RESUMO
Investigam-se os avanços de inovações incluídas na reestruturação curricular da Faculdade de Serviço Social da Universidade de Colima, a partir da introdução de novas modalidades pedagógicas no currículo. Considera-se a importância de que, na formação de trabalhadores sociais, estes sejam vistos como atores sociais que participam da resolução de problemas da sociedade. Neste sentido, o corpo acadêmico da Faculdade analisou o processo e os resultados da implemantação de um modelo de ensino centrado no aluno no período de 2001 a 2005, para sustentar a reestruturação curricular. Resultados obtidos confirmam a pertinência dos modelos adotados e indicam algumas exigências para consolidação das inovações curriculares implementadas.
Assuntos
Humanos , Masculino , Feminino , Currículo/tendências , Universidades , EnsinoRESUMO
Knee articular cartilage samples obtained by arthroscopy from ten patients with well defined knee osteoarthritis (OA) were studied by light and transmission electron microscopy. The morphological phenotype of cells from fibrillated and non-fibrillated regions of OA cartilage was characterized. Three different cell sub-populations were identified. Type 1 cells were found in the superficial and upper middle zones and comprised single chondrocytes and cells organized in aggregates or "clones' that showed a typical chondrocyte phenotype. Type 2 cells displayed a secretory phenotype. Type 3 cells comprised chondrocytes undergoing a degenerative process and were distributed throughout all zones of the cartilage. Changes in the cytoskeletal arrangement, presence of abundant filopodia, peripheral localization of centrioles, and presence of primary cilia were found in many chondrocytes suggesting that they are active motile cells. No mitotic figures were found in this study. Morphometrical analysis was performed to determine the total number of cells and the number of chondrocytes per lacuna in the superficial and upper middle zones of fibrillated and non-fibrillated OA cartilage. There were no statistically significant differences in the total number of cells. In contrast, fibrillated OA cartilage contained a statistically significantly higher percentage of lacunae containing four of more chondrocytes than non-fibrillated OA cartilage samples. The absence of mitotic figures and the presence of motile elements in many chondrocytes raise the possibility that cell aggregates or "clones' in damaged OA cartilage originate by an active process of cell migration rather than by cellular division.
Assuntos
Cartilagem Articular/patologia , Osteoartrite/patologia , Idoso , Citoesqueleto/ultraestrutura , Feminino , Humanos , Masculino , Microscopia Eletrônica , Pessoa de Meia-IdadeRESUMO
OBJECTIVE: To characterize a kindred of Chiloe Islanders with spondyloepiphyseal dysplasia tarda (SEDT), brachydactyly, precocious osteoarthritis (OA), and intraarticular calcification. METHODS: Sixteen family members underwent a complete physical examination, anthropometric measurements, radiographic studies of the spine and peripheral joints, and analysis of the type II procollagen gene (COL2A1). RESULTS: Seven family members presented with SEDT, brachydactyly, precocious OA, and periarticular calcification while 2 others had the same syndrome but without brachydactyly. The inheritance was autosomal dominant, and the disease cosegregated with a base substitution in the COL2A1 gene. CONCLUSION: The syndrome o SEDT, precocious OA, and brachydactyly in a kindred of Chiloe Islanders is associated with a point mutation in 1 allele of the COL2A1 gene. The relationship of this type of SEDT to familial calcium pyrophosphate dihydrate deposition disease and idiopathic hip dysplasia, both endemic in Chiloe Islanders, needs to be further investigated.
Assuntos
Deformidades Congênitas do Pé/genética , Deformidades Congênitas da Mão/genética , Osteoartrite/genética , Osteocondrodisplasias/genética , Pró-Colágeno/genética , Adulto , Arginina/genética , Chile/epidemiologia , Cisteína/genética , DNA/análise , DNA/sangue , Feminino , Deformidades Congênitas do Pé/epidemiologia , Mãos/diagnóstico por imagem , Deformidades Congênitas da Mão/epidemiologia , Quadril/diagnóstico por imagem , Humanos , Joelho/diagnóstico por imagem , Leucócitos/química , Osteoartrite/epidemiologia , Osteocondrodisplasias/epidemiologia , Linhagem , Mutação Puntual , Reação em Cadeia da Polimerase , RadiografiaRESUMO
Lyophilized mid-wall left ventricular myocardial tissues of the long-tailed non-human primate, Macaca fascicularis, were examined for the presence of glycosaminoglycans and chondroitin/dermatan sulfate proteoglycans. Mean uronic acid concentration in all samples was 0.97 +/- 0.27 micrograms per mg dry weight myocardium. The distribution of the glycosaminoglycans in the myocardium, determined by cellulose acetate strip electrophoresis was 62 +/- 4% heparan sulfate, 20 +/- 6% hyaluronan, and 16 +/- 5% chondroitin/dermatan sulfate. The analysis of chondroitin/dermatan sulfate proteoglycans, done directly on the extracts of lyophilized myocardium using agarose-acrylamide gel electrophoresis and Western blotting with monoclonal antibodies to various carbohydrate epitopes and with polyclonal antibodies to the protein core, showed the presence of biglycan and decorin. That these two and no other chondroitin/dermatan sulfates were present was established by core protein analysis using SDS PAGE and Western blotting. Quantification of chondroitin/dermatan sulfate proteoglycans uncovered high individual specific variability of the chondroitin/dermatan sulfate epitopes, but only moderate variability of biglycan and decorin core proteins. The variability of the chondroitin/dermatan sulfate epitopes is most likely related to individual specific differences in chain number, iduronate content and sulfation patterns of biglycan and decorin.
Assuntos
Sulfatos de Condroitina/metabolismo , Dermatan Sulfato/metabolismo , Glicosaminoglicanos/metabolismo , Macaca fascicularis/metabolismo , Miocárdio/metabolismo , Proteoglicanas/metabolismo , Animais , Anticorpos Monoclonais , Eletroforese em Gel de Ágar , Eletroforese em Acetato de Celulose , Eletroforese em Gel de Poliacrilamida , ImmunoblottingRESUMO
Four patients with stable systemic sclerosis and limited skin involvement received radiation for the treatment of solid malignant neoplasms. Following localized irradiation, each patient developed an exaggerated cutaneous and internal fibrotic reaction in the irradiated areas. The surface area of fibrosis extended beyond the radiation portals employed, and the fibrotic process was poorly responsive to antifibrotic therapy. Three of the patients died of complications caused by fibrous encasement of internal organs. The extent and severity of postradiation fibrosis in these patients was distinctly unusual. These observations suggest that patients with systemic sclerosis are particularly susceptible to developing excessive radiation-induced fibrosis.
Assuntos
Radioterapia/efeitos adversos , Esclerose/patologia , Pele/patologia , Adulto , Feminino , Fibrose/etiologia , Humanos , Pessoa de Meia-Idade , Doses de Radiação , Pele/efeitos da radiaçãoRESUMO
It has recently become apparent that several cytokines and growth factors are capable of modulating fibroblast proliferation and biosynthetic activity. To understand the role of these factors in connective tissue regulation, we examined the effects of the simultaneous addition of interferon-gamma (IFN-gamma) and transforming growth factor-beta (TGF-beta) on normal human dermal fibroblast collagen and fibronectin production. In addition, in vitro transcription rates and steady-state mRNA levels for these molecules were determined by nuclear run-off assays and Northern and dot-blot hybridization using specific human cDNA probes. Treatment of cultures with TGF-beta caused stimulation of collagen and fibronectin production. Addition of IFN-gamma to the TGF-beta-treated cultures abrogated the stimulatory effects of TGF-beta on collagen production in a dose-dependent manner and resulted in a net inhibition of collagen production. In contrast, the increase in fibronectin synthesis induced by TGF-beta was augmented further by IFN-gamma. These changes in collagen and fibronectin production were accompanied by parallel changes in the steady-state mRNA levels for these proteins. The effects of TGF-beta plus IFN-gamma on fibronectin gene expression appeared to be mediated entirely by transcriptional mechanisms, whereas the effects on collagen gene expression resulted from a combination of transcriptional and post-transcriptional events.
Assuntos
Fibroblastos/efeitos dos fármacos , Interferon gama/farmacologia , Fator de Crescimento Transformador beta/antagonistas & inibidores , Células Cultivadas , Colágeno/biossíntese , Colágeno/genética , Fibroblastos/metabolismo , Fibronectinas/biossíntese , Fibronectinas/genética , Expressão Gênica/efeitos dos fármacos , Humanos , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Fator de Crescimento Transformador beta/farmacologiaAssuntos
Eosinofilia/complicações , Doenças Musculares/complicações , Adulto , Idoso , Idoso de 80 Anos ou mais , Eosinofilia/fisiopatologia , Eosinofilia/terapia , Feminino , Gastroenteropatias/complicações , Cardiopatias/complicações , Humanos , Artropatias/complicações , Pneumopatias/complicações , Masculino , Pessoa de Meia-Idade , Músculos/enzimologia , Músculos/fisiopatologia , Doenças Musculares/fisiopatologia , Doenças Musculares/terapia , Dor , Doenças do Sistema Nervoso Periférico/complicações , Dermatopatias/complicações , SíndromeRESUMO
Hereditary arthro-ophthalmopathy (AO), or Stickler syndrome, is a dominantly inherited disorder characterized by vitreo-retinal degeneration and frequently accompanied by epiphyseal dysplasia and premature degenerative joint disease. Three large families with AO were analyzed for clinical manifestations of the disease and for coinheritance of the genetic defect with RFLPs in the type II procollagen gene (COL2A1). Genetic linkage between AO and COL2A1 was demonstrated in the largest family, with a maximum LOD score of 3.52 at a recombination distance of zero. Data from a second family also supported linkage of AO and COL2A1, with a LOD score of 1.20 at a recombination distance of zero. These results are consistent with the conclusion that mutations in the COL2A1 gene are responsible for AO in these two families. In a third AO family, however, recombination between AO and COL2A1 occurred in at least one meiosis, and the data were inconclusive with respect to linkage.