Supervise-Assisted Self-Supervised Deep-Learning Method for Hyperspectral Image Restoration.

Hyperspectral image (HSI) restoration is a challenging research area, covering a variety of inverse problems. Previous works have shown the great success of deep learning in HSI restoration. However, facing the problem of distribution gaps between training HSIs and target HSI, those data-driven methods falter in delivering satisfactory outcomes for the target HSIs. In addition, the degradation process of HSIs is usually disturbed by noise, which is not well taken into account in existing restoration methods. The existence of noise further exacerbates the dissimilarities within the data, rendering it challenging to attain desirable results without an appropriate learning approach. To track these issues, in this article, we propose a supervise-assisted self-supervised deep-learning method to restore noisy degraded HSIs. Initially, we facilitate the restoration network to acquire a generalized prior through supervised learning from extensive training datasets. Then, the self-supervised learning stage is employed and utilizes the specific prior of the target HSI. Particularly, to restore clean HSIs during the self-supervised learning stage from noisy degraded HSIs, we introduce a noise-adaptive loss function that leverages inner statistics of noisy degraded HSIs for restoration. The proposed noise-adaptive loss consists of Stein's unbiased risk estimator (SURE) and total variation (TV) regularizer and fine-tunes the network with the presence of noise. We demonstrate through experiments on different HSI tasks, including denoising, compressive sensing, super-resolution, and inpainting, that our method outperforms state-of-the-art methods on benchmarks under quantitative metrics and visual quality. The code is available at https://github.com/ying-fu/SSDL-HSI.

Electrocatalysis Boosts the Methanol Thermocatalytic Dehydrogenation for High-Purity H2 and CO Production.

Hydrogen production from methanol represents an energy-sustainable way to produce ethanol, but it normally results in heavy CO2 emissions. The selective conversion of methanol into H2 and valuable chemical feedstocks offers a promising strategy; however, it is limited by the harsh operating conditions and low conversion efficiency. Herein, we realize efficient high-purity H2 and CO production from methanol by coupling the thermocatalytic methanol dehydrogenation with electrocatalytic hydrogen oxidation on a bifunctional Ru/C catalyst. Electrocatalysis enables the acceleration of C-H cleavage and reduces the partial pressure of hydrogen at the anode, which drives the chemical equilibrium and significantly enhances methanol dehydrogenation. Furthermore, a bilayer Ru/C + Pd/C electrode is designed to mitigate CO poisoning and facilitate hydrogen oxidation. As a result, a high yield of H2 (558.54 mmol h-1 g-1) with high purity (99.9%) was achieved by integrating an applied cell voltage of 0.4 V at 200 °C, superior to the conventional thermal and electrocatalytic processes, and CO is the main product at the anode. This work presents a new avenue for efficient H2 production together with valuable chemical synthesis from methanol.

Efficient Low-temperature Hydrogen Production by Electrochemical-assisted Methanol Steam Reforming.

Methanol steam reforming (MSR) provides an alternative way for efficient production and safe transportation of hydrogen but requires harsh conditions and complicated purification processes. In this work, an efficient electrochemical-assisted MSR reaction for pure H2 production at lower temperature (~140 °C) is developed by coupling the electrocatalysis reaction into the MSR in a polymer electrolyte membrane electrolysis reactor. By electrochemically assisted, the two critical steps including the methanol dehydrogenation and water-gas shift reaction are accelerated, which is attributed to decreasing the methanol dehydrogenation energy and promoting the dissociation of H2 O to OH* by the applied potential. Furthermore, the reduced H2 partial pressure by the hydrogen oxidation and reduction process further promotes MSR. The combination of these advantages not only efficiently decreases the MSR temperature but also achieves the high rate of hydrogen production of 505 mmol H2 g Pt -1 h-1 with exceptionally high H2 selectivity (99 %) at 180 °C and a low voltage (0.4 V), and the productivity is about 30-fold than that of traditional MSR. This study opens up a new avenue to design novel electrolysis cells for hydrogen production.

Combined Ganoderma lucidum polysaccharide and ciprofloxacin therapy alleviates Salmonella enterica infection, protects the intestinal barrier, and regulates gut microbiota.

Clinical antibiotics used worldwide could diminish the intestinal barrier, enhance contact with microbiota and intestinal immune cells, and induce inflammation. We found that ciprofloxacin treatment of Salmonella enterica serovar Typhimurium infection resulted in the destruction of the intestinal barrier, with decreased concentrations of MUC2, ZO-1, and occludin in the jejunum and colon. Ganoderma lucidum ethanol extracts (GLE), as a prebiotic food extract, significantly decreased inflammation-related enzymes, including COX-2, MPO, and iNOS, and pro-inflammatory cytokines (IL-6, IL-1ß, IL-17, and TNF-α), and protected the intestinal barrier by increasing the concentration of MUC2, ZO-1, and occludin. Meanwhile it significantly increased the abundances of Salmonella, Parabacteroides, Acinetobacter, Enterococcus, and Escherichia-Shigella, which increased the risk of pathogenic bacterial infections. Prebiotic G. lucidum polysaccharide (GLP) provided a significant intestinal barrier, improving the concentration of ZO-1, occludin, and MUC2 in the colon and jejunum. The synergistic effects of GLP and ciprofloxacin were hypothesized to reverse the negative effects resulting from ciprofloxacin alone, as the concentrations of ZO-1, occludin, and MUC2 were significantly increased in the jejunum and colon, especially in the colon. Also, the synergistic effect increased the abundances of probiotic bacteria Lachnospiraceae NK4A136, Ruminococcaceae UGG-014, Lactobacillus, and Parabacteroides. In conclusion, combined GLP and ciprofloxacin therapy against Salmonella infection alleviated the side effects resulting from the clinical application of the antibiotic alone, and increased the probiotic bacterial population.

A Low-Protein, High-Carbohydrate Diet Exerts a Neuroprotective Effect on Mice with 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson's Disease by Regulating the Microbiota-Metabolite-Brain Axis and Fibroblast Growth Factor 21.

Parkinson's disease (PD) is closely linked to lifestyle factors, particularly dietary patterns, which have attracted interest as potential disease-modifying factors. Eating a low-protein, high-carbohydrate (LPHC) diet is a promising dietary intervention against brain aging; however, its protective effect on PD remains elusive. Here, we found that an LPHC diet ameliorated 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-induced motor deficits, decreased dopaminergic neuronal death, and increased the levels of striatal dopamine, serotonin, and their metabolites in PD mice. Levels of fibroblast growth factor 21 (FGF-21), a member of the fibroblast growth factor family, were elevated in PD mice following LPHC treatment. Furthermore, the administration of FGF-21 exerted a protective effect on MPTP-induced PC12 cells, similar to the effect of an LPHC diet in MPTP-induced mice. Sequencing of the 16S rDNA from fecal microbiota revealed that an LPHC diet normalized the gut bacterial composition imbalance in PD mice, as evidenced by the increased abundance of the genera Bifidobacterium, Ileibacterium, Turicibacter, and Blautia and decreased abundance of Bilophila, Alistipes, and Bacteroides. PICRUSt-predicted fecal microbiome function revealed that an LPHC diet suppressed lipopolysaccharide biosynthesis and the citrate cycle (TCA cycle), biosynthesis of ubiquinone and other terpenoid-quinones, and oxidative phosphorylation pathways caused by MPTP, and enhanced the biosynthesis of amino acids, carbohydrate metabolism, and biosynthesis of other secondary metabolites. A nonmetabolomic analysis of the serum and feces showed that an LPHC diet significantly increased the levels of aromatic amino acids (AAAs), including tryptophan, tyrosine, and phenylalanine. In addition, an LPHC diet elevated the serum concentrations of bile acids (BAs), particularly tauroursodeoxycholic acid (TUDCA) and taurine. Collectively, our current findings point to the potential mechanism of administering an LPHC diet in attenuating movement impairments in MPTP-induced PD mice, with AAAs, microbial metabolites (TUDCA and taurine), and FGF-21 as key mediators along the gut-microbiota-brain axis.

Effect of water-soluble polysaccharides from Morchella esculenta on high-fat diet-induced obese mice: changes in gut microbiota and metabolic functions.

Morchella esculenta polysaccharides exhibit numerous probiotic activities, but their regulatory effects on the gut microbiota are unclear. This study was conducted to explore whether M. esculenta polysaccharides can regulate dysbacteriosis caused by a high-fat diet and relieve obesity. We extracted a water-soluble polysaccharide from M. esculenta (MPF, purity: 96.19%, consisting of 55.97% glucose, 9.63% xylose, and 22% mannose) that reduces mouse fat accumulation, alleviates obesity, and relieves liver injury, after 90 days of high-fat diet intake. This polysaccharide reversed dysbiosis and regulated the abundance of gut microbiota caused by a high-fat diet (restoring the ratio of Firmicutes/Bacteroidetes and changing the abundances of Lactobacillus, Dubosiella, and Faecalibaculum), increasing short-chain fatty acids and decreasing gene expression in the liver (glucose 6-phosphatase, glucose transporter 1, peroxisome proliferator-activated receptor gamma (PPAR) receptor-1α, PPARα, PPARγ, and CCAAT enhancer binding protein α). We identified a regulatory relationship between polysaccharides, gut microbiota, and the liver as a potential mechanism by which polysaccharides can alleviate obesity.

Pt-Based Rare Earth Alloy as Efficient and Robust Electrocatalyst for High-Temperature Proton Exchange Membrane Fuel Cells.

High-temperature proton exchange membrane fuel cells (HT-PEMFCs) are crucial in future energy systems. However, the activity and stability of the electrocatalysts are severely restricted by high temperature and phosphoric acid poisoning. Herein, PtCe alloy as oxygen reduction reaction (ORR) electrocatalyst for HT-PEMFCs exhibits fantastic performance. Ce can increase the electronic density of Pt, weakening phosphoric acid poisoning and improving ORR activity. The optimized electronic structure can also reduce the dipole effect between Pt and O, which suppresses the irreversible oxidation of Pt. Additionally, the dramatically negative heat of formation in PtCe catalyst brings high kinetic barrier of metal diffusion and dissolution. With this electrocatalyst, the HT-PEMFCs show a preeminent peak power of 605 mW cm-2 with 0.3 mgPt cm-2 . After 30000 cycles of accelerated stability test, the peak power density only decreases by 31.6%, achieving the goal of Department of Energy in 2020 (<40% loss).

Durable High-Temperature Proton Exchange Membrane Fuel Cells Enabled by the Working-Temperature-Matching Palladium-Hydrogen Buffer Layer.

The durability degradation during stack-operating conditions seriously deteriorates the lifetime and performance of the fuel cell. To alleviate the rapid potential rise and performance degradation, an anode design is proposed to match the working temperature of high-temperature proton exchange membrane fuel cells (HT-PEMFCs) with the release temperature of hydrogen from palladium. The result is significantly enhanced hydrogen oxidation reaction (HOR) activity of Pd and superior performance of the Pd anode. Furthermore, Pd as hydrogen buffer and oxygen absorbent layer in the anode can provide additional in situ hydrogen and absorb infiltrated oxygen during local fuel starvation to maintain HOR and suppress reverse-current degradation. Compared with the traditional Pt/C anode, the Pd/C also greatly improved HT-PEMFCs durability during start-up/shut-down and current mutation. The storage/release of hydrogen provides innovative guidance for improving the durability of PEMFCs.

Ganoderma lucidum Ethanol Extraction Promotes Dextran Sulphate Sodium Induced Colitis Recovery and Modulation in Microbiota.

Popular edible mushrooms Ganoderma lucidum and Gloeostereum incarnatum can improve physical health as a prebiotic and positively alter intestinal microbiota. Our research investigated the prebiotic effects of Ganoderma lucidum and Gloeostereum incarnatum on colon inflammation through G. lucidum water extraction polysaccharides (GLP), G. incarnatum water extraction polysaccharides (GIP), G. lucidum ethanol extraction (GLE), and G. incarnatum ethanol extraction (GIE) administered in mice after 7 days of dextran sulphate sodium (DSS) administration. Among the extracts, GLE showed reduced mortality rates, prevention of weight loss, mitigated colon length shortening, and decreased disease activity indices and histological scores. COX-2, MPO, and iNOS activities and the inflammatory cytokines' expressions were determined to demonstrate the inhibition inflammation by GLE. Meanwhile, GLE upregulated the levels of MUC2, ZO-1, claudin-3, and occluding to protect the intestinal barrier. Furthermore, GLE modulated the composition of gut microbiota disturbed by DSS, as it decreased the abundance of Bacteroides, Staphylococcus, and Escherichia_Shigella, and increased Turicibacter and Bifidobacterium. Through cell experiment, GLE had a positive influence on adherens junction, tight junction, and TRAF6/MyD88/NF-κB signaling pathways. In conclusion, GLE supplementation promotes DSS-induced colitis recovery by regulating inflammatory cytokines, preserving the intestinal mucosal barrier, positively modulating microbiota changes, and positively influences immune response in TRAF6/MyD88/NF-κB signaling pathways.

Genome-wide association study for wattles trait in the dairy goat breed.

Dairy goats are significant livestock that provide high-quality milk sources in the world. The wattles trait is an evident phenotypic character on the neck of a dairy goat, which is considered to be under genetic control. We collected samples of 189 dairy goats, including 94 with wattles and 95 without wattles, from four different farms and multiple dairy goat breeds. The samples were genotyped with the GeneSeek Genomic Profiler Goat 70 K SNP chip. Genome-wide association studies (GWAS) in wattles have identified associations with single nucleotide polymorphisms (SNPs) at chromosome 10. In this area, an extremely strong association locus was assigned to FMN1 (Formin 1) belongs to the formin homology family and is associated with limb deformity, other candidate genes of interest confirmed for wattles were ARHGAP11A (Rho GTPase Activating Protein 11 A) and GJD2 (Gap Junction Protein Delta 2). Meanwhile, we found the presence or absence of wattles had no significant effect on milk yield. This research will provide genetic resources useful to explore genetic factors affecting the trait.

Ganoderma applanatum polysaccharides and ethanol extracts promote the recovery of colitis through intestinal barrier protection and gut microbiota modulations.

Inflammatory bowel disease is associated with intestinal homeostasis dysregulation and gut microbiota dysbiosis. This study aimed to investigate the protective effect of Ganoderma applanatum extracts (G. applanatum polysaccharides (GAP) and 75% ethanol extracts (GAE)) on colon inflammation and elucidate the therapeutic mechanism. GAP and GAE showed considerable protective effects against dextran sodium sulfate (DSS)-induced colitis, as demonstrated by reduced mortality, body weight, disease activity index score, colon length, and histological score. Through GAP and GAE administration, the destroyed intestinal barrier recovered to normal, as did intestinal inflammation. We also confirmed that GAP administration promoted the recovery of colitis in a gut microbiota-dependent manner. The similarity between GAP and GAE administration was that they both altered the disordered gut microbiota damaged by DSS, exhibiting reduced abundance of Escherichia_Shigella, Enterococcus, and Staphylococcus, but the modulation of the gut microbiota was distinct between GAP and GAE.

Behavioral disorders caused by nonylphenol and strategies for protection.

Nonylphenol (NP) is widely used in daily production and life due to its good emulsification. In this review, we discuss toxicology studies that examined behavioral disorders caused by NP, the corresponding toxicological mechanisms in the central nervous system (CNS), and strategies for protection. Available in vitro and in vivo evidence suggests that exposure to NP during adulthood or early childhood is associated with cognitive dysfunction, including depression-like behaviors, anxiety-like behaviors, and impaired learning and memory. The main mechanisms underlying NP-related cognitive disorders include inflammation, destruction of synaptic plasticity, and destruction of important signaling pathways that affect the synthesis and secretion of neurotransmitters. The effects and mechanisms of NP exposure on CNS-mediated reproductive function, including interference with the expression of hormones, proteins, and enzymes, are discussed. Other abnormal behaviors such as locomotor activity and swimming behavior are also described. Several measures to prevent NP neurotoxicity are summarized. These measures are based on the toxicological mechanisms underlying NP exposure and include external protection and internal self-regulation of the nervous system. Finally, a new treatment idea is proposed based on the gut-brain axis. Characterizing the behavioral changes and underlying toxicity mechanisms associated with NP exposure and investigating the possible methods of treatment will help to expand the understanding of these mechanisms and could lead to more effective treatments.

Plant productivity and microbial composition drive soil carbon and nitrogen sequestrations following cropland abandonment.

Understanding the variations in soil organic carbon (SOC) and total nitrogen (STN) stocks in the different ages of abandoned cropland ecosystems of different ages is essential for land use decisions to maximize C sinks or improve ecosystem services. However, knowledge of the dynamics of SOC and STN stocks and their controlling factors after cropland abandonment is limited. Thus, this study investigated the changes in the SOC and STN stocks of loessal soil (Calcaric Regosols) with a chronosequence of 3, 8, 13, 18, 23 and 30 years following cropland abandonment on the Loess Plateau. As a whole, we examined 42 field plots and implemented multivariable linear regression analysis (MLRA) and structural equation modeling (SEM) using 22 influencing variables related to plant, soil and microbial properties to quantify the controls of SOC and STN stocks. The results revealed that SOC and STN stocks significantly increased after cropland abandonment for 30 years, and there were minor decreases in C and N sequestrations in the early restoration stage (<18 years). The SOC and STN changes had significant positive correlations, in which that exhibited STN stocks shifted concurrently with the rate of relative SOC stock changes. The MLRA models demonstrated that the SOC stocks were primarily controlled by aboveground biomass, STN, fungi, and the ratio of fungi to bacteria, while STN stocks were mainly driven by root biomass, above-ground biomass, STN, fungi and the ratio of fungi to bacteria after cropland abandonment. The SEM models further demonstrated that plant productivity not only directly determined the variations in SOC and STN stocks but also changed the microbial community following post-cropland restoration. These results suggest that long-term (>18 years) cropland abandonment can be a successful approach for reinstating SOC and STN stocks, while plants and microbes together mediate microbial C and N stocks during vegetation succession in a semiarid region.

Effects of 3-benzidino-6-phenylpyridazine, as an acetylcholinesterase inhibitor, on outward potassium current in acutely isolated rat hippocampal pyramidal neurons.

As an acetylcholinesterase (AChE) inhibitor, the effects of 3-benzidino-6-phenylpyridazine (BPP) on outward potassium current including delayed rectifier potassium current (I(K(DR))) and transient outward potassium current (I(K(A))) in acutely isolated rat hippocampal pyramidal neurons were studied, using the whole cell patch-clamp technique. BPP reversibly inhibited electric eel AChE as an inhibitor, with IC(50) of 1.43 microM. BPP (0.10-100 microM) decreased I(K(DR)) and I(K(A)) in a concentration-dependent, voltage-independent and partial reversible manner, with IC(50) of 0.47 and 0.31 microM, respectively. 10 microM BPP did not affect steady-state activation of I(K(DR)) and I(K(A)). In addition, 10 microM BPP shifted the voltage dependence of steady-state inactivation of I(K(A)) towards negative potential. In conclusion, BPP potently inhibits I(K(DR)) and I(K(A)) in rat hippocampal pyramidal neurons, which may contribute to BPP's restoring the damaged central nervous system.

3-Benzidino-6(4-chlorophenyl) pyridazine blocks delayed rectifier and transient outward potassium current in acutely isolated rat hippocampal pyramidal neurons.

3-[(beta-morpholinoethyl)amino]-4-methyl-6-phenylpyridazine (minaprine) is an acetylcholinesterase (AChE) inhibitor. 3-Benzidino-6(4-chlorophenyl) pyridazine (BCP) and minaprine have a central pyridazine ring in common. In this study, we investigated the effects of BCP on delayed rectifier potassium current (IK(DR)) and transient outward potassium current (IK(A)) in acutely isolated rat hippocampal pyramidal neurons by using whole-cell patch-clamp technique. IK(DR) and IK(A) were inhibited by BCP (0.01-500 microM) in a concentration-dependent and voltage-dependent manner. The IC50 value for the blocking action of BCP on IK(DR) and IK(A) was calculated as 7.13+/-0.18 microM and 0.55+/-0.11 microM, respectively. At the concentration of 10 microM, BCP shifted the activation curve of IK(DR) to positive potential by 29.09 mV. Meanwhile, at the concentration of 10 microM, BCP also shifted the activation and inactivation curve of IK(A) to positive potential by 34.18 and 22.47 mV, respectively. In conclusion, BCP potently inhibits IK(DR) and IK(A) in rat hippocampal pyramidal neurons.