Classifying Aerosols Based on Fuzzy Clustering and Their Optical and Microphysical Properties Study in Beijing, China

Classification of Beijing aerosol is carried out based on clustering optical properties obtained from three Aerosol Robotic Network (AERONET) sites. The fuzzy c-mean (FCM) clustering algorithm is used to classify fourteen-year (2001–2014) observations, totally of 6,732 records, into six aerosol types. They are identified as fine particle nonabsorbing, two kinds of fine particle moderately absorbing (fine-MA1 and fine-MA2), fine particle highly absorbing, polluted dust, and desert dust aerosol. These aerosol types exhibit obvious optical characteristics difference. While five of them show similarities with aerosol types identified elsewhere, the polluted dust aerosol has no comparable prototype. Then the membership degree, a significant parameter provided by fuzzy clustering, is used to analyze internal variation of optical properties of each aerosol type. Finally, temporal variations of aerosol types are investigated. The dominant aerosol types are polluted dust and desert dust in spring, fine particle nonabsorbing aerosol in summer, and fine particle highly absorbing aerosol in winter. The fine particle moderately absorbing aerosol occurs during the whole year. Optical properties of the six types can also be used for radiative forcing estimation and satellite aerosol retrieval. Additionally, methodology of this study can be applied to identify aerosol types on a global scale

Sugarcane bagasse dietary fiber as an adjuvant therapy for stable chronic obstructive pulmonary disease: a four-center, randomized, double-blind, placebo-controlled study

AbstractObjectiveTo evaluate the efficacy and safety of sugarcane bagasse dietary fiber as an adjuvant therapy for improving quality of life in patients with stable chronic obstructive pulmonary disease (COPD).MethodsThis was a multicenter, randomized, double-blind, placebo-controlled trial. A total of 196 participants were randomized into a trial group (treated with 6 g/day sugarcane bagasse plus conventional treatment, n = 98) and a control group (treated with placebo plus conventional treatment, n = 98). All efficacy analyses were performed according to the intention-to-treat (ITT) principle. A per-protocol analysis set (PPS) was used to analyze the cases that completed the clinical trial with good compliance. The trial period was 30 days, with a 6-month follow-up. Pre- and post-treatment pulmonary symptom scores (cough, sputum, wheezing, and dyspnea) were recorded for both groups. The St. George's Respiratory Questionnaire (SGRQ) and the modified Medical Research Council (mMRC) dyspnea scale were assessed before treatment and at the end of the 6-month follow-up.ResultsThe ITT population was 178 and the PPS population was 166. Post-treatment pulmonary clinical symptoms and severity of dyspnea (mMRC and SGRQ evaluation) were significantly improved in both the trial group and the control group (ITT and PPS: P < 0.05). However, there was no statistical difference between the two groups in post-treatment pulmonary symptoms and mMRC. There was a greater reduction in the SGRQ subscales of activity, effect and total score in the trial group compared with the control group (ITT and PPS: P < 0.01). There was no statistical difference in pre- and post-treatment safety variables in either group.ConclusionSugarcane bagasse combined with conventional treatment improved quality of life in patients with stable COPD. Sugarcane bagasse appears to be a safe herbal medicine with potential for treating patients with stable COPD when taken orally as an adjuvant therapy

Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis

Homeostasis; PathogenesisHomeostasis; PatogénesisHomeòstasi; PatogènesiProgressive hepatic damage and fibrosis are major features of chronic liver diseases of different etiology, yet the underlying molecular mechanisms remain to be fully defined. N-RAS, a member of the RAS family of small guanine nucleotide-binding proteins also encompassing the highly homologous H-RAS and K-RAS isoforms, was previously reported to modulate cell death and renal fibrosis; however, its role in liver damage and fibrogenesis remains unknown. Here, we approached this question by using N-RAS deficient (N-RAS−/−) mice and two experimental models of liver injury and fibrosis, namely carbon tetrachloride (CCl4) intoxication and bile duct ligation (BDL). In wild-type (N-RAS+/+) mice both hepatotoxic procedures augmented N-RAS expression in the liver. Compared to N-RAS+/+ counterparts, N-RAS−/− mice subjected to either CCl4 or BDL showed exacerbated liver injury and fibrosis, which was associated with enhanced hepatic stellate cell (HSC) activation and leukocyte infiltration in the damaged liver. At the molecular level, after CCl4 or BDL, N-RAS−/− livers exhibited augmented expression of necroptotic death markers along with JNK1/2 hyperactivation. In line with this, N-RAS ablation in a human hepatocytic cell line resulted in enhanced activation of JNK and necroptosis mediators in response to cell death stimuli. Of note, loss of hepatic N-RAS expression was characteristic of chronic liver disease patients with fibrosis. Collectively, our study unveils a novel role for N-RAS as a negative controller of the progression of liver injury and fibrogenesis, by critically downregulating signaling pathways leading to hepatocyte necroptosis. Furthermore, it suggests that N-RAS may be of potential clinical value as prognostic biomarker of progressive fibrotic liver damage, or as a novel therapeutic target for the treatment of chronic liver disease.This work was supported by the MICINN Retos RTI2018-095673-B-I00, PID2020-11782RB-I00, PID2020-117941RB-I00, all of which were co-funded with FEDER funds, AMMF 2018/117, COST Action CA17112 and Comunidad de Madrid S2022/BMD-7409. This project has received funding from the European Horizon’s research and innovation program HORIZON-HLTH-2022-STAYHLTH-02 under agreement No. 101095679. The research group belongs to the validated Research Groups Ref. 970935 Liver Pathophysiology, 920631 Lymphocyte Immunobiology and IBL-6 (imas12-associated). KZ was supported by the China Scholarship Council. SM-G was supported by a predoctoral scholarship from Complutense University

Pu-erh Tea Regulates Fatty Acid Metabolism in Mice Under High-Fat Diet

Pu-erh tea has been extensively reported to possess lipid lowering effects but the underlying mechanisms remained unclear. Free fatty acids (FFAs) are generally correlated with the development of obesity, leading to increased risk for type 2 diabetes mellitus and cardiovascular diseases. To investigate whether Pu-erh tea treatment alters FA metabolism, we treated HFD induced obese mice with Pu-erh tea for 22 weeks and analyzed FFA profiles of experimental mice using a UPLC-QTOF-MS platform. Results showed remarkable changes in metabolic phenotypes and FFA compositions in mice treated with or without Pu-erh tea. HFD induced a marked obese phenotype in mice as revealed by significantly increased body weight, liver and adipose tissue weight, lipid levels in serum and liver, and these parameters were markedly reduced by Pu-erh tea treatment. Several FFA or FFA ratios, such as DGLA, palmitoleic acid, and OA/SA ratio, were significantly increased while the levels of SA/PA and AA/DGLA were significantly reduced in HFD-induced obese mice. Interestingly, these differential FFAs or FFA ratios were previous identified as key markers in human obese subjects, and their changes observed in the HFD group were reversed by Pu-erh tea treatment. Moreover, a panel of FFA markers including C20:3 n6/C18:3 n6 and C20:3 n6/C20:2 n6, C18:3 n6/C18:2 n6, C18:3 n3/C18:2 n6 and C24:1 n9/C22:1 n9, which were previously identified as biomarkers in predicting the remission of obesity and diabetes in human subjects who underwent metabolic surgery procedures, were reversed by Pu-erh tea intervention. Pu-erh tea significantly improved glucose homeostasis and insulin tolerance compared to the HFD group. Additionally, Pu-erh tea treatment significantly decreased FFA synthesis genes and increased the expression of genes involved in FFA uptake and β-oxidation including FATP2, FATP5, PPARα, CPT1α, and ACOX-1. These finding confirmed the beneficial effects of Pu-erh tea on regulating lipid and glucose metabolism, and further validated a panel of FFA markers with diagnostic and prognostic value for obesity and diabetes

Weathering Characteristics of Sloping Fields in the Three Gorges Reservoir Area, China

For the purpose of understanding the weathering characteristics of surface layers in purple mudstone sloping fields of the Three Gorges Reservoir area of China, oxide content of major elements, composition of clay minerals, magnetic susceptibility, and difference in weathering characteristics of surface layers under different slope gradients were determined. The results showed that the oxide content of Si, Al, and Fe ranged from 60% to 75% and the weathering coefficient with depth showed no trend along the slope gradient. Also, for gentle (10° and 15°) and intermediate (25° and 40°) slopes the clay relative diffraction peak for kaolinite at the surface between 0–10 cm and 10–20 cm declined with an increase in slope gradient, while the relative diffraction peak for kaolinite in weathered layers on steep slopes (50° and 60°) disappeared altogether. Magnetic susceptibility decreased with increasing depth and, for a given depth layer, decreased with an increase in slope gradient. Analysis of the oxide content, weathering coefficients, clay minerals, and magnetic susceptibility showed that in the Three Gorges Reservoir area, the pedogenesis of the weathering layer in purple mudstone sloping fields was weak with weaker soil formation going from gentle slope to steep slope

Intestinal Epithelial Cell-Derived Extracellular Vesicles Modulate Hepatic Injury via the Gut-Liver Axis During Acute Alcohol Injury.

Binge drinking, i.e., heavy episodic drinking in a short time, has recently become an alarming societal problem with negative health impact. However, the harmful effects of acute alcohol injury in the gut-liver axis remain elusive. Hence, we focused on the physiological and pathological changes and the underlying mechanisms of experimental binge drinking in the context of the gut-liver axis. Eight-week-old mice with a C57BL/6 background received a single dose (p.o.) of ethanol (EtOH) [6 g/kg b.w.] as a preclinical model of acute alcohol injury. Controls received a single dose of PBS. Mice were sacrificed 8 h later. In parallel, HepaRGs and Caco-2 cells, human cell lines of differentiated hepatocytes and intestinal epithelial cells intestinal epithelial cells (IECs), respectively, were challenged in the presence or absence of EtOH [0-100 mM]. Extracellular vesicles (EVs) isolated by ultracentrifugation from culture media of IECs were added to hepatocyte cell cultures. Increased intestinal permeability, loss of zonula occludens-1 (ZO-1) and MUCIN-2 expression, and alterations in microbiota-increased Lactobacillus and decreased Lachnospiraceae species-were found in the large intestine of mice exposed to EtOH. Increased TUNEL-positive cells, infiltration of CD11b-positive immune cells, pro-inflammatory cytokines (e.g., tlr4, tnf, il1β), and markers of lipid accumulation (Oil Red O, srbep1) were evident in livers of mice exposed to EtOH, particularly in females. In vitro experiments indicated that EVs released by IECs in response to ethanol exerted a deleterious effect on hepatocyte viability and lipid accumulation. Overall, our data identified a novel mechanism responsible for driving hepatic injury in the gut-liver axis, opening novel avenues for therapy.This work was supported by the MINECO Retos SAF2016-78711, SAF2017-87919-R, EXOHEP-CM S2017/BMD-3727, NanoLiver-CM Y2018/NMT-4949, ERAB Ref. EA 18/14, AMMF 2018/117, UCM-25-2019 and COST Action CA17112, the German Research Foundation (SFB/TRR57/P04, SFB 1382-403224013/A02, and DFG NE 2128/2-1). FC and YN are Ramón y Cajal Researchers RYC-2014-15242 and RYC-2015-17438. FC is a Gilead Liver Research 2018. KZ is a recipient of a Chinese Scholarship Council (CSC). BK20170127 from the Natural Science Foundation of Jiangsu Province to JP.S

Pairing symmetry and properties of iron-based high temperature superconductors

Pairing symmetry is important to indentify the pairing mechanism. The analysis becomes particularly timely and important for the newly discovered iron-based multi-orbital superconductors. From group theory point of view we classified all pairing matrices (in the orbital space) that carry irreducible representations of the system. The quasiparticle gap falls into three categories: full, nodal and gapless. The nodal-gap states show conventional Volovik effect even for on-site pairing. The gapless states are odd in orbital space, have a negative superfluid density and are therefore unstable. In connection to experiments we proposed possible pairing states and implications for the pairing mechanism.Comment: 4 pages, 1 table, 2 figures, polished versio

Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis.

Progressive hepatic damage and fibrosis are major features of chronic liver diseases of different etiology, yet the underlying molecular mechanisms remain to be fully defined. N-RAS, a member of the RAS family of small guanine nucleotide-binding proteins also encompassing the highly homologous H-RAS and K-RAS isoforms, was previously reported to modulate cell death and renal fibrosis; however, its role in liver damage and fibrogenesis remains unknown. Here, we approached this question by using N-RAS deficient (N-RAS-/-) mice and two experimental models of liver injury and fibrosis, namely carbon tetrachloride (CCl4) intoxication and bile duct ligation (BDL). In wild-type (N-RAS+/+) mice both hepatotoxic procedures augmented N-RAS expression in the liver. Compared to N-RAS+/+ counterparts, N-RAS-/- mice subjected to either CCl4 or BDL showed exacerbated liver injury and fibrosis, which was associated with enhanced hepatic stellate cell (HSC) activation and leukocyte infiltration in the damaged liver. At the molecular level, after CCl4 or BDL, N-RAS-/- livers exhibited augmented expression of necroptotic death markers along with JNK1/2 hyperactivation. In line with this, N-RAS ablation in a human hepatocytic cell line resulted in enhanced activation of JNK and necroptosis mediators in response to cell death stimuli. Of note, loss of hepatic N-RAS expression was characteristic of chronic liver disease patients with fibrosis. Collectively, our study unveils a novel role for N-RAS as a negative controller of the progression of liver injury and fibrogenesis, by critically downregulating signaling pathways leading to hepatocyte necroptosis. Furthermore, it suggests that N-RAS may be of potential clinical value as prognostic biomarker of progressive fibrotic liver damage, or as a novel therapeutic target for the treatment of chronic liver disease