RESUMO
Objective: To evaluate the recognition of acute respiratory infection (ARI) by a pretrained model based on electronic medical records (EMRs). Methods: 38 581 EMRs were obtained from Chongqing University Three Gorges Hospital in December 2021. Bidirectional encoder representation from transformers (BERT) pretrained model was used to identify ARI in EMRs. The results of medical professionals were considered as the gold standard to calculate the sensitivity, specificity, Kappa value, and area under the curve of the receiver operating characteristic (AUC). Results: There were 3 817 EMRs in the test set, with 1 200 ARIs. A total of 1 205 cases were determined as ARI by the model, with a sensitivity of 92.67% (1 112/1 200) and a specificity of 96.45% (2 524/2 617). The model identified ARI with similar accuracy in males and females (AUCs 0.95 and 0.94, respectively), and was more accurate in identifying ARI cases in those aged less than 18 than in adults 18-59 and adults 60 and older (AUCs 0.94, 0.89 and 0.94, respectively). The current model had a better identification of ARIs in outpatient patients than that in hospitalized patients, with AUCs of 0.74 and 0.95, respectively. Conclusion: The use of the BERT pretrained model based on EMRs has a good performance in the recognition of ARI cases, especially for the outpatients and juveniles. It shows a great potential to be applied to the monitoring of ARI cases in medical institutions.
Assuntos
Registros Eletrônicos de Saúde , Infecções Respiratórias , Adulto , Masculino , Feminino , Humanos , Infecções Respiratórias/diagnóstico , Pacientes AmbulatoriaisRESUMO
BACKGROUND: Both animals and plants respond rapidly to pathogens by inducing the expression of defense-related genes. Whether such an inducible system of innate immunity is present in the model nematode Caenorhabditis elegans is currently an open question. Among conserved signaling pathways important for innate immunity, the Toll pathway is the best characterized. In Drosophila, this pathway also has an essential developmental role. C. elegans possesses structural homologs of components of this pathway, and this observation raises the possibility that a Toll pathway might also function in nematodes to trigger defense mechanisms or to control development. RESULTS: We have generated and characterized deletion mutants for four genes supposed to function in a nematode Toll signaling pathway. These genes are tol-1, trf-1, pik-1, and ikb-1 and are homologous to the Drosophila melanogaster Toll, dTraf, pelle, and cactus genes, respectively. Of these four genes, only tol-1 is required for nematode development. None of them are important for the resistance of C. elegans to a number of pathogens. On the other hand, C. elegans is capable of distinguishing different bacterial species and has a tendency to avoid certain pathogens, including Serratia marcescens. The tol-1 mutants are defective in their avoidance of pathogenic S. marcescens, although other chemosensory behaviors are wild type. CONCLUSIONS: In C. elegans, tol-1 is important for development and pathogen recognition, as is Toll in Drosophila, but remarkably for the latter rôle, it functions in the context of a behavioral mechanism that keeps worms away from potential danger.
Assuntos
Comportamento Animal/fisiologia , Proteínas de Caenorhabditis elegans , Caenorhabditis elegans/fisiologia , Proteínas de Drosophila , Proteínas de Helminto/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Actinomycetales/patogenicidade , Sequência de Aminoácidos , Animais , Ascomicetos/patogenicidade , Sequência de Bases , Caenorhabditis elegans/microbiologia , Sequência Conservada , Proteínas de Ligação a DNA , Genes de Helmintos , Genes Letais , Proteínas de Helminto/genética , Imunidade Inata , Fungos Mitospóricos/patogenicidade , Dados de Sequência Molecular , Proteínas do Tecido Nervoso/genética , Fosfoproteínas , Proteínas Serina-Treonina Quinases , Pseudomonas aeruginosa/patogenicidade , Homologia de Sequência de Aminoácidos , Transdução de SinaisRESUMO
In the past year, a Caenorhabditis elegans-Pseudomonas aeruginosa pathogenesis model has been developed to facilitate the systematic dissection of both host and pathogen genes involved in pathogenic interactions. Analysis of the P. aeruginosa-C. elegans interaction should shed light on the larger question of how organisms interact at the molecular level in antagonistic relationships.
Assuntos
Caenorhabditis elegans/genética , Caenorhabditis elegans/microbiologia , Pseudomonas aeruginosa/genética , Pseudomonas aeruginosa/patogenicidade , Animais , Caenorhabditis elegans/imunologia , Camundongos , Modelos Biológicos , Infecções por Pseudomonas/imunologia , Infecções por Pseudomonas/fisiopatologia , VirulênciaRESUMO
This article introduces some basic concepts of psychiatric risk management and demonstrates how risk management and quality assurance can work together. Risk exposure areas and loss prevention issues identified during a review of 98 psychiatric claims managed from 1976 to 1988 by the Risk Management Foundation of the Harvard Medical Institutions are detailed.
Assuntos
Imperícia , Psiquiatria , Gestão de Riscos , Honorários Médicos , Humanos , Transtornos Mentais/diagnóstico , Transtornos Mentais/terapia , Garantia da Qualidade dos Cuidados de Saúde , Comportamento Sexual , Suicídio , ViolênciaAssuntos
Vacinas Bacterianas/normas , Leptospira/imunologia , Animais , Cricetinae , Leptospira/patogenicidade , Suínos , Vacinação , VirulênciaRESUMO
The controversial issues and numerous regulatory, ethical, financial, and liability risks that must be considered when a healthcare organization evaluates implementation of a program to reuse single-use equipment are discussed. A role for the well-informed intravenous nurse specialist in institutional policy development regarding reuse of infusion equipment is suggested. Numerous resources on this topic are referenced.
Assuntos
Reutilização de Equipamento/normas , Infusões Intravenosas/instrumentação , Infusões Intravenosas/enfermagem , Política Organizacional , Especialidades de Enfermagem/organização & administração , Análise Custo-Benefício , Reutilização de Equipamento/economia , Reutilização de Equipamento/legislação & jurisprudência , Humanos , Infusões Intravenosas/economia , Descrição de Cargo , Responsabilidade Legal , Gestão de Riscos/organização & administração , Gestão da Segurança/organização & administraçãoRESUMO
The Harvard Medical Practice Study of adverse events and professional liability has generated renewed interest in occurrence screening as a risk management strategy. Occurrence screening techniques are applicable to intravenous nursing quality assurance and risk-management programs. This article includes an original set of I.V. therapy screens plus practical implementation suggestions to help I.V. nurses begin screening in their clinical setting.
Assuntos
Hidratação/enfermagem , Garantia da Qualidade dos Cuidados de Saúde , Gestão de Riscos/métodos , Hidratação/efeitos adversos , Hidratação/normas , HumanosRESUMO
We show that a single clinical isolate of the human opportunistic pathogen Pseudomonas aeruginosa (strain PA14), which previously was shown to be pathogenic in mice and plants, also kills Caenorhabditis elegans. The rate of PA14-mediated killing of C. elegans depends on the composition of the agar medium on which PA14 is grown. When PA14 is grown on minimal medium, killing occurs over the course of several days and is referred to as "slow" killing. When PA14 is grown on high-osmolarity medium, killing occurs over the course of several hours and is referred to as "fast" killing. Several lines of evidence, including the fact that heat-killed bacteria are still capable of fast but not slow killing of C. elegans, indicate that fast and slow killing occur by distinct mechanisms. Slow killing involves an infection-like process and correlates with the accumulation of PA14 within worm intestines. Among 10 PA14 virulence-related mutants that had been shown previously to affect pathogenicity in plants and mice, 6 were less effective in killing C. elegans under both fast- and slow-killing conditions, indicating a high degree of commonalty among the P. aeruginosa factors required for pathogenicity in disparate eukaryotic hosts. Thus, we show that a C. elegans pathogenicity model that is genetically tractable from the perspectives of both host and pathogen can be used to model mammalian bacterial pathogenesis.
Assuntos
Caenorhabditis elegans/metabolismo , Pseudomonas aeruginosa/patogenicidade , Virulência/genética , Animais , Caenorhabditis elegans/microbiologia , Divisão Celular , Meios de Cultura/química , Intestinos/microbiologia , Microscopia de Fluorescência , Mutação/genética , Pseudomonas aeruginosa/genéticaRESUMO
We are exploiting the broad host range of the human opportunistic pathogen Pseudomonas aeruginosa strain PA14 to elucidate the molecular basis of bacterial virulence in plants, nematodes, insects and mice. In this report, we characterize the role that two PA14 gene products, MucD and AlgD, play in virulence. MucD is orthologous to the Escherichia coli periplasmic protease and chaperone DegP. DegP homologues are known virulence factors that play a protective role in stress responses in various species. AlgD is an enzyme involved in the biosynthesis of the exopolysaccharide alginate, which is hyperinduced in mucD mutants. A PA14 mucD mutant was significantly impaired in its ability to cause disease in Arabidopsis thaliana and mice and to kill the nematode Caenorhabditis elegans. Moreover, MucD was found to be required for the production of an extracellular toxin involved in C. elegans killing. In contrast, a PA14 algD mutant was not impaired in virulence in plants, nematodes or mice. A mucDalgD double mutant had the same phenotype as the mucD single mutant in the plant and nematode pathogenesis models. However, the mucDalgD double mutant was synergistically reduced in virulence in mice, suggesting that alginate can partially compensate for the loss of MucD function in mouse pathogenesis.
Assuntos
Alginatos/metabolismo , Arabidopsis/microbiologia , Proteínas de Bactérias/metabolismo , Caenorhabditis elegans/microbiologia , Pseudomonas aeruginosa/patogenicidade , Serina Endopeptidases , Animais , Proteínas de Bactérias/genética , Desidrogenases de Carboidrato/genética , Desidrogenases de Carboidrato/metabolismo , Clonagem Molecular , Ácido Glucurônico , Ácidos Hexurônicos , Masculino , Camundongos , Camundongos Endogâmicos AKR , Dados de Sequência Molecular , Mariposas/microbiologia , Mutação , Infecções por Pseudomonas/microbiologia , Pseudomonas aeruginosa/genética , Pseudomonas aeruginosa/metabolismo , Análise de Sequência de DNA , VirulênciaRESUMO
Barley Rar1 is a convergence point in the signaling of resistance to powdery mildew, triggered by multiple race-specific resistance (R) genes. Rar1 is shown to function upstream of H2O2 accumulation in attacked host cells, which precedes localized host cell death. We isolated Rar1 by map-based cloning. The sequence of the deduced 25.5 kDa protein reveals two copies of a 60-amino acid domain, CHORD, conserved in tandem organization in protozoa, plants, and metazoa. CHORD defines a novel eukaryotic Zn2+-binding domain. Silencing of the C. elegans CHORD-containing gene, chp, results in semisterility and embryo lethality, suggesting an essential function of the wild-type gene in nematode development. Our findings indicate that plant R genes have recruited a fundamental cellular control element for signaling of disease resistance and cell death.
Assuntos
Caenorhabditis elegans/fisiologia , Proteínas de Transporte/fisiologia , Hordeum/fisiologia , Proteínas de Plantas , Transdução de Sinais , Zinco , Alelos , Sequência de Aminoácidos , Animais , Sequência de Bases , Caenorhabditis elegans/genética , Caenorhabditis elegans/crescimento & desenvolvimento , Proteínas de Transporte/classificação , Proteínas de Transporte/genética , Morte Celular , Clonagem Molecular , DNA Complementar , Drosophila melanogaster/genética , Células Eucarióticas , Genes de Plantas , Hordeum/genética , Humanos , Peróxido de Hidrogênio/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular , Dados de Sequência Molecular , Mutação , Doenças das Plantas , Splicing de RNA , Homologia de Sequência de Aminoácidos , Toxoplasma/genética , Transcrição GênicaRESUMO
The human opportunistic pathogen Pseudomonas aeruginosa strain PA14 kills Caenorhabditis elegans. Using systematic mutagenesis of PA14 to identify mutants that fail to kill C. elegans and a C. elegans mutant that lacks P-glycoproteins, we identified phenazines, secreted P. aeruginosa pigments, as one of the mediators of killing. Analysis of C. elegans mutants with altered responses to oxidative stress suggests that phenazines exert their toxic effects on C. elegans through the generation of reactive oxygen species. Finally, we show that phenazines and other P. aeruginosa factors required for C. elegans killing are also required for pathogenesis in plants and mice, illustrating that this model tackles the dual challenges of identifying bacterial virulence factors as well as host responses to them.
Assuntos
Caenorhabditis elegans/microbiologia , Pseudomonas aeruginosa/patogenicidade , Subfamília B de Transportador de Cassetes de Ligação de ATP/genética , Fosfatase Alcalina , Animais , Toxinas Bacterianas/toxicidade , Meios de Cultura , Humanos , Camundongos , Modelos Biológicos , Mutagênese , Concentração Osmolar , Fenazinas/metabolismo , Monoéster Fosfórico Hidrolases/genética , Pseudomonas aeruginosa/genética , Fatores de Tempo , VirulênciaRESUMO
We reported recently that the human opportunistic pathogen Pseudomonas aeruginosa strain PA14 kills Caenorhabditis elegans and that many P. aeruginosa virulence factors (genes) required for maximum virulence in mouse pathogenicity are also required for maximum killing of C. elegans. Here we report that among eight P. aeruginosa PA14 TnphoA mutants isolated that exhibited reduced killing of C. elegans, at least five also exhibited reduced virulence in mice. Three of the TnphoA mutants corresponded to the known virulence-related genes lasR, gacA, and lemA. Three of the mutants corresponded to known genes (aefA from Escherichia coli, pstP from Azotobacter vinelandii, and mtrR from Neisseria gonorrhoeae) that had not been shown previously to play a role in pathogenesis, and two of the mutants contained TnphoA inserted into novel sequences. These data indicate that the killing of C. elegans by P. aeruginosa can be exploited to identify novel P. aeruginosa virulence factors important for mammalian pathogenesis.
Assuntos
Caenorhabditis elegans/microbiologia , Infecções por Pseudomonas/fisiopatologia , Pseudomonas aeruginosa/genética , Pseudomonas aeruginosa/patogenicidade , Animais , Arabidopsis/microbiologia , Azotobacter vinelandii/genética , Proteínas de Bactérias/genética , Sequência de Bases , Primers do DNA , Elementos de DNA Transponíveis , Proteínas de Ligação a DNA/genética , Escherichia coli/genética , Genes Reguladores , Teste de Complementação Genética , Humanos , Mamíferos , Camundongos , Dados de Sequência Molecular , Mutagênese Insercional , Neisseria gonorrhoeae/genética , Transativadores/genética , Fatores de Transcrição/genética , Virulência/genéticaRESUMO
We used plants as an in vivo pathogenesis model for the identification of virulence factors of the human opportunistic pathogen Pseudomonas aeruginosa. Nine of nine TnphoA mutant derivatives of P. aeruginosa strain UCBPP-PA14 that were identified in a plant leaf assay for less pathogenic mutants also exhibited significantly reduced pathogenicity in a burned mouse pathogenicity model, suggesting that P. aeruginosa utilizes common strategies to infect both hosts. Seven of these nine mutants contain TnphoA insertions in previously unknown genes. These results demonstrate that an alternative nonvertebrate host of a human bacterial pathogen can be used in an in vivo high throughput screen to identify novel bacterial virulence factors involved in mammalian pathogenesis.
Assuntos
Arabidopsis/microbiologia , Modelos Biológicos , Pseudomonas aeruginosa/patogenicidade , Animais , Evolução Molecular , Masculino , Camundongos , Dados de Sequência Molecular , Mutagênese , Virulência/genéticaRESUMO
By exploiting the ability of Pseudomonas aeruginosa to infect a variety of vertebrate and nonvertebrate hosts, we have developed model systems that use plants and nematodes as adjuncts to mammalian models to help elucidate the molecular basis of P. aeruginosa pathogenesis. Our studies reveal a remarkable degree of conservation in the virulence mechanisms used by P. aeruginosa to infect hosts of divergent evolutionary origins.