Regeneration Effect of a New Bio-Based Warm-Mix Rejuvenator on Performance and Micro-Morphology of Aged Asphalt.

The use of warm-mix recycling technology can reduce the mixing temperature and the secondary aging of binders in reclaimed asphalt pavement (RAP), which is one of the effective ways to recycle high-content RAP. In this study, the penetration, softening point, ductility, and viscosity were used to characterize the conventional physical properties of aged asphalt after regenerating, while a dynamic shear rheometer (DSR), force ductility tester (FDT), and atomic force microscope (AFM) were used to evaluate the rheological performance and micro-morphology of aged asphalt incorporating a new bio-based warm-mix rejuvenator (BWR) and a commercial warm-mix rejuvenator (ZJ-WR). The regeneration mechanism of warm-mix rejuvenators on aged asphalt was analyzed by Fourier transform infrared spectroscopy (FTIR). The results show that the new bio-based warm-mix rejuvenator can restore the conventional physical properties, low-temperature performance, and micro-morphology of aged asphalt with an appropriate dosage, but it has a negative effect on high-temperature performance. In comparison with 2D area parameters, 3D roughness parameters were more accurate in evaluating the variation in micro-morphology of aged asphalt after regeneration. The FTIR analysis results indicate that both the new bio-based warm-mix rejuvenator and the commercial warm-mix rejuvenator regenerate aged asphalt by physical action, and AS=O and AC-H values are more reasonable than the AC=O value for the restoration evaluation of aged asphalt. And the new bio-based warm-mix rejuvenator has a better regeneration effect on the performance and micro-morphology of aged asphalt than the commercial warm-mix rejuvenator.

Gestodene causes masculinization of the western mosquitofish (Gambusia affinis): Insights from ovary metabolomics.

Gestodene (GES) is a common synthetic progesterone frequently detected in aquatic environments. Chronic exposure to GES can cause masculinization of a variety of fish; however, whether metabolism is closely related to the masculinization has yet to be explored. Hence, the ovary metabolome of adult female western mosquitofish (Gambusia affinis) after exposing to GES (0.0, 5.0, 50.0, and 500.0 ng/L) for 40 days was analyzed by using high-performance liquid chromatography ionization with quadrupole time-of-flight tandem mass spectrometry (HPLC-QTOF-MS). The results showed that GES increased the levels of cysteine, taurine, ophthalmic acid and cAMP while decreased methionine, these metabolites changes may owing to the oxidative stress of the ovaries; while taurcholic acid and uric acid were decreased along with induced oocyte apopotosis. Steroids hormone metabolism was also significantly affected, with progesterone and cortisol being the most affected. Enzyme-linked immunoassay results showed that estradiol levels were decreased while testosterone levels were increased with GES exposure. In addition, correlation analysis showed that the differential metabolites of some amino acids (e.g. leucine) were strongly correlated with the levels of steroids hormones secreted by the pituitary gland. The results of this study suggest that GES affects ovarian metabolism via the hypothalamus-pituitary-gonad and hypothalamic-pituitary-adrenal axes, impair antioxidant capacity, induce apoptosis in the ovary of G. affinis, and finally caused masculinization.

Huangqi Decoction, a compound Chinese herbal medicine, inhibits the proliferation and activation of hepatic stellate cells by regulating the long noncoding RNA-C18orf26-1/microRNA-663a/transforming growth factor-ß axis.

OBJECTIVE: Huangqi Decoction (HQD), a classical traditional Chinese medicine formula, has been used as a valid treatment for alleviating liver fibrosis; however, the underlying molecular mechanism is still unknown. Although our previous studies showed that microRNA-663a (miR-663a) suppresses the proliferation and activation of hepatic stellate cells (HSCs) and the transforming growth factor-ß/small mothers against decapentaplegic (TGF-ß/Smad) pathway, whether long noncoding RNAs (lncRNAs) are involved in HSC activation via the miR-663a/TGF-ß/Smad signaling pathway has not yet reported. The present study aimed to investigate the roles of lncRNA lnc-C18orf26-1 in the activation of HSCs and the mechanism by which HQD inhibits hepatic fibrosis. METHODS: The expression levels of lnc-C18orf26-1, miR-663a and related genes were measured by quantitative reverse transcription-polymerase chain reaction. HSCs were transfected with the miR-663a mimic or inhibitor and lnc-C18orf26-1 small interfering RNAs. The water-soluble tetrazolium salt-1 assay was used to assess the proliferation rate of HSCs. Changes in lncRNA expression were evaluated in miR-663a-overexpressing HSCs by using microarray to identify miR-663a-regulated lncRNAs. RNA hybrid was used to predict the potential miR-663a binding sites on lncRNAs. Luciferase reporter assays further confirmed the interaction between miR-663a and the lncRNA. The expression levels of collagen α-2(I) chain (COL1A2), α-smooth muscle actin (α-SMA) and TGF-ß/Smad signaling pathway-related proteins were determined using Western blotting. RESULTS: Lnc-C18orf26-1 was upregulated in TGF-ß1-activated HSCs and competitively bound to miR-663a. Knockdown of lnc-C18orf26-1 inhibited HSC proliferation and activation, downregulated TGF-ß1-stimulated α-SMA and COL1A2 expression, and inhibited the TGF-ß1/Smad signaling pathway. HQD suppressed the proliferation and activation of HSCs. HQD increased miR-663a expression and decreased lnc-C18orf26-1 expression in HSCs. Further studies showed that HQD inhibited the expression of COL1A2, α-SMA, TGF-ß1, TGF-ß type I receptor (TGF-ßRI) and phosphorylated Smad2 (p-Smad2) in HSCs, and these effects were reversed by miR-663a inhibitor treatment. CONCLUSION: Our study identified lnc-C18orf26-1 and miR-663a as promising therapeutic targets for hepatic fibrosis. HQD inhibits HSC proliferation and activation at least partially by regulating the lnc-C18orf26-1/miR-663a/TGF-ß1/TGF-ßRI/p-Smad2 axis.

Serum level of fibroblast growth factor 21 predicts long-term prognosis in patients with both diabetes mellitus and coronary artery calcification.

BACKGROUND: This study aimed to investigate the relationship between serum level of fibroblast growth factor 21 (FGF-21) and long-term prognosis in patients with both diabetes mellitus (DM) and coronary artery calcification (CAC). METHODS: The study included 1,132 patients with DM and CAC according to inclusion and exclusion criteria. Based on the baseline serum level of FGF-21, patients were divided into four groups (283 in each group): low-FGF-21 group (LFG), lower-medium-FGF-21 group (LMFG), higher-medium-FGF-21 group (HMFG), and high-FGF-21 group (HFG). Major adverse cardiovascular events (MACEs), including coronary revascularization, acute coronary syndrome (ACS), heart failure (HF), malignant arrhythmia, and sudden cardiac death (SCD), were recorded. Renal function, serum level of NT-proBNP, and left ventricular function were watched and observed during follow-up. RESULTS: All patients were followed up for 1.5-5.1 (2.7±2.2) years. The range of baseline serum level of FGF-21 was 67.5-314.7 pg/mL. The serum level of FGF-21 was ≤103.8 pg/mL in LFG, 108.6-184.9 pg/mL in LMFG, 199.3-271.2 pg/mL in LHFG, and >276.1 pg/mL in HFG. The baseline CAC score (CACS) was 83.2-524.9 and the mean CACS was 124.6±37.5, 186.8±51.9, 271.3±62.7, and 349.2±80.6, respectively. During follow-up, 481 patients underwent percutaneous coronary intervention (PCI) with 71, 107, 141, and 162 in subgroups, respectively. Malignant arrhythmia occurred in 89 patients, HF in 127, and SCD in 9. At the end of the 1-year follow-up, the average eGFR, NT-proBNP, and left ventricular ejection fraction (LVEF) differed significantly among groups. CONCLUSIONS: Lower baseline serum level of FGF-21 is a prediction for a better long-term prognosis.

[Distribution of IgG subclasses of TgAb and TPOAb in sera from patients with Graves' disease, Graves' disease plus Hashimoto's thyroiditis and Hashimoto's thyrotoxicosis].

OBJECTIVE: To evaluate the distribution of IgG subclasses of TgAb and TPOAb in sera from patients with Graves' disease (GD), Graves' disease plus Hashimoto's thyroiditis (GH) and Hashimoto's thyrotoxicosis. METHODS: Patients with GD (n = 33), GH (n = 31) or Hashimoto's thyrotoxicosis (n = 18) diagnosed by fine needle aspiration cytology at Department of Endocrinology of Peking University First Hospital, Beijing Haidian Hospital, China-Japan Friendship Hospital and Civil Aviation General Hospital during the period from January 2010 to May 2013 were enrolled. All of them had TgAb and TPOAb. The total serum IgG and IgG subclasses of TgAb and TPOAb were detected by antigen-specific enzyme-linked immunosorbent assay (ELISA). The prevalence and relative amount of IgG subclasses were calculated and compared among three groups. RESULTS: The levels of TRAb in GD group (21.80(7.53, 40) U/L) were significantly higher than those in GH (7.30(3.10, 25.40) U/L) (P = 0.000) and Hashimoto's thyrotoxicosis groups (4.90(1.69, 16.43) U/L) (P = 0.003). And no significant differences were found in the levels of TgAb and TPOAb. The prevalence of TgAb IgG3 subclass in Hashimoto's thyrotoxicosis group (66.7%) was higher than GD group (35.5%) and GH group (36.4%) and the difference was close to significance (P = 0.066). There were significant differences of relative amount of TgAb IgG2 and TgAb IgG4 among three groups (P = 0.039 and 0.013), and GD patients had higher relative amounts of TgAb IgG2 (0.59(0.34, 0.94)) and TgAb IgG4 (0.57(0.28, 0.97)) than GH patients (TgAb IgG2, 0.31(0.23, 0.34); TgAb IgG4, 0.26(0.09, 0.48)) or patients with Hashimoto's thyrotoxicosis (TgAb IgG2, 0.32(0.24, 0.83); TgAb IgG4, 0.33(0.10, 0.65)) (for TgAb IgG2, P = 0.009 and 0.167; for TgAb IgG4, P = 0.005 and 0.041 respectively). No significant difference was found in the prevalence of each TPOAb IgG subclass. The difference of relative amount of TPOAb IgG2 among three groups was close to significance (P = 0.069). And the relative amount was higher in sera from GD patients (0.39 ± 0.04) than that in GH patients (0.29 ± 0.13) or patients with Hashimoto's thyrotoxicosis (0.26 ± 0.02) (P = 0.104 and 0.002 respectively). CONCLUSION: The patients with high levels of TgAb IgG2, TgAb IgG4 and TPOAb IgG2 subclasses have a greater risk of GD. The IgG subclass distribution of TgAb and TPOAb might help to differentiate the causes of thyrotoxicosis in autoimmune thyroid diseases.

[Distribution and significance of IgG subclasses of serum antithyroglobulin antibody in Hashimoto thyroiditis].

OBJECTIVE: To evaluate the distribution and significance of IgG subclasses of antithyroglobulin antibody in sera from patients with Hashimoto thyroiditis. METHODS: Sera from 112 patients with Hashimoto thyroiditis were collected and patients were divided into 3 groups, i. e. hypothyroidism, subclinical hypothyroidism and euthyroidism. Antigen specific ELISA was used to detect the distribution of IgG subclasses of antithyroglobulin antibody. RESULTS: The positive rates of IgG subclasses of TgAb were IgG1 90.2%, IgG2 58.0%, IgG3 19.6% and IgG4 87.5% respectively. The mean geometric titers of IgG1 in sera from patients with hypothyroidism and subclinical hypothyroidism were 1: 450.8 and 1: 245.5 respectively, both being significantly higher than that with euthyroidism (1:8.7, P < 0.01). The mean geometric titers of IgG2 in sera from patients with hypothyroidism and subclinical hypothyroidism were 1: 37.3 and 1: 3.2 respectively, both being also significantly higher than that with euthyroidism (1: 0.2, P < 0.01 and P < 0.05 respectively) and that with hypothyroidism was significantly higher than that with subclinical hypothyroidism (P < 0.05). CONCLUSION: The distribution of IgG subclasses of antithyroglobulin antibody in sera from patients with Hashimoto thyroiditis was predominantly IgG1, IgG2 and IgG4. High titers of IgG1 and IgG2 implicated the possibility of development from subclinical hypothyroidism to overt hypothyroidism.