Bartlettbuckley6259

From DigitalMaine Transcription Project
Revision as of 17:21, 22 November 2024 by Bartlettbuckley6259 (talk | contribs) (Created page with "Thus, the selective catalytic route to monofunctional limonene carbonates demonstrated gives straightforward access to monomers for novel bio-based polymers. © 2020 WILEY-VCH...")
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to: navigation, search

Thus, the selective catalytic route to monofunctional limonene carbonates demonstrated gives straightforward access to monomers for novel bio-based polymers. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.BACKGROUND Characteristics and outcome of Invasive fungal infection (IFI) in critically ill burn patients have been poorly explored. OBJECTIVES We report the factors associated with 90-day mortality in a multicenter retrospective European study. PATIENTS/METHODS All burn patients with confirmed IFI admitted between 1st January 2010 to 31st December 2015 in 10 centers in France and Belgium were included. RESULTS Ninety-four patients were enrolled with 110 cases of IFIs 79 (71.8%) were yeasts IFI and 31 (28.2%) filamentous IFI. Incidence was 1% among admitted patients. The 90-day mortality was 37.2% for all IFIs combined, 52% for filamentous infection and 31.9% for yeast infection. Patients with more than one IFI had a higher 90-day mortality than patients with only one episode (61.5% vs 33.5 % (P= .006)). In multivariate analysis, higher Simplified Acute Physiology Score II (OR= 1.05 (95% CI 1.02-1.09) P= .003), bacterial co-infection (OR= 3.85 (95% CI 1.23-12.01), P= .014) and use of skin allografts at the time of IFI diagnosis (OR= 3.87 (95% CI 1.31-11.42), P = .021) were associated with 90-day mortality. CONCLUSIONS Although rare, invasive fungal infections remain associated with poor outcome in burn patients. Bacterial coinfection and presence of allograft were potentially modifiable factors independently associated with outcome. This article is protected by copyright. All rights reserved.Neurodegeneration is associated with inflammation and mismanaged iron homeostasis, leading to increased concentration of non-transferrin-bound iron (NTBI) in the brain. NTBI can be taken up by cells expressing Zrt-, Irt-like protein-14 (ZIP14), which is regulated by iron overload and pro-inflammatory cytokines, for example, interleukin-1β (IL-1β) and IL-6. Here, we focus on the astrocytic involvement and regulation of ZIP14 in an experimental model of chronic neurodegeneration with inflammation and iron overload. Rats were unilaterally injected with ibotenic acid in striatum resulting in excitotoxicity-induced neuronal loss in substantia nigra pars reticulata (SNpr). ZIP14 expression was measured in SNpr using immunohistochemistry, western blotting, and RT-qPCR. Cultures of primary astrocytes were examined for Zip14 mRNA expression after stimulation with ferric ammonium citrate (FAC), IL-6, or IL-1β. Merbarone To study the involvement of ZIP14 in astrocytic iron uptake, uptake of 59 Fe was investigated after treatment with IL-1β and siRNA-mediated ZIP14 knockdown. In the lesioned SNpr, reactive astrocytes, but not microglia, revealed increased ZIP14 expression with a main confinement to cell bodies and cellular processes. In astrocyte cultures, FAC and IL-1β stimulation increased Zip14 expression and IL-1β stimulation increased uptake of 59 Fe. Increased 59 Fe uptake was also observed after siRNA-mediated ZIP14 knockdown suggesting that lowering of ZIP14 impaired the balance between astrocytic uptake and export of iron. We conclude that astrocytes increase ZIP14 expression in response to inflammation and iron exposure and that ZIP14 seems pertinent for iron uptake in astrocytes and plays a role for a balanced astrocytic iron homeostasis. © 2020 Wiley Periodicals, Inc.Three isostructural covalent organic frameworks (COFs) with either methoxyl, hydroxyl, or both groups on the channel wall, are synthesized and served as metal-free heterogeneous catalysts for chemical fixation of CO2 . Among them, the COF decorated with both hydroxyl and methoxyl groups named OMe-OH-TPBP-COF exhibits the highest catalytic activity and efficiency for CO2 cycloaddition under mild conditions. © 2020 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.AIMS To investigate the relationship between fitness, heart failure (HF) risk factors (age, blood pressure, and obesity), and global/regional myocardial longitudinal strain in young adults undergoing stress testing. METHODS Individuals 25-55 years old without any significant medical history, not taking medications, and with a normal maximal stress echocardiogram were eligible. Global and regional longitudinal strain (LS) was evaluated by 2D speckle tracking echocardiography. RESULTS One hundred and seventy patients were included, of which 60% were males. The mean age was 43 years old, 49% had optimal blood pressure, and 30% were obese. On average, patients achieved 10.5 (3) METS, and the global LS was -19.9 (3.1) %. Reduced fitness was associated with decreased global longitudinal strain (GLS). Those in the top GLS quartile walked on average 1 minute and 21 seconds longer compared with the lowest quartile (P  less then  .001). The effect of fitness on LS was preferential to the mid and apex, such that there was an apex-to-base gradient. Obesity was also independently associated with reduced GLS. However, the reduction in LS in obese individuals was more prominent at the base and mid-walls with relative sparing of the apex. Similar to fitness, aging was also associated with an increase in the apex-to-base gradient of LS. Furthermore, diastolic filling parameters correlated distinctively with regional LS. CONCLUSIONS In young adults without cardiovascular disease, low fitness and obesity are independently associated with reduced left ventricular longitudinal strain. There is a differential effect of HF risk factors on regional longitudinal function. © 2020 Wiley Periodicals, Inc.BACKGROUND Lymphocyte activation gene 3 (LAG-3, also known as CD223) is an immune checkpoint molecule expressed on various types of lymphocytes, and it is mainly involved in maintaining immune homeostasis. However, there are currently no data on LAG-3 expression in non-small-cell lung cancer cells. METHODS Human lung cancer cells were cultured using conventional methods. The expression of LAG-3 was measured by Western blot and flow cytometry. Between April 2018 and May 2019, we collected 52 surgical specimens of stage I-III non-small-cell lung cancer (NSCLC). Fourteen samples of benign lung tissue lesions were collected as the control group, and the expression levels of LAG-3 in the lung cancer cells and tissue samples were measured via immunohistochemistry. RESULTS Western blots showed that LAG-3 was expressed in lung cancer cell lines. There was significant difference in the LAG-3 expression levels in the NSCLC cells and benign lung tissue (χ2  = 13.055, P = .0003). The LAG-3 expression level was significantly associated with the NSCLC clinical stage, and LAG-3 expression was significantly higher in stage III patients (P  less then  .