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[PMID]:28531196
[Au] Autor:Deng Z; Yang F; Bai Y; He L; Li Q; Wu Y; Luo L; Li H; Ma L; Yang Z; He Y; Cui L
[Ad] Endereço:Department of Cell Biology and Medical Genetics, Kunming Medical University, Kunming, Yunnan Province, China.
[Ti] Título:Co-inheritance of glucose-6-phosphate dehydrogenase deficiency mutations and hemoglobin E in a Kachin population in a malaria-endemic region of Southeast Asia.
[So] Source:PLoS One;12(5):e0177917, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucose-6-phosphate dehydrogenase (G6PD) deficiency and hemoglobin E (HbE, ß26 Glu-Lys) are two common red cell disorders in Southeast Asia. G6PD deficiency produces hemolytic anemia, which can be triggered by certain drugs or infections. HbE is asymptomatic or is manifested as microcytic, minimally hemolytic anemia. The association between G6PD deficiency and HbE is little understood. This study aimed to investigate G6PD deficiency and HbE in a Kachin ethnic group in the China-Myanmar border area. G6PD enzyme activity was measured using a quantitative G6PD assay, G6PD variants genotyped by the SNaPshot assay, and an HbE gene mutation identified by an amplification refractory mutation system and subsequently confirmed by using a reverse dot blot hybridization assay from 100 unrelated individuals in the study area. G6PD enzyme activity ranged from 0.4 to 24.7 U/g Hb, and six males had severe G6PD deficiency (<0.12-1.2 U/g Hb), while six males and 12 females had mild G6PD deficiency (>1.2-4.5 U/g Hb). Among the 24 G6PD-deficient subjects, 22 (92%) had the Mahidol 487G>A mutation (12 male hemizygotes, one female homozygote, and nine female heterozygotes), while the G6PD genotypes in two female subjects were unknown. HbE was identified in 39 subjects (20 males and 19 females), including 15 HbEE (seven males and eight females) and 24 HbAE (13 males and 11 females). Twenty-three subjects co-inherited both G6PD deficiency and HbE (22 with HbAE and one with HbEE). Whereas mean Hb levels were not significantly different between the HbA and HbE groups, G6PD-deficient males had significantly lower Hb levels than G6PD-normal males (P < 0.05, t-test). However, it is noteworthy that two G6PD-deficient hemizygous males with HbAE were severely anemic with Hb levels below 50 g/L. This study revealed high prevalence of co-inheritance of G6PD deficiency with HbAE in the Kachin ethnicity, and a potential interaction of the G6PD Mahidol 487G>A and HbAE in males leading to severe anemia. The presence of 6% males with severe G6PD deficiency raised a major concern in the use of primaquine for radical cure of vivax malaria.
[Mh] Termos MeSH primário: Deficiência de Glucosefosfato Desidrogenase/epidemiologia
Glucosefosfato Desidrogenase/genética
Hemoglobina E/genética
Hemoglobinúria/epidemiologia
Malária/epidemiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Criança
Pré-Escolar
China/epidemiologia
China/etnologia
Comorbidade
Doenças Endêmicas
Feminino
Genótipo
Glucosefosfato Desidrogenase/metabolismo
Deficiência de Glucosefosfato Desidrogenase/etnologia
Hemoglobinúria/etnologia
Seres Humanos
Malária/etnologia
Masculino
Meia-Idade
Mutação
Mianmar/epidemiologia
Mianmar/etnologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9034-61-1 (Hemoglobin E); EC 1.1.1.49 (Glucosephosphate Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171118
[Lr] Data última revisão:
171118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177917


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[PMID]:28438111
[Au] Autor:Navarro MA; Dutra F; Briano C; Romero A; Persiani M; Freedman JC; Morrell E; Beingesser J; Uzal FA
[Ad] Endereço:1 California Animal Health and Food Safety Laboratory System, San Bernardino Branch, University of California, Davis, San Bernardino, CA, USA.
[Ti] Título:Pathology of Naturally Occurring Bacillary Hemoglobinuria in Cattle.
[So] Source:Vet Pathol;54(3):457-466, 2017 May.
[Is] ISSN:1544-2217
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clostridium haemolyticum causes bacillary hemoglobinuria (BH), an infectious and usually fatal disease that occurs mostly in cattle, which is clinically characterized by jaundice, hemoglobinuria, and anemia. The trematode Fasciola hepatica has been commonly reported as the main predisposing factor that triggers this condition. The authors evaluated 20 naturally occurring cases of bovine BH to characterize the pathology and pathogenesis of the disease. Grossly, the most consistent finding was a large, frequently single focus of necrosis surrounded by a red to purple halo, observed most frequently on the parietal surface of the right and left hepatic lobes. Other findings were jaundice, dark-brown discoloration of kidneys, and red urine in the urinary bladder. Microscopically, characteristic lesions were locally extensive, necrotizing hepatitis with thrombosis and numerous intralesional Gram-positive rod-shaped bacteria, and acute renal tubular necrosis. By immunohistochemistry, many hepatocytes outside the necrotic focus in the liver were positive for activated caspase 3, suggesting that those cells were undergoing apoptosis. Ultrastructural evaluation revealed hepatocyte necrosis, hemolysis, and clumps of vegetative and sporulating bacilli within the liver. Polymerase chain reaction for the C. haemolyticum beta toxin gene was positive in randomly selected liver samples. No gross or microscopic lesions indicative of fascioliasis were detected in the liver of any animal, suggesting that other yet undetermined predisposing factors were associated with these cases of BH.
[Mh] Termos MeSH primário: Doenças dos Bovinos/patologia
Infecções por Clostridium/veterinária
Clostridium
Hemoglobinúria/veterinária
[Mh] Termos MeSH secundário: Animais
Apoptose
Bovinos
Doenças dos Bovinos/microbiologia
Infecções por Clostridium/microbiologia
Infecções por Clostridium/patologia
Feminino
Hemoglobinúria/microbiologia
Hemoglobinúria/patologia
Icterícia/veterinária
Rim/patologia
Fígado/patologia
Masculino
Necrose/veterinária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1177/0300985816688945


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[PMID]:28349743
[Au] Autor:Tang KY
[Ad] Endereço:a Accident and Emergency Department , Caritas Medical Centre , Sham Shui Po , Hong Kong.
[Ti] Título:A patient presented with dark brown urine after mothballs powder ingestion.
[So] Source:Clin Toxicol (Phila);55(7):674-675, 2017 Aug.
[Is] ISSN:1556-9519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We report a case who presented with dark brown urine and malaise after mothballs powder ingestion.
[Mh] Termos MeSH primário: Cor
Hemoglobinúria/urina
Hemólise/efeitos dos fármacos
Repelentes de Insetos/envenenamento
Naftalenos/envenenamento
Envenenamento/urina
Tentativa de Suicídio
Urina/química
[Mh] Termos MeSH secundário: Hidratação
Hemoglobinúria/induzido quimicamente
Hemoglobinúria/diagnóstico
Hemoglobinúria/terapia
Seres Humanos
Masculino
Meia-Idade
Envenenamento/diagnóstico
Envenenamento/etiologia
Envenenamento/terapia
Pós
Resultado do Tratamento
Urinálise
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insect Repellents); 0 (Naphthalenes); 0 (Powders); 2166IN72UN (naphthalene)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1080/15563650.2017.1305110


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[PMID]:27613607
[Au] Autor:Barber BE; Grigg MJ; William T; Yeo TW; Anstey NM
[Ad] Endereço:Menzies School of Health Research and Charles Darwin University, PO Box 41096, Casuarina, NT, 0810, Australia. bridget.barber@menzies.edu.au.
[Ti] Título:Intravascular haemolysis with haemoglobinuria in a splenectomized patient with severe Plasmodium knowlesi malaria.
[So] Source:Malar J;15:462, 2016 Sep 09.
[Is] ISSN:1475-2875
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Haemoglobinuria is an uncommon complication of severe malaria, reflecting acute intravascular haemolysis and potentially leading to acute kidney injury. It can occur early in the course of infection as a consequence of a high parasite burden, or may occur following commencement of anti-malarial treatment. Treatment with quinine has been described as a risk factor; however the syndrome may also occur following treatment with intravenous artesunate. In Malaysia, Plasmodium knowlesi is the most common cause of severe malaria, often associated with high parasitaemia. Asplenic patients may be at additional increased risk of intravascular haemolysis. CASE PRESENTATION: A 61 years old asplenic man was admitted to a tertiary referral hospital in Sabah, Malaysia, with severe knowlesi malaria characterized by hyperparasitaemia (7.9 %), jaundice, respiratory distress, metabolic acidosis, and acute kidney injury. He was commenced on intravenous artesunate, but1 day later developed haemoglobinuria, associated with a 22 % reduction in admission haemoglobin. Additional investigations, including a cell-free haemoglobin of 10.2 × 10(5) ng/mL and an undetectable haptoglobin, confirmed intravascular haemolysis. The patient continued on intravenous artesunate for a total of 48 h prior to substitution with artemether-lumefantrine, and made a good recovery with resolution of his haemoglobinuria and improvement of his kidney function by day 3. CONCLUSIONS: An asplenic patient with hyperparasitaemic severe knowlesi malaria developed haemoglobinuria after treatment with intravenous artesunate. There are plausible mechanisms for increased haemolysis with hyperparasitaemia, and following both splenectomy and artesunate. Although in this case the patient made a rapid recovery, knowlesi malaria patients with this unusual complication should be closely monitored for potential deterioration.
[Mh] Termos MeSH primário: Artemisininas/efeitos adversos
Hemoglobinúria/induzido quimicamente
Hemólise/efeitos dos fármacos
Malária/complicações
Malária/parasitologia
Plasmodium knowlesi/isolamento & purificação
Esplenectomia
[Mh] Termos MeSH secundário: Artemisininas/administração & dosagem
Hemoglobinúria/patologia
Seres Humanos
Malária/tratamento farmacológico
Malásia
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Artemisinins); 60W3249T9M (artesunate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160911
[St] Status:MEDLINE
[do] DOI:10.1186/s12936-016-1514-0


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[PMID]:27568864
[Au] Autor:Mevorach D; Reiner I; Grau A; Ilan U; Berkun Y; Ta-Shma A; Elpeleg O; Shorer Z; Edvardson S; Tabib A
[Ad] Endereço:Rheumatology Research Center and Department of Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
[Ti] Título:Therapy with eculizumab for patients with CD59 p.Cys89Tyr mutation.
[So] Source:Ann Neurol;80(5):708-717, 2016 Nov.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The objective of this work was to report on the outcome of eculizumab treatment in pediatric patients with recurrent acute predominantly motor, demyelinating neuropathy with conduction block, and chronic hemolysis attributed to p.Cys89Tyr mutation in the CD59 gene. METHODS: Four patients were recruited from our new registry of patients with homozygosity for the p.Cys89Tyr mutation on CD59. Participants received repeated intravenous eculizumab. In this 24-month open-label phase IIa study, we aimed to determine whether eculizumab reduces chronic hemolysis, and cumulative doses of steroids and intravenous immunoglobulin (IVIG), and ameliorates neurological deficits, compared to pretreatment status. Treatment response was evaluated every 2 to 4 weeks over 104 weeks and included examination with gross motor scoring by American Spinal Injury Association Impairment Scale and Inflammatory Neuropathy Cause and Treatment disability score, laboratory examination, well-being [12-item Short Form Health Survey; SF-12]). Neurological relapses and cumulative dose of IVIGs and/or corticosteroids before and after treatment were documented. Red blood cells (RBCs) and neutrophils were stained to evaluate C5b-9 deposition. ClinicalTrials.gov: NCT01579838. RESULTS: Dramatic and significant neurological amelioration in the upper limbs and trunk with more-modest amelioration in the lower limbs was observed in all patients. Corticosteroid and IVIG treatment was completely stopped. No patient relapsed during treatment despite infections, and there were no hospital admissions. Decreased C3bi and C5b-9 deposition on RBCs and neutrophils was documented (p < 0.0001). The SF-12 health questionnaires indicated significant improvement (p < 0.003). INTERPRETATION: Eculizumab was safely administered to these patients. Marked clinical improvement suggests that eculizumab may be a life-saving treatment for patients with acute predominantly motor, demyelinating neuropathy with conduction block, and secondary axonal damage attributed to primary p.Cys89Tyr mutation in the CD59 gene. Ann Neurol 2016;80:708-717.
[Mh] Termos MeSH primário: Anemia Hemolítica/complicações
Anticorpos Monoclonais Humanizados/farmacologia
Antígenos CD59/genética
Hemoglobinúria/complicações
Hemólise/efeitos dos fármacos
Polirradiculoneuropatia
Sistema de Registros
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/administração & dosagem
Pré-Escolar
Feminino
Seres Humanos
Lactente
Masculino
Mutação
Polirradiculoneuropatia/tratamento farmacológico
Polirradiculoneuropatia/etiologia
Polirradiculoneuropatia/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (CD59 Antigens); 101754-01-2 (CD59 protein, human); A3ULP0F556 (eculizumab)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160830
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24770


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[PMID]:27498996
[Au] Autor:Takagi M; Kohyama M; Ono T; Adachi S; Shirao D; Tamura H; Taniguchi M; Yabuki A; Yamato O
[Ad] Endereço:Laboratory of Theriogenology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi-shi, Yamaguchi 753-8511, Japan.
[Ti] Título:Recovery with a regular dose of antibiotics from bacillary hemoglobinuria in a Holstein cow.
[So] Source:J Vet Med Sci;78(11):1737-1740, 2016 Dec 01.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:One Holstein cow housed with 21 other cows exhibited clinical signs of pyrexia, anorexia and diarrhea along with severe hemoglobinuria. Hematological and biochemical analyses conducted before and after antibiotic therapy indicated severe hemolytic anemia and disruption of hepatic function. A general improvement in conditions was observed after an 11-day program of treatment comprising a regular dose of antibiotics and prescribed supportive therapies. A tentative diagnosis of bacillary hemoglobinuria was made based on the clinical and clinico-pathologic features on day 7. A molecular diagnosis was made by a PCR amplification of the flagellin gene of Clostridium haemolyticum using DNA extracted from the whole blood. The cow was diagnosed with the first recorded occurrence of bacillary hemoglobinuria of Holstein cattle in Japan.
[Mh] Termos MeSH primário: Antibacterianos/uso terapêutico
Doenças dos Bovinos/microbiologia
Infecções por Clostridium/veterinária
Clostridium/isolamento & purificação
Hemoglobinúria/veterinária
[Mh] Termos MeSH secundário: Anemia Hemolítica/microbiologia
Anemia Hemolítica/veterinária
Animais
Bovinos
Doenças dos Bovinos/tratamento farmacológico
Doenças dos Bovinos/urina
Infecções por Clostridium/tratamento farmacológico
Infecções por Clostridium/microbiologia
Infecções por Clostridium/urina
Feminino
Hemoglobinúria/tratamento farmacológico
Hemoglobinúria/microbiologia
Japão
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160809
[St] Status:MEDLINE


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[PMID]:27348613
[Au] Autor:Habibi A; Mekontso-Dessap A; Guillaud C; Michel M; Razazi K; Khellaf M; Chami B; Bachir D; Rieux C; Melica G; Godeau B; Galacteros F; Bartolucci P; Pirenne F
[Ad] Endereço:Unité des Maladies Génétiques du Globule Rouge, APHP, Hôpitaux Universitaire Henri-Mondor, Créteil, France.
[Ti] Título:Delayed hemolytic transfusion reaction in adult sickle-cell disease: presentations, outcomes, and treatments of 99 referral center episodes.
[So] Source:Am J Hematol;91(10):989-94, 2016 Oct.
[Is] ISSN:1096-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Delayed hemolytic transfusion reaction (DHTR) is one of the most feared complications of sickle-cell disease (SCD). We retrospectively analyzed the clinical and biological features, treatments and outcomes of 99 DHTRs occurring in 69 referral center patients over 12 years. The first clinical signs appeared a median of 9.4 [IQR, 3-22] days after the triggering transfusion (TT). The most frequent DHTR-related clinical manifestation was dark urine/hemoglobinuria (94%). Most patients (89%) had a painful vaso-occlusive crisis and 50% developed a secondary acute chest syndrome (ACS). The median [IQR] hemoglobin-concentration nadir was 5.5 [4.5-6.3] g/dL and LDH peak was 1335 [798-2086] IU/L. Overall mortality was 6%. None of the patients had been receiving chronic transfusions. Among these DHTRs, 61% were developed in previously immunized patients, 28% in patients with prior DHTR. Among Abs detected after the TT in 62% of the episodes, half are classically considered potentially harmful. No association could be established between clinical severity and immunohematological profile and/or the type and specificity of Abs detected after the TT. Management consisted of supportive care alone (53%) or with adjunctive measures (47%), including recombinant erythropoietin and sometimes rituximab and/or immunosuppressants. Additional transfusions were either ineffective or worsened hemolysis. In some cases, severe intravascular hemolysis can be likely responsible for the vascular reaction and high rates of ACS, pulmonary hypertension and (multi)organ failure. In conclusion, clinicians and patients must recognize early DHTR signs to avoid additional transfusions. For patients with a history of RBC immunization or DHTR, transfusion indications should be restricted. Am. J. Hematol. 91:989-994, 2016. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Anemia Falciforme/complicações
Hemólise
Reação Transfusional/diagnóstico
[Mh] Termos MeSH secundário: Síndrome Torácica Aguda
Adulto
Arteriopatias Oclusivas
Transfusão de Sangue
Contraindicações
Gerenciamento Clínico
Feminino
Hemoglobinúria
Seres Humanos
Isoanticorpos/sangue
Masculino
Encaminhamento e Consulta
Estudos Retrospectivos
Fatores de Tempo
Reação Transfusional/terapia
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isoantibodies)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160628
[St] Status:MEDLINE
[do] DOI:10.1002/ajh.24460


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[PMID]:27059502
[Au] Autor:Ghalwash MF; Cao XH; Stojkovic I; Obradovic Z
[Ad] Endereço:Center for Data Analytics and Biomedical Informatics, College of Science and Technology, Temple University, North 12th Street, Philadelphia, 19122, PA, USA. mohamed.ghalwash@temple.edu.
[Ti] Título:Structured feature selection using coordinate descent optimization.
[So] Source:BMC Bioinformatics;17:158, 2016 Apr 08.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Existing feature selection methods typically do not consider prior knowledge in the form of structural relationships among features. In this study, the features are structured based on prior knowledge into groups. The problem addressed in this article is how to select one representative feature from each group such that the selected features are jointly discriminating the classes. The problem is formulated as a binary constrained optimization and the combinatorial optimization is relaxed as a convex-concave problem, which is then transformed into a sequence of convex optimization problems so that the problem can be solved by any standard optimization algorithm. Moreover, a block coordinate gradient descent optimization algorithm is proposed for high dimensional feature selection, which in our experiments was four times faster than using a standard optimization algorithm. RESULTS: In order to test the effectiveness of the proposed formulation, we used microarray analysis as a case study, where genes with similar expressions or similar molecular functions were grouped together. In particular, the proposed block coordinate gradient descent feature selection method is evaluated on five benchmark microarray gene expression datasets and evidence is provided that the proposed method gives more accurate results than the state-of-the-art gene selection methods. Out of 25 experiments, the proposed method achieved the highest average AUC in 13 experiments while the other methods achieved higher average AUC in no more than 6 experiments. CONCLUSION: A method is developed to select a feature from each group. When the features are grouped based on similarity in gene expression, we showed that the proposed algorithm is more accurate than state-of-the-art gene selection methods that are particularly developed to select highly discriminative and less redundant genes. In addition, the proposed method can exploit any grouping structure among features, while alternative methods are restricted to using similarity based grouping.
[Mh] Termos MeSH primário: Algoritmos
Modelos Teóricos
[Mh] Termos MeSH secundário: Neovascularização da Córnea/diagnóstico
Neovascularização da Córnea/genética
Bases de Dados Genéticas
Regulação da Expressão Gênica
Ontologia Genética
Variação Genética
Infecções por HIV/diagnóstico
Infecções por HIV/genética
Hemoglobinúria/diagnóstico
Hemoglobinúria/genética
Seres Humanos
Melanoma/diagnóstico
Melanoma/genética
Análise em Microsséries
Mieloma Múltiplo/diagnóstico
Mieloma Múltiplo/genética
Tumores Neuroendócrinos/diagnóstico
Tumores Neuroendócrinos/genética
Nevo/diagnóstico
Nevo/genética
Estresse Fisiológico/genética
Viroses/diagnóstico
Viroses/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160410
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-016-0954-4


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[PMID]:26994986
[Au] Autor:Kobayashi T; Hayakawa K; Kato Y
[Ad] Endereço:Disease Control and Prevention Center, National Center for Global Health and Medicine.
[Ti] Título:A 41-year-old man with fever and dark-coloured urine.
[So] Source:J Travel Med;23(3), 2016 Mar.
[Is] ISSN:1708-8305
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Antimaláricos/administração & dosagem
Artemisininas/administração & dosagem
Malária Falciparum/tratamento farmacológico
Viagem
[Mh] Termos MeSH secundário: Adulto
Antimaláricos/efeitos adversos
Artemisininas/efeitos adversos
Febre/etiologia
Hemoglobinúria/etiologia
Hemólise
Seres Humanos
Malária Falciparum/diagnóstico
Masculino
Serra Leoa
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antimalarials); 0 (Artemisinins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160321
[St] Status:MEDLINE


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[PMID]:26794659
[Au] Autor:Deuel JW; Schaer CA; Boretti FS; Opitz L; Garcia-Rubio I; Baek JH; Spahn DR; Buehler PW; Schaer DJ
[Ad] Endereço:Division of Internal Medicine, University of Zürich, Zürich, Switzerland.
[Ti] Título:Hemoglobinuria-related acute kidney injury is driven by intrarenal oxidative reactions triggering a heme toxicity response.
[So] Source:Cell Death Dis;7:e2064, 2016 Jan 21.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Intravascular hemolysis can result in hemoglobinuria with acute kidney injury. In this study we systematically explored two in vivo animal models and a related cell culture system to identify hemoglobinuria-triggered damage pathways. In models of stored blood transfusion and hemoglobin (Hb) exposure in guinea pigs and beagle dogs we found that hemoglobinuria led to intrarenal conversion of ferrous Hb(Fe(2+)) to ferric Hb(Fe(3+)), accumulation of free heme and Hb-cross-linking products, enhanced 4-hydroxynonenal reactivity in renal tissue, and acute tubule injury. These changes were associated in guinea pigs with activation of a renal cortex gene expression signature indicative of oxidative stress and activation of the unfolded protein response (UPR). Tubule cells of hemolytic animals demonstrated enhanced protein expression of heme oxygenase and heat shock protein and enhanced expression of acute kidney injury-related neutrophil gelatinase-associated lipocalin. These adverse changes were completely prevented by haptoglobin treatment. The in vivo findings were extrapolated to a MS-based proteome analysis of SILAC-labeled renal epithelial cells that were exposed to free heme within a concentration range estimate of renal tubule heme exposure. These experiments confirmed that free heme is a likely trigger of tubule barrier deregulation and oxidative cell damage and reinforced the hypothesis that uncontrolled free heme could trigger the UPR as an important pathway of renal injury during hemoglobinuria.
[Mh] Termos MeSH primário: Lesão Renal Aguda/etiologia
Hemoglobinúria/etiologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Animais
Cães
Cobaias
Heme
Hemólise
Oxirredução
Estresse Oxidativo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
42VZT0U6YR (Heme)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2015.392



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