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61.
Felicita Urzi Boštjan Šimunič Elena Buzan 《Journal of the American Medical Directors Association》2017,18(11):991.e5-991.e10
Background
Sarcopenia is a major health problem of the older population. The European Working Group on Sarcopenia in Older People (EWGSOP) developed diagnostic criteria for diagnosis of sarcopenia that require assessing muscle mass and strength or physical performance. Recently, however, a rapid screening method SARC-CalF was developed.Objective
The aim of the present study was to validate the SARC-CalF test using EWGSOP sarcopenia diagnostic criteria in a sample of nursing home residents.Methods
Cross-sectional study. A sample of 80 nursing home residents [30% of men; mean age 84.3 (7.9) years]. Sarcopenia was determined as proposed by the EWGSOP diagnostic criteria, whereby muscle mass was measured by bioelectrical impedance, muscle strength by handgrip strength, and physical performance by usual gait speed and a Short Physical Performance Battery score. Sarcopenia was also assessed by the SARC-CalF screening test.Results
A total of 38.7% of sarcopenia was evaluated using EWGSOP diagnostic criteria and 36.2% using the SARC-CalF test. The SARC-CalF demonstrated a sensitivity level of 77.4% and specificity of 89.8%. The area under the receiver operating characteristic curves of SARC-CalF test was 0.84 (95% confidence interval 0.74, 0.94).Conclusions
SARC-CalF could be a useful screening test for sarcopenia in nursing home residents. The incorporation of the test as a basis for sarcopenia screening will provide additional value to current nursing home preventive measures. 相似文献62.
Felicita Pedata Marta Pazzagli Silvia Tilli Giancarlo Pepeu 《Naunyn-Schmiedeberg's archives of pharmacology》1990,342(4):447-453
Summary The release of both radioactive and endogenous purines was investigated in rat brain cortical, hippocampal and striatal slices at rest and following stimulation with electrical fields.Purities were labelled by incubating the slices with 3H-adenine. The purine efflux at rest and that evoked by electrical stimulation (10 Hz, 5 min) was analyzed by HPLC with ultraviolet absorbance detection. Both radio-active and endogenous purines in the effluent consisted mainly of hypoxanthine, xanthine, inosine and adenosine. No qualitative differences in the composition of the released purines were found in the three areas investigated. Electrical stimulation evoked a net increase in both radioactive and endogenous purine release. However the increase in 3H-adenosine following electrical stimulation was twice as large as that of endogenous adenosine. The electrically evoked release of both radioactive and endogenous purines was greatest in hippocampal slices and progressively smaller in cortical and striatal slices. In the three areas the addition of 0.5 M tetrodotoxin to the superfusing Krebs solution brought about a similar (83–100%) reduction in evoked 3H-purine and endogenous purine release. Superfusion of the slices with calcium-free Krebs solution containing 0.5 mM EGTA reduced evoked release of 3H-purines by 58–60% and that of endogenous purine components by 54–89%.The results demonstrate similar characteristics for both radioactive and endogenous purine release but indicate that the most recently synthetized adenosine is the most readily available for release. The features of the electrically evoked purine release support a neuronal origin of adenosine and derivatives and are consistent with the hypothesis of discrete regional differences in adenosine neuromodulation.
Send offprint requests to F. Pedata at the above address 相似文献
63.
Stefan D. Anker Muhammad Shariq Usman Markus S. Anker Javed Butler Michael Böhm William T. Abraham Marianna Adamo Vijay K. Chopra Mariantonietta Cicoira Francesco Cosentino Gerasimos Filippatos Ewa A. Jankowska Lars H. Lund Brenda Moura Wilfried Mullens Burkert Pieske Piotr Ponikowski Jose R. Gonzalez-Juanatey Amina Rakisheva Gianluigi Savarese Petar Seferovic John R. Teerlink Carsten Tschöpe Maurizio Volterrani Stephan von Haehling Jian Zhang Yuhui Zhang Johann Bauersachs Ulf Landmesser Shelley Zieroth Konstantinos Tsioufis Antoni Bayes-Genis Ovidiu Chioncel Felicita Andreotti Enrico Agabiti-Rosei Jose L. Merino Marco Metra Andrew J.S. Coats Giuseppe M.C. Rosano 《European journal of heart failure》2023,25(7):936-955
Heart failure with preserved ejection fraction (HFpEF) represents a highly heterogeneous clinical syndrome affected in its development and progression by many comorbidities. The left ventricular diastolic dysfunction may be a manifestation of various combinations of cardiovascular, metabolic, pulmonary, renal, and geriatric conditions. Thus, in addition to treatment with sodium–glucose cotransporter 2 inhibitors in all patients, the most effective method of improving clinical outcomes may be therapy tailored to each patient's clinical profile. To better outline a phenotype-based approach for the treatment of HFpEF, in this joint position paper, the Heart Failure Association of the European Society of Cardiology, the European Heart Rhythm Association and the European Hypertension Society, have developed an algorithm to identify the most common HFpEF phenotypes and identify the evidence-based treatment strategy for each, while taking into account the complexities of multiple comorbidities and polypharmacy. 相似文献
64.
65.
Irene Paterniti Alessia Melani Sara Cipriani Francesca Corti Tommaso Mello Emanuela Mazzon Emanuela Esposito Placido Bramanti Salvatore Cuzzocrea Felicita Pedata 《Journal of neuroinflammation》2011,8(1):31
Background
Permanent functional deficits following spinal cord injury (SCI) arise both from mechanical injury and from secondary tissue reactions involving inflammation. Enhanced release of adenosine and glutamate soon after SCI represents a component in the sequelae that may be responsible for resulting functional deficits. The role of adenosine A2A receptor in central ischemia/trauma is still to be elucidated. In our previous studies we have demonstrated that the adenosine A2A receptor-selective agonist CGS21680, systemically administered after SCI, protects from tissue damage, locomotor dysfunction and different inflammatory readouts. In this work we studied the effect of the adenosine A2A receptor antagonist SCH58261, systemically administered after SCI, on the same parameters. We investigated the hypothesis that the main action mechanism of agonists and antagonists is at peripheral or central sites. 相似文献66.
67.
Corsani L Bizzoco E Pedata F Gianfriddo M Faussone-Pellegrini MS Vannucchi MG 《Experimental neurology》2008,211(2):433-440
The hippocampus (dentate gyrus DG plus Cornu Ammonis, CA) is vulnerable to neuropathological events such as ischemia. The DG is a region where neurogenesis takes place and it has been demonstrated that ischemia stimulates neurogenesis. Nitric oxide (NO) plays a major role in ischemic damage evolution and increases in rat hippocampus after ischemia. No information is available on the presence of nNOS-immunoreactive(IR) neurons in the hippocampus of ischemic animals; whereas, the presence of the iNOS protein has been reported in the DG after focal ischemia.We evaluated, immunohistochemically, the cell types expressing nNOS and iNOS in the rat hippocampus by 24 up to 144 h after transient middle cerebral artery occlusion to ascertain whether ischemia induces changes in nNOS or iNOS expression and whether a relationship exists between these changes and the animal survival.nNOS-IR interneurons were detected in control and ischemic rats; in the latter, their number was significantly decreased at all time points. iNOS-IR interneurons appeared in the hippocampus of ischemic rats at 24 h; their number was significantly higher in the animals with longer survival and did not change at later time points. More than 50% of the nNOS-IR interneurons co-expressed iNOS-IR. All these changes were seen both in the ipsilateral and contralateral hippocampus.In conclusion, the focal ischemia affects the hippocampus which responds bilaterally to the injury. We hypothesize that the decrease in the nNOS-IR neurons is likely due to either a neuronal loss or a switching towards the iNOS production which, by inducing neurogenesis, might compensate the neuronal loss. 相似文献
68.
69.
Ignatios Ikonomidis John Lekakis Ioanna Revela Felicita Andreotti Petros Nihoyannopoulos 《European heart journal》2005,26(16):1618-1624
AIMS: We investigated, in a 6 year follow-up study, whether circulating levels of C-reactive protein (CRP) and macrophage colony stimulating factor (MCSF) have an independent or complementary prognostic value in patients with chronic coronary artery disease (CAD). METHODS AND RESULTS: MCSF and CRP were measured in 100 patients with chronic CAD. Of 95 (33%) patients, 31 who completed the 6 year follow-up presented adverse events (death, myocardial infarction, and unstable angina). In multivariable analysis (including traditional risk factors and medications), the upper tertiles of MCSF (> or =814 pg/mL) and CRP (> or =2.5 mg/L) levels were independently associated with a 13- and 6-fold increase in risk of events, respectively (P<0.01). Patients with combined high CRP and MCSF had a higher absolute risk of events than patients with elevated MCSF or CRP alone (75 vs. 59 vs. 32%, respectively, P<0.01). The mean event-free time was 39, 64, and 52 months in patients with elevated MCSF, elevated CRP, and their combination, respectively. CONCLUSION: In patients with chronic CAD, the prognostic value of MCSF is independent and complementary to that of CRP. MCSF is a particularly useful prognostic marker when CRP levels are low, but also provides additional information concerning risk and time-course of events in patients with elevated CRP. 相似文献
70.
Italo Porto Antonio Maria Leone Luisa Nanni Alessandro Sciahbasi Maria De Vita Gaetano Antonio Lanza Felicita Andreotti 《Blood coagulation & fibrinolysis》2005,16(2):97-104
Platelets play a pivotal role in thrombus formation in patients with coronary artery disease (CAD), since the high shear generated in the presence of severe coronary stenoses can increase platelet reactivity (PR) and trigger thrombogenesis. Several reports have suggested a functional effect of human platelet antigen (HPA)-1 and HPA-2 gene polymorphisms on PR. However, the true determinants of high-shear PR in CAD patients taking their usual medications are still incompletely understood. In 104 patients with stable CAD we analyzed the possible clinical, biochemical and genetic factors affecting high-shear PR, measured by the ex vivo platelet function analyzer (PFA-100) collagen-adenosine diphosphate method. In univariate analysis, a lower PR was associated with decreased plasma von Willebrand factor-ristocetin cofactor activity, increased blood levels of triglycerides, female sex, use of thienopyridines, lower platelet count, and HPA-1b carriership. All variables, except HPA-1b, remained associated with lower PR in multivariate analysis. However, the introduction in the model of the HPA-1 and HPA-2 genotypes as interaction terms led to a significant improvement in the prediction of PR, although the quantitative effect was small (about 3% improvement, P=0.046).Thus, in CAD patients, there seems to be only a mild effect of the platelet glycoprotein HPA-1 and HPA-2 polymorphisms on collagen-adenosine diphosphate-stimulated PR after the effect of well-established clinical and biochemical determinants are considered. 相似文献