Biodegradation enhancement of high concentrations formaldehyde waste gas and verification of the metabolic mechanism.

The enhanced effects of formaldehyde biodegradation in a biofilm packing tower are investigated in this study. Three experimental groups were established: a blank control group, a biochar addition group, and a lanthanum addition group. The inlet gas flow rate, the inlet gas concentration, and the structural succession characteristics of the microbial community in the tower were investigated by regular sampling. The intracellular metabolites and key enzymes of the dominant functional bacteria, Pseudomonas P1 and Methylobacterium Q1, in the tower were analyzed. The results indicated that with the biochar addition, the formaldehyde purification efficiency increased significantly from 91.67-94.67 % to 94.12 96.85 %, and the bio-elimination capacity increased with an increase in the inlet gas flow rate from 2.314 to 13.988 mg L-1h-1 to 2.697-15.051 mg L-1h-1. With the addition of lanthanum, the purification efficiency increased significantly from 90.80-93.98 % to 94.36-96.78 %, and the bio-elimination capacity increased with an increase in the inlet gas concentration from 1.099-11.284 mg L-1h-1 to 1.266-11.961 mg L-1h-1. The microbial community structure in the tower changed with system operation, and the formaldehyde degrading functional bacteria formed the dominant bacteria. It was verified that P1 and Q1 metabolized high concentrations of formaldehyde by the serine cycle and the ribulose monophosphate (RuMP) cycle.

Comparative analysis of different treatment strategies for septic spondylitis: a retrospective study of one hundred and twelve patients.

PURPOSE: To compare the clinical efficacy and prognosis differences between conservative treatment and surgical treatment in patients with non-serious neurologically intact pyogenic spondylitis (Nsi-Nsni-PS), and to provide theoretical reference for the clinical treatment of Nsi-Nsni-PS patients. METHODS: A retrospective analysis was conducted on 112 cases of Nsi-Nsni-PS patients treated in our hospital from June 2016 to June 2021. According to different treatment methods, they were divided into conservative treatment group (53 cases) and surgical treatment group (59 cases). The general data, laboratory tests, imaging examinations, length of hospital stay, duration of antibiotic use, VAS for pain before and after treatment, ODI, local kyphotic angle correction of diseased vertebrae, and recurrence rate were collected and analyzed in both groups. SPSS 26.0 statistical software was used for analysis. Measurement data were expressed as mean ± standard deviation, and independent sample t-test or rank sum test was used for comparison between groups, while variance analysis was used for intra-group comparison. Count data were expressed as number (%) and compared between groups using chi-square test or Fisher's exact test. Mann-Whitney U test was used to evaluate the changes in local kyphotic angle between the two groups. A p value < 0.05 was considered statistically significant. RESULTS: There were no significant differences in general data and imaging characteristics between the two groups (P > 0.05); there were no statistically significant differences in the positive culture rate of pathogens, length of hospital stay, duration of antibiotic use, treatment complications, WBC, CRP, ESR levels at admission and discharge, VAS and ODI at admission and last follow-up between the two groups (P > 0.05). The WBC and CRP levels of patients in the conservative group at discharge were lower than those in the surgical group (P < 0.05), and there was no significant difference in the decrease in inflammatory indicators (WBC, CRP, ESR) between the two groups (P > 0.05). By the last follow-up, the neurological function of patients in both groups had significantly improved compared to admission (P < 0.05), with 12 out of 15 ASIA grade D patients in the conservative group recovering to grade E, and 21 out of 25 grade D patients in the surgical group recovering to grade E, with no worsening of neurological function in either group. The differences in VAS and ODI scores at the last follow-up compared to before treatment were statistically significant in both groups (P < 0.05), and all patients regained normal activity. Compared with before treatment, the correction degree of local kyphotic angle in the surgical group at the last follow-up was 0.93 ± 4.94°, slightly higher than that in the conservative group (-0.83 ± 3.37°), and the difference was statistically significant(P < 0.05). CONCLUSIONS: During our follow-up, we found that both conservative and surgical treatments achieved satisfactory clinical outcomes in patients with Nsi-Nsni-PS. Compared to conservative treatment, surgical intervention did not demonstrate significant advantages in reducing hospitalization time and antibiotic usage duration, increasing pathogen culture positivity rate, lowering treatment complications, or controlling recurrence. However, surgical intervention showed superiority in correcting the local kyphotic angle of spinal lesions, albeit with relatively increased surgical trauma, risks, and treatment costs. At the last follow-up, the surgical group did not exhibit better long-term efficacy. Therefore, when formulating clinical treatment strategies for patients with Nsi-Nsni-PS, it may be preferable to prioritize conservative treatment, supplemented by the use of sensitive or empiric antibiotics for infection management, to improve patient prognosis.

Nanoparticles functionalized with stem cell secretome and CXCR4-overexpressing endothelial membrane for targeted osteoporosis therapy.

BACKGROUND: Osteoporosis is a chronic condition affecting patients' morbidity and mortality and represents a big socioeconomic burden. Because stem cells can proliferate and differentiate into bone-forming cells, stem cell therapy for osteoporosis has been widely studied. However, cells as a live drug face multiple challenges because of their instability during preservation and transportation. In addition, cell therapy has potential adverse effects such as embolism, tumorigenicity, and immunogenicity. RESULTS: Herein, we sought to use cell-mimicking and targeted therapeutic nanoparticles to replace stem cells. We fabricated nanoparticles (NPs) using polylactic-co-glycolic acid (PLGA) loaded with the secretome (Sec) from mesenchymal stem cells (MSCs) to form MSC-Sec NPs. Furthermore, we cloaked the nanoparticles with the membranes from C-X-C chemokine receptor type 4 (CXCR4)-expressing human microvascular endothelial cells (HMECs) to generate MSC-Sec/CXCR4 NP. CXCR4 can target the nanoparticles to the bone microenvironment under osteoporosis based on the CXCR4/SDF-1 axis. CONCLUSIONS: In a rat model of osteoporosis, MSC-Sec/CXCR4 NP were found to accumulate in bone, and such treatment inhibited osteoclast differentiation while promoting osteogenic proliferation. In addition, our results showed that MSC-Sec/CXCR4 NPs reduce OVX-induced bone mass attenuation in OVX rats.

Structural definition of the discrete hotspot sites of BMP-2 conformational wrist epitope and rational design of the hotspot-derived osteogenic peptides against chondrocyte senescence.

The bone morphogenetic protein-2 (BMP-2) is an essential regulator of bone formation and remodeling, which has also been implicated in the pathogenesis of osteoarthritis and its closely related chondrocyte senescence. The BMP-2 uses a conformational wrist epitope and a linear knuckle epitope to interact with type-I (BMPR-I) and type-II (BMPR-II) receptors, respectively. Previously, the knuckle epitope has been intensely studied, but the wrist epitope still remains largely unexplored due to its discontinuous nature. In the present work, the intermolecular interaction of BMP-2 with BMPR-I was investigated systematically at structural, energetic and dynamic levels. Three discrete hotspots that represent the key BMPR-I recognition sites of BMP-2 were identified; they are spatially dispersed over the two monomers of BMP-2 dimer and totally account for 83.5 % binding potency of BMP-2 to BMPR-I (hotspot 1: residues 49-70 in monomer 1; hotspot 2: residues 24-31 in monomer 2; hotspot 3: residues 88-107 in monomer 2). Therefore, we defined the three discrete hotspot sites as the core region of wrist epitope; their contribution to the binding increases in the order: hotspot 2 < hotspot 3 < hotspot 1. We demonstrated that the primary hotspot 1 site has a native U-shaped conformation in the full-length BMP-2 protein context, but it cannot maintain in the native conformation when split from the context to obtain a free hotspot-1 peptide, thus largely impairing its binding potency to BMPR-I. We further employed disulfide-bonded cyclization and head-to-tail cyclization to constrain the peptide conformation, and found that only the former can effectively constrain the peptide into native conformation, thus considerably improving its binding affinity to BMPR-I, whereas the latter totally disorders the native conformation, thus rendering the peptide as a full nonbinder of BMPR-I.

MiRNA-132 regulates the development of osteoarthritis in correlation with the modulation of PTEN/PI3K/AKT signaling.

BACKGROUND: Osteoarthritis (OA) is a commonly known prevalent joint disease, with limited therapeutic methods. This study aimed to investigate the functions of miRNA-132 (miR-132) in the modulation of PTEN/PI3K/AKT signaling pathway in the development and progression of osteoarthritis. METHODS: Eight male osteoarthritic patients and eight healthy males were recruited. Male Sprague Dawley (SD) rats were used for cellular experiments. QRT-PCR was performed to detect the expression levels of miR-132, PTEN, PI3K and AKT. MTT assay and apoptosis assay were carried out to measure the cell proliferation rate and cell apoptosis rate, respectively. Western blotting was employed to detect the protein expression of related RNAs and inflammatory factors. RESULTS: In osteoarthritic patients, the expression level of miR-132 was decreased, compared with that in the normal group. Over-expression of miR-132 elevated cell proliferation and decreased apoptosis of chondrocytes. Down-regulation of miR-132 decreased cell proliferation and induced apoptosis in chondrocytes. In addition, down-regulation of miR-132 promoted the expression of Bax protein and activated caspase-3/9, increased inflammation divisors. PTEN inhibitor antagonized the destructive effect of the miR-132 inhibitor on cell proliferation of chondrocytes. PI3K inhibitor increased the destructive effect of the miR-132 inhibitor on osteoarthritis. CONCLUSION: In conclusion, miR-132 is an important regulator of osteoarthritis in chondrocytes through the PTEN/PI3K/AKT signaling pathway.

Exosomes for gene therapy effectively inhibit the endothelial-mesenchymal transition in mouse aortic endothelial cells.

BACKGROUND: Heterotopic ossification (HO) can limit joint activity, causes ankylosis and impairs the function and rehabilitation of patients. Endothelial to mesenchymal transition (EndMT) plays an important role in the pathogenesis of HO, and high expression of SMAD7(Mothers Against Decapentaplegic Homolog 7) in endothelial cells can effectively reverse the TGF-ß1 mediated EndMT. This article studied an appropriately engineered exosome with high biocompatibility and good targeting property to administrate SMAD7 gene therapy to inhibit the EndMT. METHODS: Exosomes from mouse aortic endothelial cells were cultured and harvested. DSPE-PEG and antibody CD34 were combined to exosomes to synthesize the endothelial cell targeting exosome vector (Exosome-DSPE-PEG-AbCD34). The biocompatibility, stability, targeting and cell internalization of exosome vector were tested, then the Exosome-DSPE-PEG-AbCD34 was loaded with Smad7 plasmid and administrated to MAECs to examine its therapeutic effect on EndMT of MAEC mediated by TGF-ß1. RESULTS: The Exosome-DSPE-PEG-AbCD34 has no impact on MAEC cell viability at high concentration, and exosome-DSPE-PEG-AbCD34 could be stably stored at 4°C and 37°C for at least 8 days. Exosome-DSPE-PEG-AbCD34 has better targeting property to MAEC cells and can enter into the cells more effectively. The Exosome-DSPE-PEG-AbCD34-Smad7 could significantly increase the level of SMAD7, decrease the expression of TGF-ß1, and effectively reverse the EndMT of MAEC mediated by TGF- ß1 in MAEC cells. CONCLUSIONS: The synthesized Exosome-DSPE-PEG-AbCD34-Smad7 has good biological properties and can effectively reverse the EndMT of MAEC mediated by TGF-ß1. Thus, Exosome-DSPE-PEG-AbCD34-Smad7 may has the potential for the prevention and treatment of HO.

Superparamagnetic iron oxide (SPIO) nanoparticles labeled endothelial progenitor cells (EPCs) administration inhibited heterotopic ossification in rats.

Heterotopic ossification (HO) is a painful disease characterized by unwanted bone ectopic formation outside of the skeleton after injury. SPIO nanoparticles therapy has been widely used in diverse orthopedic diseases. However, the effect of SPIO nanoparticles on heterotopic ossification remains unknown. Here, we prepared the SPIO nanoparticles carrying mothers against decapentaplegic homolog 7 (SMAD7) and evaluated their mechanism function to HO in a rat model. The results revealed that SPIO nanoparticles containing SMAD7 treatment lead to a decrease in epithelial-mesenchymal transition (EMT) relevant protein expression in vitro. Moreover, SPIO nanoparticles labeled EPCs transplantation effectively prevented heterotopic ossification and inhibited endothelial-mesenchymal transition (EndMT) in HO rats. In addition, SPIO nanoparticles labeled EPCs transplantation suppressed osteogenic and adipogenic differentiation of embryonic fibroblasts (EFs) in HO rats. Our results demonstrated that administration of SPIO nanoparticles labeled EPCs could inhibit heterotopic ossification in rats, which might be a potential therapy method for a medical intervention to treat HO in clinic.

[In vitro evaluation, cellular uptake and anti-acute myocardial ischemia effect of puerarin PEG-PLGA micelles].

PUE@PEG-PLGA micelles has excellent characteristics such as small particle size, high drug loading and slow drug release. The results of TEM electron microscopy showed that PUE@PEG-PLGA micelles had obvious core-shell structure. The critical micelle concentration(CMC) of PEG-PLGA micelles determined by pyrene assay was about 4.8 mg·L~(-1). Laser confocal experiments showed that PEG-PLGA micelles can enhance the cellular uptake of coumarin-6 and aggregate around the mitochondria; quantitative results of extracellular drug residues also indirectly confirmed that PEG-PLGA micelles can promote cellular uptake of the drug. Acute ischemic myocardial model rats were prepared by coronary artery ligation, and then the model rats were randomly divided into six groups: Sham operation group, model group, puerarin(PUE) group, as well as low-, mid-, and high-dose PUE@PEG-PLGA micelles groups. Drugs were given by iv administration 5 min after the ligation. The ST segment changes in the electrocardiogram were monitored; serum creatine kinase(CK), lactate dehydrogenase(LDH), aspartate aminotransferase(AST), and malondialdehyde(MDA) levels were detected and myocardial infarct size was also measured. Both PUE and PUE@PEG-PLGA micelles can reduce the elevated ST segment, reduce serum CK, LDH, AST and MDA levels, and reduce myocardial infarct size. The efficacy of PUE@PEG-PLGA medium and high dose groups was significantly better than that in the PUE group, and the efficacy in PUE@PEG-PLGA low dose group was basically equivalent to that in the PUE group. PUE@PEG-PLGA micelles can greatly improve the cardiomyocytes uptake of PUE, enhance the anti-acute myocardial ischemia effect of drugs, and reduce its dosage.

MiR-34a Enhances Chondrocyte Apoptosis, Senescence and Facilitates Development of Osteoarthritis by Targeting DLL1 and Regulating PI3K/AKT Pathway.

BACKGROUND/AIMS: Osteoarthritis (OA) is the prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in the inflammation and immune response. The aim of this study was to investigate the effect of microRNA-34a (MiR-34a) on the death of chondrocytes, senescence, as well as its role in OA progression. METHODS: A series of experiments involving CCK-8, flow cytometry, ß-galactosidase staining and wound healing assays were conducted to determine the cellular capabilities of proliferation, cell apoptosis, senescence and the ability of cells to recover from injury, respectively. Binding sites between miR-34a and delta-like protein 1 (DLL1) were identified using a luciferase reporter system, whereas mRNA and protein expression of target genes was determined by RT-PCR and immunoblot, respectively. OA model was generated via surgery. RESULTS: We found that miR-34a expression was increased in the cartilage of OA patients. In rat chondrocytes and chondrosarcoma cells, miR-34a transfections noticeably inhibited the expression of DLL1, triggered cell death and senescence, suppressed proliferation, and prevented scratch assay wound closure. However, transfection of a miR-34a inhibitor displayed adverse effects. Additionally, secretion and expression of factors associated with cartilage degeneration were altered via miR-34a. Moreover, miR-34a directly inhibits DLL1 mRNA. Furthermore, concentrations of DLL1, total PI3K, and p-AKT declined in chondrocytes that overexpress miR-34a. DLL1 overexpression elevated PI3K and p-AKT levels, and eliminated cell death triggered by a miR-34a mimic. In vivo, miR-34a remarkably inhibited miR-34a up-regulation, while enhanced the level of DLL1 expression. In the knee joints of surgery-induced OA rats, articular chondrocyte death and loss of cartilage were attenuated via miR-34a antagomir injection. CONCLUSIONS: These findings indicate that miR-34a contributes to chondrocyte death, causing OA progression through DLL1 and modulation of the PI3K/AKT pathway.

Structural modeling of osteoarthritis ADAMTS4 complex with its cognate inhibitory protein TIMP3 and rational derivation of cyclic peptide inhibitors from the complex interface to target ADAMTS4.

The ADAMTS4 (a disintegrin and metalloproteinase with thrombospondin motifs 4) enzyme is a matrix-associated zinc metalloendopeptidase that plays an essential role in the degradation of cartilage aggrecan in arthritic diseases and has been recognized as one of the most primary targets for therapeutic intervention in osteoarthritis (OA). Here, we reported computational modeling of the atomic-level complex structure of ADAMTS4 with its cognate inhibitory protein TIMP3 based on high-resolution crystal template. By systematically examining the modeled complex structure we successfully identified a short inhibitory loop (62EASESLC68) in TIMP3 N-terminal inhibitory domain (NID) that directly participates in blocking the enzyme's active site, which, and its extended versions, were then broken from the full-length protein to serve as the peptide inhibitor candidates of ADAMTS4. Atomistic molecular dynamics simulation, binding energetic analysis, and fluorescence-based assay revealed that the TIMP3-derived linear peptides can only bind weakly to the enzyme (Kd = 74 ±â€¯8 µM), which would incur a considerable entropy penalty due to the high conformational flexibility and intrinsic disorder of these linear peptides. In this respect, we proposed a cyclization strategy to improve enzyme-peptide binding affinity by, instead of traditionally maximizing enthalpy contribution, minimizing entropy cost of the binding, where a disulfide bond was added across the two terminal residues of linear peptides, resulting in a number of TIMP3-derived cyclic peptides. Our studies confirmed that the cyclization, as might be expected, can promote peptide binding capability against ADAMTS4 substantially, with affinity increase by 3-fold, 9-fold and 7-fold for cyclic peptides , and , respectively.

Tea Consumption is Associated with Increased Risk of Kidney Stones in Northern Chinese: A Cross-sectional Study.

Kidney stones are a common urinary system condition that can progress to kidney disease. Previous studies on the association between tea consumption and kidney stones are inconsistent. A cross-sectional study to investigate the association between tea consumption and kidney stones was conducted from 2013 to 2014 and recruited 9,078 northern Chinese adults. A total of 8,807 participants were included in the final analysis. Participants' prevalence of kidney stones was 1.07%, 1.73%, and 2.25% based on their tea consumption frequency of never, occasionally, and often groups, respectively. Compared with the 'never' group, the odds ratios (95% confidence intervals) for the occurrence of kidney stones were 1.57 (1.00-2.46) and 1.65 (1.06-2.57) in the 'occasionally' and 'often' groups, respectively. After adjusting for sex, age, and other potential confounding factors, tea consumption still significantly increased the risk of kidney stones. Tea consumption is independently associated with an increased risk of kidney stones in the investigated population, suggesting that a decrease in the consumption of tea may be a preventive strategy for kidney stones.

Laser cooling of Yb³âº-doped LuLiF4 crystal.

In order to meet the demands for applications of optical refrigerators in the fields of spaceflight, aviation, space science, and detection, a 2 wt. % Yb3+-doped LuLiF4 crystal, as a new laser cooling material, was prepared and demonstrated by using a 178 mW diode laser centered at 1015 nm and a resonant extra-cavity scheme with an enhancement factor of 12.8. Cooling efficiency of 1.27% and a temperature drop of 14.3 K/W are obtained with 79% of the incident laser power being absorbed. Based on our results, a sample with background absorption of α=4.2×10(-4) cm(-1) can be potentially cooled down to ∼145 K. Our investigation shows that Yb3+-doped LuLiF4 crystal is potentially a promising candidate for solid-state refrigeration.

Percutaneous drainage of Morel-Lavallée lesions when the diagnosis is delayed.

SUMMARY: Morel-Lavallée lesions are a closed internal degloving, and open débridement can damage the only remaining blood supply to the skin. We performed percutaneous draining and débridement to treat 8 patients in whom the diagnosis of Morel-Lavallée lesions was delayed more than 1 week. Here we discuss our treatment procedures and the outcomes in these 8 patients. We consider percutaneous drainage to be an effective treatment for patients with delayed diagnosis of Morel-Lavallée lesions.

Comparing approaches to expose type C fractures of the distal humerus for ORIF in elderly patients: six years clinical experience with both the triceps-sparing approach and olecranon osteotomy.

BACKGROUND: Although open reduction and internal fixation (ORIF) is a standard fracture treatment method, the optimal way to expose a fracture prior to ORIF is debated. We compared the effects of two exposure methods, the triceps-sparing approach and olecranon osteotomy, on the functional outcomes of ORIF-treated type C distal humerus fractures in elderly people. METHODS: From January 2006 to January 2011, 75 elderly patients with type C distal humerus fractures were treated with ORIF, and we retrospectively reviewed their medical records, radiographs, and follow-up charts to identify any complications. Patients' Mayo Elbow Performance Score (MEPS) and range of motion were determined at their final clinic visit. RESULTS: Sixty-seven patients (89 %) attended the final visit. Of these patients, 36 received olecranon osteotomy and 31 received the triceps-sparing approach. For patients with type C1 and C2 fractures, we observed reductions in procedure times, blood loss, complication rates, and MEPS outcomes (all P < 0.01) with the triceps-sparing approach compared with olecranon osteotomy. Except for MEPS outcomes, all of these approach-related improvements were also statistically significantly for type C3 fractures (all P < 0.01). Overall, we did not observe any cases of fracture nonunion, implantation breakage or loosening, or elbow stiffening in our series. CONCLUSIONS: In our study, we found better functional outcomes for type C1 and C2 distal humerus fractures that were exposed using the triceps-sparing approach rather than olecranon osteotomy. Even for the most complex type of fracture, C3 fractures, similar recoveries in elbow function were achieved using either approach. LEVEL OF EVIDENCE: Level III.

Predicting climate change effects on surface soil organic carbon of Louisiana, USA.

This study aimed to assess the degree of potential temperature and precipitation change as predicted by the HadCM3 (Hadley Centre Coupled Model, version 3) climate model for Louisiana, and to investigate the effects of potential climate change on surface soil organic carbon (SOC) across Louisiana using the Rothamsted Carbon Model (RothC) and GIS techniques at the watershed scale. Climate data sets at a grid cell of 0.5° × 0.5° for the entire state of Louisiana were collected from the HadCM3 model output for three climate change scenarios: B2, A2, and A1F1, that represent low, higher, and even higher greenhouse gas emissions, respectively. Geo-referenced datasets including USDA-NRCS Soil Geographic Database (STATSGO), USGS Land Cover Dataset (NLCD), and the Louisiana watershed boundary data were gathered for SOC calculation at the watershed scale. A soil carbon turnover model, RothC, was used to simulate monthly changes in SOC from 2001 to 2100 under the projected temperature and precipitation changes. The simulated SOC changes in 253 watersheds from three time periods, 2001-2010, 2041-2050, and 2091-2100, were tested for the influence of the land covers and emissions scenarios using SAS PROC GLIMMIX and PDMIX800 macro to separate Tukey-Kramer (p < 0.01) adjusted means into letter comparisons. The study found that for most of the next 100 years in Louisiana, monthly mean temperature under all three emissions projections will increase; and monthly precipitation will, however, decrease. Under three emission scenarios, A1FI, A2, and B2, the mean SOC in the upper 30-cm depth of Louisiana forest soils will decrease from 33.0 t/ha in 2001 to 26.9, 28.4, and 29.2 t/ha in 2100, respectively; the mean SOC of Louisiana cropland soils will decrease from 44.4 t/ha in 2001 to 36.3, 38.4, and 39.6 t/ha in 2100, respectively; the mean SOC of Louisiana grassland soils will change from 30.7 t/ha in 2001 to 25.4, 26.6, and 27.0 t/ha in 2100, respectively. Annual SOC changes will be significantly different among the land cover classes including evergreen forest, mixed forest, deciduous forest, small grains, row crops, and pasture/hay (p < 0.0001), emissions scenarios (p < 0.0001), and their interactions (p < 0.0001).

Biomass-Derived Hard Carbon for Sodium-Ion Batteries: Basic Research and Industrial Application.

Sodium-ion batteries (SIBs) have significant potential for applications in portable electric vehicles and intermittent renewable energy storage due to their relatively low cost. Currently, hard carbon (HC) materials are considered commercially viable anode materials for SIBs due to their advantages, including larger capacity, low cost, low operating voltage, and inimitable microstructure. Among these materials, renewable biomass-derived hard carbon anodes are commonly used in SIBs. However, the reports about biomass hard carbon from basic research to industrial applications are very rare. In this paper, we focus on the research progress of biomass-derived hard carbon materials from the following perspectives: (1) sodium storage mechanisms in hard carbon; (2) optimization strategies for hard carbon materials encompassing design, synthesis, heteroatom doping, material compounding, electrolyte modulation, and presodiation; (3) classification of different biomass-derived hard carbon materials based on precursor source, a comparison of their properties, and a discussion on the effects of different biomass sources on hard carbon material properties; (4) challenges and strategies for practical of biomass-derived hard carbon anode in SIBs; and (5) an overview of the current industrialization of biomass-derived hard carbon anodes. Finally, we present the challenges, strategies, and prospects for the future development of biomass-derived hard carbon materials.

Induction of apoptosis in osteosarcoma S180 cells by polysaccharide from Dictyophora indusiata.

Polysaccharides have shown great importance in cancer therapy. The current study showed that a polysaccharide from Dictyophora indusiata (PDI) also possessed anti-cancer properties. Methyl thiazolyl tetrazolium assay revealed a dose-dependent reduction of osteosarcoma S180 growth in response to PDI treatment. Apoptosis was observed following treatments with PDI, as reflected by the appearance of the subdiploid fraction and DNA fragmentations. We then investigated effects of PDI on expression of apoptosis-associated genes and the results revealed an increase of expression of bcl-2 and decreases of cdk4 and p53 protein levels. Finally, PDI treatment significantly increased the activation of caspase-3, a key executioner of apoptosis. These findings indicate that PDI may act as a chemopreventive and/or chemotherapeutic agent in osteosarcoma cells by reducing cell viability and inducing apoptosis.

Dietary intervention reprograms bone marrow cellular signaling in obese mice.

Objectives: The current study aimed to investigate the pathogenesis of obesity-induced impaired bone mass accrual and the impact of dietary intervention on bone density in the mouse model of obesity. Methods: Mice were fed with chow diet (CD) for 10 months, high-fat-diet (HFD) for 10 months, or HFD for 6 months then transferred to chow diet for 4 months (HFDt). Results: Weight loss and decreased intrahepatic lipid accumulation were observed in mice following dietary intervention. Additionally, HFD feeding induced bone mass accrual, while diet intervention restrained trabecular bone density. These changes were further reflected by increased osteogenesis and decreased adipogenesis in HFDt mice compared to HFD mice. Furthermore, HFD feeding decreased the activity of the Wingless-related integration site (Wnt)-ß-Catenin signaling pathway, while the Wnt signaling was augmented by diet intervention in the HFDt group. Conclusions: Our findings suggest that a HFD inhibits bone formation and that dietary intervention reverses this inhibition. Furthermore, the dietary intervention was able to compensate for the suppressed increase in bone mass to a level comparable to that in the CD group. Our study suggests that targeting the Wnt signaling pathway may be a potential approach to treat obesity-induced impaired bone mass accrual.

Exploring the common diagnostic gene KCNJ15 and shared pathway of ankylosing spondylitis and ulcerative colitis through integrated bioinformatics.

Introduction: The similarity between ankylosing spondylitis (AS) and ulcerative colitis (UC) in incidence rate and pathogenesis has been revealed. But the common pathogenesis that explains the relationship between AS and UC is still lacked, and the related genetic research is limited. We purposed to explore shared biomarkers and pathways of AS and UC through integrated bioinformatics. Methods: Gene expression data of AS and UC were obtained in the GEO database. We applied weighted gene co-expression network analysis (WGCNA) to identify AS-related and UC-related co-expression gene modules. Subsequently, machine learning algorithm was used to further screen hub genes. We validated the expression level and diagnostic efficiency of the shared diagnostic gene of AS and UC in external datasets. Gene set enrichment analysis (GSEA) was applied to analyze pathway-level changes between disease group and normal group. Finally, we analyzed the relationship between hub biomarker and immune microenvironment by using the CIBERSORT deconvolution algorithm. Results: 203 genes were obtained by overlapping AS-related gene module and UC-related gene module. Through SVM-RFE algorithm, 19 hub diagnostic genes were selected for AS in GSE25101 and 6 hub diagnostic genes were selected for UC in GSE94648. KCNJ15 was obtained as a common diagnostic gene of AS and UC. The expression of KCNJ15 was validated in independent datasets, and the results showed that KCNJ15 were similarly upregulated in AS samples and UC samples. Besides, ROC analysis also revealed that KCNJ15 had good diagnostic efficacy. The GSEA analysis revealed that oxidative phosphorylation pathway was the shared pathway of AS and UC. In addition, CIBERSORT results revealed the correlation between KCNJ15 gene and immune microenvironment in AS and UC. Conclusion: We have explored a common diagnostic gene KCNJ15 and a shared oxidative phosphorylation pathway of AS and UC through integrated bioinformatics, which may provide a potential diagnostic biomarker and novel insight for studying the mechanism of AS-related UC.

Comparative proteomic analysis identifies differentially expressed proteins and reveals potential mechanisms of traumatic heterotopic ossification progression.

Background: Traumatic Heterotopic Ossification (tHO) is one of complications of elbow fractures to the detriment of patients' rehabilitation, and the severity of tHO corresponds to the size of ectopic bone. It has yet to be elucidated which proteins and pathways underlying the progression of tHO, and biomarkers to predict the severity of tHO at early stage of the disease also need further investigation. Methods: In this study, a new rat model with distinct volume of ectopic bone was established first. Then a data-independent acquisition proteomics approach was used to investigate injured site tissues sequentially obtained from these rats (2, 7, 14, and 28 days post-injury). Differentially expressed analysis, functional annotation and co-expression analysis and protein-protein interaction network were performed to explore the pathways and hub proteins in the tHO progression. Clinical samples from a nest case-control study were used to validate the selected proteins for predicting the severity of tHO. Results: The Achilles Tenotomy (AT) induced significantly larger sizes of ectopic bone compared to Partial Achilles Tenotomy (PAT) in rat models. A total of 3547 quantifiable proteins were screened for differential expression analysis among the AT, PAT and control groups. The hierarchical clustering and expression pattern analysis revealed more apparent difference in the pathways such as oxidative phosphorylation, mitochondrial function, and sirtuin signaling between AT and PAT group at the early stage (2 dpi) of tHO. The co-expression analysis identified five hub proteins, UBA1, EIF3E, RPL17, RPL27, and RPS28. qPCR assay, immunoblot assay and immunohistochemistry assay verified that these proteins had higher expression level in the tissue samples of clinically relevant HO patients and clinically irrelevant HO patients than HO negative patients. Conclusion: The new established animal model and proteome profile could serve as a solid foundation for the comprehensive investigation of the progression of traumatic heterotopic ossification. And the identified 5 proteins (UBA1, EIF3E, RPL17, RPL27, and RPS28) may serve as potential biomarkers to predict the severity of tHO. The translational potential of this article: The proteins identified in this study may be the potential biomarkers and therapeutic targets for predicting and treating the tHO at early stage.