TY  - JOUR
A1  - Chaykovska, Lyubov
A1  - Zientara, Alicja
A1  - Reser, Diana
A1  - Weise, Alexander
A1  - Reichert, Wolfgang
A1  - Hocher, Berthold
T1  - Development and validation of a macroarray system - MutaCHIP (R) ARTERO - for the detection of genetic variants involved in the pathogenesis of atherosclerosis
JF  - Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion
N2  - Background: Cardiovascular diseases are the leading cause of death in developed countries. The underlying mechanism is often atherosclerotic remodeling of blood vessels in organs such as heart, kidney, brain, and large arteries in case of peripheral arterial disease. Beside environmental and behavioral factors such as smoking or lack of physical activity, genetic variants in genes involved in lipid metabolism, blood pressure regulation, oxidative stress, and coagulation play a prominent role in the pathogenesis of atherosclerosis.
 Methods: Thus, we developed and validated for clinical use and research a macroarray system for the simultaneous detection of key genetic variants in genes involved in lipid metabolism, blood pressure regulation, oxidative stress, and coagulation.
 Results: When compared with standard PCR technologies to determine all these genetic variants in parallel, the macroarray system (MutaCHIP (R) ARTERO) was as accurate but faster, cheaper, and easier to handle compared to classical real time PCR based technologies.
 Conclusions: MutaCHIP (R) ARTERO is a gene chip for diagnostics of a complex genetic panel involved in the pathogenesis of atherosclerosis. This method is as sensitive and precise as real time PCR and is able to replicate real time PCR data previously validated in evaluation studies.
KW  - cardiovascular disease
KW  - atherosclerosis
KW  - genes
KW  - rapid detection method
KW  - macroarray
Y1  - 2014
U6  - https://doi.org/10.7754/Clin.Lab.2014.140104
SN  - 1433-6510
VL  - 60
IS  - 5
SP  - 873
EP  - 878
PB  - Clin Lab Publ., Verl. Klinisches Labor
CY  - Heidelberg
ER  - 
TY  - JOUR
A1  - Chen, You-Peng
A1  - Lu, Yong-Ping
A1  - Li, Jian
A1  - Liu, Zhi-Wei
A1  - Chen, Wen-Jing
A1  - Liang, Xu-Jing
A1  - Chen, Xin
A1  - Wen, Wang-Rong
A1  - Xiao, Xiao-Min
A1  - Reichetzeder, Christoph
A1  - Hocher, Berthold
T1  - Fetal and maternal angiotensin (1-7) are associated with preterm birth
JF  - Journal of hypertension
N2  - Background: Recent studies show that preterm birth is associated with hypertension in later life. The renin-angiotensin system (RAS) during pregnancy influences fetal growth and development. In the current study, we investigated the impact of fetal as well as maternal angiotensin (1-7) [Ang (1-7)] and angiotensin II (Ang II) plasma concentrations on the risk of preterm birth.
 Methods: Three hundred and nine pregnant women were prospectively included into the study. The pregnant women were divided into two groups, for example, preterm birth of lower than 37 gestational weeks (n = 17) and full-term birth of 37 gestational weeks or more (n = 292). Maternal and neonatal plasma Ang (1-7) and Ang II concentrations were analyzed at birth from maternal venous blood and umbilical cord blood, respectively. Risk factors for premature birth were determined by multiple logistic regression analysis.
 Results: Fetal and maternal plasma Ang (1-7) concentrations in the preterm group were lower than those of the term group fetal Ang (1-7) preterm birth: 486.15 +/- 337.34 ng/l and fetal Ang (1-7) term birth: 833.84 +/- 698.12 ng/l and maternal Ang (1-7) preterm birth: 399.86 +/- 218.93 ng/l; maternal Ang (1-7) term birth: 710.34 +/- 598.22 ng/l. Multiple logistic regression analysis considering confounding factors revealed that preeclampsia (P < 0.001), premature rupture of membranes (P = 0.001), lower concentration of maternal Ang (1-7) (P = 0.013) and fetal plasma Ang (1-7) (P = 0.032) were independently associated with preterm birth. We could furthermore demonstrate that the maternal Ang (1-7)/Ang II ratio is independently associated with gestational hypertension or preeclampsia, factors causing preterm birth.
 Conclusions: Lower concentrations of maternal and fetal Ang (1-7) are independently associated with preterm birth - a risk factor of hypertension in later life.
KW  - angiotensin (1-7)
KW  - angiotensin II
KW  - cardiovascular disease
KW  - fetal programming
KW  - intrauterine fetal growth
KW  - pregnancy
KW  - preterm delivery
Y1  - 2014
U6  - https://doi.org/10.1097/HJH.0000000000000251
SN  - 0263-6352
SN  - 1473-5598
VL  - 32
IS  - 9
SP  - 1833
EP  - 1841
PB  - Lippincott Williams & Wilkins
CY  - Philadelphia
ER  -