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[PMID]:29505523
[Au] Autor:Kang X; Zeng Y; Liang J; Li J; Ren D; Chai L; Sun Z; Yu S; Wu X; Han W; Wang W
[Ad] Endereço:Department of Dermatology.
[Ti] Título:Aberrations and clinical significance of BRAF in malignant melanoma: A series of 60 cases in Chinese Uyghur.
[So] Source:Medicine (Baltimore);97(1):e9509, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malignant melanoma (MM) is a highly malignant melanocytic tumor, it occurs mostly in the skin, the mucous membrane close to the skin, but also in the tunicae rhagoides and the pia mater. The Uyghur is the largest ethnic group living in the Xinjiang Uyghur Autonomous Region of China, accounting for 46% of the total population of 20 million. Large-scale studies on MMs in Asian countries are limited. This study aimed to investigate BRAF mRNA expression and mutations in Chinese Uyghur patients with MMs and to identify the clinical features associated with these parameters.Formalin-fixed, paraffin wax-embedded tumor sections from 60 MMs were analyzed for BRAF expression using reverse transcription polymerase chain reaction (RT-PCR). Exons 11 and 15 of BRAF were analyzed for the presence of mutations using PCR and DNA sequencing. Sixty MMs were followed by mobile phone for survival analysis.BRAF mRNA expression was higher in MMs than in pigmented moles and normal skin tissues. Fourteen of 60 MMs had BRAF mutations. The frequency of BRAF mutations was significantly higher in patients younger than 60 years (10/28, 4/32, P = .02). A significant difference was observed in the frequency of BRAF mutations among specimens of mucosal, acral, chronic sun-induced damage (CSD), and non-CSD MMs (2/10, 3/19, 8/25, 1/6, P = .002). No significant association was found among BRAF mutations, sex, ulceration, or lymph node metastasis. MMs lymph node metastasis (hazard ratio 2.54 [95% confidence interval 1.062 - 6.066], P = .01) affected survival.This study indicated that BRAF mutations and expression might serve as independent adverse prognostic factors in melanoma.
[Mh] Termos MeSH primário: Melanoma/genética
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Idoso
Grupo com Ancestrais do Continente Asiático/genética
China/epidemiologia
Feminino
Seres Humanos
Masculino
Melanoma/metabolismo
Melanoma/mortalidade
Meia-Idade
Mutação
Proteínas Proto-Oncogênicas B-raf/metabolismo
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/mortalidade
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009509


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[PMID]:29408271
[Au] Autor:Ben Khelifa S; Martinez R; Dandana A; Khochtali I; Ferchichi S; Castaño L
[Ad] Endereço:Unit of Clinical and Molecular Biology/UR17ES29, Faculty of Pharmacy, Monastir, Tunisia. Electronic address: souhaira34@gmail.com.
[Ti] Título:Maturity Onset Diabetes of the Young (MODY) in Tunisia: Low frequencies of GCK and HNF1A mutations.
[So] Source:Gene;651:44-48, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Maturity Onset Diabetes of the Young (MODY) is a monogenic form of diabetes characterized by autosomal dominant inheritance, an early clinical onset and a primary defect in ß-cell function. Mutations in the GCK and HNF1A genes are the most common cause of MODY among Caucasians. The etiology of MODY in Tunisia stills a challenge for researchers. The aim of this study was to screen for mutations in GCK, HNF1A, HNF4A and INS genes in North African Tunisians subjects, in whom the clinical profile was very suggestive of MODY. A total of 23 unrelated patients, with clinical presentation of MODY were tested for mutations in GCK, HNF1A, HNF4A and INS genes, using Denaturing High Performance Liquid Chromatography (DHPLC), Multiplex Ligation-depend Probe Amplification (MLPA) and sequencing analysis. We identified the previously reported mutation c-169C > T in one patient as well as a new mutation c-457C > T in two unrelated patients. No mutations were detected in the HNF1A and INS genes. Despite restrictive clinical criteria used for selecting patients in this study, the most common genes known for MODY do not explain the majority of cases in Tunisians. This suggests that there are others candidate or unidentified genes contributing to the etiology of MODY in Tunisians families.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/genética
Glucoquinase/genética
Fator 1-alfa Nuclear de Hepatócito/genética
Mutação
[Mh] Termos MeSH secundário: Adulto
Feminino
Frequência do Gene
Fator 4 Nuclear de Hepatócito/genética
Seres Humanos
Masculino
Polimorfismo Genético
Regiões Promotoras Genéticas
Proteínas Serina-Treonina Quinases
Tunísia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HNF1A protein, human); 0 (HNF4A protein, human); 0 (Hepatocyte Nuclear Factor 1-alpha); 0 (Hepatocyte Nuclear Factor 4); EC 2.7.1.2 (Glucokinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (germinal center kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29376607
[Au] Autor:Olefir YV; Yavorskii AN; Butnaru DV; Shatalova OV; Gorbatenko VS; Gerasimenko AS
[Ad] Endereço:I.M. Sechenov First MSMU, Moscow, Russia.
[Ti] Título:[Idiopathic hypercalciuria. Diagnosis and treatment].
[So] Source:Urologiia;(6):112-119, 2017 Dec.
[Is] ISSN:1728-2985
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Most patients with idiopathic hypercalciuria and calcium nephrolithiasis have a family history of the disease. Idiopathic hypercalciuria is a metabolic abnormality with various causes and developmental pathways. The systematic review describes specific mutations associated with idiopathic hypercalciuria and nephrolithiasis. Detection of these mutations may provide a better understanding of the pathogenesis of this heterogeneous disease and personalize patient management depending on the detected polymorphisms. A promising treatment option for a mutation in the vitamin D receptor gene is thiazide diuretics in combination with bisphosphonates. Among bisphosphonates, the drug of choice which has been most strongly supported by research evidence is alendronate.
[Mh] Termos MeSH primário: Alendronato/uso terapêutico
Mutação
Nefrolitíase
Receptores de Calcitriol
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Hipercalciúria/diagnóstico
Hipercalciúria/tratamento farmacológico
Hipercalciúria/genética
Hipercalciúria/metabolismo
Masculino
Nefrolitíase/diagnóstico
Nefrolitíase/tratamento farmacológico
Nefrolitíase/genética
Nefrolitíase/metabolismo
Receptores de Calcitriol/genética
Receptores de Calcitriol/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Calcitriol); X1J18R4W8P (Alendronate)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE


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[PMID]:29364930
[Au] Autor:Tang M; Zhang M; Yan S; Xia L; Yang Z; Du C; Cui HL; Wei D
[Ad] Endereço:Chongqing Key laboratory of Multi-Scale manufacturing Technology, Chongqing Institute of Green and Intelligent Technology, Chinese Academy of Sciences, Chongqing, China.
[Ti] Título:Detection of DNA oligonucleotides with base mutations by terahertz spectroscopy and microstructures.
[So] Source:PLoS One;13(1):e0191515, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA oligonucleotides with a 5-base mutation at the 3'-terminus were investigated by terahertz (THz) spectroscopy in a marker-free manner. The four single-stranded oligonucleotides with 17nt have been detected with specificity on a microfluidic chip, and corroborated by spectral measurements with split-ring resonators. The number of hydrogen bonds formed between the oligonucleotide and its surrounding water molecules, deemed a key contribution to the THz absorption of biological solutions, was explored by molecular dynamics simulations to explain the experimental findings. Our work underlies the feasibility of THz spectroscopy combined with microstructures for marker-free detection of DNA, which may form the basis of a prospective diagnostic tool for studying genic mutation.
[Mh] Termos MeSH primário: DNA/química
Mutação
Espectroscopia Terahertz/métodos
[Mh] Termos MeSH secundário: DNA/genética
Microfluídica
Simulação de Dinâmica Molecular
Conformação de Ácido Nucleico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9007-49-2 (DNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191515


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[PMID]:29363351
[Au] Autor:Faghfuri E; Nikfar S; Niaz K; Faramarzi MA; Abdollahi M
[Ad] Endereço:a Pharmaceutical Biotechnology, Faculty of Pharmacy , Tehran University of Medical Sciences , Tehran , Iran.
[Ti] Título:Mitogen-activated protein kinase (MEK) inhibitors to treat melanoma alone or in combination with other kinase inhibitors.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):317-330, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Malignant melanoma (MM) is an aggressive disease with a rapidly rising incidence due to neoplasm of melanocytes. Molecular targeted therapies have demonstrated lower toxicity and improved overall survival versus conventional therapies of MM. The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM. Though, progression of resistance to these agents has prompted attempts to target downstream proteins in this pathway. Trametinib, a MEK1/2 inhibitor, was approved in 2013 for the treatment of BRAF V600E/K mutation-positive unresectable or metastatic cutaneous melanoma patients. Areas covered: The aim of the current review is to present an update on the role of MEK in progressive melanomas and summarize latest results of clinical studies with innovative MEK inhibitors and/or combined approaches with other kinase inhibitors such as BRAF inhibitors in the treatment of MM. Expert opinion: Two combined treatments (i.e. trametinib plus dabrafenib and vemurafenib plus cobimetinib) target two different kinases in the BRAF/MEK/ERK pathway. The simultaneous prohibition of both MEK and BRAF is associated with more durable response rate than BRAF monotherapy and can overcome acquired resistance.
[Mh] Termos MeSH primário: Melanoma/tratamento farmacológico
Inibidores de Proteínas Quinases/administração & dosagem
Neoplasias Cutâneas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Melanoma/genética
Melanoma/patologia
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Terapia de Alvo Molecular
Mutação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432593


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[PMID]:29346447
[Au] Autor:Chang HJ; Shin HS; Kim TH; Yoo JY; Teasley HE; Zhao JJ; Ha UH; Jeong JW
[Ad] Endereço:Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI, United States of America.
[Ti] Título:Pik3ca is required for mouse uterine gland development and pregnancy.
[So] Source:PLoS One;13(1):e0191433, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The PI3K/AKT signaling pathway plays a critical role in the maintenance of equilibrium between cell survival and apoptosis. The Pik3ca gene is mutated in a range of human cancers. It has been found to be oncogenic, and mutations lead to constitutive activation of the PI3K/AKT pathway. The expression patterns of PIK3CA proteins in the uterus of mice during early pregnancy indicate that it may play a role in the regulation of glandular epithelial cells, which is required to support uterine receptivity. To further investigate the role of Pik3ca in uterine function, Pik3ca was conditionally ablated only in the PGR-positive cells (Pgrcre/+Pik3caf/f; Pik3cad/d). A defect of uterine gland development and decidualization led to subfertility observed in Pik3cad/d mice. Pik3cad/d mice showed significantly decreased uterine weight compared to Pik3caf/f mice. Interestingly, a significant decrease of gland numbers were detected in Pik3cad/d mice compared to control mice. In addition, we found a decrease of Foxa2 expression, which is a known uterine gland marker in Pik3cad/d mice. Furthermore, the excessive proliferation of endometrial epithelial cells was observed in Pik3cad/d mice. Our studies suggest that Pik3ca has a critical role in uterine gland development and female fertility.
[Mh] Termos MeSH primário: Fosfatidilinositol 3-Quinases/metabolismo
Útero/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Western Blotting
Proliferação Celular
Decídua/citologia
Decídua/crescimento & desenvolvimento
Implantação do Embrião
Feminino
Fertilidade
Camundongos
Camundongos Endogâmicos C57BL
Mutação
Fosfatidilinositol 3-Quinases/genética
Gravidez
Reação em Cadeia da Polimerase em Tempo Real
Útero/citologia
Útero/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (Pik3ca protein, mouse)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191433


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[PMID]:29339161
[Au] Autor:El Nagar S; Zindy F; Moens C; Martin L; Plassard D; Roussel MF; Lamonerie T; Billon N
[Ad] Endereço:Université Côte d'Azur, CNRS, Inserm, iBV, Nice, France.
[Ti] Título:A new genetically engineered mouse model of choroid plexus carcinoma.
[So] Source:Biochem Biophys Res Commun;496(2):568-574, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Choroid plexus carcinomas (CPCs) are highly malignant brain tumours predominantly found in children and associated to poor prognosis. Improved therapy for these cancers would benefit from the generation of animal models. Here we have created a novel mouse CPC model by expressing a stabilised form of c-Myc (MycT58A) and inactivating Trp53 in the choroid plexus of newborn mice. This induced aberrant proliferation of choroid plexus epithelial cells, leading to aggressive tumour development and death within 150 days. Choroid plexus tumours occurred with a complete penetrance in all brain ventricles, with prevalence in the lateral and fourth ventricles. Histological and cellular analysis indicated that these tumours were CPCs resembling their human counterparts. Comparison of gene expression profiles of CPCs and non-neoplastic tissues revealed profound alterations in cell cycle regulation and DNA damage responses, suggesting that dysregulation of cell division and DNA checkpoint pathways may represent key vulnerabilities. This novel animal model of CPC provides an invaluable tool to elucidate the mechanism of CPC formation and to develop successful therapies against this devastating paediatric cancer.
[Mh] Termos MeSH primário: Carcinoma/genética
Carcinoma/patologia
Neoplasias do Plexo Corióideo/genética
Neoplasias do Plexo Corióideo/patologia
Plexo Corióideo/patologia
Proteínas Proto-Oncogênicas c-myc/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Carcinogênese/patologia
Proliferação Celular
Dano ao DNA
Modelos Animais de Doenças
Seres Humanos
Camundongos
Camundongos Transgênicos
Mutação
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-myc); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29339155
[Au] Autor:Kuwabara J; Umakoshi A; Abe N; Sumida Y; Ohsumi S; Usa E; Taguchi K; Choudhury ME; Yano H; Matsumoto S; Kunieda T; Takahashi H; Yorozuya T; Watanabe Y; Tanaka J
[Ad] Endereço:Department of Gastrointestinal Surgery and Surgical Oncology, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
[Ti] Título:Truncated CD200 stimulates tumor immunity leading to fewer lung metastases in a novel Wistar rat metastasis model.
[So] Source:Biochem Biophys Res Commun;496(2):542-548, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD200 mediates immunosuppression in immune cells that express its receptor, CD200R. There are two CD200 variants; truncated CD200 that lacks the part of N-terminal sequence necessary for CD200R binding (CD200S) and full-length CD200 (CD200L). We established a novel lung metastasis model by subcutaneously transplanting C6 glioma cells into the backs of neonatal Wistar rats. All transplanted rats developed large back tumors, nearly 90% of which bore lung metastases. To compare the effects of CD200S and CD200L on tumor immunity, CD200L (C6-L)- or CD200S (C6-S)-expressing C6 cells were similarly transplanted. The results showed that 100% of rats with C6-L tumors developed lung metastases, while metastases were found in only 44% of rats with C6-S tumors (n = 25). Tumors disappeared in approximately 20% of the C6-S-bearing rats, and these animals evaded death 180 d after transplantation, while all C6-L tumor-bearing rats died after 45 d. Next generation sequencing revealed that C6-S tumors expressed chemokines and granzyme B at much higher levels than C6-L tumors. Flow cytometry revealed that C6-S tumors contained more dead cells and more CD45 cells, including natural killer cells and CD8 lymphocytes. In particular, multiple subsets of dendritic cells expressing CD11c, MHC class II, CD8, and/or CD103 were more abundant in C6-S than in C6-L tumors. These results suggested that CD200S induced the accumulation of multiple dendritic cell subsets that activated cytotoxic T lymphocytes, leading to the elimination of metastasizing tumor cells.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
Glioma/imunologia
Glioma/patologia
Neoplasias Pulmonares/imunologia
Neoplasias Pulmonares/secundário
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Células Dendríticas/imunologia
Células Dendríticas/patologia
Regulação Neoplásica da Expressão Gênica
Glioma/genética
Tolerância Imunológica
Imunidade Celular
Pulmão/imunologia
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Mutação
Ratos Wistar
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (antigens, CD200)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29332224
[Au] Autor:Tong D; Yu M; Guo L; Li T; Li J; Novakovic VA; Dong Z; Tian Y; Kou J; Bi Y; Wang J; Zhou J; Shi J
[Ad] Endereço:Department of Hematology, First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, China.
[Ti] Título:Phosphatidylserine-exposing blood and endothelial cells contribute to the hypercoagulable state in essential thrombocythemia patients.
[So] Source:Ann Hematol;97(4):605-616, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The mechanisms of thrombogenicity in essential thrombocythemia (ET) are complex and not well defined. Our objective was to explore whether phosphatidylserine (PS) exposure on blood cells and endothelial cells (ECs) can account for the increased thrombosis and distinct thrombotic risks among mutational subtypes in ET. Using flow cytometry and confocal microscopy, we found that the levels of PS-exposing erythrocytes, platelets, leukocytes, and serum-cultured ECs were significantly higher in each ET group [JAK2, CALR, and triple-negative (TN) (all P < 0.001)] than those in controls. Among ET patients, those with JAK2 mutations showed higher levels of PS-positive erythrocytes, platelets, neutrophils, and serum-cultured ECs than TN patients or those with CALR mutations, which show similar levels. Coagulation function assays showed that higher levels of PS-positive blood cells and serum-cultured ECs led to markedly shortened coagulation time and dramatically increased levels of FXa, thrombin, and fibrin production. This procoagulant activity could be largely blocked by addition of lactadherin (approx. 70% inhibition). Confocal microscopy showed that the FVa/FXa complex and fibrin fibrils colocalized with PS on ET serum-cultured ECs. Additionally, we found a relationship between D-dimer, prothrombin fragment F1 + 2, and PS exposure. Our study reveals a previously unrecognized link between hypercoagulability and exposed PS on cells, which might also be associated with distinct thrombotic risks among mutational subtypes in ET. Thus, blocking PS-binding sites may represent a new therapeutic target for preventing thrombosis in ET.
[Mh] Termos MeSH primário: Plaquetas/patologia
Endotélio Vascular/patologia
Eritrócitos/patologia
Leucócitos/patologia
Fosfatidilserinas/metabolismo
Trombocitemia Essencial/fisiopatologia
Trombose/etiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Substituição de Aminoácidos
Plaquetas/metabolismo
Calreticulina/genética
Calreticulina/metabolismo
Células Cultivadas
China/epidemiologia
Endotélio Vascular/metabolismo
Eritrócitos/metabolismo
Feminino
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Janus Quinase 2/genética
Janus Quinase 2/metabolismo
Leucócitos/metabolismo
Masculino
Meia-Idade
Mutação
Receptores de Trombopoetina/genética
Receptores de Trombopoetina/metabolismo
Risco
Propriedades de Superfície
Trombocitemia Essencial/genética
Trombocitemia Essencial/metabolismo
Trombocitemia Essencial/patologia
Trombose/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calreticulin); 0 (Phosphatidylserines); 0 (Receptors, Thrombopoietin); 0 (calreticulin, human); 143641-95-6 (MPL protein, human); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3228-6


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[PMID]:29309428
[Au] Autor:Sarika K; Hossain F; Muthusamy V; Zunjare RU; Baveja A; Goswami R; Thirunavukkarasu N; Jha SK; Gupta HS
[Ad] Endereço:Division of Genetics, ICAR-Indian Agricultural Research Institute, New Delhi, India.
[Ti] Título:Opaque16, a high lysine and tryptophan mutant, does not influence the key physico-biochemical characteristics in maize kernel.
[So] Source:PLoS One;13(1):e0190945, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The enhancement of lysine and tryptophan in maize is so far basedon opaque2(o2) mutant, that along with the endosperm-modifiersled to development of Quality Protein Maize[QPM]. Though many mutants improving the endospermic protein quality were discovered, they could not be successfully deployed. Recently discovered opaque16 (o16)mutant enhances the lysine and tryptophan content in maize endosperm. In the present study, the influence of o16 on the endosperm modification was analyzed in four F2 populations, two each segregating for o16 allele alone and in combination with o2. The recessive o16o16 seed endosperm was found to be vitreousphenotypically similar to wild-O16O16. The mutant did not influence the degree of kernel opaqueness in o2o2 genetic background as opaqueness in o2o2/O16O16 and o2o2/o16o16 was similar. Grain hardness of o16o16 was comparable with the normal and QPM maize. The pattern of microscopic organization of proteinaceous matrix and starch granules, and zein profiling of the storage protein in o16o16 were found to be similar with normal maize endosperm, but distinct from the o2o2-soft genotype. The pattern in o2o2/o16o16 was unique and different from o2o2 and o16o16 as well. Here we demonstrated the effects of o16 on physico-biochemical characteristics of endosperm and report of o16 possessing negligible influence on kernel modification and hardness, which holds a great significance in maize quality breeding programme.
[Mh] Termos MeSH primário: Lisina/metabolismo
Mutação
Proteínas de Plantas/metabolismo
Triptofano/metabolismo
Zea mays/metabolismo
[Mh] Termos MeSH secundário: Genes de Plantas
Marcadores Genéticos
Proteínas de Plantas/química
Proteínas de Plantas/genética
Zea mays/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Genetic Markers); 0 (Plant Proteins); 8DUH1N11BX (Tryptophan); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190945



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