The pathogenesis of Parkinson's disease (PD) seems to involve genetic susceptibility to neurodegeneration. APOE gene has been considered a risk factor for PD. This study aimed to evaluate the association of APOE polymorphism with PD and its influence on lipid profile. We studied 232 PD patients (PD) and 169 individuals without the disease. The studied polymorphism was analyzed by PCR/RFLP. The Fisher's exact test, chi-square, ANOVA, and t-test (P < 0.05) were applied. The APOE3/3 genotype was prevalent in PD patients and Controls (P = 0.713) followed by APOE3/4 (P = 0.772). Both groups showed recommended values for lipid profile, with increase in the values of total cholesterol and LDLc, as well as decreased values of triglycerides in PD patients compared with Controls (P < 0.05 for all of them). Increased levels of HDLc, in PD patients, were associated with the APOE3/3 versus APOE-/4 genotypes (P = 0.012). The APOE polymorphism does not distinguish PD patients from Controls, as opposed to the lipid profile alone or in association with APOE. Furthermore, a relationship between increase of HDLc levels and APOE3 in homozygous was found in PD patients only.

To study the jitter parameters in the distant (DM) and the adjacent muscle (AM) after botulinum neurotoxin type A (BoNT/A) injection in 78 patients, jitter was measured by voluntary activation in DM (n = 43), and in AM (n = 35). Patients were receiving BoNT/A injections as a treatment for movement disorders. Mean age 65.1 years (DM) and 61.9 years (AM). The mean jitter was abnormal in 13.9% (maximum 41.4 µs) of DM, and 40% (maximum 43.7 µs) of AM. Impulse blocking was sparse. We found no correlation of the mean jitter to age, BoNT/A most recent injection (days/units), number of muscles injected, total BoNT/A units summated, number of total BoNT/A sessions, beta-blockers/calcium channel blockers use, and cases with local spread symptoms such as eyelid drop/difficulty swallowing. Maximum mean jitter (41.4/43.7 µs) for DM/AM occurred 61 and 131 days since the most recent BoNT/A, respectively. The far abnormal mean jitter (32.6/36.9 µs) occurred 229 and 313 days since the most recent BoNT/A. We suggested that jitter measurement can be done after BoNT/A in a given muscle other than the injected one, after 8 (DM) and 11 (AM) months, with reference >33 µs and >37 µs, respectively.

Parkinson's disease (PD) is the second most common neurodegenerative disorder, showing high prevalence in elderly patients also in Brazil, with an incidence of 150/200 cases per 100,000 inhabitants ABSTRACT Objective:This study aimed to analyze the frequency of GSTP1-Alw26I polymorphism and to estimate its association with toxic substances in Parkinson's disease (PD). Methods: A study group with 154 patients -subdivided into familial and sporadic PD groups -and 158 elderly individuals without the disease (control group) were evaluated. GSTP1-Alw26I polymorphism was analyzed by polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP). Results: Patients were significantly more exposed to pesticides compared with the control group (p=0.0004), and the heterozygote genotype associated to exposure to pesticides also prevailed in patients (p=0.0001). Wild homozygote genotype was related to tobacco use (p=0.043) and alcoholism (p=0.033) in familial PD patients. Conclusion: Exposure to pesticides is associated to PD, whose effect can be enhanced when combined with the heterozygote genotype of GSTP1-Alw26I. Also, large genetic and environmental studies considering tobacco use, alcoholism, GSTP1 and PD are necessary to confirm our findings.Key words: glutathione transferase, genetic polymorphism, Parkinson disease, xenobiotics. RESUMOObjetivo: Analisar a frequência do polimorfismo GSTP1-Alw26I, assim como estimar sua associação com substâncias tóxicas na doença de Parkinson (DP). Métodos: A casuística avaliada foi composta por um grupo de estudo, com 154 pacientes, subdivididos em DP familial e esporádica, e outro com 158 idosos sem a doença (grupo controle). O polimorfismo GSTP1-Alw26I foi analisado por reação em cadeia da polimerase/polimorfismo de comprimento do fragmento de restrição (PCR/RFLP). Resultados: Os pacientes foram significativamente mais expostos a pesticidas, comparados com o grupo controle (p=0,0004), e o genótipo heterozigoto associado a exposição a pesticidas também prevaleceu nos pacientes (p=0,0001). O genótipo homozigoto selvagem apresentou relação com tabagismo (p=0,043) e etilismo (p=0,033) em pacientes com DP familial. Desse modo, a exposição a pesticidas está associada à DP, cujo efeito pode ser potencializado quando combinado ao genótipo heterozigoto de GSTP1-Alw26I. Estudos genético-ambientais envolvendo tabagismo, etilismo, GSTP1 e DP devem ser realizados em casuísticas numerosas, confirmando essa associação.Palavras-Chave: glutationa transferase, polimorfismo genético, doença de Parkinson, xenobióticos.

Funding Acknowledgements Type of funding sources: None. Main funding source(s): No funding. Background the Timed Up And Go test (TUG) is a form of mobility and functional capacity evaluation, but is still not well studied in cardiac patients. Objective test TUG association and prediction capacity for peak VO2. Methods cross sectional study. Patients with cardiophaties, admitted to a cardiac rehabilitation facility, who were submitted to TUG and a cardiopulmonary exercise test (CPET). Pearson correlation, multiple linear regression, ROC curves and Bland-Altman analysis were applied. From the total 2/3 were designated to the creation and 1/3 to the validation population. A p value &lt; 0.05 was admitted as significant. Results 201 patients, mean age of 67±13 years, 30% were female, 70% had ischaemic cardiopathy. Heart failure was present in 30%, 53% were NYHA I, 37% NYHA II, the mean left ventricle ejection fraction was 56±16%. Mean peak VO2 was 17±6 ml.kg-1.min-1 and mean TUG was 7±2.5 seconds (s). The correlation between TUG and peak VO2 was: r= -0.53 (IC95%= -0.62 -0.42; p&lt;0.001) with a R² of 0.28. The AUC to predict a peak VO2 ≥20 ml.kg-1.min-1 based on TUG was 0.80 (IC95% 0.74-0.86; p&lt;0.001) and the best cut point ≤5.47s (sensitivity 83% and specificity 63%). Based in 134 patients (2/3 of the total), the following equation was described to peak VO2 prediction based in TUG results: peak VO2= 33.553+ (-0.149*age) + (-0.738*TUG) + (-2.870*sex); male=0, female=1. In the validation population (1/3 of the total), the peak VO2 estimated by TUG was 18.8±3.2 ml.kg-1.min-1 and the CPET measured was 18.1±5.9 ml.kg-1.min-1 (p &gt; 0.05). Conclusion TUG and peak VO 2 were moderately but significantly associated. A equation to predict peak VO2 based on TUG was described and validated with good performance. Achieving 5.47s or less in TUG was related levels of peak VO2 that are related to better prognosis.

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