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1
Content available remote

Comparative animal study on hard tissue integration and bone formation of different Nobel Biocare implants

100%
Gedrange T., Gredes T., Gredes M., Allegrini M. R. F., Borsos G., Vegh A., Salles M. B., Heinemann F., Dominiak M., Allegrini S.,Jr
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 8
117-121
2

The adipocyte component of bone marrow in heterotopic bone induced by demineralized incisor grafts

100%
Wlodarski K. H., Galus R., Brodzikowska A., Wlodarski P. K.
Folia Histochemica et Cytobiologica
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2012
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tom 50
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nr 3
3

Influence of estrogen deficiency on the level of magnesium in rat mandible and teeth

100%
Rahnama M., Marciniak A.
Bulletin of the Veterinary Institute in Puławy
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2002
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tom 46
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nr 2
4

Mutations in type I collagen genes resulting in osteogenesis imperfecta in humans

100%
Gajko-Galicka A.
Acta Biochimica Polonica
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2002
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tom 49
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nr 2
Osteogenesis imperfecta (OI), commonly known as "brittle bone disease", is a domi­nant autosomal disorder characterized by bone fragility and abnormalities of connec­tive tissue. Biochemical and molecular genetic studies have shown that the vast major­ity of affected individuals have mutations in either the COL1A1 or COL1A2 genes that encode the chains of type I procollagen. OI is associated with a wide spectrum of phe- notypes varying from mild to severe and lethal conditions. The mild forms are usually caused by mutations which inactivate one allele of COL1A1 gene and result in a re­duced amount of normal type I collagen, while the severe and lethal forms result from dominant negative mutations in COL1A1 or COL1A2 which produce structural de­fects in the collagen molecule. The most common mutations are substitutions of glycine residues, which are crucial to formation and function of the collagen triple he­lix, by larger amino acids. Although type I collagen is the major structural protein of both bone and skin, the mutations in type I collagen genes cause a bone disease. Some reports showed that the mutant collagen can be expressed differently in bone and in skin. Since most mutations identified in OI are dominant negative, the gene therapy requires a fundamentally different approach from that used for genetic-recessive dis­orders. The antisense therapy, by reducing the expression of mutant genes, is able to change a structural mutation into a null mutation, and thus convert severe forms of the disease into mild OI type I.
5

Metaplasia of chondrocytes into osteoblasts

100%
Wlodarski K. H., Wlodarski P. K., Brodzikowska A.
Folia Biologica
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2006
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tom 54
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nr 3-4
6

Osteogenic efficiency of demineralized and lyophilized xenogeneic bone and syngeneic dentine implants in mice

80%
Wlodarski P., Galus R., Brodzikowska A., Wlodarski K. H.
Folia Biologica
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2013
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tom 61
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nr 1-2
7
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A glimpse at the ontogeny of the fossil neobatrachian frog Calyptocephalella canqueli from the Deseadan (Oligocene) of Patagonia, Argentina

80%
Muzzopappa P., Nicoli L.
Acta Palaeontologica Polonica
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2010
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tom 55
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nr 4
Two fossil tadpoles collected in the Deseadan levels (Oligocene) at the Scarritt Pocket locality of central Patagonia are studied herein. These specimens, which show different degrees of skeletal development, have been assigned to the neobatrachian Calyptocephalella canqueli based on the morphology of the frontoparietals and the presence of adult specimens of this fossil species at the same locality. The concurrent analysis of three developmental stages (Gosner Stages 35/36 and 38/39, and adult) has provided significant data about the ontogeny of this species, including the change of the pattern of exostosis of the frontoparietals, from a pitted to a tuberculated pattern, and the corroboration of the inclusion of two neural arches in the formation of the urostyle. This evidence will shed light on developmental mechanisms that might be involved in the evolution of the genus Callyptocephalella.
8

Gene expression patterns in bone following lipopolysaccharide stimulation

80%
Yang J., Su N., Du X., Chen L.
Cellular and Molecular Biology Letters
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2014
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tom 19
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nr 4
Bone displays suppressed osteogenesis in inflammatory diseases such as sepsis and rheumatoid arthritis. However, the underlying mechanisms have not yet been clearly explained. To identify the gene expression patterns in the bone, we performed Affymetrix Mouse Genome 430 2.0 Array with RNA isolated from mouse femurs 4 h after lipopolysaccharide (LPS) administration. The gene expressions were confirmed with real-time PCR. The serum concentration of the N-terminal propeptide of type I collagen (PINP), a bone-formation marker, was determined using ELISA. A total of 1003 transcripts were upregulated and 159 transcripts were downregulated (more than twofold upregulation or downregulation). Increased expression levels of the inflammation-related genes interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) were confirmed from in the period 4 h to 72 h after LPS administration using real-time PCR. Gene ontogene analysis found four bone-related categories involved in four biological processes: system development, osteoclast differentiation, ossification and bone development. These processes involved 25 upregulated genes. In the KEGG database, we further analyzed the transforming growth factor β (TGF-β) pathway, which is strongly related to osteogenesis. The upregulated bone morphogenetic protein 2 (BMP2) and downregulated inhibitor of DNA binding 4 (Id4) expressions were further confirmed by real-time PCR after LPS stimulation. The osteoblast function was determined through examination of the expression levels of core binding factor 1 (Cbfa1) and osteocalcin (OC) in bone tissues and serum PINP from 4 h to 72 h after LPS administration. The expressions of OC and Cbfa1 decreased 6 h after administration (p < 0.05). Significantly suppressed PINP levels were observed in the later stage (from 8 h to 72 h, p < 0.05) but not in the early stage (4 h or 6 h, p > 0.05) of LPS stimulation. The results of this study suggest that LPS induces elevated expressions of skeletal system development- and osteoclast differentiation-related genes and inflammation genes at an early stage in the bone. The perturbed functions of these two groups of genes may lead to a faint change in osteogenesis at an early stage of LPS stimulation. Suppressed bone formation was found at later stages in response to LPS stimulation.
9
Content available remote

A 3-year clinical and radiographic study of implants placed simultaneously with maxillary sinus floor augmentations using a new nanocrystaline hydroxyapatite

80%
Heinemann F., Mundt T., Biffar R., Gedrange T., Goetz W.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 8
91-97
10

A preliminary study in osteoinduction by a nano-crystalline hydroxyapatite in the mini pig

80%
Gotz W., Lenz S., Reichert C., Henkel K., Bienengraber V., Pernicka L., Gundlach K., Gredes T., Gerber T., Gedrange T., Heinemann F.
Folia Histochemica et Cytobiologica
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2010
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tom 48
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nr 4
11

A novel Gly to Arg substitution at position 388 of the alpha1 chain of type I collagen in lethal form of osteogenesis imperfecta

80%
Galicka A., Wolczynski S., Lesniewicz R., Chyczewski L., Gindzienski A.
Acta Biochimica Polonica
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2002
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tom 49
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nr 2
Cultured skin fibroblasts from a proband with a lethal form of osteogenesis imperfecta produce two forms of type I collagen chains, with normal and delayed elec- trophoretic migration; collagen of the proband's mother was normal. Peptide map­ping experiments localized the structural defect in the proband to a 1(I) CB8 peptide in which residues 123 to 402 are spaned. Direct sequencing of amplified cDNA covering this region revealed a G to A single base change in one allele of the al(I) chain, that converted glycine 388 to arginine. Restriction enzyme digestion of the RT-PCR prod­uct was consistent with a heterozygous COL1A1 mutation. The novel mutation con­forms to the linear gradient of clinical severity for the αl(I) chain and results in re­duced thermal stability by 3°C and intracellular retention of abnormal molecules.
12

The limitation of DEXA analysis for bone mass determination in mice

80%
Dickson G. R., Luczak M., Wlodarski K. H.
Folia Biologica
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2004
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tom 52
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nr 1-2
13

Novel model of stimulation of periosteal osteogenesis and of perichondreal chondrogenesis by oncogenic virus Mu-MSV and its application in bone research

61%
Wlodarski K. H., Wlodarski P. K., Luczak M., Galus K.
Bulletin of the Polish Academy of Sciences. Biological Sciences
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1994
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tom 42
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nr 3
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