Serum-Biomarker zur Abschätzung des Risikos einer Thrombolyse-assoziierten Blutung

2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
C Foerch ◽  
F Dvorak ◽  
M Wunderlich
Keyword(s):  
2005 ◽  
Vol 173 (4S) ◽  
pp. 383-383
Author(s):  
Rainer Kuefer ◽  
Matthias D. Hofer ◽  
Christoph Zorn ◽  
Bjoern G. Volkmer ◽  
Juergen E. Gschwend ◽  
...  

2014 ◽  
Author(s):  
Aleksandra Jawiarczyk-Przybylowska ◽  
Marek Bolanowski ◽  
Katarzyna Kolackov
Keyword(s):  

2019 ◽  
Author(s):  
Zheqiong Tan ◽  
Yaru Zou ◽  
Man Zhu ◽  
Zhenzhao Luo ◽  
Tangwei Wu ◽  
...  

Biochimie ◽  
2021 ◽  
Vol 185 ◽  
pp. 87-95
Author(s):  
Aleksandr S. Taraskin ◽  
Konstantin K. Semenov ◽  
Aleksandr V. Protasov ◽  
Alexey A. Lozhkov ◽  
Aleksandr A. Tyulin ◽  
...  

2018 ◽  
Vol 36 (28) ◽  
pp. 2887-2894 ◽  
Author(s):  
Linda D. Mellby ◽  
Andreas P. Nyberg ◽  
Julia S. Johansen ◽  
Christer Wingren ◽  
Børge G. Nordestgaard ◽  
...  

Purpose Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, with a 5-year survival of < 10% because of diffuse symptoms leading to late-stage diagnosis. That survival could increase significantly if localized tumors could be detected early. Therefore, we used multiparametric analysis of blood samples to obtain a novel biomarker signature of early-stage PDAC. The signature was derived from a large patient cohort, including patients with well-defined early-stage (I and II) PDAC. This biomarker signature was validated subsequently in an independent patient cohort. Patients and Methods The biomarker signature was derived from a case-control study, using a Scandinavian cohort, consisting of 16 patients with stage I, 132 patients with stage II, 65 patients with stage III, and 230 patients with stage IV PDAC, and 888 controls. This signature was validated subsequently in an independent case-control cohort in the United States with 15 patients with stage I, 75 patients with stage II, 15 patients with stage III, and 38 patients with stage IV PDAC, and 219 controls. An antibody microarray platform was used to identify the serum biomarker signature associated with early-stage PDAC. Results Using the Scandinavian case-control study, a biomarker signature was created, discriminating samples derived from patients with stage I and II from those from controls with a receiver operating characteristic area under the curve value of 0.96. This signature, consisting of 29 biomarkers, was then validated in an independent case-control study in the United States. The biomarker signature could discriminate patients with stage I and II PDAC from controls in this independent patient cohort with a receiver operating characteristic area under the curve value of 0.96. Conclusion This serum biomarker signature might represent a tenable approach to detecting early-stage, localized PDAC if these findings are supported by a prospective validation study.


PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0151590 ◽  
Author(s):  
Laura Lehtinen ◽  
Pia Vesterkvist ◽  
Pia Roering ◽  
Taina Korpela ◽  
Liisa Hattara ◽  
...  

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
O Gritsenko ◽  
GA Chumakova

Abstract Funding Acknowledgements Type of funding sources: None. Currently, there is no serum biomarker that is a marker of the presence of heart failure (HF) at an early stage. It is also shown that the traditional indicators used for the diagnosis diastolic dysfunction (DD) of left ventricular (LV) using echocardiography (ECG) are not informative enough. Thus, it is currently relevant to study new serum biomarkers of DD, such as sST2, as well as to study the mechanics of LV. Objective to study the relationship between mechanics of LV and the level of sST2 (bioamarker of HF) in patients with epicardial obesity (EO). Materials and methods The study included 110 men with general obesity. According to the results of echocardiography (ECG), patients were divided into 2 groups: EO (+) with epicardial fat thickness (tEAT) ≥7 mm (n = 70); EO (-) with tEAT &lt;7 mm (n = 40) without diastolic dysfunction according to the results of ECG. All patients were assessed for sST2 and NT-pro-BNP levels using enzyme immunoassay. Using speckle-tracking ECG, the mechanics of LV were studied (twist LV, peak twist ratio LV, time to peak twist of LV, peak untwist ratio LV, time to peak untwist of LV). The exclusion criteria were the presence of coronary pathology, arterial hypertension, and type 2 diabetes mellitus. Results In the group patients with EO ( + ) a statistically significant increase in the level of sST2 was revealed in comparison with the group of EO (-) [21,55 ng/ml (26,52; 15,40) and 9.89 ng/ml (11.12; 7.95); p = 0.001, respectively], while the levels of NT-pro-BNP in both groups were not statistically different [211.36 pg / ml (254.0; 156.0) and 204.81 pg / ml (268.0; 157.0), respectively, p = 0.85]. When determining the parameters of DD LV by ECG, there were no statistical differences between the EO (+) and EO (-) groups [e ", cm / sec 0.09 (0.11; 0.09) and 0.09 (0.11; 0.09), respectively, p = 0.63; E/e " , units, 7.80 (8.90; 6.55) in the EO (+) and 8.53 (9.70; 7.20) in the EO group ( - ), p = 0.08; left atrial volume index, ml / sq2, in the EO group (+) 28.39 (31.25; 24.17) and in the EO group(-) 27,82 (30,21; 25,66), p = 0.55; in the EO group ( + ), the maximum speed of tricuspid regurgitation, m / sec, is 2.78 (2.9; 2.58) in the EO group(-) 2,67 (2,87; 2,41), p = 0.13]. According to the results of speckle-tracking ECG in the EO (+) group, an increase peak untwist ratio LV to -128.31 (-142.0; -118.0) deg/s-1 (p = 0.002) and an increase time to peak untwist of LV of 476.44 (510.0; 411.0) msec was determined in comparison with the EO ( - ) group (p = 0.03). A significant relationship between peak untwist ratio LV and sST2 was revealed (r = 0.37; p = 0.02). Conclusion Thus, it can be assumed that patients with EO have DD LV at the preclinical stage, which is not diagnosed using traditional ECG indicators. The serum biomarker sST2 is an early marker of the presence of HF.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ismael Artur da Costa-Rocha ◽  
Ketty Lysie Libardi Lira Machado ◽  
Ana Carolina Campi-Azevedo ◽  
Andréa Teixeira-Carvalho ◽  
Vanessa Peruhype-Magalhães ◽  
...  

AbstractThe present study aimed to investigate whether the serum biomarkers of immune response orchestrate the seroconversion status in patients with autoimmune diseases (AID) upon planned primary 17DD-YF vaccination. For this purpose a total of 161 individuals were enrolled in a prospective study, including patients with Rheumatoid Arthritis (RA = 38), Spondyloarthritis (SpA = 51), Systemic Lupus Erythematosus (SLE = 21) and Sjögren’s Syndrome (SS = 30) along with a group of healthy controls (HC = 21). Analysis of plaque reduction neutralization test (PRNT) titers and seropositivity rates along with the 17DD-YF viremia and serum biomarkers were carried out at distinct time points (D0/D3–4/D5–6/D7/D14–28). The results demonstrated an overall lower PRNT titer and seropositivity rate (170 vs. 448; 77 vs. 95%) in AID as compared to HC, especially in SpA and SLE subgroups. No significant differences were observed in the viremia levels amongst groups. In general, a more prominent serum biomarker response was observed in AID as compared to HC, throughout the timeline kinetics. Remarkably, AID/PRNT(−) exhibited higher levels of several biomarkers at baseline as compared to AID/PRNT+. Moreover, while AID/PRNT(+) exhibited earlier increase in serum biomarkers at D3–4/D5–6, the AID/PRNT(−) displayed higher response at later time points (D7/D14–D28). Of note, a synchronic increase of IFN-γ at the peak of viremia (D5–6) was observed in HC and AID/PRNT(+) groups, whereas a later asynchronous IFN-γ response was reported for AID/PRNT(−) at D7. The biomarker profile tends to deflate at post-vaccination timeline, highlighting a putative immunomodulatory effect of live attenuated 17DD-YF vaccine in AID/PRNT(+), but not in AID/PRNT(−). Altogether these data suggested that inflammatory status prior vaccination, low IFN-γ at viremia peak and the occurrence of asynchronous biomarker storm after 17DD-YF vaccination may orchestrate the lack of neutralizing antibody response γ.


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