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1.
Future Sci OA ; 4(8): FSO329, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30271616

RESUMO

Formaldehyde is a widely used aldehyde in biomedical applications, including tissue fixation. It is this same fixative property that can result in toxicity if aldehydes are improperly discarded. A proper neutralization of aldehyde waste products can address this, thereby reducing both health and environmental toxicity concerns. In this study two commercially available products designed to neutralize formaldehyde were evaluated, including neutralization of laboratory derived tissue fixative waste. The primary selection criteria for inclusion in the study were: their ease of use (based on product instructions); the two products assert high levels of formaldehyde neutralization (below 20 ppm) relative to other neutralizing products and their lack of generation of polymeric residues that can clog drains. Both products tested were relatively easy to use and both achieved <10 ppm residual levels of formaldehyde from standard formalin and glutaraldehyde preparations used in research and clinical laboratories.

2.
Curr Opin Biotechnol ; 40: 155-163, 2016 08.
Artigo em Inglês | MEDLINE | ID: mdl-27162093

RESUMO

Stroke disability is the only major disease without an effective treatment. The substantial clinical burden of stroke in disabled survivors and the lack of a medical therapy that promotes recovery provide an opportunity to explore the use of biomaterials to promote brain repair after stroke. Hydrogels can be injected as a liquid and solidify in situ to form a gelatinous solid with similar mechanical properties to the brain. These biomaterials have been recently explored to generate pro-repair environments within the damaged organ. This review highlights the clinical problem of stroke treatment and discusses recent advances in using in situ forming hydrogels for brain repair.


Assuntos
Materiais Biocompatíveis/química , Encefalopatias/terapia , Hidrogéis/administração & dosagem , Acidente Vascular Cerebral/complicações , Animais , Encefalopatias/etiologia , Humanos , Hidrogéis/química , Cicatrização
3.
Curr Neurovasc Res ; 4(3): 216-27, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17691975

RESUMO

Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only recently coming to light. Potential mechanisms include changes in brain plasticity-promoting factors, unregulated expression of neurotoxic factors, or differences in the generation of scar tissue that impedes the formation of new axons and blood vessels in the infarcted region. Behaviorally, aged rats are more severely impaired by stroke than are young rats, and they also show diminished functional recovery. Infarct volume does not differ significantly in young and aged animals, but critical differences are apparent in the cytological response to stroke, most notably an age-related acceleration of the establishment of the glial scar. The early infarct in older rats is associated with a premature accumulation of BrdU-positive microglia and astrocytes, persistence of activated oligodendrocytes, a high incidence of neuronal degeneration, and accelerated apoptosis. Regeneration-associated mechanisms in the rat brain are active throughout life, albeit at lower levels in the aged animals. However; after stroke in aged rats, neuroepithelial marker-positive cells emanating largely from capillaries did not make a significant contribution to neurogenesis in the infarcted cortex of aged animals. Furthermore, the expression of plasticity-associated proteins, such as MAP1B, was delayed in aged rats. Tissue recovery was further delayed by the upregulation of Nogo, ephrin-A5 and MAG, which exert a powerful negative effect on axonal sprouting in the aged peri-infarct cortex, and by an age-related increase in the amount of the neurotoxic C-terminal fragment of the beta-amyloid precursor protein (betaAPP) at 2 wks post-stroke. Our findings indicate that the aged brain has the capability to mount a cytoproliferative response to injury, but the timing of the cellular and genetic response to cerebral insult is dysregulated in aged animals, thereby further compromising functional recovery. Elucidating the molecular basis of this phenomenon in the aging brain could yield novel approaches to neurorestoration following stroke or head injury in the elderly.


Assuntos
Envelhecimento , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/fisiopatologia , Animais , Apoptose , Modelos Animais de Doenças , Humanos , Acidente Vascular Cerebral/metabolismo , Acidente Vascular Cerebral/terapia
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