PPD-induced blastogenesis is auto-regulated by suppressor cells generated in vitro

Summary Suppressor cell induction can be demonstrated during antigen specific blastogenesis by using the same methods which have shown induction of suppressor cells by Con A. Since suppressor cells are rapidly generated during antigen specific blastogenesis, they must regulate the final level of blastogenesis induced during the seven day in vitro incubation.Supported by Unites States Public Health Service grants AM-13377 and CA-19266.     

PPD-induced blastogenesis is auto-regulated by suppressor cells generated in vitro.

Suppressor cell induction can be demonstrated during antigen specific blastogenesis by using the same methods which have shown induction of suppressor cells by Con A. Since suppressor cells are rapidly generated during antigen specific blastogenesis, they must regulate the final level of blastogenesis induced during the seven day in vitro incubation.     

Deoxyribozymes: useful DNA catalysts in vitro and in vivo

Deoxyribozymes (DNA enzymes; DNAzymes) are catalytic DNA sequences. Using the technique of in vitro selection, individual deoxyribozymes have been identified that catalyze RNA cleavage, RNA ligation, and a growing range of other chemical reactions. DNA enzymes have been used in vitro for applications such as biochemical RNA manipulation and analytical assays for metal ions, small organic compounds, oligonucleotides, and proteins. Deoxyribozymes have also been utilized as in vivo therapeutic agents to destroy specific mRNA targets. Although many conceptual and practical challenges remain to be addressed, deoxyribozymes have substantial promise to contribute meaningfully for applications both in vitro and in vivo.     

Fenofibrate inhibits angiogenesis in vitro and in vivo

Fenofibrate, a peroxisome proliferator-activated receptor (PPAR)-alpha activator, used as a normolipidemic agent, is thought to offer additional beneficial effects in atherosclerosis. Since angiogenesis is involved in plaque progression, hemorrhage, and instability, the main causes of ischemic events, this study was designed to evaluate the action of fenofibrate on angiogenesis. Our results show that fenofibrate (i) inhibits endothelial cell proliferation induced by angiogenic factors, followed at high concentrations by an increase in apoptosis, (ii) inhibits endothelial cell migration in a healing wound model, (iii) inhibits capillary tube formation in vitro, and (iv) inhibits angiogenesis in vivo. Concerning the mechanism of action, the inhibition of endothelial cell migration by fenofibrate can be explained by a disorganization of the actin cytoskeleton. At the molecular level, fenofibrate markedly decreased basic fibroblast growth factor-induced Akt activation and cyclooxygenase 2 gene expression. This inhibition of angiogenesis could participate in the beneficial effect of fenofibrate in atherosclerosis.     

In vivo and in vitro deiodination of silver iodide

Résumé La stabilité de l'iodure d'argent a été étudiée in vivo, par rapport à l'élimination de l'argent et du iode radioactif. Le foie semble responsable de la désiodation. Dans le foie, au bout de 6 h, 83% de l'iode est eliminé, mais seulement 16% de l'argent. Les expériences in vitro indiquent que le facteur responsable de la désiodation est thermostable et plus concentré dans le foie et dans le sang.     

Mechanisms of glial-guided neuronal migration in vitro and in vivo

Summary Our laboratory has developed an in vitro model system in which glial-guided neuronal migration can be observed in real time. Cerebellar granule neurons migrate on astroglial fibers by apposing their cell soma against the glial arm, forming a specialized migration junction, and extending a motile leading process in the direction of migration. In vitro assays indicate that the neuronal antigen astrotactin functions as a neuron-glia ligand, and is likely to play a role in the movement of neurons along glial fibers. In heterotypic recombinations of neurons and glia from mouse cerebellum and rat hippocampus, neurons migrate on heterotypic glial processes with a cytology, speed and mode of movement identical to that of neuronal migration on homotypic glial fibers, suggesting that glial fibers provide a permissive pathway for neuronal migration in developing brain. In vivo analyses of developing cerebellum demonstrate a close coordination of afferent axon ingrowth relative to target cell migration. These studies indicate that climbing fibers contact immature Purkinje neurons during the migration and settling of Purkinje cells, implicating a role for afferents in the termination of migration.     

Mechanisms of glial-guided neuronal migration in vitro and in vivo

Our laboratory has developed an in vitro model system in which glial-guided neuronal migration can be observed in real time. Cerebellar granule neurons migrate on astroglial fibers by apposing their cell soma against the glial arm, forming a specialized migration junction, and extending a motile leading process in the direction of migration. In vitro assays indicate that the neuronal antigen astrotactin functions as a neuron-glia ligand, and is likely to play a role in the movement of neurons along glial fibers. In heterotypic recombinations of neurons and glia from mouse cerebellum and rat hippocampus, neurons migrate on heterotypic glial processes with a cytology, speed and mode of movement identical to that of neuronal migration on homotypic glial fibers, suggesting that glial fibers provide a permissive pathway for neuronal migration in developing brain. In vivo analyses of developing cerebellum demonstrate a close coordination of afferent axon ingrowth relative to target cell migration. These studies indicate that climbing fibers contact immature Purkinje neurons during the migration and settling of Purkinje cells, implicating a role for afferents in the termination of migration.     

Formation of proviruses in acute infection in vitro and in vivo

Summary Formation of DNA proviruses of RNA viruses, Sendai and Newcastle disease, was studied. DNA provirus of NDV was shown to be formed in mouse L-cells and Sendai DNA provirus in Ehrlich ascites carcinoma cells within 2–3 days post infection.     

In vitro and in vivo catabolism of cholesterol in meal-fed rats

Zusammenfassung Bei männlichen Wistar-Ratten wurde der Einfluss des meal-feeding-Regimes nach täglicher 2stündlicher Fütterung an Leberschnitten auf den Katabolismus von Cholesterol-4-¹⁴C geprüft und normal befunden. Im In-vivo-Versuch unter denselben experimentellen Bedingungen zeigte weder der Katabolismus noch die Exkretion des i. p. applizierten Cholesterol-4-¹⁴C eine Veränderung.     

Antimicrobial activity of cyclacillin againstEscherichia coli in vivo and in vitro

Résumé Chez la souris, l'effet de la cyclacilline diffère peu de celui de l'ampicilline, en ce qui concerne la concentration ou localisation deE. coli dans le sang, la rate et la foie. Une différence importante est cependant notée dans les concentrations minima inhibitrices (MIC) de ces deux antibiotiques pour les bactéries gram-négatives.     

In vivo and in vitro molecular hybridization of malate dehydrogenase isozymes

Résumé Les hybrides moléculaires des isozymes de la déshydrogénase de malate de différentes espèces de poissons peuvent être engendrés in vitro en gelant puis dégelant les isozymes en présence du sel. L'isozyme hybride est identique à celle observée in vivo dans l'hybride interspécifique F₁.     

In vivo and in vitro differences between leukocytic uptake of oligodeoxynucleotides

Development and application of therapeutic oligonucleotides rely on proper analysis of binding and uptake. We have used several model oligodeoxynucleotides (ODNs) to analyze binding/uptake by rat and human leukocytes. Here we describe: (1) differences between in vivo and in vitro uptake of ODNs to rat leukocytes, (2) differences after injection of lipopolysaccharide (LPS), (3) large in vitro differences between primary mononuclear cells in PBS, plasma and blood, and (4) differences of ODN uptake between rat and human leukocytes. Our data show that ODN uptake by primary blood cells was different in PBS, plasma and blood. In addition, LPS treatment increased ODN uptake by leukocytes in blood, indicating that pathological conditions may influence ODN uptake. Furthermore, ODN uptake in rat and human blood is also different, suggesting that preclinical ODN uptake data from rat blood cannot easily be extrapolated to the human condition. Received 17 December 2007; received after revision 16 January 2008; accepted 5 February 2008