Placental expression of AChE, α7nAChR and NF-κB in patients with preeclampsia

Objectives: This study aimed to investigate placental expression of AChE, α7nAChR and NF-κB in patients with preeclampsia and discuss about its clinical significance. Material and methods: mRNA expression levels of acetylcholine (AChE), alpha-7 nicotinic acetylcholine receptor (α7nAChR) and nuclear factor-kB (NF-κB) in placenta were detected by qRT-PCR, and protein levels were determined by immunohis­tological analysis and Western Blot in 35 women with preeclampsia (including 20 cases of mild preeclampsia and 15 cases of severe preeclampsia) and 30 cases in control group, respectively. Results: The expression of AChE mRNA and protein in placenta increased significantly in patients with preeclampsia compared with the control group (p < 0.01). It was lower in patients with severe preeclampsia than in patients with mild preeclampsia (p < 0.05). The expression of α7nAChR mRNA and protein in placenta decreased significantly in patients with preeclampsia compared with the control group (p < 0.01). However, the expression of α7nAChR mRNA and protein in patients with severe preeclampsia was higher than that in patients with mild preeclampsia, without significant difference(p > 0.05). The expression of NF-κB protein in placenta decreased significantly in patients with preeclampsia compared with the control group(p < 0.01). It was higher in patients with severe preeclampsia than in patients with mild preeclampsia (p < 0.05), but there was no significant difference between preeclampsia group and control group in the expression of NF-κB mRNA in placenta (p > 0.05). The results of Western blotting assay were consistent with those of immunohistochemistry. Conclusions: Abnormal expression of AChE, α7nAChR and NF-κB in placenta may be associated with preeclampsia. Cho­linergic anti-inflammatory pathway may play an important role in the pathogenesis of preeclampsia

Reticulation is a Risk Factor of Progressive Subpleural non-Fibrotic Interstitial Lung Abnormalities

Rationale: Interstitial lung abnormalities (ILAs) are being increasingly identified in clinical practice. In particular for subpleural non-fibrotic ILAs, the risk of progression over time and the risk factors for progressive behavior are still largely unknown. Objectives: To determine the age band prevalence of ILAs and the risk of radiological progression of subpleural non-fibrotic ILAs over time in a large health check-up population, and to identify how reticulation contributes to the risk of radiological progression. Methods: Based on ILAs definition by the Fleischner Society, low-dose chest CT images from community-dwelling population undergone health check-up were evaluated for ILAs. Multivariable logistic regression was used to assess the risk of radiological progression. Measurements and Main Results: Among 155,539 individuals, 3,300 (2.1%) were confirmed to have ILAs: the vast majority (81.7%) were defined as subpleural non-fibrotic ILAs. The prevalence of ILAs increased linearly with age (P for trend<0.0001). Of 454 individuals with subpleural non-fibrotic ILAs, 198 (43.6%) had radiological progression over 4 years. The presence of reticulation on initial imaging was an independent predictor of radiological progression (OR 1.9; 95%CI 1.2-3.0, P=0.0040). No difference in radiological progression was identified between subpleural non-fibrotic ILAs with extensive reticulation and subpleural fibrotic ILAs (73.0% vs. 68.8%, P=0.7626). Conclusions: The prevalence of ILAs increases linearly with age. Nearly half of subpleural non-fibrotic ILAs progress radiologically over 4 years. The presence of reticulation is a risk factor for radiological progression. Subpleural non-fibrotic ILAs with extensive reticulation are likely to be a feature of subpleural fibrotic ILAs

Causative agent distribution and antibiotic therapy assessment among adult patients with community acquired pneumonia in Chinese urban population

<p>Abstract</p> <p>Background</p> <p>Knowledge of predominant microbial patterns in community-acquired pneumonia (CAP) constitutes the basis for initial decisions about empirical antimicrobial treatment, so a prospective study was performed during 2003–2004 among CAP of adult Chinese urban populations.</p> <p>Methods</p> <p>Qualified patients were enrolled and screened for bacterial, atypical, and viral pathogens by sputum and/or blood culturing, and by antibody seroconversion test. Antibiotic treatment and patient outcome were also assessed.</p> <p>Results</p> <p>Non-viral pathogens were found in 324/610 (53.1%) patients among whom <it>M. pneumoniae </it>was the most prevalent (126/610, 20.7%). Atypical pathogens were identified in 62/195 (31.8%) patients carrying bacterial pathogens. Respiratory viruses were identified in 35 (19%) of 184 randomly selected patients with adenovirus being the most common (16/184, 8.7%). The nonsusceptibility of <it>S. pneumoniae </it>to penicillin and azithromycin was 22.2% (Resistance (R): 3.2%, Intermediate (I): 19.0%) and 79.4% (R: 79.4%, I: 0%), respectively. Of patients (312) from whom causative pathogens were identified and antibiotic treatments were recorded, clinical cure rate with β-lactam antibiotics alone and with combination of a β-lactam plus a macrolide or with fluoroquinolones was 63.7% (79/124) and 67%(126/188), respectively. For patients having mixed <it>M. pneumoniae </it>and/or <it>C. pneumoniae </it>infections, a better cure rate was observed with regimens that are active against atypical pathogens (e.g. a β-lactam plus a macrolide, or a fluoroquinolone) than with β-lactam alone (75.8% vs. 42.9%, <it>p </it>= 0.045).</p> <p>Conclusion</p> <p>In Chinese adult CAP patients, <it>M. pneumoniae </it>was the most prevalent with mixed infections containing atypical pathogens being frequently observed. With <it>S. pneumoniae</it>, the prevalence of macrolide resistance was high and penicillin resistance low compared with data reported in other regions.</p

Low-NOx study of a 600 MW tangentially fired boiler based on pulverized coal preheating method

Boiler emissions are the primary sources of atmospheric nitrogen oxide (NOx) emissions. Exceeding the NOx emission limit can shut down the boiler, causing financial losses. Herein, a new preheated combustion method is proposed to prevent coal-fired boilers from exceeding the NOx emission limit at low loads. This is a simulation study of internal combustion burners and a 600 MW tangentially fired boiler using a pulverized coal preheating method that explores syngas production patterns after pulverized coal is preheated, the effects of flow characteristics, and variations in NOx and unburned carbon content under different preheating ratios. Our results indicated that the internal combustion burner had a stable preheating effect. The volume fractions of CH4, CO, and H2 at the burner outlet were 0.95%, 12.7%, and 0.8%, respectively. The fuel nitrogen precipitated during the preheating process was converted into N2. High-temperature char and syngas entered the furnace chamber and were mixed with air to accelerate combustion, which enhanced the jet flow intensity and improved the combustion stability at 50% load. The top burner exhibited a more significant nitrogen reduction than the bottom burner. The NO reduction from retrofitting Layers D and E accounted for 53% after retrofitting all five layers. When the preheating ratio was increased from 0 to 100%, NOx concentration was reduced by 63.6% at 6% O2, while unburned carbon content was reduced by 41%, which improved combustion efficiency. By discussing the advantages of internal combustion burners for retrofitting a 600 MW tangentially fired boiler, this study provides theoretical guidance for the application of preheating methods in peaking conditions

Efficacy and Safety of JAK Inhibitors for Rheumatoid Arthritis: A Meta-Analysis

Background: More and more trials have been conducted. We aimed to assess the efficacy and safety of different JAKinibs in RA. Methods: A systematic search of randomized controlled trials (RCTs) with JAKinib treatment in RA published in the Medline, Embase, and Cochrane databases up to May 2021 was performed. Results: 37 trials involving 15,174 patients were identified. Pooled analysis revealed that JAKinibs were associated with significant therapeutic improvement in RA patients as determined by ACR20 (RR = 2.03, 95% CI: 1.85 to 2.28) and HAQ-DI (MD = &minus;0.31, 95% CI: &minus;0.33 to &minus;0.28) over placebo. Compared to placebo, JAKinib treatment was also associated with more adverse events (RR = 1.10, p &lt; 0.001; RR = 1.29, p &lt; 0.001; RR = 1.59, p = 0.02). Baricitinib and upadacitinib were related to more frequent adverse events (RR = 1.10; 95% CI: 1.01, 1.21; RR = 1.19; 95% CI: 1.11, 1.28) and infection (RR = 1.22; 95% CI: 1.09, 1.37; RR = 1.38; 95% CI: 1.22, 1.56), whereas only baricitinib was associated with more herpes zoster (RR = 3.15; 95% CI: 1.19, 8.33). Conclusions: JAKinibs were superior to placebo for improving signs, symptoms, and health-related quality of life in RA patients at short term, whereas the overall risk of adverse events and infections were greater with baricitinib and upadacitinib, and a higher risk of herpes zoster was only associated with baricitinib. More trials are needed to investigate the long-term safety

Inhibition of Receptor Interacting Protein Kinases Attenuates Cardiomyocyte Hypertrophy Induced by Palmitic Acid

Palmitic acid (PA) is known to cause cardiomyocyte dysfunction. Cardiac hypertrophy is one of the important pathological features of PA-induced lipotoxicity, but the mechanism by which PA induces cardiomyocyte hypertrophy is still unclear. Therefore, our study was to test whether necroptosis, a receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3-) dependent programmed necrosis, was involved in the PA-induced cardiomyocyte hypertrophy. We used the PA-treated primary neonatal rat cardiac myocytes (NCMs) or H9c2 cells to study lipotoxicity. Our results demonstrated that cardiomyocyte hypertrophy was induced by PA treatment, determined by upregulation of hypertrophic marker genes and cell surface area enlargement. Upon PA treatment, the expression of RIPK1 and RIPK3 was increased. Pretreatment with the RIPK1 inhibitor necrostatin-1 (Nec-1), the PA-induced cardiomyocyte hypertrophy, was attenuated. Knockdown of RIPK1 or RIPK3 by siRNA suppressed the PA-induced myocardial hypertrophy. Moreover, a crosstalk between necroptosis and endoplasmic reticulum (ER) stress was observed in PA-treated cardiomyocytes. Inhibition of RIPK1 with Nec-1, phosphorylation level of AKT (Ser473), and mTOR (Ser2481) was significantly reduced in PA-treated cardiomyocytes. In conclusion, RIPKs-dependent necroptosis might be crucial in PA-induced myocardial hypertrophy. Activation of mTOR may mediate the effect of necroptosis in cardiomyocyte hypertrophy induced by PA

Surface structure-dependent pyrite oxidation in relatively dry and moist air: Implications for the reaction mechanism and sulfur evolution

Pyrite oxidation not only is environmentally significant in the formation of acid mine (or acid rock) drainage and oxidative acidification of lacustrine sediment but also is a critical stage in geochemical sulfur evolution. The oxidation process is always controlled by the reactivity of pyrite, which in turn is controlled by its surface structure. In this study, the oxidation behavior of naturally existing {100}, {111}, and {210} facets of pyrite was investigated using a comprehensive approach combining X-ray photoelectron spectroscopy, diffuse reflectance Fourier transform infrared spectroscopy, and time-of-flight secondary-ion mass spectrometry with periodic density functional theoretical (DFT) calculations. The experimental results show that (i) the initial oxidation rates of both pyrite {111} and {210} are much greater than that of pyrite {100}; (ii) the initial oxidation rate of pyrite {210} is greater than that of pyrite {111} in low relative humidity, which is reversed in high relative humidity; and (iii) inner sphere oxygen-bearing sulfur species are originally generated from surface reactions and then converted to outer sphere species. The facet dependent rate law can be expressed as: r({hkl}) = k({hkl})h(a)P(0.5) (t + 1)(-0.5), where r({hkl}) is the orientation dependent reaction rate, k{hkl} is the orientation dependent rate constant, h is the relative humidity, P is the oxygen partial pressure, and t is the oxidation time in seconds. {111} is the most sensitive facet for pyrite oxidation. Combined with DFT theoretical investigations, water catalyzed electron transfer is speculated as the rate-limiting step. These findings disclose the structure-reactivity dependence of pyrite, which not only presents new insight into the mechanism of pyrite oxidation but also provides fundamental data to evaluate sulfur speciation evolution, suggesting that the surface structure sensitivity should be considered to estimate the reactivity at the mineral-water interface. (C) 2018 Elsevier Ltd. All rights reserved