Impact of stent retriever size on clinical outcomes in the RECO registry.

Objective: In the RECO study, we investigated the impact of the operator's choice of stent retriever size on patients with internal carotid artery (ICA) occlusion.

Methods: Data from the RECO Registry, a prospective multicentre study, were utilized. Patients who underwent mechanical thrombectomy (MT) were divided according to the size of the stent into the RECO 4 × 20 group, the RECO 5 × 30 group and the RECO 6 × 30 group.

Dynamic pressure surface deformation measurement based on a chromatic confocal sensor: erratum.

This erratum corrects errors in Fig. 4 of the original paper, Appl. Opt.

Cilia-related diseases.

More and more attention is paid to diseases such as internal transfer and brain malformation which are caused by the abnormal morphogenesis of cilia. These cilia-related diseases are divided into two categories: ciliopathy resulting from defects of primary cilia and primary ciliary dyskinesia (PCD) caused by functional dysregulation of motile cilia. Cilia are widely distributed, and their related diseases can cover many human organs and tissues.

Dynamic pressure surface deformation measurement based on a chromatic confocal sensor.

To enable the real-time measurement of pressure deformations in sealed cavities, a high-precision method of detecting the deformation of a material surface is proposed. By combining a chromatic confocal displacement sensor with a pressure sensor, we can acquire dynamic online strain measurements that consider the effects of the deformed material and internal environmental conditions. A 90 ×90 static mechanical cylindrical cavity is simulated using finite element software.

Single-cell transcriptome analyses reveal microglia types associated with proliferative retinopathy.

Pathological angiogenesis is a major cause of irreversible blindness in individuals of all age groups with proliferative retinopathy (PR). Mononuclear phagocytes (MPs) within neovascular areas contribute to aberrant retinal angiogenesis. Due to their cellular heterogeneity, defining the roles of MP subsets in PR onset and progression has been challenging.

ATIC-Associated De Novo Purine Synthesis Is Critically Involved in Proliferative Arterial Disease.

Background: Proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of arterial diseases, especially in arterial restenosis after angioplasty or stent placement. VSMCs reprogram their metabolism to meet the increased requirements of lipids, proteins, and nucleotides for their proliferation. De novo purine synthesis is one of critical pathways for nucleotide synthesis.

Deoxynivalenol induces caspase-3/GSDME-dependent pyroptosis and inflammation in mouse liver and HepaRG cells.

Deoxynivalenol (DON), a frequent food and feed contaminant, poses a severe threat to human and livestock health. Some studies have demonstrated that DON could induce liver damage and cell death. However, novel cell death styles and detailed mechanisms to explain DON-induced liver inflammatory injury are still lacking.

Suppression of myeloid PFKFB3-driven glycolysis protects mice from choroidal neovascularization.

Background And Purpose: Pathological angiogenesis is a major cause of irreversible blindness in individuals with neovascular age-related macular degeneration (nAMD). Macrophages and microglia (MΦ) contribute to aberrant ocular angiogenesis. However, the role of glucose metabolism of MΦ in nAMD is still undefined.

Distinct gut microbiota and health outcomes in asymptomatic infection, viral nucleic acid test re-positive, and convalescent COVID-19 cases.

Gut microbiota composition is suggested to associate with coronavirus disease 2019 (COVID-19) severity, but the impact of gut microbiota on health outcomes is largely unclear. We recruited 81 individuals from Wuhan, China, including 13 asymptomatic infection cases (Group A), 24 COVID-19 convalescents with adverse outcomes (Group C), 31 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) re-positive cases (Group D), and 13 non-COVID-19 healthy controls (Group H). The microbial features of Groups A and D were similar and exhibited higher gut microbial diversity and more abundant short-chain fatty acid (SCFA)-producing species than Group C.

Endothelial AMPKα1/PRKAA1 exacerbates inflammation in HFD-fed mice.

Background And Purpose: Excess nutrient-induced endothelial cell inflammation is a hallmark of high fat diet (HFD)-induced metabolic syndrome. Pharmacological activation of the protein kinase AMP-activated α1 (PRKAA1) also known as AMPKα1, shows its beneficial effects in many studies of cardiometabolic disorders. However, AMPKα1, as a major cellular sensor of energy and nutrients in endothelial cells, has not been studied for its physiological role in excess nutrient-induced endothelial cell (EC) inflammation.

Deficiency of Myeloid Pfkfb3 Protects Mice From Lung Edema and Cardiac Dysfunction in LPS-Induced Endotoxemia.

Sepsis, a pathology resulting from excessive inflammatory response that leads to multiple organ failure, is a major cause of mortality in intensive care units. Macrophages play an important role in the pathophysiology of sepsis. Accumulating evidence has suggested an upregulated rate of aerobic glycolysis as a key common feature of activated proinflammatory macrophages.

T-2 Toxin Induces Oxidative Stress at Low Doses via Atf3ΔZip2a/2b-Mediated Ubiquitination and Degradation of Nrf2.

T-2 toxin is mainly produced by species, which is an extremely toxic mycotoxin to humans and animals. It is well known that T-2 toxin induces oxidative stress, but the molecular mechanism is still unknown. In this study, we found that T-2 toxin significantly promoted reactive oxygen species (ROS) accumulation in MCF-7 cells at low doses which maintains cell viability at least 80%.

Disruption of endothelial Pfkfb3 ameliorates diet-induced murine insulin resistance.

Overnutrition-induced endothelial inflammation plays a crucial role in high-fat diet (HFD)-induced insulin resistance in animals. Endothelial glycolysis plays a critical role in endothelial inflammation and proliferation, but its role in diet-induced endothelial inflammation and subsequent insulin resistance has not been elucidated. PFKFB3 is a critical glycolytic regulator, and its increased expression has been observed in adipose vascular endothelium of C57BL/6J mice fed with HFD in vivo, and in palmitate (PA)-treated primary human adipose microvascular endothelial cells (HAMECs) in vitro.

Prkaa1 Metabolically Regulates Monocyte/Macrophage Recruitment and Viability in Diet-Induced Murine Metabolic Disorders.

Myeloid cells, including monocytes/macrophages, primarily rely on glucose and lipid metabolism to provide the energy and metabolites needed for their functions and survival. AMP-activated protein kinase (AMPK, its gene is for human, for rodent) is a key metabolic sensor that regulates many metabolic pathways. We studied recruitment and viability of -deficient myeloid cells in mice and the phenotype of these mice in the context of cardio-metabolic diseases.

Mice with a specific deficiency of Pfkfb3 in myeloid cells are protected from hypoxia-induced pulmonary hypertension.

Background And Purpose: Macrophage infiltration into the lungs is a characteristic of pulmonary hypertension (PH). Glycolysis is the main metabolic pathway for macrophage activation. However, the effect of macrophage glycolysis on the development of PH remains unknown.

Ablation of endothelial Pfkfb3 protects mice from acute lung injury in LPS-induced endotoxemia.

Acute lung injury (ALI) is one of the leading causes of death in sepsis. Endothelial inflammation and dysfunction play a prominent role in development of ALI. Glycolysis is the predominant bioenergetic pathway for endothelial cells (ECs).

Inactivation of endothelial adenosine A receptors protects mice from cerebral ischaemia-induced brain injury.

Background And Purpose: Inactivation of the gene for adenosine A receptors (ADORA2A for humans and Adora2a for rodents) protects against brain injury in experimental stroke. However, the cell-specific pathogenic effects of A receptors in thromboembolic stroke and the underlying mechanisms remain undefined. Here, we tested the hypothesis that inhibition of endothelial A receptors after thromboembolic stroke improves post-stroke outcomes via down-regulation of inflammation.

Monitoring Avian Influenza Viruses from Chicken Carcasses Sold at Markets, China, 2016.

During 2016 in Guangzhou, China, we detected infectious avian influenza viruses (AIVs) in 39.8% of samples from chicken carcasses slaughtered at live poultry markets but none from carcasses supplied to supermarkets by facilities bypassing live poultry markets. Promoting supply chains with high biosecurity may reduce the risk for zoonotic AIV transmission.

[Comparison of differentiated endothelial cells from the embryonic stem cells with human umbilical vein endothelial cells].

To compare the differentiated endothelial cells from the embryonic stem cells in vitro with human umbilical vein endothelial cells (HUVECs).
 Methods: Induction of the stem cells HUES9 to endothelial cells follows 2 steps. Stem cells were treated with CHIR99021 (10 µmol/L) and bone morphogenetic protein 4 (25 ng/mL) for 3 days to keep mesoderm state, then subsequent exposure them to VEGF165 (200 ng/mL) and Forskolin (2 µmol/L) to differentiate into endothelial cells.

BET bromodomain is a novel regulator of TAZ and its activity.

Transcriptional coactivator with PDZ-binding motif (TAZ) is a key transcriptional mediator of Hippo signaling that has been recently reported to mediate Wnt-activated transcription and serve as a component to suppress canonical Wnt/β-catenin activity. The Bromodomain and Extra-terminal domain (BET) family of proteins can recognize the acetylated lysine chain on histones and plays a critical role in transcriptional regulation. However, the mechanisms underlying transcriptional repression by the BET bromodomain are poorly understood.

Inhibition of BET bromodomain attenuates angiotensin II induced abdominal aortic aneurysm in ApoE mice.

Background: Excessive degradation of extracellular matrix by matrix metalloproteinases (MMP) is the major pathological feature of abdominal aortic aneurysm (AAA). Suppression of extracellular matrix degradation attenuates AAA initiation and progression in preclinical models. In the present study, we wanted to test the effect of JQ1, a small chemical molecule that selectively targets bromodomain and extra-terminal domain (BET), on AngII induced AAA formation in ApoE mice.

[Y-27632 reduces the MMP2 and MMP9 expression in endothelial cell via inhibition of ROCK signal pathway].

Objective: To explore the effect of ROCK inhibitor Y-27632 on the matrix metalloproteinase 2 and 9 (MMP2 and MMP9) gene expression and activity in tumor necrosis factor α (TNF-α)-treated human umbilical vein endothelial cell (HUVEC).


Methods: HHUVEC was divided into 3 groups, a control group, a TNF-α group, and a TNF-α plus Y-27632 group. The expressions of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), MMP2 and MMP9 were examined by real-time PCR.