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Atherosclerosis, a silent chronic vascular pathology, is the cause of the majority of cardiovascular ischaemic events. Atherosclerosis is characterized by a series of deleterious changes in cellularity, including endothelial dysfunction, transmigration of circulating inflammatory cells into the arterial wall, pro-inflammatory cytokines production, lipid accumulation in the intima, vascular local inflammatory response, atherosclerosis-related cells apoptosis and autophagy. Proteins of Annexin A (AnxA) family, the well-known Ca

Accumulating evidence suggests that envelope proteins play an important role in viral secondary envelopment; however, the molecular mechanisms involved are poorly understood. To clarify these mechanisms, we studied the localization of equine herpesvirus type 1 (EHV-1) envelope proteins and found that glycoprotein D of EHV-1 (gDEHV−1) was mostly retained in the Golgi complex, unlike that of HSV-1 and PRV. We used a gene truncation and replacement strategy to investigate the determinant sequence responsible for the Golgi retention phenotype and found that Golgi retention signals exhibit multi-domain features. The extracellular domain of gDEHV−1 (ECDEHV−1) is an endoplasmic reticulum (ER)-resident domain. The transmembrane domain and cytoplasmic tail (TM-CT) of gDEHV−1 was found to help the protein reside in the Golgi complex. Once each of the dual domains was deleted or replaced, the mutant gD remained in the ER. (TM-CT)EHV−1 preferentially binds to the endomembrane and induces a large number of vesicles that may originate from the Golgi complex or ER-Golgi intermediate compartment. Membrane fusion was hardly observed between the cell membrane and the induced vesicles. These findings provide further insight into the molecular mechanism underlying the Golgi retention of gDEHV−1, enhancing our understanding of viral secondary envelopment.

Cardiovascular and related metabolic diseases are significant global health challenges. Glucagon-like peptide 1 (GLP-1) is a brain-gut peptide secreted by the ileal endocrine system and is now an established drug target in type 2 diabetes (T2DM). GLP-1 targeting agents have been shown not only to treat T2DM, but also to exert cardiovascular protective effects by regulating multiple signaling pathways. The mitogen-activated protein kinase (MAPK) pathway, a common signal transduction pathway for transmitting extracellular signals to downstream effector molecules, is involved in regulating diverse cellular physiological processes, including cell proliferation, differentiation, stress, inflammation, functional synchronization, transformation, and apoptosis. The purpose of this review is to highlight the relationship between GLP-1 and cardiovascular disease (CVD) and discuss how GLP-1 exerts cardiovascular protective effects through the MAPK signaling pathway. This review also discusses the future challenges in fully characterizing and evaluating the CVD protective effects of GLP-1 receptor agonists (GLP-1RA) at the cellular and molecular levels. A better understanding of the MAPK signaling pathway that is dysregulated in CVD may aid in the design and development of promising GLP-1RA.

Atherosclerosis is one of the chronic progressive diseases, which is caused by vascular injury and promoted by the interaction of various inflammatory factors and inflammatory cells. In recent years, kruppel-like factor 4 (KLF4), a significant transcription factor that participated in cell growth, differentiation and proliferation, has been proved to cause substantial impacts on regulating cardiovascular disease. This paper will give a comprehensive summary to highlight KLF4 as a crucial regulator of foam cell formation, vascular smooth muscle cells (VSMCs) phenotypic transformation, macrophage polarization, endothelial cells inflammation, lymphocyte differentiation and cell proliferation in the process of atherosclerosis. Recent studies show that KLF4 may be an important "molecular switch" in the process of improving vascular injury and inflammation under harmful stimulation, suggesting that KLF4 is a latent disease biomarker for the therapeutic target of atherosclerosis and vascular disease.

To evaluate the atherosclerotic cardiovascular diseases (ASCVD) risk factors in type 2 diabetes patients from the primary diabetes clinics for further comprehensive intervention in China. A cross-sectional study was conducted in 5 primary diabetes chain hospitals in Beijing, Lanzhou, Harbin, Chengdu, and Taiyuan in continuous patients with type 2 diabetes from March 2016 to December 2019. The data collected at the first visit were analyzed, and proportions of patients reached the targets (glycosylated hemoglobin [HbA1c]

Atherosclerosis is one of the most common type of cardiovascular disease and the prime cause of mortality in the aging population worldwide. However, the detail mechanisms and special biomarkers of atherosclerosis remain to be further investigated. Lately, long non-coding RNAs (lncRNAs) has attracted much more attention than other types of ncRNAs. In our work, we found and confirmed differently expressed lncRNAs and mRNAs in atherosclerosis by analyzing {"type":"entrez-geo","attrs":{"text":"GSE28829","term_id":"28829"}}GSE28829. We performed the weighted gene co-expression network analysis (WGCNA) by analyzing {"type":"entrez-geo","attrs":{"text":"GSE40231","term_id":"40231"}}GSE40231 to confirm highly correlated genes. Gene Ontology (GO) analysis were utilized to assess the potential functions of differential expressed lncRNAs in atherosclerosis. Co-expression networks were also constructed to confirm hub lncRNAs in atherosclerosis. A total of 5784 mRNAs and 654 lncRNAs were found to be dysregulated in the progression of atherosclerosis. A total of 15 lncRNA-mRNA co-expression modules were identified in this study based on WGCNA analysis. Moreover, a few lncRNAs, such as ZFAS1, LOC100506730, LOC100506691, DOCK9-AS2, RP11-6I2.3, LOC100130219, were confirmed as important lncRNAs in atherosclerosis. Taken together, bioinformatics analysis revealed these lncRNAs were involved in regulating the leukotriene biosynthetic process, gene expression, actin filament organization, t-circle formation, antigen processing, and presentation, interferon-gamma-mediated signaling pathway, and activation of GTPase activity. We believed that this study would provide potential novel therapeutic and prognostic targets for atherosclerosis.

Efficient amplification of spoof surface plasmon polaritons (SPPs) is proposed at microwave frequencies by using a subwavelength-scale amplifier. For this purpose, a special plasmonic waveguide composed of two ultrathin corrugated metallic strips on top and bottom surfaces of a dielectric substrate with mirror symmetry is presented, which is easy to integrate with the amplifier. It is shown that spoof SPPs are able to propagate on the plasmonic waveguide in broadband with low loss and strong subwavelength effect. By loading a low-noise amplifier chip produced by the semiconductor technology, the first experiment is demonstrated to amplify spoof SPPs at microwave frequencies (from 6 to 20GHz) with high gain (around 20dB), which can be directly used as a SPP amplifier device. The features of strong field confinement, high efficiency, broadband operation, and significant amplification of the spoof SPPs may advance a big step towards other active SPP components and integrated circuits.

Anti-gamma-aminobutyric acid B (anti-GABAData from patients diagnosed with anti-GABASix of the seven patients were males, and a median age at presentation of 56 years (range: 4-71 years). Seizures were the most common initial symptom, and all patients developed symptoms of typical limbic encephalitis during their disease course. Additional types of autoantibodies were identified in four patients. After presentation, three patients were found to have small cell lung cancer and one patient was eventually diagnosed with thymoma. All patients accepted first-line immune therapy, but only one chose tumor treatment. The three tumor-free patients had a good outcome, whereas those with tumors had a poor one. Finally, there were no relapses during follow-up.Anti-GABA

A 60 GHz upconversion mixer is realised in a 65 nm LP CMOS. The mixer consists of a Gilbert cell, a LO buffer and a RF buffer. To enhance the bandwidth and reduce the area, the transformer impedance matching network is used. The measured results show that the mixer covers the IEEE 802.15.3c standard four channels, from 57 to 66 GHz. In each channel, the gain flatness is

Five isoflavanquinones have been isolated from the roots of Abrus precatorius L. (Leguminosae). Three of them are new and designated as abruquinones D, E, and F. The pharmacological activities of the isoflavanquinones have been evaluated. The results indicated that abruquinones A, B, and D exhibited remarkable inhibitory effects on the platelet aggregation. The IC50 of abruquinones A and B for the inhibition of the platelet aggregation induced by arachidonic acid (AA) and collagen were less than 5 micrograms/ml, and of abruquinone D, was less than 10 micrograms/ml for that induced by AA. On the other hand, abruquinones A, B, D, and F showed strong anti-inflammatory and antiallergic effects. The IC50 of abruquinones A, B, D, and F for the inhibition of superoxide formation were less than 0.3 micrograms/ml, for the inhibition of the release of both beta-glucuronidase and lysozyme from rat neutrophils and the release of both beta-glucuronidase and histamine from mast cells were less than 1 microgram/ml.