sj-docx-1-jtt-10.1177_1357633X241235982 - Supplemental material for Efficacy of telerehabilitation in patients with nonspecific neck pain: A meta-analysis

Supplemental material, sj-docx-1-jtt-10.1177_1357633X241235982 for Efficacy of telerehabilitation in patients with nonspecific neck pain: A meta-analysis by Hui Zou, Zhoupeng Lu, Peng Zhao, Jialin Wang, and Ruirui Wang in Journal of Telemedicine and Telecare</p

sj-docx-2-jtt-10.1177_1357633X241235982 - Supplemental material for Efficacy of telerehabilitation in patients with nonspecific neck pain: A meta-analysis

Supplemental material, sj-docx-2-jtt-10.1177_1357633X241235982 for Efficacy of telerehabilitation in patients with nonspecific neck pain: A meta-analysis by Hui Zou, Zhoupeng Lu, Peng Zhao, Jialin Wang, and Ruirui Wang in Journal of Telemedicine and Telecare</p

Highly Enhanced Photoelectrochemical Water Oxidation Efficiency Based on Triadic Quantum Dot/Layered Double Hydroxide/BiVO₄ Photoanodes

The water oxidation half-reaction is considered to be a bottleneck for achieving highly efficient solar-driven water splitting due to its multiproton-coupled four-electron process and sluggish kinetics. Herein, a triadic photoanode consisting of dual-sized CdTe quantum dots (QDs), Co-based layered double hydroxide (LDH) nanosheets, and BiVO₄ particles, that is, QD@LDH@BiVO₄, was designed. Two sets of consecutive Type-II band alignments were constructed to improve photogenerated electron–hole separation in the triadic structure. The efficient charge separation resulted in a 2-fold enhancement of the photocurrent of the QD@LDH@BiVO₄ photoanode. A significantly enhanced oxidation efficiency reaching above 90% in the low bias region (i.e., <i>E</i> < 0.8 V vs RHE) could be critical in determining the overall performance of a complete photoelectrochemical cell. The faradaic efficiency for water oxidation was almost 90%. The conduction band energy of QDs is ∼1.0 V more negative than that of LDH, favorable for the electron injection to LDH and enabling a more efficient hole separation. The enhanced photon-to-current conversion efficiency and improved water oxidation efficiency of the triadic structure may result from the non-negligible contribution of hot electrons or holes generated in QDs. Such a band-matching and multidimensional triadic architecture could be a promising strategy for achieving high-efficiency photoanodes by sufficiently utilizing and maximizing the functionalities of QDs

Enhancing Photoelectrochemical Water Oxidation Efficiency of BiVO₄ Photoanodes by a Hybrid Structure of Layered Double Hydroxide and Graphene

Making solar fuels, e.g., hydrogen from water splitting, is one of the most critical pathways to developing a clean energy economy. The overall water splitting includes two half-reactions, i.e., water reduction and water oxidation, in which the latter is a speed-limiting step because of its multiproton-coupled four-electron process. It is highly desirable to improve the efficiency of the prevailing photoelectrochemical (PEC) anodes. We constructed an integrated BiVO₄ photoanode modified with a hybrid structure of CoAl-layered double hydroxides (LDHs) and graphene (G), i.e., G@LDH@BiVO₄. This triadic photoanode exhibited a remarkably enhanced performance toward PEC water oxidation, compared to LDH@BiVO₄ and pristine BiVO₄. The photocurrent density of G@LDH@BiVO₄ achieved 2.13 mA·cm^–2 (at 1.23 V vs reversible hydrogen electrode, RHE), 4 times higher than that of pristine BiVO₄. The oxidation efficiency is as high as 80% even at a low bias (<0.8 V vs RHE). The incident photon-to-current conversion efficiency (IPCE) of G@LDH@BiVO₄ reaches 52% at 400 nm, 2.5 times higher than that of BiVO₄. The photoconversion efficiency peaked at 0.55% at a bias of 0.72 V, a 25-fold increase over that of BiVO₄. The findings indicated that the improvement of charge separation efficiency is mainly ascribed to graphene. The enhanced charge transfer efficiency is a consequence of the synergy of graphene and an LDH, where the LDH is capable of expediting water oxidation kinetics and graphene promotes photogenerated charge transfer

Controlling the Structure and Photoelectrochemical Performance of BiVO₄ Photoanodes Prepared from Electrodeposited Bismuth Precursors: Effect of Zinc Ions as Directing Agent

A facile and green method was developed to control the structure of the prevailing BiVO₄ photoanodes derived from electrodeposited Bi precursors, in which Zn²⁺ ions were added as a directing agent to tune the deposition of Bi particles. The particle size and density of the Bi precursors were affected by the amount (or concentration) of Zn²⁺ ions added. The structural evolution of BiVO₄ was consistent with that of the Bi precursor particles. An optimal concentration of Zn²⁺ ions resulted in smaller particle sizes and produced appropriate interparticle spacing of BiVO₄ photoanodes, which possessed enhanced photocurrent and improved charge separation efficiency. The enhancement is mostly ascribed to the suppression of carrier recombination in the bulk. This work demonstrates an effective way to adjust the structure and the subsequent photoelectrochemical performance of BiVO₄ photoanodes by a cation-tuned Bi precursor strategy without the use of hard templates or complex directing agents

Antipyretic effects of Xiangqin Jiere granules on febrile young rats revealed by combining pharmacodynamics, metabolomics, network pharmacology, molecular biology experiments and molecular docking strategies

Xiangqin Jiere granules (XQJRG) is a proprietary Chinese medicine treating children’s colds and fevers, but its mechanism of action is unclear. The aim of this study was to explore the antipyretic mechanisms of XQJRG based on pharmacodynamics, non-targeted metabolomics, network pharmacology, molecular biology experiments, molecular docking, and molecular dynamics (MD) simulation. Firstly, the yeast-induced fever model was constructed in young rats to study antipyretic effect of XQJRG. Metabolomics and network pharmacology studies were performed to identify the key compounds, targets and pathways involved in the antipyretic of XQJRG. Subsequently, MetScape was used to jointly analyze targets from network pharmacology and metabolites from metabolomics. Finally, the key targets were validated by enzyme-linked immunosorbent assay (ELISA), and the affinity and stability of key ingredient and targets were evaluated by molecular docking and MD simulation. The animal experimental results showed that after XQJRG treatment, body temperature of febrile rats was significantly reduced, 13 metabolites were significantly modulated, and pathways of differential metabolite enrichment were mainly related to amino acid and lipid metabolism. Network pharmacology results indicated that quercetin and kaempferol were the key active components of XQJRG, TNF, AKT1, IL6, IL1B and PTGS2 were core targets. ELISA confirmed that XQJRG significantly reduced the plasma concentrations of IL-1β, IL-6, and TNF-α, and the hypothalamic concentrations of COX-2 and PGE2. Molecular docking demonstrated that the binding energies of kaempferol to the core targets were all below −5.0 kcal/mol. MD simulation results showed that the binding free energies of TNF-kaempferol, IL6-kaempferol, IL1B-kaempferol and PTGS2-kaempferol were −87.86 kcal/mol, −70.41 kcal/mol, −69.95 kcal/mol and −106.67 kcal/mol, respectively. In conclusion, XQJRG has antipyretic effects on yeast-induced fever in young rats, and its antipyretic mechanisms may be related to the inhibition of peripheral pyrogenic cytokines release by constituents such as kaempferol, the reduction of hypothalamic fever mediator production, and the amelioration of disturbances in amino acid and lipid metabolism. Communicated by Ramaswamy H. Sarma</p

Table_3_Genetically Obese Human Gut Microbiota Induces Liver Steatosis in Germ-Free Mice Fed on Normal Diet.XLSX

<p>Dysbiotic gut microbiota contributes to genetically obese phenotype in human. However, the effect of genetic obesity-associated gut microbiota on host hepatic metabolic deteriorations remains largely unknown. Gut microbiota from a genetically obese human donor before and after a dietary weight loss program was transplanted into germ-free C57BL/6J male mice, grouped as PreM and PostM groups, respectively. The gut microbiome, liver pathology and transcriptome response in the gnotobiotic mice were evaluated. After being fed on normal chow diet for 4 weeks, PreM group developed liver macrovesicular steatosis accompanied with higher concentrations of hepatic triglyceride and cholesterol, while PostM group exhibited normal hepatic physiology. The gut microbiota in PreM and PostM groups was significantly different from each other and was more resembling with their respective donor. RNA-sequencing revealed that, in comparison with PostM group, PreM group showed a foregoing pro-steatotic transcriptional response in liver featuring by the repression of lipid beta-oxidation and the activation of lipid absorption and cholesterol uptake before the pathology of liver steatosis. Moreover, peroxisome proliferator-activated receptor alpha (PPARα), which was repressed in PreM group, may act as crucial regulator of the hepatic transcriptional profile of lipid metabolism between two groups. Our results show that gut microbiota from a genetically obese human promotes the onset of liver steatosis by impacting hepatic transcriptional profile of lipid metabolism in mice. This adds new evidence that gut microbiota may play a causative role in the development of non-alcoholic fatty liver disease.</p

Table_2_Genetically Obese Human Gut Microbiota Induces Liver Steatosis in Germ-Free Mice Fed on Normal Diet.XLSX

<p>Dysbiotic gut microbiota contributes to genetically obese phenotype in human. However, the effect of genetic obesity-associated gut microbiota on host hepatic metabolic deteriorations remains largely unknown. Gut microbiota from a genetically obese human donor before and after a dietary weight loss program was transplanted into germ-free C57BL/6J male mice, grouped as PreM and PostM groups, respectively. The gut microbiome, liver pathology and transcriptome response in the gnotobiotic mice were evaluated. After being fed on normal chow diet for 4 weeks, PreM group developed liver macrovesicular steatosis accompanied with higher concentrations of hepatic triglyceride and cholesterol, while PostM group exhibited normal hepatic physiology. The gut microbiota in PreM and PostM groups was significantly different from each other and was more resembling with their respective donor. RNA-sequencing revealed that, in comparison with PostM group, PreM group showed a foregoing pro-steatotic transcriptional response in liver featuring by the repression of lipid beta-oxidation and the activation of lipid absorption and cholesterol uptake before the pathology of liver steatosis. Moreover, peroxisome proliferator-activated receptor alpha (PPARα), which was repressed in PreM group, may act as crucial regulator of the hepatic transcriptional profile of lipid metabolism between two groups. Our results show that gut microbiota from a genetically obese human promotes the onset of liver steatosis by impacting hepatic transcriptional profile of lipid metabolism in mice. This adds new evidence that gut microbiota may play a causative role in the development of non-alcoholic fatty liver disease.</p

Table_4_Genetically Obese Human Gut Microbiota Induces Liver Steatosis in Germ-Free Mice Fed on Normal Diet.XLSX

<p>Dysbiotic gut microbiota contributes to genetically obese phenotype in human. However, the effect of genetic obesity-associated gut microbiota on host hepatic metabolic deteriorations remains largely unknown. Gut microbiota from a genetically obese human donor before and after a dietary weight loss program was transplanted into germ-free C57BL/6J male mice, grouped as PreM and PostM groups, respectively. The gut microbiome, liver pathology and transcriptome response in the gnotobiotic mice were evaluated. After being fed on normal chow diet for 4 weeks, PreM group developed liver macrovesicular steatosis accompanied with higher concentrations of hepatic triglyceride and cholesterol, while PostM group exhibited normal hepatic physiology. The gut microbiota in PreM and PostM groups was significantly different from each other and was more resembling with their respective donor. RNA-sequencing revealed that, in comparison with PostM group, PreM group showed a foregoing pro-steatotic transcriptional response in liver featuring by the repression of lipid beta-oxidation and the activation of lipid absorption and cholesterol uptake before the pathology of liver steatosis. Moreover, peroxisome proliferator-activated receptor alpha (PPARα), which was repressed in PreM group, may act as crucial regulator of the hepatic transcriptional profile of lipid metabolism between two groups. Our results show that gut microbiota from a genetically obese human promotes the onset of liver steatosis by impacting hepatic transcriptional profile of lipid metabolism in mice. This adds new evidence that gut microbiota may play a causative role in the development of non-alcoholic fatty liver disease.</p

Data_Sheet_1_Genetically Obese Human Gut Microbiota Induces Liver Steatosis in Germ-Free Mice Fed on Normal Diet.PDF

<p>Dysbiotic gut microbiota contributes to genetically obese phenotype in human. However, the effect of genetic obesity-associated gut microbiota on host hepatic metabolic deteriorations remains largely unknown. Gut microbiota from a genetically obese human donor before and after a dietary weight loss program was transplanted into germ-free C57BL/6J male mice, grouped as PreM and PostM groups, respectively. The gut microbiome, liver pathology and transcriptome response in the gnotobiotic mice were evaluated. After being fed on normal chow diet for 4 weeks, PreM group developed liver macrovesicular steatosis accompanied with higher concentrations of hepatic triglyceride and cholesterol, while PostM group exhibited normal hepatic physiology. The gut microbiota in PreM and PostM groups was significantly different from each other and was more resembling with their respective donor. RNA-sequencing revealed that, in comparison with PostM group, PreM group showed a foregoing pro-steatotic transcriptional response in liver featuring by the repression of lipid beta-oxidation and the activation of lipid absorption and cholesterol uptake before the pathology of liver steatosis. Moreover, peroxisome proliferator-activated receptor alpha (PPARα), which was repressed in PreM group, may act as crucial regulator of the hepatic transcriptional profile of lipid metabolism between two groups. Our results show that gut microbiota from a genetically obese human promotes the onset of liver steatosis by impacting hepatic transcriptional profile of lipid metabolism in mice. This adds new evidence that gut microbiota may play a causative role in the development of non-alcoholic fatty liver disease.</p