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Stenotrophomonas maltophilia is a Gram-negative bacterium found in water, plant rhizospheres, animals, and foods. It is associated with a variety of infections in humans, involving respiratory tract (most common), soft tissue and bone, blood, eye, heart, and brain. This opportunistic pathogen is of serious concern to the immunocompromised patient population, and it is also being isolated with increasing frequency from the respiratory tract of individuals with cystic fibrosis. The observed increase worldwide in antibiotic resistance and the ability of this organism to make biofilms on epithelial cells and medical devices make it difficult for health-care personnel to treat infections caused by this pathogen. Recently, several genomes of S. maltophilia have been sequenced, revealing high genetic diversity among isolates. This pathogen uses a variety of molecular mechanisms to acquire and demonstrate resistance to an impressive array of antimicrobial drugs. Research has also focused on the pathogenesis of S. maltophilia in animal models and the resulting host immune response. S. maltophilia is recognized as an important organism in the plant microbiome. This environmental bacterium uses a diffusible signal mechanism for controlling its colonization and interaction with other bacteria and plants. S. maltophilia has also gained considerable research interest for its biotechnological applications, with recent studies on enzyme production, anti-biofilm strategies, biodegradation, and bioremediation. This e-book focuses on the latest developments in the areas of physiology, genomics, infection and immunity, host-pathogen interaction, pathogenesis, antimicrobial resistance and therapy, molecular epidemiology, applied and environmental microbiology, bioremediation and biotechnology.
Stenotrophomonas maltophilia --- antibiotic resistance mechanisms --- bioremediation --- cystic fibrosis --- iron --- antimicrobial activity --- biofilms --- biocontrol --- Stenotrophomonas maltophilia --- antibiotic resistance mechanisms --- bioremediation --- cystic fibrosis --- iron --- antimicrobial activity --- biofilms --- biocontrol
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Stenotrophomonas maltophilia is a Gram-negative bacterium found in water, plant rhizospheres, animals, and foods. It is associated with a variety of infections in humans, involving respiratory tract (most common), soft tissue and bone, blood, eye, heart, and brain. This opportunistic pathogen is of serious concern to the immunocompromised patient population, and it is also being isolated with increasing frequency from the respiratory tract of individuals with cystic fibrosis. The observed increase worldwide in antibiotic resistance and the ability of this organism to make biofilms on epithelial cells and medical devices make it difficult for health-care personnel to treat infections caused by this pathogen. Recently, several genomes of S. maltophilia have been sequenced, revealing high genetic diversity among isolates. This pathogen uses a variety of molecular mechanisms to acquire and demonstrate resistance to an impressive array of antimicrobial drugs. Research has also focused on the pathogenesis of S. maltophilia in animal models and the resulting host immune response. S. maltophilia is recognized as an important organism in the plant microbiome. This environmental bacterium uses a diffusible signal mechanism for controlling its colonization and interaction with other bacteria and plants. S. maltophilia has also gained considerable research interest for its biotechnological applications, with recent studies on enzyme production, anti-biofilm strategies, biodegradation, and bioremediation. This e-book focuses on the latest developments in the areas of physiology, genomics, infection and immunity, host-pathogen interaction, pathogenesis, antimicrobial resistance and therapy, molecular epidemiology, applied and environmental microbiology, bioremediation and biotechnology.
Stenotrophomonas maltophilia --- antibiotic resistance mechanisms --- bioremediation --- cystic fibrosis --- iron --- antimicrobial activity --- biofilms --- biocontrol
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Stenotrophomonas maltophilia is a Gram-negative bacterium found in water, plant rhizospheres, animals, and foods. It is associated with a variety of infections in humans, involving respiratory tract (most common), soft tissue and bone, blood, eye, heart, and brain. This opportunistic pathogen is of serious concern to the immunocompromised patient population, and it is also being isolated with increasing frequency from the respiratory tract of individuals with cystic fibrosis. The observed increase worldwide in antibiotic resistance and the ability of this organism to make biofilms on epithelial cells and medical devices make it difficult for health-care personnel to treat infections caused by this pathogen. Recently, several genomes of S. maltophilia have been sequenced, revealing high genetic diversity among isolates. This pathogen uses a variety of molecular mechanisms to acquire and demonstrate resistance to an impressive array of antimicrobial drugs. Research has also focused on the pathogenesis of S. maltophilia in animal models and the resulting host immune response. S. maltophilia is recognized as an important organism in the plant microbiome. This environmental bacterium uses a diffusible signal mechanism for controlling its colonization and interaction with other bacteria and plants. S. maltophilia has also gained considerable research interest for its biotechnological applications, with recent studies on enzyme production, anti-biofilm strategies, biodegradation, and bioremediation. This e-book focuses on the latest developments in the areas of physiology, genomics, infection and immunity, host-pathogen interaction, pathogenesis, antimicrobial resistance and therapy, molecular epidemiology, applied and environmental microbiology, bioremediation and biotechnology.
Stenotrophomonas maltophilia --- antibiotic resistance mechanisms --- bioremediation --- cystic fibrosis --- iron --- antimicrobial activity --- biofilms --- biocontrol
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Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell-wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens.
tuberculosis --- toxin-antitoxin systems --- bacterial cell death --- NAD+ --- stress-response --- toxin–antitoxin system --- mazF --- type II --- toxin --- mRNA interferase --- X-ray crystallography --- cognate interactions --- cross-interactions --- molecular insulation --- antitoxin --- TA systems --- addiction --- anti-addiction --- type I toxin–antitoxin system --- small protein toxin structure --- Fst/Ldr family --- toxin–antitoxin --- M. tuberculosis --- bacteria --- pathogenesis --- protein–protein interactions --- cross-talk --- protein interface --- tolerance --- persistence --- cross-resistance --- toxin-antitoxin system --- PemI/PemK --- Klebsiella pneumoniae --- toxin–antitoxin systems --- toxin activation --- antibacterial agents --- bacterial persistence --- Stenotrophomonas maltophilia --- opportunistic pathogen --- clinical origin --- environmental origin --- biofilm --- antibiotic resistance --- cell wall inhibition --- nucleotide hydrolysis --- uridine diphosphate-N-acetylglucosamine --- n/a --- type I toxin-antitoxin system --- toxin-antitoxin --- protein-protein interactions
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Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell-wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens.
Medicine --- tuberculosis --- toxin-antitoxin systems --- bacterial cell death --- NAD+ --- stress-response --- toxin-antitoxin system --- mazF --- type II --- toxin --- mRNA interferase --- X-ray crystallography --- cognate interactions --- cross-interactions --- molecular insulation --- antitoxin --- TA systems --- addiction --- anti-addiction --- type I toxin-antitoxin system --- small protein toxin structure --- Fst/Ldr family --- toxin-antitoxin --- M. tuberculosis --- bacteria --- pathogenesis --- protein-protein interactions --- cross-talk --- protein interface --- tolerance --- persistence --- cross-resistance --- toxin-antitoxin system --- PemI/PemK --- Klebsiella pneumoniae --- toxin-antitoxin systems --- toxin activation --- antibacterial agents --- bacterial persistence --- Stenotrophomonas maltophilia --- opportunistic pathogen --- clinical origin --- environmental origin --- biofilm --- antibiotic resistance --- cell wall inhibition --- nucleotide hydrolysis --- uridine diphosphate-N-acetylglucosamine --- tuberculosis --- toxin-antitoxin systems --- bacterial cell death --- NAD+ --- stress-response --- toxin-antitoxin system --- mazF --- type II --- toxin --- mRNA interferase --- X-ray crystallography --- cognate interactions --- cross-interactions --- molecular insulation --- antitoxin --- TA systems --- addiction --- anti-addiction --- type I toxin-antitoxin system --- small protein toxin structure --- Fst/Ldr family --- toxin-antitoxin --- M. tuberculosis --- bacteria --- pathogenesis --- protein-protein interactions --- cross-talk --- protein interface --- tolerance --- persistence --- cross-resistance --- toxin-antitoxin system --- PemI/PemK --- Klebsiella pneumoniae --- toxin-antitoxin systems --- toxin activation --- antibacterial agents --- bacterial persistence --- Stenotrophomonas maltophilia --- opportunistic pathogen --- clinical origin --- environmental origin --- biofilm --- antibiotic resistance --- cell wall inhibition --- nucleotide hydrolysis --- uridine diphosphate-N-acetylglucosamine
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This text will provide the most recent knowledge and advances in the area of molecular computing and bioinformatics. Molecular computing and bioinformatics have a close relationship, paying attention to the same object but working towards different orientations. The articles will range from topics such as DNA computing and membrane computing to specific biomedical applications, including drug R&D and disease analysis.
systems biology --- join graph --- hierarchical support vector regression --- transcription factor --- brain storm optimization --- heterogeneous information network embedding --- structural patterns --- gene fusion data --- Panax ginseng --- flowering plant --- geometric arithmetic index --- interspecies transmission --- iron-depleted --- drug discovery --- protein --- protein targeting --- recursively enumerable function --- Mycoplasma hominis --- environmental factor --- Alzheimer’s disease --- absorption --- angiogenesis --- classification --- self-organizing systems --- enzymatic numerical P system --- excretion --- atom-bond connectivity index --- molecular learning --- DNA coding --- phylogeny --- bone formation --- DCL1 --- line graph --- pseudo dinucleotide composition --- load balancing --- K2 --- efflux ratio --- osteogenesis --- distribution --- NanoString Technologies --- RAST server --- 8-bit adder/subtractor --- gene networks --- dihydrouridine --- structure information --- Cartesian product graph --- domain label --- stacking denoising auto-encoder --- DNA computing --- Stenotrophomonas maltophilia --- pattern classification --- stress --- causal direction learning --- machine learning --- adverse drug reaction prediction --- membrane computing --- support vector machine --- Brassica napus --- miRNA biogenesis --- identification of Chinese herbal medicines --- bio-inspired --- toxicity --- protein transduction domain --- RNA --- sequence information --- multiple interaction networks --- in silico --- protein complex --- drug --- low-dimensional representation --- gene coding protein --- amino acid mutation --- Bayesian causal model --- edge detection --- big data --- function prediction --- parallel computing --- resolution free --- Hamming distance --- cascade --- oligopeptide transporter --- DNA barcoding technology --- DNA strand displacement --- protein–protein interaction (PPI) --- biomedical text mining --- bioinformatics --- metabolism --- hypoxia-inducible factor-1? --- nucleotide physicochemical property --- Turing universality --- diabetes mellitus --- chaotic map --- multinetwork integration --- bacterial computing --- lignification --- penalized matrix decomposition --- ensemble classifier --- bacteria and plasmid system --- similarity network --- RNA secondary structure --- avian influenza virus --- evaluating driver partner --- image encryption --- siderophores --- meta-path-based proximity --- P-glycoprotein --- Tianhe-2 --- prostate cancer --- iron acquisition systems --- biochip technology --- gene susceptibility prioritization --- laccase --- DNA --- molecular computing --- microRNA --- clustering --- drug-target interaction prediction --- endoplasmic reticulum
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