Objetivou-se, neste trabalho, estudar a proporção de tecido conjuntivo existente na fração ventricular direita e esquerda do músculo cardíaco de cães, buscando, através da morfometria, dados referentes a inter-relação entre o tecido conjuntivo e o tecido muscular cardíaco, para o conhecimento das relações anátomo-funcionais da estrutura cardíaca, característica de determinados processos ligados a diminuição do trabalho do órgão. Utilizou-se 6 corações de cães SRD, machos e fêmeas, com idade entre 48 e 150 meses, pesando entre 18 e 30 Kg, sem alterações cardíacas, confirmado mediante exames eletrocardiográfico e ecocardiográfico. Preparou-se o material oriundo de três regiões ventriculares em relação a sua base, proximal, média e distal, tanto da face direita quanto da esquerda, segundo as técnicas histológicas convencionais e corados com Picrosirius red, Fucsina-Paraldeido e Tricromo de Gomori, para evidenciação das fibras conjuntivas. As lâminas foram analisadas com auxílio do Axioscópio Zeiss acoplado ao programa de análise de imagens KS-400 Zeiss. A quantidade de tecido conjuntivo no Ventrículo Esquerdo variou de 0,44 a 26,26%; no Ventrículo Direito variou de 0,97 a 21,18%; no ápice variou de 1,32 a 29,24% e no septo interventricular variou de 5,41 a 11,24%. Os resultados obtidos mostram que há uma complexa rede de fibras conjuntivas envolvendo as fibras do tecido muscular cardíaco e que sua quantidade e disposição é muito variada, dependendo da região estudada. / The aim of this study was to evaluate the ratio of connective tissue on the right and left ventricule of the cardiac muscle in the dog. Throughout of the morphometric study, we can gather information regarding the relationship between the connective and the muscle tissue, in order to find out the anatomic and functional relationship of the heart, which can provide information as for the diseases of the heart. In this study, we evaluated the heart of dogs, males and females, from 48 to 150 months-old, whose weight ranged from 18 to 30 kilograms, with no heart diseases confirmed by eletrocardographic and echocardiographic examinations. We got sample from 3 different regions of the ventricule, on the proximal, medial and distal faces, both on the right and left parts. We used the Picrosirius red and Gomori´s Trichrome to stain the material and bring out the connective fibers. We evaluated the slides by Axioscope Zeiss® with program KS400 analyse of images. The amount of connective tissue on the left ventricule ranged from 0,44 to 26,26%. On the right ventricule ranged from 0,97 to 21,18%. On the apex ranged from 1,32 to 29,24% and on the septo interventricular ranged from 5,41 to 11,24%. The results showed that there is a accureted connective fibers pattern surrounding the cardiac muscle tissue and it has na assorted amount and arrangement.

Para se avaliar a citoxicidade de materiais endodônticos, uma das metodologias utilizadas é a implantação de amostras dos materiais no tecido conjuntivo de pequenos animais, e para essa implantação são utilizados acondicionadores. O propósito deste estudo foi comparar as reações teciduais de alguns acondicionadores utilizados neste tipo de pesquisa, propondo desta maneira uma melhor metodologia para ser utilizada em trabalhos futuros. Foram implantados no tecido subcutâneo de 54 ratos, tubos de polietileno, bastões de dentina e cápsulas de colágeno, formando 3 grupos que permaneceram com os implantes pelos períodos de 15, 30 e 60 dias. Os espécimes dos grupos I e II foram analisados pela microscopia óptica de modo descritivo e morfométrico, considerando 5 critérios morfológicos: fibras colágenas, fibroblastos, vasos sanguíneos, células inflamatórias e outros componentes. O grupo III foi submetido, apenas, à análise descritiva. Os valores médios encontrados nos grupos I e II foram submetidos ao Teste t de Student para comparação entre os grupos nos períodos experimentais. O Teste ANOVA foi aplicado para comparar os períodos, nos grupos experimentais, e os valores significantes foram submetidos ao teste de Tukey. Os resultados obtidos revelaram que os tubos de polietileno e bastões de dentina induziram reações teciduais semelhantes, demonstrando, aos 60 dias, um comportamento de reparo. As cápsulas de colágeno foram reabsorvidas e houve recomposição morfológica do tecido subcutâneo. / With the purpose of evaluating the citotoxicity of some endodontic materials, their implantation in subcutaneous tissue of small animals is performed, with the aid of containers, which are used to carry the testing materials. The aim of this study was to compare the subcutaneous tissue response related to the implantation of polyethylene tubes, dentin tubes and collagen capsules usually used as carrier materials in this kind of methodology. 54 rats were divided in 3 groups: polyethylene tubes (Group I), dentin tubes (Group II) and collagen capsules (Group III). After 15, 30 and 60 days of implantation, the animals were killed and the specimens of group I and II were prepared for descriptive and morphometric analysis considering: collagen fibers, fibroblasts, vessels, inflammatory cells and other components. The group III (collagen capsules) was only evaluated through descriptive analyses. The average values of group I and II were submitted to T student test for comparison between the groups in the experimental periods. ANOVA-Tukey test was used to show a difference in the tissue response in the different periods to each material. The results showed similar tissue reaction between polyethylene and dentin tubes, showing organization of the tissue at 60 days. The collagen capsules were resorbed showing morphological recomposition of the subcutaneous tissue.

<p>Fibroblasts continuously strive to organize and compact the surrounding extracellular matrix (ECM). Recent data suggest that this cellular contractility controls interstitial fluid homeostasis in loose connective tissues (CT). The aim of this thesis was to study the effects of prostaglandins on fibroblast contractility and to investigate whether fibroblasts in the interstitial CT surrounding the human endolymphatic duct (ED) can modulate inner ear fluid pressure and endolymph resorption. </p><p>Paper I shows that prostaglandin E1 (PGE₁) and prostacyclin inhibit fibroblast-mediated collagen matrix compaction <i>in vitro</i> and lower the interstitial fluid pressure <i>in vivo</i> in rat dermis. Paper II demonstrates that the inhibition of collagen matrix compaction by PGE₁ is protein kinase A-dependent. Furthermore, PGE₁ induces a complete but reversible actin depolymerization in human dermal fibroblasts by affecting the phosphorylation state of regulatory actin-binding proteins. Paper III describes that the cells of the interstitial CT encompassing the human ED are organized in a network based on intercellular- and cell-ECM contacts. Paper IV shows that two distinct cell phenotypes populate this interstitial CT: one expressing the lymph endothelial marker podoplanin and the other a fibroblast marker. Furthermore, CT cells isolated from human ED tissues exhibited the same tissue compacting properties <i>in vitro</i> as dermal fibroblasts. </p><p>In conclusion, PGE₁ inhibits fibroblast contractility by interfering with the stability and dynamics of the actin cytoskeleton, which leads to a loss of integrin-mediated adhesion to the ECM. These mechanisms are supposedly involved in edema formation in skin during inflammation and might be involved in the formation of endolymphatic hydrops in the inner ear of patients with Ménière’s disease.</p>

No description available.

Fibroblasts continuously strive to organize and compact the surrounding extracellular matrix (ECM). Recent data suggest that this cellular contractility controls interstitial fluid homeostasis in loose connective tissues (CT). The aim of this thesis was to study the effects of prostaglandins on fibroblast contractility and to investigate whether fibroblasts in the interstitial CT surrounding the human endolymphatic duct (ED) can modulate inner ear fluid pressure and endolymph resorption. Paper I shows that prostaglandin E1 (PGE1) and prostacyclin inhibit fibroblast-mediated collagen matrix compaction in vitro and lower the interstitial fluid pressure in vivo in rat dermis. Paper II demonstrates that the inhibition of collagen matrix compaction by PGE1 is protein kinase A-dependent. Furthermore, PGE1 induces a complete but reversible actin depolymerization in human dermal fibroblasts by affecting the phosphorylation state of regulatory actin-binding proteins. Paper III describes that the cells of the interstitial CT encompassing the human ED are organized in a network based on intercellular- and cell-ECM contacts. Paper IV shows that two distinct cell phenotypes populate this interstitial CT: one expressing the lymph endothelial marker podoplanin and the other a fibroblast marker. Furthermore, CT cells isolated from human ED tissues exhibited the same tissue compacting properties in vitro as dermal fibroblasts. In conclusion, PGE1 inhibits fibroblast contractility by interfering with the stability and dynamics of the actin cytoskeleton, which leads to a loss of integrin-mediated adhesion to the ECM. These mechanisms are supposedly involved in edema formation in skin during inflammation and might be involved in the formation of endolymphatic hydrops in the inner ear of patients with Ménière’s disease.

Cutaneous wound healing is a complex process involving the migration of inflammatory cells to the wound site, deposition of extracellular matrix, and the reestablishment of an intact epithelial barrier. Re-epithelialization depends on the proliferation and directional migration of keratinocytes from the wound edges. Initially, keratinocytes migrate over a provisional wound matrix that is rich in fibronectin, and as the wound heals the provisional matrix becomes replaced by one consisting of collagen and proteoglycans. Re-epithelialization is tightly regulated by a variety of peptides such as growth factors, cytokines and proteases, and abnormalities may result in chronic non-healing wounds or hypertrophic scars. CCN2 (Connective Tissue Growth Factor) is a multifunctional protein with effects on cells and their interactions with the connective tissue. CCN2 is expressed in a variety of cell types and regulates numerous cell functions including proliferation, differentiation, adhesion, migration and stimulation of collagen production. While the importance of CCN2 for the fibrotic response has been well studied, its involvement in keratinocyte function has not yet been fully explored. Using an in vivo wound model, the expression of CCN2 was captured at the leading keratinocyte edge during re-epithelialization. In vitro, exogenous addition of CCN2 to human keratinocyte cultures promoted keratinocyte migration. Subsequently, integrin a5b1 was identified as an important mediator of CCN2 enhancement of keratinocyte adhesion to fibronectin. CCN2 activated the FAK-MAPK signaling pathway, and pretreatment with MEK1 specific inhibitor PD98059 markedly reduced CCN2-promoted keratinocyte migration. In vitro, CCN2 expression was induced by TGF-β1. Compared with inhibiting the SMAD pathway, blocking MAPK was more effective in reducing TGF-β1-induced CCN2 mRNA and protein expression. In addition, CCN2-induced keratinocyte spreading required FAK. Treatment with CCN2 led to actin disassembly and altered the activity of the Rho proteins and p190RhoGAP in keratinocytes. Furthermore, Cdc42 mediated CCN2-induced cell polarity. In conclusion, using in vivo and in vitro models, CCN2 was shown to regulate keratinocyte function by promoting keratinocyte adhesion, spreading and migration. A complete understanding of CCN2 expression in keratinocytes is crucial in order to develop novel therapies for wound healing.

Degenerative suspensory ligament desmitis (DSLD) is a debilitating disease of connective tissues seen in many breeds but has become prevalent in the Peruvian Pasohorse. DSLD is believed to be a genetic disorder caused by one primary founder and most likely has a recessive mode of inheritance although a dominant or co-dominant mode of inheritance has not been ruled out. A genome scan using 259 microsatellite markers was used to test for linkage disequilibrium between one or more markers and DSLD. Two groups of Peruvian Pasohorses were selected from one population including the US and Canada. The only difference between the two groups of horses besides the size of the two groups was the presence of DSLD in the affected group and the absence of DSLD in the unaffected group. It was assumed that differences seen between the two groups in homozygosity and or common allele frequency could be an indication of linkage to DSLD. As a connective tissue disorder, there were a large number of candidate genes forDSLD to consider, yet no identical human or animal model exists. The genome scan identified five chromosomal regions where statistically significant differences were seen between affected and unaffected sample populations that could be indications of linkage to DSLD. Those chromosomes were: ECA 6, 7, 11, 14, and 26. Sequencing of a portion of the G domain in the Chondroitin Sulfate Proteoglycan2 (CSPG2) gene has mostly ruled out that segment of chromosome 14 as having linkage to DSLD. Further research needs to be conducted in the regions of ECA 6,7,11 and 26 where statistically significant differences were seen between the affected and unaffected groups, especially on ECA 6 and 11 since possible candidate genes are located in those regions based on the human comparative map.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 5 uppsatser.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2007. / Härtill 4 uppsatser.

Thesis (M.S.)--Duquesne University, 2004. / Title from document title page. Abstract included in electronic submission form. Includes bibliographical references (p. 55-60) and index.