Absence of near-ambient superconductivity in LuH2±xNy.

A recent study demonstrated near-ambient superconductivity in nitrogen-doped lutetium hydride1. This stimulated a worldwide interest in exploring room-temperature superconductivity at low pressures. Here, by using a high-pressure and high-temperature synthesis technique, we have obtained nitrogen-doped lutetium hydride (LuH2±xNy), which has a dark-blue colour and a structure with the space group [Formula: see text] as evidenced by X-ray diffraction. This structure is the same as that reported in ref. 1, with a slight difference in lattice constant. Raman spectroscopy of our samples also showed patterns similar to those observed in ref. 1. Energy-dispersive X-ray spectroscopy confirmed the presence of nitrogen in the samples. We observed a metallic behaviour from 350 K to 2 K at ambient pressure. On applying pressures from 2.1 GPa to 41 GPa, we observed a gradual colour change from dark blue to violet to pink-red. By measuring the resistance at pressures ranging from 0.4 GPa to 40.1 GPa, we observed a progressively improved metallic behaviour; however, superconductivity was not observed above 2 K. Temperature dependence of magnetization at high pressure shows a very weak positive signal between 100 K and 320 K, and the magnetization increases with an increase in magnetic field at 100 K. All of these are not expected for superconductivity above 100 K. Thus, we conclude the absence of near-ambient superconductivity in this nitrogen-doped lutetium hydride at pressures below 40.1 GPa.

Distinguishing homogeneous advanced oxidation processes in bulk water from heterogeneous surface reactions in organic oxidation.

Clarifying the reaction pathways at the solid-water interface and in bulk water solution is of great significance for the design of heterogeneous catalysts for selective oxidation of organic pollutants. However, achieving this goal is daunting because of the intricate interfacial reactions at the catalyst surface. Herein, we unravel the origin of the organic oxidation reactions with metal oxide catalysts, revealing that the radical-based advanced oxidation processes (AOPs) prevail in bulk water but not on the solid catalyst surfaces. We show that such differing reaction pathways widely exist in various chemical oxidation (e.g., high-valent Mn3+ and MnOX) and Fenton and Fenton-like catalytic oxidation (e.g., Fe2+ and FeOCl catalyzing H2O2, Co2+ and Co3O4 catalyzing persulfate) systems. Compared with the radical-based degradation and polymerization pathways of one-electron indirect AOP in homogeneous reactions, the heterogeneous catalysts provide unique surface properties to trigger surface-dependent coupling and polymerization pathways of a two-electron direct oxidative transfer process. These findings provide a fundamental understanding of catalytic organic oxidation processes at the solid-water interface, which could guide the design of heterogeneous nanocatalysts.

A spatiotemporal barrier formed by Follistatin is required for left-right patterning.

How left-right (LR) asymmetry emerges in a patterning field along the anterior-posterior axis remains an unresolved problem in developmental biology. Left-biased Nodal emanating from the LR organizer propagates from posterior to anterior (PA) and establishes the LR pattern of the whole embryo. However, little is known about the regulatory mechanism of the PA spread of Nodal and its asymmetric activation in the forebrain. Here, we identify bilaterally expressed Follistatin (Fst) as a regulator blocking the propagation of the zebrafish Nodal ortholog Southpaw (Spaw) in the right lateral plate mesoderm (LPM), and restricting Spaw transmission in the left LPM to facilitate the establishment of a robust LR asymmetric Nodal patterning. In addition, Fst inhibits the Activin-Nodal signaling pathway in the forebrain thus preventing Nodal activation prior to the arrival, at a later time, of Spaw emanating from the left LPM. This contributes to the orderly propagation of asymmetric Nodal activation along the PA axis. The LR regulation function of Fst is further confirmed in chick and frog embryos. Overall, our results suggest that a robust LR patterning emerges by counteracting a Fst barrier formed along the PA axis.

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1.

Feingold syndrome type 1, caused by loss-of-function of MYCN, is characterized by varied phenotypes including esophageal and duodenal atresia. However, no adequate model exists for studying the syndrome's pathological or molecular mechanisms, nor is there a treatment strategy. Here, we developed a zebrafish Feingold syndrome type 1 model with nonfunctional mycn, which had severe intestinal atresia. Single-cell RNA-seq identified a subcluster of intestinal cells that were highly sensitive to Mycn, and impaired cell proliferation decreased the overall number of intestinal cells in the mycn mutant fish. Bulk RNA-seq and metabolomic analysis showed that expression of ribosomal genes was down-regulated and that amino acid metabolism was abnormal. Northern blot and ribosomal profiling analysis showed abnormal rRNA processing and decreases in free 40S, 60S, and 80S ribosome particles, which led to impaired translation in the mutant. Besides, both Ribo-seq and western blot analysis showed that mTOR pathway was impaired in mycn mutant, and blocking mTOR pathway by rapamycin treatment can mimic the intestinal defect, and both L-leucine and Rheb, which can elevate translation via activating TOR pathway, could rescue the intestinal phenotype of mycn mutant. In summary, by this zebrafish Feingold syndrome type 1 model, we found that disturbance of ribosomal biogenesis and blockage of protein synthesis during development are primary causes of the intestinal defect in Feingold syndrome type 1. Importantly, our work suggests that leucine supplementation may be a feasible and easy treatment option for this disease.

Functional characterization of NBS-LRR genes reveals an NBS-LRR gene that mediates resistance against Fusarium wilt.

BACKGROUND: Most disease resistance (R) genes in plants encode proteins that contain leucine-rich-repeat (LRR) and nucleotide-binding site (NBS) domains, which belong to the NBS-LRR family. The sequenced genomes of Fusarium wilt-susceptible Vernicia fordii and its resistant counterpart, Vernicia montana, offer significant resources for the functional characterization and discovery of novel NBS-LRR genes in tung tree. RESULTS: Here, we identified 239 NBS-LRR genes across two tung tree genomes: 90 in V. fordii and 149 in V. montana. Five VmNBS-LRR paralogous were predicted in V. montana, and 43 orthologous were detected between V. fordii and V. montana. The orthologous gene pair Vf11G0978-Vm019719 exhibited distinct expression patterns in V. fordii and V. montana: Vf11G0978 showed downregulated expression in V. fordii, while its orthologous gene Vm019719 demonstrated upregulated expression in V. montana, indicating that this pair may be responsible for the resistance to Fusarium wilt in V. montana. Vm019719 from V. montana, activated by VmWRKY64, was shown to confer resistance to Fusarium wilt in V. montana by a virus-induced gene silencing (VIGS) experiment. However, in the susceptible V. fordii, its allelic counterpart, Vf11G0978, exhibited an ineffective defense response, attributed to a deletion in the promoter's W-box element. CONCLUSIONS: This study provides the first systematic analysis of NBS-LRR genes in the tung tree and identifies a candidate gene that can be utilized for marker-assisted breeding to control Fusarium wilt in V. fordii.

Precise Surface Profiling at the Nanoscale Enabled by Deep Learning.

Surface topography, or height profile, is a critical property for various micro- and nanostructured materials and devices, as well as biological systems. At the nanoscale, atomic force microscopy (AFM) is the tool of choice for surface profiling due to its capability to noninvasively map the topography of almost all types of samples. However, this method suffers from one drawback: the convolution of the nanoprobe's shape in the height profile of the samples, which is especially severe for sharp protrusion features. Here, we report a deep learning (DL) approach to overcome this limit. Adopting an image-to-image translation methodology, we use data sets of tip-convoluted and deconvoluted image pairs to train an encoder-decoder based deep convolutional neural network. The trained network successfully removes the tip convolution from AFM topographic images of various nanocorrugated surfaces and recovers the true, precise 3D height profiles of these samples.

Personalized Nanovaccines Enhance Lymph Node Accumulation and Reprogram the Tumor Microenvironment for Improved Photodynamic Immunotherapy.

Tumor immunotherapy has emerged as an efficacious therapeutic approach that mobilizes the patient's immune system to achieve durable tumor suppression. Here, we design a photodynamic therapy-motivated nanovaccine (Dex-HDL/ALA-Fe3O4) co-delivering 5-aminolevulinic acid and Fe3O4 nanozyme that demonstrate a long-term durable immunotherapy strategy. After vaccination, the nanovaccine exhibits obvious tumor site accumulation, lymph node homing, and specific and memory antitumor immunity evocation. Upon laser irradiation, Dex-HDL/ALA-Fe3O4 effectively generates reactive oxygen species at the tumor site not only to induce the immunogenic cell death-cascade but also to trigger the on-demand release of full types of tumor antigens. Intriguingly, Fe3O4 nanozyme-catalyzed hydrogen peroxide generated oxygen for alleviating tumor hypoxia and modifying the inhibitory tumor microenvironment, thereby exhibiting remarkable potential as a sensitizer. The intravenous administration of nanovaccines in diverse preclinical cancer models has demonstrated remarkable tumor regression and inhibition of postoperative tumor recurrence and metastasis, thereby enabling personalized treatment strategies against highly heterogeneous tumors.

Genome assembly, resequencing and genome-wide association analyses provide novel insights into the origin, evolution and flower colour variations of flowering cherry.

Flowering cherry is a very popular species around the world. High-quality genome resources for different elite cultivars are needed, and the understanding of their origins and the regulation of key ornamental traits are limited for this tree. Here, a high-quality chromosome-scale genome of Prunus campanulata 'Plena' (PCP), which is a native and elite flowering cherry cultivar in China, was generated. The contig N50 of the genome was 18.31 Mb, and 99.98% of its contigs were anchored to eight chromosomes. Furthermore, a total of 306 accessions of flowering cherry germplasm and six lines of outgroups were collected. Resequencing of these 312 lines was performed, and 761 267 high-quality genomic variants were obtained. The origins of flowering cherry were predicted, and these 306 accessions could be classified into three clades, A, B and C. According to phylogenetic analysis, we predicted two origins of flowering cherry. Flowering cherry in clade A originated in southern China, such as in the Himalayan Mountains, while clades B and C originated in northeastern China. Finally, a genome-wide association study of flower colour was performed for all 312 accessions of flowering cherry germplasm. A total of seven quantitative trait loci (QTLs) were identified. One gene encoding glycosylate transferase was predicted as the candidate gene for one QTL. Taken together, our results provide a valuable genomic resource and novel insights into the origin, evolution and flower colour variations of flowering cherry.

Site-Specific Analysis of Core and Antenna Fucosylation on Serum Glycoproteins.

Fucosylation is an important structural feature of glycans and plays an essential role in the regulation of glycoprotein functions. Fucosylation can be classified into core- (CF) and antenna-fucosylation (AF, also known as (sialyl-) Lewis) based on the location on N-glycans, and they perform distinct biological functions. In this study, core- and antenna-fucosylated N-glycans on human serum glycoproteins that hold great clinical application values were systematically characterized at the site-specific level using StrucGP combined with the recently developed fucosylation assignment method. The results showed that fucosylation was widely distributed on serum glycoproteins, with 50% of fucosylated glycopeptides modified by AF N-glycans, 37% by CF N-glycans, and 13% by dual-fucosylated N-glycans. Interestingly, CF and AF N-glycans preferred to modify different groups of serum glycoproteins with different tissue origins and were involved in distinctive biological processes. Specifically, AF N-glycoproteins are mainly from the liver and participated in complement activation, blood coagulation, and endopeptidase activities, while CF N-glycoproteins originate from diverse tissues and are mainly involved in cell adhesion and signaling transduction. These data further enhanced our understanding of fucosylation on circulation glycoproteins.

Cell surface GRP78: A potential therapeutic target for high glucose-induced endothelial injury.

Endothelial cell inflammation and oxidative stress are critical to developing diabetic vascular complications. GRP78 translocation to the cell surface has been observed in different types of endothelial cells, but the potential role of cell surface GRP78 in modulating endothelial inflammation and oxidative stress remains uncertain. In this study, we investigated whether inhibiting cell surface GRP78 function using a novel anti-GRP78 monoclonal antibody (MAb159) could suppress high glucose (HG)-induced endothelial inflammation and oxidative stress. Our findings demonstrated that the expression of cell surface GRP78 was increased in HG-treated HUVECs. Inhibition of cell surface GRP78 using MAb159 attenuated HG-induced endothelial injury, inflammation and oxidative stress, while activation of GRP78 by recombinant GRP78 further amplified HG-induced endothelial damage, inflammation and oxidative stress. Additionally, we discovered that cell surface GRP78 promoted HG-induced inflammation and oxidative stress by activating the TLR4/NF-κB signalling pathway. Moreover, HG-induced GRP78 translocation to the cell surface is dependent on ER stress. Our data demonstrate that targeting cell surface GRP78 could be a promising therapeutic strategy for mitigating endothelial injury, inflammation and oxidative stress.

Changes in choroidal hemodynamics of form-deprivation myopia in Guinea pigs.

PURPOSE: We studied changes in the choroid, particularly variation in blood flow, during the development of myopia. The hemodynamic mechanism in play remains unclear. We evaluated blood flow by quantitating indocyanine green (ICG) fluorescence in a guinea pig model of form-deprivation myopia. METHODS: Guinea pigs were divided into form-deprivation myopia (FDM) and normal control (NC) groups. Ocular biometric and choroidal hemodynamics parameters were quantitatively derived via ICG imaging, and included the maximal ICG fluorescence intensity (Imax), rising time (Trising), blood flow index (BFI), and mean transit time (MTT). RESULTS: Form deprivation was associated with significant interocular differences in terms of both refractive error and axial length. ICG fluorescence hemodynamic maps of fundal blood flow and vasculature density were evident. In deprived eyes, the fluorescence signals exhibited significantly longer Trising and MTT but lower Imax and BFI than fellow eyes and NC group. The interocular differences in terms of the ocular biometric and hemodynamic parameters were significantly correlated. Hemodynamic analysis of choriocapillaris lobules revealed weakened fluorescence intensity and prolonged arrival and filling times in deprived eyes. Form deprivation reduced the number of lobulated choriocapillaris structures. CONCLUSION: Form-deprivation myopia triggered changes in the hemodynamic and vascular network structures of the choroid and choriocapillaris. The ICG fluorescence imaging/analysis method provides a unique tool for further myopia research.

Heterogeneous-Structured Molybdenum Diboride as a Novel and Promising Anode for Lithium-Ion Batteries.

With the development of electric vehicles, exploiting anode materials with high capacity and fast charging capability is an urgent requirement for lithium-ion batteries (LIBs). Borophene, with the merits of high capacity, high electronic conductivity and fast diffusion kinetics, holds great potential as anode for LIBs. However, it is difficult to fabricate for the intrinsic electron-deficiency of boron atom. Herein, heterogeneous-structured MoB2 (h-MoB2 ) with amorphous shell and crystalline core, is prepared by solid phase molten salt method. As demonstrated, crystalline core can encapsulate the honeycomb borophene within two adjacent Mo atoms, and amorphous shell can accommodate more lithium ions to strengthen the lithium storage capacity and diffusion kinetics. According to theoretical calculations, the lithium adsorption energy in MoB2 is about -2.7 eV, and the lithium diffusion energy barrier in MoB2 is calculated to be 0.199 eV, guaranteeing the enhanced adsorption capability and fast diffusion kinetic behavior of Li+ ions. As a result, h-MoB2 anode presents high capacity of 798 mAh g-1 at 0.1 A g-1 , excellent rate performance of 183 mAh g-1 at 5 A g-1 and long-term cyclic stability for 1200 cycles. This work may inspire ideas for the fabrication of borophene analogs and two-dimensional metal borides.

Transcription factor PbMYB80 regulates lignification of stone cells and undergoes RING finger protein PbRHY1-mediated degradation in pear fruit.

The Chinese white pear (Pyrus bretschneideri) fruit carries a high proportion of stone cells, adversely affecting fruit quality. Lignin is a main component of stone cells in pear fruit. In this study, we discovered that a pear MYB transcription factor, PbMYB80, binds to the promoters of key lignin biosynthesis genes and inhibits their expression. Stable overexpression of PbMYB80 in Arabidopsis showed that lignin deposition and secondary wall thickening were inhibited, and the expression of the lignin biosynthesis genes in transgenic Arabidopsis was decreased. Transient overexpression of PbMYB80 in pear fruit inhibited lignin metabolism and stone cell development, and the expression of some genes in the lignin metabolism pathway was reduced. In contrast, silencing PbMYB80 with VIGS increased the lignin and stone cell content in pear fruit, and increased expression of genes in the lignin metabolism pathway. By screening a pear fruit cDNA library in yeast, we found that PbMYB80 binds to a RING finger (PbRHY1) protein. We also showed that PbRHY1 exhibits E3 ubiquitin ligase activity and degrades ubiquitinated PbMYB80 in vivo and in vitro. This investigation contributes to a better understanding of the regulation of lignin biosynthesis in pear fruit, and provides a theoretical foundation for increasing pear fruit quality at the molecular level.

Short-Process Regeneration of Highly Stable Spherical LiCoO2 Cathode Materials from Spent Lithium-Ion Batteries through Carbonate Precipitation.

High-efficacy recycling of spent lithium cobalt oxide (LiCoO2 ) batteries is one of the key tasks in realizing a global resource security strategy due to the rareness of lithium (Li) and cobalt (Co) resources. However, it is of great significance to develop the innovative recycle methods for spent LiCoO2 , simultaneously realizing the efficient recovery of valuable elements and the regeneration of high-performance LiCoO2 . Herein, a novel strategy of regenerating LiCoO2 cathode is proposed, which involves the preparation of micro-spherical aluminum (Al)-doped lithium-lacked precursor (Li2x Co1-x-y Al2/3y CO3, remarked as "PLCAC") via ammonium bicarbonate coprecipitation. The comprehensive conditions affecting particle growth kinetics, morphology and particle size the has been investigated in detail by physical characterizations and electrochemical measurements. And the optimized Al-doped LiCoO2 materials with high-density sphericity (LiCo1-z Alz O2 , remarked as "LCAO") shows a high initial specific capacity of 161 mAh g-1 at 0.1 C and excellent capacity retention of 99.5 % within 100 cycles at 1 C in the voltage range of 2.8 to 4.3 V. Our work provides valuable insights into the featured design of LiCoO2 precursors and cathode materials from spent LiCoO2 batteries, potentially guaranteeing the high-efficacy recycling and utilization of strategic resources.

Constructing Hollow Microcubes SnS2 as Negative Electrode for Sodium-ion and Potassium-ion Batteries.

Sodium/potassium-ion batteries (NIBs and KIBs) are considered the most promising candidates for lithium-ion batteries in energy storage fields. Tin sulfide (SnS2) is regarded as an attractive negative candidate for NIBs and KIBs thanks to its superior power density, high-rate performance and natural richness. Nevertheless, the slow dynamics, the enormous volume change and the decomposition of polysulfide intermediates limit its practical application. Herein, microcubes SnS2 were prepared through sacrificial MnCO3 template-assisted and a facile solvothermal reaction strategy and their performance was investigated in Na and K-based cells. The unique hollow cubic structure and well-confined SnS2 nanosheets play an important role in Na+/K+ rapid kinetic and alleviating volume change. The effect of the carbon additives (Super P/C65) on the electrochemical properties were investigated thoroughly. The in operando and ex-situ characterization provide a piece of direct evidence to clarify the storage mechanism of such conversion-alloying type negative electrode materials.

Brown adipose tissue transplantation improves skin fibrosis in localized scleroderma.

Adipose tissue transplantation shows great therapeutic potential in reversing localized scleroderma-associated skin fibrosis. Brown adipose tissue (BAT) can specifically secrete various cytokines against fibrosis, but its therapeutic potential in improving skin fibrosis has not yet been demonstrated. In this study, we have demonstrated the superior therapeutic efficacy of BAT transplantation for sclerotic skin by transplanting two distinct types of adipose tissue. In comparison to the white adipose tissue (WAT) group, mice treated with BAT transplantation exhibited a significant reduction in dermal thickness. BAT transplantation effectively reverses skin sclerosis through mechanisms involving inflammation reduction, promotion of angiogenesis, inhibition of myofibroblast accumulation, and collagen deposition. This therapeutic effect can be attributed to its unique paracrine effects. Furthermore, transcriptome sequencing (RNA-Seq) revealed upregulation of pathways associated with lipogenesis and fatty acid metabolism in BAT while downregulating pathways are related to transforming growth factor ß(TGF-ß), epithelial-mesenchymal transition (EMT), and inflammatory response. These findings suggest that BAT transplantation holds great promise as a novel approach for localized scleroderma treatment.

Effect of DBD Plasma Treatment on Activity of Mo-Based Sulfur-Resistant Methanation Catalyst.

By combining the advantages of dielectric barrier discharge (DBD) low temperature plasma and fluidized bed, the effect of plasma on the performance of supported Mo-based catalyst was studied in this paper. The performance of the catalyst obtained by plasma treatment, calcined, plasma+calcined was compared, and the appropriate catalyst preparation scheme was explored. Comparing with the three catalysts, it was concluded that the catalyst average conversion after 30 W plasma treatment is 33.40 %, which was 8.94 % and 12.75 % higher than the other two, respectively. The structure and properties of the catalyst were characterized by N2-Physisorption, H2-chemisorption, XRD, TEM, XPS, Raman and NO-pulse adsorption. Then, by analyzing the characterization results, it can be seen that plasma can make the catalyst have a higher specific surface area and a more dispersed active metal with smaller grain size. Through the surface species identification characterization, it was found that plasma can produce more defective structures and expose more active sites, which is the main reason for the difference in conversion.

Isolation and the pathogenicity characterization of Decapod iridescent virus 1 (DIV1) from diseased Macrobrachium nipponense and its activation on host immune response.

The high morbidity and mortality of Macrobrachium nipponense occurred in several farms in China, with cardinal symptoms of slow swimming, loss of appetite, empty of intestine, reddening of the hepatopancreas and gills. The pathogen has been confirmed as Decapod Iridescent Virus 1 (DIV1), namely DIV1-mn, by molecular epidemiology, histopathological examination, TEM observation, challenge experiment, and viral load detection. Histopathological analysis showed severe damage in hepatopancreas and gills of diseased prawns, exhibited few eosinophilic inclusions and pyknosis, and TEM of diseased prawns revealed that icosahedral virus particles existed in hepatopancreas and gill, which confirmed the disease of the farmed prawns caused by the DIV1 infection. Besides, challenge tests showed LD50 of DIV1 to M. nipponense was determined to be 2.14 × 104 copies/mL, and real-time PCR revealed that M. nipponense had a very high DIV1 load in the hemocytes, gills and hepatopancreas after infection. Furthermore, qRT-PCR was undertaken to investigated the expression of six immune-related genes in DIV1-infected M. nipponense after different time points, and the results revealed UCHL3, Relish, Gly-Cru2, CTL, MyD88 and Hemocyanin were significantly up-regulated in hemocytes, gills and hepatopancreas, which revealed various expression patterns in response to DIV1 infection. This study revealed that DIV1 infection is responsible for the mass mortality of M. nipponense, one of the important crustacean species, indicating its high susceptibility to DIV1. Moreover, this study will contribute to exploring the interaction between the host and DIV1 infection, specifically in terms of understanding how M. nipponense recognizes and eliminates the invading of DIV1.

Refining DIIS algorithms for Si and GaAs solar cells: incorporation of weight regularization, conjugate gradient, and reverse automatic differentiation techniques.

Pivotal enhancements in electronic minimization algorithms, which are vital for the advancement of computational materials science, are introduced in this research. Our research is dedicated to refining the DIIS algorithm specifically for electronic structure calculations of silicon (Si) and gallium arsenide (GaAs) solar cells, aiming to enhance their efficiency and stability. We have enriched DIIS by integrating a weight regularization factor, significantly bolstering its convergence stability. This modification enhances iteration robustness and curtails the average iteration duration, thus streamlining the convergence process. Furthermore, we have incorporated the conjugate gradient (CG) algorithm to proficiently resolve symmetric positive definite residual matrices. This inclusion substantially accelerates the solution-finding process within the DIIS framework. A novel aspect of our research is the application of reverse automatic differentiation (AD), deployed in two distinct methodologies: the construction of the Jacobian matrix and direct chain rule application for gradient computation. These approaches involve sophisticated mathematical techniques that enhance computational precision and efficiency specifically for Si and GaAs solar cell materials in determining the optimal weights for residual combinations during DIIS iterations. The integration of these advanced methods into the DIIS algorithm not only augments its convergence stability but also ensures a substantial reduction in total computational time. Our findings demonstrate that the enhanced DIIS, CG-enhanced DIIS, and AD-integrated DIIS methods collectively lead to a more efficient electronic minimization process. This balance of stability and efficiency is crucial in high-performance computational materials science, particularly for complex systems analysis. The findings of this research represent a notable advancement in computational strategies for Si and GaAs solar cell materials, providing enhanced methodologies and insights that significantly improve the efficiency and stability of electronic structure calculations in these critical components of renewable energy technologies.

Effects of biological agents on glycogen metabolism in psoriasis patients: A systematic review and meta-analysis.

The effectiveness and safety of biological agents for treating psoriasis have been confirmed; however, their effects on glucose metabolism biomarkers in psoriasis patients remain unclear. A systematic review and meta-analysis were performed according to PRISMA guidelines. The final analysis enrolled 12 studies, including eight randomized controlled trial (RCT) (n = 5628 patients) and four observational cohort studies (OBSs) (n = 393 patients). The meta-analysis comprising nine studies (six RCTs and three OBSs) revealed a slight reduction in the levels of HOMA-IR associated with the use of biological therapies in OBS (biological therapies vs. traditional therapies: WMD = -0.2, CI = -0.10 to 0.50, p = 0.02). Although a considerable number of studies were analysed, our review did not show a significant alteration in HOMA-IR levels among patients treated with biological therapies such as IL-17 inhibitors and IL-12/23 inhibitors at weeks 12-16 in RCTs. We also did not observe remarkable alterations in the fasting plasma glucose levels of patients in both OBS and RCT. Additional RCT on a larger scale and duration is required to provide more conclusive evidence regarding the effect of biological agents on glycogen metabolism in psoriasis.