Application of Magnetic Resonance T1rho and T2 Mapping in Evaluating Cartilage Injury in Middle-aged and Elderly Patients with Knee Osteoarthritis.

Objective: To investigate magnetic resonance longitudinal relaxation time quantitative imaging (T1rho) and transverse relaxation time quantitative imaging (T2 mapping) techniques in evaluating cartilage damage in middle-aged and elderly patients with knee osteoarthritis (OA). Methods: To carry out this investigation, the researchers enrolled 65 OA patients subjects for the study. These patients were divided into 2 groups based on the severity of their OA. Thirty healthy individuals were included as the control group. All study participants underwent magnetic resonance T1rho and T2 mapping scans. OA patient scores and values from the Western Ontario and McMaster University Osteoarthritis Index (WOMAC), T2, and a T1rho MRI measurement indicating potential early indication of bone and joint diseases from each cartilage area were compared among the OA patients as well as the control group. Pearson correlation analysis was used to examine the relationships between T2 and T1rho values and WOMAC scores. Results: The WOMAC scores in the mild OA group were lower than the severe OA group (P < .05). There were no significant differences in T2 and T1rho values of lateral tibial cartilage among the 3 groups (P > .05). On the other hand, the T2 and T1rho values of medial femoral, lateral femoral, and medial tibial cartilage areas increased progressively in the control, mild OA, and severe OA groups (P < .05). A Pearson analysis found a positive correlation between the T2 values of medial, lateral, and medial tibial cartilages and the WOMAC scores. Similarly, the T1rho values of these cartilage areas were also positively correlated with the WOMAC scores. Conclusion: Magnetic resonance T1rho and T2 mapping offer good evaluation value for assessing cartilage injury in middle-aged and elderly patients with knee OA. The values obtained from T1rho and T2 mapping in various areas of the cartilage show a positive correlation with WOMAC scores.

MIR503HG Overexpression Inhibits the Malignant Behaviors of Osteosarcoma Cells by Sponging miR-103a-3p.

Osteosarcoma (OS) is the most representative primary bone tumour in children and teenagers. This study explored the regulatory effects of long noncoding RNA MIR503HG (MIR503HG) on the biological functions of OS cells, and further investigated the potential mechanism of MIR503HG function exertion by analyzing the microRNA-103a-3p (miR-103a-3p) in OS cells and tissues. The expression of MIR503HG was examined using reverse transcription-quantitative PCR. OS cell proliferation was assessed by CCK-8 assay. Transwell assay was used to evaluate the migration and invasion of OS cells. The interaction between MIR503HG and miR-103a-3p was detected using the Dual-luciferase reporter assay. Forty-six paired OS tissues were collected, and the expression and correlation of MIR503HG and miR-103a-3p were evaluated. The expression of MIR503HG were significantly decreased in both OS cells and tissues. Over-expression of MIR503HG inhibited OS cell proliferation, migration and invasion. miR-103a-3p was directly targeted by MIR503HG in OS cells, and mediated the inhibitory effects of MIR503HG on OS cell malignant behaviors. miR-103a-3p expression was upregulated in OS tissues, which was negatively correlated with MIR503HG expression levels. The expression of MIR503HG was associated with OS patients' tumor size, differentiation, distant metastasis and clinical stage. Decreased MIR503HG in OS tissues and cell lines served as a tumor suppressor by inhibiting OS cell malignant behaviors through sponging miR-103a-3p. The findings of this study may provide evidence for the development of novel therapeutic targets of OS.

Genome-wide analysis of genomic imprinting in the endosperm and allelic variation in flax.

Genomic imprinting is an epigenetic phenomenon that causes biased expression of maternally and paternally inherited alleles. In flowering plants, genomic imprinting predominantly occurs in the triploid endosperm and plays a vital role in seed development. In this study, we identified 248 candidate imprinted genes including 114 maternally expressed imprinted genes (MEGs) and 134 paternally expressed imprinted genes (PEGs) in flax (Linum usitatissimum L.) endosperm using deep RNA sequencing. These imprinted genes were neither clustered in specific chromosomal regions nor well conserved among flax and other plant species. MEGs tended to be expressed specifically in the endosperm, whereas the expression of PEGs was not tissue-specific. Imprinted single nucleotide polymorphisms differentiated 200 flax cultivars into the oil flax, oil-fiber dual purpose flax and fiber flax subgroups, suggesting that genomic imprinting contributed to intraspecific variation in flax. The nucleotide diversity of imprinted genes in the oil flax subgroup was significantly higher than that in the fiber flax subgroup, indicating that some imprinted genes underwent positive selection during flax domestication from oil flax to fiber flax. Moreover, imprinted genes that underwent positive selection were related to flax functions. Thirteen imprinted genes related to flax seed size and weight were identified using a candidate gene-based association study. Therefore, our study provides information for further exploration of the function and genomic variation of imprinted genes in the flax population.

Yttrium chloride-induced cytotoxicity and DNA damage response via ROS generation and inhibition of Nrf2/PPARγ pathways in H9c2 cardiomyocytes.

Increasing exploration of rare-earth elements (REEs) has resulted in a high REEs' exposure risk. Owing to their persistence and accumulation of REEs in the environment, their adverse effects have caused widespread concern. However, limited toxicological data are available for the adverse effects of yttrium (Y) and its underlying mechanisms of action. In the present study, H9c2 cardiomyocytes were used in vitro model to investigate the cardiotoxicity of yttrium chloride (YCl3). Results show that YCl3 treatment resulted in reactive oxygen species (ROS) overproduction, decrease in ∆Ψm, and DNA damage. Mechanistically, we detected expression levels of protein in response to cellular DNA damage and antioxidative defense. Results indicated that the phosphorylation of histone H2AX remarkably increased in a dose-dependent manner. At a high YCl3-exposure concentration (120 µM), specific DNA damage sensors ATM/ATR-Chk1/Chk2 were significantly decreased. The protein levels of key antioxidant genes Nrf2/PPARγ/HO-1 were also remarkably inhabited. Additionally, the antioxidant N-acetyl-L-cysteine (NAC) pretreatment promoted the activation of antioxidative defense Nrf2/PPARγ signaling pathways, and prevented the production of cellular ROS, thus protecting the DNA from cleavage. Altogether, our findings suggest that YCl3 can induce DNA damage through causing intracellular ROS overproduction and inhibition of antioxidative defense, leading to cytotoxicity in H9c2 cardiomyocytes.

Comprehensive Analysis of Potential miRNA-Target mRNA-Immunocyte Subtype Network in Cerebral Infarction.

INTRODUCTION: Cerebral infarction (CI) is one of the leading causes of serious long-term disability and mortality. OBJECTIVE: We aimed to identify potential miRNAs and target mRNAs and assess the involvement of immunocyte infiltration in the process of CI. METHODS: First, miRNA and mRNA data were downloaded from the Gene Expression Omnibus database, followed by differential expression analysis. Second, correlation analysis between differentially expressed mRNAs and differential immunocyte subtypes was performed through the CIBERSORT algorithm. Third, the regulatory network between miRNAs and immunocyte subtype-related mRNAs was constructed followed by the functional analysis of these target mRNAs. Fourth, correlation validation between differentially expressed mRNAs and differential immunocyte subtypes was performed in the GSE37587 dataset. Finally, the diagnostic ability of immunocyte subtype-related mRNAs was tested. RESULTS: Up to 17 differentially expressed miRNAs and 3,267 differentially expressed mRNAs were identified, among which 310 differentially expressed mRNAs were significantly associated with immunocyte subtypes. Several miRNA-target mRNA-immunocyte subtype networks including hsa-miR-671-3p-ZC3HC1-neutrophils, hsa-miR-625-CD5-monocytes, hsa-miR-122-ACOX1/DUSP1/NEDD9-neutrophils, hsa-miR-455-5p-SLC24A4-monocytes, and hsa-miR-455-5p-SORL1-neutrophils were identified. LAT, ACOX1, DUSP1, NEDD9, ZC3HC1, BIN1, AKT1, DNMT1, SLC24A4, and SORL1 had a potential diagnostic value for CI. CONCLUSIONS: The network including miRNA, target mRNA, and immunocyte subtype may be novel regulators and diagnostic and therapeutic targets in CI.

Rapamycin relieves lupus nephritis by regulating TIM-3 and CD4+CD25+Foxp3+ Treg cells in an MRL/lpr mouse model.

Lupus nephritis (LN) is a severe consequence of systemic lupus erythematosus (SLE) and is an important driver of morbidity and mortality in SLE. Treg cells and TIM-3 play an important role in the pathogenesis of LN. The beneficial effect of rapamycin on LN has been confirmed in both mouse models and patients, but the effect of rapamycin on Treg cells and TIM-3 is not yet completely understood. In this study, rapamycin treatment attenuated proteinuria, histological damage, and renal deposition of C3, and improved renal function. Spleen and renal draining lymph node weight and serum levels of anti-dsDNA antibodies were also improved by rapamycin. Furthermore, the frequency of Treg cells and Treg functional molecules, such as cytotoxic T cell antigen 4 (CTLA-4), interleukin 10 (IL-10), and transforming growth factor ß1 (TGF-ß1), increased significantly after treatment with rapamycin in MRL/lpr mice. We also found that expression of TIM-3 was significantly decreased in CD4+ T cells and Treg cells in mice treated with rapamycin. In summary, the study demonstrated that rapamycin treatment induced preferential expansion of CD4+CD25+Foxp3+ Tregs with increased expression of CTLA-4, IL-10, and TGF-ß1, and decreased TIM-3 expression, thereby ameliorating lupus nephritis in the MRL/lpr mouse model.

Impact of maternal thyroid hormone in late pregnancy on adverse birth outcomes: A retrospective cohort study in China.

The purpose of this study was to explore the impact of maternal thyroid hormone dysfunction in late pregnancy on birth outcomes in a Chinese population. We retrospectively examined hospitalisation records and laboratory data between April 2016 and March 2017 and obtained results from 11,564 consecutive pregnant women with singleton births in which serum thyroid hormone had been examined together with birth outcomes. We assessed the association between maternal thyroid level and dysfunction with adverse birth outcomes based on regression analysis. Hyperthyroidism was associated with an increased risk of preterm birth (PTB, adjusted OR: 2.41, 95% CI: 1.83-3.17) and hypothyroidism was associated with an increased risk of small for gestational age (SGA, adjusted OR: 1.56, 95% CI: 1.10-2.22), while hyperthyroxinaemia was associated with a decreased risk of large for gestational age (LGA, adjusted OR: 0.64, 95% CI: 0.45-0.90). In addition, compared to women with normal FT3 and TSH (≥the 5th and ≤the 95th percentiles), women with high free triiodothyronine (FT3 >the 95th percentile) and low thyroid-stimulating hormone (TSH

Type I collagen inhibits adipogenic differentiation via YAP activation in vitro.

Extracellular matrix (ECM) has a marked influence on adipose tissue development. Adipose tissue formation is initiated with proliferation of preadipocytes and migration before undergoing further differentiation into mature adipocytes. Previous studies showed that collagen I (col I) provides a good substratum for 3T3-L1 preadipocytes to grow and migrate. However, it remains unclear whether and how col I regulates adipogenic differentiation of preadipocytes. This study reports that lipid accumulation, representing in vitro adipogenesis of the 3T3-L1 preadipocytes or the mouse primary adipocyte precursor cells derived from subcutaneous adipose tissue in the inguinal region is inhibited by the culture on col I, owing to downregulation of adipogenic factors. Previous study shows that col I enhances 3T3-L1 cell migration via stimulating the nuclear translocation of yes-associated protein (YAP). In this study, we report that downregulation of YAP is associated with in vitro adipogenesis of preadipocytes as well as with in vivo adipose tissue of high-fat diet fed mice. Increased expression of YAP in the cells cultured on col I-coated dishes is correlated with repression of adipogenic differentiation processes. The inactivation of YAP using YAP inhibitor, verteporfin, or YAP small-interfering RNA enhanced adipogenic differentiation and reversed the inhibitory effect of col I. Activation of YAP either by the transfection of YAP plasmid or the silence of large tumor suppressor 1 (LATS1), an inhibitory kinase of YAP, inhibited adipogenic differentiation. The results indicate that col I inhibits adipogenic differentiation via YAP activation in vitro.

Natural flavonoid silibinin promotes the migration and myogenic differentiation of murine C2C12 myoblasts via modulation of ROS generation and down-regulation of estrogen receptor α expression.

Skeletal muscle regeneration is a complex process, involving the proliferation, migration, and differentiation of myoblasts. Recent studies suggest that some natural flavanones stimulate myogenesis. However, the effect of plant estrogen, silibinin, on the regulation of myoblast behaviors is unclarified. In this study, we investigated the effects of silibinin on immortalized murine myoblast C2C12 in the aspects of proliferation, migration, differentiation along with underlying mechanisms. The results show that silibinin at concentrations below 50 µM enhanced the migration and differentiation of C2C12 cells, but had no effect on cell proliferation. Silibinin significantly promoted the production of ROS, which appeared to play important roles in the migration and differentiation of the myoblasts. Interestingly, among ROS, the superoxide anion and hydroxyl radical were associated with the migration, whereas hydrogen peroxide contributed to the myogenic differentiation. We used ER agonist and antagonist to explore whether estrogen receptors (ERs), which are affected by silibinin treatment in the silibinin-enhanced C2C12 migration and differentiation. Migration was independent of ERs, whereas the differentiation was associated with decreased ERα activity. In summary, silibinin treatment increases ROS levels, leading to the promotion of migration and myogenic differentiation. Negative regulation ERα of differentiation but not of migration may suggest that ERα represses hydrogen peroxide generation. The effect of silibinin on myoblast migration and differentiation suggests that silibinin may have therapeutic benefits for muscle regeneration.

Cerium(III)-doped MoS2 nanosheets with expanded interlayer spacing and peroxidase-mimicking properties for colorimetric determination of hydrogen peroxide.

Molybdenum disulfide (MoS2) nanosheets (NSs) with an 8.1 Å interlayer spacing were heavily loaded with cerium(III) ions by a one-step hydrothermal method. The material thus obtained has a strong peroxidase-like (POx-like) activity. The introduction of the large Ce(III) ion enlarges the interlayer distance of MoS2NSs. It also supports shuttling and transport of substrate, intermediates and electrons. It also increases the specific surface of MoS2. This results in a larger number of active sites, accelerates the contact between substrate and catalytic surface, and improves the kinetics of the catalytic reaction. The nanomaterial catalyzes the oxidation of colorless 3,3',5,5'-tetramethylbenzidine by hydrogen peroxide (H2O2 ) to give a blue-green product with an absorption maximum at 652 nm. The assay has a linear response in the 1-50 µM H2O2 concentration range and a 0.47 µM limit of detection. The colorimetric method was applied to real milk samples, and high recoveries (98.4%-108.0%) and repeatability were obtained. Graphical abstractMolybdenum disulfide nanosheets loaded with cerium(III) catalyze the oxidation of colorless 3,3',5,5'-tetramethylbenzidine (TMB) by hydrogen peroxide to give a blue-green product with an absorption maximum at 652 nm.

Ratiometric fluorometric determination of mercury(II) by exploiting its quenching effect on glutathione-stabilized and tetraphenylporphyrin modified gold nanoclusters.

A ratiometric fluorometric assay for mercury(II) ion is described. It is making use of glutathione-stabilized gold nanoclusters (GSH-AuNCs) modified with tetraphenylporphyrin tetrasulfonic acid (TPPS). The resultant GSH-AuNC/TPPS nanocomposite displays dual emission (at 572 and 664 nm) under a single excitation wavelength of 365 nm. Mercury(II) ion intensively quenches the yellow fluorescence of GSH-AuNCs (peaking at 572 nm) but has a negligible effect on the red fluorescence of TPPS (at 664 nm). The ratio of fluorescence intensities at 572 and 664 nm drops linearly with Hg(II) ion concentration in the 0.02-2.0 µmol·L-1 range, and the detection limit is 7 nmol·L-1 (3sb/S). The relative standard deviation (RSD) of the assay is 2.0% at a 0.5 µmol·L-1 concentration level (n = 11). The method was successfully applied to the determination of Hg(II) ion in spiked water samples, with recoveries within the range of 87.5-107.5%. Graphical abstract Ratiometric fluorescence detection of mercury(II).

Chaetospirolactone reverses the apoptotic resistance towards TRAIL in pancreatic cancer.

The pancreatic cancer is one of the most aggressive tumors. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can trigger apoptosis by interaction with death receptors. However, in TRAIL-resistant pancreatic cancer, responsiveness to TRAIL treatment is terribly poor. In current work, we have demonstrated that a natural product chaetospirolactone (CSL) isolated from an endophytic fungus Chaetomium sp. NF00754 can enhance the susceptibility of TRAIL-resistant pancreatic cancer cells to apoptosis. CSL can induce apoptosis in TRAIL-treated pancreatic cancer cells. Furthermore, combined CSL and TRAIL treatment significantly inhibits viability and migration of pancreatic cancer cells. Combinatorial TRAIL and CSL treatment repressed xenograft tumor growth without substantially toxic side effects. CSL can specifically upregulate expression of death receptor 4 (DR4). Further study revealed that CSL represses the activities of an epigenetic regulator enhancer of zeste homolog 2 (EZH2) and consistently reduces histone H3 lysine 27 trimethylation (H3K27me3) to allow DR4 transcription. Taken together, CSL treatment may reverse TRAIL resistance in pancreatic cancer cells via epigenetic regulation of DR4 implying that administration of CSL might represent a putative strategy for pancreatic cancer therapy.

Mining and exploration of appendicitis nursing targets: An observational study.

Appendicitis is an inflammation caused by obstruction of the appendiceal lumen or termination of blood supply leading to appendiceal necrosis followed by secondary bacterial infection. The relationship between TYROBP gene and the nursing of appendicitis remains unclear. The appendicitis dataset GSE9579 profile was downloaded from the gene expression omnibus database generated from GPL571. Differentially expressed genes were screened, followed by weighted gene co-expression network analysis, functional enrichment analysis, gene set enrichment analysis, construction and analysis of protein-protein interaction network, Comparative Toxicogenomics Database analysis, and immune infiltration analysis. Heatmaps of gene expression levels were plotted. A total of 1570 differentially expressed genes were identified. According to gene ontology analysis, they were mainly enriched in organic acid metabolic process, condensed chromosome kinetochore, oxidoreductase activity. In Kyoto Encyclopedia of Gene and Genome analysis, they mainly concentrated in metabolic pathways, P53 signaling pathway, PPAR signaling pathway. The soft threshold power in weighted gene co-expression network analysis was set to 12. Through the construction and analysis of protein-protein interaction network, 5 core genes (FCGR2A, IL1B, ITGAM, TLR2, TYROBP) were obtained. Heatmap of core gene expression levels revealed high expression of TYROBP in appendicitis samples. Comparative Toxicogenomics Database analysis found that core genes (FCGR2A, IL1B, ITGAM, TLR2, TYROBP) were closely related to abdominal pain, gastrointestinal dysfunction, fever, and inflammation occurrence. TYROBP gene is highly expressed in appendicitis, and higher expression of TYROBP gene indicates worse prognosis. TYROBP may serve as a molecular target for appendicitis and its nursing.

MYC and NCAPG2 as molecular targets of colorectal cancer and gastric cancer in nursing.

Colorectal cancer is a common malignant tumor in intestinal tract, the early symptoms are not obvious. Gastric cancer is a malignant tumor originating from the gastric mucosal epithelium. However, the role of MYC and non-SMC condensin II complex subunit G2 (NCAPG2) in colorectal cancer and gastric cancer remains unclear. The colorectal cancer datasets GSE49355 and gastric cancer datasets GSE19826 were downloaded from gene expression omnibus database. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis (WGCNA) was performed. Functional enrichment analysis, gene set enrichment analysis (GSEA) and immune infiltration analysis was performed. Construction and analysis of protein-protein interactions (PPI) network. Survival analysis and comparative toxicogenomics database (CTD) were performed. A heat map of gene expression was drawn. A total of 751 DEGs were obtained. According to the gene ontology (GO) analysis, in Biological process (BP) analysis, they are mainly enriched in cell differentiation, cartilage development, and skeletal development. In cellular component (CC) analysis, they are mainly enriched in the cytoskeleton of muscle cells and actin filaments. In molecular function (MF) analysis, they are mainly concentrated in Rho GTPase binding, DNA binding, and fibronectin binding. In Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis, they are mainly enriched in the MAPK signaling pathway, apoptosis, and cancer pathways. The soft threshold power for WGCNA analysis was set to 9, resulting in the generation of 40 modules. Ultimately, 2 core genes (MYC and NCAPG2) were identified. The heatmap of core gene expression showed high expression of MYC and NCAPG2 in colorectal cancer tissue samples and low expression in normal tissue samples, while they were core molecules in gastric cancer. Survival analysis indicated that MYC and NCAPG2 were risk factors, showing an upregulation trend with increasing risk scores. CTD analysis revealed associations of MYC and NCAPG2 with colorectal cancer, gastric cancer, inflammation, and immune system diseases. MYC and NCAPG2 are highly expressed in colorectal cancer. The higher the expression of MYC and NCAPG2, the worse the prognosis. MYC and NCAPG2 are core molecules in gastric cancer.

Spinosin inhibits activated hepatic stellate cell to attenuate liver fibrosis by targeting Nur77/ASK1/p38 MAPK signaling pathway.

AIM: Liver fibrosis remains a great challenge in the world. Spinosin (SPI), a natural flavonoid-C-glycoside, possesses various pharmacological activities including anti-inflammatory and anti-myocardial fibrosis effects. In this study, we investigate whether SPI can be a potential lead for the treatment of liver fibrosis and explore whether the orphan nuclear receptor Nur77, a negative regulator of liver fibrosis development, plays a critical role in SPI's action. METHODS: A dual luciferase reporter system of α-SMA was established to evaluate the effect of SPI on hepatic stellate cell (HSC) activation in LX2 and HSC-T6 cells. A mouse model of CCl4-induced liver fibrosis was used to test the efficacy of SPI against liver fibrosis. The expression levels of Nur77, inflammatory cytokines and collagen were determined by Western blotting and qPCR. Potential kinase pathways involved were also analyzed. The affinity of Nur77 with SPI was documented by fluorescence titration. RESULTS: SPI can strongly suppress TGF-ß1-mediated activation of both LX2 and HSC-T6 cells in a dose-dependent manner. SPI increases the expression of Nur77 and reduces TGF-ß1-mediated phosphorylation levels of ASK1 and p38 MAPK, which can be reversed by knocking out of Nur77. SPI strongly inhibits collagen deposition (COLA1) and reduces inflammatory cytokines (IL-6 and IL-1ß), which is followed by improved liver function in the CCl4-induced mouse model. SPI can directly bind to R515 and R563 in the Nur77-LBD pocket with a Kd of 2.14 µM. CONCLUSION: Spinosin is the major pharmacological active component of Ziziphus jujuba Mill. var. spinosa which has been frequently prescribed in traditional Chinese medicine. We demonstrate here for the first time that spinosin is a new therapeutic lead for treatment of liver fibrosis by targeting Nur77 and blocking the ASK1/p38 MAPK signaling pathway.

Diagnostic and prognostic value of plasma and tissue ubiquitin-like, containing PHD and RING finger domains 1 in breast cancer patients.

Ubiquitin-like, containing PHD and RING finger domains 1 (UHRF1) has been reported to play an important role in breast carcinogenesis. This work investigated the correlation of UHRF1 DNA level in plasma with clinical characteristics of breast cancer and its clinical significance in breast cancer diagnosis. The expression of UHRF1 in primary breast cancer tissue was examined by Western blot. The UHRF1 DNA levels in plasma and UHRF1 mRNA expression in tissues were determined by accurate real-time quantitative PCR. The associations of UHRF1 levels with clinical variables were evaluated using standard statistical methods. The UHRF1 DNA in plasma of 229 breast cancer patients showed higher expression than healthy controls, which showed high specificity up to 76.2% at a sensitivity of 79.2%, and was significantly associated with c-erbB2 positive status, cancer stage and lymph node metastasis. High UHRF1 DNA level in plasma was significantly associated with short progression-free survival. The UHRF1 DNA level in plasma is highly correlative with breast cancer and its status and stage, and may be a potential independent diagnostic and prognostic factor for both breast cancer and the survival of breast cancer patients.

Stable Mo/1T-MoS2 Monolith Catalyst with a Metallic Interface for Large Current Water Splitting.

To achieve global carbon neutrality, the realization of highly active and stable catalysts is critical for water splitting to produce green hydrogen (H2). MoS2 is considered to be the most promising non-precious metal catalyst for H2 evolution because of its excellent properties. Herein, we report a metal-phase MoS2 (1T-MoS2) synthesized using a simple hydrothermal method. Using a similar procedure, we synthesize a monolithic catalyst (MC) in which 1T-MoS2 is vertically bonded to a metal molybdenum plate via strong covalent bonds. These properties endow the MC with an extremely low-resistance interface and mechanical robustness, equipping it with outstanding durability and fast charge transfer. Results show that the MC can achieve stable water splitting at 350 mA cm-2 current density with a low 400 mV overpotential. The MC exhibits negligible performance decay after 60 h of operation at a large current density of 350 mA cm-2. This study provides a novel possible MC with robust and metallic interfaces to achieve technically high current water splitting to produce green H2.

Effects of ambient particulate exposure on blood lipid levels in hypertension inpatients.

Background: With modernization development, multiple studies of atmospheric particulate matter exposure conducted in China have confirmed adverse cardiovascular health effects. However, there are few studies on the effect of particulate matter on blood lipid levels in patients with cardiovascular disease, especially in southern China. The purpose of this study was to investigate the association between short- and long-term exposure to ambient particulate matter and the levels of blood lipid markers in hypertension inpatients in Ganzhou, China. Methods: Data on admission lipid index testing for hypertension inpatients which were divided into those with and without arteriosclerosis disease were extracted from the hospital's big data center from January 1, 2016 to December 31, 2020, and air pollution and meteorology data were acquired from the China urban air quality real time release platform from January 1, 2015 to December 31, 2020 and climatic data center from January 1, 2016 to December 31, 2020, with data integrated according to patient admission dates. A semi-parametric generalized additive model (GAM) was established to calculate the association between ambient particulate matter and blood lipid markers in hypertension inpatients with different exposure time in 1 year. Results: Long-term exposure to particulate matter was associated with increased Lp(a) in three kinds of people, and with increased TC and decreased HDL-C in total hypertension and hypertension with arteriosclerosis. But particulate matter was associated with increased HDL-C for hypertension inpatients without arteriosclerosis, at the time of exposure in the present study. It is speculated that hypertension inpatients without arteriosclerosis has better statement than hypertension inpatients with arteriosclerosis on human lipid metabolism. Conclusion: Long-term exposure to ambient particulate matter is associated with adverse lipid profile changes in hypertension inpatients, especially those with arteriosclerosis. Ambient particulate matter may increase the risk of arteriosclerotic events in hypertensive patients.

Volatile Profiling and Transcriptome Sequencing Provide Insights into the Biosynthesis of α-Pinene and ß-Pinene in Liquidambar formosana Hance Leaves.

Liquidambar formosana Hance is a pinene-rich deciduous plant species in the Altingiaceae family that is used as a medicinal plant in China. However, the regulatory mechanisms underlying α-pinene and ß-pinene biosynthesis in L. formosana leaves remain unknown. Here, a joint analysis of the volatile compounds and transcriptomes of L. formosana leaves was performed to comprehensively explore the terpene synthase (TPS) that may participate in α-pinene and ß-pinene biosynthesis. Headspace solid-phase microextraction (HS-SPME) and gas chromatography-mass spectrometry (GC-MS) jointly detected volatile L. formosana leaves. Trees with high and low levels of both α-pinene and ß-pinene were defined as the H group and L group, respectively. RNA sequencing data revealed that DXR (1-deoxy-D-xylulose-5-phosphate reductoisomerase), HDS [(E)-4-hydroxy-3-methylbut-2-eny-l-diphosphate synthase], and TPS may be the major regulators of monoterpenoid biosynthesis. We identified three TPSs (LfTPS1, LfTPS2, and LfTPS3), which are highly homologous to α-pinene and ß-pinene synthases of other species in phylogenetic analysis. Four TPS genes (LfTPS1, LfTPS2, LfTPS4, LfTPS5) may be critically involved in the biosynthesis and regulation of α-pinene and ß-pinene in L. formosana. Bioinformatic and transcriptomic results were verified using quantitative real-time PCR. We identified LfTPS1, LfTPS2 as candidate genes for α-pinene and ß-pinene biosynthesis that significantly improve the yield of beneficial terpenoids.

Anticancer activity of Germacrone terpenoid in human osteosarcoma cells is mediated via autophagy induction, cell cycle disruption, downregulating the cell cycle regulatory protein expressions and cell migration inhibition.

Germacrone a sesquiterpene is a potential pharmacological agent with important medicinal applications. It is a potential anticancer agent and has been reported for anticancer activity against hepatoma cells and breast cancer cells, additionally, it has also shown anti-inflammatory, antioxidant, and antifungal activity. Therefore, this study was designed to testify anticancer activity of germacrone terpenoid in human osteosarcoma cells along with studying its effects of autophagy induction, cell cycle disruption, downregulating the cell cycle regulatory protein expressions and cell migration inhibition. Cell proliferation rate was examined by MTT assay and phase contrast inverted microscopy was performed for morphological analysis. Further, flowcytometry was implemented to examine different cell cycle phases. Transwell assay was executed for the monitoring of cell migratory tendency of osteosarcoma cells. Finally, the levels of pro-autophagic and cell cycle allied proteins were checked by Western blot analysis. MTT assay results designated potential inhibition of osteosarcoma cell viability by germacrone drug in a dose and time-reliant manner. Further, phase contrast inverted microscopy depicted significant morphological changes in osteosarcoma cells after germacrone exposure, which were indicative of autophagic cell death. Next, transmission electron microscopy evaluated the formation of autophagic vesicles which are the trademark for autophagy. The autophagy allied protein expressions were observed through Western blotting indicating enhanced levels of pro-autophagic proteins (Becalin-1, LC3-I and -II). Hence, it may be depicted that the anti-proliferation effects of germacrone may be of autophagy inducing potential. Next, flowcytometric analysis revealed the cell cycle inhibitory effects of germacrone in osteosarcoma cells and the results indicated cell cycle arrest at S-phase. Cell cycle allied protein levels indicated declination in their expressions after germacrone exposure. Finally, transwell assay specified inhibitory effects on cell migration of osteosarcoma cells by germacrone in a dose-reliant manner. In conclusion, the results of the present investigation specified that germacrone drug is a potential anticancer agent against osteosarcoma cells. The anticancer effects were found to be mediated via autophagy induction, cell cycle disruption, downregulating the cell cycle regulatory protein expressions, and cell migration inhibition.