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Exploring appropriate carbonisation process parameters is important for optimising the recycling of waste bamboo chopsticks as an alternative solid fuel for traditional ironmaking. The purpose of this research was to reveal the influence of the pyrolysis temperature on the structural features and combustion behaviour of waste bamboo chopstick chars. The fixed carbon content of waste bamboo chopstick chars increased from 46.57% to 82.83% and the volatile content decreased from 56.43% to 6.86% with pyrolysis temperature increasing from 573 to 973 K. At the same time, the O/C and H/C values gradually decreased from 0.23 to 0.08 and from 0.05 to 0.02, respectively. The surface area of waste bamboo chopstick chars first increased sharply from 2.15 m2/g at 773 K to 11.04 m2/g at 873 K, and then decreased to 1.96 m2/g at 973 K. The combustion behaviour had a close relationship with the pore structure of waste bamboo chopstick chars, and the best combustion properties were exhibited at a pyrolysis temperature of 873 K. It was found that volumetric model was the most suitable model for describing the combustion process of waste bamboo chopstick chars pyrolysed below 673 K, while random pore model was the best one for the chars pyrolysed above 673 K. The combustion activation energies of the waste bamboo chopstick chars ranged from 116.89 to 156.07 kJ/mol. There was an obvious kinetic compensation effect during the combustion.

Ferro-coke, as a new burden of blast furnace (BF), can not only greatly reduce the energy consumption and CO2 emission, but also promote the resource utilization by using the low-quality iron ore and low-grade coal. However, the strength of ferro-coke decreased with the increasing amount of iron ore powder. In order to maintain the strength of ferro-coke while increasing the amount of iron ore powder, it is necessary to add binder during the coking process to enhance the strength of ferro-coke. In this paper, phenolic resin, silicon metal powder, corn starch, and coal tar pitch were used as binder for the fabrication of ferro-coke. I-type drum machine (I 600), scanning electron microscope (SEM), and X-ray diffraction (XRD) were applied to test the crushing strength, morphology, and microcrystalline structure of the ferro-coke. The results showed that the increasing amount of iron ore powder resulted in lower crushing strength, higher porosity, and the worse macroscopic morphology of ferro-coke. When the amount of iron ore powder reached 40%, obvious cracks appeared on the surface of ferro-coke. When the amount of iron ore was 30%, the crushing strength of ferro-coke dropped to 18.15%. Among the four binders, coal tar pitch could significantly enhance the cold crushing strength of ferro-coke through decreasing the porosity of ferro-coke and improving the bonding effect between carbon matrix particles. In the case of the 10% coal tar pitch addition, the cold crushing strength of ferro-coke was increased from 18.15% to 76.41%; meanwhile, its hot compression strength during gasification improved by 100N.

There is increasing evidence that HFpEF is a heterogeneous clinical entity and distinct molecular pathways may contribute to pathophysiology. Leveraging unbiased proteomics to identify novel biomarkers, this study seeks to understand the underlying molecular mechanisms of HFpEF. The discovery cohort consisted of HFpEF cases and non-HF controls from the CATHGEN study (N = 176); the validation cohort consisted of participants from the TECOS trial of patients with diabetes (N = 109). Proteins associated with HFpEF were included in a LASSO model to create a discriminative multi-protein model and assessed in the validation cohort. Survival models and meta-analysis were used to test the association of proteins with incident clinical outcomes, including HF hospitalization, mortality and HFpEF hospitalization in CATHGEN, TECOS and the Jackson Heart Study. In the derivation set, 190 proteins were associated with HFpEF in univariate analysis, of which 65 remained significant in the multivariate model. Twenty (30.8%) of these proteins validated in TECOS, including LCN2, U-PAR, IL-1ra, KIM1, CSTB and Gal-9 (OR 1.93–2.77, p  < 0.01). LASSO regression yielded a 13-protein model which, when added to a clinical model inclusive of NT-proBNP, improved the AUC from 0.82 to 0.92 ( p  = 1.5 × 10 –4 ). Five proteins were associated with incident HF hospitalization, four with HFpEF hospitalization and eleven with mortality ( p  < 0.05). We identified and validated multiple circulating biomarkers associated with HFpEF as well as HF outcomes. These biomarkers added incremental discriminative capabilities beyond clinical factors and NT-proBNP.

Regular exercise leads to widespread salutary effects, and there is increasing recognition that exercise-stimulated circulating proteins can impart health benefits. Despite this, limited data exist regarding the plasma proteomic changes that occur in response to regular exercise. Here, we perform large-scale plasma proteomic profiling in 654 healthy human study participants before and after a supervised, 20-week endurance exercise training intervention. We identify hundreds of circulating proteins that are modulated, many of which are known to be secreted. We highlight proteins involved in angiogenesis, iron homeostasis, and the extracellular matrix, many of which are novel, including training-induced increases in fibroblast activation protein (FAP), a membrane-bound and circulating protein relevant in body-composition homeostasis. We relate protein changes to training-induced maximal oxygen uptake adaptations and validate our top findings in an external exercise cohort. Furthermore, we show that FAP is positively associated with survival in 3 separate, population-based cohorts.

Abstract Context Thyroid hormones play an important role in metabolic homeostasis, and higher levels have been associated with cardiometabolic risk. Objective To examine the association of cardiometabolic risk factors with TSH levels in US youth. Methods Cross-sectional study of youth aged 12 to 18 years without known thyroid abnormalities from 5 National Health and Nutrition Examination Survey cycles (n = 2818) representing 15.4 million US children. Subclinical hypothyroidism (SH) was defined as thyrotropin (TSH) levels of 4.5 to 10 mIU/L. Assessed cardiometabolic risk factors include abdominal obesity (waist circumference >90th percentile), hypertriglyceridemia (triglyceride ≥130 mg/dL), low high-density lipoprotein cholesterol (<40 mg/dL), elevated blood pressure (systolic and diastolic blood pressure ≥90th percentile), hyperglycemia (fasting blood glucose ≥100 mg/dL, or known diabetes), insulin resistance (homeostatic model for insulin resistance > 3.16), and elevated alanine transferase (≥ 50 for boys and ≥44 U/L for girls). Age and sex- specific percentiles for thyroid parameters were calculated. Results In this cohort of youth (51.3% male), 31.2% had overweight/obesity. The prevalence of SH was 2.0% (95% CI 1.2-3.1). The median TSH levels were higher in youth with overweight/obesity (P < 0.001). Adjusting for age, sex, race/ethnicity, and obesity, youth with TSH in the fourth quantile had higher odds of abdominal obesity (OR 2.53 [1.43-4.46], P = .002), insulin resistance (OR 2.82 [1.42-5.57], P = .003), and ≥2 cardiometabolic risk factors (CMRF) (OR 2.20 [1.23-3.95], P = .009). Conclusion The prevalence of SH is low in US youth. The higher odds of insulin resistance and cardiometabolic risk factors in youth with TSH levels >75th percentile requires further study.

The use of omic modalities to dissect the molecular underpinnings of common diseases and traits is becoming increasingly common. But multi-omic traits can be genetically predicted, which enables highly cost-effective and powerful analyses for studies that do not have multi-omics 1 . Here we examine a large cohort (the INTERVAL study 2 ; n  = 50,000 participants) with extensive multi-omic data for plasma proteomics (SomaScan, n  = 3,175; Olink, n  = 4,822), plasma metabolomics (Metabolon HD4, n  = 8,153), serum metabolomics (Nightingale, n  = 37,359) and whole-blood Illumina RNA sequencing ( n  = 4,136), and use machine learning to train genetic scores for 17,227 molecular traits, including 10,521 that reach Bonferroni-adjusted significance. We evaluate the performance of genetic scores through external validation across cohorts of individuals of European, Asian and African American ancestries. In addition, we show the utility of these multi-omic genetic scores by quantifying the genetic control of biological pathways and by generating a synthetic multi-omic dataset of the UK Biobank 3 to identify disease associations using a phenome-wide scan. We highlight a series of biological insights with regard to genetic mechanisms in metabolism and canonical pathway associations with disease; for example, JAK–STAT signalling and coronary atherosclerosis. Finally, we develop a portal ( https://www.omicspred.org/ ) to facilitate public access to all genetic scores and validation results, as well as to serve as a platform for future extensions and enhancements of multi-omic genetic scores. A machine learning approach is used to analyse multi-omics (proteomics, metabolomics and transcriptomics) data, producing genetic scores for more than 17,000 biomolecular traits in human blood, and identifying possible associations with disease.

Despite the wide effects of cardiorespiratory fitness (CRF) on metabolic, cardiovascular, pulmonary and neurological health, challenges in the feasibility and reproducibility of CRF measurements have impeded its use for clinical decision-making. Here we link proteomic profiles to CRF in 14,145 individuals across four international cohorts with diverse CRF ascertainment methods to establish, validate and characterize a proteomic CRF score. In a cohort of around 22,000 individuals in the UK Biobank, a proteomic CRF score was associated with a reduced risk of all-cause mortality (unadjusted hazard ratio 0.50 (95% confidence interval 0.48–0.52) per 1 s.d. increase). The proteomic CRF score was also associated with multisystem disease risk and provided risk reclassification and discrimination beyond clinical risk factors, as well as modulating high polygenic risk of certain diseases. Finally, we observed dynamicity of the proteomic CRF score in individuals who undertook a 20-week exercise training program and an association of the score with the degree of the effect of training on CRF, suggesting potential use of the score for personalization of exercise recommendations. These results indicate that population-based proteomics provides biologically relevant molecular readouts of CRF that are additive to genetic risk, potentially modifiable and clinically translatable. A proteomic risk score for cardiorespiratory fitness, comprising as few as 21 proteins, is dynamic with exercise training and helps predict the risk of mortality and a range of cardiovascular, metabolic and neurological conditions.

Introduction: Subclinical hypothyroidism (SH) is defined as elevated TSH with normal thyroid levels, and is often associated with obesity. SH has been linked to cardiometabolic risk factors such as abnormal lipids, elevated blood pressure, atherosclerosis and fatty liver. This study sought to elucidate the association of TSH level with the components of metabolic syndrome independent of BMI in children from the National Health and Nutrition Examination Survey (NHANES). Methods: NHANES surveys 1999-01 and 2007-12 that measured thyroid function tests were included in the study. Youth aged 2-18 years with TSH levels < 10 uU/mL and normal Total T4 (TT4) levels were included in the analysis. The components of metabolic syndrome were defined as abdominal obesity (waist circumference > 95th %tile), hypertriglyceridemia (TG >=100 for 0-9 years and >=130 mg/dL for > 10 years), low HDL cholesterol < 40 mg/dL), elevated blood pressure (> 95th %tile for age/sex/height) and hyperglycemia (FBG > 100 mg/dL, or diagnosis of diabetes). The association of these components with quartiles of TSH were examined by logistic and linear regression controlling for age, sex, race/ethnicity and BMI. All analyses were performed in R v3.5.1. Results: After excluding youth with TSH >10 uU/mL and TT4 levels < 12.4 mcg/dL, 2377 subjects (50% female) were included in the study. The mean age of the cohort was 15 ± 1.7 years; 28.2 % were non-hispanic whites and 38.5 % hispanic/latino. Obesity (BMI >95 %tile) was seen in 21.7% individuals. There were 44 subjects with TSH levels >4.5 uU/mL that was not different by BMI (2.5% in BMI >95%tile and 1.7% BMI < 95%tile, p = 0.29). Based on the distribution in the population, TSH levels were divided into 4 quartiles: Q1= 0.01-0.97, Q2= 0.98-1.42, Q3=1.43-2.0, Q4 = > 2.01 uU/mL. A statistically significant association of the Q4 TSH was seen with abdominal obesity, OR 2.44 (1.38-4.39), p=0.002 and elevated BP, OR 1.6 (1.06-2.44), p = 0.02 but not with high TG, OR 1.58 (0.93-2.75), p=0.09, low HDL, OR 0.84 (0.6-1.17), p = 0.31 or those with hyperglycemia and/or diabetes, OR = 1.25 (0.78-2.05), p = 0.36. Linear regression models showed statistically significant association of abdominal obesity, hypertriglyceridemia, elevated BP and hyperglycemia (and/or diabetes) with increase in TSH level. Conclusions: In children from a representative US population, the prevalence of SH defined as TSH level >4.5 uU/mL is low, even with BMI >95th %tile. The association of measures of metabolic syndrome with linear increase in TSH suggests that the current reference range may require modification.

FUNDING. NIH K08 HL161445-01A1; 5T32HL160522-03; HHSN268201600034I; HL133870.

Metformin is a widely prescribed anti-diabetic medicine that also reduces body weight. There is ongoing debate about the mechanisms that mediate metformin’s effects on energy balance. Here, we show that metformin is a powerful pharmacological inducer of the anorexigenic metabolite N -lactoyl-phenylalanine (Lac-Phe) in cells, in mice and two independent human cohorts. Metformin drives Lac-Phe biosynthesis through the inhibition of complex I, increased glycolytic flux and intracellular lactate mass action. Intestinal epithelial CNDP2 + cells, not macrophages, are the principal in vivo source of basal and metformin-inducible Lac-Phe. Genetic ablation of Lac-Phe biosynthesis in male mice renders animals resistant to the effects of metformin on food intake and body weight. Lastly, mediation analyses support a role for Lac-Phe as a downstream effector of metformin’s effects on body mass index in participants of a large population-based observational cohort, the Multi-Ethnic Study of Atherosclerosis. Together, these data establish Lac-Phe as a critical mediator of the body weight-lowering effects of metformin. Metformin is shown to trigger production and release of Lac-Phe from gut epithelial cells, which is required for its effects on food intake and loss of body weight.