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"extravasate" Definitions
  1. to force out or cause to escape from a proper vessel or channel
  2. to pass by infiltration or effusion from a proper vessel or channel (such as a blood vessel) into surrounding tissue

14 Sentences With "extravasate"

How to use extravasate in a sentence? Find typical usage patterns (collocations)/phrases/context for "extravasate" and check conjugation/comparative form for "extravasate". Mastering all the usages of "extravasate" from sentence examples published by news publications.

Angiopellosis extravasation occurs as a means for cells that are not native to the circulation to exit. This includes adult stem cells that are injected intravenously for therapies. Cells that are normally found in circulation (i.e. blood cells) either extravasate through diapedesis (white blood cells), or do not extravasate and remain in circulation (red blood cells).
Although both cell types persist in circulation, EMT cells fail to adhere to the vessel wall at the secondary site, while non- EMT cells, which have greater adhesive properties, are able to attach to the vessel wall and extravasate into the secondary site.
The word ecchymosis (; plural ecchymoses, ), comes to English from New Latin, based on Greek ἐκχύμωσις ekchymōsis, from ἐκχυμοῦσθαι ekchymousthai "to extravasate blood", from ἐκ- ek- (elided to ἐ- e-) and χυμός chymos "juice". Compare enchyma, "tissue infused with organic juice"; elaboration from chyme, the formative juice of tissues.
For example, they block the metastatic cancer cells' ability to extravasate and home to secondary sites. This has been successfully demonstrated in metastatic melanoma that hones to the lungs. In mice, when antibodies directed against CAMs in the lung endothelium were used as treatment there was a significant reduction in the number of metastatic sites.
Nanocarrier vehicles (~20–200 nm in diameter) can transport drugs and other therapeutic molecules. These therapies can be targeted to selectively extravasate through tumor vasculature via the EPR effect. Nanocarriers are now considered the gold standard of targeted cancer therapy because it can target tumors that are hypovascularized, such as prostate and pancreatic tumors. These efforts include protein capsids and liposomes.
Rupture of the urethra is an uncommon result of penile injury, incorrect catheter insertion, straddle injury, or pelvic girdle fracture. The urethra, the muscular tube that allows for urination, may be damaged by trauma. When urethral rupture occurs, urine may extravasate (escape) into the surrounding tissues. The membranous urethra is most likely to be injured in pelvic fractures, allowing urine and blood to enter the deep perineal space and subperitoneal spaces via the genital hiatus.
Enhanced permeability and retention (EPR) effect and passive targeting. Nanocarriers can extravasate into the tumors through the gaps between endothelial cells and accumulate there due to poor lymphatic drainage. Passive targeting refers to a nanocarrier's ability to travel down a tumor's vascular system, become trapped, and accumulate in the tumor. This accumulation is caused by the enhanced permeability and retention effect which refers to the poly(ethylene oxide) (PEO) coating on the outside of many nanocarriers.
Couvelaire uterus is a phenomenon where the retroplacental blood may penetrate through the thickness of the wall of the uterus into the peritoneal cavity. This may occur after abruptio placentae. The hemorrhage that gets into the decidua basalis ultimately splits the decidua, and the haematoma may remain within the decidua or may extravasate into the myometrium (the muscular wall of the uterus). The myometrium becomes weakened and may rupture due to the increase in intrauterine pressure associated with uterine contractions.
Attachment of liposomes or nanoparticles to the exterior of the lipid MB has also been explored to increase MB payload. Upon MB destruction with ultrasound, these smaller particles can extravasate into the tumor tissue. Furthermore, through attachment of these particles to MBs as opposed to co-injection, the drug is confined to the blood stream instead of accumulating in healthy tissues, and the treatment is relegated to the location of ultrasound therapy. This MB modification is particularly attractive for Doxil, a lipid formulation of Doxorubicin already in clinical use.
There are two major components stored within Weibel–Palade bodies. One is von Willebrand factor (vWF), a multimeric protein that plays a major role in blood coagulation. Storage of long polymers of vWF gives this specialized lysosomal structure an oblong shape and striated appearance on electron microscope. The other is P-selectin, which plays a central role in the ability of inflamed endothelial cells to recruit passing leukocytes (white blood cells), allowing them to exit the blood vessel (extravasate) and enter the surrounding tissue, where they can migrate to the site of infection or injury.
A circulating tumor cell (CTC) is a cell that has shed into the vasculature or lymphatics from a primary tumor and is carried around the body in the blood circulation. CTCs can extravasate and become seeds for the subsequent growth of additional tumors (metastases) in distant organs, a mechanism that is responsible for the vast majority of cancer-related deaths. The detection and analysis of CTCs can assist early patient prognoses and determine appropriate tailored treatments. Currently, there is one FDA-approved method for CTC detection, CellSearch, which is used to diagnose breast, colorectal and prostate cancer.
This is presumably due to loss of uptake of essential polyunsaturated fatty acids by the brain endothelial cells, which utilize MFSD2A as a transporter for these fats. Serum from patients showed elevated levels of essential polyunsaturated fatty acids, presumably due to the inability of vascular cells to uptake these lipids in the absence of protein function. Without the ability to uptake these fats into endothelial cells, there is breakdown of the blood-brain-barrier and loss of brain volume. This was demonstrated in a zebrafish model by intracardiac injection of dye, which was found to extravasate into the brain parenchyma following inactivating one of the paralogues of MSFD2A known as mfsd2aa.
T cell precursors extravasate from the bloodstream in cortico-medullary junction and they first migrate to the thymic cortex, where they undergo construction of TCRs and subsequently a process called T cell positive selection which is mediated by mTEC-related cells: cortical thymic epithelial cells (cTECs). This process verifies, whether newly generated TCRs are functional. About 90% of T cells displays badly rearranged TCRs, they can´t reach the positive selection and they die by neglect in the cortex. The rest starts to express CCR7, which is a receptor for mTEC-generated chemokine CCL21, and migrate after concentration gradient to the thymic medulla to encounter mTECs.
E-selectin was first discovered as an transmembrane receptor induced in endothelial cells upon inflammatory stimulation which mediated adhesion of monocytic or HL60 leukemic cells. This led to the hypothesis that cancer cells secreted inflammatory cytokines such as IL-1β or TNFα to induce E-selectin at distant metastatic sites. This induction would enable circulating tumor cells to arrest at stimulated sites, roll along activated endothelium, extravasate, and form metastases. Studies since have showed that E-selectin binding to colon cancer cells correlates with increasing metastatic potential, and that cancer cells of multiple tumor types bind E-selectin using glycoprotein or glycolipid ligands normally expressed on immune cells.

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