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1.
Environ Sci Technol ; 57(20): 7684-7697, 2023 05 23.
Artículo en Inglés | MEDLINE | ID: mdl-37167023

RESUMEN

Mounting evidence has shown that ambient PM2.5 exposure is closely associated with the development of obesity, and adipose tissue represents an important endocrine target for PM2.5. In this study, the 3T3-L1 preadipocyte differentiation model was employed to comprehensively explore the adipogenic potential of PM2.5. After 8 days of PM2.5 exposure, adipocyte fatty acid uptake and lipid accumulation were significantly increased, and adipogenic differentiation of 3T3-L1 cells was promoted in a concentration-dependent manner. Transcriptome and lipidome analyses revealed the systematic disruption of transcriptional and lipid profiling at 10 µg/mL PM2.5. Functional enrichment and visualized network analyses showed that the peroxisome proliferator-activated receptor (PPAR) pathway and the metabolism of glycerophospholipids, glycerolipids, and sphingolipids were most significantly affected during adipocyte differentiation. Reporter gene assays indicated that PPARγ was activated by PM2.5, demonstrating that PM2.5 promoted adipogenesis by activating PPARγ. The increased transcriptional and protein expressions of PPARγ and downstream adipogenesis-associated markers (e.g., Fabp4 and CD36) were further cross-validated using qRT-PCR and western blot. PM2.5-induced adipogenesis, PPARγ pathway activation, and lipid remodeling were significantly attenuated by the supplementation of a PPARγ antagonist (T0070907). Overall, this study yielded mechanistic insights into PM2.5-induced adipogenesis in vitro by identifying the potential biomolecular targets for the prevention of PM2.5-induced obesity and related metabolic diseases.


Asunto(s)
Adipogénesis , PPAR gamma , Animales , Ratones , PPAR gamma/genética , PPAR gamma/metabolismo , Células 3T3-L1 , Lípidos , Obesidad , Diferenciación Celular
2.
Ecotoxicol Environ Saf ; 256: 114852, 2023 May.
Artículo en Inglés | MEDLINE | ID: mdl-37023648

RESUMEN

Antimony (Sb) poses a significant threat to human health due to sharp increases in its exploitation and application globally, but few studies have explored the pathophysiological mechanisms of acute hepatotoxicity induced by Sb exposure. We established an in vivo model to comprehensively explore the endogenous mechanisms underlying liver injury induced by short-term Sb exposure. Adult female and male Sprague-Dawley rats were orally administrated various concentrations of potassium antimony tartrate for 28 days. After exposure, the serum Sb concentration, liver-to-body weight ratio, and serum glucose levels significantly increased in a dose-dependent manner. Body weight gain and serum concentrations of biomarkers of hepatic injury (e.g., total cholesterol, total protein, alkaline phosphatase, and the aspartate aminotransferase/alanine aminotransferase ratio) decreased with increasing Sb exposure. Through integrative non-targeted metabolome and lipidome analyses, alanine, aspartate, and glutamate metabolism; phosphatidylcholines; sphingomyelins; and phosphatidylinositols were the most significantly affected pathways in female and male rats exposed to Sb. Additionally, correlation analysis showed that the concentrations of certain metabolites and lipids (e.g., deoxycholic acid, N-methylproline, palmitoylcarnitine, glycerophospholipids, sphingomyelins, and glycerol) were significantly associated with hepatic injury biomarkers, indicating that metabolic remodeling may be involved in apical hepatotoxicity. Our study demonstrated that short-term exposure to Sb induces hepatotoxicity, possibly through a glycolipid metabolism disorder, providing an important reference for the health risks of Sb pollution.


Asunto(s)
Antimonio , Enfermedad Hepática Inducida por Sustancias y Drogas , Humanos , Ratas , Masculino , Femenino , Animales , Ratas Sprague-Dawley , Antimonio/toxicidad , Esfingomielinas/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Biomarcadores/metabolismo , Peso Corporal , Hígado/metabolismo
3.
Polymers (Basel) ; 15(19)2023 Oct 03.
Artículo en Inglés | MEDLINE | ID: mdl-37836023

RESUMEN

Additive manufacturing using continuous carbon-fibre-reinforced polymer (CCFRP) presents an opportunity to create high-strength parts suitable for aerospace, engineering, and other industries. Continuous fibres reinforce the load-bearing path, enhancing the mechanical properties of these parts. However, the existing additive manufacturing processes for CCFRP parts have numerous disadvantages. Resin- and extrusion-based processes require time-consuming and costly post-processing to remove the support structures, severely restricting the design flexibility. Additionally, the production of small batches demands considerable effort. In contrast, laser sintering has emerged as a promising alternative in industry. It enables the creation of robust parts without needing support structures, offering efficiency and cost-effectiveness in producing single units or small batches. Utilising an innovative laser-sintering machine equipped with automated continuous fibre integration, this study aims to merge the benefits of laser-sintering technology with the advantages of continuous fibres. The paper provides an outline, using a finite element model in COMSOL Multiphysics, for simulating and identifying an optimised operating point range for the automated integration of continuous fibres. The results demonstrate a remarkable reduction in processing time of 233% for the fibre integration and a reduction of 56% for the width and 44% for the depth of the heat-affected zone compared to the initial setup.

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