Binary and ternary blends composed of poly(lactic acid) (PLA), starch, and poly(ethylene glycols) (PEGs) with different molecular weights (weight-average molecular weights 5 300, 2000, 4000, 6000, and 10, 000 g/mol) were prepared, and the plasticizing effect and miscibility of PEGs in poly(lactic acid)/starch (PTPS) or PLA were intensively studied. The results indicate that the PEGs were effective plasticizers for the PTPS blends. The small-molecule plasticizers of PEG300 (i.e., the M w of PEG was 300g/mol) and glycerol presented better plasticizing effects, whereas its migration and limited miscibility resulted in significant decreases in the water resistance and elongation at break. PEG2000, with a moderate molecular weight, was partially miscible in sample PTPS3; this led to better performance in water resistance and mechanical properties. For higher molecular weight PEG, its plasticization for both starch and PLA was depressed, and visible phase separation also occurred, especially for PTPS6. It was also found that the presence of PEG significantly decreased the glass-transition temperature and accelerated the crystallization of the PLA matrix, depending on the PEG molecular weight and concentration.

Homocysteine (Hcy) is an intermediate amino acid formed during the conversion from methionine to cysteine. When the fasting plasma Hcy level is higher than 15 μmol/L, it is considered as hyperhomocysteinemia (HHcy). The vascular endothelium is an important barrier to vascular homeostasis, and its impairment is the initiation of atherosclerosis (AS). HHcy is an important risk factor for AS, which can promote the development of AS and the occurrence of cardiovascular events, and Hcy damage to the endothelium is considered to play a very important role. However, the mechanism by which Hcy damages the endothelium is still not fully understood. This review summarizes the mechanism of Hcy-induced endothelial injury and the treatment methods to alleviate the Hcy induced endothelial dysfunction, in order to provide new thoughts for the diagnosis and treatment of Hcy-induced endothelial injury and subsequent AS-related diseases.

A relatively simple and economical method to prepare linear long-chain dextrin (LLD) was created, with a resulting product that could act as a high-amylose starch for a variety of downstream applications. Native cassava starch was chosen as the starting material due to its inexpensive price and low-gelatinization temperature. A pretreatment with NaOH solution was applied to increase the susceptibility of cassava starch to pullulanase attack. The apparent amylose content of the final LLD product was extremely high (above 90%), as determined by the iodine binding colorimetric method. Using HPLC, the optimum amount of enzyme was determined to be 25 U pullulanase per gram of starch. The structure of the LLD was found to be a V6I crystalline type, and this was confirmed by multiple physical techniques, including X-ray powder diffraction, solid-state nuclear magnetic resonance, and Fourier transform infrared. Overall, this study could promote further investigations into the efficient preparation and characterization of amylose products.

BackgroundAcute myocardial infarction (AMI) can occur in patients with atherosclerotic disease, with or without plaque rupture. Previous studies have indicated a set of immune responses to plaque rupture. However, the specific circulating immune cell subsets that mediate inflammatory plaque rupture remain elusive.MethodsTen AMI patients were enrolled in our study (five with and five without plaque rupture; plaque characteristics were identified by optical coherence tomography). By single-cell RNA sequencing, we analyzed the transcriptomic profile of peripheral blood mononuclear cells.ResultsWe identified 27 cell clusters among 82,550 cells, including monocytes, T cells, NK cells, B cells, megakaryocytes, and CD34+ cells. Classical and non-classical monocytes constitute the major inflammatory cell types, and pro-inflammatory genes such as CCL5, TLR7, and CX3CR1 were significantly upregulated in patients with plaque rupture, while the neutrophil activation and degranulation genes FPR2, MMP9, and CLEC4D were significantly expressed in the intermediate monocytes derived from patients without plaque rupture. We also found that CD4+ effector T cells may contribute to plaque rupture by producing a range of cytokines and inflammatory-related chemokines, while CD8+ effector T cells express more effector molecules in patients without plaque rupture, such as GZMB, GNLY, and PRF1, which may contribute to the progress of plaque erosion. Additionally, NK and B cells played a significant role in activating inflammatory cells and promoting chemokine production in the plaque rupture. Cell–cell communication elaborated characteristics in signaling pathways dominated by inflammatory activation of classical monocytes in patients with plaque rupture.ConclusionsOur studies demonstrate that the circulating immune cells of patients with plaque rupture exhibit highly pro-inflammatory characteristics, while plaque erosion is mainly associated with intermediate monocyte amplification, neutrophil activation, and degranulation. These findings may provide novel targets for the precise treatment of patients with AMI.