Assuntos
COVID-19/patologia , Dermatologia/organização & administração , Linhas Diretas/estatística & dados numéricos , Dermatopatias/patologia , COVID-19/diagnóstico , COVID-19/epidemiologia , COVID-19/psicologia , Fundações/organização & administração , Acessibilidade aos Serviços de Saúde/tendências , Linhas Diretas/tendências , Humanos , Irlanda/epidemiologia , Papel do Profissional de Enfermagem , SARS-CoV-2/genética , Dermatopatias/diagnóstico , Dermatopatias/epidemiologiaRESUMO
Despite progress in diagnosis and treatment, invasive aspergillosis (IA) remains a principal cause of mortality due to infection after allogeneic hematopoietic stem cell transplantation (AHSCT). In order to clarify the course of IA among children receiving an AHSCT before the advent of new drugs such as voriconazole or caspofungin, we retrospectively reviewed the medical records of all proven and probable IA between January 1986 and December 2000. 1) Ten children developed IA after AHSCT, mostly long after transplantation. Overall incidence was 2.7%. Seven of those children experienced 1 or more complications after AHSCT and before IA. Mortality was 90% with a median survival of 23 days (2-90). 2) Five children underwent AHSCT after a previous episode of IA. All patients were treated with systemic antifungal therapy combined with surgery. Median time between IA and AHSCT was 110 days (73-370). Two children were diagnosed with IA relapse after transplantation. One child was cured while the other died of IA and AHSCT complications. AHSCT could be considered even in the setting of previous IA, but established strategies implementing newer less toxic antifungal agents as treatment or prophylaxis in high-risk patients are needed.
Assuntos
Aspergilose/etiologia , Transplante de Células-Tronco Hematopoéticas/efeitos adversos , Adolescente , Aspergilose/prevenção & controle , Aspergilose/terapia , Criança , Pré-Escolar , Humanos , Lactente , Estudos Retrospectivos , Transplante HomólogoAssuntos
Complexo Mycobacterium avium/isolamento & purificação , Infecção por Mycobacterium avium-intracellulare/diagnóstico , Pneumonia Bacteriana/diagnóstico , Tuberculose Pulmonar/diagnóstico , Antituberculosos/uso terapêutico , Diagnóstico Diferencial , Seguimentos , Humanos , Imunocompetência , Lactente , Infecção por Mycobacterium avium-intracellulare/tratamento farmacológico , Infecção por Mycobacterium avium-intracellulare/imunologia , Pneumonia Bacteriana/tratamento farmacológico , Pneumonia Bacteriana/imunologia , Resultado do TratamentoRESUMO
Despite the importance of fibroproliferative lung disorders, no safe and effective therapies exist for reducing the size of the fibroblast population in existing fibrotic lesions. Recent work suggests that therapies that promote fibroblast apoptosis during the repair phase following lung injury may facilitate lung repair by eliminating excess fibrotic tissue. We report here our finding that three soluble fibronectin peptides (RGD, CS-1, and FN-C/H-V) induce apoptosis in lung fibroblasts. Fibroblast susceptibility to these peptides was dose and time dependent, with a maximal effect observed at 96 h (87 +/- 16% [mean +/- SEM] apoptosis). The peptides were able to induce fibroblast apoptosis in fibrin gels, an in vitro model of early fibroproliferative lesions. Fibroblasts were difficult to kill. All three peptides were required for maximal apoptosis of anchored cells. Apoptosis occurred by disruption of adhesion (anoikis). Treatment of fibroblasts with peptides caused proteolysis of pp125FAK, a tyrosine kinase involved in integrin-mediated signaling related to cell survival. These data show that soluble fibronectin peptides trigger nontransformed fibroblast apoptosis in routine culture and in fibrin gels by a mechanism that includes disruption of an integrin-mediated survival signaling pathway. The use of small fibronectin peptides to promote fibroblast apoptosis warrants further study as possible antifibrotic therapy.
