Recent Advances in Design Strategies and Multifunctionality of Flexible Electromagnetic Interference Shielding Materials.

With rapid development of 5G communication technologies, electromagnetic interference (EMI) shielding for electronic devices has become an urgent demand in recent years, where the development of corresponding EMI shielding materials against detrimental electromagnetic radiation plays an essential role. Meanwhile, the EMI shielding materials with high flexibility and functional integrity are highly demanded for emerging shielding applications. Hitherto, a variety of flexible EMI shielding materials with lightweight and multifunctionalities have been developed. In this review, we not only introduce the recent development of flexible EMI shielding materials, but also elaborate the EMI shielding mechanisms and the index for "green EMI shielding" performance. In addition, the construction strategies for sophisticated multifunctionalities of flexible shielding materials are summarized. Finally, we propose several possible research directions for flexible EMI shielding materials in near future, which could be inspirational to the fast-growing next-generation flexible electronic devices with reliable and multipurpose protections as offered by EMI shielding materials.

High-Resolution U-Net: Preserving Image Details for Cultivated Land Extraction.

Accurate and efficient extraction of cultivated land data is of great significance for agricultural resource monitoring and national food security. Deep-learning-based classification of remote-sensing images overcomes the two difficulties of traditional learning methods (e.g., support vector machine (SVM), K-nearest neighbors (KNN), and random forest (RF)) when extracting the cultivated land: (1) the limited performance when extracting the same land-cover type with the high intra-class spectral variation, such as cultivated land with both vegetation and non-vegetation cover, and (2) the limited generalization ability for handling a large dataset to apply the model to different locations. However, the "pooling" process in most deep convolutional networks, which attempts to enlarge the sensing field of the kernel by involving the upscale process, leads to significant detail loss in the output, including the edges, gradients, and image texture details. To solve this problem, in this study we proposed a new end-to-end extraction algorithm, a high-resolution U-Net (HRU-Net), to preserve the image details by improving the skip connection structure and the loss function of the original U-Net. The proposed HRU-Net was tested in Xinjiang Province, China to extract the cultivated land from Landsat Thematic Mapper (TM) images. The result showed that the HRU-Net achieved better performance (Acc: 92.81%; kappa: 0.81; F1-score: 0.90) than the U-Net++ (Acc: 91.74%; kappa: 0.79; F1-score: 0.89), the original U-Net (Acc: 89.83%; kappa: 0.74; F1-score: 0.86), and the Random Forest model (Acc: 76.13%; kappa: 0.48; F1-score: 0.69). The robustness of the proposed model for the intra-class spectral variation and the accuracy of the edge details were also compared, and this showed that the HRU-Net obtained more accurate edge details and had less influence from the intra-class spectral variation. The model proposed in this study can be further applied to other land cover types that have more spectral diversity and require more details of extraction.

Synergetic dielectric loss and magnetic loss towards superior microwave absorption through hybridization of few-layer WS2 nanosheets with NiO nanoparticles.

WS2 nanomaterials have attracted great attention in the field of electromagnetic wave absorption due to their high specific surface area, layered structure, and peculiar electronic properties. However, further improvements on their limited electromagnetic absorbing (EMA) capacity and bandwidth are urgently required for their practical application as EMA absorbents. In this work, WS2/NiO hybrids with heterostructures are prepared by a hydrothermal method and developed into EMA absorbents. The maximum reflection loss of the hybrids with 20% NiO loading could reach -53.31 dB at a thickness of 4.30 mm; the bandwidth with a reflection loss value of less than -10 dB is determined to be 13.46 GHz (4.54-18 GHz) when the thickness of the absorbent is between 3.5 and 5.5 mm. It is found that the enhanced EMA performance of WS2/NiO hybrids is caused by the addition of magnetic NiO, which could result in the interfaces between WS2 and NiO being responsible for the synergetic magnetic loss and dielectric loss in the hybrids. This work provides a new approach for the design of excellent EMA materials for practical applications.

Differential Co-release of Two Neurotransmitters from a Vesicle Fusion Pore in Mammalian Adrenal Chromaffin Cells.

Co-release of multiple neurotransmitters from secretory vesicles is common in neurons and neuroendocrine cells. However, whether and how the transmitters co-released from a single vesicle are differentially regulated remains unknown. In matrix-containing dense-core vesicles (DCVs) in chromaffin cells, there are two modes of catecholamine (CA) release from a single DCV: quantal and sub-quantal. By combining two microelectrodes to simultaneously record co-release of the native CA and ATP from a DCV, we report that (1) CA and ATP were co-released during a DCV fusion; (2) during kiss-and-run (KAR) fusion, the co-released CA was sub-quantal, whereas the co-released ATP was quantal; and (3) knockdown and knockout of the DCV matrix led to quantal co-release of both CA and ATP even in KAR mode. These findings strongly imply that, in contrast to sub-quantal CA release in chromaffin cells, fast synaptic transmission without transmitter-matrix binding is mediated exclusively via quantal release in neurons.

Stretch-induced Ca2+ independent ATP release in hippocampal astrocytes.

KEY POINTS: Similar to neurons, astrocytes actively participate in synaptic transmission via releasing gliotransmitters. The Ca2+ -dependent release of gliotransmitters includes glutamate and ATP. Following an 'on-cell-like' mechanical stimulus to a single astrocyte, Ca2+ independent single, large, non-quantal, ATP release occurs. Astrocytic ATP release is inhibited by either selective antagonist treatment or genetic knockdown of P2X7 receptor channels. Our work suggests that ATP can be released from astrocytes via two independent pathways in hippocampal astrocytes; in addition to the known Ca2+ -dependent vesicular release, larger non-quantal ATP release depends on P2X7 channels following mechanical stretch. ABSTRACT: Astrocytic ATP release is essential for brain functions such as synaptic long-term potentiation for learning and memory. However, whether and how ATP is released via exocytosis remains hotly debated. All previous studies of non-vesicular ATP release have used indirect assays. By contrast, two recent studies report vesicular ATP release using more direct assays. In the present study, using patch clamped 'ATP-sniffer cells', we re-investigated astrocytic ATP release at single-vesicle resolution in hippocampal astrocytes. Following an 'on-cell-like' mechanical stimulus of a single astrocyte, a Ca2+ independent single large non-quantal ATP release occurred, in contrast to the Ca2+ -dependent multiple small quantal ATP release in a chromaffin cell. The mechanical stimulation-induced ATP release from an astrocyte was inhibited by either exposure to a selective antagonist or genetic knockdown of P2X7 receptor channels. Functional P2X7 channels were expressed in astrocytes in hippocampal brain slices. Thus, in addition to small quantal ATP release, larger non-quantal ATP release depends on P2X7 channels in astrocytes.

Calcium triggers exocytosis from two types of organelles in a single astrocyte.

Astrocytes release a variety of signaling molecules including glutamate, D-serine, and ATP in a regulated manner. Although the functions of these molecules, from regulating synaptic transmission to controlling specific behavior, are well documented, the identity of their cellular compartment(s) is still unclear. Here we set out to study vesicular exocytosis and glutamate release in mouse hippocampal astrocytes. We found that small vesicles and lysosomes coexisted in the same freshly isolated or cultured astrocytes. Both small vesicles and lysosome fused with the plasma membrane in the same astrocytes in a Ca(2+)-regulated manner, although small vesicles were exocytosed more efficiently than lysosomes. Blockade of the vesicle glutamate transporter or cleavage of synaptobrevin 2 and cellubrevin (both are vesicle-associated membrane proteins) with a clostridial toxin greatly inhibited glutamate release from astrocytes, while lysosome exocytosis remained intact. Thus, both small vesicles and lysosomes contribute to Ca(2+)-dependent vesicular exocytosis, and small vesicles support glutamate release from astrocytes.

Glutamate release through connexin 43 by cultured astrocytes in a stimulated hypertonicity model.

We investigated the role of connexin 43 (Cx43) hemichannels in the release of glutamate by astrocytes after hypertonic stimulus. Mechanical, osmotic and oxidative stress, and changes in the extracellular or intracellular Ca(2+) levels induce connexin hemichannels located in the plasma membrane to open and release small ions and molecules with signaling potential such as glutamate, ATP, etc. In our past studies, we primarily found that acute hypertonic stimulus induced the release of glutamate. Since glutamate release was involved with several routes, we studied its release routes by astrocytes incubated in a hypertonic media for various periods. The glutamate release was increased after hypertonic stimulus. Glutamate release in hypertonic stimulus was inhibited by gap junction or Cx43 hemichannel blockers, but not by antagonists of purinergic receptor (P2XnR), glutamate transport inhibitors, intracellular Ca(2+) blockers, and pannexin 1(Panx1) hemichannel. The results suggest that glutamate release by the Cx43 hemichannels is likely to feature in the response of cultured astrocytes to hypertonic stimulus.

Effects of vagotomy, splanchnic nerve lesion, and fluorocitrate on the transmission of acute hyperosmotic stress signals to the supraoptic nucleus.

The response to hyperosmotic stresses in the abdominal cavity is regulated, in part, by vasopressin (VP)-secreting neurons in the supraoptic nucleus (SON). How osmotic stress signals are transmitted to the brain is incompletely understood, and whether the transmission routes for osmotic stress signals differ between acute and chronic stresses is unknown. Here we investigated the role of the vagus, splanchnic nerves, and astrocytes in the SON in transducing acute hyperosmotic-stress signals from the abdominal cavity. We found that acute administration of hyperosmotic saline triggered the activation of neurons as well as astrocytes in the SON and the adjoining ventral glia limitans (SON-VGL). Severing the subdiaphragmatic vagal nerve (SDV) prevented the normal response of cells in the SON to HS treatment and attenuated the release of VP into the bloodstream. Lesioning the splanchnic nerves (SNL) diminished HS-induced release of VP, but to a much lesser extent than SDV. Furthermore, SNL did not significantly affect the up-regulation of Fos in SON neurons or the up-regulation of Fos and GFAP in SON and SON-VGL astrocytes that normally occurred in response to HS and did not affect HS-induced expansion of the SON-VGL. Inhibiting astrocytes with fluorocitrate (FCA) prevented the response of the SON to HS and attenuated the release of VP, similarly to SDV surgery. These results suggest that the vagus is the principle route for the transmission of hyperosmotic signals to the brain and that astrocytes in the SON region are necessary for the activation of SON neurons and the release of VP into the bloodstream.

Acute hyperosmotic stimulus-induced Fos expression in neurons depends on activation of astrocytes in the supraoptic nucleus of rats.

Acute hyperosmolarity induced a time-dependent expression of Fos protein in both neurons and astrocytes of the rat supraoptic nucleus, with peak Fos expression occurring at 45 min in astrocytes and at 90 min in neurons after hypertonic stimulation in vivo. To determine whether the two cell types were activated separately or in an integrated manner, animals were pretreated with fluorocitrate, a glial metabolic blocker or carbenoxolone, a gap junction blocker followed by an acute hypertonic stimulation similar to that of the controls. Antibodies against glial fibrillary acidic protein, connexin 43, vasopressin, and oxytocin were used in serial sections to identify the cellular elements of the supraoptic nucleus. It was found that interruption of astrocyte metabolism with fluorocitrate significantly reduced Fos protein expression in both astrocytes and neurons, whereas blockage of gap junctions with carbenoxolone clearly reduced Fos protein expression in neurons, but not in astrocytes. These results indicate that both neurons and astrocytes in the rat supraoptic nucleus are involved in regulating osmolarity. Astrocytes are activated first, whereas connexin 43 functional hemichannels in SON astrocytes are required for the subsequent activation of the neurons.

Hypertonic stimulation induces synthesis and release of glutamate in cultured rat hypothalamic astrocytes and C6 cells.

OBJECTIVE: To investigate whether hypertonic saline (HS) can induce the synthesis and release of glutamate in cultured hypothalamic astrocytes or C6 cell line. METHODS: Astrocytes were isolated, cultured, purified and identified from the hypothalamus of newborn rat (1 day). The astrocytes were randomly divided into five groups: isotonic (IS) and HS groups, astrocytes were incubated by IS and HS (320 mosM NaCl) medium, respectively, for 1, 3, 5, 10 or 15 min; carbenoxolone (CBX)+IS and CBX+HS groups, astrocytes were pre-treated with CBX (100 mmol/L) for 1 h at 37 degrees C in a 5% CO(2) / 95% atmosphere, then removed to IS and HS medium, respectively, for 1, 3, 5, 10 or 15 min; Ca(2+)+HS group, astrocytes were pre-incubated with Ca Ca(2+) (1,000 micromol/L) for 1 h at 37 degrees C in a 5% CO(2) / 95% atmosphere, followed by a wash with isotonic FBS/DMEM, and then removed to hypertonic saline for 1, 3, 5, 10 or 15 min. The media of five groups were collected to analyze the medium glutamate concentration with high performance liquid chromatography. The astrocytes were fixed and double immunofluorescent stained with anti-glial fibrillary acidic protein (GFAP) and anti-glutamate. The C6 cells were divided into four groups: IS, HS, CBX+IS and CBX+HS groups, and used for quantitative measurement of glutamate in cells by flow cytometry (FCM). RESULTS: (1) Anti-GFAP immunofluorescent signal revealed no significant difference among various time points in each group, or among the five groups. (2) The anti-glutamate immunofluorescent signal was increased in HS group and peaked at 5 min, and decreased and returned to the level of IS group at 15 min (P < 0.01 vs the 5 min of HS group). In CBX+HS group, the glutamate intensity was higher than that in CBX+IS and HS groups. (3) The medium glutamate concentration had no change after treatment with HS for 1 and 3 min, while increased markedly after treatment for 5 min to 15 min (P< 0.01 vs 1 min and 3 min). On the contrary, the medium glutamate concentrations in the CBX+HS or Ca(2+)+HS group were significant lower than that in the HS group (P < 0.01). (4) FCM showed HS and CBX+HS induced glutamate increase in C6 cells. CONCLUSION: HS induced cultured rat hypothalamic astrocytes or C6 cells to synthesize and release glutamate; CBX could block glutamate release, but could not disrupt glutamate synthesis.

Blocking the glial function suppresses subcutaneous formalin-induced nociceptive behavior in the rat.

This study examined whether glial cells in the trigeminal nucleus caudalis (Sp5C) were necessary for orofacial nociception and nociceptive processing induced by subcutaneously (s.c.) injection of 5% formalin into left mystacial vibrissae. The immunohistochemical, immunoelectron microscopical methods and behavior assessment were used in this study. Two hours after administration of carbenoxolone (CBX, a gap junction blocker) or fluorocistrate (FCA, a glail metabolic inhibitor) into the cerebellomedullary cistern, the nociceptive behavior and scratching-cumulative time reduced significantly (P<0.01). FCA attenuated obviously the expression of Fos/NeuN-immunoreactive (-IR) neurons (mean+/-S.E.M.=29+/-2.5) and Fos/glial fibrillary acidic protein (GFAP)-IR astrocytes (7.2+/-2.2) in Sp5C. CBX decreased the number of Fos/NeuN-IR neurons (25+/-1.7), but did not affect Fos/GFAP-IR astrocytes (16.2+/-5.4), compared with vehicle-preadministered rats (Fos/NeuN-IR neurons 135+/-4.2, and Fos/GFAP-IR astrocytes 25.8+/-4). Immunoelectron microscopy established that Cx32/Cx43 heterotypic gap junctions (HGJs) were present on junction areas between astrocytes and neurons within Sp5C. The number of HGJs increased significantly following formalin s.c. injection. It suggests that the Sp5C astrocytes may play an active regulating role in orofacial nociception via Cx32/Cx43 HGJs between astrocytes and neurons of Sp5C.

"Kiss-and-run" exocytosis in astrocytes.

Neurons and glia are the principal cellular components of the nervous system. Although the glia are 10 times more numerous than neurons, until recently they were thought to be passive cells that monitor and support the active neurons by taking up used neurotransmitters from the synapses. In the past few years, this concept has been challenged by the findings that Ca(2+) waves spread from one astrocyte to another via Ca(2+)-and SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor)-dependent gliotransmitter release in pure cultures of astrocytes, raising the possibility that glia are not so passive as previously thought. This hypothesis was further advanced by two recent reports, which demonstrated that astrocytes release glutamate via vesicular exocytosis in response to stimuli. The kinetics of single vesicle exocytosis is distinct from its neural equivalent, because in response to physiological stimulation, gliotransmitter release is exclusively in the mode of "kiss and run." These advances were made possible by newly available techniques for single vesicle recordings, which will also be briefly reviewed here.

The lumbar spinal cord glial cells actively modulate subcutaneous formalin induced hyperalgesia in the rat.

We investigated the response and relationship of glial cells and neurons in lumbar spinal cord to hyperalgesia induced by the unilateral subcutaneous formalin injection into the hindpaw of rats. It was demonstrated that Fos/NeuN immunoreactive (-IR) neurons, glial fibrillary acidic protein (GFAP)-IR astrocytes and OX42-IR microglia were distributed in dorsal horn of lumbar spinal cord, predominantly in the superficial layer. In the time-course studies, GFAP-IR astrocytes were firstly detected, OX42-IR microglia were sequentially observed, Fos/NeuN-IR neurons were found slightly late. Immunoelectron microscopy studies established that many heterotypic gap junctions (HGJs), which consisting of Cx43-IR astrocytic process on one side and Cx32-IR dendrite on the other side, were present in superficial layer of dorsal horn. Ninety-one HGJs were found in 100 areas of experimental rats and occupied 91%, while only 39% HGJs were found in control rats. In experimental rats pretreated with intrathecal (i.t.) application of the carbenoxolone (a gap junction blocker) or fluorocitrate (a glial metabolic inhibitor), the paw withdrawal thermal latency was prolonged than those application of the sterile saline (i.t.). It suggests that spinal cord glial cells may play an important role for modulation of hyperalgesia induced by noxious stimuli through HGJs which located between astrocytes and neurons.