Maintaining moderate levels of hypochlorous acid promotes neural stem cell proliferation and differentiation in the recovery phase of stroke.

JOURNAL/nrgr/04.03/01300535-202503000-00029/figure1/v/2024-06-17T092413Z/r/image-tiff It has been shown clinically that continuous removal of ischemia/reperfusion-induced reactive oxygen species is not conducive to the recovery of late stroke. Indeed, previous studies have shown that excessive increases in hypochlorous acid after stroke can cause severe damage to brain tissue. Our previous studies have found that a small amount of hypochlorous acid still exists in the later stage of stroke, but its specific role and mechanism are currently unclear. To simulate stroke in vivo, a middle cerebral artery occlusion rat model was established, with an oxygen-glucose deprivation/reoxygenation model established in vitro to mimic stroke. We found that in the early stage (within 24 hours) of ischemic stroke, neutrophils produced a large amount of hypochlorous acid, while in the recovery phase (10 days after stroke), microglia were activated and produced a small amount of hypochlorous acid. Further, in acute stroke in rats, hypochlorous acid production was prevented using a hypochlorous acid scavenger, taurine, or myeloperoxidase inhibitor, 4-aminobenzoic acid hydrazide. Our results showed that high levels of hypochlorous acid (200 µM) induced neuronal apoptosis after oxygen/glucose deprivation/reoxygenation. However, in the recovery phase of the middle cerebral artery occlusion model, a moderate level of hypochlorous acid promoted the proliferation and differentiation of neural stem cells into neurons and astrocytes. This suggests that hypochlorous acid plays different roles at different phases of cerebral ischemia/reperfusion injury. Lower levels of hypochlorous acid (5 and 100 µM) promoted nuclear translocation of ß-catenin. By transfection of single-site mutation plasmids, we found that hypochlorous acid induced chlorination of the ß-catenin tyrosine 30 residue, which promoted nuclear translocation. Altogether, our study indicates that maintaining low levels of hypochlorous acid plays a key role in the recovery of neurological function.

Cascade analysis of awareness, willingness, uptake and adherence with regard to PrEP among young men who have sex with men (YMSM) in China: A comparison between students and non-students.

INTRODUCTION: In China, young men who have sex with men (YMSM) are one of the groups most at risk of HIV/AIDS. The uptake of pre-exposure prophylaxis (PrEP) among YMSM has not been well documented. A cascade analysis of awareness, willingness, use and adherence with regard to PrEP was conducted separately among YMSM students and non-students. METHODS: From 20 October to 30 December 2021, all adolescents aged 16-24 years were selected for the study from among MSM recruited from 31 provincial administrative regions in mainland China. Participants were included in a cross-sectional study of awareness, willingness, use and adherence with regard to PrEP among YMSM. Logistic regression modelling was used to identify factors associated with the four outcomes. RESULTS: Among 1014 student and 866 non-student YMSMs, respectively, 88.07% and 81.64% had heard of PrEP; 58.16% and 50.35% were willing to use PrEP; 7.59% and 7.62% had used PrEP; and 3.16% and 3.58% had adhered to PrEP. Among students, those living in high-risk areas and pilot cities and those who had engaged in commercial sex and group sex had a positive effect on PrEP use, and the same trends were found among non-students living in high-risk areas and pilot cities and those who had engaged in group sex. 'Daily oral' and 'flexible' PrEP use positively influenced adherence among both groups. CONCLUSIONS: A differentiation strategy of PrEP promotion should be implemented among YMSM. Material support for students, such as financial resources, should increase, while non-students should increase their level of perception of HIV risk.

D-Optimal Design and Development of a Koumine-Loaded Microemulsion for Rheumatoid Arthritis Treatment: In vivo and in vitro Evaluation.

Introduction: Koumine (KME) is the most abundant active ingredient separated from Gelsemium elegans Benth and exhibits a significant therapeutic effect on rheumatoid arthritis (RA). It is a lipophilic compound with poor aqueous solubility, and there is an urgent need to develop novel dosage forms of KME and promote its clinical application for the treatment of RA. The aim of this study was to design and develop KME-loaded microemulsions (KME-MEs) for the effective management of RA. Methods: The composition of the microemulsion was selected by carrying out a solubility study and generating pseudoternary phase diagrams, and further optimized by D-Optimal design. The optimized KME-MEs was evaluated for particle size, viscosity, drug release, storage stability, cytotoxicity, cellular uptake, Caco-2 cell transport and everted gut sac investigations. In vivo fluorescence imaging and the therapeutic effects of KME and KME-MEs on collagen-induced arthritis (CIA) rats were also evaluated. Results: The optimized microemulsion contained 8% oil, 32% Smix (surfactant/cosurfactant) and 60% water and was used for in vivo and in vitro studies. The optimal KME-MEs exhibited a small globule size of 18.5 ± 0.14 nm and good stability over 3 months, and the release kinetics followed a first-order model. These KME-MEs had no toxic effect on Caco-2 cells but were efficiently internalized into the cytoplasm. Compared to KME, the KME-MEs displayed significantly increased permeability and absorption in Caco-2 cell monolayer assay and ex vivo everted gut sac experiment. As expected, the KME-MEs attenuated the progression of RA in CIA rats and were more effective than free KME with a reduced frequency of administration. Conclusion: The KME-MEs improved the solubility and therapeutic efficacy of KME by employing formulation technology. These results provide a promising vehicle for the oral delivery of KME to treat RA and have attractive potential for clinical translation.

Improvement of Corrosion and Wear Resistance of CoCrNiSi0.3 Medium-Entropy Alloy by Sputtering CrN Film.

In this study, Co, Cr, and Ni were selected as the equal-atomic medium entropy alloy (MEA) systems, and Si was added to form CoCrNiSi0.3 MEA. In order to further improve its wear and corrosion properties, CrN film was sputtered on the surface. In addition, to enhance the adhesion between the soft CoCrNiSi0.3 substrate and the super-hard CrN film, a Cr buffer layer was pre-sputtered on the CoCrNiSi0.3 substrate. The experimental results show that the CrN film exhibits a columnar grain structure, and the film growth rate is about 2.022 µm/h. With the increase of sputtering time, the increase in CrN film thickness, and the refinement of columnar grains, the wear and corrosion resistance improves. Among all CoCrNiSi0.3 MEAs without and with CrN films prepared in this study, the CoCrNiSi0.3 MEA with 3 h-sputtered CrN film has the lowest wear rate of 2.249 × 10-5 mm3·m-1·N-1, and the best corrosion resistance of Icorr 19.37 µA·cm-2 and Rp 705.85 Ω·cm2.

Ischemic accumulation of succinate induces Cdc42 succinylation and inhibits neural stem cell proliferation after cerebral ischemia/reperfusion.

Ischemic accumulation of succinate causes cerebral damage by excess production of reactive oxygen species. However, it is unknown whether ischemic accumulation of succinate affects neural stem cell proliferation. In this study, we established a rat model of cerebral ischemia/reperfusion injury by occlusion of the middle cerebral artery. We found that succinate levels increased in serum and brain tissue (cortex and hippocampus) after ischemia/reperfusion injury. Oxygen-glucose deprivation and reoxygenation stimulated primary neural stem cells to produce abundant succinate. Succinate can be converted into diethyl succinate in cells. Exogenous diethyl succinate inhibited the proliferation of mouse-derived C17.2 neural stem cells and increased the infarct volume in the rat model of cerebral ischemia/reperfusion injury. Exogenous diethyl succinate also increased the succinylation of the Rho family GTPase Cdc42 but repressed Cdc42 GTPase activity in C17.2 cells. Increasing Cdc42 succinylation by knockdown of the desuccinylase Sirt5 also inhibited Cdc42 GTPase activity in C17.2 cells. Our findings suggest that ischemic accumulation of succinate decreases Cdc42 GTPase activity by induction of Cdc42 succinylation, which inhibits the proliferation of neural stem cells and aggravates cerebral ischemia/reperfusion injury.

Mechanism and Molecular Targets of Ejiao Siwu Decoction for Treating Primary Immune Thrombocytopenia Based on High-Performance Liquid Chromatograph, Network Pharmacology, Molecular Docking and Cytokines Validation.

We explored the mechanisms and molecular targets of Ejiao Siwu Decoction (EJSW) for treating primary immune thrombocytopenia (ITP) using network pharmacology and molecular docking. Active compounds of EJSW were identified by high-performance liquid chromatography-diode array detector (HPLC-DAD) and high-performance liquid chromatography-mass spectrometry (HPLC-MS) and their targets were obtained from HERB and SwissTargetPrediction, and ITP targets were obtained from Comparative Toxicogenomics Database (CTD) and GeneCards. STRING and Cytoscape were used for protein-protein interaction (PPI) network analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses by WebGestalt yielded a gene-pathway network, Autodock molecular docking was applied to screen targets and active compounds, and cytokines were detected using a cytometric bead array (CBA) human inflammation kit. We identified 14 compounds and 129 targets, and 1,726 ITP targets. RAC-alpha serine/threonine-protein kinase (AKT1), tumour necrosis factor (TNF), interleukin-6 (IL6), caspase-3 (CASP3) and tumour suppressor protein (TP53) were core targets (nodes and edges). Functional annotation identified cofactor binding and coenzyme binding, and 20 significantly enriched pathways. Active compounds of EJSW were successfully docked with ITP targets. Tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1ß) were upregulated in ITP patients, vascular endothelial growth factor A (VEGF-A) and vascular endothelial growth factor D (VEGF-D) were downregulated, and EJSW treatment reversed these trends. EJSW may regulate key ITP targets based on the in silico analyses, and protect vascular integrity through AGE-RAGE signalling, complement and coagulation cascades, and VEGF signalling by downregulating TNF-α, IL-1ß and other inflammatory factors.

[Analysis of Differential Proteins Related to Platelet Activation in Patients with Essential Thrombocythemia Based on Label-Free Quantitative Technology].

OBJECTIVE: To analysis the specific protein markers of essential thrombocythemia (ET) based on proteomics technology, to explore and verify the differential protein related to platelet activation. METHODS: Blood samples were obtained from ET patients and healthy people and a certain protein mass spectrometry was detected using label-free quantitative technology. The proteins relative abundance increased or down-regulated by 1.3 times in the disease group compared with the control group, and the protein abundance in the two groups t test P＜0.05 were defined as differential proteins. Bioinformatics analysis of the differential proteins was performed using GO and KEGG. The difference in the average protein abundance between the two groups was analyzed by t test and P＜0.05 was considered statistically significant. Differential proteins were selected for verification by parallel reaction monitoring (PRM) technology. RESULTS: A total of 140 differential proteins were found, of which 72 were up-regulated and 68 were down-regulated. KEGG enrichment showed that the differential protein expression was related to the platelet activation pathway. The differential proteins related to platelet activation were GPV, COL1A2, GP1bα, COL1A1 and GPVI. Among them, the expressions of GPV, GP1bα and GPVI were up-regulated, and the expressions of COL1A2 and COL1A1 were down-regulated. PRM verification of COL1A1, GP1bα, GPVI and GPV was consistent with LFP proteomics testing. CONCLUSION: Differential proteins in ET patients are related to platelet activation pathway activation.Differential proteins such as GPV, GPVI, COL1A1 and GP1bα can be used as new targets related to ET platelet activation.

Cooperative P-Wave Velocity Measurement with Full Waveform Moment Tensor Inversion in Transversely Anisotropic Media.

Precise stochastic approaches to quantitatively calculate the source uncertainties offers the opportunity to eliminate the influence of anisotropy on moment tensor inversion. The effects of ignoring anisotropy were tested by using homogeneous Green's functions. Results indicate the influence of anisotropy and noise on fault plane rotation is very small for a pure shear source whether it is restricted to double couple solution or full moment tensor solution. Green's functions with different prior rough anisotropy information were tested, indicating that the complex source is more sensitive to velocity models than the pure shear source and the fault plane rotation caused by full moment tensor solution is larger than the pure double couple solution. Collaborative P-wave velocity inversion with active measurements and passive acoustic emission data using the fast-marching method were conducted, and new Green's functions established based on the tomography results. The resolved fault plane solution rotated only 3.5° when using the new Green's functions, but the presence of spurious isotropic and compensated linear vector dipole components was not completely eliminated. It is concluded that the cooperative inversion is capable of greatly improving the accuracy of the fault plane solutions and reducing the spurious components in the full moment tensor solution.

Combinational Chemoimmunotherapy for Breast Cancer by Codelivery of Doxorubicin and PD-L1 siRNA Using a PAMAM-Incorporated Liposomal Nanoplatform.

Chemoimmunotherapy can synergistically enhance the therapeutic effects and decrease the side effects by a combined method. However, the effective targeted codelivery of various chemotherapeutic agents and siRNAs remains challenging. Although nanomedicine-based chemoimmunotherapy has shown great potential in cancer treatment in recent years, further effort is needed to simplify the nanocarrier designs and maintain their effective functions. Here, we report a simple but robust multifunctional liposomal nanocarrier that contains a pH-sensitive liposome (LP) shell and a dendritic core for tumor-targeted codelivery of programmed cell death ligand 1 (PD-L1) siRNA and doxorubicin (DOX) (siPD-L1@PM/DOX/LPs). siPD-L1@PM/DOX/LPs had a suitable particle size and zeta potential, excellent stability in serum, and pH-sensitive drug release in vitro. They exhibited significant cell proliferation inhibition compared to free DOX and DOX-loaded LPs and could escape endosomes, effectively release siRNA into the cytoplasm of MCF-7 cells, and significantly reduce the PD-L1 expression on tumor cells. In vivo imaging confirmed high accumulation of siPD-L1@PM/DOX/LPs at the tumor site. More importantly, compared with siPD-L1@PM/LPs or DOX alone, siPD-L1@PM/DOX/LPs were more effective in inhibiting tumor growth and activating cytotoxic T cells in vivo. In conclusion, this nanocarrier may hold promise as a codelivery nanoplatform to improve the treatment of various solid tumors.

M2 Macrophage-Based Prognostic Nomogram for Gastric Cancer After Surgical Resection.

A good prediction model is useful to accurately predict patient prognosis. Tumor-node-metastasis (TNM) staging often cannot accurately predict prognosis when used alone. Some researchers have shown that the infiltration of M2 macrophages in many tumors indicates poor prognosis. This approach has the potential to predict prognosis more accurately when used in combination with TNM staging, but there is less research in gastric cancer. A multivariate analysis demonstrated that CD163 expression, TNM staging, age, and gender were independent risk factors for overall survival. Thus, these parameters were assessed to develop the nomogram in the training data set, which was tested in the validation and whole data sets. The model showed a high degree of discrimination, calibration, and good clinical benefit in the training, validation, and whole data sets. In conclusion, we combined CD163 expression in macrophages, TNM staging, age, and gender to develop a nomogram to predict 3- and 5-year overall survivals after curative resection for gastric cancer. This model has the potential to provide further diagnostic and prognostic value for patients with gastric cancer.

Identification of the prognostic value of ferroptosis-related gene signature in breast cancer patients.

BACKGROUND: Breast cancer (BRCA) is a malignant tumor with high morbidity and mortality, which is a threat to women's health worldwide. Ferroptosis is closely related to the occurrence and development of breast cancer. Here, we aimed to establish a ferroptosis-related prognostic gene signature for predicting patients' survival. METHODS: Gene expression profile and corresponding clinical information of patients from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database. The Least absolute shrinkage and selection operator (LASSO)-penalized Cox regression analysis model was utilized to construct a multigene signature. The Kaplan-Meier (K-M) and Receiver Operating Characteristic (ROC) curves were plotted to validate the predictive effect of the prognostic signature. Gene Ontology (GO) and Kyoto Encyclopedia of Genes, Genomes (KEGG) pathway and single-sample gene set enrichment analysis (ssGSEA) were performed for patients between the high-risk and low-risk groups divided by the median value of risk score. RESULTS: We constructed a prognostic signature consisted of nine ferroptosis-related genes (ALOX15, CISD1, CS, GCLC, GPX4, SLC7A11, EMC2, G6PD and ACSF2). The Kaplan-Meier curves validated the fine predictive accuracy of the prognostic signature (p < 0.001). The area under the curve (AUC) of the ROC curves manifested that the ferroptosis-related signature had moderate predictive power. GO and KEGG functional analysis revealed that immune-related responses were largely enriched, and immune cells, including activated dendritic cells (aDCs), dendritic cells (DCs), T-helper 1 (Th1), were higher in high-risk groups (p < 0.001). Oppositely, type I IFN response and type II IFN response were lower in high-risk groups (p < 0.001). CONCLUSION: Our study indicated that the ferroptosis-related prognostic signature gene could serve as a novel biomarker for predicting breast cancer patients' prognosis. Furthermore, we found that immunotherapy might play a vital role in therapeutic schedule based on the level and difference of immune-related cells and pathways in different risk groups for breast cancer patients.

SPARC enhances 5-FU chemosensitivity in gastric cancer by modulating epithelial-mesenchymal transition and apoptosis.

Previous studies have shown that secreted protein acidic and rich in cysteine (SPARC) proteins can inhibit the development of cancer cells in various ways, such as by inhibiting angiogenesis and inhibiting cell proliferation. In fact, SPARC proteins may have an effect on the chemoresistance of gastric cancer cells to 5-Fluorouracil (5-FU), which needs further research in the future. Therefore, the purpose of this study was to explore the relationship between SPARC proteins and the chemosensitivity of gastric cancer cells to 5-FU. In vitro, after SPARC protein levels were regulated by plasmid, siRNA and human recombinant SPARC protein transfection in MGC-803, SGC-7901 and BGC-823 cells, we detected epithelial-mesenchymal transition (EMT), apoptosis markers and cell viability after 5-FU treatment. In vivo, we implanted BGC-823 cells with stable SPARC overexpression into nude mice. Tumour size was measured to assess the effect of SPARC protein on tumour formation and 5-FU chemosensitivity. In SGC-7901 and BGC-823 cells, both endogenous and exogenous upregulation of SPARC protein levels decreased cell viability, destroyed cytoskeletal F-actin, inhibited cell migration, and downregulated a series of transcription factors to inhibit cell EMT; it also upregulated cell apoptosis-related proteins to promote cell apoptosis. However, we obtained opposite results in SPARC knockdown MGC-803 cells. In vivo, compared with the control group, the group engrafted with BGC-823 cells stably overexpressing SPARC had a significant smaller tumour size. After 5-FU treatment, the new tumour gradually decreased in size. Our results show that the SPARC protein could enhance 5-FU chemosensitivity in gastric cancer cell lines by inhibiting EMT and promoting cell apoptosis.

Micro-Crack Mechanism in the Fracture Evolution of Saturated Granite and Enlightenment to the Precursors of Instability.

To explore the potential precursors of rock instability, it is necessary to clarify the mechanism of micro-crack from fracturing to failure, which involves the evolution of fracture size, orientation, source model, and their relationships to the loading. The waveforms of acoustic emission (AE) recorded by the sensor network attached rock sample during laboratory tests provide a data basis for solving these problems, since these observations are directly related to the characteristics of the fracturing sources. Firstly, we investigated the source mechanism, looking at the rise angle and the average frequency (RA-AF) trends during five loading stages in a uniaxial compression test. Results show that the proportion of shear events significantly increases when approaching instability. Secondly, we calculated the moment tensor for each event, considering the uncertainties of P-wave polarity, azimuth, and the takeoff angles of the rays. Moment tensor solutions suggest that there are obviously more crack events than shear events in all loading stages. Moment tensor evolutions confirmed that the decreasing of isotropic component and the increment of double-couple can be used as precursors of rock fracturing development. Considering the limitations of these two methods, it is suggested that we should be concerned more about the proportions of individual failure components and their evolutions over time, instead of absolutely classifying the events into a certain source type.

Circulatory CD4-Positive T-Lymphocyte Imbalance Mediated by Homocysteine-Induced AIM2 and NLRP1 Inflammasome Upregulation and Activation Is Associated with Human Abdominal Aortic Aneurysm.

INTRODUCTION: CD4-positive T lymphocytes (CD4 cells) play a significant role in human abdominal aortic aneurysm (AAA). However, we know little about the role of the different CD4 subtypes. OBJECTIVE: We aimed to discover the circulatory CD4 phenotypic marker profile and the roles of the newly found T helper cell 9 (Th9) and follicular helper T cells (Tfh) and that of inflammasomes in CD4 cells from AAA patients. METHODS: We extracted CD4 cells from 30 AAA patients and 21 age-matched controls. Phenotype-specific transcription factors (TFs) and inflammasomes were analyzed with qRT-PCR. RESULTS: Th17-, Th1-, Th9-, and Tfh-specific TFs and inflammasome components NLRP1 (NLR family pyrin domain-containing 1), NLRP3, NLRC4, AIM2 (absent in melanoma 2), PYCARD (apoptosis speck-like protein containing a CARD), and CASP1 (caspase 1) were upregulated, and T regulatory cell- and Th2-specific TFs were downregulated in the patients' peripheral blood CD4 cells. Homocysteine was involved in Tfh and Th17 imbalance by AIM2 and NLRP1 inflammasome upregulation. Blood total cholesterol level correlated positively with NLRP1 expression, and blood low-density lipoprotein level correlated negatively with FOXP3 expression. CONCLUSIONS: Inflammasome-induced CD4 cell imbalance was involved in AAA. We thought that AAA might be a consequence of synergism between systemic immune imbalance and local autoimmunity.

Macrophage-derived SPARC Attenuates M2-mediated Pro-tumour Phenotypes.

Since the theory of seed and soil was put forward, people have increasingly recognized that the tumour microenvironment is an important regulator of tumour progression and therapeutic response. Among them, M2-type macrophages (M2, as the major macrophage subtype in the tumour foci) have important promoting effects on various biological behaviours. Secreted protein acidic and rich in cysteine (SPARC) is an important anti-tumour component in the microenvironment of gastric cancer. This study shows that macrophages are an important source of the SPARC and that SPARC overexpression in M2 can reduce M2-mediated promoting proliferation, migration and anti-apoptotic effects in gastric cancer. Additionally, the AKT/mTOR signalling pathways may participate in the malignant process.

Aminooxyacetic acid (AOAA) sensitizes colon cancer cells to oxaliplatin via exaggerating apoptosis induced by ROS.

Background: As the third confirmed gaseous transmitter, the role of hydrogen sulfide (H2S) in the pathogenesis of multiple types of cancer has been attracting increasing attention. Increased expression of cystathionine ß-synthase (CBS) and H2S in colon cancer tissue samples has been validated and tumor-derived H2S, mainly produced by CBS, stimulates bioenergetics, cell proliferation, and angiogenesis in colon cancer. Recently, the therapeutic manipulation of H2S has been proposed as a promising anticancer approach. However, the effect of aminooxyacetic acid (AOAA), which has been widely used as an inhibitor of CBS dependent synthesis of H2S, on the chemotherapeutic effect of oxaliplatin (OXA) and the underlying mechanisms remain to be illustrated. Methods: We examined the expression of CBS in human colorectal cancer specimens and matched normal mucosa by immunohistochemistry. The effect of AOAA on the sensitivity of colon cancer cells to OXA and the level of apoptosis induced by caspase cascade was investigated in both HCT116 and HT29 cell lines utilizing CCK-8 assays, flow cytometry analysis and western blot analysis. The endogenous levels of reactive oxygen species (ROS) were detected fluorescently by DCF-DA, and glutathione (GSH) levels were measured by a Total GSH Detection Kit. Tumor bearing xenograft mouse models and in vivo imaging systems were further used to investigate the effect of AOAA in vivo and immunohistochemistry (IHC) and TUNEL analysis were performed. Results: In the current study, we confirmed CBS, the main target of AOAA, is overexpressed in human colorectal cancer by immunohistochemistry. The inhibitory effect of AOAA on the synthesis of H2S was validated utilizing fluorescent probe and specific electrode. AOAA significantly reduced the IC50 values of OXA in both colon cancer cell lines. Co-incubation with AOAA elicited increased apoptosis induced by OXA, featured by increased activation of caspase cascade. Besides, AOAA further increased the levels of ROS induced by OXA and attenuated the synthesis of glutathione (GSH), which is a vital antioxidant. Besides, the results of in vivo imaging and following IHC and TUNEL analysis were in accordance with cellular experiments, indicating that AOAA sensitizes colon cancer cells to OXA via exaggerating intrinsic apoptosis. Conclusion: The results suggested that CBS is overexpressed in colorectal cancer tissues and AOAA sensitizes colon cancer cells to OXA via exaggerating apoptosis both in vitro and in vivo. Decreasing the endogenous level of GSH and consequently impaired detoxification of ROS might be one of the mechanisms underlying the effect of AOAA.

Antithermal Quenching of Luminescence in Zero-Dimensional Hybrid Metal Halide Solids.

Zero-dimensional (0D) hybrid metal halides have emerged as a new generation of luminescent phosphors owing to their high radiative recombination rates, which, akin to their three-dimensional cousins, commonly demonstrate thermal quenching of luminescence. Here, we report on the finding of antithermal quenching of luminescence in 0D hybrid metal halides. Using (C9NH20)2SnBr4 single crystals as an example system, we show that 0D metal halides can demonstrate antithermal quenching of luminescence. A combination of experimental characterizations and first-principles calculations suggests that antithermal quenching of luminescence is associated with trap states introduced by structural defects in (C9NH20)2SnBr4. Importantly, we find that antithermal quenching of luminescence is not only limited to (C9NH20)2SnBr4 but also exists in other 0D metal halides. Our work highlights the important role of defects in impacting photophysical properties of hybrid metal halides and may stimulate new efforts to explore metal halides exhibiting antithermal quenching of luminescence at higher temperatures.

Apigenin Prevent Abdominal Aortic Aneurysms Formation by Inhibiting the NF-κB Signaling Pathway.

Abdominal aortic aneurysms (AAA) is a multifactorial vascular disease with a high rate of mortality and brings heavy burden to both human and society. The pathological process behind AAA is complex. Elastin degradation, chronic inflammation, and vascular smooth muscle cell phenotypic modulation are involved in AAA formation. Apigenin (API) has gained much attention due to its specific properties, such as anti-inflammation, antioxidant, and anti-cancer effects. Previous studies have demonstrated that API exert beneficial effects on prevention of cardiovascular diseases. However, the effects of API on AAA are still unknown. Here, we for the first time evaluated API-related effects on AAA formation using a Cacl2-induced AAA model. Compared with the AAA group, treatment with API reduced the incidence of AAA, attenuated pathological expansion of the aorta, and preserved elastic fiber in a dose-dependent manner. In addition, API attenuated vascular inflammation by inhibiting activation of matrix metalloproteinase and modulated vascular smooth muscle cell contractile phenotypic transition. The preventative effect of API on AAA might be associated with the downregulation of nuclear factor-kappa B (NF-κB) activity via the IKK-dependent signaling pathway. Our findings firstly revealed that API could suppress AAA formation in a dose-dependent manner by inhibiting the NF-κB signaling pathway, and API should be considered as a promising therapeutic drug in prevention of AAA.

The intensification of metallic layered phenomena above thunderstorms through the modulation of atmospheric tides.

We present a multi-instrument experiment to study the effects of tropospheric thunderstorms on the mesopause region and the lower ionosphere. Sodium (Na) lidar and ionospheric observations by two digital ionospheric sounders are used to study the variation in the neutral metal atoms and metallic ions above thunderstorms. An enhanced ionospheric sporadic E layer with a downward tidal phase is observed followed by a subsequent intensification of neutral Na number density with an increase of 600 cm-3 in the mesosphere. In addition, the Na neutral chemistry and ion-molecule chemistry are considered in a Na chemistry model to simulate the dynamical and chemical coupling processes in the mesosphere and ionosphere above thunderstorms. The enhanced Na layer in the simulation obtained by using the ionospheric observation as input is in agreement with the Na lidar observation. We find that the intensification of metallic layered phenomena above thunderstorms is associated with the atmospheric tides, as a result of the troposphere-mesosphere-ionosphere coupling.

[Mid-term follow-up efficacy of interspinous dynamic stabilization system for lumbar degenerative diseases].

OBJECTIVE: To explore mid-term clinical efficacy and effect on adjacent segment degeneration of Wallis and Coflex interspinous implants for lumbar degenerative diseases. METHODS: From January 2011 to January 2013, 55 patients with L4, 5 degenerative lumbar spine diseases treated with interspinous devices were retrospectively analyzed, including 31 males and 24 females aged from 25 to 67 years old with an average of 43.3 years old; 21 patients were lumbar spinal stenosis and 34 patients were lumbar disc herniation. All patients were divided into Wallis group (33 cases) and Coflex group (22 cases) according to the interspinous fixation system. Visual analogue scale(VAS) was used to evaluate low back pain and lower limb pain, Japanese Orthopedic Association(JOA) score and Oswestry Disability Index(ODI) score were used to evaluate lumbar function. Surgical segment and adjacent segments, range of motion(ROM), disc height and the Pfirrmann grade of upper the adjacent segments were compared before and after operation. RESULTS: Fifty-five patients were followed up from 48 to 72 months with an average of 60.4 months. VAS score of low back pain and lower limb pain, JOA and ODI score of lumbar at 48 months after operation were improved than before operation between two groups(P<0.01), but there was no statistical difference for group comparisons(P>0.05). ROM, disc height of surgical segments were significantly lower than those before operation between two groups (P<0.05), while ROM of the upper and lower adjacent segments and disc height did not change significantly (P>0.05). There was no significant difference in ROM and disc height for group comparisons(P>0.05). There was no change in Pfirrmann grade of the upper adjacent segment degeneration between two groups(P>0.05). Four patients with primary lumbar disc herniation had a recurrence of 1 to 3 years after operation, including 3 in Wallis group and 1 in Coflex group, with an average age of 35.2 years old. CONCLUSIONS: Wallis and Coflex interspinous implants have the similar mid-term efficacy for the treatment of lumbar degenerative diseases, and could delay adjacent segment degeneration, but could not prevent recurrence of disc herniation.