colchicine/cárie dentária

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Expression of bone sialoprotein mRNA during bone formation and resorption induced by colchicine in rat tibial bone marrow cavity.

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In the rat tibial bone marrow cavity, following colchicine injection, there is a phase of osteogenesis in which bone trabeculae replace the necrotic bone marrow tissues and fill the marrow cavity. The newly formed bone is subsequently resorbed by osteoclasts and normal bone marrow is restored. In

A comparison of the anti-inflammatory activity of selective 5-lipoxygenase inhibitors with dexamethasone and colchicine in a model of zymosan induced inflammation in the rat knee joint and peritoneal cavity.

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Intraperitoneal and intra-articular (knee joint) injection of zymosan in the rat caused two phases of increased vascular permeability, a rapid increase (0.25-0.5 h) and a secondary increase (2-3 h) which was temporally associated with the onset of leukocyte infiltration. Intraperitoneal injection of

Ectopic bone formation after treatment with colchicine.

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We followed changes occurring within bone tissue and marrow cells during the process of colchicine-induced ectopic bone development and its resorption inside the marrow cavity of the rat tibia. To stimulate ectopic bone formation male Wistar rats were i.p injected with 0.5 or 1 mg/kg b.w. of

Colchicine prolongs patency of myringotomy in an animal model.

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OBJECTIVE Chronic otitis media with effusion (COME) is a frequently observed condition in childhood. The most common and effective surgical therapy for COME is myringotomy with insertion of a ventilation tube (VT). Our aims were to investigate the combined effect of myringotomy and the topical

Effects of colchicine on gap junction formation during retinal neurogenesis.

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Colchicine, injected into the amniotic cavity of 3 to 10 day-old chick embryos, has the following effects on the developing retina: 1. Cells in arrested metaphase accumulate in the ventricular portion of the matrix region. If colchicine is applied at the end of the first week of incubation, the

Oral colchicine for the treatment of experimental traction retinal detachment.

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In proliferative vitreoretinopathy and trauma, long-term reattachment of the retina is often prevented by the formation of contractile cellular membranes on the retinal surface and within the vitreous cavity. Colchicine, a well-documented inhibitor of microtubule assembly, is a potent inhibitor of

Colchicine and post-inflammatory adhesions in a rabbit model: a dose-response study.

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OBJECTIVE To determine the dose-response relationship of colchicine in reducing inflammatory adhesive disease secondary to Neisseria gonorrhoeae in the rabbit. METHODS Following intrauterine inoculation of a suspension of N gonorrhoeae, the rabbits were divided into five groups of 11 rabbits each.

Effects of colchicine on the formation and looping of the tubular heart of the embryonic chick.

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The role of microtubules in the early development of the chick embryo heart was studied. The microtubules were disrupted by treatment of the embryos with colchicine. The embryos were divided for study into three groups: (I) before the fusion of the paired cardiac primordia; (II) before the starting

[The number of the rat peritoneal cells in normal condition, blood loss, and under colchicine injection].

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The modification of peritoneal cells derivation method proposed for the peritoneum rat, and the absolute amount of peritoneal lymphocytes, monocytes, macrophages, stem and polymorphonuclear neutrophyles, mat cells was determined. The procedure of acute 2% blood loss was found to reduce the total

Inclusion complex of colchicine in hydroxypropyl-β-cyclodextrin tenders better solubility and improved pharmacokinetics.

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BACKGROUND Colchicine (CLC) causes cell death by destabilizing the tubulin unit. However, it ionizes at physiological pH resultant low bioavailability and therapeutic efficacy. OBJECTIVE We have attempted to augment the bioavailability of CLC by fabricating the inclusion complex with

Peritoneal macrophages which phagocytose autologous polymorphonuclear leucocytes in guinea-pigs. I: induction by irritants and microorgansisms and inhibition by colchicine.

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In order to examine macrophages phagocytosing polymorphonuclear leucocytes (PMNs) in detail, we established a new method, whereby a large number of PMN-phagocytosing macrophages (PPMs) were easily induced. PPMs were harvested from the peritoneal cavity after thioglycollate medium, oyster glycogen,

Morphological changes induced by colchicine in the chick optic cup in early stages of development. A stereological study.

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In this study chick embryo optic cups at HH stage 13 of development were analyzed under normal conditions and after inoculation with colchicine for 1, 2, 4, and 8 h. Several changes were seen after these periods of treatment: 1) modifications of the structure, with thicker regions in the cup and a

Dynamic and Static Water Molecules Complement the TN16 Conformational Heterogeneity inside the Tubulin Cavity.

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TN16 is one of the most promising inhibitors of α, β dimer of tubulin that occupies the cavity in the β-subunit located at the dimeric interface, known as the colchicine binding site. The experimentally determined structure of the complex (Protein Data Bank entry 3HKD) presents the conformation and

[Effects of cycloheximide, aminoglutethimide, indomethacin, cytochalasin B and colchicine on ovulation and the ultrastructure of the ovarian follicle wall in the stellate sturgeon Acipenser stellatus Pall].

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The inhibitor of protein synthesis cycloheximide, inhibitor of steroidogenesis aminoglutethimide, and inhibitor of prostaglandin synthesis indomethacin, as well as the drugs affecting the cell cytoskeleton, such as cytochalasin B and colchicine, were used for studying the mechanisms of ovulation in

Development of carrageenan pleurisy in the rat: effects of colchicine on inhibition of cell mobilization.

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Colchicine produced three effects which modified the acute inflammatory response to carrageenan in the rat pleural cavity: (i) inhibition of neutrophil mobilization and concomitant exudate formation (3 hr); (ii) inhibition of monocyte mobilization (21 hr); and (iii) augmented exudate formation (3

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