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Sayfa 1 itibaren 49 Sonuçlar
Pepstatin, an ascites retardant of L1210 tumor-bearing mice.
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The effect of pepstatin on the kinetics of ascitic fluid accumulation in L1210 tumor-bearing mice (DBA/2) was observed. Following inoculation of 1.5x10(6) tumor cells, untreated mice reached a peak of fluid accumulation on day 6 and remained at this level until death on day 9. A "lag" phase of 4
Pepstatin, an inhibitor of acid kininogenases and ascites retardant in neoplastic disease.
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Evidence is reviewed that pepstatin, an inhibitor of acid kininogenases such as cathepsin D, may be an effective therapeutic agent in retarding ascites accumulation in certain cancers. The evidence for this conclusion is based on the actions of pepstatin in retarding ascites in six different tumor
Host cathepsin D response to tumor in the normal and pepstatin-treated mouse.
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In view of the postulated role of cathepsin D in cachexia, investigations have been pursued on the host tissue response of cathepsin D activity in DBA/2 mice inoculated with 5 X 10(5) L1210 tumor cells. The results confirmed previous investigators' findings of the increase in cathepsin D activity
Effects of E-64 (cysteine-proteinase inhibitor) and pepstatin (aspartyl-proteinase inhibitor) on metastasis formation in mice with mammary and ovarian tumors.
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The effects of E-64 (Cathepsin B and L inhibitor) and Pepstatin A (Cathepsin D inhibitor) on spontaneous and experimental metastasis formation were investigated in mice with MCa mammary carcinoma, M5076 ovarian sarcoma and L1210 leukemia. Pepstatin induced a marked decrease in the number of
Large Pore Mesoporous Silica and Organosilica Nanoparticles for Pepstatin A Delivery in Breast Cancer Cells.
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(1) Background: Nanomedicine has recently emerged as a new area of research, particularly to fight cancer. In this field, we were interested in the vectorization of pepstatin A, a peptide which does not cross cell membranes, but which is a potent inhibitor of cathepsin D, an aspartic protease
Evaluation of antitumor and antimetastatic activity of pepstatin A in some experimental tumor models.
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[Cathepsins D from normal and some human neoplasms].
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Cathepsins D were isolated from human liver and spleen, from three malignant tumours (kidney cancer, sarcoma, spleen tumour caused by chronic myeloleucosis) and from one non-malignant tumour (uterine myoma). The isolation procedure involved adsorption on pepstatin-Sepharose and gel-filtration on
Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent.
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Recent studies suggest that the aryl hydrocarbon receptor (AhR) modulates susceptibilities to some pro-apoptotic agents. AhR-containing murine hepatoma 1c1c7 cultures underwent apoptosis following exposure to tumor necrosis factor-alpha (TNFalpha) + cycloheximide (CHX). In contrast, Tao cells, an
Comparative studies on antibody and lectin-dependent macrophage-mediated tumor lysis.
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Three characteristics of the mechanisms of antibody-dependent macrophage-mediated cytolysis (ADMC) and lectin-dependent macrophage-mediated cytolysis (LDMC) in a C3H/He mouse-MM46 syngeneic tumor system were compared: the role of divalent cations, the effect of cyclic nucleotides, and the role of
Rapid killing of actinomycin D-treated tumor cells by human monocytes. II. Cytotoxicity is independent of secretion of reactive oxygen intermediates and is suppressed by protease inhibitors.
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Pretreatment with Actinomycin D (ActD, 1 microgram/ml for 3 hr) rendered WEHI 164 tumor cells susceptible to killing by human monocytes in a 6-hr 51Cr release assay. The present study was designed to elucidate the role of reactive oxygen intermediates (ROI) and of proteolytic enzymes in this
Potential role for cathepsin D in p53-dependent tumor suppression and chemosensitivity.
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Cathepsin D (CD), the major intracellular aspartyl protease, is a mediator of IFN-gamma and TNF-alpha induced apoptosis. Using subtractive hybridization screening we isolated CD as an upregulated transcript in PA1 human ovarian cancer cells undergoing adriamycin-induced apoptosis. CD mRNA levels
A novel aspartyl proteinase from apocrine epithelia and breast tumors.
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GCDFP-15 (gross cystic disease fluid protein, 15 kDa) is a secretory marker of apocrine differentiation in breast carcinoma. In human breast cancer cell lines, gene expression is regulated by hormones, including androgens and prolactin. The protein is also known under different names in different
Characterization of inactive renin ("prorenin") from renin-secreting tumors of nonrenal origin. Similarity to inactive renin from kidney and normal plasma.
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Inactive renin comprises well over half the total renin in normal human plasma. There is a direct relationship between active and inactive renin levels in normal and hypertensive populations, but the proportion of inactive renin varies inversely with the active renin level; as much as 98% of plasma
BIOCHEMICAL PROPERTIES OF CARBOXYPEPTIDASE A OF THE UNTRANSFERRED TISSUE AND MALIGNANT NEOPLASM OF THE MAMMARY GLAND
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To study biochemical properties of carboxypeptidase A of the untransformed tissue and malignant neoplasm of the mammalian gland. Sampling of anatomical materials for research was conducted with compliance of ethical and legal standards. Excretion of this enzymes includes gradual fractionation with
Selective cell death of oncogenic Akt-transduced brain cancer cells by etoposide through reactive oxygen species mediated damage.
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We have established several glioma-relevant oncogene-engineered cancer cells to reevaluate the oncogene-selective cytotoxicity of previously well-characterized anticancer drugs, such as etoposide, doxorubicin, staurosporine, and carmustine. Among several glioma-relevant oncogenes (activated
Bilim tarafından desteklenen en eksiksiz şifalı otlar veritabanı
- 55 dilde çalışır
- Bilim destekli bitkisel kürler
- Görüntüye göre bitki tanıma
- Etkileşimli GPS haritası - bölgedeki bitkileri etiketleyin (yakında)
- Aramanızla ilgili bilimsel yayınları okuyun
- Şifalı bitkileri etkilerine göre arayın
- İlgi alanlarınızı düzenleyin ve haber araştırmaları, klinik denemeler ve patentlerle güncel kalın
Bir belirti veya hastalık yazın ve yardımcı olabilecek bitkiler hakkında bilgi edinin, bir bitki yazın ve karşı kullanıldığı hastalıkları ve semptomları görün.
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