Cause Of Coronary Heart Disease Research Articles

Association Between CYP2D7 and TCF20 Polymorphisms and Coronary Heart Disease.

One of the causes of coronary heart disease (CHD) is genetic factors. In this study, we explored the relationship between CYP2D7 and TCF20 gene polymorphisms and the risk of CHD in the Han Chinese population. Three single nucleotide polymorphisms (CYP2D7 rs1800754, CYP2D7 rs2743461, and TCF20 rs760648) were selected and genotyped from 490 cases and 480 controls. The odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the association between CYP2D7 and TCF20 polymorphisms and the risk of CHD. The association between clinical indicators and polymorphisms was analyzed using one-way ANOVA and Tukey's HSD. The SNP-SNP interactions were obtained by performing multifactor dimensionality reduction (MDR). CYP2D7 rs1800754 and rs2743461 were closely associated with increased risk of CHD (alleles: p = 0.014, p = 0.031). Stratified analysis showed that CYP2D7 rs1800754 and rs2743461 were associated with an increased risk of CHD in men, age > 60years, BMI ≥ 24, and smoking. Rs1800754 is also associated with an increased risk of CHD associated with alcohol consumption. In addition, TCF20 rs760648 was associated with a reduced risk of CHD in patients aged ≤ 60years and with CALs. A significant association was found between CYP2D7 rs1800754 and rs2743461 genotypes and levels of UREA, Cr, and LDL-C; TCF20 rs760648 genotypes and levels of RBC. The MDR analysis showed that the three-locus interaction model was the best in the multi-locus model. In conclusion, CYP2D7 rs1800754 and rs2743461 polymorphisms were associated with CHD risk.

Apolipoprotein E E3/E4 genotype is associated with an increased risk of premature coronary artery disease

ObjectiveDyslipidemia is one of the causes of coronary heart disease (CAD), and apolipoprotein E (APOE) gene polymorphism affects lipid levels. However, the relationship between APOE gene polymorphisms and premature CAD (PCAD, male CAD patients with ≤ 55 years old and female with ≤ 65 years old) risk had different results in different studies. The aim of this study was to assess this relationship and to further evaluate the relationship between APOE gene polymorphisms and PCAD risk in the Hakka population.MethodsThis study retrospectively analyzed 301 PCAD patients and 402 age matched controls without CAD. The APOE rs429358 and rs7412 polymorphisms were genotyped by polymerase chain reaction (PCR) -chip technique. The distribution of APOE genotypes and alleles between the case group and the control group was compared. The relationship between APOE genotypes and PCAD risk was obtained by logistic regression analysis.ResultsThe frequency of the APOE ɛ3/ɛ4 genotype (18.9% vs. 10.2%, p = 0.001) and ε4 allele (11.1% vs. 7.0%, p = 0.007) was higher in the PCAD patients than that in controls, respectively. PCAD patients with ɛ2 allele had higher TG level than those with ɛ3 allele, and controls carried ɛ2 allele had higher HDL-C level and lower LDL-C level than those carried ɛ3 allele. Regression logistic analysis showed that BMI ≥ 24.0 kg/m2 (BMI ≥ 24.0 kg/m2 vs. BMI 18.5–23.9 kg/m2, OR: 1.763, 95% CI: 1.235–2.516, p = 0.002), history of smoking (Yes vs. No, OR: 5.098, 95% CI: 2.910–8.930, p < 0.001), ɛ3/ɛ4 genotype (ɛ3/ɛ4 vs. ɛ3/ɛ3, OR: 2.203, 95% CI: 1.363–3.559, p = 0.001), ε4 allele (ε4 vs. ε3, OR: 2.125, 95% CI: 1.333–3.389, p = 0.002), and TC level (OR: 1.397, 95% CI: 1.023–1.910, p = 0.036) were associated with PCAD.ConclusionsIn summary, BMI ≥ 24.0 kg/m2, history of smoking, APOE ɛ3/ɛ4 genotype, and TC level were independent risk factors for PCAD. It means that young individuals who are overweight, have a history of smoking, and carried APOE ɛ3/ɛ4 genotype had increased risk of PCAD.

Coronary heart disease: innovative understanding from traditional Chinese medicine and treatment by classic formulas

Coronary heart disease is a common cardiovascular disease, attacking about 11.4 million patients in China. With increasing prevalence and mortality year by year, coronary heart disease has become a major factor threatening human health and public health. Although primary and secondary prevention, intervention, coronary artery bypass grafting and other interventions have reduced the death rate, there are drug(aspirin) resistance, secondary nitroglycerin failure, post-intervention fatigue, chest tightness, and an-xiety, and complication with a high risk of bleeding, which have become the key clinical and scientific issues needed to be resolved. Coronary heart disease belongs to the category of chest impediment and heart pain in traditional Chinese medicine(TCM). The TCM etiology of this disease includes external contraction of cold, emotional disorders, constitutional insufficiency, physical weakness, and labor injury, which are closely related to sympathetic nerve activity, state of cardiac and psychological diseases, family history, and cardiovascular metabolic disorders in modern medicine. The TCM causes of coronary heart disease include Qi depression, phlegm turbidity, blood stasis, fire-heat, cold congealing, and healthy Qi deficiency, which are associated with emotional factors such as anxiety and depression, abnormal lipid metabolism, abnormalities in blood circulation and coagulation, inflammatory responses, hyperactive immune responses, and heart failure, chronic wasting disease, or aging, respectively. Accordingly, the patients with Qi depression should be treated with Chaihu Longgu Muli Decoction, and those with phlegm turbidity should be treated with Wendan Decoction and Gualou Xiebai Banxia Decoction. Xuefu Zhuyu Decoction and Guizhi Fuling Pills are recommended for blood stasis, Xiaoxianxiong Decoction and Sanhuang Xiexin Decoction for fire-heat, Zhishi Xiebai Guizhi Decoction for cold congealing, and Renshen Decoction for healthy Qi deficiency. Due to the changes in the spectrum of diseases from ancient to modern times as well as the differences in physical constitution, the key cause of coronary heart disease has evolved from the chest Yang deficiency and cold congealing to Qi depression, phlegm turbidity, phlegm combined with stasis, and fire-heat, showing a shift from cold to heat and from deficiency to excess. The combination of classic formulas presents a pattern. That is, the core formula-syndrome correspondence of a disease often fixedly appears with other formula-syndrome correspondence, which may be related to the development of the pathophysiological mechanism of the disease. In the clinical application of modern pharmacological results, the research team has formulated the clinical principle of pathogenesis corresponding to pathological changes and medicinal nature corresponding pharmacological effects. The modern pharmacological research on classic formulas is conducive to targeted treatment. Moreover, classic formulas help to ameliorate aspirin resistance, clopidogrel resistance, post-intervention anxiety, and high risk of bleeding and address the lack of effective blockade of critical lesions in the coronary artery and the progression of post-infarction heart failure. The innovative understanding of the etiology and pathogenesis of co-ronary heart disease helps to improve the clinical efficacy of TCM and the clinical system for treating coronary heart disease with classic formulas.

Combinatory data-independent acquisition and parallel reaction monitoring method for revealing the lipid metabolism biomarkers of coronary heart disease and its comorbidities.

Disorders of lipid metabolism are a common cause of coronary heart disease (CHD) and its comorbidities. In this study, ultra-performance liquid chromatography-high-resolution mass spectrometry in data-independent acquisition (DIA) mode was applied to collect abundant tandem mass spectrometry data, which provided valuable information for lipid annotation. For the lipid isomers that could not be completely separated by chromatography, parallel reaction monitoring (PRM) mode was used for quantification. A total of 223 plasma lipid metabolites were annotated, and 116 of them were identified for their fatty acyl chain composition and location. In addition, 152 plasma lipids in patients with CHD and its comorbidities were quantitatively analyzed. Multivariate statistical analysis and metabolic pathway analysis demonstrated that glycerophospholipid and sphingolipid metabolism deserved more attention for CHD. This study proposed a method combining DIA and PRM for high-throughput characterization of plasma lipids. The results also improved our understanding of metabolic disorders of CHD and its comorbidities, which can provide valuable suggestions for medical intervention.

Treatment of Coronary Heart Disease from the Perspective of Liver Controlling Dispersion

The liver is in charge of distributing and regulating the movement of qi throughout the whole body, coordinating the transportation and transformation of the internal organs in the middle part of the body, promoting the biochemical circulation of qi, blood, and body fluids, and regulating emotions. Liver dysfunction can disrupt the transportation and transformation of qi, blood, and body fluids, causing phlegm turbidity, blood stasis, and other unwanted symptoms. Poor regulation of emotion further aggravates the accumulation of pathological substances, resulting in the obstruction of heart vessels, and ultimately coronary heart disease (CHD). Through regulating lipid metabolism, inflammatory reaction, vasoactive substances, platelet function, neuroendocrine, and other factors, liver controlling dispersing qi plays a comprehensive role in the prognosis of atherosclerosis, the primary cause of CHD. Therefore, it is recommended to treat CHD from the perspective of liver-controlling dispersion.

Immune Homeostasis Maintenance Through Advanced Immune Therapeutics to Target Atherosclerosis.

Atherosclerosis remains the leading cause of coronary heart disease (CHD) with enormous health and societal tolls. Traditional drug development approaches have been focused on small molecule-based compounds that aim to lower plasma lipids and reduce systemic inflammation, two primary causes of atherosclerosis. However, despite the widely available lipid-lowering and anti-inflammatory small compounds and biologic agents, CHD prevalence still remains high. Based on recent advances revealing disrupted immune homeostasis during atherosclerosis pathogenesis, novel strategies aimed at rejuvenating immune homeostasis with engineered immune leukocytes are being developed. This chapter aims to assess basic and translational efforts on these emerging strategies for the effective development of atherosclerosis treatment, as well as key challenges in this important translational field.

Association between six-minute walk distance and prognosis of atherosclerotic coronary heart disease post-cardiac rehabilitation.

Plaque accumulation in the coronary arteries is a major cause of coronary heart disease (CHD), a disease infamously known as a contributor for global death burden. Major adverse cardiac events (MACE) pose significant risks for CHD patients, highlighting the urgency of effective management and cardiac rehabilitation in CHD management. Studies have reported the role of the six-minute walk distance (6MWD) test in predicting outcomes for CHD patients; however, none have performed the investigation in Aceh setting. The aim of this study was to investigate the reliability of 6MWD as a prognostic factor for post-cardiac rehabilitation of patients with atherosclerotic CHD. A cross-sectional study was conducted in Dr. Zainoel Abidin Hospital, Banda Aceh, Indonesia. MACE was determined through in-person interviews, and phone calls with 30 atherosclerotic CHD patients who completed cardiac rehabilitation between August 2018 and September 2020. The association between 6MWD and prognosis, assessed by MACE incidence, was calculated. The results revealed that 6MWD was strongly associated with MACE occurrence during post-cardiac rehabilitation (p=0.029; prevalence ratio 4.5). Furthermore, CHD patients achieving 6MWD of more than 300 meters exhibited a lower incidence of MACE (10.5%) than patients with 6MWD of less than 300 meters (45.5%). In conclusion, the present study sheds light on the importance of improving functional capacity in patients with atherosclerotic CHD post-cardiac rehabilitation due to its significant association with the prognosis.

Dietary antioxidant intake reduces carotid intima-media thickness in coronary heart disease patients: From the CORDIOPREV study

BackgroundAtherosclerosis is the leading underlying cause of coronary heart disease (CHD). In patients with CHD, intima-media thickness of common carotid arteries (IMT-CC) is a reliable, validated, and non-invasive marker of the progression of atherosclerosis. Dietary intervention may affect IMT-CC evolution through different pathways. There is a lack of clinical trials evaluating the effect of total dietary antioxidant content of diets on IMT-CC, especially in patients with CHD. ObjectiveWe evaluated the correlation between the diet's total antioxidant content and the changes in IMT-CC produced after 5 years of dietary intervention following two healthy diet models (Mediterranean diet and low-fat diet). We also evaluated whether the diet's total antioxidant content was related to the total redox capacity of the participants. MethodsFrom the total participants of the CORDIOPREV study (clinical trial register NCT00924937), 805 participants completed the IMT-CC measurement and the dietary antioxidant evaluation at baseline and after 5 years of dietary intervention. IMT-CC was carried out by ultrasound and the dietary antioxidant evaluation was performed by the Dietary Antioxidant Index (DAI). Additionally, direct redox balance was evaluated in a subset of population by the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSH) by colorimetric assay. ResultsWe observed an inverse correlation between evolution of DAI and IMT-CC after 5-years of dietary intervention. The mean of the DAI index augmented in the Mediterranean Diet group, whereas it decreased in the Low-fat group. DAI was correlated to the GSH/GSSG ratio, supporting DAI as an adequate estimator of diet's antioxidant content. When looking for individual components of the DAI that were associated to the changes in IMT-CC, an inverse correlation was found for carotenoids, vitamin E, vitamin C, and zinc and the IMT-CC. ConclusionsOur study indicates that, after five years of dietary intervention, changes in DAI inversely correlate with changes in IMT-CC in patients with CHD. Overall effect of Mediterranean diet resulted in an increase of DAI, conversely to low-fat. Specific elements included in the DAI index were inversely correlated with IMT-CC.

Coronary Microvascular Dysfunction: Epidemiology, Clinical Presentation, Diagnosis and Treatment

In a significant number of patients with symptoms of angina pectoris or myocardial infarction with ischemic changes in the myocardium, according to the results of instrumental research methods, there is no hemodynamically significant stenosis of the coronary arteries. In these cases, vasospastic angina or microvascular dysfunction is considered the cause of coronary heart disease. Coronary microvascular dysfunction is caused by several pathological mechanisms that cause structural and functional disorders in the microvascular bed of the heart. Clinical groups of coronary microvascular dysfunction include angina pectoris and myocardial ischemia without obstructive coronary artery disease (primary coronary microvascular dysfunction), in combination with coronary atherosclerosis, with myocardial damage and iatrogenic nature. Diagnostics of microvascular disorders is carried out on the basis of the results of non-invasive and invasive methods, which make it possible to clarify the nature of the changes and choose an effective nondrug and drug treatment. The prognosis for coronary microvascular dysfunction is poor, due to the development of cardiovascular complications and death, a high risk of disability, and a decrease in the quality of life of patients.

Modeling and numerical simulation of non-Newtonian arterial blood flow for mild to severe stenosis

The fundamental cause of coronary heart disease is thought to be atherosclerosis. Blood flow in arteries under plaque formation is widely studied using both experimental and theoretical methods in literature. This paper presents a comprehensive study on the mathematical modelling and numerical simulation of non-Newtonian blood flow in an idealized stenosed artery. Non-Newtonian behavior of blood flow is assumed by Casson and Quemada fluid models. An analysis is performed for four forms of stenosis, 50%, 60%, 70%, and 80%, which are defined by a narrowing of the artery's diameter. The mathematical model for non-Newtonian fluid transport is presented in the form of highly nonlinear coupled partial differential equations. A finite-volume approach is used to solve the system of equations numerically. The solutions are obtained using a hybrid mesh with hexahedron and tetrahedron control volumes. Numerical solutions are validated first with experimental results from the literature for a Newtonian fluid, and then the results are extended to non-Newtonian fluid models. It can be observed that the non-Newtonian nature of the fluid model influences flow dynamics and is a significant aspect to consider for arteries with small diameter. The velocity and pressure drop rise as the degree of stenosis develops. Wall shear is substantially larger in stenotic passages and severity of stenosis is directly related with this increasing behavior.

The genetic etiology of critical congenital heart disease

Congenital Heart Disease (CHD) is the most common kind of birth defect. Congenital heart disease is the most common birth defect and the leading cause of death in newborns. The causes of CHD are complicated and involve both genes and the environment. Congenital heart disease includes problems with the septum, the valves, and the outflow tract. Correctional heart surgery and new strategies for managing CHD have massively enhanced life expectancy. 490 percent of CHD newborns who live through their first year will become adults. Studies of the molecular genetics of humans and animal models of development are enhancing our understanding of normal heart development and cardiac diseases. A recent study demonstrates that microRNAs are implicated in congenital heart diseases. Epigenetic variables were eventually revealed to influence heart development. Several genes are responsible for congenital cardiac abnormalities as well as genetic disorders. This paper describes the categorization, environmental, and genetic causes of Coronary Heart Disease (CHD), the role of key CHD-causing genes, and potential options for preventing CHD.

Identification of Key Genes in Atherosclerosis by Combined DNA Methylation and miRNA Expression Analyses.

Atherosclerosis is a significant cause of coronary heart disease, cerebral infarction, and peripheral vascular disease. The objective of this study was to identify the key genes aberrantly expressed in atherosclerosis, which were regulated by microRNAs and DNA methylation. We acquired data on DNA methylation and microRNA and messenger RNA expression from Gene Expression Omnibus data sets (GSE46394, GSE53675, and GSE12288, respectively) and identified differentially methylated genes, differentially expressed genes, and differentially expressed microRNAs between atherosclerosis and control samples. The miRDB, miRTarBase, and TargetScan databases were used to predict differentially expressed microRNAs-targeted genes, which were then intersected with differentially methylated genes and differentially expressed genes to identify genes associated with aberrant DNA methylation and microRNA activity. The DAVID database was used to perform functional enrichment analysis of differentially methylated genes and the key genes involved in atherosclerosis. Potential therapeutic agents for atherosclerosis were predicted by Connectivity Map analysis. In total, we identified 47 upregulated hypomethylated and 90 downregulated hypermethylated genes in atherosclerosis. Among them, 24 differentially expressed genes were found to be modulated both through aberrant DNA methylation and microRNA expression, and 10 such differentially expressed genes were defined as the key genes in atherosclerosis. Fifteen chemicals were selected for their potential effect in . We identified 10 key genes significantly associated with aberrant DNA methylation and microRNA expression in atherosclerosis and suggested 15 chemicals with potential effects on these genes, which could be further investigated as candidate drugs for atherosclerosis.

Prevalence of standard modifiable cardiovascular risk factors in patients with ST segment elevation myocardial infarction and its relation with outcomes

Abstract Background It has been recently suggested that more than 15% of patients with ST-segment–elevation myocardial infarction (STEMI) lack any of the standard modifiable risk factors (cigarette smoking, diabetes, hyperlipidemia, and hypertension -SMuRFs). This claim implies that other factors play a significant role in development of STEMI and has led to considerable interest in genetic causes of coronary heart disease including family history (FHx) Purpose To investigate whether FHx may be a significant driver for STEMI in patients without SMuRFs. Methods We analyzed 11,840 patients with ACSs, without evidence of prior cardiovascular disease (CVD) enrolled in the ISACS-TC (International Survey of Acute Coronary Syndromes in Transitional Countries) registry between January 2010 to January 2021. Main outcome measures were the adjusted rates of STEMI and 30-day mortality from STEMI using multivariable logistic regression models. Patients presenting with non-ST elevation acute coronary syndromes served as controls. Results Among patients with STEMI, at least 1 of the 4 conventional risk factors was present in 88.1% of women and 86.7% of men. Overall, 3,194 patients (27.0%) self-reported a FHx of CV disease, defined as a first-degree relative with premature CV events (men, age &amp;lt;55 years; women, age &amp;lt;65 years). There were 261 (8.2%) patients with FHx but without SMuRFs and 2,933 (91.8%) patients with FHx and SMuRFs. After adjusting for age, and standard risk factors, FHx was associated with a significantly lower incidence of STEMI in patients with SMuRFs, but not in those without SMuRFs (ORs: 0.87; 95% Cl: 0.79 to 0.97 vs 0.80; 95% Cl: 0.58 to 1.12). Prior use of evidence-based medications (aspirin, beta-blockers, ACE inhibitors/ARBs and statins) did not consistently change prior estimates on FHx and SMuRFs (OR: 0.82 95% Cl: 0.71 to 0.96 and OR 0.89 95% CI: 0.54–1.47). Patients who presented with STEMI had a 46% excess risk of 30-day mortality (OR: 1.46; 95% CI: 1.11 to 1.91; p&amp;lt;0.001) compared with controls Conclusions In direct contrast with recent findings, almost 90% of patients with STEMI have SMuRFs. Self-reported FHx is not a significant risk factor for development of STEMI and related high rate of CV mortality in patients without SMuRFs. Although research on genetic causes of heart disease is important, public health policies, and research efforts should place significant emphasis on the 4 SMuRFs and the lifestyle behaviors causing them to reduce the epidemic of STEMI. Funding Acknowledgement Type of funding sources: None.

The 1964 US Surgeon General's report on smoking and health.

The 1964 report of the US Surgeon General on smoking and health made an authoritative case that tobacco smoking was a cause of premature deaths from lung cancer and chronic bronchitis. It justified the practice of drawing causal inferences from epidemiological studies, specified influential criteria for doing so, and made use of an early form of meta-analysis.

Influence of an Interventional Health Education in Enhancing the Perceived Learning Needs of Patients with Myocardial Infarction

Background: Myocardial infarction is the leading cause of coronary heart disease and death. Because post-MI patients are more likely to have another attack, it is vital that they have enough knowledge about their health and the appropriate self-care. post-MI patients, it is critical for post-MI patients to have adequate health information and self-care, especially if they have risk factors such as smoking, hypertension, hyperlipidemia, obesity, and a lack of exercise. Objectives: To evaluate influence of an interventional health education in enhancing the perceived learning needs of patients with myocardial infarction. Methods: A quasi-experimental design was used with the application of pre and post-test approach for both studied and controlled groups. This study was conducted at cardiac advisory department on purposive sample was selected to obtain representative and accurate data consisting of (90) patients at Missan Center for Cardiac Diseases and Surgery, (10) patients were excluded for the pilot study. Data were analyzed using descriptive statistical data analysis approach of frequency, percentage, mean, mean of scores, a total of scores, range and standard deviation and inferential statistical data analysis approach T-test, and analysis of variance (ANOVA). Results: highly significant difference between pre and posttests responses at (P value &lt; .05) in the study group related to all domains of the study. Conclusions: Less than one-quarter of patients in the study group were institute graduate level, and more than one-quarter of patients in the control group were secondary level graduate, one quarter of patients in the study group were within employee level; and more than one quarters in control group were within the retired level. more than half of patients in the study group and more than two-thirds of patients in the control group were married. In pretest and posttest, there is a significant influence of an interventional health education in enhancing the perceived learning needs of patients with myocardial infarction. Recommendations: The study recommend that it is critical to update patient learning needs by encouraging and inspiring patients to participate in particular interventional health education on the perceived learning needs of patients with Myocardial Infarction. Patients should have access to continued education and resources that enhance patient's learning needs during their hospitalization. Keyword: Myocardial Infarction, Influence, Interventional, Enhance.

Effect of miR-663 on atherosclerosis by regulating the proliferation of vascular smooth muscle cells in lipid plaques.

Atherosclerosis (AS) is the main cause of coronary heart disease, cerebral infarction, and peripheral vascular disease. microRNAs (miRNAs) are widely distributed in the human body and closely related to the pathological progress of AS. This study probed into the function of miR-663 in AS. The atherosclerotic plaques, cholesterol (CHOL), low-density lipoprotein (LDL), inflammatory factors, and miR-663 expression in ApoE-/- mice on high-fat diet were evaluated. The overexpressing miR-663 adenovirus was injected into ApoE-/- mice, followed by measurement of type III collagen (Col III), matrix metalloproteinase (MMP)-2, α-SMA, osteopontin, and CD31. miR-663 mimic or inhibitor was introduced into vascular smooth muscle cells (VSMCs) stimulated by oxidized LDL (Ox-LDL), and cell proliferation and IL-6 and IL-18 secretion were evaluated. The binding relationship between miR-663 and HMGA2 was verified, followed by the determination of HMGA2 role in VSMC proliferation. Atherosclerotic plaques appeared in ApoE-/- mice on high-fat diet, with increased CHOL, LDL, osteopontin, MMP-2 and Col III and decreased miR-663, α-SMA and CD31. miR-663 overexpression downregulated osteopontin, MMP-2 and Col III and upregulated α-SMA and CD31 in ApoE-/- mice on high-fat diet. With Ox-LDL concentration increase, VSMC proliferation was promoted and miR-663 was downregulated. miR-663 overexpression inhibited proliferation of Ox-LDL-stimulated VSMCs and reduced levels of inflammatory factor levels, whereas silencing miR-663 did the opposite. miR-663 targeted HMGA2. HMGA2 overexpression partially reversed the inhibitory effect of miR-663 overexpression on VSMC proliferation. miR-663 targeted HMGA2 to inhibit VSMC proliferation and AS development, which may offer insights into AS treatment.

Ratiometric fluorescence biosensor for imaging of protein phosphorylation levels in atherosclerosis mice

Atherosclerosis (AS) is the main cause of coronary heart disease, cerebral infarction and peripheral vascular disease, which is an important disease threatening human health. Abnormal levels of protein phosphorylation are closely related to the occurrence and development of diseases. Herein, the ratiometric fluorescence nanosensor (PCN/W– B@BSA) was prepared by using metal-organic frameworks (PCN-224) and fluorescent nanocluster wool-balls, which was applied for ratiometric fluorescence imaging of protein phosphorylation level in the AS mice model. Specific recognition of phosphorylation sites was achieved via specific interaction between active center Zr(IV) and phosphate. Using the two-photon property of porphyrin, the background is significantly reduced, and the sensitivity of imaging analysis is improved by combining with ratio imaging. Bovine serum albumin (BSA) was used to modify the surface of the nanosensor to reduce the non-specific adsorption and improve the biocompatibility of the nanosensor. Finally, the fluorescence nanosensor was successfully apply to fluorescence imaging of protein phosphorylation level in AS mice model, and the results showed that the protein phosphorylation level in the AS mice model was lower than that of the normal mice. The present study provides suitable fluorescence tool for further revealing phosphorylation related signaling pathways and disease mechanisms.

A coronary artery CTA segmentation approach based on deep learning.

Presence of plaque and coronary artery stenosis are the main causes of coronary heart disease. Detection of plaque and coronary artery segmentation have become the first choice in detecting coronary artery disease. The purpose of this study is to investigate a new method for plaque detection and automatic segmentation and diagnosis of coronary arteries and to test its feasibility of applying to clinical medical image diagnosis. A multi-model fusion coronary CT angiography (CTA) vessel segmentation method is proposed based on deep learning. The method includes three network layer models namely, an original 3-dimensional full convolutional network (3D FCN) and two networks that embed the attention gating (AG) model in the original 3D FCN. Then, the prediction results of the three networks are merged by using the majority voting algorithm and thus the final prediction result of the networks is obtained. In the post-processing stage, the level set function is used to further iteratively optimize the results of network fusion prediction. The JI (Jaccard index) and DSC (Dice similarity coefficient) scores are calculated to evaluate accuracy of blood vessel segmentations. Applying to a CTA dataset of 20 patients, accuracy of coronary blood vessel segmentation using FCN, FCN-AG1, FCN-AG2 network and the fusion method are tested. The average values of JI and DSC of using the first three networks are (0.7962, 0.8843), (0.8154, 0.8966) and (0.8119, 0.8936), respectively. When using new fusion method, average JI and DSC of segmentation results increase to (0.8214, 0.9005), which are better than the best result of using FCN, FCN-AG1 and FCN-AG2 model independently.

Antioxidant potential of diet – Association between dietary antioxidant index and odds of coronary heart disease: A case-control study

BACKGROUND: Oxidative stress and chronic inflammation are among the leading causes of coronary heart disease (CHD). Studies investigated the relationship between dietary antioxidants and the risk/odds of CHD, and contradictory results have been reported. Dietary antioxidant index (DAI) is a novel and reliable nutritional tool that examines the diet’s overall antioxidant capacity. Its validity was examined using serum total antioxidant capacity and malondialdehyde. OBJECTIVE: This study aimed to investigate the relationship between DAI score and odds of CHD. METHODS: In this incidence case-control study, 320 individuals with a definitive diagnosis of CHD and 320 participants without CHD or related risk factors attending the same hospitals/polyclinics were selected as the case and control groups. We estimated the DAI by summing up six standardized intakes of major dietary antioxidants, including manganese, vitamin E, A, C, selenium, and zinc. RESULTS: Modeling DAI categorized according to the median (–0.38), in multi-adjusted model showed a significant protective association with the odd of CHD (OR = 0.72; 95%CI:0.51–0.99, p-value = 0.05). Also, modeling DAI as a continuous variable in multi-adjusted models (OR = 0.94;95%CI:0.90–0.95; p-value = 0.01) showed significant results. CONCLUSION: Using the DAI to investigate the relationship between dietary antioxidants and CHD can show more realistic results than a single study of antioxidants.

Circular RNA circCHFR downregulation protects against oxidized low-density lipoprotein-induced endothelial injury via regulation of microRNA-15b-5p/growth arrest and DNA damage inducible gamma

ABSTRACT Atherosclerosis is the leading cause of coronary heart disease. In recent years, circ_0029589 (circCHFR) has been found to be associated with atherosclerosis development. However, the molecular mechanism of circCHFR action in atherosclerosis development is unknown. This study was aimed to investigate the function and action mechanism of circCHFR in atherosclerosis development. An atherosclerosis cell model was created by exposing human vascular endothelial cells (HUVECs) to oxidized low-density lipoprotein. The expression of circCHFR, microRNA(miR)-15b-5p, growth arrest and DNA damage inducible gamma (GADD45G), and their associated proteins was evaluated using quantitative reverse transcription-polymerase chain reaction and Western blotting. Additionally, cell viability, apoptosis, and cytokine levels were determined using Cell Counting Kit-8 (CCK8) assay, flow cytometry, and enzyme-linked immunosorbent assay, respectively. circCHFR expression was upregulated in patients with atherosclerosis and oxidized low-density lipoprotein (ox-LDL)-exposed HUVECs, whereas miR-15b-5p expression was downregulated. circCHFR silencing significantly improved viability and reduced apoptosis of HUVECs. In addition, the pro-apoptotic protein Bax and atherosclerosis-associated cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) were significantly downregulated, whereas the anti-apoptotic protein Bcl-2 was upregulated. Further, we discovered that circCHFR serves as a molecular sponge of miR-15b-5p. GADD45G was found to be an important target of miR-15b-5p; miR-15b-5p mimic inhibited GADD45G expression, reduced apoptosis and proinflammatory cytokine secretion, and improved cell survival. However, these effects of miR-15b-5p on (ox-LDL) induced HUVECs were reversed with GADD45G plasmid co-transfection. In conclusion, circCHFR promotes atherosclerosis progression via the miR-15b-5p/GADD45G axis and may be an important target for atherosclerosis treatment.