Acetylated nanocellulose reinforced hydroxypropyl starch acetate realizing polypropylene replacement for green packaging application.

The use of natural starch as a replacement for petroleum-based packaging materials is limited due to its poor processability, weak mechanical properties, and strong moisture sensitivity. To address these limitations, this study adopts molecular design of hydroxypropylation and acetylation to sequentially modify natural starch, and material design of introducing acetylated cellulose nanofibers (ACNF) into the starch matrix to reinforce the material. Hydroxypropylation decreased the interaction force between the starch molecular chains, thereby reducing the glass transition temperature. Subsequent acetylation introduced hydrophobic acetyl groups that disrupted intermolecular hydrogen bonds, enhancing the mobility of the starch molecular chain, and endowed the hydroxypropyl starch acetate (HPSA) with excellent thermoplastic processability (melt index of 7.12 g/10 min) without the need for plasticizers and notable water resistance (water absorption rate of 3.0 %). The introduction of ACNF generated a strong interaction between HPSA chains, promoting the derived ACNF-HPSA to exhibit excellent mechanical strength, such as high impact strength of 2.1 kJ/m2, tensile strength of 22.89 MPa, elasticity modulus of 813.22 MPa, flexural strength of 24.18 MPa and flexural modulus of 1367.88 MPa. Its overall performance even surpassed that of polypropylene (PP) plastic, making it a potential alternative material for PP-based packaging materials.

Serum uric acid predicts the development of atherosclerosis in women but not in men: A ten-year cohort study in China.

BACKGROUND AND AIM: Atherosclerosis is becoming a significant health burden. Serum uric acid (SUA) is the final enzymatic product of purine metabolism and can contribute to the development of atherosclerosis. The aim of this study was to explore the possible predictive value of SUA in the development of atherosclerosis in a healthy Chinese population. METHODS AND RESULTS: In this study, a total of 11,222 healthy subjects with no carotid plaque at baseline were enrolled and divided into sex-specific groups, and then the occurrence of carotid plaque during the follow-up time was documented. The association between carotid plaque and SUA levels was examined using Cox proportional-hazards regression models. The mean SUA level was 5.35 ± 1.41 mg/dL. A total of 2,911 individuals (25.94%) developed carotid plaque during the follow-up time, including 1,071 females and 1,840 males. After adjusting for potential confounding factors, the hazard ratio (HR) and 95% confidence interval (95% CI) in women for the occurrence of carotid plaque associated with SUA levels were 1.163 (1.017-1.330), but no significant correlation was found in men, as the HR was 1.050 (0.965-1.143). CONCLUSION: Our results indicate that SUA levels predict the development of carotid plaque independent of traditional risk factors only in women.

Longitudinal Associations Between Serum Bilirubin Level and Carotid Atherosclerosis Plaque in a Health Screening Population.

This study aimed to determine the relationship between bilirubin levels and carotid atherosclerosis (CAS) in the health screening population. After propensity score matching, this retrospective cohort study included 4360 subjects who underwent health examinations regularly in Hebei General Hospital between January 2010 and December 2019 and had no carotid plaque at baseline. After an average follow-up of 26.76 months, the main endpoint Cox regression analysis of carotid plaques was performed. After adjusting the confounding factors, Cox regression analysis showed that when serum total bilirubin (TBIL) and unconjugated bilirubin (UCB) increased by 1 standard deviation (SD), the risk of carotid plaque decreased by 7.30% (95% confidence interval (CI): 2.80-11.60%) and 15.70% (95% CI: 11.40-19.80%), respectively. When conjugated bilirubin (CB) increased by 1 SD, the risk of carotid plaques increased by 24.3% (95% CI: 19.7-29.0%). TBIL and UCB levels were negatively associated with CAS, and CB levels were positively associated with CAS.

Integrated Analysis of Competitive Endogenous RNA Networks in Acute Ischemic Stroke.

Background: Acute ischemic stroke (AIS) is a severe neurological disease with complex pathophysiology, resulting in the disability and death. The goal of this study is to explore the underlying molecular mechanisms of AIS and search for new potential biomarkers and therapeutic targets. Methods: Integrative analysis of mRNA and miRNA profiles downloaded from Gene Expression Omnibus (GEO) was performed. We explored differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMirs) after AIS. Target mRNAs of DEMirs and target miRNAs of DEGs were predicted with target prediction tools, and the intersections between DEGs and target genes were determined. Subsequently, Gene Ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses, Gene set enrichment analysis (GSEA), Gene set variation analysis (GSVA), competitive endogenous RNA (ceRNA) (lncRNA-miRNA-mRNA) network, protein-protein interaction (PPI) network, and gene transcription factors (TFs) network analyses were performed to identify hub genes and associated pathways. Furthermore, we obtained AIS samples with evaluation of immune cell infiltration and used CIBERSORT to determine the relationship between the expression of hub genes and infiltrating immune cells. Finally, we used the Genomics of Drug Sensitivity in Cancer (GDSC) database to predict the effect of the identified targets on drug sensitivity. Result: We identified 293 DEGs and 26 DEMirs associated with AIS. DEGs were found to be mainly enriched in inflammation and immune-related signaling pathways through enrichment analysis. The ceRNA network included nine lncRNAs, 13 miRNAs, and 21 mRNAs. We used the criterion AUC >0.8, to screen a 3-gene signature (FBL, RPS3, and RPS15) and the aberrantly expressed miRNAs (hsa-miR-125a-5p, hsa-miR-125b-5p, hsa-miR-148b-3p, and hsa-miR-143-3p) in AIS, which were verified by a method of quantitative PCR (qPCR) in HT22 cells. T cells CD8, B cells naïve, and activated NK cells had statistical increased in number compared with the acute cerebral infarction group. By predicting the IC50 of the patient to the drug, AZD0530, Z.LLNle.CHO and NSC-87877 with significant differences between the groups were screened out. AIS demonstrated heterogeneity in immune infiltrates that correlated with the occurrence and development of diseases. Conclusion: These findings may contribute to a better understanding of the molecular mechanisms of AIS and provide the basis for the development of novel treatment targets in AIS.