Terhesség és akut ischaemiás stroke

Bereczki, Dániel

doi:10.1556/650.2016.30421

Cited by 4 publications

(2 citation statements)

References 30 publications

(40 reference statements)

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“…anti-angiogenic factors, pro-inflammatory cytokines, and syncytiotrophoblast debris) into the maternal circulation ( 40 , 41 , 43 , 56 – 66 ). As a consequence, the terminal pathway of preeclampsia, featuring an anti-angiogenic state and exaggerated maternal systemic inflammation, occurs in most cases, and its intensity correlates with the severity of preeclampsia, which may be coupled with damage to the maternal endothelium and to the kidneys, liver, and central nervous system during the clinical phase ( 21 , 42 , 43 , 64 , 67 – 72 ). VT development can also be impaired in preeclampsia ( 73 – 75 ), especially in the preterm form associated with SGA, where VT turnover is affected together with morphometric features ( 73 , 76 ).…”

Section: Introductionmentioning

confidence: 99%

Integrated Systems Biology Approach Identifies Novel Maternal and Placental Pathways of Preeclampsia

et al. 2018

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Preeclampsia is a disease of the mother, fetus, and placenta, and the gaps in our understanding of the complex interactions among their respective disease pathways preclude successful treatment and prevention. The placenta has a key role in the pathogenesis of the terminal pathway characterized by exaggerated maternal systemic inflammation, generalized endothelial damage, hypertension, and proteinuria. This sine qua non of preeclampsia may be triggered by distinct underlying mechanisms that occur at early stages of pregnancy and induce different phenotypes. To gain insights into these molecular pathways, we employed a systems biology approach and integrated different “omics,” clinical, placental, and functional data from patients with distinct phenotypes of preeclampsia. First trimester maternal blood proteomics uncovered an altered abundance of proteins of the renin-angiotensin and immune systems, complement, and coagulation cascades in patients with term or preterm preeclampsia. Moreover, first trimester maternal blood from preterm preeclamptic patients in vitro dysregulated trophoblastic gene expression. Placental transcriptomics of women with preterm preeclampsia identified distinct gene modules associated with maternal or fetal disease. Placental “virtual” liquid biopsy showed that the dysregulation of these disease gene modules originates during the first trimester. In vitro experiments on hub transcription factors of these gene modules demonstrated that DNA hypermethylation in the regulatory region of ZNF554 leads to gene down-regulation and impaired trophoblast invasion, while BCL6 and ARNT2 up-regulation sensitizes the trophoblast to ischemia, hallmarks of preterm preeclampsia. In summary, our data suggest that there are distinct maternal and placental disease pathways, and their interaction influences the clinical presentation of preeclampsia. The activation of maternal disease pathways can be detected in all phenotypes of preeclampsia earlier and upstream of placental dysfunction, not only downstream as described before, and distinct placental disease pathways are superimposed on these maternal pathways. This is a paradigm shift, which, in agreement with epidemiological studies, warrants for the central pathologic role of preexisting maternal diseases or perturbed maternal–fetal–placental immune interactions in preeclampsia. The description of these novel pathways in the “molecular phase” of preeclampsia and the identification of their hub molecules may enable timely molecular characterization of patients with distinct preeclampsia phenotypes.

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Section: Introductionmentioning

confidence: 99%

Integrated Systems Biology Approach Identifies Novel Maternal and Placental Pathways of Preeclampsia

et al. 2018

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“…This enhances the deleterious potential of a PFO. Although there are only anecdotal and no robust data to prove that the pregnancy risk be increased by the presence of a PFO [ 51 , 52 ], closing a PFO before a planned pregnancy cannot be wrong, considering the collateral benefits.…”

Section: Compelling and Established Indications For Pfo Closure ( ...mentioning

confidence: 99%

Every Patent Foramen Ovale Should Be Closed

Meier

2024

JCM

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At present, the patent foramen ovale (PFO) does not receive the deserved medical attention. The PFO poses a serious threat to health and even the life of mankind. The first respective case report in the medical literature dates back to the 19th century. It led to death. The fact that a PFO is present in roughly 25% of people underscores its overall potential to cause harm. Yet at the same time, the sheer number discourages the medical community from screening for it and from treating it. About 5% of the population have particularly dangerous forms of PFOs. Such PFOs portray a high enough risk for clinical events, the likes of death, stroke, myocardial infarction, or ocular, visceral, and peripheral embolism, to justify screening for them. Highly significant health incidents being at stake, it appears obvious that PFO closure should be used for primary prevention. This is supported by the fact that closing a PFO is the simplest intervention in cardiology, with presumably the highest clinical yield. Being mainly a preventive measure, PFO closure represents a mechanical vaccination. When closing PFOs for one of the rarer therapeutic indications (migraine, platypnea orthodeoxia, etc.), patients automatically profit from the collateral benefit of getting, at the same time, mechanically vaccinated for life against paradoxical embolism. Vice versa, closing a PFO for the prevention of paradoxical embolism betters or cures migraine or exercise dyspnea not infrequently, thereby improving quality of life as a collateral benefit.

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Candidate SNP markers of reproductive potential are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters

et al. 2018

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BackgroundThe progress of medicine, science, technology, education, and culture improves, year by year, quality of life and life expectancy of the populace. The modern human has a chance to further improve the quality and duration of his/her life and the lives of his/her loved ones by bringing their lifestyle in line with their sequenced individual genomes. With this in mind, one of genome-based developments at the junction of personalized medicine and bioinformatics will be considered in this work, where we used two Web services: (i) SNP_TATA_Comparator to search for alleles with a single nucleotide polymorphism (SNP) that alters the affinity of TATA-binding protein (TBP) for the TATA boxes of human gene promoters and (ii) PubMed to look for retrospective clinical reviews on changes in physiological indicators of reproductive potential in carriers of these alleles.ResultsA total of 126 SNP markers of female reproductive potential, capable of altering the affinity of TBP for gene promoters, were found using the two above-mentioned Web services. For example, 10 candidate SNP markers of thrombosis (e.g., rs563763767) can cause overproduction of coagulation inducers. In pregnant women, Hughes syndrome provokes thrombosis with a fatal outcome although this syndrome can be diagnosed and eliminated even at the earliest stages of its development. Thus, in women carrying any of the above SNPs, preventive treatment of this syndrome before a planned pregnancy can reduce the risk of death. Similarly, seven SNP markers predicted here (e.g., rs774688955) can elevate the risk of myocardial infarction. In line with Bowles’ lifespan theory, women carrying any of these SNPs may modify their lifestyle to improve their longevity if they can take under advisement that risks of myocardial infarction increase with age of the mother, total number of pregnancies, in multiple pregnancies, pregnancies under the age of 20, hypertension, preeclampsia, menstrual cycle irregularity, and in women smokers.ConclusionsAccording to Bowles’ lifespan theory—which links reproductive potential, quality of life, and life expectancy—the above information was compiled for those who would like to reduce risks of diseases corresponding to alleles in own sequenced genomes. Candidate SNP markers can focus the clinical analysis of unannotated SNPs, after which they may become useful for people who would like to bring their lifestyle in line with their sequenced individual genomes.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4478-3) contains supplementary material, which is available to authorized users.

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Terhesség és akut ischaemiás stroke

Cited by 4 publications

References 30 publications

Integrated Systems Biology Approach Identifies Novel Maternal and Placental Pathways of Preeclampsia

Integrated Systems Biology Approach Identifies Novel Maternal and Placental Pathways of Preeclampsia

Every Patent Foramen Ovale Should Be Closed

Candidate SNP markers of reproductive potential are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters

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