Screening and Identification of Pregnancy Zone Protein and Leucine‐Rich Alpha‐2‐Glycoprotein as Potential Serum Biomarkers for Early‐Onset Myocardial Infarction using Protein Profile Analysis

2018 ◽  
Vol 13 (3) ◽  
pp. 1800079 ◽  
Author(s):  
Chao Xuan ◽  
Hui Li ◽  
Le‐Le Li ◽  
Qing‐Wu Tian ◽  
Qing Wang ◽  
...  
2019 ◽  
Vol 4 (3) ◽  
pp. 120-123
Author(s):  
Ioana Cîrneală ◽  
Diana Opincariu ◽  
István Kovács ◽  
Monica Chițu ◽  
Imre Benedek

Abstract Heart failure is a clinical syndrome that appears as a consequence of a structural disease, and the most common cause of left ventricular systolic dysfunction results from myocardial ischemia. Cardiac remodeling and neuroendocrine activation are the major compensatory mechanisms in heart failure. The main objective of the study is to identify the association between serum biomarkers illustrating the extent of myocardial necrosis (highly sensitive troponin as-says), left ventricular dysfunction (NT-proBNP), and systemic inflammatory response (illustrated via serum levels of hsCRP and interleukins) during the acute phase of a myocardial infarction, and the left ventricular remodeling process at 6 months following the acute event, quantified via speckle tracking echocardiography. The study will include 400 patients diagnosed with acute myocardial infarction without signs and symptoms of heart failure at the time of enrollment that will undergo a complex clinical examination and speckle tracking echocardiography. Serum samples from the peripheral blood will be collected in order to determine the inflammatory serum biomarkers. After 6 months, patients will be divided into 2 groups according to the development of ventricular remodeling, quantified by speckle tracking echocardiography: group 1 will consist of patients with a remodeling index lower than 15%, and group 2 will consist of patients with a remodeling index higher than 15%. All clinical and imaging data obtained at the baseline will be compared between these two groups in order to determine the features associated with a higher risk of deleterious ventricular remodeling and heart failure.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
L. Ormesher ◽  
L. Warrander ◽  
Y. Liu ◽  
S. Thomas ◽  
L. Simcox ◽  
...  

AbstractAbnormal maternal serum biomarkers (AMSB), identified through the aneuploidy screening programme, are frequent incidental findings in pregnancy. They are associated with fetal growth restriction (FGR), but previous studies have not examined whether this association is with early-onset (< 34 weeks) or late-onset (> 34 weeks) FGR; as a result there is no consensus on management. The aims of this study were to determine the prevalence and phenotype of FGR in women with AMSB and test the predictive value of placental sonographic screening to predict early-onset FGR. 1196 pregnant women with AMSB underwent a 21–24 week “placental screen” comprising fetal and placental size, and uterine artery Doppler. Multivariable regression was used to calculate a predictive model for early-onset FGR (birthweight centile < 3rd/< 10th with absent umbilical end-diastolic flow, < 34 weeks). FGR prevalence was high (10.3%), however early-onset FGR was uncommon (2.3%). Placental screening effectively identified early-onset (area under the curve (AUC) 0.93, 95% confidence interval (CI) 0.87–1.00), but not late-onset FGR (AUC 0.70, 95% CI 0.64–0.75). Internal validation demonstrated robust performance for detection/exclusion of early-onset FGR. In this cohort, utilisation of our proposed algorithm with targeted fetal growth and Doppler surveillance, compared with universal comprehensive surveillance would have avoided 1044 scans, potentiating significant cost-saving for maternity services.


BMC Genomics ◽  
2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Huan-Xin Jiang ◽  
Lin-Tong Yang ◽  
Yi-Ping Qi ◽  
Yi-Bin Lu ◽  
Zeng-Rong Huang ◽  
...  

2008 ◽  
Vol 134 (2) ◽  
pp. 198 ◽  
Author(s):  
William H. Moretz ◽  
Christine G. Gourin ◽  
David J. Terris ◽  
Zhong-Sheng Xia ◽  
Zhongmin Liu ◽  
...  

BMJ ◽  
1999 ◽  
Vol 319 (7218) ◽  
pp. 1157-1162 ◽  
Author(s):  
J. Danesh ◽  
L. Youngman ◽  
S. Clark ◽  
S. Parish ◽  
R. Peto ◽  
...  

1998 ◽  
Vol 36 (10) ◽  
pp. 2957-2963 ◽  
Author(s):  
Mary Ellen Rafferty ◽  
Aldona L. Baltch ◽  
Raymond P. Smith ◽  
Lawrence H. Bopp ◽  
Carol Rheal ◽  
...  

During an outbreak of diarrhea in a general hospital in 1992, 166Clostridium difficile isolates from 102 patients were typed by restriction enzyme analysis (REA), arbitrarily primed PCR (AP-PCR), and protein profile analysis (PP) techniques. A total of 18 types and 5 subtypes were identified by REA, 32 types were identified by AP-PCR, and 9 types were identified by PP. Analysis of the data indicated the presence of a predominant strain among 76, 75, and 84% of the isolates by REA, AP-PCR, and PP, respectively. Subsequently, 45C. difficile isolates which had been collected in 1990 from 33 patients in the same hospital following a significant increase in the number of cases of diarrhea caused by C. difficile were studied by REA, AP-PCR, and PP typing techniques. Thirteen types and one subtype were identified by REA, 12 types were identified by AP-PCR, and 5 types were identified by PP. As with the isolates from 1992, a dominant strain was identified. This strain was represented by 53, 64, and 70% of the total number of isolates when the strains were typed by REA, AP-PCR, and PP, respectively. Every isolate (210 of 211) from both 1990 and 1992 that was available for typing was typeable by all three methods. Furthermore, the same dominant strain was identified in both 1990 and 1992 by each method. This study demonstrates that each of the three typing methods can be useful in epidemiologic investigations of C. difficileoutbreaks and that one strain can be dominant in an institution over a number of years.


1998 ◽  
Vol 36 (4) ◽  
pp. 1015-1019 ◽  
Author(s):  
William T. Golde ◽  
Barbara Robinson-Dunn ◽  
Mary Grace Stobierski ◽  
Daniel Dykhuizen ◽  
Ing-Nang Wang ◽  
...  

In recent years, the utility of serum-based diagnostic testing for Lyme disease has improved substantially; however, recovery by culture of the bacterium from skin biopsies of suspected patients is still the only definitive laboratory test. Reinfection of patients has been assumed to occur but as yet has not been documented by serial isolates from the same person. We present a case of culture-confirmed reinfection of a patient in Menominee County, Michigan. Borrelia burgdorferi was isolated from the skin punch biopsy specimens during each episode of erythema migrans (EM) and was subjected to molecular strain typing, genetic analysis of two outer surface protein genes, protein profile analysis, and serum antibody response testing. Results show that these isolates are distinct strains of the bacterium and that the two episodes of EM were caused by independent infections. This report describes the documented, culture-confirmed reinfection of a human by two different strains of B. burgdorferi.


2019 ◽  
Vol 115 (13) ◽  
pp. 1886-1906 ◽  
Author(s):  
Martina Gast ◽  
Bernhard H Rauch ◽  
Arash Haghikia ◽  
Shinichi Nakagawa ◽  
Jan Haas ◽  
...  

AbstractAimsInflammation is a key driver of atherosclerosis and myocardial infarction (MI), and beyond proteins and microRNAs (miRs), long noncoding RNAs (lncRNAs) have been implicated in inflammation control. To obtain further information on the possible role of lncRNAs in the context of atherosclerosis, we obtained comprehensive transcriptome maps of circulating immune cells (peripheral blood mononuclear cells, PBMCs) of early onset MI patients. One lncRNA significantly suppressed in post-MI patients was further investigated in a murine knockout model.Methods and resultsIndividual RNA-sequencing (RNA-seq) was conducted on PBMCs from 28 post-MI patients with a history of MI at age ≤50 years and stable disease ≥3 months before study participation, and from 31 healthy individuals without manifest cardiovascular disease or family history of MI as controls. RNA-seq revealed deregulated protein-coding transcripts and lncRNAs in post-MI PBMCs, among which nuclear enriched abundant transcript (NEAT1) was the most highly expressed lncRNA, and the only one significantly suppressed in patients. Multivariate statistical analysis of validation cohorts of 106 post-MI patients and 85 controls indicated that the PBMC NEAT1 levels were influenced (P = 0.001) by post-MI status independent of statin intake, left ventricular ejection fraction, low-density lipoprotein or high-density lipoprotein cholesterol, or age. We investigated NEAT1−/− mice as a model of NEAT1 deficiency to evaluate if NEAT1 depletion may directly and causally alter immune regulation. RNA-seq of NEAT1−/− splenocytes identified disturbed expression and regulation of chemokines/receptors, innate immunity genes, tumour necrosis factor (TNF) and caspases, and increased production of reactive oxygen species (ROS) under baseline conditions. NEAT1−/− spleen displayed anomalous Treg and TH cell differentiation. NEAT1−/− bone marrow-derived macrophages (BMDMs) displayed altered transcriptomes with disturbed chemokine/chemokine receptor expression, increased baseline phagocytosis (P < 0.0001), and attenuated proliferation (P = 0.0013). NEAT1−/− BMDMs responded to LPS with increased (P < 0.0001) ROS production and disturbed phagocytic activity (P = 0.0318). Monocyte-macrophage differentiation was deregulated in NEAT1−/− bone marrow and blood. NEAT1−/− mice displayed aortic wall CD68+ cell infiltration, and there was evidence of myocardial inflammation which could lead to severe and potentially life-threatening structural damage in some of these animals.ConclusionThe study indicates distinctive alterations of lncRNA expression in post-MI patient PBMCs. Regarding the monocyte-enriched NEAT1 suppressed in post-MI patients, the data from NEAT1−/− mice identify NEAT1 as a novel lncRNA-type immunoregulator affecting monocyte-macrophage functions and T cell differentiation. NEAT1 is part of a molecular circuit also involving several chemokines and interleukins persistently deregulated post-MI. Individual profiling of this circuit may contribute to identify high-risk patients likely to benefit from immunomodulatory therapies. It also appears reasonable to look for new therapeutic targets within this circuit.


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