Sediment transport rate-based model for rainfall-induced soil erosion

http://www.sciencedirect.com/science/article/B6VCG-4TP7HC2-1/2/2a6275ceb0176f80cedfb5efe5ef248

Optimizing Logical Execution Time Model for Both Determinism and Low Latency

The Logical Execution Time (LET) programming model has recently received considerable attention, particularly because of its timing and dataflow determinism. In LET, task computation appears always to take the same amount of time (called the task's LET interval), and the task reads (resp. writes) at the beginning (resp. end) of the interval. Compared to other communication mechanisms, such as implicit communication and Dynamic Buffer Protocol (DBP), LET performs worse on many metrics, such as end-to-end latency (including reaction time and data age) and time disparity jitter. Compared with the default LET setting, the flexible LET (fLET) model shrinks the LET interval while still guaranteeing schedulability by introducing the virtual offset to defer the read operation and using the virtual deadline to move up the write operation. Therefore, fLET has the potential to significantly improve the end-to-end timing performance while keeping the benefits of deterministic behavior on timing and dataflow. To fully realize the potential of fLET, we consider the problem of optimizing the assignments of its virtual offsets and deadlines. We propose new abstractions to describe the task communication pattern and new optimization algorithms to explore the solution space efficiently. The algorithms leverage the linearizability of communication patterns and utilize symbolic operations to achieve efficient optimization while providing a theoretical guarantee. The framework supports optimizing multiple performance metrics and guarantees bounded suboptimality when optimizing end-to-end latency. Experimental results show that our optimization algorithms improve upon the default LET and its existing extensions and significantly outperform implicit communication and DBP in terms of various metrics, such as end-to-end latency, time disparity, and its jitter

Bis(3-meth­oxy-6-methyl-2-pyrid­yl) ether

In the mol­ecule of the title compound, C14H16N2O3, the dihedral angle between the pyridyl rings is 87.74 (3)°. In the crystal structure, inter­molecular C—H⋯O hydrogen bonds link the mol­ecules into infinite zigzag chains

Tetrodotoxin and paralytic shellfish poisons in gastropod species from Vietnam analyzed by high-performance liquid chromatography and liquid chromatography–tandem mass spectrometry

AbstractAmong marine toxins, tetrodotoxin (TTX) and paralytic shellfish poisons (PSPs) are known as notorious neurotoxins that induce serious food poisoning incidents in the Southeast Asia region. The aim of this study was to investigate whether TTX and PSP toxins are important issues of seafood safety. Paralytic toxicity was observed in mice exposed to 34 specimens from five species of gastropods using a PSP bioassay. Five species of gastropods, Natica vitellus, Natica tumidus, Oliva hirasei, Oliva lignaria, and Oliva annulata, were collected from the coastal seawaters in Nha Trang City, Vietnam, between August 2007 and October 2007. The average lethal potency of gastropod specimens was 90 ± 40 (mean ± standard deviation) mouse units (MU) for N. vitellus, 64 ± 19 MU for N. tumidus, 42 ± 28 MU for O. hirasei, 51 ± 17 MU for O. lignaria, and 39 ± 18 MU for O. annulata. All toxic extracts from the sample species were clarified using a C18 Sep-Pak solid-phase extraction column and a microcentrifuge filter prior to analysis. High-performance liquid chromatography coupled with fluorescence detection indicated that the toxins of the olive shell (O. hirasei, O. lignaria, and O. annulata) were mainly composed of saxitoxin (STX) (73–82%), gonyautoxin (GTX) 2, 3 (12–22%), and minor levels of TTX (5–6%). The toxins of N. vitellus and N. tumidus were mainly composed of STX (76–81%) and GTX 1, 4 (19–24%). Furthermore, liquid chromatography–tandem mass spectrometry analysis was used to verify the identity of the PSPs and TTX. Our evidence shows that these gastropods have novel toxin profiles

A randomized, open-label study of the efficacy and safety of AZD4547 monotherapy versus paclitaxel for the treatment of advanced gastric adenocarcinoma with FGFR2 polysomy or gene amplification

Background:Approximately 5%-10% of gastric cancers have a fibroblast growth factor receptor-2 (FGFR2) gene amplification. AZD4547 is a selective FGFR-1, 2, 3 tyrosine kinase inhibitor with potent preclinical activity in FGFR2 amplified gastric adenocarcinoma SNU16 and SGC083 xenograft models. The randomized phase II SHINE study (NCT01457846) investigated whether AZD4547 improves clinical outcome versus paclitaxel as second-line treatment in patients with advanced gastric adenocarcinoma displaying FGFR2 polysomy or gene amplification detected by fluorescence in situ hybridization. Patients and methods:Patients were randomized 3:2 (FGFR2 gene amplification) or 1:1 (FGFR2 polysomy) to AZD4547 or paclitaxel. Patients received AZD4547 80 mg twice daily, orally, on a 2 weeks on/1 week off schedule of a 21-day cycle or intravenous paclitaxel 80 mg/m2 administered weekly on days 1, 8, and 15 of a 28-day cycle. The primary end point was progression-free survival (PFS). Safety outcomes were assessed and an exploratory biomarker analysis was undertaken. Results:Of 71 patients randomized (AZD4547 n = 41, paclitaxel n = 30), 67 received study treatment (AZD4547 n = 40, paclitaxel n = 27). Among all randomized patients, median PFS was 1.8 months with AZD4547 and 3.5 months with paclitaxel (one-sided P = 0.9581); median follow-up duration for PFS was 1.77 and 2.12 months, respectively. The incidence of adverse events was similar in both treatment arms. Exploratory biomarker analyses revealed marked intratumor heterogeneity of FGFR2 amplification and poor concordance between amplification/polysomy and FGFR2 mRNA expression. Conclusions:AZD4547 did not significantly improve PFS versus paclitaxel in gastric cancer FGFR2 amplification/polysomy patients. Considerable intratumor heterogeneity for FGFR2 gene amplification and poor concordance between FGFR2 amplification/polysomy and FGFR2 expression indicates the need for alternative predictive biomarker testing. AZD4547 was generally well tolerated

Anti-Inflammatory Activities of Cinnamomum cassia Constituents In Vitro and In Vivo

We have investigated the anti-inflammatory effects of Cinnamomum cassia constituents (cinnamic aldehyde, cinnamic alcohol, cinnamic acid, and coumarin) using lipopolysaccharide (LPS)-stimulated mouse macrophage (RAW264.7) and carrageenan (Carr)-induced mouse paw edema model. When RAW264.7 macrophages were treated with cinnamic aldehyde together with LPS, a significant concentration-dependent inhibition of nitric oxide (NO), tumor necrosis factor (TNF-α), and prostaglandin E2 (PGE2) levels productions were detected. Western blotting revealed that cinnamic aldehyde blocked protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear transcription factor kappa B (NF-κB), and IκBα, significantly. In the anti-inflammatory test, cinnamic aldehyde decreased the paw edema after Carr administration, and increased the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in the paw tissue. We also demonstrated cinnamic aldehyde attenuated the malondialdehyde (MDA) level and myeloperoxidase (MPO) activity in the edema paw after Carr injection. Cinnamic aldehyde decreased the NO, TNF-α, and PGE2 levels on the serum level after Carr injection. Western blotting revealed that cinnamic aldehyde decreased Carr-induced iNOS, COX-2, and NF-κB expressions in the edema paw. These findings demonstrated that cinnamic aldehyde has excellent anti-inflammatory activities and thus has great potential to be used as a source for natural health products

Hispolon Protects against Acute Liver Damage in the Rat by Inhibiting Lipid Peroxidation, Proinflammatory Cytokine, and Oxidative Stress and Downregulating the Expressions of iNOS, COX-2, and MMP-9

The hepatoprotective potential of hispolon against carbon tetrachloride (CCl4)-induced liver damage was evaluated in preventive models in rats. Male rats were intraperitoneally treated with hispolon or silymarin once daily for 7 consecutive days. One hour after the final hispolon or silymarin treatment, the rats were injected with CCl4. Administration with hispolon or silymarin significantly decreased the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in serum and increased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione (GSH) content and decreased the malondialdehyde (MDA) content in liver compared with CCl4-treated group. Liver histopathology also showed that hispolon reduced the incidence of liver lesions induced by CCl4. In addition, hispolon decreased nitric oxide (NO) production and tumor necrosis factor (TNF-α), inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) activation in CCl4-treated rats. We also examined the involvement of matrix metalloproteinase (MMP)-9 in the development of CCl4-induced liver damage in rats. Hispolon inhibited the expression of MMP-9 protein, indicating that MMP-9 played an important role in the development of CCl4-induced rat liver damage. Therefore, we speculate that hispolon protects rats from liver damage through their prophylactic redox balancing ability and anti-inflammation capacity