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Background The role of H. pylori infection has been reported in various extragastric diseases, particularly, the correlation between H. pylori and atherosclerosis (AS) have received lots of attention. Some scholars demonstrated that the presence of H. pylori‐specific DNA in the sclerotic plaques of atheromatous patients provides biological evidences, with indicating that H. pylori infection is a potential factor of AS. However, the underlying mechanism of H. pylori or their products cross the epithelial barriers to enter the blood circulation remains unclear. Recent studies have shown that the extracellular vesicles (EVs) derived from H. pylori‐infected gastric epithelial cells encapsulated H. pylori virulence factor cytotoxin‐associated gene A (CagA) and existed in the blood samples of patients or mice, which indicating that they can carry CagA into the blood circulation. Based on these findings, some researchers proposed a hypothesis that H. pylori is involved in the pathogenesis of AS via EVs‐based mechanisms. In addition, outer membrane vesicles (OMVs) serve as transport vehicles to deliver H. pylori virulence factors to epithelial cells. It is necessary to discuss the role of H. pylori OMVs in the development of AS. Objectives This review will focus on the correlation between H. pylori infection and AS and tried to unveil the possible role of EVs from H. pylori‐infected cells and H. pylori OMVs in the pathogenesis of AS, with a view to providing help in refining our knowledge in this aspect. Methods All of information included in this review was retrieved from published studies on H. pylori infection in AS. Results H. pylori infection may be an atherosclerotic risk factor and drives researchers to reevaluate the role of H. pylori in the pathogenesis of AS. Some findings proposed a new hypothesis that H. pylori may be involved in the pathogenesis of AS through EVs‐based mechanisms. Besides EVs from H. pylori‐infected cells, whether H. pylori OMVs may play some role in the pathogenesis of AS is still remain unclear. Conclusion Existing epidemiological and clinical evidence had shown that there is a possible association between H. pylori and AS. However, except for the larger randomized controlled trials, more basic research about EVs from H. pylori‐infected cells and H. pylori OMVs is the need of the hour to unveil the possible role of H. pylori infection in the pathogenesis of AS.

Surfactant-like peptides (SLPs) can self-assemble into various nanostructures, which have shown great potential for a variety of biomedical and biotechnological applications. In this work, two SLPs, V 4 Y, and V 4 AGY, were designed and synthesized, both of which had hydrophobic head valines (V) with large side-chain steric hindrance effect and the hydrophilic head tyrosine (Y) with a rigid ring and two negative charges in the basic solution. Fourier transform infrared and circular dichroism studies confirmed their different secondary structures, whereas atomic force microscopy and dynamic light scattering characterized the difference in their morphologies. In solution, they formed different secondary structures. Correspondingly, V 4 Y and V 4 AGY formed noncompact spherical aggregates and a spiral clubbed structure, respectively. In V 4 AGY, the introduction of alanine (A) and glycine (G) increased the molecule's flexibility and increased the distance between the tyrosine and four continuous valines, so as to weaken the synergistic action of electronic repulsion and steric hindrance and strengthen the intermolecular hydrogen bond beneficial to β-sheet formation and the axial growth of the self-assembly. Therefore, the flexibility of the molecule and the side-chain steric effect of the two heads of SLPs are non-negligible in the tuning process of peptide self-assembly, in addition to hydrogen-bonding, hydrophobic, and electrostatic interactions.

Recently, endoplasmic reticulum (ER) stress has been shown to influence tumor progression and immune cell function in the tumor microenvironment (TME). However, the underlying role of ER stress-related gene patterns in colorectal cancer (CRC) development remains unclear. We analyzed the ER stress-related gene patterns in 884 patients with CRC from the Gene Expression Omnibus database and evaluated the cell-infiltrating patterns in the TME. Two ER stress-related patterns were identified in patients with CRC that had distinct cell-infiltrating patterns in the TME and clinical characteristics. A risk score and nomogram based on 14 screened prognosis-correlated genes was built and validated to predict patient survival. Patients with a higher risk score were shown to have an unfavorable prognosis, and the risk score was associated with cell infiltration and drug sensitivity. Furthermore, spatial transcriptomics data were utilized to explore ER stress-related gene patterns in CRC tissues, and it was shown that ER stress phenotype involves in the formation of the immunosuppressive TME. This study demonstrated that ER stress-related gene patterns play a role in influencing the TME and predicting prognosis. These analyses of ER stress in the TME of CRC might deepen our understanding of CRC progression and immune escape and provide novel insights into therapeutic strategies.

The hydrolysis reactions of N- (O,O'-diisopropyl)phosphoryl-γ-amino butyric acid (DIPP-γ-Aba), were studied by HPLC and their hydrolysis reaction kinetic equations were obtained. Under acid conditions, the reaction rate of DIPP-L-α-Ala was close to that of DIPP-D-α-Ala and the same rule was true between DIPP-β-Ala and DIPP-γ-Aba. Meantime, the reaction rate of DIPP-L/D-α-Ala was as 10 times as that of DIPP-β-Ala or DIPP-γ-Aba. Under basic conditions, the hydrolysis reactions of DIPP-β-Ala and DIPP-γ-Aba almost did not take place and the reaction rate of DIPP-L/D-α-Ala was about 1/10 of that under acid conditions. Moreover, theoretical calculation further illuminated the differences of the hydrolysis rate from the view of energy. The results would provide some helpful clues to why nature chose α-amino acids but not other kinds of analogs as protein backbones.