Changes in the EEG spectral power during dual-task walking with aging and Parkinson’s disease: initial findings using Event-Related Spectral Perturbation analysis

Journal of Neurology - The ability to maintain adequate motor-cognitive performance under increasing task demands depends on the regulation and coordination of neural resources. Studies have shown...     

Inflammatory activation: cardiac, renal, and cardio-renal interactions in patients with the cardiorenal syndrome

Although inflammation is a physiologic response designed to protect us from infection, when unchecked and ongoing it may cause substantial harm. Both chronic heart failure (CHF) and chronic kidney disease (CKD) are known to cause elaboration of several pro-inflammatory mediators that can be detected at high concentrations in the tissues and blood stream. The biologic sources driving this chronic inflammatory state in CHF and CKD are not fully established. Traditional sources of inflammation include the heart and the kidneys which produce a wide range of pro-inflammatory cytokines in response to neurohormones and sympathetic activation. However, growing evidence suggests that non-traditional biomechanical mechanisms such as venous and tissue congestion due to volume overload are also important as they stimulate endotoxin absorption from the bowel and peripheral synthesis and release of pro-inflammatory mediators. Both during the chronic phase and, more rapidly, during acute exacerbations of CHF and CKD, inflammation and congestion appear to amplify each other resulting in a downward spiral of worsening cardiac, vascular, and renal functions that may negatively impact patients’ outcome. Anti-inflammatory treatment strategies aimed at attenuating end organ damage and improving clinical prognosis in the cardiorenal syndrome have been disappointing to date. A new therapeutic paradigm may be needed, which involves different anti-inflammatory strategies for individual etiologies and stages of CHF and CKD. It may also include specific (short-term) anti-inflammatory treatments that counteract inflammation during the unsettled phases of clinical decompensation. Finally, it will require greater focus on volume overload as an increasingly significant source of systemic inflammation in the cardiorenal syndrome.     

Estimation of Parkinson’s disease survival in Israeli men and women, using health maintenance organization pharmacy data in a unique approach

The aim of this work was to estimate in an incident cohort of pharmacy-based PD patients the survival of men and women accounting for age at treatment initiation and to compare their gender-specific survival with that of the general Israeli population. A population-based cohort of 4,848 incident pharmacy-based PD cases with definite/probable/possible certainty was previously identified using a drug-tracer approach for 1999–2008. Survival analysis was performed for two time scales: survival after treatment initiation (disease duration), and life-time survival (life expectancy). Kaplan–Meier curves and Cox regressions were used to compare survival across gender. Gender-specific SMRs were calculated from national rates and were compared using Poisson regression. During the follow-up from first purchase of any anti-parkinsonian drug (mean 4.0 ± 2.6 years, range 2 months–10 years), 1,266 (26 %) of the cases died. Younger age at first anti-parkinsonian drug purchase and female gender were associated with increased survival after treatment initiation (HR = 1.089, 95 % CI 1.080–1.098 for 1-year age increase; HR = 0.716, 95 % CI 0.640–0.800, females vs. males). Life-time survival increased with older age at first anti-parkinsonian drug purchase and female gender (HR = 0.759, 95 % CI 0.746–0.771 for 1-year age increase; HR = 0.694, 95 % CI 0.621–0.776, females vs. males). Sensitivity analysis on a sub-cohort of definite cases (n = 2501) yielded similar results. In comparison to the general Israeli population, mortality among pharmacy-based PD patients was significantly increased (SMR_men = 1.69, 95 % CI 1.57–1.81, SMR_women = 1.49, 95 % CI 1.37–1.62), differently between genders (p < 0.01). Female gender was associated with longer, perhaps more benign disease course, and longer life expectancy. Earlier age at anti-parkinsonian drug initiation increased disease duration, but was associated with shorter life expectancy.     

Association of Bezafibrate Treatment With Reduced Risk of Cancer in Patients With Coronary Artery Disease

ObjectiveTo evaluate the association between bezafibrate, a drug used to treat hypertriglyceridemia, and long-term cancer incidence in patients with coronary artery disease (CAD).Patients and MethodsThe study comprised 2980 patients with CAD (mean age, 60 years; 2729 [91.6%] men) who were free of cancer and were enrolled in the Bezafibrate Infarction Prevention study, a double-blind trial conducted between May 1, 1990, and January 31, 1993, in 18 cardiology departments in Israel. Patients randomized to receive 400 mg of bezafibrate (n=1486) or placebo (n=1494) daily for a median of 6.2 years (range, 4.7-7.6 years) were followed up for incidence of cancer through the Israeli National Cancer Registry and all-cause death through the Population Registry of the State of Israel until December 31, 2013. Cox proportional hazards and Fine and Gray survival models were used to assess the bezafibrate-cancer association.ResultsClinical characteristics and laboratory values were well balanced between the 2 groups at the study entry. Over a median follow-up of 22.5 years (range, 21.2-23.9 years), cancer developed in 753 patients. With death considered a competing event, the cumulative incidence of cancer at the end of the follow-up was lower in the bezafibrate vs the placebo group (23.9%; 95 CI, 21.9%-26.1% vs 27.2%; 95 CI, 25.1%-29.4%; P=.04). The hazard ratio for cancer in the bezafibrate vs placebo groups was 0.86 (95% CI, 0.74-0.99). In mediation analysis, the association between bezafibrate treatment and cancer incidence was not sensitive to adjustment for on-trial lipid levels but was attenuated on adjustment for on-trial fibrinogen levels.ConclusionBezafibrate treatment is associated with reduced risk of cancer among patients with CAD. Fibrinogen, but not lipid lowering, is linked to this association.