Objective: From data in the literature, we hypothesized that high vascular resistance values in the uterine arteries at the end of the first trimester would increase adverse pregnancy outcomes and therefore might be accompanied by changes in VEGF/VEGFR1 immunoreactivities.
Study Design: In our university hospital 82 women (Study I n=62 and Study II n=20) were divided into two groups according to their uterine vascular resistance values. Uterine vascular resistance values were measured in the 10-13th weeks of gestation by color-Doppler ultrasonography. Women were divided into low and high vascular resistance groups. In the prospective follow-up study (Study I) the data of the pregnancy outcome were recorded. In cross-sectional study (Study II), VEGF and VEGFR1 immunoreactivities were measured on the tissue samples from women who underwent termination of pregnancy.
Results: In the high vascular resistance group (PI>2.3), the probability of adverse pregnancy outcome was significantly higher (40.0% vs. 12.8%). No differences in VEGF and VEGFR1 immunoreactivities were observed between groups. In both groups, intense VEGF immunoreactivity was observed in the maternal glandular epithelium and in the decidual cells. Weak reactivity was observed in the villous trophoblast. VEGFR1 immunoreactivity was intense in all regions.
Conclusions: Our data suggest that high vascular resistance values in the first trimester are independent from VEGF/VEGFR1 immunoreactivities and markedly increase the probability of adverse pregnancy outcomes. This may be used for early screening of pregnant women in the first trimester.
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http://dx.doi.org/10.1016/j.ejogrb.2011.01.029 | DOI Listing |
Zh Nevrol Psikhiatr Im S S Korsakova
December 2024
Kazan (Volga region) Federal University, Kazan, Russia.
Cerebrovascular diseases themselves are the second most common cause of cognitive impairment (dementia). In addition, cerebral small vessel disease (CSVD) makes a significant contribution to the clinical picture of neurodegenerative diseases. Since there are currently no pharmacological treatments for CSVD, a promising method is the activation of the endogenous mechanisms of sanogenesis.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Biomedical Sciences, College of Health Sciences, Qatar University, PO Box 2713, Doha, Qatar.
Diabetes mellitus is a chronic disease characterized by metabolic defects, including insulin deficiency and resistance. Individuals with diabetes are at increased risk of developing cardiovascular complications, such as atherosclerosis, coronary artery disease, and hypertension. Conventional treatment methods, though effective, are often challenging, costly, and may lead to systemic side effects.
View Article and Find Full Text PDFCancer Genomics Proteomics
December 2024
Division of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Background/aim: Bile tract cancer (BTC) is a malignant tumor with a poor prognosis. Recent studies have reported the heterogeneity of the genomic background and gene alterations in BTC, but its genetic heterogeneity and molecular profiles remain poorly understood. Whole-genome sequencing may enable the identification of novel actionable gene mutations involved in BTC carcinogenesis, malignant progression, and treatment resistance.
View Article and Find Full Text PDFToxins (Basel)
December 2024
Univ. Angers, INSERM, CNRS, MITOVASC, Equipe CarME, SFR ICAT, 49000 Angers, France.
The vegetal alkaloid toxin veratridine (VTD) is a selective voltage-gated Na (Na) channel activator, widely used as a pharmacological tool in vascular physiology. We have previously shown that Na channels, expressed in arteries, contribute to vascular tone in mouse mesenteric arteries (MAs). Here, we aimed to better characterize the mechanisms of action of VTD using mouse cecocolic arteries (CAs), a model of resistance artery.
View Article and Find Full Text PDFJ Xenobiot
December 2024
Cancer Biology and Therapy Laboratory, School of Applied and Health Sciences, London South Bank University, London SE1 0AA, UK.
The vascular endothelial growth factor receptor 2 (VEGFR2) and the hepatocyte growth factor receptor (C-Met) are critical receptors for signaling pathways controlling crucial cellular processes such as cell growth, angiogenesis and tissue regeneration. However, dysregulation of these proteins has been reported in different diseases, particularly cancer, where these proteins promote tumour growth, invasiveness, metastasis and resistance to conventional therapies. The identification of dual inhibitors targeting both VEGFR-2 and c-Met has emerged as a strategic therapeutic approach to overcome the limitations and resistance mechanisms associated with single-target therapies in clinical settings.
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