Day Waddell (petneck37)

Aim Body awareness arises when attending to and maintaining awareness of visuospatial body representations. By the same token, focussing on representations transfers them to working memory. Body awareness and working memory seemingly rely on similar processes and recruit common parietal areas involved in perception. Therefore, we asked whether visuospatial working memory abilities would define individual differences in the perception of spontaneous sensations (SPS), i.e., bodily sensations perceived in the absence of triggers (e.g., tactile stimulation or movement), when attending to the body.Method Participants completed two visuospatial working memory tasks to assess various mechanisms (i) the decay of representations was assessed through a Brown-Peterson task in which the delay between the memorandum presentation and its recall was manipulated, and (ii) the impact of distractors' interference and cognitive load (i.e., complexity) on recall performances were assessed through a complex span task that required the processing of distractors while maintaining a memorandum. A standard SPS task involving localization and characterization of SPS perceived on the hands was completed afterwards.Results Low performance due to decay, distractors' interference and cognitive load in visuospatial working memory was associated with a decrease in the frequency of SPS. Additionally, low performance due to distractors' cognitive load predicted a decrease in the perception of surface-type sensations, and high performance despite distractors' interference led to a better perception of SPS on less sensitive areas of the hand.Conclusion We discuss how visuospatial working memory processes might contribute to body awareness and perceptual distortions of the body.Nitrate signaling integrates and coordinates the expression of a wide range of genes, metabolic pathways and ultimately, plant growth and development. Calcium signaling is proved to be involved in the primary nitrate response pathway. However, it is much less understood how calcium signaling mediates nitrate sensing and responses from the extracellular space to cytoplasm, then to the nucleus. In this review, we describe how transceptor-channel complex (cyclic nucleotide-gated channel protein 15 interacting with nitrate transceptor, CNGC15-NRT1.1), calcineurin B-like proteins (CBLs, CBL1, CBL9), CBL-interacting protein kinases (CIPKs), phospholipase C (PLC) and calcium-dependent protein kinases (CDPKs, also CPKs), acting as key players, complete a potential backbone of the nitrate-signaling pathway, from the plasma membrane to the nucleus. selleck chemical NRT1.1 together with CBL1/9-CIPK23 and CBL-CIPK8 links the NO3- signaling to cytoplasmic and nuclear regulators and triggers downstream NO3- responses. PLCs and inositol 1, 4, 5-triphosphate (IP3) connect NO3- signaling and cytoplasmic Ca2+ signature. CPK10/30/32 fill the gap between NRT1.1 and NIN-like protein (NLP) transcription factors. The arabidopsis nitrate regulated1 (ANR1) is induced from the endosome by the Ca2+-CPKs-NLPs signaling pathway activated by the unphosphorylated form of NRT1.1 (NRT1.1 T101A) at high nitrate condition. Understanding how calcium signaling interconnects the upstream nitrate sensor complex with downstream multiple sensors of the nitrate-signaling pathway is key to completing the nutrient-growth regulatory networks. The use of lycopene as a complementary medicine for Type II diabetes mellitus (T2DM) is limited and controversial. This study evaluated the effect of lycopene intake on the changes of glycaemic status and antioxidant capacity among the T2DM patients. This case-control study involved the participation of 87 patients and 122 healthy individuals. Lycopene intake was assessed by using a food frequency questionnaire. The peripheral antioxidant capacity among the T2DM patients was evaluated. Glycated haemoglobin (HbA1c) and fasting plasma glucose (FPG) were measured as indication