Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases.
Drug Information Services
National Library of Medicine (U.S.)
An agency of the NATIONAL INSTITUTES OF HEALTH concerned with overall planning, promoting, and administering programs pertaining to advancement of medical and related sciences. Major activities of this institute include the collection, dissemination, and exchange of information important to the progress of medicine and health, research in medical informatics and support for medical library development.
Drugs manufactured and sold with the intent to misrepresent its origin, authenticity, chemical composition, and or efficacy. Counterfeit drugs may contain inappropriate quantities of ingredients not listed on the label or package. In order to further deceive the consumer, the packaging, container, or labeling, may be inaccurate, incorrect, or fake.
A computerized biomedical bibliographic storage and retrieval system operated by the NATIONAL LIBRARY OF MEDICINE. MEDLARS stands for Medical Literature Analysis and Retrieval System, which was first introduced in 1964 and evolved into an online system in 1971 called MEDLINE (MEDLARS Online). As other online databases were developed, MEDLARS became the name of the entire NLM information system while MEDLINE became the name of the premier database. MEDLARS was used to produce the former printed Cumulated Index Medicus, and the printed monthly Index Medicus, until that publication ceased in December 2004.
Poetry as Topic
Early Detection of Cancer
Journal Impact Factor
Peer Review, Research
The evaluation by experts of the quality and pertinence of research or research proposals of other experts in the same field. Peer review is used by editors in deciding which submissions warrant publication, by granting agencies to determine which proposals should be funded, and by academic institutions in tenure decisions.
An organized procedure carried out by a select committee of professionals in evaluating the performance of other professionals in meeting the standards of their specialty. Review by peers is used by editors in the evaluation of articles and other papers submitted for publication. Peer review is used also in the evaluation of grant applications. It is applied also in evaluating the quality of health care provided to patients.
Critical and exhaustive investigation or experimentation, having for its aim the discovery of new facts and their correct interpretation, the revision of accepted conclusions, theories, or laws in the light of newly discovered facts, or the practical application of such new or revised conclusions, theories, or laws. (Webster, 3d ed)
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
Academies and Institutes
Palatal Expansion Technique
Pulmonary Disease, Chronic Obstructive
Lung Diseases, Obstructive
Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.
Forced Expiratory Volume
Measure of the maximum amount of air that can be expelled in a given number of seconds during a FORCED VITAL CAPACITY determination . It is usually given as FEV followed by a subscript indicating the number of seconds over which the measurement is made, although it is sometimes given as a percentage of forced vital capacity.
Access to Information
Angiostatin binds ATP synthase on the surface of human endothelial cells. (1/210)Angiostatin, a proteolytic fragment of plasminogen, is a potent antagonist of angiogenesis and an inhibitor of endothelial cell migration and proliferation. To determine whether the mechanism by which angiostatin inhibits endothelial cell migration and/or proliferation involves binding to cell surface plasminogen receptors, we isolated the binding proteins for plasminogen and angiostatin from human umbilical vein endothelial cells. Binding studies demonstrated that plasminogen and angiostatin bound in a concentration-dependent, saturable manner. Plasminogen binding was unaffected by a 100-fold molar excess of angiostatin, indicating the presence of a distinct angiostatin binding site. This finding was confirmed by ligand blot analysis of isolated human umbilical vein endothelial cell plasma membrane fractions, which demonstrated that plasminogen bound to a 44-kDa protein, whereas angiostatin bound to a 55-kDa species. Amino-terminal sequencing coupled with peptide mass fingerprinting and immunologic analyses identified the plasminogen binding protein as annexin II and the angiostatin binding protein as the alpha/beta-subunits of ATP synthase. The presence of this protein on the cell surface was confirmed by flow cytometry and immunofluorescence analysis. Angiostatin also bound to the recombinant alpha-subunit of human ATP synthase, and this binding was not inhibited by a 2,500-fold molar excess of plasminogen. Angiostatin's antiproliferative effect on endothelial cells was inhibited by as much as 90% in the presence of anti-alpha-subunit ATP synthase antibody. Binding of angiostatin to the alpha/beta-subunits of ATP synthase on the cell surface may mediate its antiangiogenic effects and the down-regulation of endothelial cell proliferation and migration. (+info)
Angiostatin formation involves disulfide bond reduction and proteolysis in kringle 5 of plasmin. (2/210)Plasmin is processed in the conditioned medium of HT1080 fibrosarcoma cells producing fragments with the domain structures of the angiogenesis inhibitor, angiostatin, and microplasmin. Angiostatin consists of kringle domains 1-4 and part of kringle 5, while microplasmin consists of the remainder of kringle 5 and the serine proteinase domain. Our findings indicate that formation of angiostatin/microplasmin involves reduction of plasmin by a plasmin reductase followed by proteolysis of the reduced enzyme. We present evidence that the Cys461-Cys540 and Cys511-Cys535 disulfide bonds in kringle 5 of plasmin were reduced by plasmin reductase. Plasmin reductase activity was secreted by HT1080 and Chinese hamster ovary cells and the human mammary carcinoma cell lines MCF-7, MDA231, and BT20 but not by the monocyte/macrophage cell line THP-1. Neither primary foreskin fibroblasts, blood monocyte/macrophages, nor macrovascular or microvascular endothelial cells secreted detectable plasmin reductase. In contrast, cultured bovine and rat vascular smooth muscle cells secreted small but reproducible levels of plasmin reductase. Reduction of the kringle 5 disulfide bonds triggered cleavage at either Arg529-Lys530 or two other positions C-terminal of Cys461 in kringle 5 by a serine proteinase. Plasmin autoproteolysis could account for the cleavage, although another proteinase was mostly responsible in HT1080 conditioned medium. Three serine proteinases with apparent Mr of 70, 50, and 39 were purified from HT1080 conditioned medium, one or more of which could contribute to proteolysis of reduced plasmin. (+info)
Effects of angiogenesis inhibitors on multistage carcinogenesis in mice. (3/210)Solid tumors depend on angiogenesis for their growth. In a transgenic mouse model of pancreatic islet cell carcinogenesis (RIP1-Tag2), an angiogenic switch occurs in premalignant lesions, and angiogenesis persists during progression to expansive solid tumors and invasive carcinomas. RIP1-Tag2 mice were treated so as to compare the effects of four angiogenesis inhibitors at three distinct stages of disease progression. AGM-1470, angiostatin, BB-94, and endostatin each produced distinct efficacy profiles in trials aimed at preventing the angiogenic switch in premalignant lesions, intervening in the rapid expansion of small tumors, or inducing the regression of large end-stage cancers. Thus, anti-angiogenic drugs may prove most efficacious when they are targeted to specific stages of cancer. (+info)
Systemic gene delivery expands the repertoire of effective antiangiogenic agents. (4/210)Cationic liposome-DNA complex (CLDC)-based intravenous gene delivery targets gene expression to vascular endothelial cells, macrophages and tumor cells. We used systemic gene delivery to identify anti-angiogenic gene products effective against metastatic spread in tumor-bearing mice. Specifically, CLDC-based intravenous delivery of the p53 and GM-CSF genes were each as effective as the potent antiangiogenic gene, angiostatin, in reducing both tumor metastasis and tumor angiogenesis. Combined delivery of these genes did not increase anti-tumor activity, further suggesting that each gene appeared to produce its antimetastatic activity through a common antiangiogenic pathway. CLDC-based intravenous delivery of the human wild type p53 gene transfected up to 80% of tumor cells metastatic to lung. Furthermore, it specifically induced the expression of the potent antiangiogenic gene, thrombospondin-1, indicating that p53 gene delivery in vivo may inhibit angiogenesis by inducing endogenous thrombospondin-1 expression. CLDC-based delivery also identified a novel anti-tumor activity for the metastasis suppressor gene CC3. Thus, CLDC-based intravenous gene delivery can produce systemic antiangiogenic gene therapy using a variety of different genes and may be used to assess potential synergy of combined anti-tumor gene delivery and to identify novel activities for existing anti-tumor genes. (+info)
Angiostatin inhibits endothelial and melanoma cellular invasion by blocking matrix-enhanced plasminogen activation. (5/210)Angiostatin, a kringle-containing fragment of plasminogen, is a potent inhibitor of angiogenesis. The mechanism(s) responsible for the anti-angiogenic properties of angiostatin are unknown. We now report that human angiostatin blocks plasmin(ogen)-enhanced in vitro invasion of tissue plasminogen activator (t-PA)-producing endothelial and melanoma cells. Kinetic analyses demonstrated that angiostatin functions as a non-competitive inhibitor of extracellular-matrix (ECM)-enhanced, t-PA-catalysed plasminogen activation, with a Ki of 0.9+/-0.03 microM. This mechanism suggests that t-PA has a binding site for the inhibitor angiostatin, as well as for its substrate plasminogen that, when occupied, prevents ternary complex formation between t-PA, plasminogen and matrix protein. Direct binding experiments confirmed that angiostatin bound to t-PA with an apparent Kd [Kd(app)] of 6.7+/-0.7 nM, but did not bind with high affinity to ECM proteins. Together, these data suggest that angiostatin in the cellular micro-environment can inhibit matrix-enhanced plasminogen activation, resulting in reduced invasive activity, and suggest a biochemical mechanism whereby angiostatin-mediated regulation of plasmin formation could influence cellular migration and invasion. (+info)
Suppression of angiogenesis and tumor growth by the inhibitor K1-5 generated by plasmin-mediated proteolysis. (6/210)Proteolytic enzymes are involved in generation of a number of endogenous angiogenesis inhibitors. Previously, we reported that angiostatin, a potent angiogenesis inhibitor, is a proteolytic fragment containing the first four kringle modules of plasminogen. In this report, we demonstrate that urokinase-activated plasmin can process plasminogen to release an angiogenesis inhibitor, K1-5 (protease-activated kringles 1-5). K1-5 inhibits endothelial-cell proliferation with a half-maximal concentration of approximately 50 pM. This inhibitory effect is endothelial-cell-specific and appears to be at least approximately 50-fold greater than that of angiostatin. A synergistic efficacy of endothelial inhibition was observed when angiostatin and kringle 5 (K5) were coincubated with capillary endothelial cells. The synergistic effect is comparable to that produced by K1-5 alone. Systemic treatment of mice with K1-5 at a low dose significantly blocked the fibroblast growth factor-induced corneal neovascularization, whereas angiostatin had no effect at the same dose. K1-5 also suppressed angiogenesis in chicken embryos. Systemic administration of K1-5 at a low dose at which angiostatin was ineffective significantly suppressed the growth of a murine T241 fibrosarcoma in mice. The antitumor effect correlates with the reduced neovascularization. These findings suggest that the plasmin-mediated proteolysis may be involved in the negative switch of angiogenesis. (+info)
Therapeutic potentials of angiostatin in the treatment of cancer. (7/210)The discovery of specific endothelial inhibitors such as angiostatin and endostatin not only increases our understanding of the functions of these molecules in the regulation of physiological and pathological angiogenesis, but also provides an important therapeutic strategy for cancer treatment. Recent studies have demonstrated that the angiostatin protein significantly suppresses the growth of a variety of tumors in mice. However, the dosages of angiostatin protein used in these animal studies seem to be too high for clinical trials. In addition, repeated injections and long-term treatment with angiostatin are required to reach its maximal antitumor effect. In this article, I will discuss several alternative approaches that may become feasible to move angiostatin therapy from animal experiments into the clinic. In particular, I will emphasize the therapeutic potentials of angiostatin gene therapy and more potent angiogenesis inhibitors that are related to angiostatin. (+info)
Liposomes complexed to plasmids encoding angiostatin and endostatin inhibit breast cancer in nude mice. (8/210)Gene therapy transfer of angiostatin and endostatin represents an alternative method of delivering angiogenic polypeptide inhibitors. We examined whether liposomes complexed to plasmids encoding angiostatin or endostatin inhibited angiogenesis and the growth of MDA-MB-435 tumors implanted in the mammary fat pads of nude mice. We determined that plasmids expressing angiostatin (PCI-Angio) or endostatin (PCI-Endo) effectively reduced angiogenesis using an in vivo Matrigel assay. We then investigated the efficacy of these plasmids in reducing the size of tumors implanted in the mammary fat pad of nude mice. Both PCI-Angio and PCI-Endo significantly reduced tumor size when injected intratumorally (P < 0.05). Compared to the untreated control group, the mice treated with PCI-Angio and PCI-Endo exhibited a reduction in tumor size of 36% and 49%, respectively. In addition, we found that i.v. injections of liposomes complexed to PCI-Endo reduced tumor growth in the nude mice by nearly 40% when compared to either empty vector (PCI) or untreated controls (P < 0.05). These findings provide a basis for the further development of nonviral delivery of antiangiogenic genes. (+info)
Therapeutic potentials of angiostatin in the treatment of cancer | Haematologica
The discovery of specific endothelial inhibitors such as angiostatin and endostatin not only increases our understanding of the functions of these molecules in the regulation of physiological and pathological angiogenesis, but also provides an important therapeutic strategy for cancer treatment. Recent studies have demonstrated that the angiostatin protein significantly suppresses the growth of a variety of tumors in mice. However, the dosages of angiostatin protein used in these animal studies seem to be too high for clinical trials. In addition, repeated injections and long-term treatment with angiostatin are required to reach its maximal antitumor effect. In this article, I will discuss several alternative approaches that may become feasible to move angiostatin therapy from animal experiments into the clinic. In particular, I will emphasize the therapeutic potentials of angiostatin gene therapy and more potent angiogenesis inhibitors that are related to angiostatin.. ...
Recombinant Human Plasminogen Angiostatin Kringles 1-3 | Cell Sciences
|p|Angiostatin is proteolytically processed from plasminogen, a secreted blood zymogen. Angiostatin reduces endothelial cell proliferation and acts as a potent inhibitor of angiogenesis and tumor growth.|/p| |p|Recombinant Human Angiostatin, Kringle doma
Human - Angiostatin - for Immunohistochemistry - Antibodies | BioVendor Research and Diagnostics Products
BioVendor - BioVendor Research and Diagnostic Products is a developer and manufacturer of immunoassays, recombinant proteins, antibodies and endotoxin-removal products.
Human - Angiostatin - for Immunohistochemistry - Antigene from Human serum - Antibodies | BioVendor Research and Diagnostics...
BioVendor - BioVendor Research and Diagnostic Products is a developer and manufacturer of immunoassays, recombinant proteins, antibodies and endotoxin-removal products.
Definition of angiostatin - NCI Drug Dictionary - National Cancer Institute
Encoded by human PLG Gene (Plasminogen Family) and expressed in the kidney, angiostatin is an angiogenesis inhibitor present in plasma and other extracellular fluids that blocks neovascularization and mediates suppression of metastases. Containing at least three kringles, angiostatin is a 38-kD internal (serine protease) proteolytic fragment of plasminogen.
Combined effects of angiostatin and ionizing radiation in antitumour therapy
Angiogenesis, the formation of new capillaries from pre-existing vessels, is essential for tumour progression. Angiostatin, a proteolytic fragment of plasminogen that was first isolated from the serum and urine of tumour-bearing mice, inhibits angiogenesis and thereby growth of primary and metastati …
KAKEN - Research Projects | The relationship between serum Angiostatin levels, tumor angiogenesis and distant metastasis of the...
Principal Investigator：OKADA Yasuo, Project Period (FY)：1998 - 2000, Research Category：Grant-in-Aid for Scientific Research (C), Section：一般, Research Field：Surgical dentistry
Migration of MAE cells transfected with angiomotin or w | Open-i
Migration of MAE cells transfected with angiomotin or with the vector alone was studied in the modified Boyden chamber assay. (A) Analysis of spontaneous migrat
Table of Contents - June 21, 1975, 2 (5972) | The BMJ
In this study, we demonstrated that both the angiogenic factor VEGF and antiangiogenic factors endostatin and angiostatin were significantly increased in the rat colon with experimental UC. The increased levels of endostatin and angiostatin were reversed significantly (75-95%) by 5-ASA treatment, whereas 5-ASA treatment did not change VEGF expression. Because 5-ASA could inhibit angiogenesis through up-regulating expression of PPAR-γ, which is a downstream inhibitor of VEGF-induced angiogenesis (Murata et al., 2000), it was not surprising that the levels of VEGF did not change. It is possible that increased VEGF and simultaneously up-regulated endostatin and angiostatin contribute to pathologic angiogenesis. This study indicates that the effectiveness of 5-ASA on UC healing may be directly related to down-regulation of the antiangiogenic factors endostatin and angiostatin in UC.. Because angiostatin and endostatin could be generated by MMP2 and MMP9 through cleavage of collagen XVIII and ...
Nucleic acids encoding plasminogen fragments - Patent # 6521439 - PatentGenius
Nucleic acid sequences encoding kringle region fragments of plasminogen. Ribonucleic and deoxyribonucleic acid sequences that encode for kringle region fragments are useful for gene therapy or recombinant expression for the treatment of angiogenesis-related diseases, specifically angiogenesis-dependent cancer.
Impaired Coronary Collateral Growth in the Metabolic Syndrome Is in Part Mediated by Matrix Metalloproteinase 12-Dependent...
Approach and Results-Rats underwent transient, repetitive left anterior descending occlusion (resultant myocardial ischemia [RI]) for 0 to 10 days. CCG was measured in the collateral-dependent and normal zones using microspheres, MMP activation by Western blot, and endostatin and angiostatin by ELISA on days 0, 3, 6, 9, or 10 of RI. Endostatin and angiostatin were increased in JCR but not in Sprague Dawley rats on days 6 and 9 of RI. Increased endostatin and angiostatin correlated with increased MMP12 (≈4-fold) activation in JCR but not in Sprague Dawley rats on days 6 and 9 of RI. Inhibition of MMP12 in JCR rats nearly completely blocked endostatin (≈85%) and angiostatin (≈90%) generation and significantly improved CCG (collateral-dependent zone flow was ≈66% of normal zone flow versus ≈12% for JCR RI).. ...
Lung Overexpression of Angiostatin Aggravates Pulmonary Hypertension in Chronically Hypoxic Mice - Inserm
Exposure to hypoxia leads to the development of pulmonary hypertension (PH) as a consequence of pulmonary smooth mus-cle hyperplasia. Hypoxia concomitantly stimulates lung expres-sion of angiogenic factors. To investigate the role of angiogenesis processes in development of hypoxic PH, we examined the effects of lung overexpression of angiostatin, an angiogenesis inhibitor, on development of hypoxic PH and lung endothelial cell (EC) density. Angiostatin delivery was achieved by a defective adeno-virus expressing a secretable angiostatin K3 molcule driven by the cytomegalovirus promoter (Ad.K3). Comparison was made with a control vector containing no gene in the expression cassette (Ad.CO1). Treatment with Ad.K3 (300 plaque-forming units [pfu]/cell) inhibited cultured human pulmonary artery EC migration by 100% and proliferation by 50%, but was without effects on human pulmonary artery smooth muscle cells. After intratracheal administration of Ad.K3 (10 9 pfu) to mice, angios-tatin protein became
Increased angiostatin levels in bronchoalveolar lavage fluids from ARDS patients and from human volunteers after lung...
TY - JOUR. T1 - Increased angiostatin levels in bronchoalveolar lavage fluids from ARDS patients and from human volunteers after lung instillation of endotoxin. AU - Lucas, Rudolf. AU - Lijnen, H. Roger. AU - Suffredini, Anthony F.. AU - Pepper, Michael S.. AU - Steinberg, Kenneth P.. AU - Martin, Thomas R.. AU - Pugin, Jérôme. PY - 2002/1/1. Y1 - 2002/1/1. N2 - Acute respiratory distress syndrome (ARDS) is characterized by a disruption of the alveolar-capillary barrier, due to both an epithelial and an endothelial dysfunction. Whereas epithelial apoptosis seems to be mainly mediated by Fas ligand, the mediators of endothelial damage remain to be identified. Angiostatin, a powerful inhibitor of angiogenesis in vivo, also specifically induces apoptosis in endothelial cells. The concentration of various enzymes that cleave angiostatin from plasminogen was reported to be significantly increased in bronchalveolar lavage (BAL) fluids from patients with ARDS. Therefore, in this study, we ...
MGCD-265 - Evolution of NADPH Oxidase Inhibitors
Angiostatin a proteolytic fragment of plasminogen is a potent endogenous antiangiogenic agent. thrombospondin-1 reinforcing its antitumor and antiangiogenic effects. Additional evidence is definitely provided for decreased infiltration and recruitment of bone tissue marrow-derived macrophages in angiostatin-treated tumors. The observed ramifications of angiostatin had been limited to the tumor site and werent observed in additional major organs from the mice indicating exclusive tumor particular bioavailability. Collectively our data recommend mitochondria like a book focus on for antiangiogenic therapy and offer mechanistic insights towards the antiangiogenic and MGCD-265 antitumor ramifications of angiostatin. Intro Human plasminogen can be an abundant proteins in blood flow. MGCD-265 Its plasma focus is 200 μg/L approximately. It really is a glycoprotein having a molecular mass of 92 kDa including 2% carbohydrate and comprising 5 kringles with a complete of 24 disulfide bonds.1 In 1994 it ...
Citation tools | Molecular & Cellular Proteomics
Wu, Tianfu et al Urinary Angiostatin - A Novel Putative Marker of Renal Pathology Chronicity in Lupus Nephritis. Molecular & Cellular Proteomics 12.5 (2013): 1170-1179. Web. 11 Aug. 2020. ...
Calories in Shop N Save Milk Skim (Fat Free Skim Milk - Calories and Nutrition Facts | MyFitnessPal.com
Calories in Shop N Save Milk Skim (Fat Free Skim Milk. Find nutrition facts for Shop N Save Milk Skim (Fat Free Skim Milk and over 2,000,000 other foods in MyFitnessPal.coms food database.
Does nitroglycerin cause orthostatic hypotension doxycycline gamma gt green tea on hair metoprolol fainting
Is acetaminophen or aspirin more soluble in water can zoloft cause permanent damage how long before geodon works celebrex side effects blood clots, Gabapentin veterinary prilosec zantac combination furosemide special considerations estrace cream price comparisons, How hard is it to get prescribed tramadol allegra d on sale this week strattera side effects hallucinations time of day to give lipitor, Zofran side effects dizziness doxepin 3000 duricef pediatric dosing 2mg ativan equivalent klonopin, Desert burn hoodia gordonii weight loss famvir vs valtrex for genital herpes clindamycin belly ache side effects of lanoxin in dogs
Beta globulins - Wikipedia
Beta globulins are a group of globular proteins in plasma that are more mobile in alkaline or electrically charged solutions than gamma globulins, but less mobile than alpha globulins. Examples of beta globulins include: beta-2 microglobulin plasminogen angiostatins properdin sex hormone-binding globulin transferrin Ren Zhang; Yan Lin & Chun-Ting Zhang (2008). Greglist: a database listing potential G-quadruplex regulated genes. Nucleic Acids Res. 36 (suppl 1): D372-D376. doi:10.1093/nar/gkm787. Phillip A. Rachwal; I. Stuart Findlow; Joern M. Werner; Tom Brown & Keith R. Fox (2007). Intramolecular DNA quadruplexes with different arrangements of short and long loops. Nucleic Acids Res. 35 (12): 4214-4222. doi:10.1093/nar/gkm316. Antonio Randazzo; Veronica Esposito; Oliver Ohlenschläger; Ramadurai Ramachandran; Antonella Virgilio & Luciano Mayol (2005). Structural studies on LNA quadruplexes. Nucleosides, Nucleotides and Nucleic Acids. 24 (5-7): 795-800. doi:10.1081/NCN-200060279. Examples ...
The angiogenic switch, a rate-limiting step in tumor progression, has already occurred by the time most human tumors are detectable. The angiogenic switch is not limited at earliest stages, but occurs also at different stages of tumor progression (2). Antiangiogenic therapy is a promising alternative for treatment of cancer, and may also be used as a maintenance therapy to prevent the metastasis or recurrence (4). Therapy with endogenous angiogenic inhibitors such as endostatin and angiostatin may reverse the angiogenic switch by preventing growth of tumor vasculature. Angiostatin can maintain metastases in a dormant state in laboratory animals when administered exogenously (34). In transgenic mice overexpressing endostatin, a small increase of circulating endostatin (approximately 1.6-fold) is sufficient to confer dramatic protection against tumor growth (11). In individuals with Down syndrome, a similar small increase of circulating endostatin is associated with a remarkably low incidence of ...
Angiogenesis inhibitor improves brain tumor survival by redu... ( The beneficial effects of anti-angio...)
Health, ...The beneficial effects of anti-angiogenesis drugs in the treatment of ... Our findings suggest that antiangiogenesis therapy can increase patie...Cediranib inhibits the potent angiogenesis factor VEGF which is known... We frequently see beneficial effects from drugs in patients without f...,Angiogenesis,inhibitor,improves,brain,tumor,survival,by,reducing,edema,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
The present study demonstrated the validity and superiority of CD105 as a marker of angiogenesis in NSCLC; the CD105-IMVD was more closely correlated with the expression of VEGF than the CD34-IMVD. Kumar et al. (11 , 13 , 15, 16, 17, 18) and others have demonstrated that anti-CD105 antibodies preferentially react with activated ECs in tissues participating in angiogenesis, such as tumor tissues, and that antibodies against pan-ECs, such as anti-CD34 antibodies, react with normal vessels, as well as activated vessels. According to the hypothesis, we tried to define the CD34-IMVD-CD105-IMVD as the baseline IMVD. As a result, the baseline IMVD proved not at all to be correlated with VEGF expression, suggesting the baseline IMVD was not a measurement of angiogenesis but a measurement of vessels just trapped within tumor tissues. Of course, it should be noted that angiogenesis is not influenced only by VEGF but also other angiogenic factors and antiangiogenic factors, such as angiostatin. Comparative ...
AMOT - Angiomotin - Homo sapiens (Human) - AMOT gene & protein
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=http://www.nrbook.com/b/bookcpdf.php>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Diabetes enhances oxidative stress-induced TRPM2 channel activity and its control by N-acetylcysteine in rat dorsal root...
N-acetylcysteine (NAC) is a sulfhydryl donor antioxidant that contributes to the regeneration of glutathione (GSH) and also scavengers via a direct reaction with free oxygen radicals. Recently, we observed a modulatory role of NAC on GSH-depleted dorsal root ganglion (DRG) cells in rats. NAC may have a protective role on oxidative stress and calcium influx through regulation of the TRPM2 channel in diabetic neurons. Therefore, we investigated the effects of NAC on DRG TRPM2 channel currents and brain oxidative stress in streptozotocin (STZ)-induced diabetic rats. Thirty-six rats divided into four groups: control, STZ, NAC and STZ + NAC. Diabetes was induced in the STZ and STZ + NAC groups by intraperitoneal STZ (65 mg/kg) administration. After the induction of diabetes, rats in the NAC and STZ + NAC groups received NAC (150 mg/kg) via gastric gavage. After 2 weeks, DRG neurons and the brain cortex were freshly isolated from rats. In whole-cell patch clamp experiments, TRPM2 currents in the DRG ...
Does Cocky Boys Model Bravo Delta Have Butt Cheek Implants? - The Sword
talk about being a jerk. with that comment you seem to fit the description pretty well. and besides being a jerk people who list things off come across as really bossy and annoying. i dont know what planet your from but here on earth if you are kissing, sucking, and fucking men and you are a man yourself i think being labeled as straight is a bit of a stretch. dont believe me, ask any real straight guy. if anything maybe hes bi. and how the hell would you know that this is literally his first male fuck? i mean who really knows what he does in private. i used to think he was hot when he just did xtube videos with his sunglasses on but now he has turned into just another dime a dozen boring gay for payer. by the way, do work for cockyboys or are you his manager? maybe his girlfriend? because you seem to consider yourself an expert when it comes to all things bravo delta.. ...
Thrombospondin-1 regulates the normal prostate in vivo through angiogenesis and TGF-beta activation
Castration experiments in rodents show that the stromal vasculature is critical to the androgen-mediated prostate growth regulation. However, the role of angiogenesis inhibitors, such as thrombospondin-1 (TSP-1), in this process is unclear. TSP-1 is a multifunctional glycoprotein that can function as a potent angiogenesis inhibitor and an in vivo activator of latent transforming growth factor-beta (TGF-beta) in some tissues. On the basis of these observations, we hypothesized that TSP-1 regulated androgen withdrawal-induced prostate regression and that this process was mediated not only through antiangiogenic activity but also through TGF-beta activation. To test this, we evaluated angiogenic activity in human prostate epithelial and stromal cells treated with androgens and hypoxia in vitro. TSP-1 knockout mice were characterized to investigate the in vivo functions of TSP-1. In vitro, we found that androgens and hypoxia differentially regulated TSP-1 and angiogenic activity. Androgens ...
Matrix metalloproteases from chondrocytes generate an antiangiogenic 16 kDa prolactin | Journal of Cell Science
These studies demonstrate for the first time that MMPs cleave PRL to generate antiangiogenic 16K-PRL. 16K-PRL blocks a variety of endothelial cell functions (Corbacho et al., 2002; Gonzalez et al., 2004; Lee et al., 2005) and inhibits angiogenesis in ocular tissues (Dueñas et al., 1999; Pan et al., 2004; Aranda et al., 2005) and in tumors (Bentzien et al., 2001; Kim et al., 2003). The specific enzymes responsible for generating 16K-PRL are largely unknown. MMPs cleave various proteins to release their bioactive forms, including the antiangiogenic fragments angiostatin (Patterson and Sang, 1997; Lijnen et al., 1998; OReilly et al., 1999) and endostatin (Lin et al., 2001). Considering that the release of antiangiogenic fragments occurs in avascular tissues such as cartilage (Pufe et al., 2004), we focused on whether chondrocyte MMPs could process PRL to 16K-PRL.. We demonstrate that MMPs produced and secreted by chondrocytes cleave PRL to generate biologically active 16K-PRL. Cleavage occurs at ...
run dream cook: molasses kringles
Ive made gingerbread for the past 10 years, every single Christmas. Its delicious, but definitely a lot of work. This year I decided to branch out a little bit and instead of doing the roll and decorate gingerbread, I wanted to try a chewy molasses cookie. After searching foodgawker for what seemed like hours, I decided to go with a recipe from What Megans Making for molasses kringles. They certainly did not disappoint. They are soft, chewy, spicy and just a bit sweet. I when I make them again Ill ditch the glaze though. I think it made them just a bit too sweet. If you want the recipe for the glaze, check out Megans original recipe ...
Study to the Optimal Duration of Therapy With Oral Angiogenesis Inhibitors - Full Text View - ClinicalTrials.gov
Until now, in trials it is common to stop therapy when progressive disease occurs; RECIST criteria are used, in which progressive disease is defined as ,20% increase of the sum of the longest diameter of the lesions, or occurence of new lesions. However, angiogenesis inhibitors have a rather cytostatic than cytotoxic effect compared to chemotherapeutics, as a result of which less frequently reduction of tumor volume is being seen.. Often in the centre of the lesion necrosis is shown. Sometimes accompanied with edema; so even tumor volume increase can be the result without real progression being the case. Recently, in our clinic, we found a number of patients, treated with oral angiogenesis inhibitors, a remarkable quickening of progressive disease and complaints after stopping this treatment. Reintroduction of the same or another type of angiogenesis inhibitor subsequently lead to a new stabilization. The causality of this phenomenon is unknown. Perhaps that the inhibitory effect of the ...
The p130 Isoform of Angiomotin Is Required for Yap-Mediated Hepatic Epithelial Cell Proliferation and Tumorigenesis | Science...
The Hippo-Yap signaling pathway regulates a number of developmental and adult cellular processes, including cell fate determination, tissue growth, and tumorigenesis. Members of the scaffold protein angiomotin (Amot) family interact with several Hippo pathway components, including Yap (Yes-associated protein), and either stimulate or inhibit Yap activity. We used a combination of genetic, biochemical, and transcriptional approaches to assess the functional consequences of the Amot-Yap interaction in mice and in human cells. Mice with a liver-specific Amot knockout exhibited reduced hepatic oval cell proliferation and tumorigenesis in response to toxin-induced injury or when crossed with mice lacking the tumor suppressor Nf2. Biochemical examination of the Amot-Yap interaction revealed that the p130 splicing isoform of Amot (Amot-p130) and Yap interacted in both the cytoplasm and nucleus, which involved binding of PPxY and LPxY motifs in Amot-p130 to WW domains of Yap. In the cytoplasm, ...
Anti-Angiogenesis Drug Discovery and Development:: volume 3 | BenthamScience
The inhibition of angiogenesis is an effective mechanism of slowing down tumor growth and malignancies. The process of induction or pro-angiogenesis is highly desirable for the treatment of cardiovascular diseases, wound healing disorders, etc. Efforts to understand the molecular basis, both for inhibition and induction, have yielded fascinating results. Anti-angiogenesis Drug Discovery and Development provides an excellent compilation of well-written reviews on various aspects of the anti-angiogenesis process. These reviews have been contributed by leading practitioners in drug discovery science and highlight the major developments in this exciting field in the last two decades. The feast of these reader-friendly reviews on topics of great scientific importance - many of which are considered significant medical breakthroughs, makes this book excellent reading both for the novice as well as for expert medicinal chemists and clinicians. This volume brings together 5 reviews on these topics: ...
Brain Tumor Response to Anti-Angiogenesis Therapy Revealed Via New MR Analysis Technique
New research indicates that a new way of analyzing data acquired in MR imaging appears to be able to identify whether or not tumors are responding to anti-angiogenesis therapy.
Angiogenesis Inhibitors | Johns Hopkins Medicine Health Library
Sometimes called antiangiogenic therapy, this treatment may prevent the growth of cancer by blocking the formation of new blood vessels.
Antiangiogenic therapies in colorectal cancer | springermedizin.at
Angiogenesis is a very important step in the development of cancer. Several antiangiogenic biological agents have been studied during the past two …
T103N Summary Report | CureHunter
T103N: alteplase variant; contains additional glycosylation site in the first kringle domain; causes substantial reduction in clearance rate
Chile, Mining, Seawater, Reverse Osmosis, Water Quality, Malta from Water. desalination + reuse
Browse Chile, Mining, Seawater, Reverse Osmosis, Water Quality, Malta items by tag, keyword or phrase on Water. desalination + reuse. Click on a keyword to refine the search further
Moreover, NK4 is structurally similar to angiostatins, which is why it possesses anti-angiogenic activity. Neutralizing anti- ...
Angiostatins at the US National Library of Medicine Medical Subject Headings (MeSH) v t e. ...
Examples of beta globulins include: beta-2 microglobulin plasminogen angiostatins properdin sex hormone-binding globulin ...
List of MeSH codes (D12.776)
... angiostatins MeSH D12.776.377.715.182.624 - properdin MeSH D12.776.377.715.182.800 - sex hormone-binding globulin MeSH D12.776. ... angiostatins MeSH D12.776.467.100.450.750 - endostatins MeSH D12.776.467.100.800.200 - vascular endothelial growth factor a ...
List of MeSH codes (D12.776.124)
... angiostatins MeSH D12.776.124.790.223.624 - properdin MeSH D12.776.124.790.223.800 - sex hormone-binding globulin MeSH D12.776. ...
List of MeSH codes (D08)
... angiostatins MeSH D08.811.074.124 - deoxyribodipyrimidine photo-lyase MeSH D08.811.074.249 - dna glycosylases MeSH D08.811. ...
List of MeSH codes (D23)
... angiostatins MeSH D23.348.479.311.200.750 - endostatins MeSH D23.348.479.311.300 - fibroblast growth factor 1 MeSH D23.348. ...
List of MeSH codes (D12.644)
... angiostatins MeSH D12.644.276.100.450.750 - endostatins MeSH D12.644.276.100.800 - vascular endothelial growth factors MeSH ...
Role of angiostatins in diabetic complications
Angiostatins, which are kringle-containing fragments of plasminogen/plasmin, are known to be powerful physiological inhibitors ... Also, role of angiostatins in the pathogenesis of typical diabetic complications, including retinopathies, nephropathies and ... Reference: Tykhomyrov A.A., Shram S.I., Grinenko T.V., Role of angiostatins in diabetic complications, Biomeditsinskaya khimiya ... In the present review, current literature data on peculiarities of production of angiostatins and their functioning at diabetes ...
Kringle 1 of human hepatocyte growth factor inhibits bovine aortic endothelial cell proliferation stimulated by basic...
Hepatocyte growth factor (HGF), also known as scatter factor, is a mesenchymal or stromal-derived mediator with angiogenic activity. There are four kringle domains in its amino terminus. They display considerable sequence similarity with those of angiostatin, an angiogenesis inhibitor. We now descri …
Combined effects of angiostatin and ionizing radiation in antitumour therapy
Search | IOVS | ARVO Journals
Corneal Neovascularization Summary Report | CureHunter
C-Met - Wikipedia
Angiostatin - Wikipedia
Drug Information Portal - U.S. National Library of Medicine - Quick Access to Quality Drug Information
Why a Cure For Cancer Is So Elusive - Slashdot
JoVE | Peer Reviewed Scientific Video Journal - Methods and Protocols
US20050149161A1 - Edge protection and bifurcated stent delivery system - Google Patents
Extracts from Fly Maggots and Fly Pupae as a "Wound Healer" | SpringerLink
Zack Z. Wang - Research Output - Johns Hopkins University
Yeast two-hybrid screening for angiostatin-binding prot | Open-i
US10285831B2 - Endovascular implant - Google Patents
iTRAQ-Based Quantitative Proteomic Analysis of Tear Fluid in a Rat Penetrating Keratoplasty Model With Acute Corneal Allograft...
Patent US20050137715 - Methods and devices for maintaining patency of surgically created channels ... - Google Patents
Antivascular Therapy for Epithelial Ovarian Cancer
Find Grants - Northwestern Scholars
Retinoschisis 1, X-Linked, Juvenile disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials
highly vascular glioma drug therapy 2000:2010[pubdate] *count=100 - BioMedLib™ search engine
Macrophage elastase suppresses white adipose tissue expansion with cigarette smoking<...
TY - JOUR. T1 - Macrophage elastase suppresses white adipose tissue expansion with cigarette smoking. AU - Tsuji, Takao. AU - Kelly, Neil J.. AU - Takahashi, Saeko. AU - Leme, Adriana S.. AU - Houghton, A. Mc Garry. AU - Shapiro, Steven D.. PY - 2014/12/1. Y1 - 2014/12/1. N2 - Macrophage elastase (MMP12) is a key mediator of cigarette smoke (CS)-induced emphysema, yet its role in other smoking related pathologies remains unclear. The weight suppressing effects of smoking are a major hindrance to cessation efforts, and MMP12 is known to suppress the vascularization on which adipose tissue growth depends by catalyzing the formation of antiangiogenic peptides endostatin and angiostatin. The goal of this study was to determine the role of MMP12 in adipose tissue growth and smoking-related suppression of weight gain. Whole body weights and white adipose depots from wild-type and Mmp12-deficient mice were collected during early postnatal development and after chronic CS exposure. Adipose tissue ...
Robert Duvoisin - Publications - Oregon Health & Science University
Sansig, G., Bushell, T. J., Clarke, V. R. J., Rozov, A., Burnashev, N., Portet, C., Gasparini, F., Schmutz, M., Klebs, K., Shigemoto, R., Flor, P. J., Kuhn, R., Knoepfel, T., Schroeder, M., Hampson, D. R., Collett, V. J., Zhang, C., Duvoisin, R. M., Collingridge, G. L. & Van Der Putten, H., Nov 15 2001, In: Journal of Neuroscience. 21, 22, p. 8734-8745 12 p.. Research output: Contribution to journal › Article › peer-review ...
Monica Rodolfo - Research Output - Italian Ministry of Health
Iles, M. M., Law, M. H., Stacey, S. N., Han, J., Fang, S., Pfeiffer, R., Harland, M., MacGregor, S., Taylor, J. C., Aben, K. K., Akslen, L. A., Avril, M. F., Azizi, E., Bakker, B., Benediktsdottir, K. R., Bergman, W., Scarrà, G. B., Brown, K. M., Calista, D., Chaudru, V. & 70 others, Fargnoli, M. C., Cust, A. E., Demenais, F., De Waal, A. C., Dȩbniak, T., Elder, D. E., Friedman, E., Galan, P., Ghiorzo, P., Gillanders, E. M., Goldstein, A. M., Gruis, N. A., Hansson, J., Helsing, P., Hočevar, M., Höiom, V., Hopper, J. L., Ingvar, C., Janssen, M., Jenkins, M. A., Kanetsky, P. A., Kiemeney, L. A., Lang, J., Lathrop, G. M., Leachman, S., Lee, J. E., Lubiński, J., MacKie, R. M., Mann, G. J., Martin, N. G., Mayordomo, J. I., Molven, A., Mulder, S., Nagore, E., Novaković, S., Okamoto, I., Olafsson, J. H., Olsson, H., Pehamberger, H., Peris, K., Grasa, M. P., Planelles, D., Puig, S., Puig-Butille, J. A., Randerson-Moor, J., Requena, C., Rivoltini, L., Rodolfo, M., Santinami, M., Sigurgeirsson, B., ...
Make it Viral? - Reading WhitneyReading Whitney
- Angiostatins, which are kringle-containing fragments of plasminogen/plasmin, are known to be powerful physiological inhibitors of neovascularization. (msk.ru)
- Aisina RB, Mukhametova LI, Gulin DA, Levashov MY, Prisyazhnaya NV, Gershkovich KB, Varfolomeyev SD (2009) Inhibitory effect of angiostatins on activity of the plasminogen/plasminogen activator system. (springer.com)
- Afternoon sessions will consist of hands-on laboratory exercises and demonstrations covering basic quantitative molecular biology protocols and tools, e.g QRTPCR quantitation of p21/p53 expression in fibroblast cultures after UV exposure, tissue culture systems (including growth factor dependent and 3D systems) and surrogate in vivo tumor model systems, e.g. perturbations of chick growth and angiogenesis by angiostatins/VEGF. (uci.edu)