Amorphous RuPd bimetallene for hydrogen evolution reaction in acidic and alkaline conditions: a first-principles study.

Metallene materials can provide a large number of active catalytic sites for the efficient use of noble metals as catalysts for hydrogen evolution reaction (HER), whereas the intrinsic activity on the surface is insufficient in crystal phase. The amorphous phase with an inherent long-range disorder can offer a rich coordinate environment and charge polarization on the surface is proposed for promoting the intrinsic catalytic activity on the surface of noble metals. Herein, we designed an amorphous RuPd (am-RuPd) structure by the first principles molecular dynamics method. The performance of the acidic HER on am-RuPd can have a huge enhancement due to the free energy change of hydrogen adsorption close to zero. In alkaline conditions, the H2O dissociation energy barrier on am-RuPd is just 0.49 eV, and it is predicted that the alkaline HER performance of am-RuPd will largely exceed that of Pt nanocrystalline sheets. This work provides a strategy for enhancing the intrinsic catalytic activity on the surface and a way to design an efficient HER catalyst based on metallene materials used in both acidic and alkaline conditions.

Protective effects of oyster polypeptide on cyclophosphamide-induced immunosuppressed rats.

BACKGROUND: Oyster polypeptide (OP) is a mixture of oligopeptides extracted from oysters through enzyme lysis, separation, and purification. It is associated with immunomodulatory effects, but the underlying mechanisms are not known. This study therefore combined proton nuclear magnetic resonance (1H-NMR) urinary metabolomics and 16S rRNA gene sequencing of the gut microbiome to determine the immunoprotective mechanisms of OP in rats subjected to cyclophosphamide-induced immunosuppression. RESULTS: Oyster polypeptide restored the body weight and the structure of spleen and thymus in rats with cyclophosphamide-induced immunosuppression. It upregulated the levels of white blood cells (WBCs), hemoglobin (HGB), platelets (PLT), red blood cells (RBCs), immunoglobulin G (IgG), immunoglobulin M (IgM), cytokines such as interleukin­6 (IL-6) and tumor necrosis factor-α (TNF-α), and increased the numbers of CD3+ and CD4+ T cells in the immunosuppressed rats. The 1H-NMR metabolomics results showed that OP significantly reversed the levels of ten metabolites in urine, including 2-oxoglutarate, citrate, dimethylamine, taurine, N-phenylacetylglycine, alanine, betaine, creatinine, uracil, and benzoate. The 16S rRNA gene sequencing results showed that OP restored the gut microbiome homeostasis by increasing the abundance of beneficial bacteria and reducing the abundance of pathogenic bacteria. Finally, a combination of metabolomics and microbiomics found that the metabolism of taurine and hypotaurine, and the metabolism of alanine, aspartate, and glutamate were disturbed, but these metabolic pathways were restored by OP. CONCLUSION: This study demonstrated that OP had immunoprotective effects in rats with cyclophosphamide-induced immunosuppression by restoring key metabolic pathways and the gut microbiome homeostasis. Our findings provide a framework for further research into the immunoregulatory mechanisms of OP and its potential use in drugs and nutritional supplements. © 2024 Society of Chemical Industry.

Myeloid cyclooxygenase-2/prostaglandin E2/E-type prostanoid receptor 4 promotes transcription factor MafB-dependent inflammatory resolution in acute kidney injury.

Following acute injury to the kidney, macrophages play an important role in recovery of functional and structural integrity, but organ fibrosis and progressive functional decline occur with incomplete recovery. Pro-resolving macrophages are characterized by increased cyclooxygenase 2 (COX-2) expression and this expression was selectively increased in kidney macrophages following injury and myeloid-specific COX-2 deletion inhibited recovery. Deletion of the myeloid prostaglandin E2 (PGE2) receptor, E-type prostanoid receptor 4 (EP4), mimicked effects seen with myeloid COX-2-/- deletion. PGE2-mediated EP4 activation induced expression of the transcription factor MafB in kidney macrophages, which upregulated anti-inflammatory genes and suppressed pro-inflammatory genes. Myeloid Mafb deletion recapitulated the effects seen with either myeloid COX-2 or EP4 deletion following acute kidney injury, with delayed recovery, persistent presence of pro-inflammatory kidney macrophages, and increased kidney fibrosis. Thus, our studies identified a previously unknown mechanism by which prostaglandins modulate macrophage phenotype following acute organ injury and provide new insight into mechanisms underlying detrimental kidney effects of non-steroidal anti-inflammatory drugs that inhibit cyclooxygenase activity.

Deletion of Myeloid Interferon Regulatory Factor 4 (Irf4) in Mouse Model Protects against Kidney Fibrosis after Ischemic Injury by Decreased Macrophage Recruitment and Activation.

BACKGROUND: AKI is characterized by abrupt and reversible kidney dysfunction, and incomplete recovery leads to chronic kidney injury. Previous studies by us and others have indicated that macrophage infiltration and polarization play key roles in recovery from AKI. The role in AKI recovery played by IFN regulatory factor 4 (IRF4), a mediator of polarization of macrophages to the M2 phenotype, is unclear. METHODS: We used mice with myeloid or macrophage cell-specific deletion of Irf4 (MΦ Irf4-/- ) to evaluate Irf4's role in renal macrophage polarization and development of fibrosis after severe AKI. RESULTS: Surprisingly, although macrophage Irf4 deletion had a minimal effect on early renal functional recovery from AKI, it resulted in decreased renal fibrosis 4 weeks after severe AKI, in association with less-activated macrophages. Macrophage Irf4 deletion also protected against renal fibrosis in unilateral ureteral obstruction. Bone marrow-derived monocytes (BMDMs) from MΦ Irf4-/- mice had diminished chemotactic responses to macrophage chemoattractants, with decreased activation of AKT and PI3 kinase and increased PTEN expression. PI3K and AKT inhibitors markedly decreased chemotaxis in wild-type BMDMs, and in a cultured macrophage cell line. There was significant inhibition of homing of labeled Irf4-/- BMDMs to postischemic kidneys. Renal macrophage infiltration in response to AKI was markedly decreased in MΦ Irf4-/- mice or in wild-type mice with inhibition of AKT activity. CONCLUSIONS: Deletion of Irf4 from myeloid cells protected against development of tubulointerstitial fibrosis after severe ischemic renal injury in mice, due primarily to inhibition of AKT-mediated monocyte recruitment to the injured kidney and reduced activation and subsequent polarization into a profibrotic M2 phenotype.

Enhanced Hydrogen Evolution Reactivity of T'-Phase Tungsten Dichalcogenides (WS2, WSe2, and WTe2) Materials: A DFT Study.

The hydrogen evolution reaction (HER) plays a crucial role in hydrogen gas production. Layers of transition-metal dichalcogenides (TMDs) possess adjustable electronic structures, and TMDs with H-phase structures have been proposed as substitute HER catalysts. Nonetheless, there are few systematic theoretical analyses of the HER catalytic properties of TMDs with T'-phase structures. Using a DFT calculation, we investigated the electrocatalytic properties of W-based dichalcogenides (WS2, WSe2, and WTe2) through defect engineering. It was found that the interaction of H atoms with the basal plane can be tuned using non-metallic atomic doping, especially with P, thereby enhancing catalytic activity. Furthermore, the computation results demonstrated that high P-doping concentrations can enhance the number of active sites and exhibit a suitable ΔGH*.

Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction.

Ischemic heart disease is the leading cause of death worldwide and is frequently comorbid with chronic kidney disease. Physiological communication is known to occur between the heart and the kidney. Although primary dysfunction in either organ can induce dysfunction in the other, a clinical entity known as cardiorenal syndrome, mechanistic details are lacking. Here, we used a model of experimental myocardial infarction (MI) to test effects of chronic cardiac ischemia on acute and chronic kidney injury. Surprisingly, chronic cardiac damage protected animals from subsequent acute ischemic renal injury, an effect that was accompanied by evidence of chronic kidney hypoxia. The protection observed post-MI was similar to protection observed in a separate group of healthy animals housed in ambient hypoxic conditions prior to kidney injury, suggesting a common mechanism. There was evidence that chronic cardiac injury activates renal hypoxia-sensing pathways. Increased renal abundance of several glycolytic enzymes following MI suggested that a shift toward glycolysis may confer renal ischemic preconditioning. In contrast, effects on chronic renal injury followed a different pattern, with post-MI animals displaying worsened chronic renal injury and fibrosis. These data show that although chronic cardiac injury following MI protected against acute kidney injury via activation of hypoxia-sensing pathways, it worsened chronic kidney injury. The results further our understanding of cardiorenal signaling mechanisms and have implications for the treatment of heart failure patients with associated renal disease.NEW & NOTEWORTHY Experimental myocardial infarction (MI) protects from subsequent ischemic acute kidney injury but worsens chronic kidney injury. Observed protection from ischemic acute kidney injury after MI was accompanied by chronic kidney hypoxia and increased renal abundance of hypoxia-inducible transcripts. These data support the idea that MI confers protection from renal ischemic injury via chronic renal hypoxia and activation of downstream hypoxia-inducible signaling pathways.

Ammonia Gas Sensor Based on Graphene Oxide-Coated Mach-Zehnder Interferometer with Hybrid Fiber Structure.

A graphene oxide-coated in-fiber Mach-Zehnder interferometer (MZI) formed with a multimode fiber-thin core fiber-multimode fiber (MMF-TCF-MMF) is proposed and experimentally demonstrated for ammonia gas (NH3) sensing. The MZI structure is composed of two segments of MMF of length 2 mm, with a flame-tapered TCF between them as the sensing arm. The MMFs act as mode couplers to split and recombine light owing to the core diameter mismatch with the other fibers. A tapered TCF is formed by the flame melting taper method, resulting in evanescent wave leakage. A layer of graphene oxide (GO) is applied to the tapered region of the TCF to achieve gas adsorption. The sensor operates on the principle of changing the effective refractive index of the cladding mode of a fiber through changing the conductivity of the GO coating by adsorbed NH3 molecules, which gives rise to a phase shift and shows as the resonant dip shifts in the transmission spectrum. So the concentration of the ammonia gas can be obtained by measuring the dip shift. A wavelength-shift sensitivity of 4.97 pm/ppm with a linear fit coefficient of 98.9% is achieved for ammonia gas concentrations in the range of 0 to 151 ppm. In addition, we performed a repetitive dynamic response test on the sensor by charging/releasing NH3 at concentration of 200 ppm and a relative humidity test in a relative humidity range of 35% to 70%, which demonstrates the reusability and stability of the sensor.

In-depth serum virome analysis in patients with acute liver failure with indeterminate etiology.

In clinical virome research, whole-genome/transcriptome amplification is required when starting material is limited. An improved method, named "template-dependent multiple displacement amplification" (tdMDA), has recently been developed in our lab (Wang et al. in BioTechniques 63:21-25. https://doi.org/10.2144/000114566, 2017). In combination with Illumina sequencing and bioinformatics pipelines, its application in virome sequencing was explored using a serum sample from a patient with chronic hepatitis C virus (HCV) infection. In comparison to an amplification-free procedure, virome sequencing via tdMDA showed a 9.47-fold enrichment for HCV-mapped reads and, accordingly, an increase in HCV genome coverage from 28.5% to 70.1%. Eight serum samples from acute patients liver failure (ALF) with or without known etiology were then used for virome sequencing with an average depth at 94,913x. Both similarity-based (mapping, NCBI BLASTn, BLASTp, and profile hidden Markov model analysis) and similarity-independent methods (machine-learning algorithms) identified viruses from multiple families, including Herpesviridae, Picornaviridae, Myoviridae, and Anelloviridae. However, their commensal nature and cross-detection ruled out an etiological interpretation. Together with a lack of detection of novel viruses in a comprehensive analysis at a resolution of single reads, these data indicate that viral agents might be rare in ALF cases with indeterminate etiology.

Genome-wide capture sequencing to detect hepatitis C virus at the end of antiviral therapy.

BACKGROUND: Viral relapse is a major concern in hepatitis C virus (HCV) antiviral therapy. Currently, there are no satisfactory methods to predict viral relapse, especially in the era of direct acting antivirals in which the virus often quickly becomes undetectable using PCR-based approaches that focus on a small viral region. Next-generation sequencing (NGS) provides an alternative option for viral detection in a genome-wide manner. However, owing to the overwhelming dominance of human genetic content in clinical specimens, direct detection of HCV by NGS has a low sensitivity and hence viral enrichment is required. METHODS: Based on template-dependent multiple displacement amplification (tdMDA), an improved method for whole genome amplification (Wang et al., 2017. Biotechniques 63, 21-27), we evaluated two strategies to enhance the sensitivity of NGS-based HCV detection: duplex-specific nuclease (DSN)-mediated depletion of human sequences and HCV probe-based capture sequencing. RESULTS: In DSN-mediated depletion, human sequences were significantly reduced in the two HCV serum samples tested, 65.3% → 55.6% → 33.7% (#4727) and 68.6% → 56% → 21% (#4970), respectively for no normalization, self- and driver-applied normalization. However, this approach was associated with a loss of HCV sequences perhaps due to its micro-homology with the human genome. In capture sequencing, HCV-mapped sequencing reads occupied 96.8% (#4727) and 22.14% (#4970) in NGS data, equivalent to 1936x and 7380x enrichment, respectively. Capture sequencing was then applied to ten serum samples collected at the end of HCV antiviral therapy. Interestingly, the number of HCV-mapped reads was significantly higher in relapsed patients (n = 5) than those from patients with sustained virological response (SVR) (n = 5), 102.4 ± 72.3 vs. 2.6 ± 0.55, p = 0.014. CONCLUSIONS: Our data provides concept evidence for a highly sensitive HCV detection by capture sequencing. The abundance difference of HCV sequencing reads at the end of HCV antiviral therapy could be applied to predict treatment outcomes.

The Role of the EGF Receptor in Sex Differences in Kidney Injury.

BACKGROUND: Sex differences mediating predisposition to kidney injury are well known, with evidence indicating lower CKD incidence rates and slower decline in renal function in nondiabetic CKD for premenopausal women compared with men. However, signaling pathways involved have not been elucidated to date. The EGF receptor (EGFR) is widely expressed in the kidney in glomeruli and tubules, and persistent and dysregulated EGFR activation mediates progressive renal injury. METHODS: To investigate the sex differences in response to renal injury, we examined EGFR expression in mice, in human kidney tissue, and in cultured cell lines. RESULTS: In wild type mice, renal mRNA and protein EGFR levels were comparable in males and females at postnatal day 7 but were significantly lower in age-matched adult females than in adult males. Similar gender differences in renal EGFR expression were detected in normal adult human kidneys. In Dsk5 mutant mice with a gain-of-function allele that increases basal EGFR kinase activity, males had progressive glomerulopathy, albuminuria, loss of podocytes, and tubulointerstitial fibrosis, but female Dsk5 mice had minimal kidney injury. Oophorectomy had no effect on renal EGFR levels in female Dsk5 mice, while castration protected against the kidney injury in male Dsk5 mice, in association with a reduction in EGFR expression to levels seen in females. Conversely, testosterone increased EGFR expression and renal injury in female Dsk5 mice. Testosterone directly stimulated EGFR expression in cultured kidney cells. CONCLUSIONS: These studies indicate that differential renal EGFR expression plays a role in the sex differences in susceptibility to progressive kidney injury that may be mediated at least in part by testosterone.

Lattice -Mismatch-Induced Ultrastable 1T-Phase MoS2-Pd/Au for Plasmon-Enhanced Hydrogen Evolution.

Metallic 1T-phase transition metal dichalcogenides (TMDs) are of considerable interest in enhancing catalytic applications due to their abundant active sites and good conductivity. However, the unstable nature of 1T-phase TMDs greatly impedes their practical applications. Herein, we developed a new approach for the synthesis of highly stable 1T-phase Au/Pd-MoS2 nanosheets (NSs) through a metal assembly induced ultrastable phase transition for achieving a very high electrocatalytic activity in the hydrogen evolution reaction. The phase transition was evoked by a novel mechanism of lattice-mismatch-induced strain based on density functional theory (DFT) calculations. Raman spectroscopy and transmission electron microscopy (TEM) were used to confirm the phase transition on experimental grounds. A novel heterostructured 1T MoS2-Au/Pd catalyst was designed and synthesized using this mechanism, and the catalyst exhibited a 0 mV onset potential in the hydrogen evolution reaction under light illumination. Therefore, this method can potentially be used to fabricate 1T-phase TMDs with remarkably enhanced activities for different applications.

Improving Polysulfides Adsorption and Redox Kinetics by the Co4 N Nanoparticle/N-Doped Carbon Composites for Lithium-Sulfur Batteries.

Improved conductivity and suppressed dissolution of lithium polysulfides is highly desirable for high-performance lithium-sulfur (Li-S) batteries. Herein, by a facile solvent method followed by nitridation with NH3 , a 2D nitrogen-doped carbon structure is designed with homogeneously embedded Co4 N nanoparticles derived from metal organic framework (MOF), grown on the carbon cloth (MOF-Co4 N). Experimental results and theoretical simulations reveal that Co4 N nanoparticles act as strong chemical adsorption hosts and catalysts that not only improve the cycling performance of Li-S batteries via chemical bonding to trap polysulfides but also improve the rate performance through accelerating the conversion reactions by decreasing the polarization of the electrode. In addition, the high conductive nitrogen-doped carbon matrix ensures fast charge transfer, while the 2D structure offers increased pathways to facilitate ion diffusion. Under the current density of 0.1C, 0.5C, and 3C, MOF-Co4 N delivers reversible specific capacities of 1425, 1049, and 729 mAh g-1 , respectively, and retains 82.5% capacity after 400 cycles at 1C, as compared to the sample without Co4 N (MOF-C) values of 61.3% (200 cycles). The improved cell performance corroborates the validity of the multifunctional design of MOF-Co4 N, which is expected to be a potentially promising cathode host for Li-S batteries.

Full annotation of serum virome in Chinese blood donors with elevated alanine aminotransferase levels.

BACKGROUND: A serum alanine aminotransferase (ALT) test is currently demanded for blood donation in China. One of the major reasons to include such a test is possible etiology of known or unknown hepatotropic viruses. However, this hypothesis has never been examined convincingly. STUDY DESIGN AND METHODS: The study recruited 90 Chinese blood donors that were divided into three groups based on their ALT values. Serum virome from these donors was explored using a metagenomics approach with enhanced sensitivity resolved at single sequencing reads. RESULTS: Anellovirus and pegivirus C (GBV-C) were detected among these donors. None of them were found solely in donors with abnormal liver enzyme. Anellovirus was highly prevalent (93.3%) and the co-infection with multiple genera (alpha, beta, and gammatorquevirus) were more common in the donors with normal ALT values in comparison to those with elevated ALT (single/double/triple Anellovirus genera, 1/3/24 vs. 7/7/14 or 6/7/13, p = 0.009). For unmapped reads that accounted for 15 ± 14.9% of the data, similarity-based (BLASTN, BLASTP, and HMMER3) and similarity-independent (k-mer frequency) analysis identified several circular rep encoding ssDNA (CRESS-DNA) genomes. Direct PCR testing indicated these genomes were likely reagent contaminants. CONCLUSION: Viral etiology is not responsible for elevated ALT levels in Chinese blood donors. The ALT test, if not abandoned, should be adjusted for its cutoff in response to donor shortage in China.

Adsorption of metal atoms on silicene: stability and quantum capacitance of silicene-based electrode materials.

We explore the adsorption stability and quantum capacitance of transition metal atoms on silicene based on first-principles calculations. Silicene with a buckled atomic layer has a high surface/volume ratio and silicene-based materials are expected to have potential applications for supercapacitors. We find that the most favorable adsorption sites on pristine silicene are valley sites for Al and Ti, and hollow sites for Ag, Cu and Au, respectively. Among all these systems with the doping of metal atoms, silicene is modulated to possess a quasi-metallic characteristic, accompanied by an appreciable electron transfer and the formation of defect states near the Fermi level. Due to the low density of states near the Fermi level, the quantum capacitance of pristine silicene has been limited. By the doping of metal atoms, especially Ti atoms, with the introduction of localized defect states near the Fermi level, quantum capacitance is found to be enhanced significantly. In addition, the quantum capacitance is found to increase monotonically following the increase of doping concentrations.

First principles study on 2H-1T' transition in MoS2 with copper.

The electronic properties of MoS2 are strongly controlled by the structure, providing a route to their modulation. We report, based on first principles calculations, that the adsorption of metal atom Cu on the surface can induce the phase transition of MoS2 from the semiconducting 2H to the metallic 1T' phase. Cu adsorption results in effective n-type doping of MoS2 by charge transfer from Cu in the case of the 1T' phase. This is distinct from the behavior in the 2H phase, where Cu does not donate any charge, and it is also distinct from alkali metal adsorption, where charge is donated to both 2H and 1T' MoS2. Charge donation to the 1T' phase by Cu stabilizes it with respect to the 2H structure and importantly, it also reduces the energy barrier between the 2H and 1T' structures. This difference reflects the higher electronegativity of Cu, which also indicates that Cu-modified MoS2 can be expected to be less chemically reactive than MoS2 with alkali metal adatoms. The main atomic mechanism of the structural transition is the gliding of S atoms on the upper surface. Finally, we report the energetics of the 2H to 1T' transition with several other adatoms, Ag, Au, Ni, Pt and Pd, but none of them are as effective as Cu in inducing the transition.

Adsorption of Li on single-layer silicene for anodes of Li-ion batteries.

We report an investigation of the interactions of Li with silicene. We find silicene to be a promising anode material for high energy density lithium-ion batteries. Based on first-principles calculations, we study the interaction between Li and silicene and explore the microscopic mechanism of Li storage on silicene. We find that Li ion is adsorbed on hollow sites at a very low concentration of less than 1.56%. At a high concentration of Li, the Li chains with up-down pairs on top sites become popular. With the formation of the Li chains, the local structure of silicene is modulated. In addition, the electronic states near the Fermi level are found to be renormalized. There is no obvious charge transfer from Li to Si, distinct from the C based materials, although the local charge distributions are polarized under the trapping of Li, implying a greater chemical interaction than that of the weak interaction with graphene. It is predicted that the capacity of silicene can reach 1196 mA h g-1 due to Li intercalation without the breaking of the Si-Si bonds.

In Situ Observation and Electrochemical Study of Encapsulated Sulfur Nanoparticles by MoS2 Flakes.

Sulfur is an attractive cathode material for next-generation lithium batteries due to its high theoretical capacity and low cost. However, dissolution of its lithiated product (lithium polysulfides) into the electrolyte limits the practical application of lithium sulfur batteries. Here we demonstrate that sulfur particles can be hermetically encapsulated by leveraging on the unique properties of two-dimensional materials such as molybdenum disulfide (MoS2). The high flexibility and strong van der Waals force in MoS2 nanoflakes allows effective encapsulation of the sulfur particles and prevent its sublimation during in situ TEM studies. We observe that the lithium diffusivities in the encapsulated sulfur particles are in the order of 10-17 m2 s-1. Composite electrodes made from the MoS2-encapsulated sulfur spheres show outstanding electrochemical performance, with an initial capacity of 1660 mAh g-1 and long cycle life of more than 1000 cycles.

Interpatient mutational spectrum of human coronavirus-OC43 revealed by illumina sequencing.

Human coronaviruses (HCoV) are RNA viruses that cause respiratory tract infections with viral replication of limited duration. The host and viral population heterogeneity could influence clinical phenotypes. Employing long RT-PCR with Illumina sequencing, we quantified the gene mutation load at 0.5% mutation frequency for the 4529 bp-domain spanning the Spike gene (4086 bp) of HCoV-OC43 in four upper respiratory clinical specimens obtained during acute illness. There were a total of 121 mutations for all four HCoV samples with the average number of mutations at 30.3 ± 10.2, which is significantly higher than that expected from the Illumina sequencing error rate. There were two mutation peaks, one at the 5' end and the other near position 1 550 in the S1 subunit. Two coronavirus samples were genotype B and two were genotype D, clustering with HCoV-OC43 strain AY391777 in neighbor-joining tree phylogenetic analysis. Nonsynonymous mutations were 76.1 ± 14% of mutation load. Although lower than other RNA viruses such as hepatitis C virus, HCoV-OC43 did exhibit quasi-species. The rate of nonsynonymous mutations was higher in the HCoV-OC43 isolates than in hepatitis C (HCV) virus genotype 1a isolates analyzed for comparison in this study. These characteristics of HCoV-OC43 may affect viral replication dynamics, receptor binding, antigenicity, evolution, transmission, and clinical illness.