Food-borne bacteria analysis using a diatomite bioinspired SERS platform.

Rapid and sensitive detection of food-borne bacteria has remained challenging over the past few decades. We propose a surface-enhanced Raman scattering sensing strategy based on a novel bioinspired surface-enhanced Raman scattering substrate, which can directly detect dye molecular residues and food-borne pathogen microorganisms in the environment. The surface-enhanced Raman scattering platform consists of a natural diatomite microporous array decorated with a metal-phenolic network that enables the in situ reduction of gold nanoparticles. The as-prepared nanocomposites display excellent surface-enhanced Raman scattering activity with the lowest limit of detection and the maximum Raman enhancement factor of dye molecules up to 10-11 M and 1.18 × 107, respectively. For food-borne bacterial detection, a diatomite microporous array decorated with a metal polyphenol network and gold nanoparticle-based surface-enhanced Raman scattering analysis is capable of distinguishing the biochemical fingerprint information of Staphylococcus aureus and Escherichia coli, indicating the great potential for strain identification.

Detoxification and Activating Blood Circulation Decoction Promotes Reendothelialization of Damaged Blood Vessels via VEGF Signaling Pathway Activation by miRNA-126.

The occurrence of in-stent restenosis (ISR) poses a significant challenge for percutaneous coronary intervention (PCI). Thus, the promotion of vascular reendothelialization is essential to inhibit endothelial proliferation. In this study, we clarified the mechanism by which Detoxification and Activating Blood Circulation Decoction (DABCD) promotes vascular reendothelialization to avoid ISR by miRNA-126-mediated modulation of the vascular endothelial growth factor (VEGF) signaling pathway. A rat model of post-PCI restenosis was established by balloon injury. The injured aortic segment was collected 14 and 28 d after model establishment. Our findings indicate that on the 14th and 28th days following balloon injury, DABCD reduced intimal hyperplasia and inflammation and promoted vascular reendothelialization. Additionally, DABCD markedly increased nitric oxide (NO) expression and significantly decreased ET-1 production in rat serum. DABCD also increased the mRNA level of endothelial nitric oxide synthase (eNOS) and the protein expression of VEGF, p-Akt, and p-extracellular signal-regulated kinase (ERK)1/2 in vascular tissue. Unexpectedly, the expression of miR-126a-5p mRNA was significantly lower in the aortic tissue of balloon-injured rats than in the aortic tissue of control rats, and higher miR-126a-5p levels were observed in the DABCD groups. The results of this study indicated that the vascular reendothelialization effect of DABCD on arterial intimal injury is associated with the inhibition of neointimal formation and the enhancement of vascular endothelial activity. More specifically, the effects of DABCD were mediated, at least in part, through miR-126-mediated VEGF signaling pathway activation.

Role of epidural fat in the local milieu: what we know and what we don't.

PURPOSE: Traditionally, the epidural fat (EF) is known as a physical buffer for the dural sac against the force and a lubricant facilitating the relative motion of the latter on the osseous spine. Along with the development of the studies on EF, controversies still exist on vital questions, such as the underlying mechanism of the spinal epidural lipomatosis. Meanwhile, the scattered and fragmented researches hinder the global insight into the seemingly dispensable tissue. METHODS: Herein, we reviewed literature on the EF and its derivatives to elucidate the dynamic change and complex function of EF in the local milieu, especially at the pathophysiological conditions. We start with an introduction to EF and the current pathogenic landscape, emphasizing the interlink between the EF and adjacent structures. We generally categorize the major pathological changes of the EF into hypertrophy, atrophy, and inflammation. RESULTS AND CONCLUSIONS: It is acknowledged that not only the EF (or its cellular components) may be influenced by various endogenic/exogenic and focal/systematic stimuli, but the adjacent structures can also in turn be affected by the EF, which may be a hidden pathogenic clue for specific spinal disease. Meanwhile, the unrevealed sections, which are also the directions the future research, are proposed according to the objective result and rational inference. Further effort should be taken to reveal the underlying mechanism and develop novel therapeutic pathways for the relevant diseases.

Cycloolivil Isolated from Nardostachys jatamansi Inhibits TNF-α/IFN-γ-Induced Chemokine Production by Blocking NF-κB and JAK/STAT Activation in HaCaT Keratinocytes.

Nardostachys jatamansi is widely used as a traditional medicine in Asian countries. Numerous recent studies have reported the biological activities of its secondary metabolites and extracts. In this study, a total of 14 components were isolated, including cycloolivil and 2-(3'-hydroxy-5'-ethoxyphenyl)-3-hydroxylmethyl-7-methoxy-2,3-dihydrobenzofuran-5-carboxylic acid, which were first discovered in N. jatamansi. The isolated compounds were investigated for their anti-inflammatory effects on HaCaT keratinocytes and their potential to alleviate skin inflammation. The results of the screening revealed that cycloolivil and 4ß-hydroxy-8ß-methoxy-10-methylene-2,9-dioxatricyclo[4.3.1.03,7]decane reduced the production of inflammatory cytokines induced by TNF-α/IFN-γ, such as IL-6, IL-8, and RANTES, in keratinocytes. This study focused on exploring the biological effects of cycloolivil, and the results suggested that cycloolivil inhibits the expression of COX-2 proteins. Further mechanistic evaluations confirmed that the anti-inflammatory effects of cycloolivil were mediated by blockage of the NF-κB and JAK/STAT signaling pathways. These results suggest that cycloolivil isolated from N. jatamansi could be used to treat skin inflammatory diseases.

Hetastarch-stabilized polypyrrole with hyperthermia-enhanced release and catalytic activity for synergistic antitumor therapy.

Fenton catalytic medicine that catalyzes the production of ·OH without external energy input or oxygen as a substrate has reshaped the landscape of conventional cancer therapy in recent decades, yet potential biosafety concerns caused by non-safety-approved components restrict their clinical translation from the bench to the bedside. Herein, to overcome this dilemma, we elaborately utilizate safety-approved hetastarch, which has been extensively employed in the clinic as a plasma substitute, as a stabilizer participating in the copper chloride-initiated polymerization of pyrrole monomer before loading it with DOX. The constructed DOX-loaded hetastarch-doped Cu-based polypyrrole (HES@CuP-D) catalyzes the excess H2O2 in tumor cells to ·OH through a Cu+-mediated Fenton-like reaction, which not only causes oxidative damage to tumor cells but also leads to the structural collapse and DOX release. Additionally, HES@CuP-D together with laser irradiation reinforces tumor killing efficiency by hyperthermia-enhanced catalytic activity and -accelerated drug release. As a result, the developed HES@CuP-D provides a promising strategy for Fenton catalytic therapy with negligible toxicity to the body.

Downregulation of UBB potentiates SP1/VEGFA-dependent angiogenesis in clear cell renal cell carcinoma.

Clear cell renal cell carcinoma (ccRCC) presents a unique profile characterized by high levels of angiogenesis and robust vascularization. Understanding the underlying mechanisms driving this heterogeneity is essential for developing effective therapeutic strategies. This study revealed that ubiquitin B (UBB) is downregulated in ccRCC, which adversely affects the survival of ccRCC patients. UBB exerts regulatory control over vascular endothelial growth factor A (VEGFA) by directly interacting with specificity protein 1 (SP1), consequently exerting significant influence on angiogenic processes. Subsequently, we validated that DNA methyltransferase 3 alpha (DNMT3A) is located in the promoter of UBB to epigenetically inhibit UBB transcription. Additionally, we found that an unharmonious UBB/VEGFA ratio mediates pazopanib resistance in ccRCC. These findings underscore the critical involvement of UBB in antiangiogenic therapy and unveil a novel therapeutic strategy for ccRCC.

Quercetin inhibits necroptosis in cardiomyocytes after ischemia-reperfusion via DNA-PKcs-SIRT5-orchestrated mitochondrial quality control.

We investigated the mechanism by which quercetin preserves mitochondrial quality control (MQC) in cardiomyocytes subjected to ischemia-reperfusion stress. An enzyme-linked immunosorbent assay was employed in the in vivo experiments to assess myocardial injury markers, measure the transcript levels of SIRT5/DNAPK-cs/MLKL during various time intervals of ischemia-reperfusion, and observe structural changes in cardiomyocytes using transmission electron microscopy. In in vitro investigations, adenovirus transfection was employed to establish a gene-modified model of DNA-PKcs, and primary cardiomyocytes were obtained from a mouse model with modified SIRT5 gene. Reverse transcription polymerase chain reaction, laser confocal microscopy, immunofluorescence localization, JC-1 fluorescence assay, Seahorse energy analysis, and various other assays were applied to corroborate the regulatory influence of quercetin on the MQC network in cardiomyocytes after ischemia-reperfusion. In vitro experiments demonstrated that ischemia-reperfusion injury caused changes in the structure of the myocardium. It was seen that quercetin had a beneficial effect on the myocardial tissue, providing protection. As the ischemia-reperfusion process continued, the levels of DNA-PKcs/SIRT5/MLKL transcripts were also found to change. In vitro investigations revealed that quercetin mitigated cardiomyocyte injury caused by mitochondrial oxidative stress through DNA-PKcs, and regulated mitophagy and mitochondrial kinetics to sustain optimal mitochondrial energy metabolism levels. Quercetin, through SIRT5 desuccinylation, modulated the stability of DNA-PKcs, and together they regulated the "mitophagy-unfolded protein response." This preserved the integrity of mitochondrial membrane and genome, mitochondrial dynamics, and mitochondrial energy metabolism. Quercetin may operate synergistically to oversee the regulation of mitophagy and the unfolded protein response through DNA-PKcs-SIRT5 interaction.

Photo-induced Oriented Crystallization of Intracellular Nanocrystals Based on Phase Separation for Diagnostic Bioimaging and Analysis.

Biomineral crystals form complex nonequilibrium structures based on the multistep nucleation theory, via transient amorphous precursors. However, the intricate nature of the biological system results in the inconsistent frequency of nucleation and crystallization, which making it problematic to obtain homogeneous nanocrystals, limits their application in biomedicine. Here, it is reported that homogeneous nanocrystals of photoinduced oriented crystallization with protein coronas are based on intracellular liquid-liquid phase separation for in situ analysis and mapping of surface-enhanced Raman spectroscopy (SERS). Near-infrared light promotes the formation of intracellular dense phases, accelerates the nucleation of gold atoms at secondary structure sites of proteins, and promotes the growth of crystals. Homogeneous gold nanocrystals with stable SERS signals can be used to analysis different cell cycles and acquire in situ molecular information of metastatic tumor cells. Of note are tag molecule is embedded in protein coronas of gold nanocrystals to enable the mapping of patient tumor tissue samples and the portable recognition of tumor cells. Thus, this study proposes a new strategy for biomineralization of intracellular homogeneous gold nanocrystals and its potential application.

Bio-Based Alkali Lignin Cooperative Systems for Improving the Flame Retardant and Mechanical Properties of Rigid Polyurethane Foam.

Lignin was utilized as an environmentally friendly synergistic agent to augment the fire resistance and mechanical characteristics of rigid polyurethane foam (PUF)/melamine-formaldehyde resin ammonium polyphosphate (MFAPP). The incorporation of lignin significantly enhanced the charring capability and flame retardancy of PUF/MFAPP. Specifically, PUF/MFAPP12/A-lignin3 exhibited a charring residue of 23.1% at 800 °C, accompanied by an increase in the limiting oxygen index (LOI) to 23.1%, resulting in a UL-94 V-0 rating. The cone calorimeter test (CCT) revealed that the peak heat release rate (PHRR), total heat release (THR), smoke production rate (SPR), and total smoke production (TSP) values of PUF/MFAPP12/A-lignin3 were all lower than for pure PUF. MFAPP and alkali lignin exerted a noticeable influence on the physical and mechanical properties, leading to increases in density (35.4 kg/m3), thermal conductivity (32.68 mW/(m·K)), and compressive strength (160.5 kPa). Observations of the morphology and elemental composition of char residues after combustion indicated the formation of an intact, thick, and continuous char layer enriched with nitrogen and phosphorus elements, which acted as a protective shield for the underlying foam.

Anti-Inflammatory Activity of 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone Isolated from Cudrania tricuspidata via NF-κB, MAPK, and HO-1 Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 and BV2 Cells.

Neuroinflammation activated by microglia affects inflammatory pain development. This study aimed to explore the anti-inflammatory properties and mechanisms of 1,6,7-trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone (THMX) from Cudrania tricuspidata in microglia activation-mediated inflammatory pain. In RAW 264.7 and BV2 cells, THMX has been shown to reduce lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory mediators and cytokines, including nitric oxide (NO), prostaglandin (PG) E2, interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α). THMX also decreased LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK) and the activation of p65 nuclear factor kappa B (NF-κB). Interestingly, THMX also activated heme oxygenase (HO)-1 expression. These findings suggest that THMX is a promising biologically active compound against inflammation through preventing MAPKs and NF-ĸB and activating HO-1 signaling pathways.

Improvement of Pulmonary Function and Reconstructed 3-Dimensional Lung Volume After Halo-Pelvic Traction Combined With Posterior Correction for Severe Rigid Spinal Scoliosis: A Multicenter Study.

BACKGROUND AND OBJECTIVES: Severe rigid spinal scoliosis (SRSS) leads to severe restrictive ventilation dysfunction. Currently, the reports about the influence of preoperative halo-pelvic traction (HPT) combined with correction surgery on pulmonary function in patients with SRSS were relatively few. This study aims to investigate (1) the influence of preoperative HPT on lung volume and pulmonary function, (2) the further influence of the following correction surgery on lung volume and pulmonary function, and (3) the relationship among deformity correction, pulmonary function test outcomes, and computed tomography-based lung volume. METHODS: A total of 135 patients with SRSS who underwent preoperative HPT and followed low-grade osteotomy correction surgery were reviewed. Spinal parameters, including proximal thoracic curve, main thoracic curve (MTC), lumbar curve, coronal balance, thoracic kyphosis, lumbar lordosis, sagittal vertical axis, pulmonary function test outcomes (forced vital capacity [FVC], the percentage of predicted forced vital capacity [FVC%], forced expiratory volume in 1 second [FEV1], total lung capacity [TLC]), and lung volume (Vin), were analyzed before, after HPT and at the final follow-up, respectively. RESULTS: The mean FVC, FVC%, FEV1, and TLC increased from 1.67 L, 51.13%, 1.47 L, and 2.37 L to 1.95 L, 64.35%, 1.75 L, and 2.78 L, respectively, after HPT and further improved to 2.22 L, 72.14%, 1.95 L, and 3.15 L, respectively, at the final follow-up. The mean Vin increased from 1.98 L to 2.42 L after traction and further increased to 2.76 L at the final follow-up. The variation of MTC was correlated with the improvement of FVC (r = 0.429, P = .026), FVC% (r = 0.401, P = .038), FEV1 (r = 0.340, P = .043), and TLC (r = 0.421, P = .029) and the variation of Vin (r = 0.425, P = .015) before HPT and after surgery. CONCLUSION: Preoperative HPT can improve preoperative pulmonary function and enhance the preoperative lung volume. There were significant correlations among the variations of MTC, pulmonary function indexes, and lung volume before HPT and after surgery in patients with SRSS.

The contribution of preoperative balanced halo-pelvic traction to severe rigid spinal deformity correction.

PURPOSE: The aim of this study was to assess the clinical efficacy of balanced halo-pelvic traction (HPT) and evaluate its contribution to the correction surgery in treating adult severe rigid spinal deformity. METHODS: One hundred and eight adult patients with severe rigid spinal deformity who underwent preoperative HPT and correction surgery were reviewed. The main coronal curve, segmental kyphotic angle, coronal balance (CB), sagittal balance (SVA), and the length of spine were measured before HPT, after HPT, post-operatively, and at final follow-up. The HPT contribution rates to deformity correction were calculated. RESULTS: The pre-HPT main coronal curve was 103.4 ± 10.6°, improved to 61.0 ± 13.4° after traction and further improved to 44.2 ± 10.2° after surgical correction, and maintained at 50.3 ± 9.9° at final follow-up. CB started at 4.2 ± 4.8 cm, improved to 2.1 ± 2.5 cm after HPT, 0.8 ± 1.2 cm after operation, and 0.7 ± 0.9 cm at final follow-up. The pre-HPT sagittal segmental kyphotic angle was 67.3 ± 17.7°, was then improved to 42.2 ± 27.5° after traction and further improved to 34.9 ± 10.2° after surgery, and maintained at 35.4 ± 10.4° at final follow-up. The length of spine improved from 35.9 ± 5.9 to 42.6 ± 6.0 cm via HPT, reached up to 45.0 ± 6.0 cm after operation, and maintained at 44.3 ± 5.2 cm at final follow-up. CONCLUSION: HPT is effective for the treatment of severe rigid spinal deformity. Balanced HPT can dramatically improve coronal and sagittal deformity as well as spinal length before corrective surgery.

Effect of Ball-Milling Process on Microwave Absorption Behaviors of Flaky Carbonyl Iron Powders.

Electromagnetic (EM) wave absorption performance is greatly affected by the microscopic morphology of the absorbing material particles. In this study, a facile and efficient ball-milling method was applied to increase the aspect ratio of particles and prepare flaky carbonyl iron powders (F-CIPs), one of the most readily commercially available absorbing materials. The effect of ball-milling time and rotation speed on the absorption behaviors of the F-CIPs was investigated. The microstructures and compositions of the F-CIPs were determined using scanning electron microscopy (SEM) and X-ray diffraction (XRD). The EM parameters were measured using a vector network analyzer (VNA) in the frequency range of 2-18 GHz. The results indicated that the ball-milled flaky CIPs exhibited a better absorption ability than the raw spherical CIPs. Among all the samples, the sample milled at 200 r/min for 12 h and the sample milled at 300 r/min for 8 h showed remarkable EM parameters. The ball-milling sample with 50 wt.% F-CIPs had a minimum reflection loss peak of -14.04 dB at a thickness of 2 mm and a maximum bandwidth (RL < -7 dB) of 8.43 GHz at a thickness of 2.5 mm, a result that conformed with the transmission line theory. Hence, the ball-milled flaky CIPs were considered to be beneficial for microwave absorption.

Label-Free Surface-Enhanced Raman Scattering Bioanalysis Based on Au@Carbon Dot Nanoprobes.

Surface-enhanced Raman scattering (SERS) technology has attracted more and more attention in the biomedical field due to its ability to provide molecular fingerprint information of biological samples, as well as its potential in single-cell analysis. This work aims to establish a simple strategy for label-free SERS bioanalysis based on Au@carbon dot nanoprobes (Au@CDs). Here, polyphenol-derived CDs are utilized as the reductant to rapidly synthesize core-shell Au@CD nanostructures, which allows powerful SERS performance even when the concentration of methylene blue (MB) is as low as 10-9 M, due to the cooperative Raman enhancement mechanism. For bioanalysis, Au@CDs can serve as a unique SERS nanosensor to identify the cellular components of biosamples (e.g., cancer cells and bacteria). The molecular fingerprints from different species can be further distinguished after combination with the principal component analysis. In addition, Au@CDs also enable label-free SERS imaging to analyze intracellular composition profiles. This strategy offers a feasible, label-free SERS bioanalysis, opening up a new prospect for nanodiagnosis.

Synergistic effect and mechanism of Cd(II) and As(III) adsorption by biochar supported sulfide nanoscale zero-valent iron.

Biochar derived from bamboo was used to support sulfide nanoscale zero-valent iron (S-nZVI@BC) for simultaneous removal of Cd(II) and As (III) from aqueous media. Scanning electron microscopy (SEM) and X-ray diffraction spectroscopy (XRD) characterization confirmed the successful synthesis of the S-nZVI@BC. Adsorption kinetics and isotherms indicated that co-adsorption of Cd(II) and As(III) onto S-nZVI@BC was well represented by pseudo-second-order model (R2Cd(II) = 0.990, R2As(III) = 0.995) and Langmuir model (R2Cd(II) = 0.954, R2As(III) = 0.936). The maximum adsorption was 162.365 and 276.133 mg/g for Cd(II) and As(III), respectively, in a co-adsorption system, which was significantly higher than that in a single adsorption system (103.195 and 223.736 mg/g, respectively). Batch experiments showed that the Cd(II)-to-As(III) concentration ratio significantly affected the co-adsorption with the optimal ratio of 1:2. Ca2+ and Mg2+ significantly inhibited Cd(II) removal. In contrast, phosphate and humic acid significantly inhibited As(III) removal. Electrochemical analysis indicated S-nZVI@BC had a lower corrosion potential and resistance than nZVI@BC, making it more conducive to electron transfer and chemical reaction. Electrostatic adsorption, complexation, co-precipitation, and redox were the primary mechanisms for Cd(II) and As(III) removal. Overall, the present study provides new insights into the synergistic removal of Cd(II) and As(III) by S-nZVI@BC, which is a very promising adsorbent for the effective removal of Cd(II) and As(III) from contaminated wastewater.

Anti-Skin Inflammatory and Anti-Oxidative Effects of the Neoflavonoid Latifolin Isolated from Dalbergia odorifera in HaCaT and BJ-5ta Cells.

Skin is the first line of defense in the body against external stimulation and injury. Inflammation and oxidative stress in skin cells are the initiators and promoters of several skin diseases. Latifolin is a natural flavonoid isolated from Dalbergia odorifera T. Chen. This study aimed to evaluate the anti-inflammatory and antioxidant properties of latifolin. The anti-inflammatory effects were evaluated using tumor necrosis factor-α/interferon-γ (TNF-α/IFN-γ)-treated HaCaT cells, revealing that latifolin inhibited the secretion of Interleukin 6 (IL-6); Interleukin 8 (IL-8); Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES); and Macrophage-derived chemokine (MDC) while decreasing the expression of Intercellular Adhesion Molecule 1 (ICAM-1). The results of western blots and immunofluorescence demonstrated that the activation of Janus kinase 2 (JAK2), Signal transducer and activator of transcription 1 (STAT1), Signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) cells signaling pathways were significantly inhibited by latifolin. The antioxidant properties were evaluated using t-BHP-induced BJ-5ta cells. Latifolin increased the viability of t-BHP-induced BJ-5ta cells. Additionally, fluorescent staining of reactive oxygen species (ROS) showed that the production of ROS was inhibited by latifolin. Additionally, latifolin reduced the phosphorylation of p38 and JNK. The results indicate that latifolin has potential anti-inflammatory and antioxidant properties, and may be a candidate natural compound for the treatment of skin diseases.

Linderone Isolated from Lindera erythrocarpa Exerts Antioxidant and Anti-Neuroinflammatory Effects via NF-κB and Nrf2 Pathways in BV2 and HT22 Cells.

Linderone is a major compound in Lindera erythrocarpa and exhibits anti-inflammatory effects in BV2 cells. This study investigated the neuroprotective effects and mechanisms of linderone action in BV2 and HT22 cells. Linderone suppressed lipopolysaccharide (LPS)-induced inducible nitric oxide synthase, cyclooxygenase-2, and pro-inflammatory cytokines (e.g., tumor necrosis factor alpha, interleukin-6, and prostaglandin E-2) in BV2 cells. Linderone treatment also inhibited the LPS-induced activation of p65 nuclear factor-kappa B, protecting against oxidative stress in glutamate-stimulated HT22 cells. Furthermore, linderone activated the translocation of nuclear factor E2-related factor 2 and induces the expression of heme oxygenase-1. These findings provided a mechanistic explanation of the antioxidant and anti-neuroinflammatory effects of linderone. In conclusion, our study demonstrated the therapeutic potential of linderone in neuronal diseases.

LncRNA HOXB-AS3 binding to PTBP1 protein regulates lipid metabolism by targeting SREBP1 in endometrioid carcinoma.

Endometrial cancer (EC) is a malignant tumor with a high incidence in women, and the survival rate of high-risk patients decreases significantly after disease progression. The regulatory role of long non-coding RNAs (LncRNAs) in tumors has been widely appreciated, but there have been few studies in EC. To investigate the effect of HOXB-AS3 in EC, we used bioinformatics tools for prediction and collected clinical samples to detect the expression of HOXB-AS3. Colony formation assay, MTT assay, flow cytometry and apoptosis assay, and transwell assay were used to verify the role of HOXB-AS3 in EC. HOXB-AS3 was upregulated in EC, promoted the proliferation and invasive ability of EC cells, and inhibited apoptosis. In addition, the ROC curve illustrated its diagnostic value. We explored experiments via lentiviral transduction, FISH, Oil Red O staining, TC and FFA content detection, RNA-pulldown, RIP, and other mechanisms to reveal that HOXB-AS3 can bind to PTBP1 and co-regulate the expression of SREBP1, thereby regulating lipid metabolism in EC cells. To the best of our knowledge, this is the first study on HOXB-AS3 in disorders of lipid metabolism in EC. In addition, we believe HOXB-AS3 has the potential to be a neoplastic marker or a therapeutic target.

Molybdenum disulfide co-catalysis boosting nanoscale zero-valent iron based Fenton-like process: Performance and mechanism.

The conventional Fenton process has the drawbacks of low efficiency of Fe3+/Fe2+ conversion, low utilization of H2O2, and narrow range of pH. In this paper, molybdenum sulfide (MoS2) was used as a co-catalyst to boost the nanoscale zero-valent iron (nZVI) based heterogeneous Fenton-like process for the degradation of Rhodamine B (RhB). The catalytic performance, influences of parameters, degradation mechanism, and toxicity of intermediates were explored. Compared with the conventional like-Fenton process, the existence of MoS2 accelerated the decomposition of H2O2 and the RhB degradation rate constant of MoS2/nZVI/H2O2 reached more than six times that of nZVI/H2O2. In addition, the effective pH range of MoS2/nZVI/H2O2 was broadened to 9.0 with 84.9% of RhB being removed within 15 min. The co-catalytic system of MoS2 and nZVI was stable and had high reusability according to the results of four consecutive runs. Quenching tests and electron paramagnetic resonance (EPR) demonstrated that hydroxyl radical (·OH), superoxide anions (·O2-), and singlet oxygen (1O2) were all involved in MoS2/nZVI/H2O2. Compared with nZVI/H2O2 system, MoS2 not only increased the corrosion of nZVI but also accelerated the conversion of Fe3+/Fe2+. ECOSAR analysis suggested that the overall acute and chronic toxicity of the degradation products decreased after treatment. Hence, this MoS2 co-catalytic nZVI based Fenton-like process can be used as a promising alternative for the treatment of organic wastewater.

Identification of key genes involved in neural regeneration and the repairing effect of BDNF-overexpressed BMSCs on spinal cord ischemia-reperfusion injury in rats.

Bone marrow mesenchymal stem cells (BMSCs) can repair spinal cord ischemia-reperfusion injury (SCII); however, only a few BMSCs are usually located in the injured spinal cord. Since the brain-derived neurotrophic factor (BDNF) can promote neural development and maturation, we hypothesised that BDNF-overexpressed BMSCs can ameliorate SCII more effectively than BMSCs alone. To determine the effect of BDNF overexpression on SCII repair, BDNF-overexpressed BMSCs and BMSCs were transplanted into SCII rats. Our results revealed that BDNF-overexpressed BMSCs can better promote the recovery of damaged spinal cords than BMSCs alone. Gene chip detection of spinal cord tissues showed 803 differentially expressed genes in all groups. BTG anti-proliferation factor 2 (Btg2), FOS like 2 (Fosl2), early growth response protein 1 (Egr1), and serpin family E member 1 (Serpine1) were identified as key interrelated genes based on their expression trends, as validated via quantitative PCR and protein-protein interaction network analysis. A co-expression network was constructed to further explore the role of the candidate key genes using Pearson correlation analysis. Cluster 5 was identified as the key cluster using community discovery algorithms. Functional analysis of Cluster 5 genes revealed that this cluster was mainly involved in the stress-activated MAPK cascade, p38MAPK cascade, and apoptosis. Notably, Egr1 may play an important role in SCII repair as the top hub gene in Cluster 5. Therefore, the repair activity of transplanted BDNF-overexpressed BMSCs in SCII rats is better than that of BMSCs alone, which may be regulated by the interactions between Btg2, Fosl2, Egr1, Serpine1, and BDNF.