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The arrival of the era of artificial intelligence is constantly advancing the development of flexible electronic materials. However, low mechanical properties, nonflexible signal transmission, and insensitive signal output have restricted their development as sensors. In this study, a superstretching MXene composite conductive hydrogel was developed with a tensile strain of more than 1800%. The hydrogel was used as a flexible wearable sensor to detect human motion signals in real time. High sensitivity was achieved using the sensor to discern multidirectional human motions, such as bending of human joints, throat vocalization, swallowing, and pulse beat. In addition, rapid resilience was observed for the MXene composite hydrogel after unloading reverse compressive stress, which can quickly cause a specific current response in the micropressure area without leaving any traces. This thixotropic sensor achieves a rapid response to bidirectional stress and has huge application prospects in the field of human body motion detection and national defense information encryption.

A simple and highly efficient method is developed for in situ one-step preparation of carbon co-encapsulated anatase and rutile TiO2 nanocrystals (TiO2@C) with core-shell structure for lithium-ion battery anode. The synthesis is depending on the solid-phase reaction of titanocene dichloride with ammonium persulfate in an autoclave at 200 °C for 30 min. The other three titanocene complexes including bis(cyclopentadienyl)dicarbonyl titanium, cyclopentadienyltitanium trichloride, and cyclopentadienyl(cycloheptatrienyl)titanium are used instead to comprehensively investigate the formation mechanism and to improve the microstructure of the product. The huge heat generated during the explosive reaction cleaves the cyclopentadiene ligands into small carbon fragments, which form carbon shell after oxidative dehydrogenation coating on the TiO2 nanocrystals, resulting in the formation of core-shell structure. The TiO2 nanocrystals prepared by titanocene dichloride have an equiaxed morphology with a small diameter of 10–55 nm and the median size is 30.3 nm. Hundreds of TiO2 nanocrystals are encapsulated together by the worm-like carbon shell, which is amorphous and about 20–30 nm in thickness. The content of TiO2 nanocrystals in the nanocomposite is about 31.1 wt.%. This TiO2@C anode shows stable cyclability and retains a good reversible capacity of 400 mAh g−1 after 100 cycles at a current density of about 100 mA g−1, owing to the enhanced conductivity and protection of carbon shell.

The pathogenesis of stress-induced gastroduodenal mucosal injury is complex and incompletely understood. The aim of this investigation was to examine the involvement of gastric and duodenal capsaicin-sensitive neurons in mucosal damage associated with water-restraint stress (WRS) in rats. Following WRS, gastroduodenal mucosal injury was quantitated by macroscopic and microscopic methods. Calcitonin gene-related peptide (CGRP) content was measured by radioimmunoassay. WRS-induced mucosal erosive injury in the stomach and duodenum (40.9 +/- 4.2 and 5.1 +/- 0.6 mm2, respectively) was reduced significantly (by 88% and 67%, respectively) by acute intragastric capsaicin administration prior to WRS. In contrast, sensory denervation by chronic capsaicin significantly increased the area of gastric injury and duodenal damage. WRS alone caused a significant reduction (by 52% and -35%, respectively) in gastric and duodenal CGRP content, which was prevented by acute capsaicin treatment. The data suggest that gastric and duodenal sensory neurons and CGRP are involved in the pathogenesis of stress-induced mucosal injury to the stomach and duodenum.

Background & Aims: Acid has been shown to stimulate calcitonin gene-related peptide (CGRP) release from peripheral sensory afferent nerve endings in the stomach. The aim of this study was to determine whether endogenous CGRP was involved, by a neurocrine mechanism, in acid-mediated stimulation of somatostatin and inhibition of gastrin release. Methods: A two-compartment sleeve of antral mucosal/submucosal tissue was perfused to determine sensory nerve and endocrine cell responses to luminal acid. CGRP receptor antagonist, CGRP 8–37 , was used to inhibit the actions of endogenously released CGRP. Results: Perfusion of the antral sleeve lumen with media of increasing hydrogen ion concentration caused pH-dependent increases in CGRP and somatostatin release and decrease in gastrin release. CGRP 8–37 inhibited significantly basal somatostatin (−36%) and stimulated basal gastrin (+65%) release ( P 8–37 administration prevented luminal acid-mediated inhibition of gastrin release and stimulation of somatostatin release. These results indicate that CGRP 8–37 prevented acid-mediated feedback inhibition of gastrin release and acid-induced feedforward somatostatin release. Conclusions: These results suggest that CGRP plays an important role in the response of antral D and G cells to luminal acid and that local effector action of endogenous CGRP participates in regulation of antral regulatory peptide secretion.

The core-shell nanostructures have the advantages of combining distinctive properties of varied materials and improved properties over their single-component counterparts. Synthesis approaches for this class of nanostructures have been intensively explored, generally involving multiple steps. Here, a general and convenient strategy is developed for one-step in situ synthesis of various carbon-encapsulated nanocrystals with a core-shell structure via a solid-state reaction of metallocene complexes with (NH4)2S2O8 in an autoclave at 200 °C. A variety of near-spherical and equiaxed nanocrystals with a small median size ranging from 6.5 to 50.6 nm are prepared as inner cores, including Fe7S8, Ni3S4 and NiS, CoS, TiO2, TiO2 and S8, ZrO2, (NH4)3V(SO4)3 and VO2, Fe7S8 and Fe3O4, MoS2 and MoO2. The worm-like carbon shell provides exclusive room for hundreds of nanocrystals separated from each other, preventing nanocrystal aggregation. The synergistic effect of ammonium and a strong oxidizing anion on the electrophilic oxidation of metallocene complexes containing a metal-ligand π bond contributes to the carbon formation at low temperature. It is considered that the cyclopentadienyl ligand in a metallocene complex will decompose into highly reactive straight chain olefinic pieces and the metal-olefin π interaction enables an ordered self-assembly of olefinic pieces on nanocrystals to partially form graphitizable carbon and a core-shell structure. The high capacity, good cycling behavior and rate capability of Fe7S8@C and Ni3S4 and NiS@C electrodes are attributed to the good protection and electrical conductivity of the carbon shell.

Calcitonin gene-related peptide (CGRP) is a 37-amino acid peptide localized to primary sensory afferent nerves in the rat stomach. The actions of CGRP in regulating antral neuroendocrine function were examined in vitro through the use of capsaicin, an agent capable of evoking neuropeptide release from peripheral sensory nerve endings. These results were compared with the effects of exogenous CGRP and CGRP antagonist, CGRP8-37.Rat antral mucosal/submucosal fragments were incubated in either static or dynamic perifusion experiments. Media were assayed for gastrin, somatostatin, CGRP, and acetylcholine.Capsaicin, like exogenous CGRP, stimulated antral somatostatin release and inhibited both gastrin release and acetylcholine discharge. Low dose capsaicin (1 x 10(-5) mol/L) caused significant stimulation of CGRP release: 33 +/- 0.2 vs. 14 +/- 1 pg/mL protein; P0.001. Tetrodotoxin blocked capsaicin-induced inhibition of acetylcholine release and prevented partially capsaicin-mediated stimulation of CGRP release. The CGRP receptor antagonist CGRP8-37 prevented capsaicin-induced D-cell stimulation and inhibition of G-cell secretion and cholinergic discharge.The effects of capsaicin-induced changes in antral D- and G-cell secretion and acetylcholine discharge are due primarily to release of CGRP. Antral CGRP release from primary sensory afferent nerve terminals may act as a local effector substance to regulate antral neuroendocrine function.

In the present study we developed an experimental model for direct assessment of antral endocrine cell and cholinergic neural responses to luminal stimulation. A sleeve of antral mucosal/submucosal tissue was prepared from rat antrum, mounted in perfusion chamber, and perfused in both luminal and submucosal compartments. Morphological and functional integrity of the antral sleeve were confirmed by histological examination and measurement of protein synthesis. Antral gastrin release was assessed in response to luminal stimulation with acid, peptone and distension. Luminal acid (pH3) inhibited basal gastrin release by -70.4% and luminal peptone stimulated gastrin release to 210% above control (p0.02). Distention of the antral sleeve by hydrostatic pressure (3-25cm H2O) caused stepwise and significant increase in gastrin release that was reversible. 3H-acetylcholine was stimulated significantly by KCl (56mM) to values twice control. In summary, these results establish the integrity and responsiveness of the antral sleeve to pharmacological and luminal stimulation. The antral sleeve may be a useful model in assessing antral function in response to luminal stimulation.

The ability of exogenous calcitonin gene-related peptide (CGRP) to regulate gastric somatostatin and gastrin messenger RNA was studied in vitro in rat antral mucosal/submucosal tissues. Somatostatin and gastrin mRNA were quantified by Northern and dot blot hybridization and regulatory peptides were measured by radioimmunoassay. Incubation of antral tissues in the presence of CGRP [1 x 10(-7) M] for 60 min resulted in a reciprocal increase in somatostatin and a decrease in gastrin release: 214.7+/-28.5 vs. control of 81.7+/-5.9 pg somatostatin per gram of tissue and 2.2+/-0.3 vs. control of 5.5+/-0.7 ng gastrin per gram of tissue (P0.001). CGRP caused parallel changes in somatostatin and gastrin mRNA levels: somatostatin mRNA increased by 212% from 0.40+/-0.02 to 1.25+/-0.09 absorbance units (AU) (P0.001) and gastrin mRNA decreased by 73% from 0.55+/-0.08 to 0.15+/-0.02 AU (P0.001). Somatostatin monoclonal antibody prevented CGRP-mediated inhibition of both gastrin release and gastrin mRNA levels. In conclusion, CGRP is capable of modulating both the secretion and gene expression of regulatory peptides from antral G and D cells. Somatostatin immunoneutralization studies suggest that the actions of CGRP on gastrin release and gene expression are indirect and mediated through the paracrine influences of somatostatin.

This study addressed the role of the incretin hormone GLP-l in regulating fundic motor functions using the specific antagonist exendin(9-39)amide (Ex-9). To assess cholinergic mediation of motor effects, we combined Ex-9 with the muscarinic receptor antagonist atropine. Methods: In 9 healthy volunteers, fundic motility was recorded by a barostat technique against background infusions of Ex-9 (300 pmolekg-1emin-1), atropine (5 fJ.gekg·'eh,I), Ex-9 + atropine or saline. Antro-pyloro-duodenal motility and TMPD were recorded in parallel using a sleeve technique. 60 interdigestive min were followed by 70 min with duodenal perfusion of a mixed liquid meal (250 kcal) at variable rates imitating the exponential pattern of gastric empyting. Results: In the interdigestive state, Ex-9 neither influenced fundic tone nor compliance but increased volume waves. This effect was abolished by concomitant atropine. Postprandially, Ex-9 enhanced volume waves and fundic tone, it reduced gastric compliance. Against a background of atropine, the increase of tone was abolished, whereas effects on volume waves and compliance were partially maintained. Atropine per se markedly reduced postprandial fundic tone and volume waves. Conclusions: GLP-l is a physiological inhibitory modulator of tonic and phasic motor events of the fundus. In terms of volume waves even basal circulating levels are effective. Inhibition of cholinergic pathways is a major mediator of motor effects with GLP-\. This mechanism may be activated by receptors at vagal afferents and circumventricular organs.