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Depressive symptoms are a source of significant morbidity in Parkinson's disease (PD). Electroconvulsive therapy (ECT) is a promising treatment for depression in PD (dPD); however, data remain limited, including data on optimal electrode placement. In this retrospective study, the investigators aimed to characterize the effects of bifrontal ECT for dPD on psychiatric and motor symptoms, as well as autonomic response.

Clinical data were retrieved from a university-affiliated ECT service in Vancouver, British Columbia, for patients with dPD receiving bifrontal ECT between 2014 and 2018. Clinical Global Impression (depressive symptoms) and Unified Parkinson's Disease Rating Scale (motor symptoms) scores and cardiovascular measurements during ECT, as well as doses of dopaminergic medications, were recorded.

Eight patients met criteria for inclusion. Six patients (75%) met response criteria for improvement of depressive symptoms, including 83% of patients who completed a full ECT course. Five patients went o; however, further investigation is needed.

Instantaneous wave-free ratio (iFR) has emerged as the strategy of choice for the assessment of intermediate coronary lesions. The impact of preprocedural β-blockers therapy on the iFR was the aim of this study.

We included patients undergoing functional assessment of intermediate (40%-70%) coronary lesions in 2 centers. The iFR measurement was performed by pressure-recording guidewire and calculated at the core laboratory using the manufacturers' dedicated software. Minimal luminal diameter, reference diameter, percent diameter stenosis, and length of the lesion were measured. Positive iFR was considered for values <0.90.

We included 197 patients undergoing functional evaluation of 223 coronary lesions. Patients on β-blockers (69%) had more frequently hypertension (

= .05); previous myocardial infarction (

= .01); therapy with clopidogrel (

= .02), statins, and aspirin; and acute coronary syndrome at presentation (

< .001, respectively). Mean iFR values were slightly higher in patients on β-blockers (0.94 ± 0.06 vs 0.92 ± 0.06,

= .11). The rate of positive iFR was significantly lower with β-blockers (14.9% vs 27.5%,

= .04). On multivariate analysis, β-blockers use was a predictor of the significance of coronary stenoses (odds ratio [OR] = 0.48; 95% CI = 0.23-0.98;

= .05) together with lesion length (OR = 1.04; 95% CI = 1.01-1.07;

= .007).

Among patients undergoing iFR, preprocedural β-blockers are associated with higher absolute values and a lower rate of positive iFR.

Among patients undergoing iFR, preprocedural β-blockers are associated with higher absolute values and a lower rate of positive iFR.The prediction of human toxicities from animal toxicity tests is often poor, and is now discouraged and in some cases banned, especially those involving the LD50 test. However, there is a vast number of historical LD50 data in both public and in-house repositories that are being put to little use. This study examined the correlations between human lethality (doses and concentrations) of 36 MEIC chemicals and the median values of a large number of mouse and rat LD50 values obtained for four different routes of administration. The best correlations were found with mouse and rat intraperitoneal LD50 values (r2 = 0.838 and 0.810 for human lethal dose, and r2 = 0.753 and 0.785 for human lethal concentration). selleck chemicals The results show that excellent prediction of human lethal dose and concentration can be made, for this series of chemicals at least, by using uncurated rodent LD50 values, thus offering some reparation for the millions of rodent lives sacrificed in LD50 testing.

Coronary artery disease (CAD) is a multifactorial condition with both genetic and exogenous causes. The contribution of tissue-specific functional networks to the development of atherosclerosis remains largely unclear. The aim of this study was to identify and characterize central regulators and networks leading to atherosclerosis.

Based on several hundred genes known to affect atherosclerosis risk in mouse (as demonstrated in knockout models) and human (as shown by genome-wide association studies), liver gene regulatory networks were modeled. The hierarchical order and regulatory directions of genes within the network were based on Bayesian prediction models, as well as experimental studies including chromatin immunoprecipitation DNA-sequencing, chromatin immunoprecipitation mass spectrometry, overexpression, small interfering RNA knockdown in mouse and human liver cells, and knockout mouse experiments. Bioinformatics and correlation analyses were used to clarify associations between central genes and CA CNC homolog 1) assists MAFF in the presence of lipopolysaccharide stimulation with respective heterodimers binding at the MAF recognition element of the LDLR promoter to transcriptionally downregulate LDLR expression.

The transcription factor

was identified as a novel central regulator of an atherosclerosis/CAD-relevant liver network.

triggered context-specific expression of

and other genes known to affect CAD risk. Our results suggest that

is a missing link between inflammation, lipid and lipoprotein metabolism, and a possible treatment target.

The transcription factor MAFF was identified as a novel central regulator of an atherosclerosis/CAD-relevant liver network. MAFF triggered context-specific expression of LDLR and other genes known to affect CAD risk. Our results suggest that MAFF is a missing link between inflammation, lipid and lipoprotein metabolism, and a possible treatment target.Globally, stroke is a leading cause of death and disability. Traditional risk factors like hypertension, diabetes, and obesity do not fully account for all stroke cases. Recent infection is regarded as changes in systemic immune signaling, which can increase thrombosis formation and other stroke risk factors. We have previously shown that administration of lipopolysaccharide (LPS) 30-minutes prior to stroke increases in infarct volume. In the current study, we found that animals intermittently exposed to LPS have larger cortical infarcts when compared to saline controls. To elucidate the mechanism behind this phenomenon, several avenues were investigated. We observed significant upregulation of tumor necrosis factor-alpha (TNF-α) mRNA, especially in the ipsilateral hemisphere of both saline and LPS exposed groups compared to sham surgery animals. We also observed significant reductions in expression of genes involved in autophagy in the ipsilateral hemisphere of LPS stroke animals. In addition, we assessed DNA methylation of autophagy genes and observed a significant increase in the ipsilateral hemisphere of LPS stroke animals.