Aqueous batteries: from laboratory to market.

This perspective discusses the fundamental benefits and drawbacks of aqueous batteries and the challenges of the development of such battery technology from laboratory scale to industrial applications.

Boosting Output Performance of Sliding Mode Triboelectric Nanogenerator by Shielding Layer and Shrouded-Tribo-Area Optimized Ternary Electrification Layered Architecture.

Sliding mode triboelectric nanogenerator (S-TENG) is effective for low-frequency mechanical energy harvesting owing to their more efficient mechanical energy extraction capability and easy packaging. Ternary electrification layered (TEL) architecture is proven useful for improving the output performance of S-TENG. However, the bottleneck of electric output is the air breakdown on the interface of tribo-layers, which seriously restricts its further improvement. Herein, a strategy is adopted by designing a shielding layer to prevent air breakdown on the central surface of tribo-layers. And the negative effects of air breakdown on the edge of sliding layer are averted by increasing the shrouded area of tribo-layers on slider. Output charge of this shielding-layer and shrouded-tribo-area optimized ternary electrification layered triboelectric nanogenerator (SS-TEL-TENG) achieves 3.59-fold enhancement of traditional S-TENG and 1.76-fold enhancement of TEL-TENG. Furthermore, even at a very low speed of 30 rpm, output charge, current, and average power of the rotation-type SS-TEL-TENG reach 4.15 µC, 74.9 µA, and 25.4 mW (2.05 W m-2 Hz-1 ), respectively. With such high-power output, 4248 LEDs can be lighted brightly by SS-TEL-TENG directly. The high-performance SS-TEL-TENG demonstrated in this work will have great applications for powering ubiquitous sensor network in the Internet of Things (IoT).

Cypermethrin and/or sulfamethoxazole exposure effect on apoptosis and endoplasmic reticulum of grass carp cardiomyocyte.

With the soar use range of pesticides and antibiotics in agricultural production, the pollution of surrounding runoff has become more severe; thus, the health and safety of non-target species such as fish are at risk. Excessive amounts of cypermethrin (CMN, 0.651 mg/l) and sulfamethoxazole (SMZ, 0.3 mg/l) are known to trigger oxidative stress and endoplasmic reticulum stress, resulting in toxic effects on cells. The damage degree of poisons on grass carp and the effect of the corresponding axis pathway PERK/eif2α/CHOP are still unknown. Therefore, our study set up two single poison groups (CMN/SMZ) and a combined poison group (CMN&SMZ) to detect this pathway and related indicators. After detection, the content of MDA both in CMN and SMZ group myocardium tissue was increased, while the SOD, CAT activity and GSH levels were decreased. Apoptosis-related genes (Bax, PUMA, P53 and Caspase-3/9), inflammation-related genes (TNF-α, iNOS and IL-1ß/6/8), ER stress pathway PERK/eif2α/CHOP and related genes (ATF6, IRE1a and GRP78) were all increased; in contrast, the anti-apoptotic gene Bcl-2 was down-regulated. From the overall trend observation, the apoptosis proportion of cardiomyocytes in the combined poison group was higher than that of the single poison. In summary, this study shows that CMZ and SMZ can induce oxidative stress and subsequent ER stress in grass carp cardiomyocytes by regulating the PERK/eif2α/CHOP signaling axle, thereby inducing apoptosis, and followed by inflammatory responses. The combined effect of the CMZ and SMZ mixture was severer than that of a single poison (CMZ or SMZ), so it can be inferred that the damage degree of grass carp myocardium tissue would be aggravated with the appearance of CMZ or/and SMZ. The experimental results of this study have suggestions and warnings for the toxicological research of CMZ and SMZ and the management of industrial and ecological balance.

Arthrobacter rhizosphaerae sp. nov., isolated from wheat rhizosphere.

Gram-stain-positive, aerobic, non-spore-forming strains CCNWLXL 1-35T, CCNWLXL 12-2 and CCNWLXL 21-a, were isolated from wheat rhizosphere from Yangling, Shaanxi Province, China. Comparison of the 16S rRNA gene sequences showed that they belonged to the genus Arthrobacter and were closely related to Arthrobacter globiformis NBRC 12137T (97.95% similarity). Genomic relatedness analyses based on the average nucleotide identity and the genome-to-genome distance showed these strains constituted a single species. The major fatty acids was anteiso-C15:0. The polar lipids consist of diphosphatidylglycerol, phsophatidylethanolamine, phosphatidylglycerol, phosphatidylinositol and glycolipid. The predominant menaquinone was MK-9. The peptidoglycan type was A4α. Thus, these strains were classified as representing a novel species in the genus Arthrobacter, for which the name Arthrobacter rhizosphaerae sp. nov. is proposed. The type strain is CCNWLXL 1-35T (=JCM 34638T, =CCTCC AB 2021087T) and additional strains are CCNWLXL 12-2 (=JCM 35018, =CCTCC AB 2021546), CCNWLXL 21-a (=JCM 35019, =CCTCC AB 2021545).

Knockdown of TRIM27 alleviated sepsis-induced inflammation, apoptosis, and oxidative stress via suppressing ubiquitination of PPARγ and reducing NOX4 expression.

BACKGROUND: Sepsis is a global fatal disease and leads to severe lung injury due to dysfunction of inflammation response. TRIM27 is closely related to the diseased with dysfunction of inflammation response. The aim of this study was to clarify the role and mechanism of TRIM27 in sepsis-induced lung injury. METHODS: The lipopolysaccharide (LPS)-induced septic mouse model was successfully established. The lung injury was evaluated by lung wet/dry (W/D) ratio and hematoxylin-eosin (H&E) staining. The cell apoptosis was evaluated by TUNEL assay. The inflammatory cytokines were measured by quantitative real time-PCR (qRT-PCR) assay and commercial enzyme-linked immunosorbent assay (ELISA). The oxidative stress was assessed by the contents of superoxide dismutase (SOD) and malondialdehyde (MDA), and the expression of dihydroethidium (DHE). RESULTS: In this study, we demonstrated that TRIM27 was up-regulated in LPS-induced septic mice. In loss-of-function experiments, knockdown of TRIM27 alleviated sepsis-induced lung injury, inflammation, apoptosis, and oxidative stress. More importantly, knockdown of TRIM27 was observed to reduce p-p65/NOX4 expression via suppressing ubiquitination of PPARγ. In rescue experiments, overexpression of NOX4 abolished the effect of sh-TRIM27 on alleviating sepsis-induced inflammation, apoptosis, and oxidative stress. CONCLUSION: These findings highlighted that knockdown of TRIM27 alleviated sepsis-induced inflammation, oxidative stress and apoptosis via suppressing ubiquitination of PPARγ and reducing NOX4 expression, which supports the potential utility of TRIM27 as a therapeutic target in septic lung injury.

Deep Learning Enabled Neck Motion Detection Using a Triboelectric Nanogenerator.

The state of neck motion reflects cervical health. To detect the motion state of the human neck is of important significance to healthcare intelligence. A practical neck motion detector should be wearable, flexible, power efficient, and low cost. Here, we report such a neck motion detector comprising a self-powered triboelectric sensor group and a deep learning block. Four flexible and stretchable silicon rubber based triboelectric sensors are integrated on a neck collar. With different neck motions, these four sensors lead-out voltage signals with different amplitudes and/or directions. Thus, the combination of these four signals can represent one motion state. Significantly, a carbon-doped silicon rubber layer is attached between the neck collar and the sensors to shield the external electric field (i.e., electrical changes at the skin surface) for a far more robust identification. Furthermore, a deep learning model based on the convolutional neural network is designed to recognize 11 classes of neck motion including eight directions of bending, two directions of twisting, and one resting state with an average recognition accuracy of 92.63%. This developed neck motion detector has promising applications in neck monitoring, rehabilitation, and control.

Zinc Alleviates Arsenic-Induced Inflammation and Apoptosis in the Head Kidney of Common Carp by Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress.

Arsenic (As) pollution is ubiquitous in water, which shows immunotoxicity to aquatic organisms. As an indispensable regulator of gene transcription and enzymatic modification, zinc (Zn) may play a preventive and therapeutic effect on As toxicity. The purpose of this study was to investigate the interactions of As and Zn on the head kidney of common carp Cyprinus carpio. Herein the carp were treated alone or in combination with waterborne As3+ (2.83 mg/L) and/or Zn2+ (1 mg/L). Results suggested a head kidney-toxic effect of As exposure, which was manifested by the histopathological damage of the head kidney, elevation of nuclear translocation of pro-inflammatory nuclear factor-kappa light chain enhancer of B cells (NF-κB), and blockage of the anti-oxidative nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. The global activation of three endoplasmic reticulum (ER) stress pathways led to the execution of programmed cell death, including ER apoptosis mediated by C/EBP-homologous protein (CHOP), death receptor-mediated exogenous cell apoptosis, and the endogenous apoptosis executed by Caspases9. The combined application of Zn can significantly improve the histopathological damage of the head kidney, the imbalance of the antioxidant system, and the apoptosis outcomes due to ER stress. In conclusion, this study indicates that Zn has an antagonistic effect on the head kidney injury of common carp induced by sub-chronic As exposure. The results of this study provide basic data for the risk assessment of As accumulation in an aquatic environment and a reference for the use of Zn preparation in aquaculture.

Taxonomic Compositions and Co-occurrence Relationships of Protists in Bulk Soil and Rhizosphere of Soybean Fields in Different Regions of China.

As the main consumers of bacteria and fungi in farmed soils, protists remain poorly understood. The aim of this study was to explore protist community assembly and ecological roles in soybean fields. Here, we investigated differences in protist communities using high-throughput sequencing and their inferred potential interactions with bacteria and fungi between the bulk soil and rhizosphere compartments of three soybean cultivars collected from six ecological regions in China. Distinct protist community structures characterized the bulk soil and rhizosphere of soybean plants. A significantly higher relative abundance of phagotrophs was observed in the rhizosphere (25.1%) than in the bulk soil (11.3%). Spatial location (R 2 = 0.37-0.51) explained more of the variation in protist community structures of soybean fields than either the compartment (R 2 = 0.08-0.09) or cultivar type (R 2 = 0.02-0.03). The rhizosphere protist network (76 nodes and 414 edges) was smaller and less complex than the bulk soil network (147 nodes and 880 edges), indicating a smaller potential of niche overlap and interactions in the rhizosphere due to the increased resources in the rhizosphere. Furthermore, more inferred potential predator-prey interactions occur in the rhizosphere. We conclude that protists have a crucial ecological role to play as an integral part of microbial co-occurrence networks in soybean fields.

Paclitaxel alleviates the sepsis-induced acute kidney injury via lnc-MALAT1/miR-370-3p/HMGB1 axis.

AIMS: To investigate the effects of paclitaxel on lipopolysaccharide (LPS)-induced acute kidney injury (AKI) and its related mechanisms. MAIN METHODS: The sepsis-associated AKI was induced by LPS using HK-2 cells. Then the mRNA and protein expression levels of relevant genes in the serum of sepsis patients and HK-2 cells with LPS-induced AKI were detected by qRT-PCR and western blot analyses before and after paclitaxel treatment, respectively. Subsequently, the cell counting kit-8 (CCK-8) and flow cytometry assays were performed to estimate the effects of paclitaxel, lnc-MALAT1, miR-370-3p and HMGB1 on the proliferation and apoptosis of HK-2 cells injured by LPS. KEY FINDINGS: Lnc-MALAT1 was increased both in the serum of sepsis patients and cells injured by LPS, which could inhibit the cell proliferation, promote the cell apoptosis and increase the expression of TNF-α, IL-6 and IL-1ß caused by paclitaxel. Moreover, lnc-MALAT1 was sponged with miR-370-3p which had the inverse effects with lnc-MALAT1 in LPS induced HK-2 cells. What's more, miR-370-3p targeted HMGB1 which was induced in serum and cells of sepsis. Knockdown of miR-370-3p inhibited the expression of HMGB1 and suppressed the proliferation but promoted the apoptosis of HK-2 cells injured by LPS as well as the expression of TNF-α, IL-6 and IL-1ß. Besides, paclitaxel restrained the expression of HMGB1 via regulating lnc-MALAT1/miR-370-3p axis. SIGNIFICANCE: Paclitaxel could protect against LPS-induced AKI via the regulation of lnc-MALAT1/miR-370-3p/HMGB1 axis and the expression of TNF-α, IL-6 and IL-1ß, revealing that paclitaxel might act as a therapy drug in reducing sepsis-associated AKI.

LncRNA MIAT Promotes Inflammation and Oxidative Stress in Sepsis-Induced Cardiac Injury by Targeting miR-330-5p/TRAF6/NF-κB Axis.

Sepsis is a whole-body inflammation and main cause of death in intensive care units worldwide. We aimed to investigate the roles of lncRNA MIAT and miR-330-5p in modulating inflammatory responses and oxidative stress in lipopolysachariden (LPS)-induced septic cardiomyopathy. Serum and heart tissue were collected from in vivo septic mice model, ELISA and qRT-PCR were used to measure the expression of pro-inflammation cytokines, MIAT and miR-330-5p, respectively. The knockdown of MIAT and overexpression of miR-330-5p were conducted to assess their effects on regulating inflammation response and intracellular oxidative stress in LPS-stimulated HL-1 cells. The reactive oxygen (ROS) level, mitochondrial membrane potential (MMP), GSH/GSSH ratio, and lipid peroxidation assessment (MDA) were used to evaluate the intracellular oxidative stress. Dual-luciferase reporter assay was performed to identify the association between MIAT and miR-330-5p, TRAF6 and miR-330-5p, respectively. In septic mice, the expression of MIAT and pro-inflammation cytokines was elevated while the expression of miR-330-5p decreased. Knockdown of MIAT or overexpression of miR-330-5p restrained inflammation and oxidative stress induced by LPS in vitro; MIAT directly targeted miR-330-5p to regulate NF-κB signaling, and miR-330-5p targeted against TRAF6 to suppress the activation of NF-κB signaling. We determined that lncRNA MIAT directly binds to miR-330-5p to activate TRAF6/NF-κB signaling axis and further promotes inflammation response as well as oxidative stress in LPS-induced septic cardiomyopathy. This finding suggests the potential therapeutic role of lncRNA MIAT and miR-330-5p in LPS-induced myocardial injury.

A Cd-MOF as a fluorescent probe for highly selective, sensitive and stable detection of antibiotics in water.

Recently, the pollution and damage caused by antibiotics in water have aroused serious concerns. In this situation, it is extremely important to develop a highly effective approach to detect antibiotics in water. In this contribution, we built a Cd-MOF material with stable fluorescence properties, using bbi = 1,4-bis(2-methyl-imidazol-1-yl)butane and H2L = 1,2-phenylenediacetic acid as organic ligands and Cd(NO3)2·4H2O as the metal node. The highly selective response of this MOF probe to ceftriaxone sodium (an antibiotic) can reach up to the ppb level in water, along with a fast response time, acid and alkali resistance, and anti-interference ability.

Protective effect of polysaccharide peptide on cerebral ischemia­reperfusion injury in rats.

In the present study, the protective effects and regulatory mechanism of polysaccharide peptide (PSP) were investigated in rats with cerebral ischemia­reperfusion (IR) injury. Neuroblastoma N2a cells were divided into five groups: Negative control; IR injury; PSP low dose treatment; PSP middle dose treatment; and PSP high dose treatment. In vitro, the cell viability was detected by an MTT assay. ELISA was performed to determine the activity of lactate dehydrogenase (LDH) and caspase­3. A cerebral IR injury model in vivo was established, and hematoxylin and eosin (H&E) staining, western blotting, neurological deficit score and cerebral infarction were assessed. The cell viability was markedly improved following treatment with PSP and the activity of LDH and caspase­3 was decreased following PSP administration (P<0.05). The in vivo studies determined that the neurological deficit score and cerebral infarction volume were reduced with the concentration of PSP increasing between 150 and 250 mg/kg. The H&E staining indicated that PSP was able to protect the nerve cells against the cerebral IR injury. In addition, PSP upregulated the decreased silent information regulator protein 1, peroxisome proliferator­-activated receptor γ coactivator­1α and apoptosis regulator B­cell lymphoma 2 expression induced by cerebral IR injury. The protein expression level of caspase­3 and apoptosis regulator apoptosis regulator Bcl­2­like protein 4 was downregulated following PSP administration. These results suggested that PSP may improve nerve cell viability, enhance the neuroprotective role in cerebral IR injury and provide a novel approach for the treatment of cerebral IR injury.

The protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury.

PURPOSE: To investigate the effect of hyperbaric oxygen therapy (HBOT) on traumatic brain injury (TBI) outcome. METHODS: The modified Marmarou's weight drop device was used to generate non-lethal moderate TBI rat model, and further developed in vitro astrocytes culturing system. Then, we analyzed the expression changes of interested genes and protein by quantitative PCR and western blot. RESULTS: Multiple HBO treatments significantly reduced the expression of apoptosis promoting genes, such as c-fos, c-jun, Bax and weakened the activation of Caspase-3 in model rats. On the contrary, HBOT alleviated the decrease of anti-apoptosis gene Bcl-2 and promoted the expression of neurotrophic factors (NTFs), such as NGF, BDNF, GDNF and NT-3 in vivo. As a consequent, the neuropathogenesis was remarkably relied with HBOT. Astrocytes from TBI brain or those cultured with 21% O2 density expressed higher NTFs than that of corresponding controls, from sham brain and cultured with 7% O2, respectively. The NTFs expression was the highest in astrocytes form TBI brain and cultured with 21% O2, suggesting a synergistic effect existed between TBI and the following HBO treatment in astrocytes. CONCLUSION: Our findings provided evidence for the clinical usage of HBO treating brain damages.

The protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury

Abstract Purpose: To investigate the effect of hyperbaric oxygen therapy (HBOT) on traumatic brain injury (TBI) outcome. Methods: The modified Marmarou's weight drop device was used to generate non-lethal moderate TBI rat model, and further developed in vitro astrocytes culturing system. Then, we analyzed the expression changes of interested genes and protein by quantitative PCR and western blot. Results: Multiple HBO treatments significantly reduced the expression of apoptosis promoting genes, such as c-fos, c-jun, Bax and weakened the activation of Caspase-3 in model rats. On the contrary, HBOT alleviated the decrease of anti-apoptosis gene Bcl-2 and promoted the expression of neurotrophic factors (NTFs), such as NGF, BDNF, GDNF and NT-3 in vivo. As a consequent, the neuropathogenesis was remarkably relied with HBOT. Astrocytes from TBI brain or those cultured with 21% O2 density expressed higher NTFs than that of corresponding controls, from sham brain and cultured with 7% O2, respectively. The NTFs expression was the highest in astrocytes form TBI brain and cultured with 21% O2, suggesting a synergistic effect existed between TBI and the following HBO treatment in astrocytes. Conclusion: Our findings provided evidence for the clinical usage of HBO treating brain damages.