26 research outputs found

    Mitigating intensive care unit noise: Design-led modeling solutions, calculated acoustic outcomes, and cost implications

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    Objectives, Purpose, or Aim: The study aimed to decrease noise levels in the ICU, anticipated to have adverse effects on both patients and staff, by implementing enhancements in acoustic design. Background: Recognizing ICU noise as a significant disruptor of sleep and a potential hindrance to patient recovery, this study was conducted at a 40-bed ICU in Fiona Stanley Hospital in Perth, Australia. Methods: A comprehensive mixed-methods approach was employed, encompassing surveys, site analysis, and acoustic measurements. Survey data highlighted the importance of patient sleep quality, emphasizing the negative impact of noise on work performance, patient connection, and job satisfaction. Room acoustics analysis revealed noise levels ranging from 60 to 90 dB(A) in the presence of patients, surpassing sleep disruption criteria. Results: Utilizing an iterative 3D design modeling process, the study simulated significant acoustic treatment upgrades. The design integrated effective acoustic treatments within patient rooms, aiming to reduce noise levels and minimize transmission to adjacent areas. Rigorous evaluation using industry-standard acoustic software highlights the design’s efficacy in reducing noise transmission in particular. Additionally, cost implications were examined, comparing standard ICU construction with acoustically treated options for new construction and refurbishment projects. Conclusions: This study provides valuable insights into design-based solutions for addressing noise-related challenges in the ICU. While the focus is on improving the acoustic environment by reducing noise levels and minimizing transmission to adjacent areas. It is important to clarify that direct measurements of patient outcomes were not conducted. The potential impact of these solutions on health outcomes, particularly sleep quality, remains a crucial aspect for consideration

    Differences in genotype and virulence among four multidrug-resistant <i>Streptococcus pneumoniae</i> isolates belonging to the PMEN1 clone

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    We report on the comparative genomics and characterization of the virulence phenotypes of four &lt;i&gt;S. pneumoniae&lt;/i&gt; strains that belong to the multidrug resistant clone PMEN1 (Spain&lt;sup&gt;23F&lt;/sup&gt; ST81). Strains SV35-T23 and SV36-T3 were recovered in 1996 from the nasopharynx of patients at an AIDS hospice in New York. Strain SV36-T3 expressed capsule type 3 which is unusual for this clone and represents the product of an in vivo capsular switch event. A third PMEN1 isolate - PN4595-T23 - was recovered in 1996 from the nasopharynx of a child attending day care in Portugal, and a fourth strain - ATCC700669 - was originally isolated from a patient with pneumococcal disease in Spain in 1984. We compared the genomes among four PMEN1 strains and 47 previously sequenced pneumococcal isolates for gene possession differences and allelic variations within core genes. In contrast to the 47 strains - representing a variety of clonal types - the four PMEN1 strains grouped closely together, demonstrating high genomic conservation within this lineage relative to the rest of the species. In the four PMEN1 strains allelic and gene possession differences were clustered into 18 genomic regions including the capsule, the blp bacteriocins, erythromycin resistance, the MM1-2008 prophage and multiple cell wall anchored proteins. In spite of their genomic similarity, the high resolution chinchilla model was able to detect variations in virulence properties of the PMEN1 strains highlighting how small genic or allelic variation can lead to significant changes in pathogenicity and making this set of strains ideal for the identification of novel virulence determinant

    Des Forêts pour le Nouveau Millénaire - DES FORÊTS À GÉRER DANS L’INTÉRÊT DES GENS ET DE LA NATURE

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    LA FAÇON DONT LES FORÊTS SONT PERÇUES ET LEURS UTILISATIONS ONT BEAUCOUP CHANGÉ AU COURS DES DERNIÈRES ANNÉES. LES FORÊTS NE SONT PLUS CONSIDÉRÉES COMME ÉTANT UNIQUEMENT DES SOURCES DE BOIS MAIS DES ÉCOSYSTÈMES COMPLEXES QUI PERMETTENT À DES COMMUNAUTÉS DE SE DÉVELOPPER ET OFFRENT TOUTE UNE GAMME DE PRODUITS ET DE SERVICES ENVIRONNEMENTAUX. ON RECONNAÎT AUJOURD’HUI QUE LES FORÊTS PEUVENT CONTRIBUER AU DÉVELOPPEMENT RURAL ET À LA LUTTE CONTRE LA PAUVRETÉ.Forêt, économie

    Bosques para el Nuevo Milenio - BOSQUES QUE BENEFICIEN A LA GENTE Y SUSTENTEN LA NATURALEZA

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    LAS MANERAS DE PERCIBIR Y USAR LOS BOSQUES HAN CAMBIADO DRAMÁTICAMENTE DURANTE LOS ÚLTIMOS AÑOS. YA NO SE CONSIDERA MÁS A LOS BOSQUES SÓLO COMO UNA FUENTE DE MADERA, SINO COMO ECOSISTEMAS COMPLEJOS QUE SUSTENTAN LAS FORMAS DE VIDA HUMANA Y SUMINISTRAN UNA GAMA DE PRODUCTOS Y SERVICIOS AMBIENTALES. AHORA ES AMPLIAMENTE RECONOCIDO QUE LOS BOSQUES PUEDEN CONTRIBUIR AL DESARROLLO RURAL Y AYUDAN A ALIVIAR LA POBREZA.Forest, economics, livelihoods

    In vivo capsular switch in Streptococcus pneumoniae--analysis by whole genome sequencing.

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    <p>Two multidrug resistant strains of Streptococcus pneumoniae - SV35-T23 (capsular type 23F) and SV36-T3 (capsular type 3) were recovered from the nasopharynx of two adult patients during an outbreak of pneumococcal disease in a New York hospital in 1996. Both strains belonged to the pandemic lineage PMEN1 but they differed strikingly in virulence when tested in the mouse model of IP infection: as few as 1000 CFU of SV36 killed all mice within 24 hours after inoculation while SV35-T23 was avirulent.Whole genome sequencing (WGS) of the two isolates was performed (i) to test if these two isolates belonging to the same clonal type and recovered from an identical epidemiological scenario only differed in their capsular genes? and (ii) to test if the vast difference in virulence between the strains was mostly - or exclusively - due to the type III capsule. WGS demonstrated extensive differences between the two isolates including over 2500 single nucleotide polymorphisms in core genes and also differences in 36 genetic determinants: 25 of which were unique to SV35-T23 and 11 unique to strain SV36-T3. Nineteen of these differences were capsular genes and 9 bacteriocin genes.Using genetic transformation in the laboratory, the capsular region of SV35-T23 was replaced by the type 3 capsular genes from SV36-T3 to generate the recombinant SV35-T3* which was as virulent as the parental strain SV36-T3* in the murine model and the type 3 capsule was the major virulence factor in the chinchilla model as well. On the other hand, a careful comparison of strains SV36-T3 and the laboratory constructed SV35-T3* in the chinchilla model suggested that some additional determinants present in SV36 but not in the laboratory recombinant may also contribute to the progression of middle ear disease. The nature of this determinants remains to be identified.</p

    <em>In Vivo</em> Capsular Switch in <em>Streptococcus pneumoniae</em> – Analysis by Whole Genome Sequencing

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    <div><p>Two multidrug resistant strains of <em>Streptococcus pneumoniae</em> – SV35-T23 (capsular type 23F) and SV36-T3 (capsular type 3) were recovered from the nasopharynx of two adult patients during an outbreak of pneumococcal disease in a New York hospital in 1996. Both strains belonged to the pandemic lineage PMEN1 but they differed strikingly in virulence when tested in the mouse model of IP infection: as few as 1000 CFU of SV36 killed all mice within 24 hours after inoculation while SV35-T23 was avirulent.</p> <p>Whole genome sequencing (WGS) of the two isolates was performed (i) to test if these two isolates belonging to the same clonal type and recovered from an identical epidemiological scenario only differed in their capsular genes? and (ii) to test if the vast difference in virulence between the strains was mostly – or exclusively – due to the type III capsule. WGS demonstrated extensive differences between the two isolates including over 2500 single nucleotide polymorphisms in core genes and also differences in 36 genetic determinants: 25 of which were unique to SV35-T23 and 11 unique to strain SV36-T3. Nineteen of these differences were capsular genes and 9 bacteriocin genes.</p> <p>Using genetic transformation in the laboratory, the capsular region of SV35-T23 was replaced by the type 3 capsular genes from SV36-T3 to generate the recombinant SV35-T3* which was as virulent as the parental strain SV36-T3* in the murine model and the type 3 capsule was the major virulence factor in the chinchilla model as well. On the other hand, a careful comparison of strains SV36-T3 and the laboratory constructed SV35-T3* in the chinchilla model suggested that some additional determinants present in SV36 but not in the laboratory recombinant may also contribute to the progression of middle ear disease. The nature of this determinants remains to be identified.</p> </div
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