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Paola Forti Fabiola Maioli Elisabetta Magni Letizia Ragazzoni Roberto Piperno Marco Zoli Maura Coveri Gaetano Procaccianti 《Archives of physical medicine and rehabilitation》2018,99(3):477-483
Objective
To investigate whether oldest-old age (≥85y) is an independent predictor of exclusion from stroke rehabilitation.Design
Retrospective cohort study.Setting
Stroke unit (SU) of a tertiary hospital.Participants
Elderly patients (N=1055; aged 65–74y, n=230; aged 75–84y, n=432; aged ≥85y, n=393) who, between 2009 and 2012, were admitted to the SU with acute stroke and evaluated by a multiprofessional team for access to rehabilitation. The study excluded patients for whom rehabilitation was unnecessary or inappropriate.Interventions
Not applicable.Main Outcome Measures
Access to an early mobilization (EM) protocol during SU stay and subsequent access to postacute rehabilitation after SU discharge. Analyses were adjusted for prestroke and stroke-related characteristics.Results
32.2% of patients were excluded from EM. Multivariable-adjusted odds ratios (ORs) of EM exclusion were 1.30 (95% confidence interval [CI], .76–2.21) for ages 75 to 84 years and 2.07 (95% CI, 1.19–3.59) for ages ≥85 years compared with ages 65 to 74 years. Of 656 patients admitted to EM and who, at SU discharge, had not yet fully recovered their prestroke functional status, 18.4% were excluded from postacute rehabilitation. For patients able to walk unassisted at SU discharge, the probability of exclusion did not change across age groups. For patients unable to walk unassisted at SU discharge, ORs of exclusion from postacute rehabilitation were 3.74 (95% CI, 1.26–11.13) for ages 75 to 84 years and 9.15 (95% CI, 3.05–27.46) for ages ≥85 years compared with ages 65 to 74 years.Conclusions
Oldest-old age is an independent predictor of exclusion from stroke rehabilitation. 相似文献14.
Maggi M Filippi S Ledda F Magini A Forti G 《European journal of endocrinology / European Federation of Endocrine Societies》2000,143(2):143-154
Research on penile smooth muscle physiology has increased the number of drugs available for treating erectile dysfunction (ED). Penile erection involves the relaxation of smooth muscle in the corpus cavernosum. The key mediator of smooth muscle relaxation is nitric oxide (NO), which acts by increasing the cellular level of cGMP. Another cyclic nucleotide, cAMP, is involved in smooth muscle cell relaxation; cAMP formation is stimulated by a number of compounds, such as alprostadil. An increase in cAMP and/or cGMP levels can also be induced by inhibition of phosphodiesterases (PDEs), the enzymes involved in cyclic nucleotide breakdown. Both papaverine and sildenafil are PDE inhibitors. Papaverine is a non-specific inhibitor of these enzymes; sildenafil is an orally active, potent and selective inhibitor of GMP-specific PDE5, the predominant isoenzyme metabolizing cGMP in the cells of the corpus cavernosum. Penile smooth muscle contraction, induced by adrenergic fibers through alpha(1) adrenoceptors, produces detumescence, thus making alpha adrenoceptor antagonists suitable for maintenance of penile erection. The orally active drug yohimbine is a mixed alpha(1)-alpha(2) adrenoceptor antagonist that works by a dual mechanism; it facilitates sexual arousal by acting on alpha(2) adrenoceptors in the central nervous system and blocks adrenergic influences at peripheral level. 相似文献
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Pleiotropic activities of human interferons are mediated by multiple response pathways. 总被引:1,自引:0,他引:1 下载免费PDF全文
R L Forti W M Mitchell W C Hubbard R J Workman J T Forbes 《Proceedings of the National Academy of Sciences of the United States of America》1984,81(1):170-174
Among the pleiotropic effects of human interferon are the inhibition of viral replication, the activation of natural killer cells, and the inhibition of cellular growth. Oxyphenbutazone, a nonsteroidal antiinflammatory agent, is a potent inhibitor of the antiviral activity of human alpha and beta interferons as determined by cytopathic effect and vesicular stomatitis virus synthesis and release in human foreskin fibroblasts. The inhibition of interferon activity is dose dependent with maximal inhibition at 25-50 microM and minimal inhibition at 1 microM. In contrast, oxyphenbutazone at concentrations as high as 100 microM has no effect on the activation of natural killer cells by human interferon. Similarly, oxyphenbutazone has no inhibitory effect on interferon-induced antigrowth activity in the human breast carcinoma cell line MDA-MB-231. This cell line is sensitive to oxyphenbutazone inhibition of interferon-induced antiviral activity in vitro. In another human cell line, the vulvar carcinoma A431, oxyphenbutazone apparently augments the antigrowth activity of interferon. Although oxyphenbutazone inhibits the fatty acid cyclooxygenase enzyme in these systems, other inhibitors of cyclooxygenase fail to inactivate the antiviral activity of human interferon. Thus, oxyphenbutazone appears to inhibit the interferon antiviral cascade at a site distinct from prostaglandin biosynthesis. Moreover, the failure to inhibit natural killer cell activation or cellular antigrowth effects of human interferon suggests a pathway different from that associated with the antiviral effect of human interferon. 相似文献
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Mortality After Admission to Stroke Unit for Intracerebral Hemorrhage: Effect of Age 80 and Older and Multimorbidity 下载免费PDF全文
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M. R. Laurent M. J. Cook E. Gielen K. A. Ward L. Antonio J. E. Adams B. Decallonne G. Bartfai F. F. Casanueva G. Forti A. Giwercman I. T. Huhtaniemi K. Kula M. E. J. Lean D. M. Lee N. Pendleton M. Punab F. Claessens F. C. W. Wu D. Vanderschueren S. R. Pye T. W. O’Neill EMAS Group 《Osteoporosis international》2016,27(11):3227-3237