory effects by suppression of p38 and NF-kappa B but activation of ERK. In addition, HF6-FC significantly decreased the expression of NFATc1 and c-Fos, the master regulator of osteoclast differentiation. The data indicate that components of HF6-FC may have therapeutic effects on bone-destructive processes such as osteoporosis, rheumatoid arthritis, and periodontal bone resorption.Y

A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana

A smoke-derived compound, karrikin (KAR), and an endogenous but as yet unidentified KARRIKIN INSENSITIVE2 (KAI2) ligand (KL) have been identified as chemical cues in higher plants that impact on multiple aspects of growth and development. Genetic screening of light-signaling mutants in Arabidopsis thaliana has identified a mutant designated as ply2 (pleiotropic long hypocotyl2) that has pleiotropic light-response defects. In this study, we used positional cloning to identify the molecular lesion of ply2 as a missense mutation of KAI2/HYPOSENSITIVE TO LIGHT, which causes a single amino acid substitution, Ala219Val. Physiological analysis and genetic epistasis analysis with the KL-signaling components MORE AXILLARY GROWTH2 (MAX2) and SUPPRESSOR OF MAX2 1 suggested that the pleiotropic phenotypes of the ply2 mutant can be ascribed to a defect in KL-signaling. Molecular and biochemical analyses revealed that the mutant KAI2 ply2 protein is impaired in its ligand-binding activity. In support of this conclusion, X-ray crystallography studies suggested that the KAI2 ply2 mutation not only results in a narrowed entrance gate for the ligand but also alters the structural flexibility of the helical lid domains. We discuss the structural implications of the Ala219 residue with regard to ligand-specific binding and signaling of KAI2, together with potential functions of KL-signaling in the context of the light-regulatory network in Arabidopsis thaliana. © The Author(s) 2018. Published by Oxford University Press on behalf of the Society for Experimental Biology.1