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Real-time chatter detection is important in improving the surface quality of workpieces in milling. Since the process from stable cutting to chatter is characterized by the progressive variation of the vibration energy distribution, entropy has been utilized to capture the decreasing randomness of vibration signals when chatter occurs. To make such an index more sensitive to transitions of the cutting state, the entropy can be computed based on signal components obtained through signal decomposition techniques. However, the classic empirical mode decomposition (EMD) is difficult to put into practice due to its weak robustness to noises. The up-to-date variational mode decomposition (VMD) has strict requirements on a priori information about the signal and thus is not applicable either. In this paper, a novel method named the iterative Vold-Kalman filter (I-VKF) is proposed under the framework of the greedy algorithm, where the Vold-Kalman filter (VKF), a classic order tracker for rotating machinery, is improved to recursively extract each signal component. In the meantime, a spectrum concentration index–based technique is developed for the estimation of the instantaneous chatter frequency to adaptively determine the filter parameter. Numerical examples demonstrate the superiority of the I-VKF over the original VKF, EMD, and VMD, especially in the presence of strong noises. Combined with the energy entropy of extracted components and an automatically calculated threshold, the proposed strategy greatly helps in timely chatter detection, which has been verified by dynamic simulation and experiments.

Myeloid-derived suppressor cells (MDSCs) are a series of innate cells that play a significant role in inhibiting T cell-related responses. This heterogeneous population of immature cells is involved in tumor immunity. Recently, the function and importance of MDSCs in transplantation have garnered the attention of scientists and have become an important focus of transplantation immunology research because MDSCs play a key role in establishing immune tolerance in transplantation. In this review, we summarize recent studies of MDSCs in different types of transplantation. We also focus on the influence of immunosuppressive drugs on MDSCs as well as future obstacles and research directions in this field.

Acute kidney injury (AKI) and chronic kidney disease (CKD) represent different stages of renal failure; thus, CKD can be regarded as a result of AKI deterioration. Previous studies have demonstrated that immune cell infiltration, oxidative stress, and metabolic mentalism can support renal fibrosis progression in AKI cases. However, the most important triggers and cell types involved in this pathological progression remain unclear. This study was conducted to shed light into the underlying cellular and molecular features of renal fibrosis progression through the analysis of three mouse whole kidney and one human single-cell RNA-sequencing datasets publicly available. According to the different causes of AKI (ischemia reperfusion injury [IRI] or cisplatin), the mouse samples were divided into the CIU [control-IRI-unilateral ureteral obstruction (UUO)] and CCU (control-cisplatin-UUO) groups. Comparisons between groups revealed eight different modules of differentially expressed genes (DEGs). A total of 1,214 genes showed the same expression pattern in both CIU and CCU groups; however, 1,816 and 1,308 genes were expressed specifically in the CCU and CIU groups, respectively. Further assessment of the DEGs according to the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment pathway and Gene Ontology (GO) showed that T-cell activation, fatty acid metabolic process, and arachidonic acid metabolism were involved in the fibrosis progression in CIU and CCU. Single-cell RNA-sequencing data along with the collected DEGs information also revealed that the T-cell activation mainly happened in immune cells, whereas the fatty acid metabolic process and arachidonic acid metabolism occurred in tubule cells. Taken together, these findings suggest that the fibrosis process differed between the CIU and CCU stages, in which immune and tubule cells have different functions. These identified cellular and molecular features of the different stages of fibrosis progression may pave the way for exploring novel potential therapeutic strategies in the clinic.

Thoracic aortic aneurysm and dissection (TAAD) is a life-threatening cardiovascular disorder lacking effective clinical pharmacological therapies. The underlying molecular mechanisms of TAAD still remain elusive with participation of versatile cell types and components including endothelial cells (ECs), smooth muscle cells (SMCs), fibroblasts, immune cells, and the extracellular matrix (ECM). The main pathological features of TAAD include SMC dysfunction, phenotypic switching, and ECM degradation, which is closely associated with inflammation and immune cell infiltration. Among various types of immune cells, macrophages are a distinct participator in the formation and progression of TAAD. In this review, we first highlight the important role of inflammation and immune cell infiltration in TAAD. Furthermore, we discuss the role of macrophages in TAAD from the aspects of macrophage origination, classification, and functions. On the basis of experimental and clinical studies, we summarize key regulators of macrophages in TAAD. Finally, we review how targeting macrophages can reduce TAAD in murine models. A better understanding of the molecular and cellular mechanisms of TAAD may provide novel insights into preventing and treating the condition.

Erythropoietin (EPO) is not only an erythropoiesis hormone but also an immune-regulatory cytokine. The receptors of EPO (EPOR) 2 and tissue-protective receptor (TPR), mediate EPO’s immune regulation. Our group firstly reported a non-erythropoietic peptide derivant of EPO, cyclic helix B peptide (CHBP), which could inhibit macrophages inflammation and dendritic cells (DCs) maturation. As a kind of innate immune regulatory cell, myeloid-derived suppressor cells (MDSCs) share a common myeloid progenitor with macrophages and DCs. In this study, we investigated the effects on MDSCs differentiation and immunosuppressive function via CHBP induction. CHBP promoted MDSCs differentiate toward M-MDSCs with enhanced immunosuppressive capability. Infusion of CHBP-induced M-MDSCs significantly prolonged murine skin allograft survival compared to its counterpart without CHBP stimulation. In addition, we found CHBP increased the proportion of CD11b + Ly6G − Ly6C high CD127 + M-MDSCs, which exerted a stronger immunosuppressive function compared to CD11b + Ly6G − Ly6C high CD127 − M-MDSCs. In CHBP induced M-MDSCs, we found that EPOR downstream signal proteins Jak2 and STAT3 were upregulated, which had a strong relationship with MDSC function. In addition, CHBP upregulated GATA-binding protein 3 (GATA-3) protein translation level, which was an upstream signal of CD127 and regulator of STAT3. These effects of CHBP could be reversed if Epor was deficient. Our novel findings identified a new subset of M-MDSCs with better immunosuppressive capability, which was induced by the EPOR-mediated Jak2/GATA3/STAT3 pathway. These results are beneficial for CHBP clinical translation and MDSC cell therapy in the future.

Renal fibrosis is inevitable in all progressive chronic kidney diseases (CKDs) and represents a serious public health problem. Immune factors contribute to the progression of renal fibrosis. Thus, it is very possible that immunosuppression cells, such as myeloid-derived suppressor cells (MDSCs), could bring benefits to renal fibrosis. Herein, this study investigated the antifibrotic and reno-protective effect of MDSCs and the possible mechanisms. Murine and cell models of unilateral ureter obstruction (UUO) renal fibrosis were used. Bone marrow-induced MDSCs and granulocyte-macrophage colony-stimulating factor (GM-CSF) were pretreated before surgery. Kidney weight, pathological injury, extracellular matrix deposition, and epithelial-mesenchymal transition progression were examined. Transforming growth factor (TGF)-β1)/Smad/Snail signaling pathway involvement was investigated through Western blotting and quantitative PCR (qPCR). Accumulation of MDSC, CD4+ T cell, regulatory T (Treg), and T helper 1 (T 1) cell accumulation, and CCL5 and CCR5 expression level in MDSCs and non-MDSCs were evaluated using flow cytometry. - and induced MDSCs significantly ameliorated UUO-induced tubulointerstitial fibrosis, inhibited the TGF-β1/Smad/Snail signaling pathway, and enhanced MDSC and Treg infiltration in the kidney while downregulating the T 1 cells. Both and experiments confirmed CCL5 elevation in the two MDSC-treated groups. - and -induced MDSCs alleviated renal fibrosis similarly through promoting the CCL5-CCR5 axis interaction and TGF-β1/Smad/Snail signaling pathway inhibition. Our results indicate an alternative treatment for renal fibrosis.

Background Obesity may increase perioperative mortality of acute Stanford type A aortic dissection (ATAAD). However, the available evidence was limited. This study aimed to systematically review published literatures about body mass index (BMI) and perioperative mortality of ATAAD. Methods Electronic literature search was conducted in PubMed, Medline, Embase and Cochrane Library databases. All observational studies that investigated BMI and perioperative mortality of ATAAD were included. Pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using a random-effects model. Meta-regression analysis was performed to assess the effects of different clinical variables on BMI and perioperative mortality of ATAAD. Sensitivity analysis was performed to determine the sources of heterogeneity. Egger’s linear regression method and funnel plot were used to determine the publication bias. Results A total of 12 studies with 5,522 patients were eligible and included in this meta-analysis. Pooled analysis showed that perioperative mortality of ATAAD increased by 22% for each 1 kg/m 2 increase in BMI (OR = 1.22, 95% CI: 1.10–1.35). Univariable meta-regression analysis indicated that age and female gender significantly modified the association between BMI and perioperative mortality of ATAAD in a positive manner (meta-regression on age: coefficient = 0.04, P  = 0.04; meta-regression on female gender: coefficient = 0.02, P  = 0.03). Neither significant heterogeneity nor publication bias were found among included studies. Conclusions BMI is closely associated with perioperative mortality of ATAAD. Optimal perioperative management needs to be further explored and individualized for obese patient with ATAAD, especially in elderly and female populations. Trial registration PROSPERO (CRD42022358619). Graphical Abstract BMI and perioperative mortality of ATAAD.

Background: Aortic dissection (AD) is a cardiovascular emergency with high mortality; however, the underlying molecular pathophysiology of AD remains incompletely understood. Pyroptosis, a proinflammatory form of programmed cell death, contributes to vascular injury; nonetheless, the upstream transcriptional regulation of pyroptosis in AD is similarly poorly defined. Methods: Differentially expressed genes were identified in aortic tissues from AD patients (Gene Expression Omnibus (GEO) datasets) using bioinformatics analyses, with a focus on cell death-related candidates. In vivo AD mouse models and in vitro vascular smooth muscle cell (VSMC) systems were employed to investigate the roles of these genes in AD. Potential transcription factors for pyruvate kinase M2 (PKM2) were predicted using the Just Another Simple Array Retrieval/Simple API for Repository (JASPAR) and University of California, Santa Cruz (UCSC) databases, and validated by luciferase reporter and chromatin immunoprecipitation assays. Gain- and loss-of-function approaches were used to dissect the zinc finger protein 460 (ZNF460)–PKM2–gasdermin E (GSDME) axis and the associated impact on pyroptosis and AD progression. Results: PKM2 expression was markedly elevated in AD tissues. PKM2 silencing suppressed GSDME cleavage, attenuated VSMC pyroptosis, and mitigated experimental AD, whereas PKM2 overexpression aggravated these outcomes. GSDME upregulation rescued pyroptosis in PKM2-depleted cells. Mechanistically, the transcription factor ZNF460 directly bound to the PKM2 promoter, enhancing PKM2 transcription and activating downstream GSDME-mediated pyroptosis. ZNF460 knockdown reduced pyroptotic cell death and preserved aortic wall integrity in vivo. Conclusions: This study identifies ZNF460 as a novel upstream regulator of PKM2 that drives GSDME-dependent pyroptosis, thereby exacerbating AD progression. Targeting the ZNF460–PKM2–GSDME axis may represent a promising therapeutic strategy for preventing pyroptosis-driven vascular damage in AD.

Ischemia reperfusion injury (IRI) is commonly seen in surgical procedures involving cardiopulmonary bypass and post-shock reperfusion. Sudden restoration of blood flow after a period of ischemia triggers a rapid accumulation of reactive oxygen species (ROS) and oxidative stress that promote pathological injury. Macrophage-derived inflammatory responses are also thought to contribute to such injury, but how ROS influences tissue macrophages and their elaboration of inflammatory cytokines in IRI remains poorly understood. In this study, we showed that macrophages mobilize mitochondrial adaptations during reoxygenation, including mitochondrial fission and ubiquitin proteasome system (UPS) flux. Furthermore, the transcription factor Nuclear Factor Erythroid 2 Like 1 (NRF1) is rapidly induced during reoxygenation in response to rising levels of ROS. Induction of NRF1 upregulates ubiquitin proteasome system (UPS) and mitophagy pathways to mediate mitochondrial fusion/fission dynamics and dampen ROS production, allowing for alleviation of oxidative stress and the inflammatory response. Conversely, the absence of myeloid NRF1 leads to increased ROS, driving enhanced inflammation and kidney injury in a mouse model of IRI. We thus identify macrophage NRF1 as a master regulator of mitochondrial homeostasis, antioxidant defense, and inflammatory responses in IRI.

In this retrospective study, we investigated the incidence of postoperative acute kidney injury (AKI) and determined the predictors associated with AKI in patients underwent surgeries for acute type A aortic dissection (ATAAD). We enrolled patients diagnosed with ATAAD and received operation. AKI was defined based on the Kidney Disease: Improving Global Outcomes criteria. Potential perioperative predictors were evaluated for postoperative AKI. Univariate and multivariate regression analyses were conducted to identify predictors associated with AKI following surgery. The primary end point was the incidence of postoperative AKI, while the secondary end points included in-hospital mortality and other major surgical complications. This study enrolled 224 patients in all. There were 155 (69.2%) patients with postoperative AKI, including 55 (24.6%) with KDIGO stage 1, 45 (20.1%) with stage 2 and 55 (24.6%) with stage 3. Twenty-eight patients (12.5%) needed renal replacement therapy after surgery. The total in-hospital mortality was 2.7% (AKI vs. non-AKI: 3.2% vs. 1.4%,  = 0.669). Multivariate regression analysis found total protein concentrations [odds ratio (OR) 1.136, 95% confidence interval (CI): 1.032-1.250,  = 0.009], intraoperative blood loss (OR 1.002, 95% CI: 1.000-1.004,  = 0.042) and ventilation time (OR 1.011, 95% CI: 1.001-1.021,  = 0.026) were independently associated with AKI. The area under the receiver operating characteristic curve was 0.688 (95% CI: 0.617-0.759). Our predictive model demonstrated a sensitivity of 72.5% and a specificity of 57.4%. The ordinal logistic regression analysis found that age (OR 1.055, 95% CI: 1.027-1.084,  < 0.001), body mass index (OR 1.194, 95% CI: 1.104-1.291,  < 0.001), a high total protein to albumin ratio (OR 2.615, 95% CI: 1.234-5.540,  = 0.012) and ventilation time (OR 1.005, 95% CI: 1.001-1.008,  = 0.005) were independently associated with the severity of AKI. A higher preoperative total protein to albumin ratio independently predicted more severe postoperative AKI in patients undergoing surgical treatment for ATAAD. Monitoring preoperative total protein concentrations and the total protein to albumin ratio may assist in identifying patients at higher risk of progressing to severe AKI, though further multicenter validation is required.