Biosensor Strip for Rapid On-site Assessment of Levodopa Pharmacokinetics along with Motor Performance in Parkinson's Disease.

While levodopa (L-Dopa) is the primary treatment for alleviating Parkinson's disease (PD), its efficacy is hindered by challenges such as a short half-life and inconsistent plasma levels. As PD progresses, the rising need for increased and more frequent L-Dopa doses coupled with symptom fluctuations and dyskinesias underscores the urgency for improved comprehension of the interplay between L-Dopa levels and PD motor symptoms. Addressing this critical need, we present a decentralized testing method using a disposable biosensor strip and a universal slope (U-slope) calibration-free approach. This enables reliable, rapid, simple, and cost-effective decentralized L-Dopa measurements from capillary blood. A pilot study with PD persons demonstrates the ability to monitor real-time L-Dopa pharmacokinetics from fingerstick blood after oral L-Dopa-Carbidopa (C-Dopa) tablet administration. Correlating capillary blood L-Dopa levels with PD motor scores revealed a well-defined inverse correlation with temporal motor fluctuations. We compared the resulting dynamic capillary blood L-Dopa levels with plasma L-Dopa levels using the traditional but clinically impractical high-performance liquid chromatography technique. By providing timely feedback on a proper L-Dopa dosing regimen in a decentralized and rapid fashion, this new biosensing platform will facilitate tailored optimal L-Dopa dosing, towards improving symptom management and enhancing health-related quality of life.

Evaluation of curcumin as add-on therapy in patients with Parkinson's disease: A pilot randomized, triple-blind, placebo-controlled trial.

BACKGROUND AND OBJECTIVE: Preclinical studies suggest that curcumin might be a potential neuroprotective agent in Parkinson's disease (PD). This clinical trial aimed to evaluate the efficacy of adding nanomicelle curcumin on improving the motor and non-motor symptoms of PD patients and their quality of life. MATERIAL AND METHODS: Idiopathic PD patients aged ≥30≥ 30 whose symptoms were under control were included in this pilot, randomized, triple-blind, placebo-controlled, add-on trial. Eligible patients were randomly assigned to either the curcumin (n = 30, 80 mg/day) or placebo (n = 30) groups and were followed for nine months. Primary outcomes were the Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS) and Parkinson's Disease Questionnaire (PDQ-39). These variables, along with demographic data, drug history, and possible side effects of curcumin, were gathered at the beginning of the study and every three months. A mixed effects model was used to compare the group-by-time interaction, followed by post hoc analysis. RESULTS: Although the mean MDS-UPDRS and PDQ-39 scores were not significantly different between the curcumin and placebo groups at any time points, MDS-UPDRS part III (P = 0.04) showed a significant difference in its overall trend between the study groups. However, post hoc analysis failed to spot this difference at study time points. The most common side effects of curcumin were nausea and vomiting (P = 0.25) and gastroesophageal reflux (P = 0.42). CONCLUSION: While curcumin is a well-tolerated natural compound, this trial was unsuccessful in showing its efficacy in quality of life and clinical symptoms of PD patients.

Evaluation of combining Alberta Stroke Program Early CT Score (ASPECTS) with mean platelet volume, plateletcrit, and platelet count in predicting short- and long-term prognosis of patients with acute ischemic stroke.

BACKGROUND: There is controversy regarding Alberta Stroke Program Early CT Score (ASPECTS) and platelet indices as predictors of outcome in patients with acute ischemic stroke (AIS). We aimed to assess the prognostic value of ASPECTS, mean platelet volume (MPV), plateletcrit (PCT), and platelet count (Plt) in 3-month and 1-year functional outcomes of AIS patients, both independently and in combination. METHODS: This prospective study was conducted in Shams Al-shomuos and Ghaem hospitals of Mashhad, Iran from June 2019 to January 2021. Overall, 553 patients above 18 years old with first-ever anterior circulation AIS met the eligibility criteria and were included. Clinical, hematologic, radiologic, and demographic data of patients were recorded at baseline. The 3-month and 1-year functional outcome was evaluated by modified Rankin Scale (mRS). Multivariate logistic regression was used to determine the independent predictors of poor functional outcome (mRS>2) and mortality. RESULTS: The mean age of the patients was 65.50 ± 14.41 years and 282 patients (51%) were male. ASPECTS ≤ 7 was an independent predictor of both poor function (OR=1.94, 95%CI=1.04-3.62, P = 0.04) and mortality (OR=2.02, 95%CI=1.14-3.58, P = 0.02) at 1 year. MPV was also a strong predictor of 3-month (OR=3.88, 95%CI=2.04-7.38, P = 0.02) and 1-year (OR=3.32, 95%CI=1.91-5.78, P = 0.01) mortality, as well as 3-month (OR=3.25, 95%CI=1.80-5.86, P < 0.001) and 1-year (OR=4.35, 95%CI=2.36-8.02, P < 0.001) poor function. For 1-year poor function (OR=9.33, 95%CI=2.19-39.73, P = 0.003) and mortality (OR=6.40, 95%CI=2.09-19.64, P = 0.001), ASPECTS combined with all platelet indices found to be a more robust independent predictor compared to each variable alone. CONCLUSION: Although MPV is an independent predictor of both 3-month and 1-year poor function and mortality in AIS patients, ASPECTS ≤ 7 was found to be a risk factor for 1-year poor function and mortality. Moreover, the prognostic value of both platelet indices and ASPECTS are greater when they are combined together in AIS patients.

Association between smoking and non-alcoholic fatty liver disease: A systematic review and meta-analysis.

BACKGROUND/AIMS: Non-alcoholic fatty liver disease is one of the most common chronic liver diseases. Some risk factors are known to influence the development of non-alcoholic fatty liver disease, but the effect of tobacco smoking on the progression of non-alcoholic fatty liver disease is controversial. The main goal of this systematic review and meta-analysis is to investigate the association between smoking and non-alcoholic fatty liver disease. METHOD: Electronic databases (PubMed, Scopus, and ISI Web of Science) were searched to find published articles on non-alcoholic fatty liver disease and smoking until December 2016. All relevant studies were screened by inclusion and exclusion criteria and compatible studies were chosen. The Newcastle-Ottawa Scale was used to assess the methodological quality of eligible articles. Subsequently, information was gathered based on the following: author, publication year, keywords, country, inclusion and exclusion criteria, main results, study design, conclusion, and confounder variables (age, body mass index, gender, ethnicity, and diabetes). Finally, analyses were performed using Comprehensive Meta-Analysis Software. RESULTS: Data were extracted from 20 observational studies (9 cross-sectional, 6 case-control, 4 cohort studies, and 1 retrospective cohort study). A significant association was observed between smoking and non-alcoholic fatty liver disease with a pooled odds ratio of 1.110 (95% confidence interval, 1.028-1.199), p-value = 0.008. The statistical heterogeneity was medium with an I2 of 40.012%, p-heterogeneity = 0.074. Also there was a significant relation between non-alcoholic fatty liver disease and passive smoking with a pooled odds ratio of 1.380 (95% confidence interval, 1.199-1.588; p-value = 0.001; I2 = 59.41; p-heterogeneity = 0.117). CONCLUSION: Our meta-analysis demonstrated that smoking is significantly associated with non-alcoholic fatty liver disease. Further prospective studies exploring the underlying mechanisms of this association should be pursued. Also passive smoking increases the risk of non-alcoholic fatty liver disease about 1.38-fold. The effects of smoking cigarettes on active smokers (current smoker, former smoker, and total smoker) are less than passive smokers. Further studies are needed to compare the of effects of passive and active smoking on non-alcoholic fatty liver disease.