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1.
Arthrosc Sports Med Rehabil ; 3(2): e411-e419, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-34027449

RESUMO

PURPOSE: To compare publicly available rehabilitation protocols designated for meniscal repairs published online to determine the variability in meniscus repair protocols including different types of tears (radial vs nonradial repairs). METHODS: From the Fellowship and Residency Electronic Interactive Database Access System (FREIDA), a list of publicly available academic residency programs and orthopaedic sports medicine fellowships was obtained. With this list, an electronic search using Google was performed looking for meniscal repair rehabilitation protocols. In addition to academic institutions, private practice organizations with published meniscus repair rehabilitation protocols found during the search also were examined. RESULTS: Of 189 academic institutions, a total of 30 academic institutions had protocols that were included. Another 29 private practice programs were subsequently found and included. In total, 59 rehabilitation protocols fit the inclusion criteria. Six of the 59 specified radial repair and 53 did not. For return to full range of motion, nonradial protocols averaged 6.7 weeks and radial protocols averaged 7.3 weeks. For return to full weight-bearing, nonradial protocols averaged 6.2 weeks and radial protocols averaged 7.5 weeks. For return to sport, nonradial protocols averaged 17.8 weeks and radial protocols averaged 23.3 weeks. For time spent in a brace, nonradial protocols averaged 5.7 weeks and radial protocols averaged 6.7 weeks. CONCLUSIONS: Of publicly available meniscal repair rehabilitation protocols, a small percentage (10.2%) changed their protocol in relation to tear type and there was a wide range of timeframes for each rehabilitation component. Protocols for radial tears tended to brace patients longer, limit their range of motion longer, delay full weight-bearing, and delay return to sport. However, it is recognized that some surgeons could be modifying their protocols in relation to tear type without publishing that information online. CLINICAL RELEVANCE: As stated in the purpose, the point of this study was to access only the protocols that would be available to the public. If anything, awareness should be raised for surgeons to look at their existing protocols and update them if they are truly incomplete and outdated. More research needs to be done to structure a rehabilitation protocol that is specific to the meniscal tear type, as the current protocols have a wide range of variance.

2.
Crit Care Med ; 41(5): 1305-15, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23474678

RESUMO

OBJECTIVES: To establish the molecular background for glucocorticoid insensitivity, that is, failure to reduce edema formation and to protect blood-brain barrier integrity after acute traumatic brain injury. DESIGN: Controlled animal study. SETTING: University research laboratory. SUBJECTS: Male C57Bl/6N mice. INTERVENTIONS: Mechanical brain lesion by controlled cortical impact. MEASUREMENTS AND MAIN RESULTS: Our study demonstrates that 1) proteasomal glucocorticoid receptor degradation is established in brain endothelial cells after traumatic brain injury as a form of posttranslational glucocorticoid receptor modification; 2) inhibition of the proteasomal degradation pathway with bortezomib (0.2 mg/kg) in combination with the glucocorticoid dexamethasone (10 mg/kg) by subcutaneous injection 30 minutes postinjury restores levels of barrier sealing glucocorticoid receptor target occludin in brain endothelial cells, improves blood-brain barrier integrity, reduces edema formation, and limits neuronal damage after brain trauma. CONCLUSIONS: The results indicate that the stabilizing effect of glucocorticoids on the blood-brain barrier is hampered after cerebral lesions by proteasomal glucocorticoid receptor degradation in brain endothelial cells and restored by inhibition of proteasomal degradation pathways. The results provide underlying mechanisms for the clinically observed inefficacy of glucocorticoids. The novel combined treatment strategy might help to attenuate trauma-induced brain edema formation and neuronal damage as secondary effects of brain trauma.


Assuntos
Barreira Hematoencefálica/efeitos dos fármacos , Lesões Encefálicas/tratamento farmacológico , Dexametasona/farmacologia , Complexo de Endopeptidases do Proteassoma/metabolismo , RNA Mensageiro/metabolismo , Receptores de Glucocorticoides/efeitos dos fármacos , Animais , Gasometria , Western Blotting , Ácidos Borônicos/farmacologia , Bortezomib , Edema Encefálico/tratamento farmacológico , Edema Encefálico/prevenção & controle , Lesões Encefálicas/metabolismo , Modelos Animais de Doenças , Imuno-Histoquímica , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Análise Multivariada , Complexo de Endopeptidases do Proteassoma/efeitos dos fármacos , Pirazinas/farmacologia , Distribuição Aleatória , Reação em Cadeia da Polimerase em Tempo Real , Receptores de Glucocorticoides/metabolismo , Valores de Referência , Sensibilidade e Especificidade , Estatísticas não Paramétricas
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