Atherosclerosis as the leading cause of the cardiovascular disease is closely related to cholesterol deposition within subendothelial areas of the arteries. Significantly, early atherosclerosis intervention is the critical phase for its reversal. As atherosclerosis progresses, early foam cells formation may evolve into fibrous plaques and atheromatous plaque, ulteriorly rupture of atheromatous plaque increases risks of myocardial infarction and ischemic stroke, resulting in high morbidity and mortality worldwide. Notably, amphiphilic apolipoproteins (Apos) can concomitantly combine with lipids to form soluble lipoproteins that have been demonstrated to associate with atherosclerosis. Apos act as crucial communicators of lipoproteins, which not only can mediate lipids metabolism, but also can involve in pro-atherogenic and anti-atherogenic processes of atherosclerosis via affecting subendothelial retention and aggregation of low-density lipoprotein (LDL), oxidative modification of LDL, foam cells formation and reverse cholesterol transport (RCT) in macrophage cells. Correspondingly, Apos can be used as endogenous and/or exogenous targeting agents to effectively attenuate the development of atherosclerosis. The article reviews the classification, structure, and relationship between Apos and lipids, how Apos serve as communicators of lipoproteins to participate in the pathogenesis progression of early atherosclerosis, as well as how Apos as the meaningful targeting mass is used in early atherosclerosis treatment.

High levels of M2 macrophage infiltration invariably contribute to poor cancer prognosis and can be manipulated by metabolic reprogramming in the tumor microenvironment. However, the metabolism-related genes (MRGs) affecting M2 macrophage infiltration and their clinical implications are not fully understood. In this study, we identified 173 MRGs associated with M2 macrophage infiltration in cases of gastric cancer (GC) using the TCGA and GEO databases. Twelve MRGs were eventually adopted as the prognostic signature to develop a risk model. In the high-risk group, the patients showed poorer survival outcomes than patients in the low-risk group. Additionally, the patients in the high-risk group were less sensitive to certain drugs, such as 5-Fluorouracil, Oxaliplatin, and Cisplatin. Risk scores were positively correlated with the infiltration of multiple immune cells, including CD8+ T cells and M2 macrophages. Furthermore, a difference was observed in the expression and distribution between the 12 signature genes in the tumor microenvironment through single-cell sequencing analysis. In vitro experiments proved that the M2 polarization of macrophages was suppressed by Sorcin-knockdown GC cells, thereby hindering the proliferation and migration of GC cells. These findings provide a valuable prognostic signature for evaluating clinical outcomes and corresponding treatment options and identifying potential targets for GC treatment.

Background: Ionocytes are rare cells in airway epithelium characterized by a high expression of CFTR. Objectives: To investigate the morphology and distribution of ionocytes and the function of CFTR in the nasal mucosal epithelium of children. Methods: The exfoliated cells of nasal mucosa from 101 children were detected using flow cytometry to analyze the number of ionocytes and CFTR and the difference of CFTR function. Nasal mucosa and polyps were collected from 10 children with CRSwNP. The RNAscope of FOXI1 and CFTR was detected in pathological paraffin sections. The expression and distribution of ionocytes and CFTR in nasal mucosa and polyp epithelium were observed. Results: In CRS patients, the number of ionocytes in the nasal epithelium was lower and the number of ionocytes that did not express CFTR was higher, and the function of CFTR was also decreased. The expression of CFTR in the nasal mucosa of CRS showed the characteristics of local dense distribution and increased as the inflammation expanded. The ionocytes were “tadpole-shaped” in the epithelium and gathered in the area of high CFTR expression, the intracellular CFTR was expanded in clusters. Ionocytes that did not express CFTR was more common in the nasal polyps. Conclusions: The number of ionocytes and the function of CFTR in nasal mucosa of CRS patients decreased. With the expansion of inflammation, CFTR and ionocytes showed more obvious dense distribution. Some ionocytes lost the expression of CFTR and did not show the "tadpole" shape, which may be related to the occurrence of polyps.

No-reflow post-recanalization is a challenge in ischemic stroke. Our prior study demonstrated that Chinese medicine Tongxinluo capsule (TXL) improves no-reflow in stroke by suppressing leukocyte-endothelium interactions. However, it remains unclear which leukocyte subpopulation plays a major role. This study aimed to further explore the mechanisms of TXL improving no-reflow in stroke. The mouse model of stroke with recanalization treatment was induced by transient middle cerebral artery occlusion (tMCAO). Neutrophil depletion was performed by injecting Ly6G-specific monoclonal antibody (anti-Ly6G). The mice were orally administered with TXL suspension. We examined the following parameters: cerebral blood flow (CBF) determined by laser speckle perfusion imaging, neutrophil percentages and apoptosis examined by flow cytometry, and granulocyte colony-stimulating factor (G-CSF) measured by cytometric bead array. We confirmed our prior conclusion that TXL could significantly reduce blood neutrophil percentages (by up to 35 %) as well as improving no-reflow in stroke (increasing CBF in the ischemic area by 9 %). Interestingly, neutrophil depletion also suppressed no-reflow (increasing CBF by 15 %). These results suggest a causal role for neutrophil reduction in TXL's improvement of no-reflow. Subsequently, we found that tMCAO led to a 15 % increase in the percentage of bone marrow neutrophils but caused a 30 % decrease in the percentage of spleen neutrophils. However, TXL did not significantly affect the percentage of bone marrow neutrophils but interestingly increased the percentage of spleen neutrophils by up to 27 %. Importantly, tMCAO induced the increased granulocyte colony-stimulating factor (G-CSF) in the plasma and ischemic brain tissue, while both TXL and anti-Ly6G decreased the cytokine level. Moreover, TXL increased neutrophil apoptosis in the spleen without affecting their apoptosis in the blood and bone marrow. Our study has elucidated an important mechanism of post-stroke no-reflow: the overproduction of G-CSF by ischemic brain triggers a massive release of neutrophils from the bone marrow and spleen into the circulation, consequently obstructing the cerebral microvasculature. Interestingly, TXL counteracts post-stroke no-reflow by targeting the pathogenic surge of circulating neutrophils via a dual mechanism: inhibiting cerebral G-CSF production to reduce splenic neutrophil release; and facilitating splenic neutrophil homing to promote their clearance.