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Early-onset colorectal cancer (EOCRC) has been increasing worldwide. Potential risk factors may have occurred in childhood or adolescence. We investigated the associations between early-life factors and EOCRC risk, with a particular focus on long-term or recurrent antibiotic use (LRAU) and its interaction with genetic factors. Data on the UK Biobank participants recruited between 2006 and 2010 and followed up to February 2022 were used. We used logistic regression to estimate adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) of the associations between LRAU during early life and EOCRC risk overall and by polygenic risk score (constructed by 127 CRC-related genetic variants) and Fucosyltransferase 2 (FUT2), a gut microbiota regulatory gene. We also assessed the associations for early-onset colorectal adenomas, as precursor lesion of CRC, to examine the effect of LRAU during early-life and genetic factors on colorectal carcinogenesis. A total of 113 256 participants were included in the analysis, with 165 EOCRC cases and 719 EOCRA cases. LRAU was nominally associated with increased risk of early-onset CRC (OR = 1.48, 95% CI = 1.01-2.17, P = .046) and adenomas (OR = 1.40, 95% CI = 1.17-1.68, P < .001). When stratified by genetic polymorphisms of FUT2, LRAU appeared to confer a comparatively greater risk for early-onset adenomas among participants with rs281377 TT genotype (OR = 1.10, 95% CI = 0.79-1.52, P = .587, for CC genotype; OR = 1.75, 95% CI = 1.16-2.64, P = .008, for TT genotype; Pinteraction = .089). Our study suggested that LRAU during early life is associated with increased risk of early-onset CRC and adenomas, and the association for adenomas is predominant among individuals with rs281377 TT/CT genotype. Further studies investigating how LRAU contributes together with genetic factors to modify EOCRC risk, particularly concerning the microbiome-related pathway underlying colorectal carcinogenesis, are warranted.
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Adenoma , Neoplasias Colorretais , Humanos , Genótipo , Neoplasias Colorretais/genética , Fatores de Risco , Adenoma/genética , Carcinogênese , Galactosídeo 2-alfa-L-FucosiltransferaseRESUMO
BACKGROUND: Tobacco smoking is suggested as a risk factor for colorectal cancer (CRC), but the complex relationship and the potential pathway are not fully understood. METHODS: We performed two-sample Mendelian randomisation (MR) analyses with genetic instruments for smoking behaviours and related DNA methylation in blood and summary-level GWAS data of colorectal cancer to disentangle the relationship. Colocalization analyses and prospective gene-environment interaction analyses were also conducted as replication. RESULTS: Convincing evidence was identified for the pathogenic effect of smoking initiation on CRC risk and suggestive evidence was observed for the protective effect of smoking cessation in the univariable MR analyses. Multivariable MR analysis revealed that these associations were independent of other smoking phenotypes and alcohol drinking. Genetically predicted methylation at CpG site cg17823346 [ZMIZ1] were identified to decrease CRC risk; while genetically predicted methylation at cg02149899 would increase CRC risk. Colocalization and gene-environment interaction analyses added further evidence to the relationship between epigenetic modification at cg17823346 [ZMIZ1] as well as cg02149899 and CRC risk. DISCUSSION: Our study confirms the significant association between tobacco smoking, DNA methylation and CRC risk and yields a novel insight into the pathogenic effect of tobacco smoking on CRC risk.
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Neoplasias Colorretais , Fumar , Humanos , Fumar/efeitos adversos , Metilação de DNA , Estudos Prospectivos , Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Fumar Tabaco , Estudo de Associação Genômica Ampla , Polimorfismo de Nucleotídeo ÚnicoRESUMO
BACKGROUND: We performed phenome-wide Mendelian randomization analysis (MR-PheWAS), two-sample MR analysis, and systemic review to comprehensively explore the health effects of milk consumption in the European population. METHODS: Rs4988235 located upstream of the LCT gene was used as the instrumental variable for milk consumption. MR-PheWAS analysis was conducted to map the association of genetically predicted milk consumption with 1081 phenotypes in the UK Biobank study (n=339,197). The associations identified in MR-PheWAS were examined by two-sample MR analysis using data from the FinnGen study (n=260,405) and international consortia. A systematic review of MR studies on milk consumption was further performed. RESULTS: PheWAS and two-sample MR analyses found robust evidence in support of inverse associations of genetically predicted milk consumption with risk of cataract (odds ratio (OR) per 50 g/day increase in milk consumption, 0.89, 95% confidence interval (CI), 0.84-0.94; p=3.81×10-5), hypercholesterolemia (OR, 0.91, 95% CI 0.86-0.96; p=2.97×10-4), and anal and rectal polyps (OR, 0.85, 95% CI, 0.77-0.94; p=0.001). An inverse association for type 2 diabetes risk (OR, 0.92, 95% CI, 0.86-0.97; p=0.003) was observed in MR analysis based on genetic data with body mass index adjustment but not in the corresponding data without body mass index adjustment. The systematic review additionally found evidence that genetically predicted milk consumption was inversely associated with asthma, hay fever, multiple sclerosis, colorectal cancer, and Alzheimer's disease, and positively associated with Parkinson's disease, renal cell carcinoma, metabolic syndrome, overweight, and obesity. CONCLUSIONS: This study suggests several health effects of milk consumption in the European population.
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Diabetes Mellitus Tipo 2 , Neoplasias Renais , Humanos , Animais , Análise da Randomização Mendeliana , Leite , Diabetes Mellitus Tipo 2/epidemiologia , Polimorfismo de Nucleotídeo ÚnicoRESUMO
The environmental toxicity of Pb in organic-inorganic hybrid perovskite solar cells remains an issue, which has triggered intense research on seeking alternative Pb-free perovskites for solar applications. Halide perovskites based on group-VA cations of Bi3+ and Sb3+ with the same lone-pair ns2 state as Pb2+ are promising candidates. Herein, through a joint experimental and theoretical study, we demonstrate that Cl-incorporated methylammonium Sb halide perovskites (CH3NH3)3Sb2ClXI9-X show promise as efficient solar absorbers for Pb-free perovskite solar cells. Inclusion of methylammonium chloride into the precursor solutions suppresses the formation of the undesired zero-dimensional dimer phase and leads to the successful synthesis of high-quality perovskite films composed of the two-dimensional layered phase favored for photovoltaics. Solar cells based on the as-obtained (CH3NH3)3Sb2ClXI9-X films reach a record-high power conversion efficiency over 2%. This finding offers a new perspective for the development of nontoxic and low-cost Sb-based perovskite solar cells.
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Organometal halide perovskites have shown excellent optoelectronic properties and have been used to demonstrate a variety of semiconductor devices. Colorful solar cells are desirable for photovoltaic integration in buildings and other aesthetically appealing applications. However, the realization of colorful perovskite solar cells is challenging because of their broad and large absorption coefficient that commonly leads to cells with dark-brown colors. Herein, for the first time, we report a simple and efficient strategy to achieve colorful perovskite solar cells by using the transparent conducting polymer (poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate), PEDOT:PSS) as a top electrode and simultaneously as an spectrally selective antireflection coating. Vivid colors across the visible spectrum are attained by engineering optical interference effects among the transparent PEDOT:PSS polymer electrode, the hole-transporting layer and the perovskite layer. The colored perovskite solar cells display power conversion efficiency values from 12.8 to 15.1% (from red to blue) when illuminated from the FTO glass side and from 11.6 to 13.8% (from red to blue) when illuminated from the PEDOT:PSS side. The new approach provides an advanced solution for fabricating colorful perovskite solar cells with easy processing and high efficiency.
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Thick, uniform, easily processed, highly conductive polymer films are desirable as electrodes for solar cells as well as polymer capacitors. Here, a novel scalable strategy is developed to prepare highly conductive thick poly(3,4-ethylenedioxythiophene):polystyrene sulfonate (HCT-PEDOT:PSS) films with layered structure that display a conductivity of 1400â S cm(-1) and a low sheet resistance of 0.59â ohm sq(-1). Organic solar cells with laminated HCT-PEDOT:PSS exhibit a performance comparable to the reference devices with vacuum-deposited Ag top electrodes. More importantly, the HCT-PEDOT:PSS film delivers a specific capacitance of 120â F g(-1) at a current density of 0.4â A g(-1). All-solid-state flexible symmetric supercapacitors with the HCT-PEDOT:PSS films display a high volumetric energy density of 6.80â mWh cm(-3) at a power density of 100â mW cm(-3) and 3.15â mWh cm(-3) at a very high power density of 16160â mW cm(-3) that outperforms previous reported solid-state supercapacitors based on PEDOT materials.
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We report perovskite solar cells with a new device structure that employ highly conductive polymer poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) ( PEDOT: PSS) as the top electrode replacing commonly used metal electrodes. The PEDOT: PSS top electrode is prepared from its aqueous solution through a transfer-lamination technique rather than direct spin-coating, which converts the CH(3)NH(3)PbI(3) into PbI(2). Perovskite solar cells with the structure of glass/FTO/c-TiO(2)/m-TiO(2)/CH(3)NH(3)PbI(3)/spiro-OMeTAD/PEDOT:PSS yield a maximum open-circuit voltage (V(OC)) of 1.02 V, and a maximum power conversion efficiency (PCE) of 11.29% under AM1.5 100 mW/cm(2) illumination. The whole device was fabricated in air without high-vacuum deposition which simplifies the processing and lowers the threshold of both scientific research and industrial production of perovskite solar cells.
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BACKGROUND: Elevated allostatic load (AL) has been associated with the risk and poor prognosis of many chronic diseases. The association between AL and inflammatory bowel disease (IBD) is unknown. AIMS: The aim of this study is to investigate the associations between AL and the risk and prognosis of IBD. METHODS: We included 326,345 adults and 3767 patients with IBD from the UK Biobank. AL served as the exposure, estimated using the AL biomarker panel, with the primary outcomes including the risk and prognosis of IBD. We used Cox regression models to examine the associations. RESULTS: High AL biomarker panel was associated with a greater risk of IBD (hazard ratio: 1.19, 95% CI: 1.08-1.31), ulcerative colitis (1.17, 95%CI: 1.04-1.32), and Crohn's disease (1.25, 95%CI: 1.05-1.49). Risk of developing IBD increased by 12% in quartile 2, 20% in quartile 3, and 37% in quartile 4 as AL biomarker panel increased. The all-cause mortality risk in IBD compared with quartile 1 rose by 54% for quartile 2, 72% for quartile 3, and 82% for quartile 4, as AL biomarker panel increased. Similar effects were also observed for ulcerative colitis and Crohn's disease. An increase in AL biomarker panel count was associated with an elevated risk of intestinal resection and colorectal cancer in IBD. CONCLUSIONS: Increased AL is associated with IBD risk, as well as the risks of intestinal resection, colorectal cancer and mortality.
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Alostase , Biomarcadores , Doenças Inflamatórias Intestinais , Humanos , Masculino , Feminino , Alostase/fisiologia , Pessoa de Meia-Idade , Prognóstico , Adulto , Doenças Inflamatórias Intestinais/fisiopatologia , Reino Unido/epidemiologia , Incidência , Fatores de Risco , Idoso , Doença de Crohn/fisiopatologia , Colite Ulcerativa/fisiopatologia , Modelos de Riscos ProporcionaisRESUMO
BACKGROUND: Dietary advanced glycation end products (AGEs) may promote oxidative stress and inflammation in the gastrointestinal tract. AIMS: The aim of this study is to investigate the association between dietary AGE intake and the risk of inflammatory bowel disease (IBD). METHODS: We included 121,978 participants without IBD at baseline from the UK Biobank. We estimated consumption of three common AGEs (Nε-(carboxymethyl)-lysine (CML), Nε-(1-carboxyethyl)-lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1)) by matching 24-h dietary questionnaires to a validated dietary AGE database. We used Cox proportional hazards regression models to calculate the hazard ratio (HR) and 95% CI of the association between dietary AGEs and IBD risk. RESULTS: During a median follow-up of 13.72 years, 671 participants developed IBD (192 with Crohn's disease (CD) and 478 with ulcerative colitis (UC)). Among the assessed dietary AGEs, only CEL was associated with an increased risk of IBD (HR = 1.09, 95% CI: 1.01-1.18, p = 0.020) and CD (HR = 1.18, 95% CI: 1.03-1.36, p = 0.014), particularly for participants who were overweight, physically inactive, and non-smokers. Among participants at a high genetic risk of CD, HRs (95% CI) of CD were 1.26 (1.00-1.57) for CML, 1.41 (1.12-1.77) for CEL, and 1.28 (1.01-1.62) for MG-H1 (p < 0.05 for each). However, none of the dietary AGEs was significantly associated with UC risk, irrespective of genetic predisposition. CONCLUSIONS: Dietary CEL was associated with an increased risk of IBD and CD, but not UC. Further interventional studies are required to support the potential benefit of AGE restriction, especially for individuals at a high genetic risk of CD.
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Dieta , Produtos Finais de Glicação Avançada , Humanos , Feminino , Masculino , Estudos Prospectivos , Pessoa de Meia-Idade , Dieta/efeitos adversos , Adulto , Fatores de Risco , Reino Unido/epidemiologia , Doenças Inflamatórias Intestinais/genética , Lisina , Predisposição Genética para Doença , Idoso , Doença de Crohn/genética , Estudos de Coortes , Colite Ulcerativa/genética , Modelos de Riscos ProporcionaisRESUMO
BACKGROUND: The proteome is an important reservoir of potential therapeutic targets for cancer. This study aimed to examine the causal associations between plasma proteins and cancer risk and to identify proteins with cross-cancer effects. METHODS: Genetic instruments for 3991 plasma proteins were extracted from a large-scale proteomic study. Summary-level data of 13 site-specific cancers were derived from publicly available datasets. Proteome-wide Mendelian randomization and colocalization analyses were used to investigate the causal effect of circulating proteins on cancers. Protein-protein interactions and druggability assessment were conducted to prioritize potential therapeutic targets. Finally, systematical Mendelian randomization analysis between healthy lifestyle factors and cancer-related proteins was conducted to identify which proteins could act as interventional targets by lifestyle changes. RESULTS: Genetically determined circulating levels of 58 proteins were statistically significantly associated with 7 site-specific cancers. A total of 39 proteins were prioritized by colocalization, of them, 11 proteins (ADPGK, CD86, CLSTN3, CSF2RA, CXCL10, GZMM, IL6R, NCR3, SIGLEC5, SIGLEC14, and TAPBP) were observed to have cross-cancer effects. Notably, 5 of these identified proteins (CD86, CSF2RA, CXCL10, IL6R, and TAPBP) have been targeted for drug development in cancer therapy; 8 proteins (ADPGK, CD86, CXCL10, GZMM, IL6R, SIGLEC5, SIGLEC14, TAPBP) could be modulated by healthy lifestyles. CONCLUSION: Our study identified 39 circulating protein biomarkers with convincing causal evidence for 7 site-specific cancers, with 11 proteins demonstrating cross-cancer effects, and prioritized the proteins as potential intervention targets by either drugs or lifestyle changes, which provided new insights into the etiology, prevention, and treatment of cancers.
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Neoplasias , Proteoma , Humanos , Proteômica , Desenvolvimento de Medicamentos , Estilo de Vida Saudável , Análise da Randomização Mendeliana , Neoplasias/tratamento farmacológico , Neoplasias/epidemiologia , Neoplasias/genética , Proteínas Sanguíneas , Estudo de Associação Genômica Ampla , Polimorfismo de Nucleotídeo Único , Proteínas de Ligação ao Cálcio , Proteínas de MembranaRESUMO
Large prospective studies are required to better elucidate the associations of physical activity, sedentary behaviors (SBs), and sleep with overall cancer and site-specific cancer risk, accounting for the interactions with genetic predisposition. The study included 360,271 individuals in UK Biobank. After a median follow-up of 12.52 years, we found higher total physical activity (TPA) level and higher sleep scores were related to reduced risk of cancer while higher SB level showed a positive association with cancer. Compared with high TPA-healthy sleep group and low SB-healthy sleep group, low TPA-poor sleep group and high SB-poor sleep group had the highest risk for overall cancer, breast cancer, and lung cancer. Adherence to a more active exercise pattern was associated with a lower risk of cancer irrespective of genetic risk. Our study suggests that improving the quality of sleep and developing physical activity habits might yield benefits in mitigating the cancer risk.
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BACKGROUND: Coeliac disease (CeD) has been associated with a broad range of diseases in observational data; however, whether these associations are causal remains undetermined. We conducted a phenome-wide Mendelian randomization analysis (MR-PheWAS) to investigate the comorbidities of CeD. METHODS: Single nucleotide polymorphisms (SNPs) associated with CeD at the genome-wide significance threshold and without linkage disequilibrium (R2 <0.001) were selected from a genome-wide association study including 12,041 CeD cases as the instrumental variables. We first constructed a polygenic risk score for CeD and estimated its associations with 1060 unique clinical outcomes in the UK Biobank study (N = 385,917). We then used two-sample MR analysis to replicate the identified associations using data from the FinnGen study (N = 377,277). We performed a secondary analysis using a genetic instrument without extended MHC gene SNPs. FINDINGS: Genetic liability to CeD was associated with 68 clinical outcomes in the UK Biobank, and 38 of the associations were replicated in the FinnGen study. Genetic liability to CeD was associated with a higher risk of several autoimmune diseases (type 1 diabetes and its complications, Graves' disease, Sjögren syndrome, chronic hepatitis, systemic and cutaneous lupus erythematosus, and sarcoidosis), non-Hodgkin's lymphoma, and osteoporosis and a lower risk of prostate diseases. The associations for type 1 diabetes and non-Hodgkin's lymphoma attenuated when excluding SNPs in the MHC region, indicating shared genetic aetiology. INTERPRETATION: This study uncovers multiple clinical outcomes associated with genetic liability to CeD, which suggests the necessity of comorbidity monitoring among this population. FUNDING: This project was funded by Karolinska Institutet and the Swedish Research Council.
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BACKGROUND: This study investigates the associations between air pollution and colorectal cancer (CRC) risk and survival from an epigenomic perspective. METHODS: Using a newly developed Air Pollutants Exposure Score (APES), we utilized a prospective cohort study (UK Biobank) to investigate the associations of individual and combined air pollution exposures with CRC incidence and survival, followed by an up-to-date systematic review with meta-analysis to verify the associations. In epigenetic two-sample Mendelian randomization analyses, we examine the associations between genetically predicted DNA methylation related to air pollution and CRC risk. Further genetic colocalization and gene-environment interaction analyses provided different insights to disentangle pathogenic effects of air pollution via epigenetic modification. FINDINGS: During a median 12.97-year follow-up, 5767 incident CRC cases among 428,632 participants free of baseline CRC and 533 deaths in 2401 patients with CRC were documented in the UK Biobank. A higher APES score was associated with an increased CRC risk (HR, 1.03, 95% CI = 1.01-1.06; P = 0.016) and poorer survival (HR, 1.13, 95% CI = 1.03-1.23; P = 0.010), particularly among participants with insufficient physical activity and ever smokers (Pinteraction > 0.05). A subsequent meta-analysis of seven observational studies, including UK Biobank data, corroborated the association between PM2.5 exposure (per 10 µg/m3 increment) and elevated CRC risk (RR,1.42, 95% CI = 1.12-1.79; P = 0.004; I2 = 90.8%). Genetically predicted methylation at PM2.5-related CpG site cg13835894 near TMBIM1/PNKD and cg16235962 near CXCR5, and NO2-related cg16947394 near TMEM110 were associated with an increased CRC risk. Gene-environment interaction analysis confirmed the epigenetic modification of aforementioned CpG sites with CRC risk and survival. INTERPRETATION: Our study suggests the association between air pollution and CRC incidence and survival, underscoring the possible modifying roles of epigenomic factors. Methylation may partly mediate pathogenic effects of air pollution on CRC, with annotation to epigenetic alterations in protein-coding genes TMBIM1/PNKD, CXCR5 and TMEM110. FUNDING: Xue Li is supported by the Natural Science Fund for Distinguished Young Scholars of Zhejiang Province (LR22H260001), the National Nature Science Foundation of China (No. 82204019) and Healthy Zhejiang One Million People Cohort (K-20230085). ET is supported by a Cancer Research UK Career Development Fellowship (C31250/A22804). MGD is supported by the MRC Human Genetics Unit Centre Grant (U127527198).
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Poluição do Ar , Neoplasias Colorretais , Metilação de DNA , Epigênese Genética , Análise da Randomização Mendeliana , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Neoplasias Colorretais/genética , Neoplasias Colorretais/mortalidade , Neoplasias Colorretais/etiologia , Exposição Ambiental/efeitos adversos , Epigenômica/métodos , Interação Gene-Ambiente , Incidência , Estudos Prospectivos , Fatores de RiscoRESUMO
BACKGROUND: The global burden of metabolic dysfunction-associated steatotic liver disease (MASLD) is growing, but its subsequent health consequences have not been thoroughly examined. METHODS: A phenome-wide association study was conducted to map the associations of MASLD with 948 unique clinical outcomes among 361,021 Europeans in the UK Biobank. Disease trajectory and comorbidity analyses were applied to visualize the sequential patterns of multiple comorbidities related to the occurrence of MASLD. The associations jointly verified by observational and polygenic phenome-wide analyses were further replicated by two-sample Mendelian randomization analysis using data from the FinnGen study and international consortia. FINDINGS: The observational and polygenic phenome-wide association study revealed the associations of MASLD with 96 intrahepatic and extrahepatic diseases, including circulatory, metabolic, genitourinary, neurological, gastrointestinal, and hematologic diseases. Sequential patterns of MASLD-related extrahepatic comorbidities were primarily found in circulatory, metabolic, and inflammatory diseases. Mendelian randomization analyses supported the causal associations between MASLD and the risk of several intrahepatic disorders, metabolic diseases, cardio-cerebrovascular disease, and ascites but found no associations with neurological diseases. CONCLUSIONS: This study elucidated multisystem comorbidities and health consequences of MASLD, contributing to the development of combination interventions targeting distinct pathways for health promotion among patients with MASLD. FUNDING: X.L. was funded by the Natural Science Fund for Distinguished Young Scholars of Zhejiang Province (LR22H260001) and the National Nature Science Foundation of China (82204019) and Y.D. was funded by the Key Project of Traditional Chinese Medicine Science and Technology Plan of Zhejiang Province (GZY-ZJ-KJ-24077) and the National Natural Science Foundation of China (82001673 and 82272860).
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BACKGROUND: Metabolic dysfunction-associated fatty liver disease (MAFLD) is a significant health problem. Dietary intervention plays an important role in patients with MAFLD. OBJECTIVES: We aimed to provide a reference for dietary patterns in patients with MAFLD. METHODS: The presence of MAFLD was determined in the United Kingdom Biobank cohort. Nine dietary pattern scores were derived from the dietary records. Multivariable Cox regression models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs). The contrast test was employed to calculate the heterogeneity across MAFLD statuses. RESULTS: We identified 175,300 patients with MAFLD at baseline. Compared with non-MAFLD, MAFLD was significantly associated with chronic liver disease (CLD) (HR: 3.48; 95% CI: 3.15, 3.84), severe liver disease (SLD) (HR: 2.87; 95% CI: 2.63, 3.14), liver cancer (HR: 1.93; 95% CI: 1.67, 2.23), and liver-related death (LRD) (HR: 1.93; 95% CI: 1.67, 2.23). In the overall cohort, the alternate Mediterranean diet (aMED) (HRCLD: 0.53; 95% CI: 0.37, 0.76; HRSLD: 0.52; 95% CI: 0.37, 0.72), planetary health diet (PHD) (HRCLD: 0.62; 95% CI: 0.47, 0.81; HRSLD: 0.65; 95% CI: 0.51, 0.83), plant-based low-carbohydrate diet (pLCD) (HRCLD: 0.65; 95% CI: 0.49, 0.86; HRSLD: 0.66; 95% CI: 0.51, 0.85), and healthful plant-based diet index (hPDI) (HRCLD: 0.63; 95% CI: 0.47, 0.84; HRSLD: 0.61; 95% CI: 0.47, 0.78) were associated with a lower risk of CLD and SLD. Additionally, unhealthful plant-based diet index (uPDI) was associated with increased risk of CLD (HR: 1.42; 95% CI: 1.09,1.85), SLD (HR: 1.50; 95% CI: 1.19, 1.90), and LRD (HR: 1.88; 95% CI: 1.28-2.78). The aforementioned associations remained consistently strong within the MAFLD subgroup while exhibiting less pronounced in the non-MAFLD group. However, no significant heterogeneity was observed across different MAFLD statuses. CONCLUSIONS: These findings highlight the detrimental effects of MAFLD on the development of subsequent liver diseases and the importance of dietary patterns in managing MAFLD.
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Dieta , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Estudos Prospectivos , Idoso , Estudos de Coortes , Adulto , Reino Unido/epidemiologia , Progressão da Doença , Fígado Gorduroso/etiologia , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatias/etiologia , Hepatopatias/epidemiologia , Padrões DietéticosRESUMO
In this work, we study the kinetics of photoinduced halide migration in FA0.8Cs0.2Pb(I0.8Br0.2)3 wide (â¼1.69 eV) bandgap perovskites and show that halide migration slows down following surface passivation with (3-aminopropyl) trimethoxysilane (APTMS). We use scanning Kelvin probe microscopy (SKPM) to probe the contact potential difference (CPD) shift under illumination and the kinetics of surface potential relaxation in the dark. Our results show that APTMS-passivated perovskites exhibit a smaller CPD shift under illumination and a slower surface potential relaxation in the dark. We compare the evolution of the photoluminescence spectra of APTMS-passivated and unpassivated perovskites under illumination. We find that APTMS-passivated perovskites exhibit more than 5 times slower photoluminescence red-shift, consistent with the slower surface potential relaxation as observed by SKPM. These observations provide evidence for kinetic suppression of photoinduced halide migration in APTMS-passivated samples, likely due to reduced halide vacancy densities, opening avenues to more efficient and stable devices.
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Solar-driven interfacial evaporation has been considered one of the most promising approaches to tackle the issue of water scarcity. The salt resistance and water transport capacity of solar evaporation materials are essential to evaluate desalination performance. Herein, a 3D-porous N-doped lignosulfonate/graphene oxide (GO) aerogel (NLGA) was facilely prepared by a one-step hydrothermal method. By introducing ethylenediamine (EDA) as a nitrogen source, the wettability and water transport capacity of the aerogel were enhanced; by introducing lignosulfonate (LS), its porous structure was regulated, and its light absorption capability was significantly improved. The obtained aerogel exhibited an outstanding evaporation rate (1.57 kg m-2 h-1) and efficiency (95.2 %) under 1 sun illumination, which is significantly better than some reported foam-based solar evaporators. In addition, NLGA maintained a stable evaporation rate over long-term cyclic evaporation without visible salt accumulation on the surface. The good salt rejection performance is due to the rich-pore structure and superhydrophilicity of NGLA, which provides sufficient water supply to dissolve the salts during water evaporation. NLGA has enormous potential as a solar evaporator based on its excellent performance in solar vapor generation.
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Vapor , Água , Porosidade , Cloreto de SódioRESUMO
The presence of multiple pollutants in wastewater, often with complex interactions, poses a significant challenge for conventional membranes to effectively remove multiple pollutants simultaneously. Herein, a lignin microparticles-reinforced cellulose filter paper (FP@AL-LS-DA) was fabricated via an aldol condensation between lignin and cellulose filter paper and cross-linking with dopamine hydrochloride (DA), which showed desired rejection of oil-in-water emulsions and dyes. Characterizations revealed that the addition of lignin and DA effectively narrowed the pore size (from 4.45 µm to 2.01 µm) and enhanced the rigidity and stability of the cellulose filter paper, thus making it not easily damaged in the water environment and showing excellent tolerance to strong acid and high-salt environments. The oil-in-water emulsions removal efficiency was higher than 99 % even after ten times usage, and the oil flux was kept stable at 52.54 L·m-2·h-1, indicating that FP@AL-LS-DA had outstanding reusability and stability. Remarkably, FP@AL-LS-DA showed excellent removal efficiency (>99 %) for complex pollutants containing dyes and oil-in-water emulsions. In this work, we demonstrate a lignin microparticles-reinforced cellulose filter paper that is simple to prepare and can efficiently separate oil-in-water emulsions and remove dyes.
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Celulose , Poluentes Ambientais , Lignina , Corantes , Óleos , Água , EmulsõesRESUMO
A new N, S-CQDs@Fe3O4@HTC composite was prepared by loading N, S carbon quantum dots (N, S-CQDs) derived from lignin on magnetic hydrotalcite (HTC) via an in-situ growth method. The characterization results showed that the catalyst had a mesoporous structure. These pores facilitate the diffusion and mass transfer of pollutant molecules inside the catalyst, allowing them to approach the active site smoothly. The catalyst performed well in the UV degradation of Congo red (CR) over a wide pH range (3-11), with efficiencies over 95.43 % in all cases. Even at a high NaCl content (100 g/L), the catalyst showed extraordinary CR degradation (99.30 %). ESR analysis and free radical quenching experiments demonstrated that OH and O2- were the main active species governing CR degradation. Besides, the composite had outstanding removal efficiency for Cu2+ (99.90 %) and Cd2+ (85.08 %) simultaneously due to the electrostatic attraction between the HTC and metal ions. Moreover, the N, S-CQDs@Fe3O4@HTC had excellent stability and recyclability during five cycles, making it free of secondary contamination. This work provides a new environment-friendly catalyst for the simultaneous removal of multiple pollutants and a waste-to-waste strategy for the value-added utilization of lignin.