Noblebuckner0005

Mindfulness has been shown to improve attentional performance, which is known to decline in aging. Long-latency electroencephalographic (EEG) event-related potential (ERP) changes have been reported immediately after mindfulness training, however the enduring stability of these effects is unknown. Furthermore, the ability of mindfulness to impact earlier stages of information processing is unclear. We examined neural activation using high density EEG in older adults engaged in mindfulness training to examine the long-term stability of training effects. After 6 months of training, mindfulness practitioners displayed enhanced neural activation during sensory encoding and perceptual processing of a visual cue. Enhanced perceptual processing of a visual cue was associated with increased neural activation during post-perceptual processing of a subsequent target. Similar changes were not observed in a control group engaged in computer-based attention training over the same period. Neural changes following mindfulness training were accompanied by behavioural improvements in attentional performance. Our results are suggestive of increased efficiency of the neural pathways subserving bottom-up visual processing together with an enhanced ability to mobilise top-down attentional processes during perceptual and post-perceptual processing following mindfulness training. These results indicate that mindfulness may enhance neural processes known to deteriorate in normal aging and age-related neurodegenerative diseases.Youth at clinical high risk (CHR) are a unique population enriched for precursors of major psychiatric disorders, especially schizophrenia (SCZ). Recent neuroimaging findings point to abnormalities in the thalamus of patients with SCZ, including chronic and early course patients, as well as in CHR individuals relative to healthy comparison groups, thus suggesting that thalamic dysfunctions are present even before illness onset. Furthermore, modeling data indicate that alteration between excitatory and inhibitory control, as reflected by alteration in GABAergic and glutamatergic balance (i.e., GABA/Glu), may underlie thalamic deficits linked to the risk and development of psychosis. There is, however, a lack of in vivo evidence of GABA/Glu thalamic abnormalities in the CHR state. Magnetic resonance spectroscopic imaging (MRSI) 7 Tesla (7 T) provides enhanced resolution to quantify GABA and Glu levels in the thalamus of CHR individuals. In this study, we performed 7 T MRSI in 15 CHR and 20 healthy control (HC) participants. We found that GABA/Glu was significantly reduced in the right medial anterior and right medial posterior thalamus of CHR relative to HC groups. The GABA/Glu reduction was negatively correlated with general symptoms in the right medial anterior thalamus, as well as with disorganization symptoms in the right medial posterior thalamus. Altogether, these findings indicate that GABA/Glu abnormalities are present in the thalamus before the onset of full-blown psychosis and are associated with symptom severity, thus providing putative molecular and neuronal targets for early interventions in youth at CHR.Early life trauma (ELT) exposure and posttraumatic stress disorder (PTSD) both affect neural structure, which predicts a variety of mental health concerns throughout the lifespan and may present differently between adolescents and adults. However, few studies have identified the relationship between ELT, PTSD, development, and brain structure using cortical thickness (CT). CT may reveal previously obscured alterations that are potentially clinically relevant and, furthermore, could identify specific structural correlates distinct to ELT from PTSD. Two hundred and fifty-three female adolescent and adult survivors of interpersonal violence and non-trauma-exposed demographically matched controls underwent structural MRI at two different sites. Images were processed and CT was estimated using FreeSurfer. Vertex-wise linear model tests were conducted across the cortical surface to investigate whether PTSD and ELT exposure uniquely affect CT, controlling for scanner site. Planned follow-up tests included second-level analyses of clinical symptoms for CT clusters that were significantly related to PTSD or ELT. CT in the middle cingulate cortex was inversely related to ELT in both age groups, such that individuals with more ELT demonstrated less CT in this region. Additionally, CT was significantly greater in the bilateral intraparietal sulcus and left angular gyrus in both adolescents and adults with PTSD. Furthermore, CT in these clusters was also significantly related to clinical symptom severity in the adult PTSD group. This study provides evidence for distinct CT correlates of ELT and PTSD that are present across adolescents and adults, suggesting consistent markers related to ELT and PTSD on gray matter structure in trauma-exposed individuals.Sensing satiety is a crucial survival skill for all animal species including human. Despite the discovery of numerous neuromodulators that regulate food intake in Drosophila, the mechanism of satiety sensing remains largely elusive. CDK inhibitor review Here, we investigated how neuropeptidergic circuitry conveyed satiety state to influence flies' food consumption. Drosophila tackykinin (DTK) and its receptor TAKR99D were identified in an RNAi screening as feeding suppressors. Two pairs of DTK+ neurons in the fly brain could be activated by elevated D-glucose in the hemolymph and imposed a suppressive effect on feeding. These DTK+ neurons formed a two-synapse circuitry targeting insulin-producing cells, a well-known feeding suppressor, via TAKR99D+ neurons, and this circuitry could be rapidly activated during food ingestion and cease feeding. Taken together, we identified a novel satiety sensor in the fly brain that could detect specific circulating nutrients and in turn modulate feeding, shedding light on the neural regulation of energy homeostasis.Saroglitazar, a dual peroxisome proliferator activated receptor α/γ agonist, approved for diabetic dyslipidemia (DD), is potential therapeutic option for non-alcoholic fatty liver disease (NAFLD). This prospective, observational, real-world study aimed to determine efficacy and safety of Saroglitazar in patients with NAFLD and DD. We included patients with DD and NAFLD who received Saroglitazar 4 mg once daily for 24 weeks. Blood investigations, liver stiffness measurement (LSM) and controlled attenuation parameter (CAP) (FibroScan) were compared at baseline and 24 weeks. Of 163 patients screened, 107 were included, and 101 completed 24 weeks treatment (mean age 50.4 ± 12.3 years, 78.5% males, mean body mass index 28.8 ± 4.2). After 24 weeks, alanine transaminase (ALT) reduced significantly from 94 (47-122) to 39 (31-49) (p  less then  0.0001) and aspartate aminotransferase (AST) (U/L) from 89 (43-114) to 37 (30-47) (p  less then  0.0001) and LSM (kPa) from 8.4 (7.1-9.3) to 7.5 (6.4-8.4) (p = 0.0261). CAP, glycated hemoglobin and lipid parameters also improved significantly.