Aim: The normal endovascular invasion of trophoblast cells and spiral artery remodeling are impaired in pre-eclampsia. Neither the circulating factor secreted by the placenta nor the cause of the widespread endothelial dysfunction in pre-eclampsia has yet been identified. In an attempt to identify novel factors, we performed a gene expression profiling study of placental tissue from women with and without pre-eclampsia.
Material And Methods: The study group comprised two pre-eclamptic patients with intrauterine growth restriction while the control group comprised three healthy women with uncomplicated pregnancies. Gene expression was studied using Affymetrix Human Genome U133 Plus 2 micro arrays. We focused on genes associated with angiogenesis. Some of the micro array analysis results were verified using real-time reverse transcription polymerase chain reaction (RT-PCR).
Results: Gene expression profiling revealed that the expression level of nine genes--ECGF1, JAG1, Palladin, COL18A1, TNFSF12, VEGF, ANPEP, PDGFRA and SERPIN12 - was downregulated whereas the level of four genes--EPAS1, FLT1, SIGLE10 and ANG4--was upregulated in the study group compared with the control group. The real-time RT-PCR results from JAG1, COL18A1 and FLT1 genes were in accordance with the gene expression results.
Conclusion: Our results show new targets for research to understand the mechanisms leading to pre-eclampsia.
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http://dx.doi.org/10.1080/09513590701350291 | DOI Listing |
Cell Signal
January 2025
Department of Breast and Thyroid Surgery, The Qinghai Provincial People's Hospital, Xining 810007, China. Electronic address:
This study utilizes single-cell RNA sequencing data to reveal the transcriptomic characteristics of breast cancer and normal epithelial cells. Nine significant cell populations were identified through stringent quality control and batch effect correction. Further classification of breast cancer epithelial cells based on the PAM50 method and clinical subtypes highlighted significant heterogeneity between triple-negative breast cancer (TNBC) and non-triple-negative breast cancer (NTNBC).
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Radiation Epidemiology Branch, National Cancer Institute, MD 20892-9778, USA; Faculty of Health, Science and Technology, Oxford Brookes University, Headington Campus, OX3 0BP, UK.
Biological effects of ionizing radiation vary with radiation quality, which is often expressed as the amount of energy deposited per unit length, i.e., linear energy transfer (LET).
View Article and Find Full Text PDFAnn Endocrinol (Paris)
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Univ. Lille, Inserm, CHU Lille, U1286 - Infinite, F-59045 Lille Cedex, Department of Biochemistry and Molecular Biology, Lille University Hospital, Lille, France. Electronic address:
Around 10% of cases of primary hyperparathyroidism are thought to be genetic in origin, some of which are part of a syndromic form such as multiple endocrine neoplasia types 1, 2A or 4 or hyperparathyroidism-jaw tumor syndrome, while the remainder are cases of isolated familial primary hyperparathyroidism. Recognition of these genetic forms is important to ensure appropriate management according to the gene and type of variant involved, but screening for a genetic cause is not justified in all patients presenting primary hyperparathyroidism. The indications for genetic analysis have made it possible to propose a decision tree that takes into account whether the presentation is familial or sporadic, syndromic or isolated, patient age, and histopathological type of parathyroid lesion.
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Imaging Department, Nuclear Medicine Service, Gustave Roussy, Université Paris-Saclay, F-94805, Villejuif, France.
Parathyroid carcinoma is extremely rare, affecting 1% of cases of primary hyperparathyroidism. For this reason, management is poorly codified and requires expertise in specialized center. PC is genetically determined in a quarter to a third of cases, notably involving the CDC73 gene coding for parafibromin.
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January 2025
Department of Urology Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China; Department of Microbiome Laboratory, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450003, China. Electronic address:
Background: ARPC1B has been identified as a key regulator of malignant biological behavior in various tumors. However, its specific role in clear cell renal cell carcinoma (ccRCC) remains poorly understood. This study aims to evaluate the influence of ARPC1B on the prognosis and disease progression in ccRCC patients.
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