Twin‐engined diagnosis of discrete‐event systems

Diagnosis of discrete-event systems (DESs) is computationally complex. This is why a variety of knowledge compilation techniques have been proposed, the most notable of them rely on a diagnoser. However, the construction of a diagnoser requires the generation of the whole system space, thereby making the approach impractical even for DESs of moderate size. To avoid total knowledge compilation while preserving efficiency, a twin-engined diagnosis technique is proposed in this paper, which is inspired by the two operational modes of the human mind. If the symptom of the DES is part of the knowledge or experience of the diagnosis engine, then Engine 1 allows for efficient diagnosis. If, instead, the symptom is unknown, then Engine 2 comes into play, which is far less efficient than Engine 1. Still, the experience acquired by Engine 2 is then integrated into the symptom dictionary of the DES. This way, if the same diagnosis problem arises anew, then it will be solved by Engine 1 in linear time. The symptom dic- tionary can also be extended by specialized knowledge coming from scenarios, which are the most critical/probable behavioral patterns of the DES, which need to be diagnosed quickly

Xenin, a Gastrointestinal Peptide, Regulates Feeding Independent of the Melanocortin Signaling Pathway

OBJECTIVE—Xenin, a 25–amino acid peptide, was initially isolated from human gastric mucosa. Plasma levels of xenin rise after a meal in humans, and administration of xenin inhibits feeding in rats and chicks. However, little is known about the mechanism by which xenin regulates food intake. Signaling pathways including leptin and melanocortins play a pivotal role in the regulation of energy balance. Therefore, we addressed the hypothesis that xenin functions as a satiety factor by acting through the melanocortin system or by interacting with leptin

Role of aryl hydrocarbon receptor (AHR) in overall retinoid metabolism : Response comparisons to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure between wild-type and AHR knockout mice

Young adult wild-type and aryl hydrocarbon receptor knockout (AHRKO) mice of both sexes and the C57BL/6J background were exposed to 10 weekly oral doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; total dose of 200 ?g/kg bw) to further characterize the observed impacts of AHR as well as TCDD on the retinoid system. Unexposed AHRKO mice harboured heavier kidneys, lighter livers and lower serum all-trans retinoic acid (ATRA) and retinol (REOH) concentrations than wild-type mice. Results from the present study also point to a role for the murine AHR in the control of circulating REOH and ATRA concentrations. In wild-type mice, TCDD elevated liver weight and reduced thymus weight, and drastically reduced the hepatic concentrations of 9-cis-4-oxo-13,14dihydro-retinoic acid (CORA) and retinyl palmitate (REPA). In female wild-type mice, TCDD increased the hepatic concentration of ATRA as well as the renal and circulating REOH concentrations. Renal CORA concentrations were substantially diminished in wild-type male mice exclusively following TCDD-exposure, with a similar tendency in serum. In contrast, TCDD did not affect any of these toxicity or retinoid system parameters in AHRKO mice. Finally, a distinct sex difference occurred in kidney concentrations of all the analysed retinoid forms. Together, these results strengthen the evidence of a mandatory role of AHR in TCDD-induced retinoid disruption, and suggest that the previously reported accumulation of several retinoid forms in the liver of AHRKO mice is a line-specific phenomenon. Our data further support participation of AHR in the control of liver and kidney development in mice.Peer reviewe

Inhibitory effects of the macrolide antimicrobial tylosin on anaerobic treatment

A laboratory-scale anaerobic sequencing batch reactor (ASBR) was operated using a glucose-based synthetic wastewater to study the effects of tylosin, a macrolide antimicrobial commonly used in swine production, on treatment performance. The experimental period was divided into three consecutive phases with different influent tylosin concentrations (0, 1.67, and 167 mg/L). The addition of 1.67 mg/L tylosin to the reactor had negligible effects on the overall treatment performance, that is, total methane production and effluent chemical oxygen demand did not change significantly ( P  < 0.05), yet analyses of individual ASBR cycles revealed a decrease in the rates of both methane production and propionate uptake after tylosin was added. The addition of 167 mg/L tylosin to the reactor resulted in a gradual decrease in methane production and the accumulation of propionate and acetate. Subsequent inhibition of methanogenesis was attributed to a decrease in the pH of the reactor. After the addition of 167 mg/L tylosin to the reactor, an initial decrease in the rate of glucose uptake during the ASBR cycle followed by a gradual recovery was observed. In batch tests, the specific biogas production with the substrate butyrate was completely inhibited in the presence of tylosin. This study indicated that tylosin inhibited propionate- and butyrate-oxidizing syntrophic bacteria and fermenting bacteria resulting in unfavorable effects on methanogenesis. Biotechnol. Biotechnol. Bioeng. 2008;101: 73–82. © 2008 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/60471/1/21864_ftp.pd

Antibiotic resistance in the environment, with particular reference to MRSA

The introduction of β-lactam antibiotics (penicillins and cephalosporins) in the 1940s and 1950s probably represents the most dramatic event in the battle against infection in human medicine. Even before widespread global use of penicillin, resistance was already recorded. E. coli producing a penicillinase was reported in Nature in 1940 (Abraham, 1940) and soon after a similar penicillinase was discovered in Staphylococcus aureus (Kirby, 1944). The appearance of these genes, so quickly after the discovery and before the widespread introduction of penicillin, clearly shows that the resistance genes pre-dated clinical use of the antibiotic itself

Unexpected effect of a Bacteroides conjugative transposon, CTnDOT, on chromosomal gene expression in its bacterial host

Foreign DNA elements such as plasmids and conjugative transposons are constantly entering new bacterial hosts. A possible outcome of such events that has not been considered previously is that regulatory genes carried on some of them might affect the expression of chromosomal genes of the new host. To assess this possibility, we investigated the effect of the Bacteroides conjugative transposon CTnDOT on expression of chromosomal genes in Bacteroides thetaiotaomicron 5482 (BT4001). Most of the upregulated genes were genes of unknown function, but a number of them were associated with a region of the chromosome that contained a putative conjugative transposon, which had been tentatively designated as CTn4-bt. Upregulation of CTn4-bt genes and other chromosomal genes affected by CTnDOT was controlled by two regulatory genes on CTnDOT, rteA and rteB, which encode a two-component regulatory system. Transfer of CTn4-bt was also mediated by rteA and rteB. Three other putative CTns, CTn1-bt, CTn2-bt and CTn3-bt, were mobilized by CTnERL, a CTn closely related to CTnDOT, but genes from CTnERL other than rteA and rteB were also required. Unexpectedly, homologous recombination was required for CTn1-bt, CTn2-bt, CTn3-bt and CTn4-bt to integrate in the recipient. Our results show that regulatory genes on an incoming mobile element can have multiple effects on its new host, including the activation of previously non-transmissible elements