Integrating genomic profiling to clinical data: assessing the impact of CD147 expression on plaque stability.

Background: Acute Coronary Syndrome (ACS) continues to be a leading cause of death and illness worldwide. Differentiating stable from unstable coronary plaques is essential for enhancing patient outcomes. This research investigates the role of CD147 as a biomarker for plaque stability among coronary artery disease patients.

Integrated analysis of differentially expressed genes and miRNA expression profiles in dilated cardiomyopathy.

Background: Although dilated cardiomyopathy (DCM) is a prevalent form of cardiomyopathy, the molecular mechanisms underlying its pathogenesis and progression remain poorly understood. It is possible to identify and validate DCM-associated genes, pathways, and miRNAs using bioinformatics analysis coupled with clinical validation methods.

Methods: Our analysis was performed using 3 mRNA datasets and 1 miRNA database.

Machine learning-based prediction model for myocardial ischemia under high altitude exposure: a cohort study.

High altitude exposure increases the risk of myocardial ischemia (MI) and subsequent cardiovascular death. Machine learning techniques have been used to develop cardiovascular disease prediction models, but no reports exist for high altitude induced myocardial ischemia. Our objective was to establish a machine learning-based MI prediction model and identify key risk factors.

Automatic Corneal Ulcer Segmentation Combining Gaussian Mixture Modeling and Otsu Method.

In this paper, we proposed and validated a novel and accurate pipeline for automatically segmenting flaky corneal ulcer areas from fluorescein staining images. The ulcer area was segmented within the cornea by employing a joint method of Otsu and Gaussian Mixture Modeling (GMM). In the GMM based segmentation, the total number of Gaussians was determined intelligently using an information theory based algorithm.

Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22.

Cell death and inflammation play critical roles in atherosclerosis. Pyroptosis, a novel proinflammatory programmed cell death process, participates in atherosclerosis pathogenesis. Recently, MALAT1 was identified as a pyroptosis-related long noncoding RNA (lncRNA).

Uncertainty evaluation in clinical chemistry, immunoassay, hematology and coagulation analytes using only external quality assessment data.

Background: Measurement uncertainty (MU) is a parameter associated with the result of a measurement that characterizes its dispersion. We report results for estimating MU following the application of a top-down procedure using only proficiency test data to establish uncertainty levels for various analytes.

Methods: Data were obtained from 142 laboratories participating in the Beijing Center for Clinical Laboratory (BCCL) proficiency testing/external quality assessment (PT/EQA) schemes.

Yunnanterpene G, a spiro-triterpene from the roots of , downregulates the expression of CD147 and MMPs in PMA differentiated THP-1 cells.

A new cycloartane triterpene, yunnanterpene G (1), containing an oxaspiro[5.4]decane moiety, was purified from the roots of . The new structure was determined from spectroscopic data and the X-ray diffraction method.

The Role of FAK in the Secretion of MMP9 after CD147 Stimulation in Macrophages.

To investigate whether focal adhesion kinase (FAK) can participate in the secretion of matrix metalloproteinase 9 (MMP9) after CD147 stimulation in THP-1 induced macrophages; thus, to explore the potential treatment perspectives for acute coronary syndrome (ACS).Phorbol-12-myristate-13-acetate (PMA) was used to induce THP-1 cells to differentiate into macrophages. To confirm the peak mRNA and protein expression of FAK and MMP9 after the stimulation of CD147, the macrophages were divided into 5 groups (0, 3, 6, 9, and 12 hours), with 0 hours group as control group.

Ox-LDL-Induced MicroRNA-155 Promotes Autophagy in Human Endothelial Cells via Repressing the Rheb/ mTOR Pathway.

Background/aims: Autophagy, an evolutionary conserved biological process, is activated in cells to cope with various types of stress. MicroRNAs control several activities related to autophagy. However, the role of autophagy-related microRNAs during atherosclerosis is far from known.

Atorvastatin attenuates plaque vulnerability by downregulation of EMMPRIN expression via COX-2/PGE2 pathway.

Extracellular matrix metalloproteinase inducer (EMMPRIN) reportedly has a key regulatory role in matrix metalloproteinase (MMP) activities and the progression of atherosclerosis. Statins, which are anti-atherosclerotic pharmacological agents, are widely applied in clinical settings. The aim of the present study was to investigate the pharmaceutical effect of atorvastatin on EMMPRIN expression in atherosclerotic plaques.

miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis.

Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS.

microRNA-155 is inversely associated with severity of coronary stenotic lesions calculated by the Gensini score.

Objectives: This study aimed to investigate the association between microRNA-155 (miR-155) and the severity and extent of coronary stenotic lesions.

Patients And Methods: We measured the miR-155 expression by real-time PCR in 110 consecutive patients undergoing coronary angiography for suspected coronary artery disease. The severity and extent of coronary stenotic lesions were evaluated on the basis of coronary angiography findings by the Gensini score.

miR-155 inhibits oxidized low-density lipoprotein-induced apoptosis of RAW264.7 cells.

Macrophage apoptosis is a prominent feature of advanced atherosclerotic plaques. Here, we examined the hypothesis that the apoptotic machinery is regulated by microRNA-155 (miR-155). Constitutive expression of miR-155 was detected in RAW264.

Functional blockage of EMMPRIN ameliorates atherosclerosis in apolipoprotein E-deficient mice.

Background: Extracellular matrix metalloproteinase inducer (EMMPRIN), a 58-kDa cell surface glycoprotein, has been identified as a key receptor for transmitting cellular signals mediating metalloproteinase activities, as well as inflammation and oxidative stress. Clinical evidence has revealed that EMMPRIN is expressed in human atherosclerotic plaque; however, the relationship between EMMPRIN and atherosclerosis is unclear. To evaluate the functional role of EMMPRIN in atherosclerosis, we treated apolipoprotein E-deficient (ApoE(-/-)) mice with an EMMPRIN function-blocking antibody.

Role of Krüppel-like factor 2 and protease-activated receptor-1 in vulnerable plaques of ApoE(-/-) mice and intervention with statin.

Background: Krüppel-like factor 2 (KLF2) and protease-activated receptor-1 (PAR-1) are 2 novel factors that play important roles in inflammation and coagulation, yet their relationship with vulnerable plaques and statin remains uncertain. The purpose of this study was to explore the expression of KLF2 and PAR-1 in vulnerable plaques of ApoE gene knockout (ApoE(-/-)) mice and the pharmaceutical effect of statin on the expression of KLF2 and PAR-1.

Methods: ApoE(-/-) mice were randomized into an early-treatment group and a late-treatment group.

Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells.

Knockdown of stromal interaction molecule 1 (STIM1) significantly suppresses neointima hyperplasia after vascular injury. Endothelial progenitor cells (EPCs) are the major source of cells that respond to endothelium repair and contribute to re-endothelialization by reducing neointima formation after vascular injury. We hypothesized that the effect of STIM1 on neointima hyperplasia inhibition is mediated through its effect on the biological properties of EPCs.

Knockdown of stromal interaction molecule 1 attenuates hepatocyte growth factor-induced endothelial progenitor cell proliferation.

Increased Ca(2+) entry through store-operated Ca(2+) channels (SOCCs) plays an essential role in the regulation of hepatocyte growth factor (HGF)-induced cell proliferation. Stromal interaction molecule 1 (STIM1) is thought to transmit endoplasmic reticulum (ER) Ca(2+) store depletion signals to the plasma membrane (PM), causing the opening of SOCCs in the PM. However, the relationship between HGF and STIM1 in endothelial progenitor cell (EPC) proliferation remains uncharacterized.

Inhibitor of DNA binding-1 promotes the migration and proliferation of endothelial progenitor cells in vitro.

Migration and proliferation of endothelial progenitor cells (EPCs) are the key mechanisms in re-endothelialization after vascular injury. Inhibitor of DNA binding-1 (Id1) function has been linked to the proliferation, migration, and senescence of cells, and studies have shed light on the relationship between Id1 and the biological functions of EPCs. On the basis of the available data concerning Id1 and the behavior of EPCs, we hypothesized that Id1 was an important regulator in modulating the migration and proliferation of EPCs.

Role of TRPC1 and NF-kappaB in mediating angiotensin II-induced Ca2+ entry and endothelial hyperpermeability.

Endothelial dysfunction is associated with cardiovascular diseases. The Ca(2+) influx occurring via activation of plasmalemma Ca(2+) channels was shown to be critical in signaling the increase in endothelial permeability in response to a variety of permeability-increasing mediators. It has been reported that angiotensin II (AngII) could induce Ca(2+) signaling in some cells, and transient receptor potential canonical 1 (TRPC1) had an important role in this process.

[Association between plasma macrophage migration inhibitory factor concentration and coronary artery lesion severity.].

Objective: To investigate the relationship between the plasma macrophage migration inhibitory factor (MIF), activator protein-1 (AP-1) and MMP-9 concentrations and the severity of coronary artery lesions in coronary heart disease (CHD) patients.

Methods: Patients were divided into normal controls (n = 35), stable angina pectoris (SAP, n = 32) and acute coronary syndrome (ACS, n = 75) according to the coronary angiography (CAG), clinical and laboratory examinations. The CAG severity and extent of coronary lesions were analyzed by means of Gensini coronary score system.

[The role of activator protein-1 in unstable coronary atherosclerotic changes].

Objective: To investigate the relation between activator protein-1 (AP-1) and coronary atherosclerotic changes and the potential role of AP-1 in the stabilization of atherosclerotic plaques in patients with coronary heart disease (CHD).

Method: 142 patients were included in this study and divided into CHD group (107) and control group (35) according to coronary angiography (CAG). The CHD group was further divided into a stable angina pectoris (SAP) group (32) and an acute coronary syndrome (ACS) group (75) according to the clinical manifestations.

[Association between murine double minute 2 expression and AngII and ceramide induced endothelial cells apoptosis].

Objective: To observe the relationship between murine double minute 2 (mdm2) expression and AngII and ceramide induced human umbilical endothelial cells apoptosis.

Method: Human umbilical endothelial cells (ECs) were cultured in vitro and treated with angiotensin II alone or in combination with losartan (an inhibitor of AT1), PD123319 (an inhibitor of AT2) and FB1 (an inhibitor of ceramidase) respectively. ECs were also treated with different doses of C2-ceramide.

[Angiotensin II up-regulates expression of inducible nitric oxide synthase in human umbilical endothelial cells: roles of AT1 and AT2].

Objective: Angiotensin II is an important pro inflammation factor in the cardiovascular system. This experiment is aimed to study the effects of angiotensin II on inducible nitric oxide synthase expression in human umbilical endothelial cells.

Methods: Human umbilical endothelial cells were cultured in vitro and treated with angiotensin II alone or in combination with AT1, AT2 and NF-kappaB inhibitors respectively.