Juvenile hormone regulates the reproductive diapause through Methoprene-tolerant gene in Galeruca daurica.

Juvenile hormone (JH) signalling plays an important role in regulation of reproductive diapause in insects. However, its underlying molecular mechanism has been unclear. Methoprene-tolerant (Met), as a universal JH receptor, is involved in JH action. To gain some insight into its function in the reproductive diapause of Galeruca daurica, a serious pest on the Inner Mongolia grasslands undergoing obligatory summer diapause at the adult stage, we cloned the complete open-reading frame (ORF) sequences of Met and other 7 JH signalling-related genes, including JH acid methyltransferase (JHAMT), JH esterase (JHE), JH epoxide hydrolase (JHEH), Krüppel homologue 1 (Kr-h1), vitellogenin (Vg), forkhead box O (FOXO) and fatty acid synthase 2 (FAS2), from this species. GdMet encoded a putative protein, which contained three domains typical of the bHLH-PAS family. Expression patterns of these eight genes were developmentally regulated during adult development. Topical application of JH analogue (JHA) methoprene into the 3-day-old and 5-day-old adults induced the expression of GdMet. Silencing GdMet by RNAi inhibited the expression of JHBP, JHE, Kr-h1 and Vg, whereas promoted the FAS2 expression, which enhanced lipid accumulation and fat body development, and finally induced the adults into diapause ahead. Combining with our previous results, we conclude that JH may regulate reproductive diapause through a conserved Met-dependent pathway in G. daurica.

MiRNA-203a-3p inhibits inflammatory response in preeclampsia through regulating IL24.

OBJECTIVE: This study aims to investigate the protective role of miRNA-203a-3p in preeclampsia (PE) patients via inhibiting the inflammatory key protein IL24. PATIENTS AND METHODS: Serum samples of 36 PE pregnant women and 30 normal pregnant volunteers hospitalized between 2015 and 2019 were collected to extract placental mononuclear cells and exosomes. Relative levels of microRNA-203a-3p and IL24 were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In addition, the interaction between microRNA-203a-3p and IL24 was analyzed through bioinformatics analysis and Luciferase reporting assay. Finally, the underlying molecular mechanisms were further explored via immunofluorescence and Western blotting. RESULTS: Compared with normal pregnant volunteers, microRNA-203a-3p expression in serum exosomes and placental mononuclear cells of PE patients were dramatically reduced, while IL24 was conversely up-regulated, indicating a negative correlation between microRNA-203a-3p and IL24 levels. In addition, IL24, which was down-regulated in mononuclear macrophages overexpressing microRNA-203a-3p, was indicated as a target of microRNA-203a-3p. At the same time, microRNA-203a-3p was able to suppress the proliferation capacity of LPS-stimulated mononuclear macrophages, and it exerted anti-inflammatory effects via down-regulating IL24 in THP-1 cells. CONCLUSIONS: MicroRNA-203a-3p plays an anti-inflammatory role in PE pregnant women by down-regulating IL24 level.

LncRNA MIF-AS1 aggravates the progression of ovarian cancer by sponging miRNA-31-5p.

OBJECTIVE: The aim of this study was to uncover the role of lncRNA MIF-AS1 in influencing the biological phenotypes of ovarian cancer (OC) and the underlying mechanism. PATIENTS AND METHODS: OC tissues and adjacent normal tissues were collected from 50 OC patients. The expression level of lncRNA MIF-AS1 in OC tissues and cells was determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). The prognostic potential of MIF-AS1 in OC patients was assessed by the Kaplan-Meier method. Subsequently, the regulatory effects of MIF-AS1 on proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells were evaluated by a series of functional experiments. Dual-Luciferase reporter gene assay, qRT-PCR, and Western blot were further conducted to verify the interaction in the regulatory loop MIF-AS1/miRNA-31-5p/PLCB1. RESULTS: MIF-AS1 was significantly upregulated in OC tissues and cell lines (p<0.05). Higher level of MIF-AS1 predicted significantly worse prognosis of OC patients (p<0.05). The knockdown of MIF-AS1 markedly attenuated the proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells (p<0.05). Dual-Luciferase reporter gene assay verified that MIF-AS1 competed with PLCB1 to bind miRNA-31-5p. In addition, MIF-AS1 negatively regulated miRNA-31-5p expression cells, and miRNA-31-5p negatively regulated PLCB1 expression in OC. CONCLUSIONS: MIF-AS1 was significantly upregulated in OC, which accelerated the proliferative, migratory, and invasive abilities of OC cells. Furthermore, the regulatory loop MIF-AS1/miRNA-31-5p/PLCB1 could be utilized as a therapeutic target for OC.

Mechanism of decorin protein inhibiting invasion and metastasis of non-small cell lung cancer.

OBJECTIVE: To detect the protein level of Decorin in non-small cell lung cancer (NSCLC) patients, and to study the mechanism of Decorin inhibiting invasion and metastasis of non-small cell lung cancer from the perspective of in vitro cells, and provide some theoretical support for the treatment of non-small cell lung cancer. MATERIALS AND METHODS: Immunohistochemical staining was used to detect the expression of Decorin protein in 332 cases of stage I-IIIA clinical NSCLC and 70 cases of adjacent tissues. Then, in vitro cell experiments (cell scratch assay and transwell assay) were used to further study the effects of Decorin on migration and invasion of human lung cancer cell line A549; the effect of transforming growth factor-ß on the expression of Decorin and Ets-1 protein was verified by Western blotting. The binding sites of Ets-1 and Decorin promoter were analyzed by bioinformatics. RESULTS: Exogenous Decorin inhibited invasion and metastasis of lung adenocarcinoma cells in vitro. Immunohistochemical staining showed that Decorin was lowly expressed in non-small cell lung cancer and Decorin had a certain effect on lung fibroblast activation. Western blotting results showed that TGF-ß affects the expression of Decorin and Ets-1. Bioinformatics results showed that Ets-1 and Decorin gene DNA promoter regions have 18 binding sites. CONCLUSIONS: Decorin inhibits invasion and metastasis of non-small cell lung cancer through the TGF-ß signaling pathway.

Introduction to CAUSES: Description of Weather and Climate Models and Their Near-Surface Temperature Errors in 5 day Hindcasts Near the Southern Great Plains.

We introduce the Clouds Above the United States and Errors at the Surface (CAUSES) project with its aim of better understanding the physical processes leading to warm screen temperature biases over the American Midwest in many numerical models. In this first of four companion papers, 11 different models, from nine institutes, perform a series of 5 day hindcasts, each initialized from reanalyses. After describing the common experimental protocol and detailing each model configuration, a gridded temperature data set is derived from observations and used to show that all the models have a warm bias over parts of the Midwest. Additionally, a strong diurnal cycle in the screen temperature bias is found in most models. In some models the bias is largest around midday, while in others it is largest during the night. At the Department of Energy Atmospheric Radiation Measurement Southern Great Plains (SGP) site, the model biases are shown to extend several kilometers into the atmosphere. Finally, to provide context for the companion papers, in which observations from the SGP site are used to evaluate the different processes contributing to errors there, it is shown that there are numerous locations across the Midwest where the diurnal cycle of the error is highly correlated with the diurnal cycle of the error at SGP. This suggests that conclusions drawn from detailed evaluation of models using instruments located at SGP will be representative of errors that are prevalent over a larger spatial scale.

Analysis of serum microRNA expression in male workers with occupational noise-induced hearing loss

Occupational noise-induced hearing loss (ONIHL) is a prevalent occupational disorder that impairs auditory function in workers exposed to prolonged noise. However, serum microRNA expression in ONIHL subjects has not yet been studied. We aimed to compare the serum microRNA expression profiles in male workers of ONIHL subjects and controls. MicroRNA microarray analysis revealed that four serum microRNAs were differentially expressed between controls (n=3) and ONIHL subjects (n=3). Among these microRNAs, three were upregulated (hsa-miR-3162-5p, hsa-miR-4484, hsa-miR-1229-5p) and one was downregulated (hsa-miR-4652-3p) in the ONIHL group (fold change >1.5 and Pbon value <0.05). Real time quantitative PCR was conducted for validation of the microRNA expression. Significantly increased serum levels of miR-1229-5p were found in ONIHL subjects compared to controls (n=10 for each group; P<0.05). A total of 659 (27.0%) genes were predicted as the target genes of miR-1229-5p. These genes were involved in various pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway. Overexpression of miR-1229-5p dramatically inhibited the luciferase activity of 3′ UTR segment of MAPK1 (P<0.01). Compared to the negative control, HEK293T cells expressing miR-1229-5p mimics showed a significant decline in mRNA levels of MAPK1 (P<0.05). This preliminary study indicated that serum miR-1229-5p was significantly elevated in ONIHL subjects. Increased miR-1229-5p may participate in the pathogenesis of ONIHL through repressing MAPK1 signaling.

Discovery and characterization of a first set of polymorphic microsatellite markers in Siganus oramin.

Nine microsatellite DNA markers were developed and characterized for Siganus oramin by the 5'-anchored polymerase chain reaction technique. A total of 42 alleles were identified in 30 individuals, and the number of alleles per locus ranged from 3 to 7, with an average of 4.7. The observed and expected heterozygosity per locus ranged from 0.5333 to 1.0000 and from 0.5254 to 0.8474, respectively, with an average of 0.7422 and 0.6906, respectively. A significant deviation from the Hardy-Weinberg equilibrium was detected at one microsatellite locus after a Bonferroni's correction (P < 0.0056). No significant linkage disequilibrium was found between any of the pairs of the nine loci. The microsatellite loci developed in this study will improve our understanding of the genetic background of S. oramin.

Molecular identification of the genus Thryssa based on DNA barcoding.

DNA barcoding is an effective method for identifying species by analyzing one or a few short standardized DNA sequences. In this study, we examined the utility of mitochondrial cytochrome oxidase subunit I (COI) sequences as a DNA barcode for the identification of six species belonging to the genus Thryssa: T. dussumieri, T. hamiltonii, T. kammalensis, T. mystax, T. setirostris, and T. vitrirostris. We obtained an intraspecific distance of 0.000 for T. vitrirostris and T. hamiltonii, 0.006 for T. mystax, 0.002 for T. dussumieri, and 0.005 for T. kammalensis. The average intraspecific distance was 0.002, while the average interspecific distance was 0.137. Thus, the interspecific genetic distance was approximately 67-fold larger than the intraspecific genetic distance; the average genetic distance among species was greater than the minimum of 0.020 between species suggested elsewhere. The genetic distance between T. vitrirostris and T. mystax was 0.003. A maximum-likelihood phylogenetic tree constructed using best-fitting tree topology showed distinct clusters corresponding to the species (except for T. vitrirostris and T. mystax). The closest relationship was found between T. vitrirostris and T. mystax. These two species clustered together in the phylogenetic tree. This conclusion contradicts the evolutionary relationship based on morphological classification.

A comparison of clinical outcomes of Chinese sirolimus-eluting stents versus foreign sirolimus-eluting stents for the treatment of coronary artery disease.

BACKGROUND: Chinese sirolimus-eluting stents (SES) have been widely used in recent years. However, the comparison of clinical outcomes between Chinese and foreign SES remains unknown. OBJECTIVES: To compare the outcomes of Chinese SES (Firebird) with foreign SES (Cypher Select) in the treatment of patients undergoing percutaneous coronary intervention (PCI). METHODS: 4000 consecutive patients treated with SESs from January 2008 to December 2009 were included in this study. Based on the differences of the stents, the patients were divided into a Chinese SES group (Firebird; n = 2008) and a foreign SES group (Cypher Select; n = 1992). Outcomes were monitored for 1 year. The primary clinical endpoint was major adverse cardiac events (MACE): a composite of death, non-fatal myocardial infarction (MI) and target-vessel revascularisation (TVR). RESULTS: No differences were observed in the incidence of MACE (17.8% vs. 18.6%, p = 0.514) and TVR rate (9.0% vs. 8.6%, p = 0.632) during 1-year follow-up. CONCLUSIONS: Chinese SES and foreign SES have similar effects on 1-year clinical outcomes and safety.

Microsatellite-centromere mapping in Cynoglossus semilaevis using gynogenetic diploid families produced by the use of homologous and non-homologous sperm.

Twenty-one microsatellite markers were studied in three meiogynogenetic families of Cynoglossus semilaevis gunther for centromere mapping using half-tetrad analysis. Among the 13 mapped loci, 10 were estimated to be located in the telomeric region, one in the centromeric region, and two in the intermediate region of the chromosome. This study provides a basis for constructing a linkage map of C. semilaevis.

Lipid peroxidation and cell death mechanisms in rats and human cells induced by chloral hydrate.

Chloral hydrate (CH) is widely used as a sedative and hypnotic in pediatric medicine. It is also a by-product of water chlorination and a metabolite of trichloroethylene. We examined the toxicological effects and cell death mechanisms of CH in rats and human Chang liver cells and lymphocytes. Monitoring of urinary 8-epi-PGF2alpha and serum levels of TNF-alpha served as index of lipid peroxidation and cytokine stimulation. The results indicated that a single intraperitoneal injection of 100 mg/kg CH in rats led to a nearly five-fold increase in urinary 8-epi-PGF2alpha on day 1, and a mild decrease on day 2 and day 3. The same treatment also induced significantly higher amounts of serum TNF-alpha on day 2 (about seven-fold). When the rats were treated with CH and vitamin E simultaneously, the amount of urinary 8-epi-PGF2alpha and serum TNF- were significantly lower than that in the rats treated with CH alone. CH caused a greater cytotoxic effect in human Chang liver cells than in comparison with lymphocytes. After treatment with CH, apoptosis features were observed in human lymphocytes, but not Chang liver cells. CH-induced cell damage in lymphocytes may offer signals for the induction of caspases activation. Further studies are needed to evaluate the relationship between caspases activation and the cleavage of other death substrates during postmitotic apoptosis in human lymphocytes.