Search

Different combinations of normalizing and tempering were carried out to optimize the microstructure and enhance the high-temperature mechanical properties of HRB400FR fire-resistant steel bars. The results showed that with the increasing of the tempering temperature from 400 to 600°C, the steel bar’s hardness decreases linearly, mainly due to the formation of quasi-polygon ferrite and granular bainite. Besides, the reduced width and the dissolution of the lath bainite also undermine the performance of the tempered steel bars. The highest Vickers hardness of 380 HV is achieved when the steel is normalized at 950°C and then tempered at 400°C, mainly due to precipitation strengthening and bainite strengthening. The hardness of the test steel tempered at 600°C gives the lowest value, only 230 HV since the least amount of bainite is obtained. When the tempering temperature reaches 650°C, the hardness rises to 260 HV due to the formation of the lath bainite. The emergence of needle bainite generally reduces the matrix grain size, and the appearance of lath martensite refines the precipitated carbides.

Aim: The association of overweight/obesity and metabolic dysfunction‐associated steatotic liver disease (MASLD) in young adulthood with subclinical atherosclerosis [coronary artery calcification (CAC) and abdominal aortic calcification (AAC)] by middle age is unknown. Method: In total, 2274 participants aged 28‐39 years from the coronary artery risk development in young adults study at year 10 (1995‐1996) who were re‐examined 15 years later were included. CAC and AAC were measured at year 25 using computed tomography. We examined the utility of three young adult phenotypes (lean group; overweight/obese group; overweight/obese MASLD group) at year 10 in predicting CAC or AAC by middle age. Modified Poisson regression was used to estimate the association between groups and CAC, and AAC. Independent determinates of CAC and AAC were determined with linear regression models. Results: Compared with individuals categorized as lean in young adulthood, the relative risk for CAC by middle age was 1.09 (95% confidence interval: 0.93‐1.28) for those with overweight/obesity and 1.32 (95% confidence interval: 1.08‐1.61) for those with overweight/obesity‐related MASLD. For AAC, no difference was observed between these three groups. Group, systolic blood pressure and group × systolic blood pressure interaction were all the independent determinates for CAC. Conclusion: In this study, young adults with overweight/obesity‐related MASLD have a higher risk of developing CAC by middle age. These abnormalities are only partially explained by traditional cardiovascular risk factors, and overweight/obesity‐related MASLD has an independent impact on CAC. Our study provides evidence for identifying young adults at higher risk of developing subclinical atherosclerosis. [ABSTRACT FROM AUTHOR]

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) increases the risk of cardiovascular disease and existing evidence indicates that MASLD affects the cardiovascular system through systemic inflammation. Our aim was to assess the association of hematological biomarkers of inflammation with the 10-year risk of major adverse cardiovascular events (MACE) and all-cause mortality in MASLD patients. Methods: A total of 1858 MASLD participants from the Atherosclerosis Risk in Communities cohort study at visit 2 (1990– 1992) were included. A total of 1338 non-MASLD participants were also included in the comparison. At baseline, hematological biomarkers of inflammation such as leukocytes, neutrophils, lymphocytes, monocytes, and C-reactive protein (CRP) were measured. Participants were followed up for MACE and all-cause mortality for a period of 10 years. Multivariate adjusted Cox models were used to estimate hazard ratios (HR). Results: The 10-year MACE was higher in MASLD participants than in non-MASLD participants (20.8% vs 9.3%). Monocytes (HR 1.114, [95% CI, 1.022– 1.216] per 1-SD, P=0.015) and CRP (HR 1.109 [95% CI, 1.032– 1.190] per 1-SD, P=0.005) were associated with an increased 10-year risk of MACE, independent of other cardiovascular risk factors. This association was specific to the MASLD population. None of these hematological biomarkers demonstrated a significant association with 10-year all-cause mortality. Conclusion: Increased levels of monocytes and CRP were associated with an increased 10-year risk of MACE in the MASLD population. Hematological biomarkers of inflammation may help identify MASLD populations at higher risk for cardiovascular events. [ABSTRACT FROM AUTHOR]