Highly efficient removal of aqueous phosphate via iron-manganese fabricated biochar: Performance and mechanism.

Biochar (BC) has emerged as a potential solution to phosphate removal from wastewater primarily resulting from global overuse of fertilizers. Further modification by embedment of iron (Fe)-manganese (Mn) oxides on BC can enhance phosphate removal; however, the modification method serves as a vital factor underlying distinctive removal performances and mechanisms, which have yet been systematically examined. Herein, two Fe-Mn modified BC, Fe/MnBC (comprised of Fe3O4 and MnO2) and Fe-MnBC (comprised of MnFe2O4), were comprehensively investigated for gaining insights into the unsolved perspectives. The results indicated that Fe-MnBC exhibited a markedly greater maximum phosphate adsorption capacity of 135.88 mg g-1 than that of Fe/MnBC with 17.93 mg g-1. The comparative results based on microstructure and spectroscopic analyses suggested that different Fe and Mn oxides were successfully loaded, which played a distinctive role in phosphate removal. Further characterizations unveiled that the key mechanisms for phosphate removal by Fe/MnBC are inner-sphere complexation and precipitation, while electrostatic interaction and outer-sphere complexation are the dominant mechanisms underlying the notable performance of Fe-MnBC. The delicately designed Fe-MnBC with special structure and property also enabled a superior regeneration capacity, which presented a promisingly high phosphate removal efficacy of over 81.34% after five cycles. These results enhance comprehension regarding the impact of biochar modification techniques on phosphate removal, offering positive indications for the remediation of excessive phosphate and other pollutant-containing water through feasible design and green chemicals.

Regio- and enantioselective nickel-alkyl catalyzed hydroalkylation of alkynes.

The migratory insertion of metal-hydride into alkene has allowed regioselective access to organometallics, readily participating in subsequent functionalization as one conventional pathway of hydroalkylation, whereas analogous process with feedstock alkyne is drastically less explored. Among few examples, the regioselectivity of metal-hydride insertion is mostly governed by electronic bias of alkynes. To alter the regioselectivity and drastically expand the intermediate pools that we can access, one aspirational design is through alternative nickel-alkyl insertion, providing opposite regioselectivity induced by steric demand. Leveraging in situ formed nickel-alkyl species, we herein report the regio- and enantioselective hydroalkylation of alkynes with broad functional group tolerance, excellent regio- and enantioselectivity, enabling efficient route to diverse valuable chiral allylic amines motifs. Preliminary mechanistic studies indicate the aminoalkyl radical species can participate in metal-capture and lead to formation of nickel-alkyl, of which the migratory insertion is key to reverse regioselectivity observed in metal-hydride insertion.

Bone marrow mesenchymal stem cell-derived exosomal miR-221-3p promotes angiogenesis and wound healing in diabetes via the downregulation of forkhead box P1.

AIM: Impaired wound healing in patients with diabetes can develop into nonhealing ulcerations. Because bone marrow mesenchymal stem cells (BMSCs) exosomes can promote wound healing, this study aims to investigate the mechanism of BMSCs-isolated exosomal miR-221-3p in angiogenesis and diabetic wound healing. METHODS: To mimic diabetes in vitro, human umbilical vein endothelial cells (HUVECs) were subjected to high glucose (HG). Exosomes were derived from BMSCs and identified by transmission electron microscopy (TEM), western blot analysis and dynamic light scattering (DLS). The ability to differentiate BMSCs was assessed via Oil red O staining, alkaline phosphatase (ALP) staining and alizarin red staining. The ability to internalise PKH26-labelled exosomes was assessed using confocal microscopy. Migration, cell viability and angiogenesis were tested by scratch, MTT and tube formation assays separately. The miRNA and protein levels were analysed by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) or western blotting. The relationship among miR-221-3p, FOXP1 and SPRY1 was determined using the dual-luciferase reporter, ChIP and RIP assays. RESULTS: Exosomal miR-221-3p was successfully isolated from BMSCs and delivered into HUVECs. HG was found to suppress the angiogenesis, cell viability and migration of HUVECs and exosomal miR-221-3p separated from BMSCs inhibited the above phenomenon. FOXP1 could transcriptionally upregulate SPRY1, and the silencing of FOXP1 reversed the HG-stimulated angiogenesis inhibition, cell viability and migration in HUVECs via the downregulation of SPRY1. Meanwhile, miR-221-3p directly targeted FOXP1 and the overexpression of FOXP1 reversed the positive effect of exosomal miR-221-3p on HUVEC angiogenesis. CONCLUSION: Exosomal miR-221-3p isolated from BMSCs promoted angiogenesis in diabetic wounds through the mediation of the FOXP1/SPRY1 axis. Furthermore, the findings of this study can provide new insights into probing strategies against diabetes.

The significance of m6A RNA methylation regulators in diagnosis and subtype classification of HBV-related hepatocellular carcinoma.

In recent years, abnormal m6A alteration in hepatocellular carcinoma (HCC) has been a focus on investigating the biological implications. In this study, our objective is to determine whether m6A modification contributes to the progression of HBV-related HCC. To achieve this, we employed a random forest model to screen top 8 characteristic m6A regulators from 19 candidate genes. Subsequently, we developed a nomogram model that utilizes these 8 characteristic m6A regulators to predict the prevalence of HBV-related HCC. According to decision curve analysis, patients may benefit from the nomogram model. The clinical impact curves exhibited a robust predictive capability of the nomogram models. Additionally, consensus molecular subtyping was employed to identify m6A modification patterns and m6A-related gene signature. The quantification of immune cell subsets was accomplished through the implementation of ssGSEA algorithms. PCA algorithms were developed to compute the m6A score for individual tumors. Two distinct m6A modification patterns, namely cluster A and cluster B, exhibited significant correlations with distinct immune infiltration patterns and biological pathways. Notably, patients belonging to cluster B demonstrated higher m6A scores compared to those in cluster A, as determined by the m6A score metric. Furthermore, the expression of IGFBP3 proteins was validated through immunofluorescence, revealing their pronounced lower expression in tumor tissues. In summary, our study underscores the importance of m6A modification in the advancement of HBV-related HCC. This research has the potential to yield novel prognostic biomarkers and therapeutic targets for the identification of HBV-related HCC.

Integrating artificial intelligence in osteosarcoma prognosis: the prognostic significance of SERPINE2 and CPT1B biomarkers.

The principal aim of this investigation is to identify pivotal biomarkers linked to the prognosis of osteosarcoma (OS) through the application of artificial intelligence (AI), with an ultimate goal to enhance prognostic prediction. Expression profiles from 88 OS cases and 396 normal samples were procured from accessible public databases. Prognostic models were established using univariate COX regression analysis and an array of AI methodologies including the XGB method, RF method, GLM method, SVM method, and LASSO regression analysis. Multivariate COX regression analysis was also employed. Immune cell variations in OS were examined using the CIBERSORT software, and a differential analysis was conducted. Routine blood data from 20,679 normal samples and 437 OS cases were analyzed to validate lymphocyte disparity. Histological assessments of the study's postulates were performed through immunohistochemistry and hematoxylin and eosin (HE) staining. AI facilitated the identification of differentially expressed genes, which were utilized to construct a prognostic model. This model discerned that the survival rate in the high-risk category was significantly inferior compared to the low-risk cohort (p < 0.05). SERPINE2 was found to be positively associated with memory B cells, while CPT1B correlated positively with CD8 T cells. Immunohistochemical assessments indicated that SERPINE2 was more prominently expressed in OS tissues relative to adjacent non-tumorous tissues. Conversely, CPT1B expression was elevated in the adjacent non-tumorous tissues compared to OS tissues. Lymphocyte counts from routine blood evaluations exhibited marked differences between normal and OS groups (p < 0.001). The study highlights SERPINE2 and CPT1B as crucial biomarkers for OS prognosis and suggests that dysregulation of lymphocytes plays a significant role in OS pathogenesis. Both SERPINE2 and CPT1B have potential utility as prognostic biomarkers for OS.

Identifying CTH and MAP1LC3B as ferroptosis biomarkers for prognostic indication in gastric cancer decoding.

Gastric cancer (GC), known for its high incidence and poor prognosis, urgently necessitates the identification of reliable prognostic biomarkers to enhance patient outcomes. We scrutinized data from 375 GC patients alongside 32 non-cancer controls, sourced from the TCGA database. A univariate Cox Proportional Hazards Model (COX) regression was employed to evaluate expressions of ferroptosis-related genes. This was followed by the application of Least Absolute Shrinkage and Selection Operator (LASSO) and multivariate COX regression for the development of prognostic models. The composition of immune cell subtypes was quantified utilizing CIBERSORT, with their distribution in GC versus control samples being comparatively analyzed. Furthermore, the correlation between the expressions of Cystathionine Gamma-Lyase (CTH) and Microtubule Associated Protein 1 Light Chain 3 Beta (MAP1LC3B) and the abundance of immune cell subtypes was explored. Our bioinformatics findings underwent validation through immunohistochemical analysis. Our prognostic models integrated CTH and MAP1LC3B. Survival analysis indicated that patients categorized as high-risk, as defined by the model, exhibited significantly lower survival rates compared to their low-risk counterparts. Notably, CTH expression inversely correlated with monocyte levels, while MAP1LC3B expression showed an inverse relationship with the abundance of M2 macrophages. Immunohistochemical validation corroborated lower expressions of CTH and MAP1LC3B in GC tissues relative to control samples, in concordance with our bioinformatics predictions. Our study suggests that the dysregulation of CTH, MAP1LC3B, and the accompanying monocyte-macrophage dynamics could be pivotal in the prognosis of GC. These elements present potential targets for prognostic assessment and therapeutic intervention.

Cholinergic Anti-inflammatory Pathway Attenuates Acute Liver Failure Through Inhibiting MAdCAM1/α4ß7-mediated Gut-derived Proinflammatory Lymphocytes Accumulation.

BACKGROUND & AIMS: The function of cholinergic anti-inflammatory pathway (CAP) in acute liver failure (ALF) with inflammatory storm remains indefinite. The liver-gut axis has been proved to be crucial for liver homeostasis. Investigation about CAP regulation on liver-gut axis would enrich our understanding over cholinergic anti-inflammatory mechanism. METHODS: Co-injection of lipopolysaccharide and D-galactosamine was used to establish the model of ALF. PNU-282987 was used to activate the CAP. Histological staining, real-time polymerase chain reaction, Western blotting, RNA sequencing, and flow cytometry were conducted. Liver biopsy specimens and patients' serum from patients with liver failure were also analyzed. RESULTS: We confirmed that activating the CAP alleviated hepatocyte destruction, accompanied by a significant decrease in hepatocyte apoptosis, pro-inflammatory cytokines, and NLRP3 inflammasome activation. Moreover, hepatic MAdCAM1 and serum MAdCAM1 levels were induced in ALF, and MAdCAM1 levels were positively correlated with the extent of liver damage and the expression of pro-inflammatory markers. Furthermore, activating the CAP mainly downregulated ectopic expression of MAdCAM1 on endothelial cells, and inhibition of NF-κB p65 nuclear translocation was partly attributed to the decreased MAdCAM1. Notably, in ALF, the aberrant hepatic expression of MAdCAM1 subsequently recruited gut-derived α4ß7+ CD4+T cells to the liver, which exhibited an augmented IFN-γ-secreting and IL-17-producing phenotype. Finally, we revealed that the levels of serum and hepatic MAdCAM1 were elevated in patients with liver failure and closely correlated with clinical course. Increasing hepatic infiltration of ß7+ cells were also confirmed in patients. CONCLUSIONS: Activating the CAP attenuated liver injury by inhibiting MAdCAM1/α4ß7 -mediated gut-derived proinflammatory lymphocytes infiltration, which provides a potential therapeutic target for ALF.

Nickel-Catalyzed Asymmetric Decarboxyarylation with NHP Esters of α-Amino Acid to Chiral Benzylamines.

A nickel-catalyzed asymmetric decarboxyarylation of NHP esters via reductive cross-coupling has been established. Utilizing the NHP of amino acid esters as radical precursors furnishes a new protocol in which structurally diverse chiral benzylamines could be accessible. This method has demonstrated excellent catalytic efficiency, high enantioselective control, mild conditions, and good functional group tolerance, thus enabling the late-stage modification of bioactive molecules and pharmaceuticals.

Prognostic and immunological significance of an M1 macrophage-related gene signature in osteosarcoma.

As the most abundant infiltrating immune cells in the tumor microenvironment (TME), tumor-associated macrophages (TAMs) are pivotal in tumor development and treatment. The present investigation endeavors to explore the potential of M1 macrophage-related genes (MRGs) as biomarkers for assessing risk in individuals with osteosarcoma. RNA-sequence data and clinical data were derived from TCGA and GEO databases. The CIBERSORT method was utilized to discern subtypes of tumor-infiltrating immune cells. Identification of MRGs was achieved through Pearson correlation analysis. A prognostic risk model for MRGs was developed using Cox and LASSO regression analyses. A tripartite gene signature comprising CD37, GABRD, and ARHGAP25 was an independent prognostic indicator and was employed to develop a risk score model. The internal and external validation cohort confirmed the results. The area under the ROC curve (AUC) was determined for survival periods of 1 year, three years, and five years, yielding values of 0.746, 0.839, and 0.850, respectively. The C-index of the risk score was found to be superior to clinicopathological factors. GO/KEGG enrichment showed that the differences between high- and low-risk groups were predominantly associated with immune response pathways. Immune-related analysis related to proportions of immune cells, immune function, and expression levels of immune checkpoint genes all showed differences between the high- and low-risk groups. The qRT-PCR and Western blotting results indicate that CD37 expression was markedly higher in MG63 and U2OS cell lines when compared to normal osteoblast hFOB1.19. In U2OS cell line, GABRD expression levels were significantly upregulated. ARHGAP25 expression levels were elevated in both 143B and U2OS cell lines. In summary, utilizing a macrophage genes signature demonstrates efficacy in predicting both the prognosis and therapy response of OS. Additionally, immune analysis confirms a correlation between the risk score and the tumor microenvironment. Our findings, therefore, provide a cogent account for the disparate prognoses observed among patients and furnish a justification for further inquiry into biomarkers and anti-tumor treatment strategies.

Clinical isolates of hepatitis B virus genotype C have higher in vitro transmission efficiency than genotype B isolates.

Serum samples were collected from 54 hepatitis B e antigen (HBeAg)-positive Chinese patients infected with hepatitis B virus (HBV) subgenotype B2 or C2. They were compared for transmission efficiency using same volume of samples or infectivity using same genome copy number. Adding polyethylene glycol (PEG) during inoculation did not increase infectivity of fresh samples but markedly increased infectivity following prolonged sample storage. Differentiated HepaRG cells infected without PEG produced more hepatitis B surface antigen (HBsAg) and higher HBsAg/HBeAg ratio than sodium taurocholate cotransporting polypeptide (NTCP)-reconstituted HepG2 cells infected with PEG. They better supported replication of core promoter mutant in contrast to wild-type (WT) virus by HepG2/NTCP cells. Overall, subgenotype C2 samples had higher viral load than B2 samples, and in general produced more HBeAg, HBsAg, and replicative DNA following same-volume inoculation. Precore mutant was more prevalent in subgenotype B2 and had reduced transmission efficiency. When same genome copy number of viral particles was inoculated, viral signals were not necessarily higher for three WT C2 isolates than four WT B2 isolates. Using viral particles generated from cloned HBV genome, three WT C2 isolates showed slightly reduced infectivity than three B2 isolates. In conclusion, subgenotype C2 serum samples had higher transmission efficiency than B2 isolates in association with higher viral load and lower prevalence of precore mutant, but not necessarily higher infectivity. PEG-independent infection by HBV viremic serum samples is probably attributed to a labile host factor.

Nitrogen and sulfur co-doped porous carbon derived from polypyrrole-polythiophene for efficient peroxydisulfate activation towards degradation of aniline.

To enhance the catalytic activity of carbon materials and streamline their synthesis process, it is necessary to optimize the doping of heteroatoms and reduce the dependence on organic solvents. This can be achieved by utilizing carbonized Polypyrrole-Polythiophene (C(Ppy-Pth)), which is obtained through simultaneous and in-situ co-doping of N and S. This material can serve as an effective activator of peroxydisulfate (PDS) for the degradation of aniline (AN). The results showed that Ppy-Pth could be efficiently synthesized by using cetyltrimethyl ammonium bromide, pyrrole, thiophene, FeCl3, and H2O2 in water. Based on the price, self-decomposition and oxidation efficiency, the performance of PDS activated by C(Ppy-Pth) was superior to that of peroxymonosulfate (PMS) in degrading AN. The optimum conditions for catalyzing PDS and degrading 30 mg/L AN by C(Ppy-Pth) were 0.10 g/L C(Ppy-Pth)-1000-1/1, 2.10 mM PDS, and pH0 = 3.00, which resulted in 86.69% AN removal in 30 min. Carbonation temperature, N/S ratio and pyridine N content are the key factors affecting the catalytic activity of C(Ppy-Pth). Quenching, probe, and electrochemical experiment revealed that in the catalytic PDS system with C(Ppy-Pth)-1000-1/1 (pH0 = 3.00), the oxidation of AN mainly occurred through the generation of hydroxyl radical (·OH), superoxide anion (O2·-), and electron transfer on the C(Ppy-Pth)-1000-1/1 surface. The steady-state concentration of ·OH and O2·- were 2.65 × 10-14 M and 1.97 × 10-13 M, respectively, and the contribution rate of ·OH oxidation was 31.28%. The oxidation of AN by sulfate radical (SO4·-) and singlet oxygen (1O2) could be neglected. This study provides a promising strategy for the construction of PDS catalyst and wastewater treatment.

Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils.

At present, the impact of cuproptosis-related genes in the study of osteosarcoma is largely unknown. Genome-wide data of osteosarcoma and controls were downloaded from 3 different databases, and specific diagnostic models associated with cuproptosis in osteosarcoma were constructed by support vector machines with artificial intelligence, random forest trees and LASSO regression. Differential analysis of immune cell infiltration was examined using routine blood data from 25,665 cases. Differential expression was examined using immunohistochemistry and PCR. PDHA1 and CDKN2A were obtained as specific cuproptosis-related biomarkers for osteosarcoma after artificial intelligence analysis. PDHA1, CDKN2A and neutrophils were differentially expressed in OS and control groups. PDHA1 and CDKN2A are significantly dysregulated in OS and are able to serve as biomarkers of OS.

Incidence of traumatic sciatic nerve injury in patients with acetabular fractures and factors affecting recovery: a retrospective study.

BACKGROUND: Reports on traumatic sciatic nerve injury associated with acetabular fracture are rare. In this study, we investigated the demographics of these injuries, their clinical characteristics, management, and factors potentially influencing neurological recovery. METHODS: We retrospectively reviewed all patients diagnosed to have acetabular fracture at our trauma center between January 2014 and June 2021. Data on patient demographics, characteristics of sciatic nerve injury, neurological recovery, factors potentially influencing neurological recovery were analyzed. RESULTS: Eighteen patients (bilateral in one case) met the diagnostic criteria. All these injuries involved the posterior wall or posterior column, and most patients had posterior dislocation of the hip joint. Four of the 19 sides with traumatic sciatic nerve injury involved the common peroneal nerve division and 15 involved both the common peroneal and tibial nerve divisions. Seventeen patients (18 sides) underwent intraoperative nerve exploration, which revealed abnormalities in 7 sides and no obvious abnormality in 11 sides. At the last follow-up, 10 sides (52.6%) had complete recovery and 9 (47.4%) had partial recovery; the difference was statistically significant between those with or without abnormal nerve damage during exploration (P = 0.046). Linear regression analysis showed that a nerve abnormality detected intraoperatively was a predictor of nerve recovery (P = 0.009). The mean recovery time was significantly longer for partial recovery than for complete recovery (13.78 months vs. 6.70 months; P = 0.001). CONCLUSIONS: All the injuries in this series involved the posterior wall or posterior column, and most patients had posterior dislocation of the hip joint. Damage to the common peroneal nerve division was more severe than that to the tibial nerve division preoperatively. However, the degree of recovery of the common peroneal division was not worse than that of the tibial division. There was a relationship between the degree of neurological recovery and whether there was an abnormality at the time of intraoperative nerve exploration. Patients with partial recovery took longer to recover.

Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1ß.

BACKGROUND: Osteoarthritis (OA) is the main cause of older pain and disability. Intra-articular injections of ozone (O3) commonly have been found to have antioxidative and anti-inflammatory effects to reduce pain and improve function in knee osteoarthritis. It has been reported that reduced autophagy in chondrocytes plays an important role in the development of OA. This study aimed to probe the role of O3 on the autophagy in chondrocytes treated with IL-1ß. METHODS: Primary chondrocytes were isolated from Wistar rats cartilage within 3 days. The OA chondrocytes model was induced via treatment with IL-1ß for 24 h. Then the cells were treated with O3 and GW9662, the inhibitor of PPARγ. Cell viability was assessed by CCK-8. Further, the cells subjected to Western blot analysis, qRT-PCR and immunofluorescence assay. The numbers of autophagosomes were observed via transmission electron microscopy. RESULTS: 30 µg/ml O3 improved the viability of chondrocytes treated with IL-1ß. The decreased level of autophagy proteins and the numbers of autophagosomes improved in IL-1ß-treated chondrocytes with O3 via activating PPARγ/mTOR. In addition, the qRT-PCR results showed that O3 decreased the levels of IL-6, TNF-α and MMP-3, MMP-13 in chondrocytes treated with IL-1ß. CONCLUSIONS: 30 µg/ml O3 improved autophagy via activating PPARγ/mTOR signaling and suppressing inflammation in chondrocytes treated with IL-1ß.

Association between age, gender, body mass index, and pulmonary function in preoperative patients with lung cancer.

INTRODUCTION: Many confounding factors such as sex, age, and body mass index (BMI) affect pulmonary function parameters, but there are limited data about the direct and/or indirect effects of small airway function on lung function for differences in confounding factors. OBJECTIVES: This study aimed to use structural equation model (SEM) to explain the influence of the confounding factors (age, sex, and BMI) on the relationship between small airway function and lung function in patients with lung cancer. METHODS: A cross-sectional observational study was conducted in a single medical center. Subjects were assessed; small airway function was specified by MEF25% and MEF50%; lung function by FVC; pulmonary obstruction by FEV1, FEV1%, and FEV1/FVC; and PEF and PEF% reflected the strength of abdominal muscles. The measurement model was analyzed by confirmatory factor analysis. The SEM was conducted to analyze the structural models of the effects of the confounding factors. RESULTS: In the measurement model, variables were fit to their domains, the path linking age and sex to pulmonary obstruction was positive and statistically significant, and the path linking sex to muscle strength was also positive and statistically significant. Muscle strength positively and significantly mediates the path between sex and FVC. As a moderator, BMI increased the effects of small airway function on FVC. CONCLUSION: Age and sex were directed to pulmonary obstruction, and muscle strength as a mediator between sex and lung function was novel, and BMI adjusted the effects of small airway function on FVC.

Comparison of effects of high- and low-frequency electromagnetic fields on proliferation and differentiation of neural stem cells.

To compare the effects of high- (HF-EMF) and low-frequency electromagnetic fields (LF-EMF) on the proliferation and differentiation of neural stem cells (NSCs). NSCs were obtained from SD rat hippocampus and cultured in suspension and adherent differentiation media. NSCs were exposed to LF-EMF (5 m T, 50 Hz, 30 min daily), HF-EMF (maximum magnetic induction 2.5 T, 40 % MO, 50 Hz, 10 min daily) and no electromagnetic field. At 3 d, cell viability and quantity of NSCs in suspension were detected by CCK-8 assay and cell counting plate. Immunofluorescence staining and qRT-PCR were performed to detect the percentage of Tuj-1 and GFAP-positive NSCs and the expression of Tuj-1 and GFAP mRNA. The P3 NSCs were positive with Nestin and induced NSCs expressed Tuj-1, GFAP and oligodendrocyte markers (MBP). CCK-8 assay and cell counting showed that the OD value and quantity of LF-EMF group were significantly higher than those in other two groups (both P < 0.05). Compared with the control group, the OD value and quantity were significantly higher in the HF-EMF group (P < 0.05). Immunofluorescence staining and qRT-PCR revealed that the percentage of Tuj-1 positive cells and the expression of Tuj-1 mRNA of NSCs exposed to LF-EMF were the highest (both P < 0.05). The proportion of GFAP-positive NSCs and the expression of GFAP mRNA did not significantly differ among three groups (all P> 0.05). Both 50 Hz LF-EMF and HF-EMF can promote the proliferation of NSCs in vitro and LF-EMF can accelerate NSCs to differentiate into neurons.

Long non-coding RNA maternally expressed gene 3 inhibits osteogenic differentiation of human dental pulp stem cells via microRNA-543/smad ubiquitin regulatory factor 1/runt-related transcription factor 2 axis.

OBJECTIVE: The aim of the present study was to investigate the biological roles and underlying mechanism of the long non-coding RNA maternally expressed gene 3 (MEG3) on osteogenic differentiation of human dental pulp stem cells (hDPSCs). METHODS: The expression levels of MEG3, microRNA-543 (miR-543), osterix, osteopontin, osteocalcin and runt-related transcription factor 2 (RUNX2) were measured by quantitative real-time PCR (qRT-PCR). Alkaline phosphatase (ALP) activity assay and alizarin red S staining (ARS) were used to measure the impacts exerted by MEG3, miR-543 on osteogenic differentiation. Cell proliferation was measured by MTT assay. In addition, the targeted relationships between miR-543, MEG3, and Smad ubiquitin regulatory factor 1 (SMURF1) were assessed through dual luciferase reporter assay. RESULTS: During osteogenic induction, the expression of MEG3 was gradually reduced, whereas the expression of miR-543, osterix, osteopontin, osteocalcin and RUNX2 were gradually increased. Functional analysis implied that MEG3 overexpression or miR-543 inhibition reduced the cell proliferation, ALP activity, ARS levels, and decreased the expression of osteoblast-related proteins. Moreover, MEG3 promoted SMURF1 expression by directly targeting miR-543 as a competing endogenous RNA. Furthermore, overexpression of miR-543 or silencing SMURF1 could reverse the inhibitory effects of MEG3 on the osteogenic differentiation of hDPSCs. CONCLUSIONS: In conclusion, our study revealed that overexpression of MEG3 inhibited hDPSCs osteogenic differentiation via miR-543/SMURF1/RUNX2 regulatory network, which may contribute to the functional regulation and clinical applications of hDPSCs.

Isolation and Characterization of Neural Progenitor Cells From Bone Marrow in Cell Replacement Therapy of Brain Injury.

Many studies supported that bone marrow mesenchymal stem cells (BM-MSCs) can differentiate into neural cells, but few researchers detected mature and function of nerve cells, especially in vivo study. Some researchers even suggested that BM-MSCs transplantation would not be able to differentiate into functional neural cells. To figure out the dispute, this study examined bone marrow-derived sphere-like cells, harvested via neural stem cell suspension culture, then identified as bone marrow-derived neural progenitor cells (BM-NPCs) by finding the expression of neural progenitor cells genes and proteins, neural progenitor cells characteristic and nerve cell differentiation induced through both methods. Moreover, BM-NPCs transplantation showed long-term survival and improved the ethological and histological indexes of brain injury rats, demonstrating functional nervous cells differentiated from BM-NPCs. These in vitro and in vivo results confirmed BM-NPCs differentiating into mature and functional nerve cells. This study provided valuable experimental data for BM-NPCs, suggesting a potential alternative treatment of central nervous injury disease.

[Association of metabolic syndrome with chronic kidney disease in premenopausal and postmenopausal women].

OBJECTIVE: To explore the relationship between metabolic syndrome (MS) and the risk for chronic kidney disease (CKD) in premenopausal and postmenopausal women. METHODS: We conducted a cross-sectional study among 1346 community-based women from June to October 2012 and collected the data of personal history, lifestyle, physical measures and laboratory indicators. The diagnosis of CKD was established for an eGFR of less than 60 mL/min per 1.73 m2 or albuminuria. The diagnosis of metabolic syndrome was based on the International Diabetes Federation Guide. According to an epidemiological survey in Guangdong province, women older than 48.9 years were classified as having a postmenopausal status. The prevalence of MS and CKD was determined in both the premenopausal and postmenopausal women, and the association between MS and CKD was analyzed using logistic regression models. RESULTS: MS was significantly correlated with CKD in premenopausal women in both unadjusted analyses (OR=3.10, 95% CI: 1.32-7.28, P=0.009) and in analysis after adjustment for potential confounders (OR=4.09, 95% CI: 1.63- 10.32, P=0.003). When adjusted for diabetes, hypertension, and hyperuricemia, no correlation was found between MS and CKD in premenopausal women (OR=1.56, 95% CI: 0.31-7.63, P= 0.592); in the unadjusted analyses, MS was significantly correlated with CKD in postmenopausal women (P < 0.001). After further adjustment for age, education status, current smoking, physical inactivity, and current drinking, MS was still significantly correlated with CKD (OR=2.60, 95% CI: 1.69-3.99, P < 0.001). When adjusted for diabetes, hypertension, and hyperuricemia, the correlation between MS and CKD was still significant (OR=1.61, 95% CI: 1.09-2.37, P=0.018). In the unadjusted model, a high blood pressure (OR=2.77, 95%CI: 1.57-4.89, P < 0.001), an elevated serum triglyceride level (OR=1.84, 95%CI: 1.16-2.90, P=0.009) and a high fast glucose level (OR=2.07, 95%CI: 1.30-3.28, P=0.002) were all significantly correlated with CKD in postmenopausal women. After adjusting for age, current smoking, current alcohol use, education status and physical inactivity, a high blood pressure (OR=2.28, 95%CI: 1.22-4.26, P=0.01), a high serum triglyceride level (OR=1.71, 95%CI: 1.03-2.86, P=0.039) and a high fast glucose (OR=2.25, 95%CI: 1.36-3.73, P=0.002) were still significantly correlated with CKD in postmenopausal women. Blood pressure, serum triglyceride level, fast glucose, serum HDL cholesterol level and central obesity were not correlated with CKD in either the unadjusted model or adjusted model in premenopausal women (P > 0.05). CONCLUSIONS: MS is correlated with CKD in both premenopausal and postmenopausal women, and the association is dependent on diabetes, hypertension, and hyperuricemia in premenopausal women but not in postmenopausal women.

Efficacy of 50 Hz electromagnetic fields on human epidermal stem cell transplantation seeded in collagen sponge scaffolds for wound healing in a murine model.

To explore the possible efficacy of electromagnetic fields (EMF) for skin tissue engineering, effects of EMF exposure on epidermal stem cells (ESC) seeded in collagen sponge scaffolds for wound healing in a murine model were investigated. The wound models of a full-thickness defect established with 36 7 ∼ 8-week-old nude mice were randomly divided into three groups: a control group, an ESC-only group, and an ESC with EMF exposure group (frequency of 50 Hz, magnetic induction of 5 mT, 60 min per day for 20 days). ESC were separated from human foreskin and cultured in vitro, and then transplanted with collagen sponge scaffolds as a delivery vehicle to wounds of the ESC-only group, and ESC with EMF exposure group was exposed to EMF after ESC transplantation. Effects of EMF on morphological changes and expression of ß1 integrin in regenerated skins were observed. Wound healing rates and healing times were collected to evaluate the efficacy of repairment. Results showed that human ESC were successfully transplanted to nude mice, which facilitated the formation of intact skin on nude mice. In contrast to other groups, the wound healing of ESC with EMF exposure group was the fastest (P < 0.05), the structure of regenerated skins was more mature, and it contained more continuity in the number of viable cell layers and rich hair follicles' structure. These results suggest that the use of 50 Hz EMF as a non-invasive treatment can accelerate wound healing of ESC transplantation, and restore structural integrity of regenerated skin. Bioelectromagnetics. 38:204-212,2017. © 2017 Wiley Periodicals, Inc.