Trends in prevalence and all-cause mortality of metabolic dysfunction-associated fatty liver disease among adults in the past three decades: Results from the NHANES study.

BACKGROUND: Given the escalating epidemic of obesity and diabetes coupled with redefined diagnostic criteria, it is critical to identify the prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD). We sought to determine the prevalence and mortality outcomes of MAFLD subtypes based on diagnostic criteria in the USA over the past three decades. METHODS: Eleven cycles of the National Health and Nutrition Examination Surveys (NHANES; 1988-1994 and 1999-2020) were used, and 72,224 participants were included. MAFLD was defined according to the 2020 International Expert Consensus. Based on diagnostic criteria and risk factors, MAFLD was categorized into seven subtypes: type 1 (obesity subtype), 2 (metabolic unhealthy subtype), 3 (diabetes subtype), 4 (metabolic unhealthy non-diabetes subtype), 5 (obesity and diabetes subtype), 6 (metabolic unhealthy non-obesity subtype), and 7 (mixed subtype). RESULTS: Over the study period, the estimated prevalence of MAFLD increased significantly from 22% in 1988-1994 to 36% in 2017-2020. The prevalence of Type 4 was the highest, followed by that of Type 7, whereas other types were low and almost unchanged over time. Individuals with MAFLD had 19% and 38% increased mortality risks from all causes and cardiovascular disease, respectively. Among them, the metabolically unhealthy participants with normal weight demonstrated a 116% higher risk for all-cause mortality [hazard ratio (HR): 2.16, 95% CI: 1.52-3.08] and a 222% higher risk for cardiovascular mortality (HR: 3.22, 95% CI: 1.72-6.04). Interestingly, stratification and interaction analyses demonstrated a significant impact of metabolic parameters on the relationship between MAFLD and all-cause mortality. CONCLUSIONS: In conclusion, our study identified an increase in MAFLD prevalence and a significant association between metabolic derangements in MAFLD and all-cause or cardiovascular mortality.

Investigation of the Oxidation Behavior of Cr20Mn17Fe18Ta23W22 and Microdefects Evolution Induced by Hydrogen Ions before and after Oxidation.

The oxidation behavior of body-centered cubic (bcc) structure Cr20Mn17Fe18Ta23W22 refractory high-entropy alloy (RHEA) and the microdefects induced by hydrogen ions before and after oxidation were investigated. The results revealed that compared with oxidizing Cr20Mn17Fe18Ta23W22 at 800 °C (6.7 °C/min) for 4 h (ST3, Ar:O2 = 3:1), the heating procedure of oxidizing Cr20Mn17Fe18Ta23W22 at 300 °C (6 °C/min) for 2 h and then increased to 800 °C (5 °C/min) for 4 h is more conducive to the production of oxides without spalling on the surface, i.e., HT1 (Ar:O2 = 1:1), HT2 (Ar:O2 = 2:1) and HT3 (Ar:O2 = 3:1) samples. The oxidation of Cr20Mn17Fe18Ta23W22 RHEA is mainly controlled by the diffusion of cations instead of affinities with O. Additionally, HT1 and HT3 samples irradiated with a fluence of 3.9 × 1022 cm-2 hydrogen ions (60 eV) were found to have a better hydrogen irradiation resistance than Cr20Mn17Fe18Ta23W22 RHEA. The microdefects in irradiated Cr20Mn17Fe18Ta23W22 mainly existed as hydrogen bubbles, hydrogen-vacancy (H-V) complexes and vacancy/vacancy clusters. The microdefects in irradiated HT3 were mainly vacancies and H-V complexes, while the microdefects in irradiated HT1 mainly existed as vacancies and vacancy clusters, as large amounts of hydrogen were consumed to react with oxides on the HT1 surface. The oxides on the surface of the HT3 sample were more stable than those on HT1 under hydrogen irradiation.

A (U)MP2(full) and (U)CCSD(T) theoretical investigation into the substituent effects on the intermolecular T-shaped F-H...π interactions between HF and LBBL (L = -H, : CO, :NN, -Cl, -CN and -NC).

The substituent effects on the intermolecular T-shaped F-H...π interactions are investigated between HF and LBBL (L = -H, : CO, :NN, -Cl, -CN and -NC) using the (U)MP2(full) and (U)CCSD(T) methods with the 6-311++G(2 d,p) basis set. The B ≡ B triple-bond contraction is found in the complexes with lone-pair-electron donors while the B = B double-bond is lengthened in the systems with the single-electron substituents upon complexation. The T-shaped F-H...π interaction energies follow the order of ClB = BCl...HF>HB = BH...HF>NNB ≡ BNN...HF>OCB ≡ BCO...HF>CNB = BNC...HF>NCB = BCN...HF. The electron-donating substituents : CO and :NN increases electron density of the B ≡ B triple bond by the delocalization interaction E ((2)) π ((CO/NN) → Lp(B)) while the electron-withdrawing substituents -CN and -NC decrease electron density of the B = B double bond by means of the π-π conjugative effect. The analyses of the APT atomic charge, "truncated" model, natural bond orbital (NBO), atoms in molecules (AIM) and electron density shifts reveal the nature of the substituent effect and explain the origin of the B ≡ B bond contraction.