Finally, we use the model to study protein inhibition and to suggest molecular targets for anti-angiogenic therapies. (C)
2010 Elsevier Ltd. All rights reserved.”
“BACKGROUND: Cerebral arteriovenous malformations (AVMs) do not seem to be static congenital vascular malformations, but rather are dynamically changing SGC-CBP30 in vitro pathologies. It is well-known from clinical situations that these AVMs can enlarge or shrink. Nuclear factor kappa B (NF-kappa B) is a nuclear transcription factor that regulates a number of physiological processes, such as inflammation, apoptosis, and cellular growth.
OBJECTIVE: To analyze phosphorylation of NF-kappa B and related molecules in cerebral AVM specimens.
METHODS: We examined 19 specimens of cerebral AVMs from 18 patients. Immunohistochemical analysis
was performed using an NF-kappa B p65 (C22B4) rabbit monoclonal antibody, the phosphorylated form of NF-kappa B (PNF-kappa B) p65 (Ser276) rabbit antibody, and an I kappa B alpha mouse monoclonal antibody.
RESULTS: Expression of NF-kappa B was mainly confined to the endothelial lining and the Torin 1 chemical structure infiltrating inflammatory cells in the perivascular regions. PNF-kappa B showed the highest level of expression in both endothelial cells and perivascular infiltrating cells. PNF-kappa B was intensely expressed in the endothelium and perivascular infiltrating cells of 15 specimens (78.9%). NF-kappa B and I kappa B were also expressed in endothelial cells and perivascular
infiltrating inflammatory cells, but at lower levels than PNF-kappa B. Immunohistochemical studies revealed that PNF-kappa B was mainly concentrated in the nuclei of endothelial and infiltrating inflammatory cells. On the contrary, expression of both NF-kappa B and I kappa B was mainly concentrated in the cytoplasm of endothelial and inflammatory cells.
CONCLUSION: We detected Thiamet G activation of NF-kappa B in the endothelium and perivascular infiltrating inflammatory cells within the cerebral AVM nidus, suggesting a role in the pathophysiology of cerebral AVM.”
“We propose a new model describing the production and the establishment of the stable gradient of the Bicoid protein along-the antero-posterior axis of the embryo of Drosophila. In this model, we consider that bicoid mRNA diffuses along the antero-posterior axis of the embryo and the protein is produced in the ribosomes localized near the syncytial nuclei. Bicoid protein stays localized near the syncytial nuclei as observed in experiments. We calibrate the parameters of the mathematical model with experimental data taken during the cleavage stages 11-14 of the developing embryo of Drosophila. We obtain good agreement between the experimental and the model gradients, with relative errors in the range 5-8%. The inferred diffusion coefficient of bicoid mRNA is in the range 4.6 x 10(-12)-1.