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1.
Arch Orthop Trauma Surg ; 143(5): 2317-2324, 2023 May.
Artigo em Inglês | MEDLINE | ID: mdl-35359162

RESUMO

PURPOSE: Vertebral osteomyelitis (VO) is a severe clinical entity associated with significant morbidity and mortality. Several studies have showed that successful treatment of VO patients leads to significantly improved quality of life (QoL). Nevertheless, QoL levels of these patients remained below those of the general population. There are rarely studies focusing on predicting factors for favourable QoL after surgically treated VO. The aim of this study was to identify factors influencing positively the QoL of patients undergoing surgery for VO. METHODS: We conducted a prospective monocentric study including surgically treated VO patients from 2008 to 2016. Data were collected before (T0) and 1 year (T1) after surgery. Primary outcome was favourable QoL defined as back pain with disability restricting normal life activity with a cutoff value ≥ 12 on Oswestry Disability Index (ODI). ETHICS: Ethical approval was given by the Faculty of Medicine at the University of Cologne (09-182). RESULTS: A total of 119 patients surviving 1 year after surgically treated VO were analysed. Favourable QoL was achieved in 35/119 patients. On multivariate analysis, younger age (hazard ratio = HR: 0.95; 95% CI 0.91-0.99; p = 0.022), lower albumin (HR: 0.9; 0.83-0.98; p = 0.019) an ASA score ≤ 2 (HR:4.24; 95%CI 1.42-12.68; p = 0.010), and a lower preoperative leg pain on the VAS (HR: 0.86; 95% CI 0.76-0.97; p = 0.018) were identified as independent risk factors for favourable QoL. Interestingly, the absence of neurological deficits was not predictive for a favourable outcome by means of QoL. CONCLUSION: One-third of surgically treated VO patients (29%) in our cohort achieved favourable QoL by means of ODI. Our findings can facilitate an estimation of the prognosis when informing the patient before surgery, and underscore that spine disability questionnaires, such as ODI, measuring QoL, are mandatory to evaluate comprehensively the outcome of this entity.


Assuntos
Qualidade de Vida , Coluna Vertebral , Humanos , Estudos Prospectivos , Resultado do Tratamento , Coluna Vertebral/cirurgia , Dor nas Costas/epidemiologia , Dor nas Costas/cirurgia , Vértebras Lombares/cirurgia , Avaliação da Deficiência
2.
Scand J Rheumatol ; 51(4): 279-283, 2022 07.
Artigo em Inglês | MEDLINE | ID: mdl-35023427

RESUMO

OBJECTIVE: Studies indicate that caffeine uptake may be a risk factor for rheumatoid arthritis (RA), but a definitive link between caffeine consumption and RA has not been established. This study aimed to investigate the interplay between caffeine, adenosine receptor A2a, and interferon-γ (IFN-γ) production in CD4+ T cells from RA patients. METHOD: Peripheral blood mononuclear cells were obtained from the peripheral blood of healthy individuals and patients with RA. CD4+ T cells were isolated using the magnetic activated cell sorting technique and cultured in vitro with caffeine or mock control. In addition, adenosine was used as a competitive inhibitor of caffeine. After 48 h, expression of IFN-γ and interleukin-17 (IL-17) was analysed by flow cytometry. Ex vivo expression levels of adenosine receptor A2a were also assessed. RESULTS: Caffeine promoted IFN-γ production in Th1 cells in vitro. Significantly higher concentrations of caffeine were required to increase IFN-γ levels in Th1 cells from healthy individuals compared to Th1 cells from patients with RA. Moreover, ex vivo levels of adenosine receptor A2a expression on CD4+ T cells were significantly higher in RA than in healthy individuals. Caffeine-driven IFN-γ production was completely reversed by adenosine, a competitive agonist of adenosine receptor A2a. In contrast to IFN-γ, production of IL-17 was not affected by caffeine. CONCLUSION: Caffeine promotes IFN-γ production in Th1 cells from RA patients in vitro by competitive inhibition of adenosine receptor A2a. Excessive coffee consumption could contribute to T-cell activation and inflammation in RA.


Assuntos
Antagonistas do Receptor A2 de Adenosina , Artrite Reumatoide , Cafeína , Interferon gama , Células Th1 , Antagonistas do Receptor A2 de Adenosina/farmacologia , Artrite Reumatoide/imunologia , Cafeína/farmacologia , Humanos , Interferon gama/metabolismo , Leucócitos Mononucleares/metabolismo , Células Th1/metabolismo , Células Th2/metabolismo
3.
J Evol Biol ; 23(8): 1581-96, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20561138

RESUMO

Ecological opportunity--through entry into a new environment, the origin of a key innovation or extinction of antagonists--is widely thought to link ecological population dynamics to evolutionary diversification. The population-level processes arising from ecological opportunity are well documented under the concept of ecological release. However, there is little consensus as to how these processes promote phenotypic diversification, rapid speciation and adaptive radiation. We propose that ecological opportunity could promote adaptive radiation by generating specific changes to the selective regimes acting on natural populations, both by relaxing effective stabilizing selection and by creating conditions that ultimately generate diversifying selection. We assess theoretical and empirical evidence for these effects of ecological opportunity and review emerging phylogenetic approaches that attempt to detect the signature of ecological opportunity across geological time. Finally, we evaluate the evidence for the evolutionary effects of ecological opportunity in the diversification of Caribbean Anolis lizards. Some of the processes that could link ecological opportunity to adaptive radiation are well documented, but others remain unsupported. We suggest that more study is required to characterize the form of natural selection acting on natural populations and to better describe the relationship between ecological opportunity and speciation rates.


Assuntos
Adaptação Fisiológica , Evolução Biológica , Seleção Genética , Animais , Biodiversidade , Ecossistema , Lagartos/classificação , Lagartos/fisiologia , Filogenia
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