ABSTRACT
BACKGROUND: Compared with a classic wrist puncture for radial artery catheterization, a distal radial artery puncture has the advantage of reducing the incidence of radial artery occlusion in anatomic and physiological procedures. This study aimed to explore the difference in clinical effects between the distal radial artery and classic radial artery approaches in percutaneous coronary intervention. METHODS: A total of 620 patients who underwent coronary angiography and/or percutaneous coronary intervention in our hospital from December 2017 to December 2018 were enrolled in this study. These patients were divided into two groups based on the puncture site: a distal radial artery group and a classic radial artery group. There were 312 patients in the radial artery group and 308 patients in the classic radial artery group. The puncture time, puncture success rate, surgery time, implanted stents, puncture site hemorrhage, hematoma, aneurysm, and iliac artery occlusion rate were observed. RESULTS: There was no significant difference in puncture time, puncture success rate, surgery time, implanted stent, puncture site hemorrhage, hematoma and aneurysm (P>0.05), while the radial artery occlusion rate was lower in the distal radial artery group, and the difference was statistically significant (P<0.05). CONCLUSIONS: The results of this study showed that the distal radial artery approach had a lower rate of brachial artery occlusion, indicating that it could be used as an alternative to the classic radial artery approach.
Subject(s)
Percutaneous Coronary Intervention , Radial Artery , Coronary Angiography , Humans , Incidence , PuncturesABSTRACT
Aging can cause retinal degeneration, which leads to visual impairment among the elderly population. Age-dependent increases in amyloid beta (Aß) inducesinflammatory cytokine overexpression in the retinal pigment epithelium (RPE), which promotes the progression of age-related retinal degeneration. However, whether dietary antioxidants are useful for the treatment of RPE degeneration remains to be clarified. This study exposited the protective activities and underlying mechanisms of grape seed extracts (GSEs) against Aß-induced proinflammatory events in mouse retinas and ARPE-19 cells. The experimental data demonstrated that GSEs attenuated the increases in messenger RNA (mRNA) levels of interleukin 12 (IL-12), interleukin 6 (IL-6), interleukin 1ß (IL-1ß), and interleukin 18 (IL-18) in the retinal tissues of Aß-treated mice. The experimental results in mice were confirmed by findings in ARPE-19 cells with or without treatment with GSEs. GSEs affected the protein expression levels of endoplasmic reticulum stress markers in ARPE-19 cells exposed to Aß. Knockdown of Bip blocked the inhibitory activities of GSEs on mRNA levels of IL-6, IL-1ß, IL-18, and IL-8. We conclude that GSEs may suppress proinflammatory cytokines partly by increasing the expression of Bip.
Subject(s)
Amyloid beta-Peptides/analysis , Endoplasmic Reticulum Stress/drug effects , Grape Seed Extract/therapeutic use , Interleukins/analysis , Retinal Pigment Epithelium/drug effects , Animals , Cell Line , Dietary Supplements , Mice , Mice, Inbred C57BL , VitisABSTRACT
Objective: Hyperglycemia-mediated cardiomyocyte damage is associated with inflammation and AMPK inactivation.Aim: The aim of our study is to explore the protective effects exerted by liraglutide on AMPK pathway and glucagon-like peptide 1 receptor in diabetic cardiomyopathy.Methods: Cardiomyocytes were treated with high-glucose stress and cardiomyocyte viability was determined via (3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide assay. Besides, LDH release, immunofluorescence, and qPCR were used to verify the influence of liraglutide on hyperglycemia-treated cardiomyocytes.Results: Hyperglycemia treatment caused inflammation response and oxidative stress were significantly elevated in cardiomyocytes. This alteration could be reversed by liraglutide. Besides, cell viability was reduced whereas apoptosis was increased after exposure to high glucose treatment. However, liraglutide treatment could attenuate apoptosis and reverse cell viability in cardiomyocyte. Further, we found that AMPK pathway was also activated and glucagon-like peptide 1 receptor expression was increased in response to liraglutide treatment.Conclusions: Liraglutide could attenuate hyperglycemia-mediated cardiomyocyte damage through reversing AMPK pathway and upregulating glucagon-like peptide 1 receptor.
Subject(s)
Glucagon-Like Peptide-1 Receptor/genetics , Hyperglycemia/drug therapy , Inflammation/drug therapy , Liraglutide/pharmacology , Protein Kinases/genetics , AMP-Activated Protein Kinase Kinases , Animals , Cell Death/drug effects , Cell Survival/drug effects , Glucose/toxicity , Humans , Hyperglycemia/genetics , Hyperglycemia/pathology , Inflammation/chemically induced , Inflammation/genetics , Inflammation/pathology , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology , Oxidative Stress/drug effects , RatsABSTRACT
Context: Although many studies have investigated the molecular mechanisms underlying hypoxia-related cardiomyocyte damage, the role of necrosis in cardiomyocyte death.Objective: The aim of our study is to explore the pathological role of nuclear receptor related 1 protein (NURR1) in regulating cardiomyocyte viability under hypoxia stress.Materials and methods: Cardiomyocyte was treated with hypoxia and siRNA against NURR1 was transfected into cardiomyocyte. Pathway agonist was used to activate the Mst1-JNK-mPTP pathway in cardiomyocyte.Results: In our study, the expression of NURR1 was rapidly increased in cardiomyocyte transfected with NURR1. Knockout of NURR1 could promote cardiomyocyte survival, reduce cell death and repress inflammation response. Mechanistically, NURR1 upregulation was associated with an activation of Mst1-JNK pathway and the latter promoted the mPTP opening in cardiomyocyte. Excessive mPTP opening was followed by cardiomyocyte necrosis and this effect could be reversed by NURR1 deletion. Besides, re-activation of Mst1-JNK pathway could abolish the protective effects of NURR1 deletion on cardiomyocytes, as evidenced by increased cell survival and decreased necrosis. Besides, re-activation of Mst1-JNK pathway also abolished NURR1 deletion-mediated mPTP opening.Conclusions: Hypoxia-mediated cardiomyocyte death is associated with NURR1 upregulation which contributes to the activation Mst1-JNK-mPTP pathways.
Subject(s)
Hepatocyte Growth Factor/antagonists & inhibitors , Hypoxia/physiopathology , Inflammation/prevention & control , MAP Kinase Kinase 4/antagonists & inhibitors , Mitochondrial Membrane Transport Proteins/antagonists & inhibitors , Myocytes, Cardiac/pathology , Necrosis , Nuclear Receptor Subfamily 4, Group A, Member 2/metabolism , Proto-Oncogene Proteins/antagonists & inhibitors , Animals , Cells, Cultured , Hepatocyte Growth Factor/genetics , Hepatocyte Growth Factor/metabolism , Inflammation/etiology , Inflammation/metabolism , Inflammation/pathology , MAP Kinase Kinase 4/genetics , MAP Kinase Kinase 4/metabolism , Mice , Mitochondrial Permeability Transition Pore , Myocytes, Cardiac/metabolism , Nuclear Receptor Subfamily 4, Group A, Member 2/genetics , Proto-Oncogene Proteins/genetics , Proto-Oncogene Proteins/metabolism , Signal TransductionABSTRACT
A new method has been developed to simultaneously determine 7 pyrethroid residues in tea brew using gas chromatography-mass spectrometry (GC-MS) combined with solid phase microextraction (SPME) with multiwalled carbon nanotubes (MWCNTs) coated fiber. The MWCNTs coated fiber of SPME was homemade by using stainless steel wire as coating carrier and polyacrylonitrile (PAN) solution as adhesive glue. Under the optimized conditions, a good linearity was shown for bifenthrin, fenpropathrin, permethrin, and cyfluthrin in 1-50 ng mL-1 and for cypermethrin, fenvalerate, and deltamethrin in 5-50 ng mL-1. The correlation coefficients were in the range of 0.9948-0.9999. The average recoveries of 7 pyrethroids were 94.2%-107.3% and the relative standard deviations (RSDs) were less than 15%. The detection limit of the method ranged from 0.12 to 1.65 ng mL-1. The tea brew samples made from some commercial tea samples were analyzed. Among them, bifenthrin, fenpropathrin, and permethrin were found. The results show that the method is rapid and sensitive and requires low organic reagent consumption, which can be well used for the detection of the pyrethroids in tea brew.
