Review on strategies for improving the added value and expanding the scope of CO2 electroreduction products.

The electrochemical reduction of CO2 into value-added chemicals has been explored as a promising solution to realize carbon neutrality and inhibit global warming. This involves utilizing the electrochemical CO2 reduction reaction (CO2RR) to produce a variety of single-carbon (C1) and multi-carbon (C2+) products. Additionally, the electrolyte solution in the CO2RR system can be enriched with nitrogen sources (such as NO3-, NO2-, N2, or NO) to enable the synthesis of organonitrogen compounds via C-N coupling reactions. However, the electrochemical conversion of CO2 into valuable chemicals still faces challenges in terms of low product yield, poor faradaic efficiency (FE), and unclear understanding of the reaction mechanism. This review summarizes the promising strategies aimed at achieving selective production of diverse carbon-containing products, including CO, formate, hydrocarbons, alcohols, and organonitrogen compounds. These approaches involve the rational design of electrocatalysts and the construction of coupled electrocatalytic reaction systems. Moreover, this review presents the underlying reaction mechanisms, identifies the existing challenges, and highlights the prospects of the electrosynthesis processes. The aim is to offer valuable insights and guidance for future research on the electrocatalytic conversion of CO2 into carbon-containing products of enhanced value-added potential.

Enhancing cowpea wilt resistance: insights from gene coexpression network analysis with exogenous melatonin treatment.

BACKGROUND: Cowpea wilt is a harmful disease caused by Fusarium oxysporum, leading to substantial losses in cowpea production. Melatonin reportedly regulates plant immunity to pathogens; however the specific regulatory mechanism underlying the protective effect of melatonin pretreated of cowpea against Fusarium oxysporum remains known. Accordingly, the study sought to evaluate changes in the physiological and biochemical indices of cowpea following melatonin treated to facilitate Fusarium oxysporum resistance and elucidate the associated molecular mechanism using a weighted gene coexpression network. RESULTS: Treatment with 100 µM melatonin was effective in increasing cowpea resistance to Fusarium oxysporum. Glutathione peroxidase (GSH-PX), catalase (CAT), and salicylic acid (SA) levels were significantly upregulated, and hydrogen peroxide (H2O2) levels were significantly downregulated in melatonin treated samples in roots. Weighted gene coexpression network analysis of melatonin- and Fusarium oxysporum-treated samples identified six expression modules comprising 2266 genes; the number of genes per module ranged from 9 to 895. In particular, 17 redox genes and 32 transcription factors within the blue module formed a complex interconnected expression network. KEGG analysis revealed that the associated pathways were enriched in secondary metabolism, peroxisomes, phenylalanine metabolism, flavonoids, and flavonol biosynthesis. More specifically, genes involved in lignin synthesis, catalase, superoxide dismutase, and peroxidase were upregulated. Additionally, exogenous melatonin induced activation of transcription factors, such as WRKY and MYB. CONCLUSIONS: The study elucidated changes in the expression of genes associated with the response of cowpea to Fusarium oxysporum under melatonin treated. Specifically, multiple defence mechanisms were initiated to improve cowpea resistance to Fusarium oxysporum.

High-sensitivity long-range surface plasmon resonance sensing assisted by gold nanoring cavity arrays and nanocavity coupling.

In many of the existing refractive index (RI) sensing works, only the shape and size of plasmonic structures are usually taken into account, while the parameters of spacer layers are ignored. In this publication, we explored the long-range surface plasmon resonance (LRSPR) and Fabry-Pérot resonance coupling effects of our proposed gold nanoring cavity array/spacer layer/Au mirror/glass substrate. Both the RI sensitivity and full width at half-maximum (FWHM) values were superior than those of conventional surface plasmon resonance substrates. We discussed the tunability of the RI sensitivity through changing the RI and thickness of the spacer layer. Then, under the optimized parameter conditions of the spacer layer, the geometry parameters (including size, gap and periodicity) of gold nanoring cavity arrays were tuned to optimize the best RI sensitivity. Finally, we broke the structural symmetry of a nanoring cavity to introduce Fano resonances into our system, and a high RI sensitivity and figure-of-merit (FOM) of 695 nm per RIU (refractive index unit) and 96.5, respectively, were achieved when the breaking angle θ was 30°. This study opens up many possibilities for boosting the FOM of RI sensing by taking into account the hybridization effects of localized surface plasmon resonance, LRSPR, and Fabry-Pérot and Fano resonances.

Shape- and Size-Dependent Refractive Index Sensing and SERS Performance of Gold Nanoplates.

Plasmonic sensors are promising for ultrasensitive chemical and biological analysis. Gold nanoplates (Au NPLs) show unique geometrical structures with high ratios of surface to bulk atoms, which display fascinating plasmonic properties but require optimization. This study presented a systematic investigation of the influence of different parameters (shape, aspect ratio, and resonance mode) on localized surface plasmon resonance properties, refractive index (RI, n) sensitivities, and surface-enhanced Raman scattering (SERS) enhancement ability of different types of Au NPLs through finite-difference time-domain (FDTD) simulations. As a proof of concept, triangular, circular, and hexagonal Au NPLs with varying aspect ratios were fabricated via a three-step seed-mediated growth method by the experiment. Both FDTD-simulated and measured experimental results confirm that the RI sensitivities increase with the aspect ratio. Furthermore, choosing a lower order resonance mode of Au NPLs benefits higher RI sensitivities. The SERS enhancement abilities of Au NPLs also predicted to be highly dependent on the shape and aspect ratio. The triangular Au NPLs showed the highest SERS enhancement ability, while it drastically decreased for circular Au NPLs after the rounding process. The SERS enhancement ability gradually became more intense as the hexagonal Au NPLs overgrown on circular Au NPLs with increasing volumes of HAuCl4 solution. The results are expected to help develop effective biosensors.

Tumor Microenvironment following Gemcitabine Treatment Favors Differentiation of Immunosuppressive Ly6Chigh Myeloid Cells.

Regulation of myeloid-derived suppressor cells (MDSC) by ongoing inflammation following repeated chemotherapy remain elusive. In this study, we show that a multidose clinical regimen of gemcitabine (GEM) treatment enhances the immunosuppressive function of monocytic MDSC (M-MDSC), although tumor development is delayed in E0771 tumor-bearing mice. Accordingly, effector IFN-γ-producing CD4 and CD8 T cells are significantly decreased in the tumor microenvironment (TME) of GEM-treated mice. The conditioned medium of GEM-treated tumor cells enhances differentiation of mouse bone marrow cells and human PBMC into immunosuppressive M-MDSC. Cytokine profiling of GEM-treated tumor cells identifies GM-CSF as one of the most differentially expressed cytokines. Blockade or knockdown of GM-CSF can partially reduce immunosuppression of Ly6Chigh cells induced by GEM-conditioned medium. Knockdown of GM-CSF in tumor cells also delays tumor progression with decreased accumulation of M-MDSC in the TME. Mechanistically, enhanced production of reactive oxygen species and activation of NF-κB are observed in GEM-treated tumor cells. Treatment with the mitochondrial-targeted antioxidant and inhibitor of NF-κB signaling can abrogate GEM-induced hyperexpression of GM-CSF in E0771 cells. In addition, the phagocytic clearance of apoptotic tumor cells (efferocytosis) enhances the immunosuppressive function of bone marrow Ly6Chigh myeloid cells. Further, GEM treatment results in metabolic changes in residual tumor cells, leading to the resistance to T cell-mediated killing. Together, our results define an undesired effect of repeated GEM treatment promoting immunosuppression in TME via upregulation of GM-CSF and efferocytosis as well as deregulation of lipid metabolism in residual tumor cells.

DNA Structure-Stabilized Liquid-Liquid Self-Assembled Ordered Au Nanoparticle Interface for Sensitive Detection of MiRNA 155.

Au nanoparticles (Au NPs) can be self-assembled in a bottom-up orderly manner at the oil-water interface, which is widely used as SERS platforms, but the stability of the Au NP interface needs to be improved due to shaking or shifting and the Brownian motion. The DNA structure with unique sequence specificity, excellent programmability, and flexible end-group modification capability owns good potential to precisely control the plasmonic structure's distance. In this study, a large area of the SERS substrate is obtained from the DNA structure-stabilized self-assembled ordered Au NPs on the cyclohexane-water interface. Combining with the exonuclease III (exo III)-assisted DNA recycling amplification strategy, we construct a liquid-phase SERS biosensor for efficient detection of microRNA 155 (miRNA 155). Compared with the traditional randomly assembled Au NPs on the two-phase interface, the SERS signal is significantly enhanced and more stable. The detection limit of the SERS biosensor for miRNA 155 reached 1.45 fmol/L, which has a very wide linear range (100 fmol/L-5 nmol/L). This work gives an efficient approach to stabilize the self-assembly Au NPs on the liquid-liquid interface, which can broaden the application of SERS analysis.

Tumor Microenvironment Modulates Immunological Outcomes of Myeloid Cells with mTORC1 Disruption.

The role of the mTOR signaling pathway in different myeloid cell subsets is poorly understood in the context of tumor development. In this study, myeloid cell-specific Raptor knockout (KO) mice were used to determine the roles of mechanistic target of rapamycin complex 1 (mTORC1) in regulating macrophage function from Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastasis. We found no difference in tumor growth between conditional Raptor KO and control mice in the s.c. tumor models, although depletion of mTORC1 decreased the immunosuppressive function of tumor-associated macrophages (TAM). Despite the decreased immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c. tumor microenvironment of mTORC1 conditional Raptor KO mice due to downregulated CD115 expression on macrophages. In addition, TNF-α production by mTORC1-deficient myeloid cells was also decreased in the s.c. LLC tumors. On the contrary, disruption of mTORC1 in myeloid cells promoted lung cancer metastasis. Accordingly, immunosuppressive interstitial macrophages/metastasis-associated macrophages (CD11b+F4/80high) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to decreased Th1 responses. Taken together, our results demonstrate that differential tumor microenvironment dictates the immunological outcomes of myeloid cells, with mTORC1 disruption leading to different tumor growth phenotypes.

Liquid Phase Interfacial Surface-Enhanced Raman Scattering Platform for Ratiometric Detection of MicroRNA 155.

The self-assembly of gold nanoparticles (Au NPs) on a liquid phase interface is often employed as a surface-enhanced Raman scattering (SERS) platform with advantages of simple preparation, high reproducibility, and a defect-free character, but they are limited to only detect a target with Raman signals. To overcome this problem, microRNA 155 without a Raman signal can be detected by a liquid phase interfacial ratiometric SERS platform. Compared with the typical solid phase SERS platform, we propose a distinctive strategy not only owning the advantages of the liquid phase interfacial platform but also breaking the limitation of recent liquid-liquid interfacial SERS analysis. This platform presents a fabulous sensitivity with a limit of detection (LOD) of 1.10 aM for microRNA 155. By simply altering the duplex-specific nuclease (DSN) enzyme amplification, our strategy can realize detection of a variety of microRNAs, paving the way to practical applications of a liquid phase SERS platform.

Target-triggered configuration change of DNA tetrahedron for SERS assay of microRNA 122.

A surface-enhanced Raman scattering (SERS) method is proposed for the assay of microRNA 122 based on configuration change of DNA tetrahedron. Firstly, a DNA tetrahedron was self-assembled with one vertex labeled with toluidine blue (TB). Then, it was immobilized on the porous Ni/SiO2@PEI@Au as a SERS platform, which was characterized by scanning electron microscopy (SEM) and X-ray diffraction (XRD). At this time, the DNA tetrahedron was contracted; so, the TB is close to AuNPs and the Raman signal is high. When target microRNA 122 existed, with the nicking enzyme amplification strategy, a great deal of DNA signal chains (S5) was obtained, which can extend the contracted DNA tetrahedron and change it into a three-dimensional DNA tetrahedron. In this case, the TB was far from AuNPs, resulting in a lower Raman signal. Due to the configuration change of DNA tetrahedron, the Raman signal at 1624 cm-1 (with the excitation wavelength of 633 nm) has a linear relationship with the logarithm concentration of microRNA 122. This SERS assay has high sensitivity for microRNA 122 with a determination range from 0.01 aM to 10 fM and a detection limit of 0.009 aM. The recoveries from spiked samples were in the range 95 to 109%. This SERS strategy is designed based on the target-triggered configuration change of DNA tetrahedron, which can give new insight for DNA structures in bioanalysis. Graphical abstract A sensitive surface-enhanced Raman scattering (SERS) biosensor was developed to detect microRNA 122 using the configuration change of DNA tetrahedron to indirectly control the position of TB and hot spot.

Systemic immune-inflammation index predicts prognosis of patients with advanced pancreatic cancer.

BACKGROUND: Systemic inflammation and immune dysfunction have been proved to be associated with cancer progression and metastasis in various malignancies. The aim of this retrospective study was to evaluate the prognostic significance of pre-treatment systemic immune-inflammation index (SII) in patients with advanced pancreatic cancer. METHODS: In total, 419 patients diagnosed with advanced pancreatic cancer, between January 2011 and December 2015, were retrospectively enrolled. The SII was developed based on a training set of 197 patients from 2011 to 2013 and validated in an independent cohort of 222 patients from 2014 to 2015. Data on baseline clinicopathologic characteristics; pre-treatment laboratory variables such as absolute neutrophil, lymphocyte, and platelet counts; and carbohydrate antigen 19-9 (CA19-9), total bilirubin (TBIL), albumin (ALB), alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) levels were collected. The association between clinicopathologic characteristics and SII was assessed. The overall survival was calculated using the Kaplan-Meier survival curves and compared using the log-rank test. Univariate and multivariate Cox proportional hazard regression models were used to analyze the prognostic value of the SII. RESULT: An optimal cutoff point for the SII of 440 stratified the patients with advanced pancreatic cancer into high (> 440) and low (≤ 440) SII groups in the training cohort. Univariate and multivariate analyses revealed that the SII was an independent predictor for overall survival. The prognostic significance of the SII was confirmed in both normal and elevated CA19-9 levels. CONCLUSION: The baseline SII serves as an independent prognostic marker for patients with advanced pancreatic cancer and can be used in patients with both normal and elevated CA19-9 levels.

A novel scoring system based on hemostatic parameters predicts the prognosis of patients with advanced pancreatic cancer.

OBJECTIVE: The aim of this study was to evaluate the prognostic value of pre-treatment plasma hemostatic parameters in patients with advanced pancreatic cancer. METHODS: A total of 320 patients diagnosed with advanced pancreatic cancer between January 1, 2011 to December 31, 2015 were enrolled in this retrospective study. The prognostic significance of hemostatic parameters such as prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FBG), platelet count (PLT), mean platelet volume (MPV), plateletcrit (PCT), and platelet distribution width (PDW) was determined by univariate and multivariate Cox hazard models. Then, Kaplan-Meier methods and log-rank tests were performed to compare the survival of patients in different risk groups. RESULT: Univariate and multivariate analyses showed that prolonged PT, high FBG, and high MPV were independent prognostic factors for poor overall survival (PT > 11.3 s, HR = 1.46, 95%CI = 1.10-1.94, p = 0.009; FBG>2.5 g/L, HR = 1.41, 95%CI = 1.08-1.84, p = 0.011; MPV>12.2 fL, HR = 1.52, 95%CI = 1.13-2.04, p = 0.005). Moreover, all the patients were stratified into three groups by a scoring system based on these three hemostatic markers. The median survival time of the three groups was 8.8 months, 6.3 months and 4.3 months (P < 0.001). CONCLUSION: PT, FBG and MPV were independent prognostic factors in advanced pancreatic cancer. A novel scoring system based on these hemostatic parameters could be used to predict the survival of patients with advanced pancreatic cancer.

N-terminus plus linker domain of Mg-chelatase D subunit is essential for Mg-chelatase activity in Oryza sativa.

Mg chelatase, a key enzyme in chlorophyll biosynthesis, is comprised of I, D and H subunits. Among these subunits, the D subunit was regarded to mediate protein interactions due to its unique protein domains. However, the functional roles of the different domains of the D subunit in vivo remain unclear. In this study, we dissected the rice (Oryza sativa) D subunit (OsCHLD) into three peptide fragments: the putative chloroplast transit peptide (TP, Met1 to Arg45), the N-terminus plus linker domain (OsCHLDN + L, Ala46 to Leu485) and the C-terminus (OsCHLDC, Ile486 to Ser754), to explore the roles of these fragments. The results of the yeast two-hybrid assay and the in vitro reconstitution of the Mg-chelatase activity showed that only OsCHLDN + L interacted with the I and H subunits and maintained most of the Mg-chelatase activity in vitro. Furthermore, artificial TP-OsCHLDN + L and TP-OsCHLDC were overexpressed in rice. Interestingly, an incomplete co-suppression had occurred in both of the overexpressed (OsCHLDN + L-ox and OsCHLDC-ox) plants, resulting in a significantly downregulated expression of endogenous OsCHLD. Therefore, these transgenic plants had adequate OsCHLDN + L and OsCHLDC instead of endogenous OsCHLD, providing ideal models to study the function of different domains of the D subunit in vivo. The OsCHLDN + L-ox plants showed an identical phenotype to that of the wild type, while the OsCHLDC-ox plants demonstrated a yellowish phenotype that resembled the D subunit mutants. These results indicated that only OsCHLDN + L could complement the function of endogenous OsCHLD, providing direct evidence that OsCHLDN + L is essential for Mg-chelatase activity in vivo.

Epigenetic modifications of the VH region after DJH recombination in Pro-B cells.

The variable region of murine immunoglobulin heavy chain (Igh) is assembled by sequential DH -JH and VH -DJH recombination. The accessibility of the Igh locus determines the order of rearrangement. Because of the large number of VH genes and the lack of a suitable model, the epigenetic modifications of VH genes after DJH recombination have not previously been characterized. Here, we employed two v-Abl pro-B cell lines, in which the Igh locus is in germline and DJH -recombined configurations, respectively. The DJH junction displays the characteristics of a recombination centre, such as high levels of activation-associated histone modifications and recombination-activating gene protein (RAG) binding in DJH -rearranged pro-B cells, which extend the recombination centre model proposed for the germline Igh locus. The different domains of the VH region have distinct epigenetic characteristics after DJH recombination. Distal VH genes have higher levels of active histone modifications, germline transcription and Pax5 binding, and good quality recombination signal sequences. Proximal VH genes are relatively close to the DJH recombination centre, which partially compensates for the low levels of the above active epigenetic modifications. DJH recombination centre might serve as a cis-acting element to regulate the accessibility of the VH region. Furthermore, we demonstrate that RAG weakly binds to functional VH genes, which is the first detailed assessment of RAG dynamic binding to VH genes. We provide a way for VH -DJH recombination in which the VH gene is brought into close proximity with the DJH recombination centre for RAG binding by a Pax5-dependent chromosomal compaction event, and held in this position for subsequent cleavage and VH -DJH joining.

TIGIT overexpression diminishes the function of CD4 T cells and ameliorates the severity of rheumatoid arthritis in mouse models.

Rheumatoid arthritis (RA) is an immune-mediated disease with a pathogenesis that involves CD4 T cell activation. Multiple immune regulatory molecules expressed on CD4(+) T cells were involved in RA pathogenesis. In this study, we investigated the role of T cell immunoglobulin and ITIM (immunoreceptor tyrosine-based inhibition motif) domain (TIGIT) in RA. The frequency of TIGIT-positive CD4(+) T cells in the synovial fluid (SF) of active RA patients was lower than that of inactive RA patients. And a negative correlation between RA disease activity and TIGIT expression was found. In CD4(+) T cells isolated from SF of active RA patients, TIGIT upregulation significantly decreased cell proliferation, as shown by MTT assay. TIGIT overexpression also significantly decreased the production of IFN-γ and IL-17, and increased that of IL-10, as determined by ELISA and qRT-PCR. In CD4(+) T cells isolated from SF of inactive RA patients, TIGIT was silenced by siRNA transfection. As expected, TIGIT knockdown resulted in an opposite effect on cell proliferation and the production of cytokines, including IFN-γ, IL-17 and IL-10. A RA mouse model was established using type II collagen induction. TIGIT was upregulated in RA mouse by lentivector infection. As expected, TIGIT overexpression in vivo significantly alleviated the disease severity and deceased the levels of anti-collagen II antibodies. TIGIT upregulation in the early stage was more effective to alleviate disease severity. Our data suggested the potential therapeutic role of TIGIT in RA patients.

Effects of Shen-Fu injection on coagulation-fibrinolysis disorders in a porcine model of cardiac arrest.

OBJECTIVE: The objective of the study is to investigate the effects of Shen-Fu injection (SFI) on coagulation-fibrinolysis disorders in a porcine model of cardiac arrest. MATERIALS AND METHODS: Thirty Wuzhishan pigs were randomly assigned into the sham operation group (SO group, n = 6), epinephrine group (EP group, n = 12), and SFI group (n = 12). After 8 minutes of untreated ventricular fibrillation (VF), pigs in the EP group or SFI group were administered with either EP (0.02 mg/kg) or SFI (1.0 mL/kg), respectively. Plasma levels of tissue factor, thrombin-antithrombin complex, tissue factor pathway inhibitor, antithrombin III, protein C, tissue plasminogen activator, plasminogen activator inhibitor 1, soluble thrombomodulin, and soluble endothelial protein C receptor were measured at baseline, 1, 6, 12, and 24 hours after return of spontaneous circulation (ROSC). In addition, arterial lactate levels were measured at baseline, 1, 6, 12, and 24 hours after ROSC, and lactate clearance was calculated at 1, 6, 12, and 24 hours after ROSC. RESULTS: Compared with the EP group, tissue factor, thrombin-antithrombin complex, tissue factor pathway inhibitor, tissue plasminogen activator, and plasminogen activator inhibitor 1 levels were significantly lower, whereas antithrombin III and protein C levels were significantly higher in the SFI group (all P < .05). In addition, soluble thrombomodulin and soluble endothelial protein C receptor levels in the SFI group were significantly lower in comparison to the EP group (all P < .01). Furthermore, arterial lactate levels were significantly lower, and lactate clearance was higher in the SFI group (all P < .01). CONCLUSIONS: This study demonstrates that SFI can inhibit coagulation-fibrinolysis disorders after cardiac arrest, which may be associated with alleviating endothelial damage and improving systemic metabolism.

[Protective Effect of Shenfu Injection on Postresuscitation Lung Injury in a Porcine Model of As- physia-induced Cardiac Arrest].

Objective To observe the protective effect of Shenfu Injection ( SFI) on post-resusci- tation lung injury in a porcine model of asphyxia-induced cardiac arrest. Methods Thirty-four anaesthe- tized Wuzhi Mountain inbred miniature piglets of both sexes were subjected to asphyxia by intubation clip- ping, followed by standard cardiopulmonary resuscitation. Eighteen successfully resuscitated pigs [with recovery of return of spontaneous circulation ( ROSC) ] were divided into the SFI group and the normal saline (NS) group according to random digit table, 9 in each group. SFI at 0. 24 mg/min was intravenously pumped to piglets in the SFI group immediately from ROSC to 6 h after resuscitation, while NS at 0. 24 mg/min was intravenously pumped to piglets in the NS group immediately from ROSC to 6 h after resusci- tation. Oxygen metabolism, respiratory mechanics indices including oxygenation index (ΟI) , respiration index ( RI) , oxygen delivery ( DO2), oxygen consumption ( VO2), oxygen extraction ratio (Ο2 ER), PaCO2, lactic acid (LAC) were detected using blood gas analyzer at basic state, immediately after ROSC, 15 and 30 min, 1, 2, 4, and 6 h after ROSC. Dynamic lung compliance (Cdyn) , airway resistance (Raw), external vascular lung water index (EVLWI) , pulmonary vascular permeability index (PVPI) were monitored at each aforesaid time point. Activities of Na+-K +-ATPase and Ca² +-ATPase, contents of SOD and MDA, concentrations of TNF-α, IFN-γ, and IL-4 were determined using ELISA.IFN-γ/IL-4 ratio was calculated. Cell apoptosis was detected using TUNEL and apoptotic index (Al) calculated. Protein concentrations of Bcl-2 and Bax were detected using immunohistochemical assay, and Bax/Bcl-2 ratio calculated. Caspase-3 protein was quantitatively detected using Western blot. Results The survival rate was 88. 9% (8/9) in the SFI group and 66. 7% (6/9) in the NS group at 6 h after ROSC. The mean survival time was (5. 77 ±0. 71) h in the SFI group, longer than that in the NS group [ (4. 77 ±0. 59) h, P >0. 05]. Compared with the basic state, 01 and Cdyn obviously decreased immediately after ROSC (P <0. 05) ; RI, DO2, VΟ2, O2ER, Raw, EVLWI, PVPI, PaCO2, and LAC obviously increased immediately after ROSC (P<0. 05). All indices were recovered as time went by. Compared with the NS group, ΟI, Cdyn, DO2, VΟ2, and Ο2 ER at each time points after ROSC were significantly higher in the SFI group than in the NS group (P <0. 05, P <0. 01); RI, Raw, EVLWI, PVPI, PaCO2, and LAC were significantly lower in the SFI group than in the NS group (P <0. 05, P <0. 01 ). Compared with the NS group, activities of Na'-K '-AT- Pase and Ca² +-ATPase, contents of SOD, level of IFN-γ, IFN-γ/IL-4 ratio, concentrations of Bcl-2 in- creased more; MDA, TNF-α, IL-4 level, Al, Bax/Bcl-2 ratio, Caspase-3 protein level decreased more (P <0. 05, P <0. 01). Conclusion SFI could improve cell energy metabolism, enhance antioxidant ca- pacity of cells, reduce the release of inflammatory mediators, regulate the Thl/Th2 balance, and attenu- ate cell apoptosis of lung tissue, thereby protecting post-resuscitation lung injury.

MiR-21 overexpression improves osteoporosis by targeting RECK.

Osteoporosis is a kind of metabolic bone disorder. MicroRNA-21 (miR-21) has been proven to play an important role in bone formation, whereas its role in osteoporosis is unclear. In the present study, miR-21 expression was inhibited by TNF-α in mesenchymal stem cells (MSCs). TNF-α induced cell apoptosis, and inhibited cell proliferation and differentiation of MSCs. Whereas the effect was reversed by miR-21 mimics. Expression of reversion-inducing cysteine-rich protein with Kazal motifs (RECK) which is a predicted target of miR-21 was inhibited by miR-21 mimics. A luciferase reporter gene assay showed that miR-21 directly bound to RECK 3'-UTR. The effect of TNF-α on MSCs was reversed by RECK siRNA which was consistent with miR-21 mimics. The expression of MT1-MMP was inhibited by TNF-α and enhanced by RECK siRNA and miR-21 mimics. For the in vivo study, an osteoporosis model (OVX) was established by bilateral oophorectomy in mice. The expression of miR-21 decreased and RECK increased in the OVX mice. When treated with lentiviral RECK shRNA, the osteocalcin concentration and alkaline phosphate activity of the OVX mice decreased. The bone mineral density of the right femur mid-diaphysis was improved by RECK shRNA. Collectively, miR-21 modulated the osteoporosis by targeting RECK. These results emphasize the role of miR-21 during osteoporosis and suggest RECK might be a new medical target for osteoporosis.

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1.

MicroRNAs (miRNAs) have been reported to have diverse biological roles in regulating many biological processes, including osteogenic differentiation. In the present study, we identified that miR-24 was a critical regulator during osteogenic differentiation. We found that overexpression of miR-24 significantly inhibited osteogenic differentiation, which decreased alkaline phosphatase activity, matrix mineralization and the expression of osteogenic differentiation markers. In contrast, inhibition of miR-24 exhibited an opposite effect. Furthermore, we delineated that miR-24 regulates post-transcriptionals of T-cell factor-1 (Tcf-1) via targeting the 3'-untranslated region (UTR) of Tcf-1 mRNA. MiR-24 was further found to regulate the protein expression of Tcf-1 in the murine osteoprogenitors cells and bone mesenchymal stem cells. Additionally, the positive effect of miR-24 suppression on osteoblast differentiation was apparently abrogated by Tcf-1 silencing. Taken together, our data suggest that miR-24 participates in osteogenic differentiation by targeting and regulating Tcf-1 expression in osteoblastic cells.

Acute kidney injury after cardiac arrest of ventricular fibrillation and asphyxiation swine model.

PURPOSES: The purposes of the study are to investigate the renal function in ventricular fibrillation (VF) and asphyxiation cardiac arrest in a swine model and to estimate the value of novel biomarkers in the acute kidney injury (AKI) after cardiac arrest. METHOD: Thirty-two healthy inbred Wu-Zhi-Shan miniature piglets were randomized into 2 groups (n = 16 per group). Cardiac arrest was induced by programmed electric stimulation and clamping the endotracheal tube in the VF group and asphyxiation group, respectively. Cardiopulmonary resuscitation was done for return of spontaneous circulation (ROSC). RESULTS: One hundred percent (16/16) ROSC was observed in the VF group, and 50% (8/16) in the asphyxiation group (P < .01). All AKI biomarkers elevated significantly after ROSC. The novel biomarkers changed much earlier than the creatinine. The concentration of novel biomarkers in the asphyxiation group was higher than the VF group. Live animals had an oliguria and developed AKI. Characteristic morphological injuries in renal tissues were observed under light microscope and transmission electron microscope and were more serious in the asphyxiation group. CONCLUSIONS: Acute kidney injury at early stage of postresuscitation is common in different causes of cardiac arrest. Asphyxiation has more severe kidney injury and gets worse prognosis.

Ratio-fluorescence sensor based on carbon dots and PtRu/CN nanozyme for efficient detection of melatonin in tablet.

The identification and quantification of melatonin (MT) are crucial for early diagnosis of disorders associated with circadian rhythm disruption. Herein, novel blue-emissive carbon dots (BCDs) were synthesized through an improved hydrothermal treatment using serine and malic acid as reductant and carbon source. The excellent optical properties of the as-obtained BCDs were used for ratiometric sensing by strategically constructing a MT sensing system integrating BCDs with C3N4 nanosheets loaded with platinum/ruthenium nanoparticles (PtRu/CN). In this system, H2O2 activated the peroxidase-like activity of PtRu/CN to generate •OH and 1O2 for oxidizing the colorless o-phenylenediamine (OPD) into yellow 2,3-diaminophenazine (DAP) with fluorescence emission at 565 nm. Concurrently, the fluorescence emission of BCDs at 439 nm was quenched by the generated DAP via the static quenching and inner filter effect (IFE) process. However, MT rapidly scavenged the generated free radicals to reverse the ratio fluorescence signal. The developed BCDs/PtRu/CN/OPD/H2O2 sensing platform enabled quantitative analysis of MT at concentrations ranging from 0.06 to 600 µmol/L with a low detection limit of 23.56 nmol/L. Moreover, smartphone-based RGB sensing of MT was successfully developed for rapid visualization and portable processing. More broadly, novel insights into the preparation of carbon dots with sensitive fluorescence sensing properties were presented, promising for future considerations.