RESUMO
OBJECTIVE: To investigate patient experience with probiotics and factors that influence probiotic use among adult patients. METHOD: Patients were invited to complete a questionnaire that assessed their experiences and opinions regarding probiotics. Questionnaires were distributed to patients seeking primary health care services at a family and community medicine practice site and a community pharmacy. Patients were invited to complete the questionnaire while awaiting the physician or waiting for prescriptions to be filled. RESULTS: Overall, 162 surveys were completed and returned (66% response rate) from patients aged 18 to 89 years of age (mean 49.5 years). Most patients (n=107; 65%) were familiar with the term "probiotic", and 49 patients (29.9%) had personally used the supplements in the past. Of those who had used probiotics, the majority (57%) had used the supplements to maintain "good gastrointestinal health" and most (59%) felt that the supplements had been beneficial. However, most (59%) had not informed their health care provider about their use of the supplements. CONCLUSION: Use of probiotic supplements is common among consumers, but may not be reported to health care providers.
RESUMO
AIMS: Decoy receptors bind with TNF related apoptosis inducing ligands (TRAIL) but do not contain the cytoplasmic domains necessary to transduce apoptotic signals. We hypothesized that decoy receptors may confer neuronal protection against lethal ischemia after ischemic preconditioning (IPC). MAIN METHOD: Mixed cortical neurons were exposed to IPC one day prior to TRAIL treatment or lethal ischemia. KEY FINDINGS: IPC increased decoy receptor but reduced death receptor expression compared to lethal ischemia. IPC-induced increase in decoy receptor expression was reduced by prior treatment with CAPE, a nuclear factor-kappa B inhibitor (NFκB). SIGNIFICANCE: Expression of decoy molecules, dependent on NFκB, may mediate neuronal survival induced by IPC.
Assuntos
Precondicionamento Isquêmico/métodos , Neurônios/metabolismo , Ligante Indutor de Apoptose Relacionado a TNF/metabolismo , Receptores Chamariz do Fator de Necrose Tumoral/metabolismo , Animais , Animais Recém-Nascidos , Apoptose , Ácidos Cafeicos/farmacologia , Córtex Cerebral/metabolismo , Regulação da Expressão Gênica , NF-kappa B/antagonistas & inibidores , NF-kappa B/metabolismo , Álcool Feniletílico/análogos & derivados , Álcool Feniletílico/farmacologia , Ratos , Receptores de Morte Celular/metabolismoRESUMO
BACKGROUND: Caveolae are small, flask-like invaginations of the plasma membrane. Caveolins are structural proteins found in caveolae that have scaffolding properties to allow organization of signaling. The authors tested the hypothesis that delayed cardiac protection induced by volatile anesthetics is caveolae or caveolin dependent. METHODS: An in vivo mouse model of ischemia-reperfusion injury with delayed anesthetic preconditioning (APC) was tested in wild-type, caveolin-1 knockout, and caveolin-3 knockout mice. Mice were exposed to 30 min of oxygen or isoflurane and allowed to recover for 24 h. After 24 h recovery, mice underwent 30-min coronary artery occlusion followed by 2 h of reperfusion at which time infarct size was determined. Biochemical assays were also performed in excised hearts. RESULTS: Infarct size as a percent of the area at risk was reduced by isoflurane in wild-type (24.0 +/- 8.8% vs. 45.1 +/- 10.1%) and caveolin-1 knockout mice (27.2 +/- 12.5%). Caveolin-3 knockout mice did not show delayed APC (41.5 +/- 5.0%). Microscopically distinct caveolae were observed in wild-type and caveolin-1 knockout mice but not in caveolin-3 knockout mice. Delayed APC increased the amount of caveolin-3 protein but not caveolin-1 protein in discontinuous sucrose-gradient buoyant fractions. In addition, glucose transporter-4 was increased in buoyant fractions, and caveolin-3/glucose transporter-4 colocalization was observed in wild-type and caveolin-1 knockout mice after APC. CONCLUSIONS: These results show that delayed APC involves translocation of caveolin-3 and glucose transporter-4 to caveolae, resulting in delayed protection in the myocardium.