Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
1.
Neth J Med ; 77(3): 109-115, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31012428

RESUMO

BACKGROUND: The seasonal influenza epidemic poses a significant burden on hospitals, both in terms of capacity and costs. Beds that are occupied by isolated influenza patients result in hospitals temporary being closed to admissions and elective operations being cancelled. Improving hospital and emergency department (ED) patient flow during the influenza season could solve these problems. Microbiological point-of-care-testing (POCT) could reduce unnecessary patient isolation by providing a positive/negative result before admission, but has not yet broadly been implemented. METHODS: A clinical pathway for patients with acute respiratory tract infection presenting at the ED was implemented, including a PCR-based POCT for influenza, operated by nurses and receptionists. In parallel, a temporary ward equipped with 15 beds for influenza-positive patients was established. In this retrospective observational study, we describe the results of implementing this pathway by comparison with the previous epidemic. RESULTS: Clinical performance of the POCT within the clinical pathway was good with strongly decreased time from ED presentation to sample collection (194 vs 47 min) and time from sample collection to result (1094 vs 62 min). Hospital patient flow was improved by a decreased percentage of admitted influenza-positive patients (91% vs 73%) and shorter length of subsequent stay (median 5.86 vs 4.61 days) compared to the previous influenza epidemic. In addition, 430 patient-days of unnecessary isolation have been prevented within a time span of 18 weeks. Roughly estimated savings were almost 400,000 euros. CONCLUSION: We recommend that hospitals explore possibilities for improving patient flow during an influenza epidemic.


Assuntos
Procedimentos Clínicos/estatística & dados numéricos , Serviço Hospitalar de Emergência/estatística & dados numéricos , Influenza Humana/diagnóstico , Testes Imediatos , Infecções Respiratórias/diagnóstico , Adulto , Idoso , Idoso de 80 Anos ou mais , Epidemias , Feminino , Implementação de Plano de Saúde , Hospitalização/estatística & dados numéricos , Humanos , Influenza Humana/epidemiologia , Masculino , Pessoa de Meia-Idade , Países Baixos/epidemiologia , Estudos Retrospectivos
2.
Circulation ; 113(1): 98-107, 2006 Jan 03.
Artigo em Inglês | MEDLINE | ID: mdl-16365196

RESUMO

BACKGROUND: Cathepsin K (catK), a lysosomal cysteine protease, was identified in a gene-profiling experiment that compared human early plaques, advanced stable plaques, and advanced atherosclerotic plaques containing a thrombus, where it was highly upregulated in advanced stable plaques. METHODS AND RESULTS: To assess the function of catK in atherosclerosis, catK(-/-)/apolipoprotein (apo) E(-/-) mice were generated. At 26 weeks of age, plaque area in the catK(-/-)/apoE(-/-) mice was reduced (41.8%) owing to a decrease in the number of advanced lesions as well as a decrease in individual advanced plaque area. This suggests an important role for catK in atherosclerosis progression. Advanced plaques of catK(-/-)/apoE(-/-) mice showed an increase in collagen content. Medial elastin fibers were less prone to rupture than those of apoE(-/-) mice. Although the relative macrophage content did not differ, individual macrophage size increased. In vitro studies of bone marrow derived-macrophages confirmed this observation. Scavenger receptor-mediated uptake (particularly by CD36) of modified LDL increased in the absence of catK, resulting in an increased macrophage size because of increased cellular storage of cholesterol esters, thereby enlarging the lysosomes. CONCLUSIONS: A deficiency of catK reduces plaque progression and induces plaque fibrosis but aggravates macrophage foam cell formation in atherosclerosis.


Assuntos
Aterosclerose/etiologia , Catepsinas/deficiência , Catepsinas/fisiologia , Fibrose/etiologia , Células Espumosas/patologia , Animais , Apolipoproteínas E/deficiência , Apolipoproteínas E/genética , Aterosclerose/patologia , Antígenos CD36/fisiologia , Catepsina K , Catepsinas/genética , Tamanho Celular , Células Cultivadas , Colágeno/análise , Progressão da Doença , Lipoproteínas LDL/metabolismo , Macrófagos/patologia , Camundongos , Camundongos Knockout
3.
Ned Tijdschr Geneeskd ; 160: D107, 2016.
Artigo em Holandês | MEDLINE | ID: mdl-27378260

RESUMO

BACKGROUND: Infection with hepatitis E virus genotype 3 (HEV3) is an emerging zoonosis in the industrialized world. The infection usually proceeds asymptomatically. Extrahepatic sequelae including neurological symptoms have been described. CASE DESCRIPTION: A 52-year-old man presented at the emergency department with pain, muscle weakness and sensory disorders in both shoulders and arms. He was found to have bilateral neuralgic amyotrophy accompanying an HEV3 infection. CONCLUSION: An HEV3 infection can have neurological sequelae, but very little is known about its incidence and spectrum of symptoms.


Assuntos
Neurite do Plexo Braquial/virologia , Hepatite E/diagnóstico , Animais , Neurite do Plexo Braquial/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade
4.
J Pathol ; 210(3): 334-43, 2006 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-16972305

RESUMO

Recently, we showed that cathepsin K deficiency reduces atherosclerotic plaque progression, induces plaque fibrosis, but aggravates macrophage foam cell formation in the ApoE -/- mouse. To obtain more insight into the molecular mechanisms by which cathepsin K disruption evokes the observed phenotypic changes, we used microarray analysis for gene expression profiling of aortic arches of CatK -/-/ApoE -/- and ApoE -/- mice on a mouse oligo microarray. Out of 20 280 reporters, 444 were significantly differentially expressed (p-value of < 0.05, fold change of > or = 1.4 or < or = - 1.4, and intensity value of > 2.5 times background in at least one channel). Ingenuity Pathway Analysis and GenMAPP revealed upregulation of genes involved in lipid uptake, trafficking, and intracellular storage, including caveolin - 1, - 2, - 3 and CD36, and profibrotic genes involved in transforming growth factor beta (TGFbeta) signalling, including TGFbeta2, latent TGFbeta binding protein-1 (LTBP1), and secreted protein, acidic and rich in cysteine (SPARC), in CatK -/-/ApoE -/- mice. Differential gene expression was confirmed at the mRNA and protein levels. In vitro modified low density lipoprotein (LDL) uptake assays, using bone marrow derived macrophages preincubated with caveolae and scavenger receptor inhibitors, confirmed the importance of caveolins and CD36 in increasing modified LDL uptake in the absence of cathepsin K. In conclusion, we suggest that cathepsin K deficiency alters plaque phenotype not only by decreasing proteolytic activity, but also by stimulating TGFbeta signalling. Besides this profibrotic effect, cathepsin K deficiency has a lipogenic effect owing to increased lipid uptake mediated by CD36 and caveolins.


Assuntos
Aterosclerose/genética , Catepsinas/deficiência , Perfilação da Expressão Gênica/métodos , Animais , Apolipoproteínas E/genética , Antígenos CD36/genética , Catepsina K , Catepsinas/genética , Caveolinas/genética , Fibrose/genética , Regulação da Expressão Gênica/genética , Imuno-Histoquímica/métodos , Proteínas de Ligação a TGF-beta Latente/genética , Metabolismo dos Lipídeos/genética , Lipoproteínas LDL/metabolismo , Macrófagos/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Análise de Sequência com Séries de Oligonucleotídeos/métodos , Fenótipo , RNA Mensageiro/análise , Fator de Crescimento Transformador beta/genética , Regulação para Cima/genética
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA