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1.
Biogerontology ; 8(5): 483-98, 2007 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-17372845

RESUMO

Articular cartilage defects, an exceedingly common problem closely correlated with advancing age, is characterized by lack of spontaneous resolution because of the limited regenerative capacity of adult articular chondrocytes. Medical and surgical therapies yield unsatisfactory short-lasting results. Recently, cultured autologous chondrocytes have been proposed as a source to promote repair of deep cartilage defects. Despite encouraging preliminary results, this approach is not yet routinely applicable in clinical practice, but for young patients. One critical points is the isolation and ex vivo expansion of large enough number of differentiated articular chondrocytes. In general, human articular chondrocytes grown in monolayer cultures tend to undergo dedifferentiation. This reversible process produces morphological changes by which cells acquire fibroblast-like features, loosing typical functional characteristics, such as the ability to synthesize type II collagen. The aim of this study was to isolate human articular chondrocytes from elderly patients and to carefully characterize their morphological, proliferative, and differentiative features. Cells were morphologically analyzed by optic and transmission electron microscopy (TEM). Production of periodic acid-schiff (PAS)-positive cellular products and of type II collagen mRNA was monitored at different cellular passages. Typical chondrocytic characteristics were also studied in a suspension culture system with cells encapsulated in alginate-polylysine-alginate (APA) membranes. Results showed that human articular chondrocytes can be expanded in monolayers for several passages, and then microencapsulated, retaining their morphological and functional characteristics. The results obtained could contribute to optimize expansion and redifferentiation sequences for applying cartilage tissue engineering in the elderly patients.


Assuntos
Cartilagem Articular/citologia , Senescência Celular/fisiologia , Condrócitos/citologia , Modelos Biológicos , Idoso , Idoso de 80 Anos ou mais , Cartilagem Articular/fisiologia , Membrana Celular/fisiologia , Membrana Celular/ultraestrutura , Células Cultivadas , Condrócitos/fisiologia , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Colágeno Tipo II/genética , Colágeno Tipo II/metabolismo , Composição de Medicamentos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , RNA Mensageiro/metabolismo , Regeneração/fisiologia
2.
Neuro Endocrinol Lett ; 20(1-2): 91-100, 1999.
Artigo em Inglês | MEDLINE | ID: mdl-11473235

RESUMO

Brunetto Tarquini became professor of medical semeiotics and cardiology in 1981, and chief of an internal medicine department in 1990, a position he held until his untimely death. As director of the Inter-University Center for Clinical Chronobiology and as coordinator of a post-doctoral school in chronobiology, Brunetto influenced many young Italian physicians. He became the leader of a budding specialty of chronomedicine, coordinating an international group. His focus included temporal aspects of vascular diseases from womb-to-tomb as well as oncological risk factors. His research thus ranged from neonatology over neuroendocrinology to geriatrics, by studies on the pineal in particular, documenting the signature of heliogeomagnetic master switches for circulating human melatonin.

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