Ultra-high Q resonances based on zero group-velocity modes accompanied by bound states in the continuum in 2D photonic crystal slabs.

Optical resonators made of 2D photonic crystal (PhC) slabs provide efficient ways to manipulate light at the nanoscale through small group-velocity modes with low radiation losses. The resonant modes in periodic photonic lattices are predominantly limited by nonleaky guided modes at the boundary of the Brillouin zone below the light cone. Here, we propose a mechanism for ultra-high Q resonators based on the bound states in the continuum (BICs) above the light cone that have zero-group velocity (ZGV) at an arbitrary Bloch wavevector. By means of the mode expansion method, the construction and evolution of avoided crossings and Friedrich-Wintgen BICs are theoretically investigated at the same time. By tuning geometric parameters of the PhC slab, the coalescence of eigenfrequencies for a pair of BIC and ZGV modes is achieved, indicating that the waveguide modes are confined longitudinally by small group-velocity propagation and transversely by BICs. Using this mechanism, we engineer ultra-high Q nanoscale resonators that can significantly suppress the radiative losses, despite the operating frequencies above the light cone and the momenta at the generic k point. Our work suggests that the designed devices possess potential applications in low-threshold lasers and enhanced nonlinear effects.

Common alterations in parallel metabolomic profiling of serum and spinal cord and mechanistic studies on neuropathic pain following PPARα administration.

Neuropathic pain (NP) is usually treated with analgesics and symptomatic therapy with poor efficacy and numerous side effects, highlighting the urgent need for effective treatment strategies. Recent studies have reported an important role for peroxisome proliferator-activated receptor alpha (PPARα) in regulating metabolism as well as inflammatory responses. Through pain behavioral assessment, we found that activation of PPARα prevented chronic constriction injury (CCI)-induced mechanical allodynia and thermal hyperalgesia. In addition, PPARα ameliorated inflammatory cell infiltration at the injury site and decreased microglial activation, NOD-like receptor protein 3 (NLRP3) inflammasome production, and spinal dendritic spine density, as well as improved serum and spinal cord metabolic levels in mice. Administration of PPARα antagonists eliminates the analgesic effect of PPARα agonists. PPARα relieves NP by inhibiting neuroinflammation and functional synaptic plasticity as well as modulating metabolic mechanisms, suggesting that PPARα may be a potential molecular target for NP alleviation. However, the effects of PPARα on neuroinflammation and synaptic plasticity should be further explored.

Ficus hirta Vahl. alleviate LPS induced apoptosis via down-regulating of miR-411 in orange-spotted grouper (Epinephelus coioides) spleen cell.

Ficus hirta Vahl. (FhV) has been shown to have antimicrobial and antiviral efficacy. To further ascertain the pharmacological properties of FhV., and to search for alternatives to antibiotics. An in vitro experiment was carried out to evaluate what influence FhV. would have on LPS-induced apoptosis. In this study, Fas, an apoptosis receptor, was cloned, which included a 5'-UTR of 39 bp, an ORF of 951 bp, a protein of 316 amino acids, and a 3'-UTR of 845 bp. EcFas was most strongly expressed in the spleen tissue of orange-spotted groupers. In addition, the apoptosis of fish spleen cells induced by LPS was concentration-dependent. Interestingly, appropriate concentrations of FhV. alleviated LPS-induced apoptosis. Inhibition of miR-411 further decreased the inhibitory effect of Fas on apoptosis, which reduced Bcl-2 expression and mitochondrial membrane potential, enhanced the protein expression of Bax and Fas. More importantly, the FhV. could activate miR-411 to improve this effect. In addition, luciferase reporter assays showed that miR-411 binds to Fas 3'-UTR to inhibit Fas expression. These findings provide evidence that FhV. alleviates LPS-induced apoptosis by activating miR-411 to inhibit Fas expression and, therefore, provided possible strategies for bacterial infections in fish.

[Improvement effect of cinnamaldehyde on reserpine-induced Parkinson's disease rat model].

In order to study the neuroprotective mechanism of cinnamaldehyde on reserpine-induced Parkinson's disease(PD) rat models, 72 male Wistar rats were randomly divided into blank group, model group, Madopar group, and cinnamaldehyde high-, medium-, and low-dose groups. Except for the blank group, the other groups were intraperitoneally injected with reserpine of 0.1 mg·kg~(-1) once every other morning, and cinnamaldehyde and Madopar solutions were gavaged every afternoon. Open field test, rotarod test, and oral chewing movement evaluation were carried out in the experiment. The brain was taken and fixed. The positive expression of dopamine receptor D1(DRD1) was detected by TSA, and the changes in neurotransmitters such as dopamine(DA) and 3,4-dihydroxyphenylacetic acid(DOPAC) in the brain were detected by enzyme-linked immunosorbent assay(ELISA). The protein and mRNA expression levels of tyrosine hydroxylase(TH) and α-synuclein(α-Syn) in substantia nigra(SN) were detected by RT-PCR and Western blot. The results showed that after the injection of reserpine, the hair color of the model group became yellow and dirty; the arrest behavior was weakened, and the body weight was reduced. The spontaneous movement and exploration behavior were reduced, and the coordination exercise ability was decreased. The number of oral chewing was increased, but the cognitive ability was decreased, and the proportion of DRD1 positive expression area in SN was decreased. The expression of TH protein and mRNA was down-regulated, and that of α-Syn protein and mRNA was up-regulated. After cinnamaldehyde intervention, it had an obvious curative effect on PD model animals. The spontaneous movement behavior, the time of staying in the rod, the time of movement, the distance of movement, and the number of standing times increased, and the number of oral chewing decreased. The proportion of DRD1 positive expression area in SN increased, and the protein and mRNA expression levels of α-Syn were down-regulated. The protein and mRNA expression levels of TH were up-regulated. In addition, the levels of DA, DOPAC, and homovanillic acid(HVA) neurotransmitters in the brain were up-regulated. This study can provide a new experimental basis for clinical treatment and prevention of PD.

Combining fecal 16 S rRNA sequencing and spinal cord metabolomics analysis to explain the modulatory effect of PPARα on neuropathic pain.

BACKGROUND: Existing evidence suggests that the composition of the gut microbiota is associated with neuropathic pain (NP), but the mechanistic link is elusive. Peroxisome proliferator-activated receptor α (PPARα) has been shown to be a pharmacological target for the treatment of metabolic disorders, and its expression is also involved in inflammatory regulation. The aim of this study was to investigate the important modulatory effects of PPARα on gut microbiota and spinal cord metabolites in mice subjected to chronic constriction injury. METHODS: We analyzed fecal microbiota and spinal cord metabolic alterations in mice from the sham, CCI, GW7647 (PPARα agonist) and GW6471 (PPARα antagonist) groups by 16 S rRNA amplicon sequencing and untargeted metabolomics analysis. On this basis, the intestinal microbiota and metabolites that were significantly altered between treatment groups were analyzed in a combined multiomics analysis. We also investigated the effect of PPARα on the polarization fractionation of spinal microglia. RESULTS: PPARα agonist significantly reduce paw withdrawal threshold and paw withdrawal thermal latency, while PPARα antagonist significantly increase paw withdrawal threshold and paw withdrawal thermal latency. 16 S rRNA gene sequencing showed that intraperitoneal injection of GW7647 or GW6471 significantly altered the abundance, homogeneity and composition of the gut microbiome. Analysis of the spinal cord metabolome showed that the levels of spinal cord metabolites were shifted after exposure to GW7647 or GW6471. Alterations in the composition of gut microbiota were significantly associated with the abundance of various spinal cord metabolites. The abundance of Licheniformes showed a significant positive correlation with nicotinamide, benzimidazole, eicosanoids, and pyridine abundance. Immunofluorescence results showed that intraperitoneal injection of GW7647 or GW6471 altered microglial activation and polarization levels. CONCLUSION: Our study shows that PPARα can promote M2-type microglia polarization, as well as alter gut microbiota and metabolites in CCI mice. This study enhances our understanding of the mechanism of PPARα in the treatment of neuropathic pain.

Development of a novel Ba2BiV3O11 photocatalyst with dual functions of both water oxidation and proton reduction performance.

To overcome the limitation of photocatalysts with dual functionality of water oxidation and proton reduction, we proposed a novel bismuth-based Ba2BiV3O11 (BBVO) photocatalyst, which can simultaneously drive the proton reduction reaction under UV light and water oxidation reaction under visible light. After doping with sulfur through an in situ vulcanization strategy, the light absorption and charge separation efficiencies of the sulfur-doped BBVO were significantly improved, thus boosting its oxygen evolution activity (64 µmol h-1) by more than 16 times compared with independent BBVO. The experimental results demonstrate that BBVO can be employed as a very promising bismuth-based photocatalyst for solar energy conversion.

Photoelectron Migration Boosted by Hollow Double-Shell Dyads Based on Covalent Organic Frameworks for Highly Efficient Photocatalytic Hydrogen Generation.

Photocatalytic hydrogen production based on noble metal-free systems is a promising technology for the conversion of solar energy into green hydrogen, it is pivotal and challenging to tailor-make photocatalysts for achieving high photocatalytic efficiency. Herein, we reported a hollow double-shell dyad through uniformly coating covalent organic frameworks (COFs) on the surface of hollow Co9S8. The double shell architecture enhances the scattering and refraction efficiency of incident light, shortens the transmission distance of the photogenerated charge carriers, and exposes more active sites for photocatalytic conversion. The hydrogen evolution rate is as high as 23.15 mmol g-1 h-1, which is significantly enhanced when compared with that of their physical mixture (0.30 mmol g-1 h-1) and Pt-based counterpart (11.84 mmol g-1 h-1). This work provides a rational approach to the construction of noble-metal-free photocatalytic systems based on COFs to enhance hydrogen evolution performance.

Hydrogen alleviated cognitive impairment and blood‒brain barrier damage in sepsis-associated encephalopathy by regulating ABC efflux transporters in a PPARα-dependent manner.

Hydrogen (H2) can protect against blood‒brain barrier (BBB) damage in sepsis-associated encephalopathy (SAE), but the mechanism is still unclear. We examined whether it is related to PPARα and its regulatory targets, ABC efflux transporters. After injection with DMSO/GW6471 (a PPARα inhibitor), the mice subjected to sham/caecal ligation and puncture (CLP) surgery were treated with H2 for 60 min postoperation. Additionally, bEnd.3 cells were grown in DMSO/GW6471-containing or saline medium with LPS. In addition to the survival rates, cognitive function was assessed using the Y-maze and fear conditioning tests. Brain tissues were stained with TUNEL and Nissl staining. Additionally, inflammatory mediators (TNF-α, IL-6, HMGB1, and IL-1ß) were evaluated with ELISA, and PPARα, ZO-1, occludin, VE-cadherin, P-gp, BCRP and MRP2 were detected using Western blotting. BBB destruction was assessed by brain water content and Evans blue (EB) extravasation. Finally, we found that H2 improved survival rates and brain dysfunction and decreased inflammatory cytokines. Furthermore, H2 decreased water content in the brain and EB extravasation and increased ZO-1, occludin, VE-cadherin and ABC efflux transporters regulated by PPARα. Thus, we concluded that H2 decreases BBB permeability to protect against brain dysfunction in sepsis; this effect is mediated by PPARα and its regulation of ABC efflux transporters.

Thiadiazole-Derived Covalent Organic Framework Macroscopic Ultralight Aerogel.

Shaping covalent organic frameworks (COFs) into macroscopic objects for practical application remains a huge challenge. Herein, a new thiadiazole-derived COF macroscopic ultralight aerogel (NNS-VCOF) was prepared through acid-catalyzed aldol condensation between 2,5-dimethyl-1,3,4-thiadiazole and a tritopic aromatic aldehyde derivative. NNS-VCOF aerogel shows extremely low density (ca. 0.020 g cm-3), excellent mechanical properties (compression modulus of 16.65 kPa), thermal insulation properties (low thermal conductivity of 0.03270 W m-1 K-1 at 25 °C), and flame retardancy (quickly self-extinguishing after ignition) due to its three-dimensional sponge-like architecture and special nitrogen heterocyclic framework. To our delight, NNS-VCOF aerogel not only can be used as an outstanding macroscopic material but also shows efficient photocatalytic hydrogen evolution properties in a powder state because of the superhydrophilicity and appropriate optical properties.

Screening Serum Biomarkers for Rats Preconditioned with Hyperbaric Oxygen: Potential of Predicting Prognosis for Stroke.

BACKGROUND: Stroke is a major health concern and a leading cause of mortality and morbidity. We and other groups have documented that hyperbaric oxygen preconditioning could significantly alleviate neuronal damage in ischemia‒reperfusion models through various mechanisms. However, we found that some of the subjects did not benefit from preconditioning with hyperbaric oxygen. The preconditioning phenomenon is similar to vaccination, in which the endogenous survival system is activated to fight against further injuries. However, with vaccine inoculations, we could test for specific antibodies against the pathogens to determine if the vaccination was successful. Likewise, this experiment was carried out to explore a biomarker that can reveal the effectiveness of the preconditioning before neuronal injury occurs. METHODS: Middle cerebral artery occlusion (MCAO) was used to induce focal cerebral ischemia-reperfusion injury. 2D-DIGE-MALDI-TOF-MS/MS proteomic technique was employed to screen the differentially expressed proteins in the serum of rats among the control (Con) group (MCAO model without hyperbaric oxygen (HBO) preconditioning), hyperbaric oxygen protective (HBOP) group (in which the infarct volume decreased after HBO preconditioning vs. Con), and hyperbaric oxygen nonprotective (HBOU) group (in which the infarct volume remained the same or even larger after HBO preconditioning vs. Con). Candidate biomarkers were confirmed by western blot and enzyme linked immunosorbent assay (ELISA), and the relationship between the biomarkers and the prognosis of cerebral injury was further validated. RESULTS: Among the 15 differentially expressed protein spots detected in the HBOP group by Two-dimensional fluorescence difference gel electrophoresis (2D-DIGE), 3 spots corresponding to 3 different proteins (haptoglobin, serum albumin, and haemopexin) products were identified by MALDI-TOF-MS/MS. Serum albumin and haemopexin were upregulated, and haptoglobin was downregulated in the HBOP group (p < 0.05 vs. Con and HBOU groups). After the western blot study, only the changes in haemopexin were validated and exhibited similar changes in subjects from the HBOP group in accordance with MALDI-TOF-MS/MS proteomic analysis and enzyme linked immunosorbent assay (ELISA) analysis. The serum level of the hemopexin (HPX) at 2 h after HBO preconditioning was correlated with the infarct volume ratio after MCAO. CONCLUSIONS: Haemopexin may be developed as a predictive biomarker that indicated the effectiveness of a preconditioning strategy against cerebral ischaemic injury.

Zwitterionic and Hydrophilic Vinylene-Linked Covalent Organic Frameworks for Efficient Photocatalytic Hydrogen Evolution.

Developing effective synthetic strategies as well as broadening functionalities for zwitterionic materials that comprise moieties with equimolar cationic and anionic groups still remains a huge challenge. Herein, we develop two zwitterionic vinylene-linked covalent organic frameworks (Zi-VCOF-1 and Zi-VCOF-2) that are a type of novel hydrophilic material. Zi-VCOF-1 and Zi-VCOF-2 are obtained directly through the convenient Knoevenagel condensation of new sulfonic-pyridinium zwitterionic monomers with aromatic aldehyde derivatives. This is the first report on zwitterionic COFs being constructed by the bottom-up functionalization approach from predesigned zwitterionic monomers. Both Zi-VCOFs exhibit a high photocatalytic hydrogen evolution rate (HER) because of their appropriate optical property and outstanding hydrophilicity. Specifically, Zi-VCOF-1 and Zi-VCOF-2 show photocatalytic HER of 13,547 and 5057 µmol h-1 g-1, respectively. Interestingly, the photocatalytic HER of Zi-VCOF-1 is about 2.68 times of that of Zi-VCOF-2, although they differ by only one methyl group in sulfonic-pyridinium zwitterionic pairs. The photocatalytic HER of Zi-VCOF-1 is not only the highest in the vinylene-linked COFs but also outstanding among the most reported COFs. This is the first application of zwitterionic COFs for photocatalytic hydrogen evolution, which would open a new frontier in zwitterionic COFs and be helpful for the design of other photocatalytic materials.

c-Jun N-terminal kinase activation contributes to improving low temperature tolerance via regulating apoptosis in the Pacific white shrimp Penaeus vannamei.

Temperature is an essential environmental factor for the survival of aquatic animals. Low temperature stress can induce mitochondria to produce excessive ROS and free radicals, and destroy homeostasis. c-Jun N-terminal kinase (JNK) is involved in regulating various physiological processes, including inflammatory responses, cell cycle, reproduction, and apoptosis. Here, we investigated the mechanism of ROS/JNK pathway under low temperature stress both in vitro and in vivo. In this study, transcriptome analysis revealed that apoptosis, autophagy, calcium channel, and antioxidant were involved in the mediation of low temperature tolerance in Pacific white shrimp (penaeus vannamei). PvJNK was activated in response to low temperature stress. Treatments with different temperature caused oxidative stress as demonstrated by increased intensity of the ROS indicator H2DCF-DA, and induced apoptosis as confirmed by indicator FITC. Pretreatment with N-acetylcysteine, an ROS scavenger, attenuated low temperature induced apoptosis, and inhibited the expression of PvJNK. In addition, we demonstrate that mediator PvJNK translocated to nuclear through interacting with PvRheb. By using flow cytometry, inhibiting PvJNK can increase the expression of apoptosis related genes, accelerate tissue damage, and induce ROS and cell apoptosis. The ultimate inhibition of PvJNK accelerates the mortality of shrimp under low temperature stress. Overall, these findings suggest that during low temperature stress, PvJNK was activated by ROS to regulates apoptosis via interacting with PvRheb to promote PvJNK into the nucleus and to improve low temperature tolerance of shrimp.

Insecticide resistance monitoring of Cnaphalocrocis medinalis (Lepidoptera: Pyralidae) and its mechanism to chlorantraniliprole.

BACKGROUND: The rice leaffolder, Cnaphalocrocis medinalis (Guenée), has become an increasingly occurring pest in Asia in recent years. Chemical control remains the most efficient and primary tool for controlling this pest. In this study, we report the resistance status of C. medinalis in China to multiple insecticides including chlorantraniliprole and the main resistance mechanism. RESULTS: Significant variations among field populations of C. medinalis in their resistance to 10 insecticides were observed during 2019-2022. Most of the tested field populations have developed low-to-moderate levels of resistance to abamectin (RR = 2.4-22.2), emamectin benzoate (RR = 1.9-40.3) and spinetoram (RR = 4.2-24.8). Some field populations have developed low resistance to chlorpyrifos (RR = 0.9-6.8). Indoxacarb, metaflumizone, methoxenozide and Bacillus thuringiensis (Bt) potency against all tested populations remained similar. For diamides, significantly higher levels of resistance to chlorantraniliprole (RR = 64.9-113.7) were observed in 2022, whereas all tested field populations in 2019-2021 exhibited susceptible or moderate resistance level to chlorantraniliprole (RR = 1.3-22.1). Cross-resistance between chlorantraniliprole and tetraniliprole was significant. Analysis of ryanodine receptor (RyR) mutations showed that mutation of I4712M was present in resistant populations of C. medinalis with different levels of chlorantraniliprole resistance and was the main mechanism conferring diamide resistance. Mutation of Y4621D also was detected in one tested population. Resistance management strategies for the control of C. medinalis are discussed. CONCLUSION: C. medinalis has developed high level of resistance to chlorantraniliprole. RyR mutations were deemed as the mechanism. © 2023 Society of Chemical Industry.

HHL1 and SOQ1 synergistically regulate nonphotochemical quenching in Arabidopsis.

Nonphotochemical quenching (NPQ) is an important photoprotective mechanism that quickly dissipates excess light energy as heat. NPQ can be induced in a few seconds to several hours; most studies of this process have focused on the rapid induction of NPQ. Recently, a new, slowly induced form of NPQ, called qH, was found during the discovery of the quenching inhibitor suppressor of quenching 1 (SOQ1). However, the specific mechanism of qH remains unclear. Here, we found that hypersensitive to high light 1 (HHL1)-a damage repair factor of photosystem II-interacts with SOQ1. The enhanced NPQ phenotype of the hhl1 mutant is similar to that of the soq1 mutant, which is not related to energy-dependent quenching or other known NPQ components. Furthermore, the hhl1 soq1 double mutant showed higher NPQ than the single mutants, but its pigment content and composition were similar to those of the wildtype. Overexpressing HHL1 decreased NPQ in hhl1 to below wildtype levels, whereas NPQ in hhl1 plants overexpressing SOQ1 was lower than that in hhl1 but higher than that in the wildtype. Moreover, we found that HHL1 promotes the SOQ1-mediated inhibition of plastidial lipoprotein through its von Willebrand factor type A domain. We propose that HHL1 and SOQ1 synergistically regulate NPQ.

Flux-assisted synthesis of tungsten-doped layered perovskite oxychloride with promoted visible-light-responsive O2 evolution performance.

Here, we successfully prepared Ba2Bi3Ta2O11Cl via a simple one-step molten salt method and adjusted its crystal morphology and structure, based on which the O2-evolving activity was significantly improved. In addition, W doping promotes the charge separation efficiency, lowers the energy barrier for water oxidation reaction, and thus improves the activity. Finally, the optimized W-doped sample after molten salt treatment shows the best O2 production activity (55 µmol h-1) without loading any cocatalyst, which is 6 times higher than that of pristine Ba2Bi3Ta2O11Cl and 2 times higher than that of the undoped Ba2Bi3Ta2O11Cl treated with molten salt, respectively.

scRNA-seq analysis reveals toxicity mechanisms in shrimp hemocytes subjected to nitrite stress.

In shrimp, hemocytes play an important role in detoxification and immune defense, and are where nitrite accumulates during exposure to this toxic environmental pollutant. However, the heterogeneity mechanisms of toxicity have not been reported under nitrite expose in shrimp. Here, we used single-cell RNA-seq to resolve 24,000 cells, which the responses of different cell populations of hemocytes under nitrite exposure in Penaeus vannamei. We identified 394 specific nitrite-responsive genes in 9 clusters of hemocytes, and found heterogeneity in the nitrite response of the three subpopulations of hemocytes (hyaline, semi-granular and granular cells). In hyaline, the response appeared modest, whereas nitrite-related dysregulation of metabolic processes in granular and semi-granular was pronounced. Ammonia nitrogen will rapidly accumulate in hemocytes of shrimp under nitrite stress. In semi-granular, excessive ammonia will interfere with oxidative phosphorylation and antioxidant system, thus inducing the production of reactive oxygen species. In granular, the abnormality of urea cycle caused by ammonia accumulation is the main toxic factor, which by inhibits arginase and arginine kinase. Collectively, our data provide a single-cell atlas for the dissection of shrimp hemocyte complexity, and reveal the toxicity mechanisms associated with nitrite exposure.

Effect of molecular hydrogen treatment on Sepsis-Associated encephalopathy in mice based on gut microbiota.

INTRODUCTION: In our experiments, male wild-type mice were randomly divided into four groups: the sham, SAE, SAE + 2% hydrogen gas inhalation (H2 ), and SAE + hydrogen-rich water (HW) groups. The feces of the mice were collected for 16 S rDNA analysis 24 h after the models were established, and the serum and brain tissue of the mice were collected for nontargeted metabolomics analysis. AIM: Destruction of the intestinal microbiota is a risk factor for sepsis and subsequent organ dysfunction, and up to 70% of severely ill patients with sepsis exhibit varying degrees of sepsis-associated encephalopathy (SAE). The pathogenesis of SAE remains unclear. We aimed to explore the changes in gut microbiota in SAE and the regulatory mechanism of molecular hydrogen. RESULTS: Molecular hydrogen treatment significantly improved the functional outcome of SAE and downregulated inflammatory reactions in both the brain and the gut. In addition, molecular hydrogen treatment improved gut microbiota dysbiosis and partially amended metabolic disorder after SAE. CONCLUSIONS: Molecular hydrogen treatment promotes functional outcomes after SAE in mice, which may be attributable to increasing beneficial bacteria, repressing harmful bacteria, and metabolic disorder, and reducing inflammation.

Expression pattern and clinical value of Key RNA methylation modification regulators in ischemic stroke.

Ischemic stroke (IS) is one of the major causes of death and disability worldwide, and effective diagnosis and treatment methods are lacking. RNA methylation, a common epigenetic modification, plays an important role in disease progression. However, little is known about the role of RNA methylation modification in the regulation of IS. The aim of this study was to investigate RNA methylation modification patterns and immune infiltration characteristics in IS through bioinformatics analysis. We downloaded gene expression profiles of control and IS model rat brain tissues from the Gene Expression Omnibus database. IS profiles were divided into two subtypes based on RNA methylation regulators, and functional enrichment analyses were conducted to determine the differentially expressed genes (DEGs) between the subtypes. Weighted gene co-expression network analysis was used to explore co-expression modules and genes based on DEGs. The IS clinical diagnosis model was successfully constructed and four IS characteristic genes (GFAP, GPNMB, FKBP9, and CHMP5) were identified, which were significantly upregulated in IS samples. Characteristic genes were verified by receiver operating characteristic curve and real-time quantitative PCR analyses. The correlation between characteristic genes and infiltrating immune cells was determined by correlation analysis. Furthermore, GPNMB was screened using the protein-protein interaction network, and its regulatory network and the potential therapeutic drug chloroquine were predicted. Our finding describes the expression pattern and clinical value of key RNA methylation modification regulators in IS and novel diagnostic and therapeutic targets of IS from a new perspective.

Phosphorylation-mediated PI3K-Art signalling pathway as a therapeutic mechanism in the hydrogen-induced alleviation of brain injury in septic mice.

Our previous studies illustrated that 2% H2 inhalation can protect against sepsis-associated encephalopathy (SAE) which is characterized by high mortality and has no effective treatment. To investigate the underlying role of protein phosphorylation in SAE and H2 treatment, a mouse model of sepsis was constructed by caecal ligation and puncture (CLP), then treated with H2 (CLP + H2 ). Brain tissues of the mice were collected to be analysed with tandem mass tag-based quantitative proteomics coupled with IMAC enrichment of phosphopeptides and LC-MS/MS analysis. In proteomics and phosphoproteomics analysis, 268 differentially phosphorylated proteins (DPPs) showed a change in the phosphorylated form in the CLP + H2 group (p < 0.05). Gene ontology analysis revealed that these DPPs were enriched in multiple cellular components, biological processes, and molecular functions. KEGG pathway analysis revealed that they were enriched in glutamatergic synapses, tight junctions, the PI3K-Akt signalling pathway, the HIF-1 signalling pathway, the cGMP-PKG signalling pathway, the Rap1 signalling pathway, and the vascular smooth muscle contraction. The phosphorylated forms of six DPPs, including ribosomal protein S6 (Rps6), tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma (Ywhag/14-3-3), phosphatase and tensin homologue deleted on chromosome ten (Pten), membrane-associated guanylate kinase 1 (Magi1), mTOR, and protein kinase N2 (Pkn2), were upregulated and participated in the PI3K-Akt signalling pathway. The WB results showed that the phosphorylation levels of Rps6, Ywhag, Pten, Magi1, mTOR, and Pkn2 were increased. The DPPs and phosphorylation-mediated molecular network alterations in H2 -treated CLP mice may elucidate the biological roles of protein phosphorylation in the therapeutic mechanism of H2 treatment against SAE.

Bismuth Gadolinium Oxychloride with a Remarkable Visible-Light-Responsive O2 Evolution Activity Promoted by Iodine Doping.

Visible-light-responsive bismuth-based oxyhalide has recently attracted extensive attention, however, the promotion of its charge separation is still challenging. Herein, we introduce iodine into Bi2 GdO4 Cl to synthetize I-doped Bi2 GdO4 Cl (denoted as yI-Bi2 GdO4 Cl, 0≤y≤2). The incorporation of I- ions is found to enhance light absorption and to accelerate charge separation by combining various characterizations such as density functional theory calculation, photoelectrochemical test, electrochemical impedance spectroscopy, photoluminescence spectrum, and open-circuit voltage decay. The O2 -evolving performances of 1I-Bi2 GdO4 Cl with optimized dopant concentration of I- ion and IrO2 loaded 1I-Bi2 GdO4 Cl are tremendously enhanced by ca. 4 and 45 times compared to pristine Bi2 GdO4 Cl. Notably, The O2 evolution rate reaches as high as 154.8 µmol ⋅ h-1 with an apparent quantum efficiency of ∼1.1 % at 420 nm. The synthetic iodine-doped photocatalyst remains stable after long-term photoreaction, demonstrating its potential in the field of photocatalysis.