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1.
Ecotoxicol Environ Saf ; 187: 109866, 2020 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-31677568

RESUMO

The combined effects of cobalt (Co) and copper (Cu) in their toxicity to plants is poorly studied although these two metals co-exist commonly in soil. In this study, a hydroponic experiment was carried out to investigate the effect of longer exposure of two barley genotypes differing in Co tolerance to the combined Co and Cu stress. The results confirmed the previous findings that Co accumulation in plant tissues was reduced by Cu presence, while Cu accumulation was stimulated by Co presence. Moreover, both single and combined treatments of Co and Cu reduced the mineral (Mn, Zn and K) uptake. Co and Cu applied alone or in combination at rate of 50 µM resulted in the significant reduction of plant growth and increase of oxidative stress (ROS and MDA), and meanwhile the capacity of scavenging active oxygen species (AOS) was enhanced, reflected by increased phytochelatin (PC) and glutathione (GSH and GSSG) content, as well as expression of the related genes (HvPCS1 and HvGR1). Yan66, a Co tolerant genotype was less affected in oxidative stress, and had higher AOS scavenging capacity in comparison with Ea52, a Co sensitive one. Among three HvSOD isoforms, only HvFeSOD expression was up-regulated in the combined treatment relative to control as well as the treatment of Co or Cu alone, while HvCuZnSOD and HvMnSOD were down-regulated and unaffected, respectively. In addition, the expressions of metal transporter genes (HvHMA2, HvHMA3 and HvHMA5) varied with genotype and metal treatments, with the extent being greater in Yan66 on the whole. The results suggest that upon longer exposure to the combined stress of Co and Cu, the greater phyto-toxicity than each element alone is associated with more Cu accumulation stimulated by Co and that, the higher regulation of transporter genes observed in Yan66 could in part explain for its higher metal tolerance ability.


Assuntos
Cobalto/toxicidade , Cobre/toxicidade , Resistência a Medicamentos/genética , Hordeum/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Poluentes do Solo/toxicidade , Interações de Medicamentos , Genótipo , Glutationa/metabolismo , Hordeum/genética , Hordeum/crescimento & desenvolvimento , Hidroponia , Fitoquelatinas/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Especificidade da Espécie
2.
Ecotoxicol Environ Saf ; 180: 234-241, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31096127

RESUMO

Cobalt (Co) commonly co-exists with copper (Cu) in natural soils, but the information about their combined effects on plants is poorly available. In this study, we hydroponically investigated the combined effects of Co and Cu on two barley genotypes differing in Co toxicity tolerance to reveal the interaction pattern of these two metals. The results showed that single treatment of Co or Cu at the dose of 100 µM led to a significant decrease of growth and photosynthetic rate, and a significant increase of lipid peroxidation, ROS radicals as well as anti-oxidative enzyme (SOD, CAT and GR) activities and glutathione content, with the extent of effect being less in Yan66 than Ea52. The combined treatment of Co and Cu alleviated the toxicity of both metals in comparison with each metal treatment alone, as reflected by improved growth and photosynthesis, and much slight oxidative stress. The alleviation of metal toxicity upon combined treatment is mainly attributed to a drastic reduction of Co uptake and its translocation from roots to shoots. It may be suggested that interaction of Co and Cu on their uptake and movement in plants is antagonistic.


Assuntos
Cobalto/toxicidade , Cobre/toxicidade , Hordeum/efeitos dos fármacos , Poluentes do Solo/toxicidade , Antioxidantes/metabolismo , Interações de Medicamentos , Glutationa/metabolismo , Hordeum/enzimologia , Hordeum/metabolismo , Peroxidação de Lipídeos , Estresse Oxidativo/efeitos dos fármacos , Fotossíntese/efeitos dos fármacos
3.
FASEB J ; 33(2): 2910-2927, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30332299

RESUMO

We previously demonstrated that membrane type 1 (MT1) matrix metalloproteinase (MMP) was up-regulated in the hippocampus of the model of transgenic mice bearing 5 familial mutations on human amyloid precursor protein (APP) and presenilin 1 of Alzheimer disease (AD), and that the proteinase increased the levels of amyloid ß peptide (Aß) and its APP C-terminal fragment of 99 aa in a heterologous cell system. Here we provide further evidence that MT1-MMP interacts with APP and promotes amyloidogenesis in a proteolytic-dependent manner in Swedish APP-expressing human embryonic kidney 293 (HEKswe) cells. MT1-MMP-mediated processing of APP releases a soluble APP fragment, sAPP95. This process partly requires the activation of endogenous MMP-2 but is independent of ß-site APP cleaving enzyme 1 (BACE-1) or α-secretase activities. In contrast, MT1-MMP-mediated increase of Aß levels involved BACE-1 activity and was inhibited by tissue inhibitor of MMP-2, a natural inhibitor of both MT1-MMP and MMP-2. Interestingly, near abolishment of basal Aß production upon BACE-1 inhibition was rescued by MT1-MMP, indicating that the latter could mimic ß-secretase-like activity. Moreover, MT1-MMP promoted APP/Aß localization in endosomes, where Aß production mainly occurs. These data unveil new mechanistic insights to support the proamyloidogenic role of MT1-MMP based on APP processing and trafficking, and reinforce the idea that this proteinase may become a new potential therapeutic target in AD.-Paumier, J.-M., Py, N. A., González, L. G., Bernard, A., Stephan, D., Louis, L., Checler, F., Khrestchatisky, M., Baranger, K., Rivera, S. Proamyloidogenic effects of membrane type 1 matrix metalloproteinase involve MMP-2 and BACE-1 activities, and the modulation of APP trafficking.


Assuntos
Secretases da Proteína Precursora do Amiloide/metabolismo , Precursor de Proteína beta-Amiloide/metabolismo , Amiloide/química , Ácido Aspártico Endopeptidases/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Metaloproteinase 14 da Matriz/farmacologia , Metaloproteinase 2 da Matriz/metabolismo , Doença de Alzheimer , Secretases da Proteína Precursora do Amiloide/genética , Precursor de Proteína beta-Amiloide/genética , Animais , Ácido Aspártico Endopeptidases/genética , Células HEK293 , Humanos , Metaloproteinase 2 da Matriz/genética , Camundongos , Camundongos Transgênicos , Transporte Proteico
4.
Sci Rep ; 8(1): 10706, 2018 Jul 16.
Artigo em Inglês | MEDLINE | ID: mdl-30013052

RESUMO

Uropathogenic Escherichia coli (UPEC), the most prevalent bacteria isolated in urinary tract infections (UTI), is now frequently resistant to antibiotics used to treat this pathology. The antibacterial properties of cranberry and propolis could reduce the frequency of UTIs and thus the use of antibiotics, helping in the fight against the emergence of antibiotic resistance. Transcriptomic profiles of a clinical UPEC strain exposed to cranberry proanthocyanidins alone (190 µg/mL), propolis alone (102.4 µg/mL) and a combination of both were determined. Cranberry alone, but more so cranberry + propolis combined, modified the expression of genes involved in different essential pathways: down-expression of genes involved in adhesion, motility, and biofilm formation, and up-regulation of genes involved in iron metabolism and stress response. Phenotypic assays confirmed the decrease of motility (swarming and swimming) and biofilm formation (early formation and formed biofilm). This study showed for the first time that propolis potentiated the effect of cranberry proanthocyanidins on adhesion, motility, biofilm formation, iron metabolism and stress response of UPEC. Cranberry + propolis treatment could represent an interesting new strategy to prevent recurrent UTI.


Assuntos
Regulação Bacteriana da Expressão Gênica/efeitos dos fármacos , Extratos Vegetais/farmacologia , Própole/farmacologia , Escherichia coli Uropatogênica/patogenicidade , Vaccinium macrocarpon/química , Biofilmes/efeitos dos fármacos , Sinergismo Farmacológico , Quimioterapia Combinada/métodos , Infecções por Escherichia coli/tratamento farmacológico , Infecções por Escherichia coli/microbiologia , Infecções por Escherichia coli/urina , Proteínas de Escherichia coli/genética , Frutas/química , Perfilação da Expressão Gênica , Humanos , Extratos Vegetais/química , Extratos Vegetais/uso terapêutico , Proantocianidinas/farmacologia , Proantocianidinas/uso terapêutico , Própole/uso terapêutico , Infecções Urinárias/tratamento farmacológico , Infecções Urinárias/microbiologia , Infecções Urinárias/urina , Urina/microbiologia , Escherichia coli Uropatogênica/efeitos dos fármacos , Escherichia coli Uropatogênica/genética , Escherichia coli Uropatogênica/isolamento & purificação , Virulência/efeitos dos fármacos , Virulência/genética , Fatores de Virulência/genética
5.
J Infect Dis ; 216(6): 771-775, 2017 09 15.
Artigo em Inglês | MEDLINE | ID: mdl-28934429

RESUMO

Cerebral malaria, a reversible encephalopathy affecting young children, is a medical emergency requiring urgent clinical assessment and treatment. We performed a whole-transcriptomic analysis of blood samples from Malian children with cerebral or uncomplicated malaria. We focused on transcripts from pathways for which dysfunction has been associated with neurodegenerative disorders. We found that SNCA, SIAH2, UBB, HSPA1A, TUBB2A, and PINK1 were upregulated (fold-increases, ≥2.6), whereas UBD and PSMC5 were downregulated (fold-decreases, ≤4.39) in children with cerebral malaria, compared with those with uncomplicated malaria. These findings provide the first evidence for pathogenic mechanisms common to human cerebral malaria and neurodegenerative disorders.


Assuntos
Malária Cerebral/genética , Malária Falciparum/genética , Doenças Neurodegenerativas/genética , ATPases Associadas a Diversas Atividades Celulares , Proteínas Adaptadoras de Transdução de Sinal/genética , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Criança , Pré-Escolar , Regulação para Baixo , Feminino , Perfilação da Expressão Gênica , Proteínas de Choque Térmico HSP70/genética , Proteínas de Choque Térmico HSP70/metabolismo , Humanos , Proteínas com Domínio LIM/genética , Proteínas com Domínio LIM/metabolismo , Leucócitos Mononucleares/parasitologia , Malária Cerebral/diagnóstico , Malária Falciparum/diagnóstico , Masculino , Doenças Neurodegenerativas/diagnóstico , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Plasmodium falciparum , Estudos Prospectivos , Complexo de Endopeptidases do Proteassoma , Proteínas Quinases/genética , Proteínas Quinases/metabolismo , Reprodutibilidade dos Testes , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Tubulina (Proteína)/genética , Tubulina (Proteína)/metabolismo , Ubiquitina/genética , Ubiquitina/metabolismo , Ubiquitina-Proteína Ligases/genética , Ubiquitina-Proteína Ligases/metabolismo , Ubiquitinas/genética , Ubiquitinas/metabolismo , Regulação para Cima , alfa-Sinucleína/genética , alfa-Sinucleína/metabolismo
6.
Sci Rep ; 7(1): 8277, 2017 08 15.
Artigo em Inglês | MEDLINE | ID: mdl-28811647

RESUMO

Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported that sirtuin-1 (SIRT1) deficiency drives accelerated senescence and dysfunction of endothelial colony-forming cells (ECFC) in PT neonates. Because preterm birth (PT) increases the risk for cardiovascular diseases during neonatal period as well as at adulthood, we hypothesized that SIRT1 deficiency could control the biogenesis of microparticles as part of a senescence-associated secretory phenotype (SASP) of PT-ECFC and investigated the related molecular mechanisms. Compared to control ECFC, PT-ECFC displayed a SASP associated with increased release of endothelial microparticles (EMP), mediating a paracrine induction of senescence in naïve endothelial cells. SIRT1 level inversely correlated with EMP release and drives PT-ECFC vesiculation. Global transcriptomic analysis revealed changes in stress response pathways, specifically the MAPK pathway. We delineate a new epigenetic mechanism by which SIRT1 deficiency regulates MKK6/p38MAPK/Hsp27 pathway to promote EMP biogenesis in senescent ECFC. These findings deepen our understanding of the role of ECFC senescence in the disruption of endothelial homeostasis and provide potential new targets towards the control of cardiovascular risk in individuals born preterm.


Assuntos
Micropartículas Derivadas de Células/metabolismo , Senescência Celular , Células Progenitoras Endoteliais/metabolismo , Epigênese Genética , Regulação da Expressão Gênica , MAP Quinase Quinase 6/genética , Nascimento Prematuro , Sirtuína 1/metabolismo , Células Endoteliais/metabolismo , Deleção de Genes , Perfilação da Expressão Gênica , Humanos , Recém-Nascido , Modelos Biológicos , Comunicação Parácrina , Transdução de Sinais , Sirtuína 1/genética , Transcriptoma , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
7.
Int J Parasitol ; 47(13): 823-830, 2017 11.
Artigo em Inglês | MEDLINE | ID: mdl-28739251

RESUMO

MicroRNAs (miRNAs) are short, non-coding RNAs that repress the translation of target gene transcripts. They have been implicated in various activities such as cell proliferation, survival, differentiation, migration and metabolism. We report here the first known miRNome and transcriptome analysis of human livers displaying advanced fibrosis due to Schistosoma japonicum infection. We present evidence that hsa-miR-150-5p, hsa-miR-10a-5p, hsa-miR-199a-3p, hsa-miR-4521, hsa-miR-222/221, hsa-miR-663b and hsa-miR-143-3p (associated without correction) play an important role in hepatic fibrosis by acting on metabolism, organization of the extracellular matrix proteins, lipid mobilization and limitation of oxidative damage stress.


Assuntos
Cirrose Hepática/genética , MicroRNAs/fisiologia , Esquistossomose Japônica/patologia , Adulto , Animais , Estudos de Casos e Controles , Regulação para Baixo , Feminino , Expressão Gênica , Humanos , Fígado/química , Fígado/patologia , Cirrose Hepática/etiologia , Cirrose Hepática/parasitologia , Masculino , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase em Tempo Real , Transcrição Reversa , Schistosoma japonicum/fisiologia , Esquistossomose Japônica/complicações , Esquistossomose Japônica/genética , Regulação para Cima , Adulto Jovem
8.
Clin Infect Dis ; 65(7): 1103-1111, 2017 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-28575239

RESUMO

Background: Chagas disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America and affects 10 million people worldwide. Approximately 12000 deaths attributable to Chagas disease occur annually due to chronic Chagas disease cardiomyopathy (CCC), an inflammatory cardiomyopathy presenting with heart failure and arrythmia; 30% of infected subjects develop CCC years after infection. Genetic mechanisms play a role in differential progression to CCC, but little is known about the role of epigenetic modifications in pathological gene expression patterns in CCC patients' myocardium. DNA methylation is the most common modification in the mammalian genome. Methods: We investigated the impact of genome-wide cardiac DNA methylation on global gene expression in myocardial samples from end-stage CCC patients, compared to control samples from organ donors. Results: In total, 4720 genes were differentially methylated between CCC patients and controls, of which 399 were also differentially expressed. Several of them were related to heart function or to the immune response and had methylation sites in their promoter region. Reporter gene and in silico transcription factor binding analyses indicated promoter methylation modified expression of key genes. Among those, we found potassium channel genes KCNA4 and KCNIP4, involved in electrical conduction and arrythmia, SMOC2, involved in matrix remodeling, as well as enkephalin and RUNX3, potentially involved in the increased T-helper 1 cytokine-mediated inflammatory damage in heart. Conclusions: Results support that DNA methylation plays a role in the regulation of expression of pathogenically relevant genes in CCC myocardium, and identify novel potential disease pathways and therapeutic targets in CCC.


Assuntos
Cardiomiopatia Chagásica/genética , Doença de Chagas/genética , Metilação de DNA/genética , Adolescente , Adulto , Idoso , Cardiomiopatia Chagásica/parasitologia , Doença de Chagas/parasitologia , Doença Crônica , Impressões Digitais de DNA/métodos , Feminino , Expressão Gênica/genética , Coração/parasitologia , Humanos , Inflamação/genética , Inflamação/parasitologia , Masculino , Pessoa de Meia-Idade , Miocárdio/metabolismo , Canais de Potássio/genética , Regiões Promotoras Genéticas/genética , Trypanosoma cruzi/patogenicidade , Adulto Jovem
9.
PLoS One ; 10(6): e0128847, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26086818

RESUMO

Epidemiological studies have associated environmental exposure to polychlorinated biphenyls (PCBs) with an increased risk of type 2 diabetes; however, little is known about the underlying mechanisms involved in the metabolic side-effects of PCB. Our study evaluated the transcriptional effects of a subchronic exposure (gavage at Day 0 and Day 15 with 10 or 100 µmol/Kg bw) to PCB118 (dioxin-like PCB), PCB153 (non-dioxin-like PCB), or an equimolar mixture of PCB118 and PCB153 on various tissues (liver, visceral adipose tissue, muscle, and colon) in mice. Our results showed that a short-term exposure to PCB118 and/or PCB153 enhanced circulating triglyceride levels but did not affect glycemia. Among the studied tissues, we did not observe any modification of the expression of inflammation-related genes, such as cytokines or chemokines. The main transcriptional effects were observed in visceral adipose and liver tissues. We found a downregulation of lipin1 and glut4 expression in these two target organs. In adipose tissue, we also showed a downregulation of Agpat2, Slc25a1, and Fasn. All of these genes are involved in lipid metabolism and insulin resistance. In muscles, we observed an induction of CnR1 and Foxo3 expression, which may be partly involved in PCB metabolic effects. In summary, our results suggest that lipin1 and glut4, notably in adipose tissue, are the main targeted genes in PCB-induced metabolic disorders, however, further studies are required to fully elucidate the mechanisms involved.


Assuntos
Tecido Adiposo/efeitos dos fármacos , Colo/efeitos dos fármacos , Transportador de Glucose Tipo 4/efeitos dos fármacos , Fígado/efeitos dos fármacos , Doenças Metabólicas/induzido quimicamente , Músculo Esquelético/efeitos dos fármacos , Proteínas Nucleares/efeitos dos fármacos , Fosfatidato Fosfatase/efeitos dos fármacos , Bifenilos Policlorados/efeitos adversos , Tecido Adiposo/metabolismo , Animais , Glicemia/efeitos dos fármacos , Colo/metabolismo , Relação Dose-Resposta a Droga , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Músculo Esquelético/metabolismo , Análise de Sequência com Séries de Oligonucleotídeos , Reação em Cadeia da Polimerase em Tempo Real , Transcrição Genética/efeitos dos fármacos , Triglicerídeos/sangue
10.
Am J Med Genet A ; 164A(9): 2344-50, 2014 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-24845202

RESUMO

Waardenburg syndrome (WS) is characterized by an association of pigmentation abnormalities and sensorineural hearing loss. Four types, defined on clinical grounds, have been delineated, but this phenotypic classification correlates imperfectly with known molecular anomalies. SOX10 mutations have been found in patients with type II and type IV WS (i.e., with Hirschsprung disease), more complex syndromes, and partial forms of the disease. The phenotype induced by SOX10 mutations is highly variable and, except for the neurological forms of the disease, no genotype-phenotype correlation has been characterized to date. There is no mutation hotspot in SOX10 and most cases are sporadic, making it particularly difficult to correlate the phenotypic and genetic variability. This study reports on three independent families with SOX10 mutations predicted to result in the same missense mutation at the protein level (p.Met112Ile), offering a rare opportunity to improve our understanding of the mechanisms underlying phenotypic variability. The pigmentation defects of these patients are very similar, and the neurological symptoms showed a somewhat similar evolution over time, indicating a potential partial genotype-phenotype correlation. However, variability in gastrointestinal symptoms suggests that other genetic factors contribute to the expression of these phenotypes. No correlation between the rs2435357 polymorphism of RET and the expression of Hirschsprung disease was found. In addition, one of the patients has esophageal achalasia, which has rarely been described in WS.


Assuntos
Mutação/genética , Polimorfismo de Nucleotídeo Único/genética , Fatores de Transcrição SOXE/genética , Síndrome de Waardenburg/genética , Síndrome de Waardenburg/patologia , Adolescente , Adulto , Criança , Pré-Escolar , Família , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Pessoa de Meia-Idade , Linhagem , Fenótipo
11.
PLoS One ; 8(12): e82702, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24358217

RESUMO

BACKGROUND: The control of gene expression in the course of chronic kidney disease (CKD) is not well addressed. Alternative splicing is a common way to increase complexity of proteins. More than 90% of human transcripts are alternatively spliced. We hypothesised that CKD can induce modification of the alternative splicing machinery. METHODS: During mutation screening in autosomal dominant polycystic kidney disease, we identified in mononuclear cells (PBMC), an alternative splicing event on the exon 30 of PKD1 gene, the gene implicated in this disease. This alternative splice variant was not correlated with the cystic disease but with CKD. To confirm the association between this variant and CKD, a monocentric clinical study was performed with 3 different groups according to their kidney function (CKD5D, CKD3-5 and normal kidney function). An exon microarray approach was used to highlight splicing events in whole human genome in a normal cell model (fibroblasts) incubated with uremic serum. Alternative splicing variants identified were confirmed by RT-PCR. RESULTS: The splicing variant of the exon 30 of PKD1 was more frequent in PBMCs from patients with CKD compared to control. With the microarray approach, despite the analysis of more than 230 000 probes, we identified 36 genes with an abnormal splicing index evocating splicing event in fibroblasts exposed to uremic serum. Only one abnormal splicing event in one gene, ADH1B, was confirmed by RT-PCR. CONCLUSION: We observed two alternative spliced genes in two different cell types associated with CKD. Alternative splicing could play a role in the control of gene expression during CKD but it does not seem to be a major mechanism.


Assuntos
Processamento Alternativo/fisiologia , Regulação da Expressão Gênica , Uremia/genética , Idoso , Estudos de Casos e Controles , Células Cultivadas , Feminino , Perfilação da Expressão Gênica , Humanos , Masculino , Análise em Microsséries , Pessoa de Meia-Idade , Insuficiência Renal Crônica/genética , Canais de Cátion TRPP/genética
12.
Respir Res ; 8: 11, 2007 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-17302979

RESUMO

BACKGROUND: Limited data are available concerning patients admitted to the intensive care unit (ICU) for severe haemoptysis. We reviewed a large series of patients managed in a uniform way to describe the clinical spectrum and outcome of haemoptysis in this setting, and better define the indications for bronchial artery embolisation (BAE). METHODS: A retrospective chart review of 196 patients referred for severe haemoptysis to a respiratory intermediate care ward and ICU between January 1999 and December 2001. A follow-up by telephone interview or a visit. RESULTS: Patients (148 males) were aged 51 (+/- sd, 16) years, with a median cumulated amount of bleeding averaging 200 ml on admission. Bronchiectasis, lung cancer, tuberculosis and mycetoma were the main underlying causes. In 21 patients (11%), no cause was identified. A first-line bronchial arteriography was attempted in 147 patients (75%), whereas 46 (23%) received conservative treatment. Patients who underwent BAE had a higher respiratory rate, greater amount of bleeding, persistent bloody sputum and/or evidence of active bleeding on fiberoptic bronchoscopy. When completed (n = 131/147), BAE controlled haemoptysis in 80% of patients, both in the short and long (> 30 days) terms. Surgery was mostly performed when bronchial arteriography had failed and/or bleeding recurred early after completed BAE. Bleeding was controlled by conservative measures alone in 44 patients. The ICU mortality rate was low (4%). CONCLUSION: Patients with evidence of more severe or persistent haemoptysis were more likely to receive BAE rather than conservative management. The procedure was effective and safe in most patients with severe haemoptysis, and surgery was mostly reserved to failure of arteriography and/or early recurrences after BAE.


Assuntos
Cuidados Críticos/métodos , Hemoptise/diagnóstico , Hemoptise/terapia , Angiografia , Artérias Brônquicas/diagnóstico por imagem , Artérias Brônquicas/cirurgia , Embolização Terapêutica/métodos , Seguimentos , França , Humanos , Unidades de Terapia Intensiva , Tempo de Internação , Masculino , Pessoa de Meia-Idade , Encaminhamento e Consulta , Estudos Retrospectivos , Resultado do Tratamento
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