Notes

Cytokine gene variations as well as socio-demographic characteristics since predictors of cervical most cancers: A product studying approach.
Anxiety is frequent in Parkinson's disease (PD) and has a negative impact on disease symptoms and quality of life. The underlying mechanisms remain largely unknown. The aim of this study was to identify anatomical and functional changes associated to PD-related anxiety by comparing the volume, shape and texture of the amygdala, the cortical thickness as well as the functional connectivity (FC) of the fear circuit in patients with and without clinically relevant anxiety.

Non-demented PD patients were recruited, and anxiety was quantified using the Parkinson Anxiety Scale. Structural MRI was used to compare cortical thickness and amygdala structure and resting-state functional MRI to compare FC patterns of the amygdala and resting-state functional networks in both groups.

We included 118 patients 34 with (A+) and 84 without (A-) clinically relevant anxiety. Clusters of cortical thinning were identified in the bilateral fronto-cingulate and left parietal cortices of the A+ group. The texture and the shape of the left amygdala was different in the A+ group but the overall volume did not differ between groups. FC between the amygdala and the whole brain regions did not differ between groups. The internetwork resting-state FC was higher between the "fear circuit" and salience network in the A+ group.

Anxiety in PD induces structural modifications of the left amygdala, atrophy of the bilateral fronto-cingulate and the left parietal cortices, and a higher internetwork resting-state FC between the fear circuit and the salience network.
Anxiety in PD induces structural modifications of the left amygdala, atrophy of the bilateral fronto-cingulate and the left parietal cortices, and a higher internetwork resting-state FC between the fear circuit and the salience network.
Approximately forty percent of all dopaminergic neurons in SNpc are located in five dense neuronal clusters, named nigrosomes. CDK inhibitor T
- or T
*-weighted images are used to delineate the largest nigrosome, named nigrosome-1. In these images, nigrosome-1 is a hyperintense region in the caudal and dorsal portion of the T
- or T
*-weighted substantia nigra. In PD, nigrosome-1 experiences iron accumulation, which leads to a reduction in T
-weighted hyperintensity. Here, we examine neuromelanin-depletion and iron deposition in regions of interest (ROIs) derived from quantitative-voxel based morphometry (qVBM) on neuromelanin-sensitive images and compare the ROIs with nigrosome-1 identified in T
*-weighted images.

Neuromelanin-sensitive and multi-echo gradient echo imaging data were obtained. R
* was calculated from multi-echo gradient echo imaging data. qVBM analysis was performed on neuromelanin-sensitive images and restricted to SNpc. Mean neuromelanin-sensitive contrast and R
* was measured from the resulting qVBM clusters. Nigrosome-1 was segmented in T
*-weighted images of control subjects and its location was compared to the spatial location of the qVBM clusters.

Two bilateral clusters emerged from the qVBM analysis. These clusters showed reduced neuromelanin-sensitive contrast and increased mean R
* in PD as compared to controls. Cluster-1 from the qVBM analysis was in a similar spatial location as nigrosome-1, as seen in T
*-weighted images.

qVBM cluster-1 shows reduced neuromelanin-sensitive contrast and is in a similar spatial position as nigrosome-1. This region likely corresponds to nigrosome-1 while the second cluster may correspond to nigrosome-2.
qVBM cluster-1 shows reduced neuromelanin-sensitive contrast and is in a similar spatial position as nigrosome-1. This region likely corresponds to nigrosome-1 while the second cluster may correspond to nigrosome-2.The gastrointestinal tract (GIT) hosts a large number of diverse microorganisms, with mutualistic interactions with the host. Here, in two separate experiments, we investigated whether light at night (LAN) would affect GIT microbiota and, in turn, the host physiology in diurnal zebra finches (Taeniopygia guttata). Experiment I assessed the effects of no-night (LL) and dimly illuminated night (dim light at night, dLAN) on fecal microbiota diversity and host physiology of birds born and raised under 12 h photoperiod (LD; 12 h light 12 h darkness). Under LL and dLAN, compared to LD, we found a significant increase in the body mass, subcutaneous fat deposition and hepatic accumulation of lipids. Although we found no difference in total 24 h food consumption, LL/ dLAN birds ate also at night, suggesting LAN-induced alteration in daily feeding times. Concurrently, there were marked differences in amplicon sequence and bacterial species richness between LD and LAN, with notable decline in Lactobacillus richness in birds under LL and dLAN. We attributed declined Lactobacillus population as causal (at least partially) to negative effects on the host metabolism. Therefore, in experiment II with similar protocol, birds under LL and dLAN were fed on diet with or without Lactobacillus rhamnosus GG (LGG) supplement. Clearly, LGG supplement ameliorated LL- and dLAN-induced negative effects in zebra finches. These results demonstrate adverse effects of unnatural lighting on GIT bacterial diversity and host physiology, and suggest the role of GIT microbiota in the maintenance of metabolic homeostasis in response to LAN environment in diurnal animals.Neurogenic orthostatic hypotension (OH) is a disabling disorder caused by impairment of the normal autonomic compensatory mechanisms that maintain upright blood pressure. Nonpharmacologic treatment is always the first step in the management of this condition, but a considerable number of patients will require pharmacologic therapies. Denervation hypersensitivity and impairment of baroreflex buffering makes these patients sensitive to small doses of pressor agents. Understanding the underlying pathophysiology can help in selecting between treatment options. In general, patients with low "sympathetic reserve", i.e., those with peripheral noradrenergic degeneration (pure autonomic failure, Parkinson's disease) and low plasma norepinephrine, tend to respond better to "norepinephrine replacers" (midodrine and droxidopa). On the other hand, patients with relatively preserved "sympathetic reserve", i.e., those with impaired central autonomic pathways but spared peripheral noradrenergic fibers (multiple system atrophy) and normal or slightly reduced plasma norepinephrine, tend to respond better to "norepinephrine enhancers" (pyridostigmine, atomoxetine, and yohimbine).
Website: https://www.selleckchem.com/CDK.html