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Abdominal aortic aneurysms (AAAs) are local dilations of infrarenal segment of aortas. Molecular mechanisms underlying the pathogenesis of AAA remain not fully clear. However, inflammation has been considered as a central player in the development of AAA. In the past few decades, studies demonstrated a host of inflammatory cells, including T cells, macrophages, dendritic cells, neutrophils, B cells, and mast cells, etc. infiltrating into aortic walls, which implicated their crucial roles. In addition to direct cell contacts and cytokine or protease secretions, special structures like inflammasomes and neutrophil extracellular traps have been investigated to explore their functions in aneurysm formation. The above-mentioned inflammatory cells and associated structures may initiate and promote AAA expansion. Understanding their impacts and interaction networks formation is meaningful to develop new strategies of screening and pharmacological interventions for AAA. In this review, we aim to discuss the roles and mechanisms of these inflammatory cells in AAA pathogenesis.

Cathepsin B (CatB) is a cysteine proteolytic enzyme widely expressed in various cells and mainly located in the lysosomes. It contributes to the pathogenesis and development of many diseases. However, the role of CatB in viral myocarditis (VMC) has never been elucidated. Here we generated the VMC model by intraperitoneal injection of coxsackievirus B3 (CVB3) into mice. At day 7 and day 28, we found CatB was significantly activated in hearts from VMC mice. Compared with the wild-type mice receiving equal amount of CVB3, genetic ablation of CatB (Ctsb-/-) significantly improved survival, reduced inflammatory cell infiltration, decreased serum level of cardiac troponin I, and ameliorated cardiac dysfunction, without altering virus titers in hearts. Conversely, genetic deletion of cystatin C (Cstc-/-), which markedly enhanced CatB levels in hearts, distinctly increased the severity of VMC. Furthermore, compared with the control, we found the inflammasome was activated in the hearts of wild-type mice with VMC, which was attenuated in the hearts of Ctsb-/- mice but was further enhanced in Cstc-/- mice. Consistently, the inflammasome-initiated pyroptosis was reduced in Ctsb-/- mice hearts and further increased in Cstc-/- mice. These results suggest that CatB aggravates CVB3-induced VMC probably through activating the inflammasome and promoting pyroptosis. This finding might provide a novel strategy for VMC treatment.

Asia giant hornet is a predator of European honeybees, invading and destroying their nests. Nowadays, the State of Washington is suffering the attack of this hornet. Due to the potential severe impact on local honeybee populations, it will probably cause a great deal of anxiety. The most informative factors we consider are Detection Date,latitude and longitude. We propose a “time-space-state model” to evaluate the information evaluated by these two indicators. The time-space-state model can be divided into two kinds: the general model of time discretization and space continuum; The general model of space discretization and time semi-continuity. In the previous model, we mainly use K-means algorithm to determine the nest position in discrete time. In the latter model, we use the improved K-means algorithm to obtain the distribution model of hornets with seasonal variation. Through research, we have discovered the temporal and spatial laws of hornets’ nests, which are of great significance for maintaining the stability of agricultural production.

Necrotizing enterocolitis (NEC) is a life-threatening inflammatory disease in newborns, but the mechanisms remain unclear. Interferon regulatory factor 5 (IRF5) is a master regulator of macrophage function and is essential for proinflammatory M1 macrophage polarization. Our previous data indicated that M1 macrophages promote NEC injury. Here, we investigated whether IRF5 is involved in the pathogenesis of NEC. First, we found that IRF5 was upregulated in infiltrated macrophages in human neonates with NEC compared to controls. We further confirmed IRF5 upregulation in macrophages in experimental murine NEC and that the infiltrated macrophages were predominantly polarized into the M1 but not the M2 phenotype. Myeloid-specific deficiency of Irf5, which was associated with reduced M1 macrophage polarization and systematic inflammation, dramatically prevented experimental NEC. Moreover, we found that the ablation of Irf5 in myeloid cells markedly suppressed intestinal epithelial cell apoptosis and further prevented intestinal barrier dysfunction in experimental NEC. Bioinformatic and chromatin immunoprecipitation analysis further showed that IRF5 binds to the promoters of the M1 macrophage-associated genes Ccl4, Ccl5, Tnf, and Il12b. Overall, our study provides evidence that IRF5 participates in the pathogenesis of NEC, while the deletion of Irf5 in myeloid cells prevents NEC via inhibiting M1 macrophage polarization.

Objectives Long QT syndrome (LQTS) is one of the primary causes of sudden cardiac death (SCD) in youth. Studies have identified mutations in ion channel genes as key players in the pathogenesis of LQTS. However, the specific etiology in individual families remains unknown. Methods Three unrelated Chinese pedigrees diagnosed with LQTS or Jervell and Lange-Nielsen syndrome (JLNS) were recruited clinically. Whole exome sequencing (WES) was performed and further validated by multiplex ligation-dependent probe amplification (MLPA) and Sanger sequencing. Results All of the probands in our study experienced syncope episodes and featured typically prolonged QTc-intervals. Two probands also presented with congenital hearing loss and iron-deficiency anemia and thus were diagnosed with JLNS. A total of five different variants in KCNQ1, encoding a subunit of the voltage-gated potassium channel, were identified in 3 probands. The heterozygous variants, KCNQ1 c.749T > C was responsible for LQTS in Case 1, transmitting in an autosomal dominant pattern. Two patterns of compound heterozygous variants were responsible for JLNS, including a large deletion causing loss of the exon 16 and missense variant c.1663 C > T in Case 2, and splicing variant c.605-2 A > G and frame-shift variant c.1265del in Case 3. To our knowledge, the compound heterozygous mutations containing a large deletion and missense variant were first reported in patients with JLNS. Conclusion Our study expanded the LQTS genetic spectrum, thus favoring disease screening and diagnosis, personalized treatment, and genetic consultation.

Background Transseptal puncture (TSP) is a crucial technique for catheter ablation of atrial fibrillation (AF). Although intracardiac echo (ICE) facilitates a safe and accurate TSP, it is not widely used in developing countries because of the expense. This study evaluated the efficiency and safety of a novel cardiac multidetector computed tomography (MDCT)‐guided TSP during AF catheter ablation. Methods The study consisted of two cohorts. In the index cohort, TSP procedure was performed under the guidance of ICE, and we recorded the angulation of right anterior oblique of X‐ray projection. In the validation cohort, we compared the efficiency and safety of TSP guided by MDCT‐calculated angulation with propensity‐score‐matched patients who underwent TSP guided by ICE. Results We included 50 patients in the index cohort, and the mean angles of interatrial septum (IAS) measured from MDCT and ICE were 34.8 ± 6.3 and 35.1 ± 6.5, respectively. In the validation cohort, 376 patients were enrolled in the MDCT‐guided group and ICE‐guided group. Both groups had 1 case of cardiac tamponade. The mean axial plane angle was 35.46 ± 6.17 degrees, which was not influenced by age, gender, BMI, and LA size, while a moderate positive linear correlation between EF and the axial plane angle (R2 = 0.14, p = .006). Conclusion Cardiac MDCT can provide a clear vision of IAS orientation, and provide the appropriate RAO angle and height for TSP. The efficiency and safety of our MDCT‐guided TSP were comparable to ICE‐guided TSP, which may serve as an alternative method for TSP with ICE unavailable. Cardiac MDCT can provide a clear vision of IAS orientation, and provide the appropriate RAO angle and height for TSP. MDCT‐guided TSP may serve as an alternative method for TSP when ICE unavailable.

A 55‐year‐old woman of I‐IVC complicated with PLSVC underwent catheter ablation for atrial fibrillation through right jugular vein access. TSP was achieved by electrocautery and the J‐tip guidewire with the help of deflectable sheath and ICE. After PVI, the CS‐PLSVC and LA‐PLSVC connections were ablated within PLSVC.

Vascular calcification (VC) is characterized by calcium phosphate deposition in blood vessel walls and is associated with many diseases, as well as increased cardiovascular morbidity and mortality. However, the molecular mechanisms underlying of VC development and pathogenesis are not fully understood, thus impeding the design of molecular-targeted therapy for VC. Recently, several studies have shown that endoplasmic reticulum (ER) stress can exacerbate VC. The ER is an intracellular membranous organelle involved in the synthesis, folding, maturation, and post-translational modification of secretory and transmembrane proteins. ER stress (ERS) occurs when unfolded/misfolded proteins accumulate after a disturbance in the ER environment. Therefore, downregulation of pathological ERS may attenuate VC. This review summarizes the relationship between ERS and VC, focusing on how ERS regulates the development of VC by promoting osteogenic transformation, inflammation, autophagy, and apoptosis, with particular interest in the molecular mechanisms occurring in various vascular cells. We also discuss, the therapeutic effects of ERS inhibition on the progress of diseases associated with VC are detailed.

Ethanol infusion of the vein of Marshall (EIVOM) has emerged as a promising adjunct to pulmonary vein isolation (PVI) for atrial fibrillation (AF). Patients undergoing catheter ablation for persistent AF (>3 months) were enrolled in this study. After PVI, high-density mapping (HD-Grid, Abbott, St Paul, MN) was performed during coronary sinus pacing (100 bpm) to assess left atrial conduction velocity (CV) and voltage. EIVOM was then performed (1-3 mL ethanol × 3 doses), followed by repeat mapping. The CV and voltage were analyzed in the left lateral wall (mitral isthmus/appendage base), with ≥300 points collected per region. A post-EIVOM electrophysiological study with isoprenaline was conducted to induce arrhythmias. Twenty patients with AF (mean age, 64.30 [SD, 7.97] years, five women [25.0%]) with 24 (interquartile range: 6-60) months of AF duration underwent EIVOM (7.8 ± 2.1 mL). Voltage dropped from 1.92 (1.12-2.61) to 1.24 (0.91-2.05) mV postprocedure (  < 0.05), particularly in the atrial ridge regions. CV remained unchanged (1.00 [0.92-1.10] vs. 1.02 [0.95-1.14] m/s,  = 0.15). Atrial flutter was induced in three patients (one mitral isthmus-dependent, one tricuspid isthmus-dependent, and one roof-dependent). All patients maintained sinus rhythm at discharge without complications. In the acute setting, EIVOM induces localized voltage reduction in the atrial ridge regions without markedly affecting conduction velocity in the mitral isthmus areas.

Vascular calcification (VC) is an urgent worldwide health issue with no available medical treatment. It is an active cell-driven process by osteogenic differentiation of vascular cells with complex mechanisms. The AMP-activated protein kinase (AMPK) serves as the master sensor of cellular energy status. Accumulating evidence reveals the vital role of AMPK in VC progression. AMPK is involved in VC in various ways, including inhibiting runt-related transcription factor 2 signaling pathways, triggering autophagy, attenuating endoplasmic reticulum stress and dynamic-related protein 1-mediated mitochondrial fission, and activating endothelial nitric oxide synthase. AMPK activators, like metformin, are associated with reduced calcification deposits in certain groups of patients, indicating that AMPK is a potential therapeutic target for VC.