Reinforcement of Electrocatalytic Oxygen Evolution Activity Enabled by Constructing Silver-Incorporated NiCo-PBA@NiFe-LDH Hierarchical Nanoboxes.

Complicated oxygen evolution reaction (OER) poses the bottleneck in improving the efficiency of hydrogen production through water electrolysis. Herein, an integrated strategy to modulate the electronic structure of NiFe layered double hydroxide (NiFe-LDH) is reported by constructing Ag-incorporated NiCo-PBA@NiFe-LDH heterojunction with a hierarchical hollow structure. This "double heterojunction" facilitates local charge polarization at the interface, thereby promoting electron transfer and reducing the adsorption energy of intermediates, ultimately enhancing the intrinsic activity of the catalyst. It is noteworthy that an exchange bias field is observed between NiCo-PBA and NiFe-LDH, which will be conducive to regulating the electron spin states of metals and facilitating the production of triplet oxygen. Additionally, the unique hierarchical nanoboxes provide a large specific surface area that ensures adequate exposure to adsorption sites and active sites. Profiting from the synergistic advantages, the overpotential is as low as 190 mV at a current density of 10 mA cm-2, with a low Tafel slope of 21 mV dec-1. Moreover, density functional theory (DFT) calculation further substantiated that the incorporation of Ag in the heterojunction can effectively reduce the adsorption energy of reactant intermediates and enhance the conductivity.

A nomogram for predicting food allergy in infants with feeding problems and malnutrition.

BACKGROUND AND OBJECTIVE: As oral food challenge (OFC) cannot be performed routinely in the general outpatient, this study aimed to construct a nomogram to predict the odds of food allergy in infants with idiopathic feeding problems and malnutrition. METHODS: From August 2018 to December 2021, 289 infants (median age, 6 months; P25-P75, 4-8) with idiopathic feeding problems and malnutrition were enrolled from seven hospitals in Shanghai, China. Food allergy was defined as a positive response to a skin prick test or OFC, with gastrointestinal, dermatologic, or respiratory symptom improvement after 4 weeks of avoidance of the suspected food. Demographic characteristics, Cow's Milk-related Symptom Scores (CoMiSS), and blood eosinophil amounts were evaluated for their associations with food allergy. Multivariable logistic regression analysis was used to identify variables to develop a nomogram model with the bootstrapped-concordance index as an assessment metric. RESULTS: Totally 249 of 289 infants had food allergy (86.2%). After logistic regression analysis, the feeding pattern (odds ratio [OR] = 5.28, 95% confidence interval [CI]: 2.13-13.09), a family history of allergy (OR = 1.79, 95% CI: 0.71-4.51), CoMiSS (OR = 1.45, 95% CI: 1.19-1.77), and eosinophil percentage (OR = 1.33, 95% CI: 1.11-1.60) were used to develop the model, which had a good performance with an area under the curve of 0.868 (95% CI: 0.792-0.944) and a bootstrapped-concordance index of 0.868. CONCLUSION: Food allergy is common in infants with idiopathic feeding problems and malnutrition. The developed nomogram may help identify infants with food allergy for further diagnosis.

HNRNPA2B1-mediated m6A modification of lncRNA MEG3 facilitates tumorigenesis and metastasis of non-small cell lung cancer by regulating miR-21-5p/PTEN axis.

BACKGROUND: Accumulating data indicate that N6-methyladenosine (m6A) RNA methylation and lncRNA deregulation act crucial roles in cancer progression. Heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1) as an m6A "reader" has been reported to be an oncogene in multiple malignancies. We herein aimed to elucidate the role and underlying mechanism by which HNRNPA2B1-mediated m6A modification of lncRNAs contributes to non-small cell lung cancer (NSCLC). METHODS: The expression levels of HNRNPA2B1 and their association with the clinicopathological characteristics and prognosis in NSCLC were determined by RT-qPCR, Western blot, immunohistochemistry and TCGA dataset. Then, the role of HNRNPA2B1 in NSCLC cells was assessed by in vitro functional experiments and in vivo tumorigenesis and lung metastasis models. HNRNPA2B1-mediated m6A modification of lncRNAs was screened by m6A-lncRNA epi-transcriptomic microarray and verified by methylated RNA immunoprecipitation (Me-RIP). The lncRNA MEG3-specific binding with miR-21-5p was evaluated by luciferase gene report and RIP assays. The effects of HNRNPA2B1 and (or) lncRNA MEG3 on miR-21-5p/PTEN/PI3K/AKT signaling were examined by RT-qPCR and Western blot analyses. RESULTS: We found that upregulation of HNRNPA2B1 was associated with distant metastasis and poor survival, representing an independent prognostic factor in patients with NSCLC. Knockdown of HNRNPA2B1 impaired cell proliferation and metastasis in vitro and in vivo, whereas ectopic expression of HNRNPA2B1 possessed the opposite effects. Mechanical investigations revealed that lncRNA MEG3 was an m6A target of HNRNPA2B1 and inhibition of HNRNPA2B1 decreased MEG3 m6A levels but increased its mRNA levels. Furthermore, lncRNA MEG3 could act as a sponge of miR-21-5p to upregulate PTEN and inactivate PI3K/AKT signaling, leading to the suppression of cell proliferation and invasion. Low expression of lncRNA MEG3 or elevated expression of miR-21-5p indicated poor survival in patients with NSCLC. CONCLUSIONS: Our findings uncover that HNRNPA2B1-mediated m6A modification of lncRNA MEG3 promotes tumorigenesis and metastasis of NSCLC cells by regulating miR-21-5p/PTEN axis and may provide a therapeutic target for NSCLC.

Achieving Ultra-Wideband NIR-II Emission in Cr3+-Doped Li(Sc,In)(Si,Ge)O4 Phosphors Based on Host Composition Engineering.

Realizing ultra-wideband and tunable near-infrared (NIR) emission remains a great challenge in NIR phosphor development. The luminescence of most reported NIR phosphors exhibits a peak wavelength shorter than 1000 nm and the corresponding FWHM is <200 nm. Here, a series of Cr3+-activated Li(Sc,In)(Si,Ge)O4 phosphors with ultra-wideband and tunable NIR-II emission are successfully developed based on the host composition engineering strategy. Significant spectral engineering in the NIR-II region is achieved with a peak wavelength changing from 1110 to 1253 nm. The olivine host structure could provide Cr3+ activator a highly distorted octahedral site with very weak crystal field strength, which results in NIR-II ultra-wideband emission with FWHM > 300 nm. A detailed discussion on the relationship between structural variation, crystal field splitting, and NIR luminescence has been applied. As far as we know, it is the first report about Cr3+ NIR luminescence engineering in such a long wavelength and wide range. The application of these NIR-II phosphors is demonstrated in intensity-based luminescent thermometry with a relative sensitivity of >2.0% K-1 in the physiological temperature range.

Genotoxicity, oxidative stress and transcriptomic effects of Nitenpyram on human bone marrow mesenchymal stem cells.

Despite of the global contamination and ubiquitous exposure to nitenpyram (NIT), little knowledge is available on the adverse effects to human health, with some evidence referring to its genotoxic potency to non-target organisms and esophageal squamous papilloma in rats. Human bone marrow mesenchymal stem cells (hBMSCs) was employed as an in vitro model more relevant to humans to assess the potential genotoxicity of NIT and to understand the underlying mechanisms at cellular and molecular levels. Noncytotoxic concentrations of NIT, 50-2500 µg/mL, dose-dependently elevated micronucleus (MN) and nuclear bud (NB) frequencies to 8.7-29‰ and 15-35‰, respectively. Additional metabolism by rat liver S9 fraction decreased chromosome impairment by 27-52% on MN frequencies and 63-76% on NB frequencies. A commercial NIT product, containing 20% of NIT and 60% of pymetrozine, caused higher cytotoxicity and chromosome impairment in comparison with NIT alone. Expressions of genes responses to DNA damage, ATM, ATR, p53, p21, Bax, H2AX, and GADD45A were disturbed by NIT treatment. Reactive oxygen species (ROS) amount and superoxide dismutase (SOD) activity were enhanced by NIT. Comet assay showed that lower concentrations of NIT, 12.5-100 µg/mL, induced the DNA damage. Transcriptomic analysis identified 468 differentially expressed genes (p < 0.05, |log2(Foldchange)| ≥ 1), from which 22 pathways were enriched. Multiple affected pathways were related to cancer including viral carcinogenesis and bladder cancer. NIT may produce genotoxicity via inducing oxidative stress and deregulating PI3K/Akt, AMPK and mTOR signaling pathways, associated with carcinogenetic potency. While environmental levels of NIT alone may pose little risk to human health, attention should be paid to the health risk arose from the synergistic or additive effects that may exist among NEOs and other types of pesticides.

Simulation and Analysis of Mie-Scattering Lidar-Measuring Atmospheric Turbulence Profile.

Based on the residual turbulent scintillation theory, the Mie-scattering lidar can measure the intensity of atmospheric turbulence by detecting the light intensity scintillation index of the laser return signal. In order to evaluate and optimize the reliability of the Mie-scattering lidar system for detecting atmospheric turbulence, the appropriate parameters of the Mie-scattering lidar system are selected and optimized using the residual turbulent scintillation theory. Then, the Fourier transform method is employed to perform the numerical simulation of the phase screen of the laser light intensity transformation on the vertical transmission path of atmospheric turbulence. The phase screen simulation, low-frequency optimization, and scintillation index calculation methods are provided in detail, respectively. Based on the phase distribution of the laser beam, the scintillation index is obtained. Through the relationship between the scintillation index and the atmospheric turbulent refractive index structure constant, the atmospheric turbulence profile is inverted. The simulation results show that the atmospheric refractive index structure constant profile obtained by the iterative method is consistent with the input HV5/7 model below 6500 m, which has great guiding significance to carry out actual experiments to measure atmospheric turbulence using the Mie lidar.

Recent Advances in the Synthesis, Characterization, and Application of Carbon Nanomaterials for the Removal of Endocrine-Disrupting Chemicals: A Review.

The large-scale production and frequent use of endocrine-disrupting chemicals (EDCs) have led to the continuous release and wide distribution of these pollutions in the natural environment. At low levels, EDC exposure may cause metabolic disorders, sexual development, and reproductive disorders in aquatic animals and humans. Adsorption treatment, particularly using nanocomposites, may represent a promising and sustainable method for EDC removal from wastewater. EDCs could be effectively removed from wastewater using various carbon-based nanomaterials, such as carbon nanofiber, carbon nanotubes, graphene, magnetic carbon nanomaterials, carbon membranes, carbon dots, carbon sponges, etc. Important applications of carbon nanocomposites for the removal of different kinds of EDCs and the theory of adsorption are discussed, as well as recent advances in carbon nanocomposite synthesis technology and characterization technology. Furthermore, the factors affecting the use of carbon nanocomposites and comparisons with other adsorbents for EDC removal are reviewed. This review is significant because it helps to promote the development of nanocomposites for the decontamination of wastewater.

Ajuforrestin A, an Abietane Diterpenoid from Ajuga ovalifolia var. calanthe, Induces A549 Cell Apoptosis by Targeting SHP2.

The Src-homology 2 domain-containing phosphatase 2 (SHP2), which is encoded by PTPN11, participates in many cellular signaling pathways and is closely related to various tumorigenesis. Inhibition of the abnormal activity of SHP2 by small molecules is an important part of cancer treatment. Here, three abietane diterpenoids, named compounds 1-3, were isolated from Ajuga ovalifolia var. calantha. Spectroscopic analysis was used to identify the exact structure of the compounds. The enzymatic kinetic experiment and the cellular thermal shift assay showed compound 2 selectively inhibited SHP2 activity in vitro. Molecular docking indicated compound 2 targeted the SHP2 catalytic domain. The predicted pharmacokinetic properties by SwissADME revealed that compound 2 passed the majority of the parameters of common drug discovery rules. Compound 2 restrained A549 proliferation (IC50 = 8.68 ± 0.96 µM), invasion and caused A549 cell apoptosis by inhibiting the SHP2-ERK/AKT signaling pathway. Finally, compound 2 (Ajuforrestin A) is a potent and efficacious SHP2 inhibitor and may be a promising compound for human lung epithelial cancer treatment.

Distribution of HLA-DQA1, -DQB1 and -DRB1 genes and haplotypes in Han, Uyghur, Kazakh and Hui populations inhabiting Xinjiang Uyghur Autonomous Region, China.

Genetic polymorphisms of human leucocyte antigen (HLA)-DRB1, -DQA1 and -DQB1 among four main ethnic groups including Han (n = 70), Uyghur (n = 71), Kazakh (n = 52) and Hui (n = 40) subjects from Xinjiang Uyghur Autonomous Region were investigated using a polymerase chain reaction-sequence-based typing (PCR-SBT). In total, 32 HLA-DRB1 alleles, eight HLA-DQA1 alleles and 14 HLA-DQB1 alleles were identified. The most predominant HLA-DRB1, -DQA1 and -DQB1 alleles were DRB1*15:01 (12.50%), DQA1*01:02 (21.43%) and DQB1*03:01 (19.29%) in Han; DRB1*07:01 (18.48%), DQA1*05:01/03/05 (24.65%) and DQB1*02:01/02 (31.69%) in Uyghur; and DRB1*13:01 (13.64%), DQA1*05:01/03/05 (28.85%) and DQB1*02:01/02 (27.88%) in Kazakh, respectively. In Hui, DRB1*07:01, DRB1*11:01 and DRB1*14:01 were the most dominant alleles with the same frequency of 11.8%, while the predominant DQA1 and DQB1 alleles were DQA1*03:01/02/03 (23.75%) and DQB1*02:01/02 (16.25%), respectively. In addition, the most common two-locus haplotypes were DQA1*05:01/03/5-DQB1*03:01 (10.0%) in Han; DQA1*02:01-DQB1*02:01/02 (18.31%) in Uyghur; DQA1*05:01/03/05-DQB1*02:01/02 (15.38%) in Kazakh; and DQA1*03:01/02/03-DQB1*03:03 (11.25%) in Hui. The phylogenetic dendrograms constructed based on the allele frequencies of HLA-DRB1, -DQA1 and -DQB1 in 13 populations (e.g. Asian, Central Asian and European) revealed that the Han and Hui populations were clustered together and closest to Han population from China, while the Kazakh and Uyghur populations were closest to each other and two ethnic groups were clustered together with Central Asian and European populations.

Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review.

The existence of the neural control of mast cell functions has long been proposed. Mast cells (MCs) are localized in association with the peripheral nervous system (PNS) and the brain, where they are closely aligned, anatomically and functionally, with neurons and neuronal processes throughout the body. They express receptors for and are regulated by various neurotransmitters, neuropeptides, and other neuromodulators. Consequently, modulation provided by these neurotransmitters and neuromodulators allows neural control of MC functions and involvement in the pathogenesis of mast cell-related disease states. Recently, the roles of individual neurotransmitters and neuropeptides in regulating mast cell actions have been investigated extensively. This review offers a systematic review of recent advances in our understanding of the contributions of neurotransmitters and neuropeptides to mast cell activation and the pathological implications of this regulation on mast cell-related disease states, though the full extent to which such control influences health and disease is still unclear, and a complete understanding of the mechanisms underlying the control is lacking. Future validation of animal and in vitro models also is needed, which incorporates the integration of microenvironment-specific influences and the complex, multifaceted cross-talk between mast cells and various neural signals. Moreover, new biological agents directed against neurotransmitter receptors on mast cells that can be used for therapeutic intervention need to be more specific, which will reduce their ability to support inflammatory responses and enhance their potential roles in protecting against mast cell-related pathogenesis.

Monitoring and predicting Fusarium wilt disease in cucumbers based on quantitative analysis of kinetic imaging of chlorophyll fluorescence.

Cucumber (Cucumis sativus L.) is a widely cultivated and economically profitable crop. However, Fusarium wilt disease can seriously affect cucumber yields, as it is difficult to prevent and eliminate. Therefore, a reliable method is needed for the rapid and early detection of Fusarium infection in cucumbers, which could be provided via the kinetic imaging of chlorophyll fluorescence (ChlF). In this study, ChlF imaging and kinetic parameters were utilized with gray and radial basis function models to monitor cucumber Fusarium wilt disease. The results indicate that the disease can be detected and predicted using this imaging technique before symptoms become visible.

Ratiometric fluorescent nanoprobe based on CdTe/SiO2/folic acid/silver nanoparticles core-shell-satellite assembly for determination of 6-mercaptopurine.

A sensitive and robust fluorescent assay of 6-MP is described which relies on the facile assembly of a fluorescence nanoprobe by design of silica nanosphere encapsulated CdTe quantum dots (CdTe QDs) as scaffold, coupling with chemically tethered folic acid (FA)-protected silver nanoparticles (AgNPs) that function as responsive element. In this way a stable ternary core-shell-satellite nanostructure with dual-emission signals can be established. On binding to the target molecules, 6-MP, FA molecules initially occupied by AgNPs are liberated to give dose-dependent fluorescence emission, which can further form a self-calibration ratiometric fluorescence assay using CdTe QDs as an internal reference. The nanoprobe color vividly changes from red to blue, enabling the direct visual detection. The linear concentration range is 0.15~50 µM with the detection limit of 67 nM. By virtue of the favorable selectivity and robust assays, the nanoprobe was applied to 6-MP detection in urine samples, with recoveries from 97.3 to 106% and relative standard deviations (RSD) less than 5%. Graphical abstract.

ISL1 and JMJD3 synergistically control cardiac differentiation of embryonic stem cells.

ISL1 is expressed in cardiac progenitor cells and plays critical roles in cardiac lineage differentiation and heart development. Cardiac progenitor cells hold great potential for clinical and translational applications. However, the mechanisms underlying ISL1 function in cardiac progenitor cells have not been fully elucidated. Here we uncover a hierarchical role of ISL1 in cardiac progenitor cells, showing that ISL1 directly regulates hundreds of potential downstream target genes that are implicated in cardiac differentiation, through an epigenetic mechanism. Specifically, ISL1 promotes the demethylation of tri-methylation of histone H3K27 (H3K27me3) at the enhancers of key downstream target genes, including Myocd and Mef2c, which are core cardiac transcription factors. ISL1 physically interacts with JMJD3, a H3K27me3 demethylase, and conditional depletion of JMJD3 leads to impaired cardiac progenitor cell differentiation, phenocopying that of ISL1 depletion. Interestingly, ISL1 is not only responsible for the recruitment of JMJD3 to specific target loci during cardiac progenitor differentiation, but also modulates its demethylase activity. In conclusion, ISL1 and JMJD3 partner to alter the cardiac epigenome, instructing gene expression changes that drive cardiac differentiation.

Nuclear hormone receptor BmFTZ-F1 is involved in regulating the fibroin heavy chain gene in the silkworm, Bombyx mori.

BACKGROUND: The synthesis of silk protein is controlled by hormones. The expression of the nuclear hormone Bmftz-f1 in the posterior silk gland (PSG) is induced by 20-hydroxyecdysone in vivo and in vitro. However, whether Bmftz-f1 regulates silk protein expression is unknown. METHODS: In our study, western blotting and quantitative polymerase chain reactions were conducted to detect the expression of FTZ-F1 in the PSG. Electrophoretic mobility shift, chromatin immunoprecipitation, far-western blotting, bimolecular fluorescence complementation, and dual luciferase reporter assays were performed to investigate the effect of FTZ-F1 on the fibH promoter. RESULTS: (1) The expression of the hormone receptor BmFTZ-F1 was opposite to that of fibH. It was highly expressed in the PSG during the fourth molting stage and the beginning of the fifth instar, and then its expression decreased gradually until it disappeared at the end of the fifth instar and the wandering stage. (2) We identified a FTZ-F1 response element 390bp upstream of the transcription initiation site of the fibH promoter. (3) BmFTZ-F1 interacted with the basic helix-loop-helix transcription factor Bmdimm. (4) BmFTZ-F1 down-regulated fibH promoter activity and counteracted the effect of Bmdimm on fibH expression. CONCLUSIONS: Integrating these results, we conclude that BmFTZ-F1 regulates the transcription of fibH by binding to the FTZ-F1 response element in the fibH promoter and counteracts the effect of Bmdimm on fibH expression. GENERAL SIGNIFICANCE: These findings provide new insights into the mechanism of regulation of the silk protein gene.

Prevalence of Celiac Disease Autoimmunity Among Adolescents and Young Adults in China.

BACKGROUND & AIMS: In China, epidemiologic information on celiac disease autoimmunity is scarce and fragmented. We investigated the prevalence of celiac disease autoimmunity in the general Chinese population. METHODS: In a cross-sectional prospective study, 19,778 undiagnosed Chinese adolescents and young adults (age, 16-25 y) were recruited from consecutive new students who underwent routine physical examinations at 2 universities in Jiangxi, China, from September 2010 through October 2013; the students were from 27 geographic regions in China. All subjects were tested for serum IgG, IgG against deamidated gliadin peptides (IgG anti-DGP), and IgA anti-tissue transglutaminase antibodies (IgA anti-tTG). We also analyzed HLA genotypes in subgroups of participants with different results from tests for serum markers of celiac disease. RESULTS: A total of 434 students (2.19%) tested positive for serum markers for celiac disease (95% confidence interval [CI], 1.99%-2.41%), 0.36% of the students tested positive for anti-tTG IgA (95% CI, 0.28%-0.46%), and 1.88% tested positive for anti-DGP IgG (95% CI, 1.70%-2.09%). The prevalence of celiac disease autoimmunity (positive results in assays for anti-tTG IgA and anti-DGP-IgG) was 0.06% (95% CI, 0.03%-0.10%). Celiac disease autoimmunity was associated with the consumption of wheat and female sex. The prevalence in the Shandong province in north China, where wheat is a staple in the diet, was 0.76% (95% CI, 0.21%-1.95%). The frequencies of the HLA-DQ2/-DQ8 genotypes associated with celiac disease were higher in subjects with celiac disease autoimmunity, based on detection of both serum markers, than in subjects with positive results from a single test (P < .01). All subjects with positive results from both assays carried the HLA-DQ2 genotype. CONCLUSIONS: Approximately 2% of adolescents or young adults in China had positive results from assays for serum markers for celiac disease. The prevalence of celiac disease autoimmunity in the Shandong province in north China, where wheat is a staple in the diet, was 0.76%.

ß-cyclodextrin-ionic liquid polymer based dynamically coating for simultaneous determination of tetracyclines by capillary electrophoresis.

Tetracyclines are a group of broad spectrum antibiotics widely used in animal husbandry to prevent and treat diseases. However, the improper use of tetracyclines may result in the presence of their residues in animal tissues or waste. Recently, great attention has been drawn towards the green solvents ionic liquids. Ionic liquids have been employed as a coating material to modify the electroosmotic flow in capillary electrophoresis. In this study, a functionalized ionic liquid, mono-6-deoxy-6-(3-methylimidazolium)-ß-cyclodextrin tosylate, was synthesized and used for the simultaneous separation and quantification of tetracyclines by capillary electrophoresis. Good separation efficiency could be achieved due to the multiple functions of ß-cyclodextrin derived ionic liquid, including the electrostatic interaction, the hydrogen bonding, and the cavity structure in ß-cyclodextrin ionic liquid which can entrap the tetracyclines to form inclusion complex. After optimization, baseline separation achieved in 25 min with the running buffer consisted of 10 mmol/L, pH 7.2 phosphate buffer and 20 mmol/L ß-cyclodextrin ionic liquid. The satisfied result demonstrated that the ß-cyclodextrin ionic liquid is an ideal background electrolyte modifier in the separation of tetracyclines with high stability and good reproducibility. And it is an effective strategy to design and synthesize specific ILs as additive applied in separation.

The TMSB4 Pseudogene LncRNA Functions as a Competing Endogenous RNA to Promote Cartilage Degradation in Human Osteoarthritis.

Mechanical stress plays a key role in the development of cartilage degradation in osteoarthritis (OA). Nevertheless, the role of long noncoding RNAs in mechanical stress-induced regulation of chondrocytes remains unclear. The aim of this study was to explore the function of mechanical stress-related long noncoding RNAs in cartilage. Tissue samples were collected from 50 patients and chondrocytes were exposed to cyclic tensile strain (CTS). A total of 107 lncRNAs were differentially expressed in damaged cartilage versus intact cartilage. Of these lncRNAs, 51 were upregulated and 56 were downregulated in the damaged tissue. The TMSB4 pseudogene, lncRNA-MSR, was upregulated in the damaged cartilage and was activated in chondrocytes in response to mechanical stress. Furthermore, lncRNA-MSR regulated the expression of TMSB4 by competing with miRNA-152 in chondrocytes. Our results demonstrated that upregulation of lncRNA-MSR initiates pathological changes that lead to cartilage degradation, and the inhibition of lncRNA-MSR could represent a potential therapeutic target for OA.

Six-channel multi-wavelength polarization Raman lidar for aerosol and water vapor profiling.

Aerosols and water vapor are important atmospheric components, and have significant effects on both atmospheric energy conversion and climate formation. They play the important roles in balancing the radiation budget between the atmosphere and Earth, while water vapor also directly affects rainfall and other weather processes. To further research atmospheric aerosol optical properties and water vapor content, an all-time six-channel multi-wavelength polarization Raman lidar has been developed at Beifang University of Nationalities. In addition to 1064, 532, and 355 nm Mie scattering channels, the lidar has a polarization channel for 532 nm return signals, a 660 nm water vapor channel, and a 607 nm nitrogen detection channel. Experiments verified the lidar's feasibility and return signals from six channels were detected. Using inversion algorithms, extinction coefficient profiles at 1064, 532 and 355 nm, Ångström exponent profiles, depolarization ratio profiles, and water vapor mixing ratio profiles were all obtained. The polarization characteristics and water vapor content of cirrus clouds, the polarization characteristics of dusty weather, and the water vapor profiles over different days were also analyzed. Results show that the lidar has the full-time detection capability for atmospheric aerosol optical properties and water vapor profiles, and real-time measurements of aerosols and water vapor over the Yinchuan area were realized, providing important information for studying the environmental quality and climate change in this area.

SOX6 and PDCD4 enhance cardiomyocyte apoptosis through LPS-induced miR-499 inhibition.

Sepsis-induced cardiac apoptosis is one of the major pathogenic factors in myocardial dysfunction. As it enhances numerous proinflammatory factors, lipopolysaccharide (LPS) is considered the principal mediator in this pathological process. However, the detailed mechanisms involved are unclear. In this study, we attempted to explore the mechanisms involved in LPS-induced cardiomyocyte apoptosis. We found that LPS stimulation inhibited microRNA (miR)-499 expression and thereby upregulated the expression of SOX6 and PDCD4 in neonatal rat cardiomyocytes. We demonstrate that SOX6 and PDCD4 are target genes of miR-499, and they enhance LPS-induced cardiomyocyte apoptosis by activating the BCL-2 family pathway. The apoptosis process enhanced by overexpression of SOX6 or PDCD4, was rescued by the cardiac-abundant miR-499. Overexpression of miR-499 protected the cardiomyocytes against LPS-induced apoptosis. In brief, our results demonstrate the existence of a miR-499-SOX6/PDCD4-BCL-2 family pathway in cardiomyocytes in response to LPS stimulation.

Silencing of miR-101 Prevents Cartilage Degradation by Regulating Extracellular Matrix-related Genes in a Rat Model of Osteoarthritis.

Osteoarthritis (OA) is a common, degenerative joint disease characterized by articular cartilage degradation. Currently, clinical trials based on microRNA therapy have been performed to treat various diseases. However, no treatment has been found for arthritis. This study investigated the functions of miR-101 in cartilage degradation in vivo and evaluated the feasibility of using miR-101 as a therapeutic agent for OA. Mono-iodoacetate-induced arthritis (MIA) rats were used as an animal model of OA. miR-101 mimic or miR-101 inhibitor was injected into the rats' knees to evaluate its effects on cartilage degradation. Cartilage degradation aggravated at 14 days after the injection of miR-101 mimic. By contrast, miR-101 silencing reduced cartilage degradation. Moreover, the administration of miR-101 mimic is sufficient to cause cartilage degradation in the normal cartilage of rats. By contrast, miR-101 inhibitor could prevent this change. Microarray and qPCR were used to investigate the different expressed genes after injecting miR-101 mimic and miR-101 inhibitor in the rats' articular cartilage. Several cartilage degradation-related genes were selected and validated to function in cartilage degradation with miR-101. Our results demonstrated the therapeutic effect of miR-101 inhibition on cartilage degradation in MIA rats by regulating several cartilage degradation-related genes.