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1.
J Eur Acad Dermatol Venereol ; 36(1): 126-132, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34592030

RESUMO

BACKGROUND: In order to successfully treat scabies and to prevent its spread, it is important to identify the factors that can influence the outcome of scabies treatment. OBJECTIVES: This study was designed to evaluate the risk factors associated with treatment resistance scabies during use of an effective topical medication. METHODS: A retrospective cohort study was performed in patients with scabies infestations confirmed by potassium hydroxide (KOH) examinations. Patient characteristics, clinical features and treatment history were collected. The treatment resistance group included patients with persistent scabies infestations for more than 28 days after initiation of antiscabies treatment with 5% permethrin cream. RESULTS: In total, 138 patients with scabies infestations treated between January 2017 and December 2020 were included in this study. Of these, 100 (72.5%) patients were treated successfully, while 38 (27.5%) patients experienced treatment resistance. In the univariable analysis, risk factors for treatment resistance scabies included impaired cognitive function (OR = 2.66, 95% CI, 1.15-6.14), limited mobility (OR = 2.97, 95% CI, 1.30-6.83), inpatient status (vs. outpatient, OR = 3.3, 95% CI, 1.28-8.54), topical steroid use before diagnosis (OR = 3.52, 95% CI, 1.61-7.81), systemic steroid use before diagnosis (OR = 3.57, 95% CI, 1.26-10.34) and a positive KOH exam after the first treatment (OR = 7.25, 95% CI, 3.24-17.11). In the multivariable analysis, limited mobility (OR = 3.46, 95% CI, 1.02-12.11) and topical steroid use before diagnosis (OR = 3.65, 95% CI, 1.41-9.75) were significant predictive factors for treatment resistance scabies. CONCLUSIONS: Scabies patients with limited mobility and topical steroid use before diagnosis are at high risk of treatment resistance. Dermatologists should take these findings into consideration when treating patients with scabies infestations.


Assuntos
Inseticidas , Escabiose , Humanos , Ivermectina , Permetrina , Estudos Retrospectivos , Fatores de Risco , Escabiose/tratamento farmacológico , Escabiose/epidemiologia , Resultado do Tratamento
2.
J Hosp Infect ; 151: 69-78, 2024 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-38740300

RESUMO

BACKGROUND: The healthcare water environment is a potential reservoir of carbapenem-resistant organisms (CROs). AIM: To report the role of the water environment as a reservoir and the infection control measures applied to suppress a prolonged outbreak of Klebsiella pneumoniae carbapenemase-producing Serratia marcescens (KPC-SM) in two intensive care units (ICUs). METHODS: The outbreak occurred in the ICUs of a tertiary hospital from October 2020 to July 2021. Comprehensive patient contact tracing and environmental assessments were conducted, and a case-control study was performed to identify factors associated with the acquisition of KPC-SM. Associations among isolates were assessed via pulsed-field gel electrophoresis (PFGE). Antibiotic usage was analysed. FINDINGS: The outbreak consisted of two waves involving a total of 30 patients with KPC-SM. Multiple environmental cultures identified KPC-SM in a sink, a dirty utility room, and a communal bathroom shared by the ICUs, together with the waste bucket of a continuous renal replacement therapy (CRRT) system. The genetic similarity of the KPC-SM isolates from patients and the environment was confirmed by PFGE. A retrospective review of 30 cases identified that the use of CRRT and antibiotics was associated with acquisition of KPC-SM (P < 0.05). There was a continuous increase in the use of carbapenems; notably, the use of colistin has increased since 2019. CONCLUSION: Our study demonstrates that CRRT systems, along with other hospital water environments, are significant potential sources of resistant micro-organisms, underscoring the necessity of enhancing infection control practices in these areas.


Assuntos
Antibacterianos , Proteínas de Bactérias , Infecção Hospitalar , Surtos de Doenças , Unidades de Terapia Intensiva , Infecções por Serratia , Serratia marcescens , beta-Lactamases , Humanos , Serratia marcescens/genética , Serratia marcescens/efeitos dos fármacos , Serratia marcescens/isolamento & purificação , Serratia marcescens/enzimologia , Infecção Hospitalar/microbiologia , Infecção Hospitalar/epidemiologia , Infecções por Serratia/epidemiologia , Infecções por Serratia/microbiologia , Antibacterianos/farmacologia , Antibacterianos/uso terapêutico , Masculino , Estudos de Casos e Controles , beta-Lactamases/metabolismo , beta-Lactamases/genética , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Feminino , Idoso , Pessoa de Meia-Idade , Estudos Retrospectivos , Centros de Atenção Terciária , Klebsiella pneumoniae/efeitos dos fármacos , Klebsiella pneumoniae/genética , Klebsiella pneumoniae/enzimologia , Klebsiella pneumoniae/isolamento & purificação , Microbiologia da Água , Controle de Infecções/métodos , Idoso de 80 Anos ou mais , Adulto
6.
Eur J Immunogenet ; 29(5): 449-52, 2002 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-12358859

RESUMO

Previously, we prepared two different monoclonal antibodies (mAbs) against human 4-1BB (CD137): an agonistic mAb BBK-1 and an antagonistic mAb BBK-2. In this paper, we describe the molecular cloning of these two mAbs and present comparisons of their amino acid sequences. cDNAs encoding the heavy (H) and light (L) chains of the two mAbs were cloned by screening of cDNA libraries constructed from hybridomas secreting these mAbs. Comparisons of amino acid sequences of the two mAbs showed that, while the constant regions of the H and L chains were identical between the two mAbs, the variable region showed 45% identity in H chains and 48% identity in L chains. This suggests that these two mAbs recognize different epitopes of 4-1BB and may have different effects on the activity of 4-1BB.


Assuntos
Anticorpos Monoclonais/imunologia , Receptores de Fator de Crescimento Neural/imunologia , Receptores do Fator de Necrose Tumoral/imunologia , Sequência de Aminoácidos , Anticorpos Monoclonais/genética , Antígenos CD , Clonagem Molecular , DNA Complementar , Genes de Imunoglobulinas , Humanos , Dados de Sequência Molecular , Receptores de Fator de Crescimento Neural/agonistas , Receptores de Fator de Crescimento Neural/antagonistas & inibidores , Receptores do Fator de Necrose Tumoral/agonistas , Receptores do Fator de Necrose Tumoral/antagonistas & inibidores , Alinhamento de Sequência , Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral
7.
Genes Immun ; 4(8): 564-9, 2003 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-14647196

RESUMO

The gene encoding the natural ligand of murine glucocorticoid-induced tumor necrosis factor receptor (GITR) was cloned and characterized. The putative GITR ligand (GITRL) is composed of 173 amino acids with features resembling those of type II membrane proteins and is 51% identical to the human activation-inducible TNF receptor (AITR) ligand, TL6. Expression of the GITRL is restricted to immature and mature splenic dendritic cells. GITRL binds GITR expressed on HEK 293 cells and triggers NF-kappaB activation. Functional studies reveal that soluble CD8-GITRL prevents CD4+CD25+ regulatory T-cell-mediated suppressive activities.


Assuntos
Proteínas de Transporte/genética , Proteínas de Transporte/metabolismo , Expressão Gênica , Receptores de Fator de Crescimento Neural/metabolismo , Receptores do Fator de Necrose Tumoral/metabolismo , Sequência de Aminoácidos , Animais , Primers do DNA , DNA Complementar/genética , Células Dendríticas/metabolismo , Citometria de Fluxo , Componentes do Gene , Proteína Relacionada a TNFR Induzida por Glucocorticoide , Humanos , Ligantes , Luciferases , Linfócitos/metabolismo , Camundongos , Dados de Sequência Molecular , NF-kappa B/metabolismo , Plasmídeos/genética , Proteínas Recombinantes , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Análise de Sequência de DNA , Fatores Supressores Imunológicos/antagonistas & inibidores , Fatores de Necrose Tumoral
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