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First-trimester screening for aneuploidy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Mark I. Evans, Howard S. Cuckle
Sequential screening can also be carried out within trimester. One contingent approach suggested by Nicolaides et al. has the potential to further increase detection while completing all screening within the first trimester (35). It is proposed that women with borderline risk based on PAPP-A, free β-hCG, and NT are offered a more specialist scan to determine, among other things nasal bone, and reassess the risk. Nasal bone hypoplasia is a very powerful marker of aneuploidy but requires appropriate training not generally available. Another approach might be to measure additional biochemical markers in a very early serum sample at about 8 weeks of gestation in addition to the 10-week sample; one possible very early marker is ADAM12 (36).
The locomotor system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Osteoarthritis is not a single disease, but the end-result of joint damage from many causes. In the past, osteoarthritis was considered to be a degenerative disease. A more modern approach is to regard it as an active disease process – as the response of a joint to injury. There is both synthesis of new components and loss of existing tissue in the process of remodelling. It is most likely that osteoarthritis results from the failure of chondrocytes to maintain homeostasis between synthesis and degradation of extracellular matrix components. Local low-grade inflammation appears to be important and there is evidence that cytokines such as IL-1 and TNF act on the chondrocyte, causing it to release metalloproteases, which degrade the matrix. Genetic factors are also important. Mutations of type II collagen genes are found in some families with osteoarthritis and mutation of the ADAM12 gene (encoding a protease enzyme) also appears to be important.
Omics and coagulation disorders in pregnancy
Published in Moshe Hod, Vincenzo Berghella, Mary E. D'Alton, Gian Carlo Di Renzo, Eduard Gratacós, Vassilios Fanos, New Technologies and Perinatal Medicine, 2019
Sara Ornaghi, Michael J. Paidas
Aiming to identify novel serological protein markers to predict preeclampsia with a multi-omic-based discovery approach, Liu and coworkers identified three upregulated and six downregulated biomarkers in preeclamptic sera, associated with lipid homeostasis (APO-E), inflammation (α-2-macroglobin, A2M), and coagulation (disintegrin and ADAM12) (54). Two optimal biomarker panels were then developed for early and late-onset preeclampsia assessment, showing a superior detection rate as compared with the well-known sFlt-1/PIGF ratio.
The role of extracellular matrix components in angiogenesis and fibrosis: Possible implication for Systemic Sclerosis
Published in Modern Rheumatology, 2018
Vasiliki Liakouli, Paola Cipriani, Paola Di Benedetto, Piero Ruscitti, Francesco Carubbi, Onorina Berardicurti, Noemi Panzera, Roberto Giacomelli
A disintegrin and metalloprotease (ADAM) molecules can degrade ECM and shed the membrane-bound precursors that modulate cell–cell and cell–matrix interactions. ADAM-12 is a complex, multi-domain protein that regulates cell proliferation and migration and promotes angiogenesis [93]. Furthermore, increased serum ADAM12 levels are associated with elevated serum inflammatory marker, severity of skin fibrosis, and activity of lung involvement in dcSSc, suggesting the possible contribution of ADAM12 to the pathological events in SSc [94]. Recently, we provided evidence of activated ADAM12 expression in SSc perivascular cells, suggesting their tendency toward pro-fibrotic activity [7].
ADAM12 abrogation alters immune cell infiltration and improves response to checkpoint blockade therapy in the T11 murine model of triple-negative breast cancer
Published in OncoImmunology, 2023
Guanpeng Wang, Yeni Romero, Indhujah Thevarajan, Anna Zolkiewska
Retroviral expression vector Adam12-pBabePuro was used for the expression of ADAM12-wildtype (ADAM12-WT) protein.48 The Adam12-Δ6 construct was generated using the QuickChange kit (Agilent Technologies). Phoenix-Eco cells were transfected using calcium phosphate precipitation method (20 μg DNA/100-mm plate), in the presence of 25 μM chloroquine. Viral supernatants were harvested 48 hours later, supplemented with 8 μg/ml polybrene, and used without further dilution for infection of T11 cells. After 48 hours, cells with stable overexpression of ADAM12-WT or ADAM12-Δ6 were selected with 2 μg/ml puromycin for 8 days.