CCAAT/Enhancer-Binding Protein Beta Nitration Participates in Hyperhomocysteinemia-Induced Cardiomyocyte Autophagic Flux Blockage by Inhibiting Transcription Factor EB Transcription.

Autophagy is a protective mechanism of cardiomyocytes. Hyperhomocysteinemia (HHcy) elevates oxidative and nitrosative stress levels, leading to an abnormal increase in nitration protein, possibly leading to abnormal autophagy regulation in cardiomyocytes. However, the regulatory effect of HHcy on autophagy at the post-translational modification level is still unclear.

Endogenous sulfur dioxide deficiency as a driver of cardiomyocyte senescence through abolishing sulphenylation of STAT3 at cysteine 259.

Objective: Cardiomyocyte senescence is an important contributor to cardiovascular diseases and can be induced by stressors including DNA damage, oxidative stress, mitochondrial dysfunction, epigenetic regulation, etc. However, the underlying mechanisms for the development of cardiomyocyte senescence remain largely unknown. Sulfur dioxide (SO) is produced endogenously by aspartate aminotransferase 2 (AAT2) catalysis and plays an important regulatory role in the development of cardiovascular diseases.

Electronic parking algorithm of new energy vehicle on slope based on FMPC.

Since the unique structure and transmission mode of new energy vehicles, the problem of parking prediction and control has always been the focus of its research. Therefore, to handle the predictive control problem of new energy vehicles in slope environments, the FMPC algorithm is applied to replace the core PID controller of new energy vehicles, and it is effectively validated using automotive simulation software on different slopes and vehicle masses. The experimental results indicate that new energy vehicles with FMPC algorithm can complete parking in about 6 s under different slopes and vehicle masses, while the PID algorithm may experience shaking and displacement.

Improvement and application of electromagnetic vibration and noise suppression method for electric vehicle motor.

Motor induced Electromagnetic Vibration and Noise (EVN) are mainly affected by Radial Electromagnetic Force Wave (REFW) and related harmonic amplitude. Therefore, in the past discussion on the suppression of motor induced EVN, it usually starts from this aspect. For this reason, this study proposes a method to suppress EVN.

Endogenous Hydrogen Sulfide Persulfidates Caspase-3 at Cysteine 163 to Inhibit Doxorubicin-Induced Cardiomyocyte Apoptosis.

Doxorubicin (DOX) is an efficient antitumor anthracycline drug, but its cardiotoxicity adversely affects the prognosis of the patients. In this study, we explored whether endogenous gasotransmitter hydrogen sulfide (HS) could protect against DOX-induced cardiomyocyte apoptosis and its mechanisms. The results indicated that DOX significantly downregulated endogenous HS production and endogenous synthetase cystathionine -lyase (CSE) expression and obviously stimulated the apoptosis in H9C2 cells.

Nitric oxide inhibits endothelial cell apoptosis by inhibiting cysteine-dependent SOD1 monomerization.

Endothelial cell apoptosis is an important pathophysiology in many cardiovascular diseases. The gasotransmitter nitric oxide (NO) is known to regulate cell survival and apoptosis. However, the mechanism underlying the effect of NO remains unclear.

Endothelial Cell-Derived SO Controls Endothelial Cell Inflammation, Smooth Muscle Cell Proliferation, and Collagen Synthesis to Inhibit Hypoxic Pulmonary Vascular Remodelling.

Hypoxic pulmonary vascular remodelling (PVR) is the major pathological basis of aging-related chronic obstructive pulmonary disease and obstructive sleep apnea syndrome. The pulmonary artery endothelial cell (PAEC) inflammation, and pulmonary artery smooth muscle cell (PASMC) proliferation, hypertrophy and collagen remodelling are the important pathophysiological components of PVR. Endogenous sulfur dioxide (SO) was found to be a novel gasotransmitter in the cardiovascular system with its unique biological properties.

Abnormal nitration and S-sulfhydration modification of Sp1-CSE-HS pathway trap the progress of hyperhomocysteinemia into a vicious cycle.

Sp1-CSE-HS pathway plays an important role in homocysteine-metabolism, whose disorder can result in hyperhomocysteinemia. HS deficiency in hyperhomocysteinemia has been reported, while the underlying mechanism and whether it in turn affects the progress of hyperhomocysteinemia are unclear. This study focused on the post-translational modification of Sp1/CSE and revealed four major findings: (1) Homocysteine-accumulation augmented CSE's nitration, inhibited its bio-activity, thus caused HS deficiency.

Nitrative Stress-Related Autophagic Insufficiency Participates in Hyperhomocysteinemia-Induced Renal Aging.

The kidneys are important organs that are susceptible to aging. Hyperhomocysteinemia (HHcy) is a risk factor for nephropathy and is associated with chronic nephritis, purpuric nephritis, and nephrotic syndrome. Numerous studies have shown that elevated serum homocysteine levels can damage the kidneys; however, the underlying mechanism of HHcy on kidney damage remains unclear.

Omi/HtrA2 Participates in Age-Related Autophagic Deficiency in Rat Liver.

Liver is a vital organ with many important functions, and the maintenance of normal hepatic function is necessary for health. As an essential mechanism for maintaining cellular homeostasis, autophagy plays an important role in ensuring normal organ function. Studies have indicated that the degeneration of hepatic function is associated with autophagic deficiency in aging liver.

Cyclic peptide RD808 reduces myocardial injury induced by β-adrenoreceptor autoantibodies.

Autoantibodies against the second extracellular loop of β-adrenergic receptor (β-AA) have been shown to be involved in the development of cardiovascular diseases. Recently, there has been considerable interest in strategies to remove these autoantibodies, particularly therapeutic peptides to neutralize β-AA. Researchers are investigating the roles of cyclic peptides that mimic the structure of relevant epitopes on the β-AR-EC in a number of immune-mediated diseases.

[Hydroxysafflor yellow A inhibits rat vascular smooth muscle cells proliferation possibly via blocking signal transduction of MEK-ERK1/2].

Objective: To elucidate the effect of hydroxysafflor yellow A ( HYSA) on the proliferation of vascular smooth muscle cells (VSMCs) and the related mechanism.

Methods: VSMCs derived from SD rats were treated with DMEC culture medium (Control), 10 ng/ml PDGF (PDGF group), pretreatment with HYSA at different doses (1, 5, 10, 20, 40, 60 µmol/L) for 24 h then cotreatment with PDGF. After 24 h, MTT assay, Western blot and immunohistochemical staining were performed to evaluate the inhibitory effects of HYSA on VSMCs proliferation.

Meta-analysis of phospholipase C epsilon 1 polymorphism and cancer risk.

Background: Phospholipase C epsilon 1 (PLCE1) plays crucial roles in carcinogenesis and progression of several cancers. A single nucleotide polymorphism (SNP, rs2274223) in PLCE1 has been identified as a novel susceptibility locus.

Methods: To evaluate the role of the Phospholipase C epsilon 1 (PLCE1) polymorphism in cancer susceptibility.

Genetic polymorphisms in key DNA repair genes and risk of head and neck cancer in a Chinese population.

Although tobacco and alcohol consumption are the major risk factors of head and neck cancer (HNC), genetic variations of genes involved in several biological pathways, such as DNA repair genes, may affect an individual's susceptibility to HNC. However, few studies have investigated the associations between polymorphisms in DNA repair genes and HNC risk in the Chinese population. Thus, we genotyped five common, non-synonymous single-nucleotide polymorphisms (SNPs) [APEX1 (Asp148Glu), XRCC1 (Arg399Gln), ADPRT (Val762Ala), XPD (Lys751Gln) and XPG (His1104Asp)] in a hospital-based, case-control study of 397 HNC cases and 900 cancer-free controls in China.