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Information wants upon cancer of the breast anatomical and also non-genetic risk factors within family members of ladies using a BRCA1/2 or PALB2 pathogenic alternative.
Moreover, our finding demonstrated that ectopic miR-155-5p expression alleviated RIPF in mice by the GSK-3β/NF-κB pathway. Thus, radiation downregulates miR-155-5p in alveolar epithelial cells that induces EMT, which contributes to RIPF using GSK-3β/NF-κB pathway. Our observation provides further understanding on the regulation of RIPF and identifies potential therapeutic targets.Proper assembly of mitotic spindles requires microtubule nucleation not only at the centrosomes but also around chromatin. In this study, we found that the Drosophila tubulin-specific chaperone dTBCE is required for the enrichment of tubulin in the nuclear space after nuclear envelope breakdown and for subsequent promotion of spindle microtubule nucleation. These events depend on the CAP-Gly motif found in dTBCE and are regulated by Ran and lamin proteins. Our data suggest that during early mitosis, dTBCE and nuclear pore proteins become enriched in the nucleus, where they interact with the Ran GTPase to promote dynamic tubulin enrichment. We propose that this novel mechanism enhances microtubule nucleation around chromatin, thereby facilitating mitotic spindle assembly.Activity-dependent persistent changes in neuronal intrinsic excitability and synaptic strength are underlying learning and memory. Voltage-gated potassium (Kv) channels are potential regulators of memory and may be linked to age-dependent neuronal disfunction. MinK-related peptides (MiRPs) are conserved transmembrane proteins modulating Kv channels; however, their possible role in the regulation of memory and age-dependent memory decline are unknown. Here, we show that, in C. elegans, mps-2 is the sole member of the MiRP family that controls exclusively long-term associative memory (LTAM) in AVA neuron. In addition, we demonstrate that mps-2 also plays a critical role in age-dependent memory decline. In young adult worms, mps-2 is transcriptionally upregulated by CRH-1/cyclic AMP (cAMP)-response-binding protein (CREB) during LTAM, although the mps-2 baseline expression is CREB independent and instead, during aging, relies on nhr-66, which acts as an age-dependent repressor. Deletion of nhr-66 or its binding element in the mps-2 promoter prevents age-dependent transcriptional repression of mps-2 and memory decline. Finally, MPS-2 acts through the modulation of the Kv2.1/KVS-3 and Kv2.2/KVS-4 heteromeric potassium channels. Altogether, we describe a conserved MPS-2/KVS-3/KVS-4 pathway essential for LTAM and also for a programmed control of physiological age-dependent memory decline.Wounding and infection trigger a protective innate immune response that includes the production of antimicrobial peptides in the affected tissue as well as increased sleep. Little is known, however, how peripheral wounds or innate immunity signal to the nervous system to increase sleep. We found that, during C. elegans larval molting, an epidermal tolloid/bone morphogenic protein (BMP)-1-like protein called NAS-38 promotes sleep. NAS-38 is negatively regulated by its thrombospondin domain and acts through its astacin protease domain to activate p38 mitogen-activated protein (MAP)/PMK-1 kinase and transforming growth factor β (TGF-β)-SMAD/SMA-3-dependent innate immune pathways in the epidermis that cause STAT/STA-2 and SLC6 (solute carrier)/SNF-12-dependent expression of antimicrobial peptide (AMP) genes. Selleckchem CNQX We show that more than a dozen epidermal AMPs act as somnogens, signaling across tissues to promote sleep through the sleep-active RIS neuron. In the adult, epidermal injury activates innate immunity and turns up AMP production to trigger sleep, a process that requires epidermal growth factor receptor (EGFR) signaling that is known to promote sleep following cellular stress. We show for one AMP, neuropeptide-like protein (NLP)-29, that it acts through the neuropeptide receptor NPR-12 in locomotion-controlling neurons that are presynaptic to RIS and that depolarize this neuron to induce sleep. Sleep in turn increases the chance of surviving injury. Thus, we found a novel mechanism by which peripheral wounds signal to the nervous system to increase protective sleep. Such a cross-tissue somnogen-signaling function of AMPs might also boost sleep in other animals, including humans.A delayed eating schedule is associated with increased risk of obesity and metabolic dysfunction in humans.1-9 However, there are no prolonged, highly controlled experimental studies testing the effects of meal timing on weight and metabolism in adults with a body mass index (BMI) of 19-27 kg/m2.10-18 Twelve healthy adults (age 26.3 ± 3.4 years; BMI 21.9 ± 1.7 kg/m2; 5 females) participated in a randomized crossover study in free-living conditions. Three meals and two snacks with comparable energy and macronutrient contents were provided during two, 8-week, counterbalanced conditions separated by a 2-week washout period (1) daytime (intake limited to 0800 h-1900 h) and (2) delayed (intake limited to 1200 h-2300 h). Sleep-wake cycles and exercise levels were held constant. Weight, adiposity, energy expenditure, and circadian profiles of hormones and metabolites were assessed during four inpatient visits occurring before and after each condition. Body weight, insulin resistance (homeostatic model assessment of insulin resistance [HOMA-IR]), trunk-to-leg fat ratio, resting energy expenditure, respiratory quotient, and fasting glucose, insulin, total and high-density lipoprotein (dHDL) cholesterol, and adiponectin decreased on the daytime compared to the delayed schedule. These measures, as well as triglycerides, increased on the delayed compared to the daytime schedule (effect size range d = 0.397-1.019). Circadian phase and amplitude of melatonin, cortisol, ghrelin, leptin, and glucose were not differentially altered by the eating schedules. Overall, an 8-week daytime eating schedule, compared to a delayed eating schedule, promotes weight loss and improvements in energy metabolism and insulin in adults with BMI 19-27 kg/m2, underscoring the efficacy and feasibility of daytime eating as a behavioral modification for real-world conditions.
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