Metamorphosis Insectorum Surinamensium Ofte Verandering Der Surinaamsche Insecten : Waar in de Surinaamsche Rupsen en Wormen met alle des zelfs Veranderingen na het leven afgebeeld en beschreeven worden, zynde elk geplaast ob die Gewassen, Bloemen en Vruchten, daar sy op gevonden zyn ...

door Maria Sibylla Merian. [J. Mulder Sculp. ; P. Sluyter Sculp.]

De Europische Insecten : Naauwkeurig onderzogt, na't leven geschildert, en in print gebragt door Maria Sibilla Merian; Met een korte Beschryving, waar in door haar gehandelt word van der Rupsen begin, Voedzel en wonderbare Verandering; En Ook Vertoont Word De Oorspronk, Spys en Gestalt-verwisseling, de Tyd, Plaats en Eigenschappen der Rupzen, Uiltjes, Vliegen en andere diergelyke bloedeloose Beesjes; Hier Is Nog Bygevoegt Een naauwkeurige Beschryving van de Planten, in dit Werk voorkomende; ... In't Frans beschreven door J. Marret, Medicinæ Doctor, En door een voornaam Liefhebber in't Nederduits vertaalt

Die Illustrationen sind Kupferstiche

Mus Hs 7 - Psalmboek : voor orgel en clavicimbel, behelzende de CL psalmen, en gewoone lofzangen, op de ordinaire & sleute gesteld, en met een bas daar egens, en een bas continuo daar booven geteekent, met noch een twééde loopende bas, ofte bas obligato, dienende tot een variatio ; alsmede ider Psalm in zyn toon getransponeert, waar in dezelve moet gespeelt, en gezongen werden, voor't orgel, clavecimbel, en andre instrumenten

door Hk: Radeker

Catalogus van de tentoonstelling van Joodsche oorlogslitteratuur : gehouden te Amsterdam in de bibliotheek van het Portugeesch Israelietisch Seminarium "Ets Haim" ... van zondag 23 Nissan 5677 (15 April 1917) tot en met vrijdag 28 Nissan 5677 (20 April 1917) ten bate van het inzamelingswerk voor de Joodsche oorlogsslachtoffers

[bewerkt door J.S. Da Silva Rosa]

The survival role and the potential therapeutic targeting of MET in multiple myeloma

Multiple myeloma (MM) is a debilitating and incurable B-cell malignancy. Previous studies have documented that the hepatocyte growth factor (HGF) plays a role in the pathobiology of MM. The receptor tyrosine kinase MET induced signaling initiates when its ligand HGF binds to the MET receptor. However, the direct importance of MET in MM has not been elucidated. The present work used three different but complementary approaches to reduce MET protein levels or its activity to demonstrate the importance of MET in MM. ^ In the first approach, MET transcript and protein levels were reduced by directly targeting the cellular MET transcripts using shRNA retroviral infection techniques. This direct reduction of MET mRNA leads to a reduction of MET protein levels, which caused an inhibition of growth and induction of cell death. ^ In the second approach, a global transcription inhibitor flavopiridol was used as a potential pharmacological tool to reduce MET levels. MET has a short half-life of 30 min for mRNA and 4 hours for protein; therefore using a RNA pol II inhibitor such as flavopiridol would be a viable option to reduce MET levels. When using flavopiridol in MM cell lines, there was a reduction of MET transcript and protein levels, which was associated with the induction of cell death. ^ Finally in the last strategy, MET kinase activity was suppressed by MP470, a small molecule inhibitor that binds to the ATP binding pocket in the kinase domain. At concentrations where phosphorylation of MET was inhibited there was induction of cell death in MM cell lines and primary cells from patients. In addition, in MM cell lines there was a decrease in phosphorylation of AKT (ser473) and caspase-9 (ser196); downstream of MET, suggesting that the mechanism of action for survival may be through these cascade of events. ^ Overall, this study provides a proof-of-principle that MET is important for the survival of MM cell lines as well as primary plasma cells obtained from patients. Therefore, targeting MET therapeutically may be a possible strategy to treat patients with this debilitating disease of MM. ^

Activation of c -Met contributes to growth and metastasis of human colorectal carcinoma

c-Met is the protein tyrosine kinase receptor for hepatocyte growth factor/scatter factor (HGF/SF) and mediates several normal cellular functions including proliferation, survival, and migration. Overexpression of c-Met correlates with progression and metastasis of human colorectal carcinoma (CRC). The goals of this study were to determine if overexpression of c-Met directly contributes to tumorigenicity and liver metastatic potential of colon cancer, and what are the critical pathways regulated by c-Met in this process. The studies used two colon tumor cell lines, KM12SM and KM20, which express high levels of constitutively active c-Met and are highly metastatic in nude mice. To examine the effects of c-Met overexpression, subclones of theses lines with reduced c-Met expression were obtained following transfection with a c-Met specific targeting ribozyme. Reduction of c-Met in KM12SM cells abolished liver metastases when cells were injected intrasplenically in an experimental metastasis assay. However, c-Met downregulation in theses clones was unstable. Three stable KM20 clones with a 25–35% reduction in c-Met protein levels but 60–90% reduction in basal c-Met autophosphorylation and kinase activity were obtained. While HGF increased c-Met kinase activity in the clones with reduced c-Met, the activity was less than that observed in parental or control transfected cells. Correlating with the reduction in c-Met kinase activity, subclones with reduced c-Met expression had significantly reduced in vitro growth rates, soft-agar colony forming abilities, and increased apoptosis. HGF/SF treatment did not affect anchorage-dependent growth or soft-agar colony forming abilities. Further, c-Met downregulation significantly impaired the ability of HGF/SF to induce migration. To examine the effects of reduced c-Met on tumor formation, parental and c-Met reduced KM20 cells were grown subcutaneously and intrahepatically in nude mice. c-Met downregulation delayed, but did not abolish growth at the subcutaneous site. When these cells were injected intrahepatically, both tumor incidences and size were significantly reduced. To further understand the molecular basis of c-Met in promoting tumor growth, the activation of several signaling intermediates that have been implicated in c-Met mediated growth, survival and migration were compared between KM20 parental cells and subclones with reduced c-Met expression levels. The expression and activity (as determined by phosphorylation) of AKT and Erk1/2 were unaltered. In contrast, Src kinase activity, as measured by immune complex kinase assay, was reduced 2–5 fold following c-Met downregulation. As Src has been implicated in growth, survival and migration, Src activation in c-Met overexpressing lines is likely contributing to the tumorigenic and metastatic capabilities of colon tumor cell lines that overexpress c-Met. Collectively, these results suggest that c-Met overexpression plays a causal role in the development of CRC liver metastases, and that c-Src and c-Met inhibitors may be of potential therapeutic benefit for late-stage colon cancer. ^

Sic amet ipse licet, sic non potiatur amato (Ov., MET. III, 405) : Narciso en las redes de la inversión

Fil: Tola, Eleonora.