PubMed · 13373605
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M DELP. 1956. Ascites.. https://pubmed.ncbi.nlm.nih.gov/13373605/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Malignant ovarian ascites are rich in cellular components, membrane-bound vesicles, and soluble proteins. This study focused on the structure of membrane-bound vesicles and their ability to promote invasion in cultured malignant ovarian epithelium. Membrane vesicles were derived from women with stage I-IV malignant ovarian ascites and from nonmalignant gynecologic ascites. Isolated vesicles were characterized by immunofluorescence and Western blot analysis. Using gel zymography for matrix metalloproteinase (MMP) detection and a colorimetric assay for urokinase-type plasminogen activator (uPA) analysis, we analyzed the proteinase activities of MMP-2, MMP-9, and uPA from the prepared vesicles, whole cells isolated from ascites, and the cell-free ultracentrifuged supernatant. The invasiveness of established cultured malignant ovarian epithelium on addition of ascites-derived vesicles was tested using a Matrigel-based invasion assay. Fractionation of malignant ascites revealed that extracellular matrix-degrading proteinases including MMPs and uPA are localized preferentially in membrane vesicles. All malignant vesicles tested, regardless of cancer stage, stimulated invasion. Furthermore, the combination of ovarian cancer cells and membrane vesicles resulted in greater uPA activation than that of cells or vesicles alone. Membrane vesicles from malignant ascites were also found to contain activated MMP-2, MMP-9, and uPA. Our data suggest that vesicle-stimulated proteinase activation leads to increased extracellular matrix degradation, which may facilitate tumor cell invasion and metastasis.
Explore the source record for details and available documents.
INTRODUCTION: We report a series of infants with optic chiasmal hypothalamic astrocytomas (OCHAs) who developed abdominal ascites following ventriculo-peritoneal (VP) shunting. The mechanism of ascites development among these patients with OCHA remains speculative and unclear. METHODS: We treated four infants with hypothalamic tumors who were shunted for hydrocephalus using standard VP shunts and who subsequently experienced symptomatic ascites. RESULTS: In three patients the gallbladder proved an effective alternative site for shunting prior to conversion to other sites, and in one patient the gallbladder shunt remains functional and revision-free. CONCLUSIONS: Several aspects of the gallbladder as a reservoir for CSF make this approach appealing. Ventricular gallbladder shunting provided an effective (at least temporarily) receptacle for CSF in these patients.