State Estimation for Time-Delay Systems with Markov Jump Parameters and Missing Measurements

This paper is concerned with the state estimation problem for a class of time-delay systems with Markovian jump parameters and missing measurements, considering the fact that data missing may occur in the process of transmission and its failure rates are governed by random variables satisfying certain probabilistic distribution. By employing a new Lyapunov function and using the convexity property of the matrix inequality, a sufficient condition for the existence of the desired state estimator for Markovian jump systems with missing measurements can be achieved by solving some linear matrix inequalities, which can be easily facilitated by using the standard numerical software. Furthermore, the gain of state estimator can also be derived based on the known conditions. Finally, a numerical example is exploited to demonstrate the effectiveness of the proposed method

Activation of an AMP-activated protein kinase is involved in post-diapause development of Artemia franciscana encysted embryos

<p>Abstract</p> <p>Background</p> <p>Cysts of <it>Artemia </it>can remain in a dormant state for long periods with a very low metabolic rate, and only resume their development with the approach of favorable conditions. The post-diapause development is a very complicated process involving a variety of metabolic and biochemical events. However, the intrinsic mechanisms that regulate this process are unclear.</p> <p>Results</p> <p>Herein we report the specific activation of an AMP-activated protein kinase (AMPK) in the post-diapause developmental process of <it>Artemia</it>. Using a phospho-AMPKα antibody, AMPK was shown to be phosphorylated in the post-diapause developmental process. Results of kinase assay analysis showed that this phosphorylation is essential for AMPK activation. Using whole-mount immunohistochemistry, phosphorylated AMPK was shown to be predominantly located in the ectoderm of the early developed embryos in a ring shape; however, the location and shape of the activation region changed as development proceeded. Additionally, Western blotting analysis on different portions of the cyst extracts showed that phosphorylated AMPKα localized to the nuclei and this location was not affected by intracellular pH. Confocal microscopy analysis of immunofluorescent stained cyst nuclei further showed that AMPKα localized to the nuclei when activated. Moreover, cellular AMP, ADP, and ATP levels in developing cysts were determined by HPLC, and the results showed that the activation of <it>Artemia </it>AMPK may not be associated with cellular AMP:ATP ratios, suggesting other pathways for regulation of <it>Artemia </it>AMPK activity.</p> <p>Conclusion</p> <p>Together, we report evidence demonstrating the activation of AMPK in <it>Artemia </it>developing cysts and present an argument for its role in the development-related gene expression and energy control in certain cells during post-diapause development of <it>Artemia</it>.</p

Modelling of a hybrid system for on-site power generation from solar fuels

201906 bcmaVersion of RecordPublishe

Prognostic significance of hemoglobin A1c level in patients hospitalized with coronary artery disease. A systematic review and meta-analysis

<p>Abstract</p> <p>Background</p> <p>The prognostic value of hemoglobin A1c (HbA1c) in coronary artery disease (CAD) remains controversial. Herein, we conducted a systematic review to quantify the association between elevated HbA1c levels and all-cause mortality among patients hospitalized with CAD.</p> <p>Methods</p> <p>A systematic search of electronic databases (PubMed, EMBASE, OVID, Web of Science, The Cochrane Library) for studies published from 1970 to May 2011 was performed. Cohort, case-control studies, and randomized controlled trials that examined the effect of HbA1c on all-cause mortality were included.</p> <p>Results</p> <p>Twenty studies met final inclusion criteria (total n = 13, 224). From the pooled analyses, elevated HbA1c level was significantly associated with increased short-term (OR 2.32, 95% CI, 1.61 to 3.35) and long-term (OR 1.54, 95% CI, 1.23 to 1.94) mortality risk. Subgroup analyses suggested elevated HbA1c level predicted higher mortality risk in patients without diabetes (OR 1.84, 95% CI, 1.51 to 2.24). In contrast, in patients with diabetes, elevated HbA1c level was not associated with increased risk of mortality (OR 0.95, 95% CI, 0.70 to 1.28). In a risk-adjusted sensitivity analyses, elevated HbA1c was also associated with a significantly high risk of adjusted mortality in patients without diabetes (adjusted OR 1.49, 95% CI, 1.24 to 1.79), but had a borderline effect in patients with diabetes (adjusted OR 1.05, 95% CI, 1.00 to 1.11).</p> <p>Conclusions</p> <p>Our findings demonstrate that elevated HbA1c level is an independent risk factor for mortality in CAD patients without diabetes, but not in patients with established diabetes. Prospective studies should further investigate whether glycemic control might improve outcomes in CAD patients without previously diagnosed diabetes.</p

Chloridobis[N′-(2-meth­oxy­benzyl­idene)-4-nitro­benzohydrazidato-κ2 O,N′](4-methyl­pyridine-κN)cobalt(III)

In the title complex, [Co(C15H12N3O4)2Cl(C6H7N)], the CoIII ion is coordinated by two N atoms and two O atoms from two deprotonated Schiff base ligands, one N atom from a 4-methyl­pyridine ligand and one Cl atom, forming a distorted octa­hedral geometry. The CoIII ion is displaced by 0.038 (2) Å from the equatorial plane towards the axial Cl atom

Structure activity related, mechanistic, and modeling studies of gallotannins containing a glucitol-core and α-glucosidase

Gallotannins containing a glucitol core, which are only produced by members of the maple (Acer) genus, are more potent α-glucosidase inhibitors than the clinical drug, acarbose. While this activity is influenced by the number of substituents on the glucitol core (e.g. more galloyl groups leads to increased activity), the mechanisms of inhibitory action are not known. Herein, we investigated ligand–enzyme interactions and binding mechanisms of a series of ‘glucitol-core containing gallotannins (GCGs)’ against the α-glucosidase enzyme. The GCGs included ginnalins A, B and C (containing two, one, and one galloyl/s, respectively), maplexin F (containing 3 galloyls) and maplexin J (containing 4 galloyls). All of the GCGs were noncompetitive inhibitors of α-glucosidase and their interactions with the enzyme were further explored using biophysical and spectroscopic measurements. Thermodynamic parameters (by isothermal titration calorimetry) revealed a 1 : 1 binding ratio between GCGs and α-glucosidase. The binding regions between the GCGs and α-glucosidase, probed by a fluorescent tag, 1,1′-bis(4-anilino-5-naphthalenesulfonic acid), revealed that the GCGs decreased the hydrophobic surface of the enzyme. In addition, circular dichroism analyses showed that the GCGs bind to α-glucosidase and lead to loss of the secondary α-helix structure of the protein. Also, molecular modeling was used to predict the binding site between the GCGs and the α-glucosidase enzyme. This is the first study to evaluate the mechanisms of inhibitory activities of gallotannins containing a glucitol core on α-glucosidase

Bis[4-amino-N-(pyrimidin-2-yl)benzene­sulfonamidato](2,2′-bipyridine)manganese(II)

The title compound, [Mn(C10H9N4O2S)2(C10H8N2)], contains a distorted octa­hedral [Mn(sdz)2(bpy)] (sdz is the sulfadiazine anion and bpy is 2,2′-bipyridine) complex mol­ecule. A three-dimensional network is generated by N—H⋯N, N—H⋯O and C—H⋯O hydrogen bonds from the sulfadiazine ligands

BAG5 Interacts with DJ-1 and Inhibits the Neuroprotective Effects of DJ-1 to Combat Mitochondrial Oxidative Damage

Loss-of-function mutations in gene encoding DJ-1 contribute to the pathogenesis of autosomal recessive early-onset familial forms of Parkinson’s disease (PD). DJ-1 is a multifunctional protein and plays a protective role against oxidative stress-induced mitochondrial damage and cell death, but the exact mechanism underlying this is not yet clearly understood. Here, using coimmunoprecipitation (Co-IP) and immunofluorescence methods, we prove that Bcl-2-associated athanogene 5 (BAG5), a BAG family member, interacts with DJ-1 in mammalian cells. Moreover, we show that BAG5 could decrease stability of DJ-1 and weaken its role in mitochondrial protection probably by influencing dimerization in stress condition. Our study reveals the relationship of BAG5 and DJ-1 suggesting a potential role for BAG5 in the pathogenesis of PD through its functional interactions with DJ-1

AUTOMATED ADVERTISEMENT CREATION SYSTEM

An advertisement creation system generates sizeless creatives and renders the creatives as display advertisements of any arbitrary dimension. The system extracts text assets and image assets from creatives provided by an advertiser. In particular, the system selects assets to display based on scores for the respective text assets and image assets. The system then combines selected text assets and image assets to generate a final creative. Finally, the system optimizes the final creative and renders the final creative for display