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[PMID]:29320581
[Au] Autor:Lian W; Liu H; Song Q; Liu YQ; Sun LY; Deng Q; Wang SP; Cao YH; Zhang XY; Jiang YY; Lv HY; Duan LB; Yu J
[Ad] Endereço:Institute for Kashin-Beck Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, China.
[Ti] Título:Prevalence of hand osteoarthritis and knee osteoarthritis in Kashin-Beck disease endemic areas and non Kashin-Beck disease endemic areas: A status survey.
[So] Source:PLoS One;13(1):e0190505, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteoarthritis (OA) is a considerable health problem worldwide, and the prevalence of OA varies in different regions. In this study, the prevalence of OA in Kashin-Beck disease (KBD) and non-KBD endemic areas was examined, respectively. According to monitoring data, 4 types of regions (including none, mild, moderate and high KBD endemic areas) in Heilongjiang and Jilin provinces were selected. All local residents were eligible for inclusion criteria have undergone X-ray images of hands and anteroposterior image of knees. A total of 1673 cases were collected, 1446 cases were analyzed after removing the KBD patients (227). The overall hand OA and knee OA detection rates were 33.3% (481/1446) and 56.6% (818/1446), respectively. After being standardized by age, the detection rate of hand OA in the KBD endemic areas was significantly higher than that in the non-endemic endemic areas. Differently, there was no significant difference in the detection rates of knee OA between the KBD endemic areas and the non-endemic area. The correlation coefficient between the severity of OA and the severity of knee OA was 0.358 and 0.197 in the KBD and non-KBD endemic areas, respectively. Where the KBD historical prevalence level was higher, the severity of the residents' hand OA was more serious. The detection rates of hand OA and knee OA increased with age. The detection rate of knee OA increased with the increase in body mass index. The prevalence of hand OA was closely related to the pathogenic factors of Kashin-Beck disease, and the prevalence of knee OA had no significant correlation with KBD pathogenic factors.
[Mh] Termos MeSH primário: Mãos/patologia
Mãos/fisiopatologia
Doença de Kashin-Bek/epidemiologia
Articulação do Joelho/patologia
Osteoartrite/epidemiologia
[Mh] Termos MeSH secundário: Doenças Endêmicas
Seres Humanos
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190505


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[PMID]:28963928
[Au] Autor:Chang Y; Wang X; Sun Z; Jin Z; Chen M; Wang X; Lammi MJ; Guo X
[Ad] Endereço:Department of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an 710061, Shaanxi, PR China.
[Ti] Título:Inflammatory cytokine of IL-1ß is involved in T-2 toxin-triggered chondrocyte injury and metabolism imbalance by the activation of Wnt/ß-catenin signaling.
[So] Source:Mol Immunol;91:195-201, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mycotoxin T-2 exerts a causative role in Kashin-Beck disease (KBD) suffering chondrocyte apoptosis and cartilage matrix homeostasis disruption. Recent research corroborated the aberrant levels of pro-inflammatory cytokine IL-1ß in KBD patients and mycotoxin environment. In the present study, we investigated the relevance of IL-1ß in T-2 toxin-evoked chondrocyte cytotoxic injury and aberrant catabolism. High levels of IL-1ß were detected in serum and cartilages from KBD patients and in T-2-stimulated chondrocytes. Moreover, knockdown of IL-1ß antagonized the adverse effects of T-2 on cytotoxic injury by enhancing cell viability and inhibiting apoptosis. However, exogenous supplementation of IL-1ß further aggravated cell damage in response to T-2. Additionally, cessation of IL-1ß rescued T-2-elicited tilt of matrix homeostasis toward catabolism by elevating the transcription of collagen II and aggrecan, promoting release of sulphated glycosaminoglycans (sGAG) and TIMP1, and suppressing matrix metalloproteinases production including MMP-1, MMP-3 and MMP-13. Conversely, IL-1ß stimulation deteriorated T-2-induced disruption of matrix metabolism balance toward catabolism. Mechanistic analysis found the high activation of Wnt/ß-catenin in KBD patients and chondrocytes upon T-2. Furthermore, this activation was mitigated after IL-1ß inhibition, but further enhanced following IL-1ß precondition. Importantly, blocking this pathway by transfection with ß-catenin alleviated the adverse roles of IL-1ß on cytotoxic injury and metabolism disorders under T-2 conditioning. Together, this study elucidates a new insight into how T-2 deteriorates the pathological progression of KBD by regulating inflammation-related pathways, indicating a promising anti-inflammation strategy for KBD therapy.
[Mh] Termos MeSH primário: Condrócitos/imunologia
Interleucina-1beta/imunologia
Toxina T-2/toxicidade
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/imunologia
[Mh] Termos MeSH secundário: Adulto
Agrecanas/biossíntese
Agrecanas/genética
Agrecanas/imunologia
Animais
Apoptose/genética
Apoptose/imunologia
Condrócitos/metabolismo
Condrócitos/patologia
Colágeno Tipo II/biossíntese
Colágeno Tipo II/genética
Colágeno Tipo II/imunologia
Colagenases/biossíntese
Colagenases/genética
Colagenases/imunologia
Matriz Extracelular/genética
Matriz Extracelular/imunologia
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Feminino
Seres Humanos
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Doença de Kashin-Bek/genética
Doença de Kashin-Bek/imunologia
Doença de Kashin-Bek/metabolismo
Doença de Kashin-Bek/patologia
Masculino
Meia-Idade
Ratos
Ratos Sprague-Dawley
Inibidor Tecidual de Metaloproteinase-1/biossíntese
Inibidor Tecidual de Metaloproteinase-1/genética
Inibidor Tecidual de Metaloproteinase-1/imunologia
Transcrição Genética/efeitos dos fármacos
Transcrição Genética/imunologia
Via de Sinalização Wnt/genética
Via de Sinalização Wnt/imunologia
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (Collagen Type II); 0 (IL1B protein, human); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (TIMP1 protein, human); 0 (Tissue Inhibitor of Metalloproteinase-1); 0 (beta Catenin); 0 (tissue inhibitor of metalloproteinase-1 protein, rat); EC 3.4.24.- (Collagenases); I3FL5NM3MO (T-2 Toxin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE


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[PMID]:28807789
[Au] Autor:Dai X; Song R; Xiong Y
[Ad] Endereço:Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission of the people's Rupublic of China, Xi'an Jiaotong University Health Science Center, No. 76 Yanta West Road, Xi'an, Shaanxi 710061, China.
[Ti] Título:The expression of ERK and JNK in patients with an endemic osteochondropathy, Kashin-Beck disease.
[So] Source:Exp Cell Res;359(2):337-341, 2017 Oct 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kashin-Beck disease (KBD) is a chronic, endemic osteochondropathy. Its etiopathogenesis is still obscure until now. Epidemiological observation has shown that low selenium play a crucial role in the pathogenesis of KBD. Extracellular signal-regulated kinases (ERKs) and C-Jun N-terminal kinase (JNK), members of the mitogen-activated protein kinase (MAPK) superfamily, play an important role in cell proliferation and differentiation. Nuclear factor-ĸB (NF-ĸB), an important signaling mediator for inflammatory and immune responses, is involved in the regulation of osteoclastogenesis. In the present study, we investigated the expression of ERK and JNK signal molecular, as well as nuclear factor-ĸB in the pathogenesis of Kashin-Beck disease, evaluated the effect of selenium on ERK signal pathway. The expression levels of ERK and JNK signal pathway, as well as nuclear factor-ĸB were investigated for 218 patients and 209 controls by immunoblot analysis in whole blood. Evaluated the effect of selenium on ERK signal pathway by Na SeO treatment. The protein levels of pRaf-1, pMek1/2 and pErk1/2 decreased significantly in KBD patients, p-JNK and NF-ĸB increased in KBD patients. Furthermore, Na SeO treatment improved the reduction of proteins in ERK signal pathway. These findings indicated that ERK and JNK signaling pathways, as well as the expression level of NF-κB signaling molecular are important contributor to the pathogenesis of KBD. Selenium stimulates the phosphorylation of the ERK signaling pathway.
[Mh] Termos MeSH primário: Cartilagem Articular/metabolismo
Doença de Kashin-Bek/genética
MAP Quinase Quinase 4/genética
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/genética
NF-kappa B/genética
Selênio/deficiência
[Mh] Termos MeSH secundário: Cartilagem Articular/patologia
Estudos de Casos e Controles
Linhagem Celular
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Feminino
Regulação da Expressão Gênica
Seres Humanos
Doença de Kashin-Bek/metabolismo
Doença de Kashin-Bek/patologia
MAP Quinase Quinase 1/genética
MAP Quinase Quinase 1/metabolismo
MAP Quinase Quinase 2/genética
MAP Quinase Quinase 2/metabolismo
MAP Quinase Quinase 4/metabolismo
Masculino
Meia-Idade
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-raf/genética
Proteínas Proto-Oncogênicas c-raf/metabolismo
Transdução de Sinais
Selenito de Sódio/farmacologia
terc-Butil Hidroperóxido/antagonistas & inibidores
terc-Butil Hidroperóxido/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 955VYL842B (tert-Butylhydroperoxide); EC 2.7.1.- (MAP2K2 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.12.2 (MAP Kinase Kinase 1); EC 2.7.12.2 (MAP Kinase Kinase 2); EC 2.7.12.2 (MAP Kinase Kinase 4); EC 2.7.12.2 (MAP2K1 protein, human); H6241UJ22B (Selenium); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28651521
[Au] Autor:Tai Z; Huang L; Lu F; Shi Y; Ma S; Cheng J; Lin H; Liu X; Li Y; Yang Z
[Ad] Endereço:The Key Laboratory for Human Disease Gene Study, Hospital of University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, China.
[Ti] Título:Association study of candidate genes for susceptibility to Kashin-Beck disease in a Tibetan population.
[So] Source:BMC Med Genet;18(1):69, 2017 Jun 26.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Many osteoarthritis (OA) susceptibility genes have been identified in recent years. Given the overlap in the phenotype of joint inflammation between OA and Kashin-Beck disease (KBD), the aim of this study is to explore whether the reported OA susceptibility genes and two genes that may link to OA pathophysiology are associated with KBD in the Tibetan population. METHOD: Fifteen single-nucleotide polymorphisms (SNPs) in 12 candidate genes previously reported as OA susceptibility loci were selected for investigation. Genotyping was performed using the SNaPshot method for these SNPs in a Tibetan population composed of 849 KBD patients and 565 normal controls. Meanwhile, the coding regions of two genes, COL10A1 and HABP2, which may involve in the pathological mechanism of OA/KBD, were sequenced by Sanger sequencing to identify susceptibility coding variants for KBD in the Tibetan population. RESULTS: The two arthritis-susceptible candidate SNPs, rs7775 (p.Arg324Gly) in the FRZB gene and rs7033979 in the ASPN gene, showed associations with KBD (OR = 1.568, P = 4 × 10 and OR = 0.744, P = 8 × 10 , respectively). The coding variants rs142463796 (p.Asp128Asn) and rs2228547 (p.Gly545Arg) in the COL10A1 gene (OR = 9.832 and P = 6 × 10 and OR = 1.242, P = 0.043, respectively) and rs548354451 (p.Asp272Glu) in the HABP2 gene (OR = 2.813, P = 0.010) were associated with KBD patients. CONCLUSION: These finding suggested that rs7775 in the FRZB gene may increase susceptibility to KBD, while rs7033979 in the ASPN gene may play a protective role in susceptibility to KBD in Tibetans. Moreover, genetic variants in chondrogenesis-related genes COL10A1 and HABP2 may play a role in the risk of developing KBD in the Tibetan population.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Doença de Kashin-Bek/genética
[Mh] Termos MeSH secundário: Colágeno Tipo X/genética
Feminino
Estudos de Associação Genética
Glicoproteínas/genética
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Análise de Sequência de DNA
Serina Endopeptidases/genética
Tibet
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type X); 0 (FRZB protein); 0 (Glycoproteins); EC 3.4.21.- (HABP2 protein, human); EC 3.4.21.- (Serine Endopeptidases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-017-0423-6


  5 / 130 MEDLINE  
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[PMID]:28549495
[Au] Autor:Zhao ZJ; Pu GL; Zhan PZ; Li Q; Wu CN; Wang LH
[Ad] Endereço:Qinghai Institute for Endemic Disease Prevention and Control, Xining 811602, Qinghai, China.
[Ti] Título:Detection of the Urinary Biomarkers PYD, CTX-II, and DPD in Patients with Kashin-Beck Disease in the Qinghai Province of China.
[So] Source:Biomed Environ Sci;30(5):380-383, 2017 May.
[Is] ISSN:0895-3988
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Kashin-Beck disease (KBD) is an endemic degenerative osteoarthropathy of uncertain etiology. The aim of our study was to identify changes in C-telopeptide of type II collagen (CTX-II), pyridinoline (PYD), and deoxypyridinoline (DPD) among KBD patients. 54 KBD patients and 78 healthy controls were included this study. Urinary samples were collected and measured by ELISA. The median quantities of PYD, CTX-II, and DPD of KBD patients were 1107.73 ng/µmol.cre, 695.11 ng/µmol.cre, and 1342.34 pml/µmol.cre, while the median quantities of healthy controls were 805.59 ng/µmol.cre, 546.47 ng/µmol.cre, and 718.15 pml/µmol.cre, respectively. The differences between KBD patients and healthy controls were statistically significant (Z = 4.405, 3.653, and 3.724; P < 0.001). The higher levels of PYD, CTX-II, and DPD detected in KBD patients indicate that they could be used as biomarkers of KBD.
[Mh] Termos MeSH primário: Aminoácidos/urina
Colágeno Tipo II/urina
Doença de Kashin-Bek/diagnóstico
Doença de Kashin-Bek/urina
Fragmentos de Peptídeos/urina
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/urina
China
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Amino Acids); 0 (Biomarkers); 0 (C-terminal cross-linking telopeptide of type II collagen, human); 0 (Collagen Type II); 0 (Peptide Fragments); 63800-01-1 (pyridinoline); 90032-33-0 (deoxypyridinoline)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.3967/bes2017.050


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[PMID]:28549491
[Au] Autor:Yang HJ; Zhang Y; Wang ZL; Xue SH; Li SY; Zhou XR; Zhang M; Fang Q; Wang WJ; Chen C; Deng XH; Chen JH
[Ad] Endereço:Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an 710061, Shaanxi, China; Xi'an Jiaotong University Hospital, Xi'an 710049, Shaanxi, Chi
[Ti] Título:Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency.
[So] Source:Biomed Environ Sci;30(5):351-362, 2017 May.
[Is] ISSN:0895-3988
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease (KBD) and in an established T-2 toxin- and selenium (Se) deficiency-induced rat model. METHODS: Cartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and mRNA levels were determined by real-time reverse transcription polymerase chain reaction. RESULTS: Increased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and mRNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet. CONCLUSION: T-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Cartilagem Articular/fisiopatologia
Condrócitos/fisiologia
Doença de Kashin-Bek/fisiopatologia
Selênio/deficiência
Toxina T-2/farmacologia
[Mh] Termos MeSH secundário: Adolescente
Animais
Biomarcadores
Criança
Feminino
Seres Humanos
Doença de Kashin-Bek/etiologia
Masculino
Proteínas Matrilinas/genética
Proteínas Matrilinas/metabolismo
Modelos Animais
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Matrilin Proteins); H6241UJ22B (Selenium); I3FL5NM3MO (T-2 Toxin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.3967/bes2017.046


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[PMID]:28292355
[Au] Autor:Yu FF; Ping ZG; Yao C; Wang ZW; Wang FQ; Guo X
[Ad] Endereço:Institute of Endemic Diseases, School of Public Health of Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an 710061, Shaanxi, China.
[Ti] Título:Evaluation of the Sensitivity and Specificity of the New Clinical Diagnostic and Classification Criteria for Kashin-Beck Disease, an Endemic Osteoarthritis, in China.
[So] Source:Biomed Environ Sci;30(2):150-155, 2017 Feb.
[Is] ISSN:0895-3988
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aimed to evaluate the sensitivity and specificity of the new clinical diagnostic and classification criteria for Kashin-Beck disease (KBD) using six clinical markers: flexion of the distal part of fingers, deformed fingers, enlarged finger joints, shortened fingers, squat down, and dwarfism. One-third of the total population in Linyou County was sampled by stratified random sampling. The survey included baseline characteristics and clinical diagnoses, and the sensitivity and specificity of the new criteria was evaluated. We identified 3,459 KBD patients, of which 69 had early stage KBD, 1,952 had stage I, 1,132 had stage II, and 306 had stage III. A screening test classified enlarged finger joints as stage I KBD, with a sensitivity and specificity of 0.978 and 0.045, respectively. Shortened fingers were classified as stage II KBD, with a sensitivity and specificity of 0.969 and 0.844, respectively, and dwarfism was classified as stage III KBD with a sensitivity and specificity of 0.951 and 0.992, respectively. Serial screening test revealed that the new clinical classification of KBD classified stages I, II, and III KBD with sensitivities of 0.949, 0.945, and 0.925 and specificities of 0.967, 0.970, and 0.993, respectively. The screening tests revealed that enlarged finger joints, shortened fingers, and dwarfism were appropriate markers for the clinical diagnosis and classification of KBD with high sensitivity and specificity.
[Mh] Termos MeSH primário: Doença de Kashin-Bek/diagnóstico
Doença de Kashin-Bek/epidemiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
China/epidemiologia
Feminino
Seres Humanos
Doença de Kashin-Bek/classificação
Doença de Kashin-Bek/patologia
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.3967/bes2017.021


  8 / 130 MEDLINE  
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[PMID]:28033256
[Au] Autor:Yu FF; Zhang YX; Zhang LH; Li WR; Guo X; Lammi MJ
[Ad] Endereço:aInstitute of Endemic Diseases, School of Public Health of Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an bDepartment of Orthopedics, Baoji People's Hospital, Baoji, China cDepartment of Integrative Medical Biology, University of Umeå, Umeå, Sweden.
[Ti] Título:Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease.
[So] Source:Medicine (Baltimore);95(52):e5669, 2016 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As environmental risk factors (ERFs) play an important role in the pathogenesis of Kashin-Beck disease (KBD), it is important to identify the interaction between ERFs and differentially expression genes (DEGs) in KBD. The environmental response genes (ERGs) were analyzed in cartilage of KBD in comparison to normal controls.We searched 5 English and 3 Chinese databases from inception to September 2015, to identify case-control studies that examined ERFs for KBD using integrative meta-analysis and systematic review. Total RNA was isolated from articular cartilage of KBD patients and healthy controls. Human whole genome microarray chip (Agilent) was used to analyze the amplified, labeled, and hybridized total RNA, and the validated microarray data were partially verified using real-time quantitative polymerase chain reaction (qRT-PCR). The ERGs were derived from the Comparative Toxicogenomics Database. The identified ERGs were subjected to KEGG pathway enrichment, biological process (BP), and interaction network analyses using the Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.7, and STRING.The trace elements (selenium and iodine), vitamin E, and polluted grains (T-2 toxin/HT-2 toxin, deoxynivalenol, and nivalenol) were identified as the ERFs for KBD using meta-analysis and review. We identified 21 upregulated ERGs and 7 downregulated ERGs in cartilage with KBD compared with healthy controls, which involved in apoptosis, metabolism, and growth and development. KEGG pathway enrichment analysis found that 2 significant pathways were involved with PI3K-Akt signaling pathway and P53 signaling pathway, and gene ontology function analysis found 3 BPs involved with apoptosis, death, and cell death in KBD cartilage.According to previous results and our own research, we suggest that the trace element selenium and vitamin E induce PI3K-Akt signaling pathway and the mycotoxins (T-2 toxin/HT-2 toxin and DON) induce P53 signaling pathway, contributing to the development of KBD, and chondrocyte apoptosis and cell death.
[Mh] Termos MeSH primário: Expressão Gênica
Interação Gene-Ambiente
Doença de Kashin-Bek/etiologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Apoptose
Cartilagem Articular/química
Cartilagem Articular/metabolismo
Estudos de Casos e Controles
Regulação para Baixo
Perfilação da Expressão Gênica
Ontologia Genética
Seres Humanos
Doença de Kashin-Bek/genética
Proteína Oncogênica v-akt/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Fatores de Risco
Proteína Supressora de Tumor p53/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Oncogene Protein v-akt)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000005669


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[PMID]:27554126
[Au] Autor:Shi XW; Shi BH; Lyu AL; Zhang F; Zhou TT; Guo X
[Ad] Endereço:Department of Pediatrics, The First Affiliated Hospital of the Medical College of Xi'an Jiaotong University, Xi'an 710061, Shannxi, China.
[Ti] Título:Exploring Genome-wide DNA Methylation Profiles Altered in Kashin-Beck Disease Using Infinium Human Methylation 450 Bead Chips.
[So] Source:Biomed Environ Sci;29(7):539-43, 2016 07.
[Is] ISSN:0895-3988
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To understand how differentially methylated genes (DMGs) might affect the pathogenesis of Kashin-Beck disease (KBD). Genome-wide methylation profiling of whole blood from 12 matched KBD and controls pairs was performed using a high-resolution Infinium 450 K methylation array. In total, 97 CpG sites were differentially methylated in KBD compared to the normal controls; of these sites, 36 sites were significantly hypermethylated (covering 22 genes) and 61 sites were significantly hypomethylated (covering 34 genes). Of these genes, 14 significant pathways were identified, the most significant P value pathway was type I diabetes mellitus pathway and pathways associated with autoimmune diseases and inflammatory diseases were included in this study. Subsequently, 4 CpG sites in HLA-DRB1 were validated using bisulfite sequencing polymerase chain reaction (BSP) in articular cartilage, and the results showed significant differences in the methylation status between KBD and controls, consistent with the results of the high-resolution array. These results suggested that differences in genome-wide DNA methylation exist between KBD and the controls, and the biological pathways support the autoimmune disease and inflammatory disease hypothesis of KBD.
[Mh] Termos MeSH primário: Metilação de DNA
Variação Genética
Estudo de Associação Genômica Ampla
Doença de Kashin-Bek/genética
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Análise por Conglomerados
Ilhas de CpG
Feminino
Seres Humanos
Meia-Idade
Análise de Sequência com Séries de Oligonucleotídeos
[Pt] Tipo de publicação:LETTER
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160825
[St] Status:MEDLINE
[do] DOI:10.3967/bes2016.072


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[PMID]:27256326
[Au] Autor:Yang L; Zhao GH; Liu H; Wang X; Guo X; Lammi MJ
[Ad] Endereço:School of Public Health, Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Xi'an, Shaanxi, People's Republic of China.
[Ti] Título:Field synopsis and meta-analyses of genetic epidemiological evidence for Kashin-Beck disease, an endemic osteoarthropathy in China.
[So] Source:Mol Genet Genomics;291(5):1823-33, 2016 Oct.
[Is] ISSN:1617-4623
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Kashin-Beck disease (KBD) is a chronic degenerative osteoarthropathy with unclear etiology. To provide current evidence supporting a genetic predisposition for KBD, we conducted a systematic review and meta-analysis of published literature on the genetic epidemiology of KBD. The PubMed, China National Knowledge Infrastructure and Wan Fang Data were searched up to August 2015 for articles published in English and Chinese. Genome-wide and exome sequencing, linkage, and case-control association studies for any genetic variants associated with KBD were included. Meta-analysis was performed for all single nucleotide polymorphisms (SNPs) that were evaluated in two or more studies. The effect size was summarized as odds ratios (ORs) with 95 % confidence intervals (CIs) by fixed and random effects models. A total of 24 articles were systematically reviewed. Eleven short tandem repeats on chromosomes 2, 11 and 12, 34 SNPs in 12 genes, as well as copy number variant 452 were identified as KBD susceptibility factors in individual studies. The meta-analysis of the GPX1 rs1050450, DIO2 rs225014, TrxR2 rs5748469 and HLA-DRB1 rs7745040 failed to reveal any associations with KBD. However, the meta-analysis of HLA-DRB1 rs9275295 allele A was associated with KBD (OR = 1.737, 95 % CI: 1.002-3.012). In addition, seven haplotypes in GPX1, GPX4, HLA-DRB1 and GDF5 genes also showed significant associations with KBD. In conclusions, our study could identify a number of genetic markers associated with KBD. However, the evidence does not currently support a strong association between the specific variants and KBD because of the limited number of studies, and in the future, more rigorous studies are needed to confirm KBD's links with these variants.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Doença de Kashin-Bek/epidemiologia
Doença de Kashin-Bek/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
China/epidemiologia
Doenças Endêmicas
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160604
[St] Status:MEDLINE
[do] DOI:10.1007/s00438-016-1222-z



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