Influencing factors and improvement paths of manufacturing innovation performance: Configuration analysis based on TOE framework.

Innovation is the first driving force to lead development, how to improve manufacturing innovation performance has become a hot topic. Based on 47 listed companies in the computer, communication and other electronic equipment manufacturing industry in the A-share market, this paper adopted the Fuzzy set qualitative comparative analysis (fsQCA) to explore the influencing factors of technology, organization and environment on the innovation performance of manufacturing industry and the improvement path. The findings are as follows: (1) A single condition is not a necessary condition for high innovation performance in manufacturing industry, but government support plays a key role in improving innovation performance in manufacturing industry.

Electrochemically Oxidative Phosphating of Aldehydes and Ketones.

Disclosed herein is the first protocol for the electrochemically oxidative phosphating of aldehydes and ketones to generate α-hydroxyphosphine oxides with diphenylphosphine as the phosphine source. Various phosphating products containing P-C bonds are basically assembled in modest to excellent yields. This electrochemical phosphating was achieved by utilizing a simple undivided cell with foam nickel electrodes at room temperature without the addition of any oxidant or metal catalyst.

CXCL16 Promotes Ly6Chigh Monocyte Infiltration and Impairs Heart Function after Acute Myocardial Infarction.

High CXCL16 levels during acute cardiovascular events increase long-term mortality. However, the mechanistic role of CXCL16 in myocardial infarction (MI) is unknown. Here we investigated the role of CXCL16 in mice with MI injury.

Polyhalogenation-Facilitated Spirolactonization at the -Position of Phenols.

A novel dearomative spirolactonization/polyhalogenation of phenols that employs hypervalent iodine PhICl (iodobenzene dichloride) as both an oxidant and chlorine source with an indispensable base, or only using NBS (-bromosuccinimide) without any additives, is presented. Halide participations are a vital factor in the cascade reaction of 3'-hydroxy-[1,1'-biphenyl]-2-carboxylic acids with good selectivities and reactivities and induced the rapid constructions of multiple C-halogen bonds and directional C═O bonds in a one-step operation under mild conditions. In gaining a good understanding of the mechanism, the increase in number of bromine atoms was inferred rationally from the spirolactonization process, assisted by DFT calculations and high-resolution mass spectrometry.

Dual Loading Antiplatelet Therapy in Patients With Acute Coronary Syndrome and High Bleeding Risk Undergoing Percutaneous Coronary Intervention: Findings From the Improving Care for Cardiovascular Disease in China Project.

Objective: Loading dose of dual antiplatelet therapy (LD) is supported by the guidelines for patients with acute coronary syndrome (ACS). However, limited data is provided in the series of high bleeding risk (HBR) patients with ACS and percutaneous coronary intervention (PCI).

Methods: Using data from the Improving Care for Cardiovascular Disease in China-Acute Coronary Syndrome registry, conducted between 2014 and 2019, we stratified all ACS patients with HBR and PCI according to LD used within 24 h of first medical contact or not.

Secreted Frizzled-Related Protein 5 Protects Against Cardiac Rupture and Improves Cardiac Function Through Inhibiting Mitochondrial Dysfunction.

Secreted frizzled-related protein 5 (Sfrp5) has been suggested to be a protective regulatory protein in coronary heart disease. However, the role of Sfrp5 in regulating ischemic injury and its consequences is not known. The aim of our study was to explore the effects of Sfrp5 on hearts after myocardial infarction (MI) and to investigate the underlying mechanisms.

Phosphodiesterase-5a Knock-out Suppresses Inflammation by Down-Regulating Adhesion Molecules in Cardiac Rupture Following Myocardial Infarction.

Cardiac rupture is a fatal complication of acute myocardial infarction (MI), associated with increased inflammation and damaged extracellular matrix. C57BL/6 J wild type (WT) and Pde5a knockout (Pde5a) mice were selected to establish MI model. The rupture rate of Pde5a mice was significantly reduced (P < 0.

Facile fabrication of highly exothermic CuO@Al nanothermites via self-assembly approach.

CuO@Al nanothermites with Al shell and CuO core were successfully fabricated via a simple self-assembly route. The composition and morphology of CuO@Al nanothermites were analyzed by x-ray diffraction and field-emission scanning electron microscopy in detail. When the equivalence ratio was 1.

Trimetazidine suppresses oxidative stress, inhibits MMP-2 and MMP-9 expression, and prevents cardiac rupture in mice with myocardial infarction.

Background/aims: Cardiac rupture (CR) is a catastrophic complication of acute myocardial infarction (MI). At present, there are no effective pharmacological strategies for preventing post-MI rupture. Here we investigated the effect of trimetazidine (TMZ) on post-MI CR.

TMEM43-S358L mutation enhances NF-κB-TGFβ signal cascade in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a genetic cardiac muscle disease that accounts for approximately 30% sudden cardiac death in young adults. The Ser358Leu mutation of transmembrane protein 43 (TMEM43) was commonly identified in the patients of highly lethal and fully penetrant ARVD subtype, ARVD5. Here, we generated TMEM43 S358L mouse to explore the underlying mechanism.

The Complement C3aC3aR Axis Promotes Development of Thoracic Aortic Dissection via Regulation of MMP2 Expression.

Thoracic aortic dissection (TAD), once ruptured, is devastating to patients, and no effective pharmaceutical therapy is available. Anaphylatoxins released by complement activation are involved in a variety of diseases. However, the role of the complement system in TAD is unknown.

Haplodeficiency of Ataxia Telangiectasia Mutated Accelerates Heart Failure After Myocardial Infarction.

Background: Cell senescence is involved in the process of organ damage and repair; however, the underlying molecular mechanism needs to be further explored.

Methods And Results: Senescence-related genes (ie, p21, p53, and ataxia telangiectasia mutated [ATM]) were shown to be elevated after myocardial infarction (MI) in both mouse and human hearts. Ten- to 12-week-old male wild-type littermates (ATM) and ATM heterozygous mice (ATM) were subjected to MI.

ER stress dependent microparticles derived from smooth muscle cells promote endothelial dysfunction during thoracic aortic aneurysm and dissection.

The degeneration of vascular smooth muscle cell(s) (SMC) is one of the key features of thoracic aortic aneurysm and dissection (TAAD). We and others have shown that elevated endoplasmic reticulum (ER) stress causes SMC loss and TAAD formation, however, the mechanism of how SMC dysfunction contributes to intimal damage, leading to TAAD, remains to be explored. In the present study, assay demonstrated that elevated mechanical stretch (18% elongation, 3600 cycles/h) stimulated the ER stress response and microparticle(s) (MP) production from both SMC and endothelial cell(s) (EC) in a time-dependent manner.

Characterization of Hemodynamics in Great Arteries of Wild-Type Mouse Using Computational Fluid Dynamics Based on Ultrasound Images.

Hemodynamic factors in cardiovascular system are hypothesized to play a significant role in causing structural heart development. It is thus important to improve our understanding of velocity characteristics and parameters. We present such a study on wild-type mouse to characterize the vessel geometry, flow pattern, and wall shear stress in great arteries.

Deficiency of IL-12p35 improves cardiac repair after myocardial infarction by promoting angiogenesis.

Aims: IL-12p35 is a pro-inflammatory cytokine that participates in a variety of inflammatory diseases. This study aimed to determine whether IL-12 regulates cardiac injury and repair following acute myocardial infarction (AMI) and investigate the underlying mechanisms.

Methods And Results: Mice with AMI showed a marked increase in IL-12p35 expression of ischaemic cardiac tissues.