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As a common method for preparing micron powder in industrial operations, the mechanical extrusion method simply pursues the particle size without considering the microstructure characteristics of sepiolite, which leads to problems such as bundles of sepiolite not being effectively dispersed, and thus the disruption of fibers is inevitably caused. In this work, a new micronization method for disaggregating these bundles while preserving the original structural integrity of the fibers is proposed based on steam pressure changes. The effects of steam pressure changes on the particle size distribution, microstructure, and properties of treated sepiolite are studied using X-ray fluorescence spectrometer (XRF), X-ray diffractometer (XRD), Field Emission Scanning Electron Microscopy (FESEM), Transmission Electron Microscopy (TEM), and a specific surface area and aperture analyzer (BET). The experimental results show that the particle size of sepiolite powder depends greatly on steam pressure, and sepiolite powder with mass ratio of 91.6% and a particle size D97 of 21.27 μm is obtained at a steam pressure of 0.6 MPa. Compared to the sepiolite after mechanical extrusion, the sepiolite treated with steam pressure changes can maintain the integrity of its crystalline structure. The specific surface area of sepiolite enhanced from 80.15 m2 g−1 to 141.63 m2 g−1 as the steam pressure increased from 0.1 to 0.6 MPa, which is about 1.6 times that of the sample treated with mechanical extrusion. [ABSTRACT FROM AUTHOR]

Summary: In this meta‐analysis, we aim to evaluate the risk of gallbladder and biliary disease of weight management strategies and investigate the association between weight reduction and risk of gallbladder or biliary disease. Randomized controlled trials (RCTs) with a duration of at least 12 weeks that compare antiobesity medications (AOMs) with placebo or bariatric surgery with less intensive weight management strategy were concluded. Weight management strategy was associated with a significant increased risk of gallbladder or biliary disease (OR 1.361, 95% CI 1.147 to 1.614, P < 0.001, I2 = 3.5%), cholelithiasis, cholecystitis, and cholecystectomy compared with placebo or controls. The increased risk of gallbladder or biliary disease was observed both in pharmacotherapies subgroup and bariatric surgery subgroup. With regards of specific pharmacotherapies, an increased risk of gallbladder or biliary disease was observed in trials with glucagon‐like peptide 1 receptor agonist (GLP‐1 RA) treatments. In addition, trials with indication of obesity and overweight treatment and trials with higher doses showed significant higher risk of gallbladder or biliary disease compared with placebo or controls. In conclusion, weight management strategy was associated with an increased risk of gallbladder or biliary disease when compared with placebo or control groups. [ABSTRACT FROM AUTHOR]

The fabrication of MnBi2Te4 family of materials has been demonstrated that intercalating magnetic MnTe layer into topological insulator Bi2Te3 is an efficient way to explore magnetic topological insulator. A natural question is that if multiple MnTe layers can be intercalated into Bi2Te3, meanwhile if the topological properties are well preserved. Based on first-principles calculations, we first confirm that multiple MnTe layers can be inserted into Bi2Te3 by forming antiferromagnetic MnnBi2Te3+n (n = 1–5) crystals, where each system is energetically stable and can be readily exfoliated down to a monolayer. Specifically, the structural phase transition from ABC to ABAC stacking happens when n ≥ 2. Further electronic band structure calculations and topological identification reveal that the magnetic MnnBi2Te3+n undergoes a topologically nontrivial to trivial phase transition when n > 2, which is attributed to that multiple MnTe layers destroy the topological property of Bi2Te3. In addition to applying compressed strain, the topological states can be restored by intercalating Bi2Te3 layers by forming (MnTe)n(Bi2Te3)m heterostructures. Most strikingly, it is found that the topological properties of (MnTe)n(Bi2Te3)m are universally determined by the ratio of n/m, once n/m ≤ 2.8, the desired topological states are recovered. Our notable findings enrich the family of magnetic topological insulator, providing opportunities to explore more intriguing topological phenomena. [ABSTRACT FROM AUTHOR]

The fabrication of MnBi2Te4 family of materials has been demonstrated that intercalating magnetic MnTe layer into topological insulator Bi2Te3 is an efficient way to explore magnetic topological insulator. A natural question is that if multiple MnTe layers can be intercalated into Bi2Te3, meanwhile if the topological properties are well preserved. Based on first-principles calculations, we first confirm that multiple MnTe layers can be inserted into Bi2Te3 by forming antiferromagnetic MnnBi2Te3+n (n = 1–5) crystals, where each system is energetically stable and can be readily exfoliated down to a monolayer. Specifically, the structural phase transition from ABC to ABAC stacking happens when n ≥ 2. Further electronic band structure calculations and topological identification reveal that the magnetic MnnBi2Te3+n undergoes a topologically nontrivial to trivial phase transition when n > 2, which is attributed to that multiple MnTe layers destroy the topological property of Bi2Te3. In addition to applying compressed strain, the topological states can be restored by intercalating Bi2Te3 layers by forming (MnTe)n(Bi2Te3)m heterostructures. Most strikingly, it is found that the topological properties of (MnTe)n(Bi2Te3)m are universally determined by the ratio of n/m, once n/m ≤ 2.8, the desired topological states are recovered. Our notable findings enrich the family of magnetic topological insulator, providing opportunities to explore more intriguing topological phenomena. [ABSTRACT FROM AUTHOR]

Aims: Whether sodium‐glucose co‐transporter 2 inhibitors are effective for heart failure caused by ATTR‐CA (transthyretin cardiac amyloidosis) remains uncertain. The aim of this study is to investigate the cardiovascular prognosis in ATTR‐CA mice model with dapagliflozin treatment. Methods and results: Humanized RBP4/TTRVal50Met and RBP4/TTR mice models were constructed with clustered regularly interspaced short palindromic repeats and associated Cas9 endonuclease (CRISPR‐Cas9) techniques and multiple generations breeding. A total of 6 RBP4/TTR mice received placebo treatment, when 12 RBP4/TTRVal50Met received dapagliflozin (1 mg/kg/day, 6 mice) and placebo (6 mice) treatment. Fasting glucose, intraperitoneal glucose tolerance test, and plasma brain natriuretic peptide (BNP) concentration were measured at Day 0, Week 2, and Week 4. BNP, transforming growth factor‐beta (TGF‐β), collagen type I alpha 1 (COL1A1) protein levels, and Cola1, TGFβ1, TNFα, IL‐1β, BNP relative quantities in cardiac, along with cardiac pathology examination including right ventricular collagen percentage, ventricular septum thickness, left ventricular wall thickness, and left ventricular internal diameter were measured at Week 4 after treatment procedure. All 18 mice completed the experiment. The baseline characteristics were balanced among three treatment groups. In placebo‐treated mice, the cardiac BNP relative quantity was significantly higher in RBP4/TTRVal50Met mice than RBP4/TTR mice (RBP4[KI/KI], TTR [KI/KI]: 0.72 ± 0.46, RBP4[KI/KI], TTRVal50Met[KI/KI]: 1.44 ± 0.60, P = 0.043), indicating more significant heart failure progression in ATTR‐CA mice than normal mice. In ATTR‐CA mice, the cardiovascular prognosis measurements including heart failure (plasma BNP concentration and relative quantities of BNP), cardiac inflammation (relative quantities of Cola1, TGFβ1, TNFα, and IL‐1β), and pathological changes (right ventricular collagen percentage, ventricular septum thickness, left ventricular wall thickness, and left ventricular internal diameter) were statistically comparable between those under dapagliflozin and placebo treatment. Conclusions: Dapagliflozin did not improve cardiovascular prognosis including the progression of heart failure, cardiac inflammation, and pathological changes in ATTR‐CA mice compared with placebo. The results of this study were not in support of dapagliflozin's therapeutic effects for ATTR‐CA. More pre‐clinical and clinical researches to validate these findings and demonstrate the underlying mechanisms are still required. [ABSTRACT FROM AUTHOR]