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1 / 2012

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[PMID]: 29040284 [Au] Autor: Lee SY; Kim EK; Kim MS; Shin SH; Chang H; Jang SY; Kim HJ; Kim DK [Ad] Endereço: Division of Cardiology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. [Ti] Título: The prevalence and clinical manifestation of hereditary thrombophilia in Korean patients with unprovoked venous thromboembolisms. [So] Source: PLoS One;12(10):e0185785, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Hereditary thrombophilia (HT) is a genetic predisposition to thrombosis. Asian mutation spectrum of HT is different from Western ones. We investigated the incidence and clinical characteristics of HT in Korean patients with unprovoked venous thromboembolism (VTE). METHODS: Among 369 consecutive patients with thromboembolic event who underwent thrombophilia tests, we enrolled 222 patients diagnosed with unprovoked VTE. The presence of HT was confirmed by DNA sequencing of the genes that cause deficits in natural anticoagulants (NAs). Median follow-up duration was 40±38 months. RESULTS: Among the 222 patients with unprovoked VTE, 66 (29.7%) demonstrated decreased NA level, and 33 (14.9%) were finally confirmed to have HT in a genetic molecular test. Antithrombin III deficiency (6.3%) was most frequently detected, followed by protein C deficiency (5.4%), protein S deficiency (1.8%), and dysplasminogenemia (1.4%). The HT group was significantly younger (37 [32-50] vs. 52 [43-65] years; P < 0.001) and had a higher proportion of male (69.7% vs. 47%; P = 0.013), more previous VTE events (57.6% vs. 31.7%; P = 0.004), and a greater family history of VTE (43.8% vs. 1.9%; P < 0.001) than the non-HT group. Age <45 years and a family history of VTE were independent predictors for unprovoked VTE with HT (odds ratio, 9.435 [2.45-36.35]; P = 0.001 and 92.667 [14.95-574.29]; P < 0.001). CONCLUSIONS: About 15% of patients with unprovoked VTE had HT. A positive family history of VTE and age <45 years were independent predictors for unprovoked VTE caused by HT. [Mh] Termos MeSH primário: Deficiência de Antitrombina III/fisiopatologia Conjuntivite/fisiopatologia Plasminogênio/deficiência Deficiência de Proteína C/fisiopatologia Deficiência de Proteína S/fisiopatologia Dermatopatias Genéticas/fisiopatologia Trombofilia/fisiopatologia Tromboembolia Venosa/fisiopatologia [Mh] Termos MeSH secundário: Adulto Idoso Antitrombina III/genética Deficiência de Antitrombina III/complicações Deficiência de Antitrombina III/diagnóstico Deficiência de Antitrombina III/genética Conjuntivite/complicações Conjuntivite/diagnóstico Conjuntivite/genética Feminino Expressão Gênica Seres Humanos Masculino Meia-Idade Plasminogênio/genética Proteína C/genética Deficiência de Proteína C/complicações Deficiência de Proteína C/diagnóstico Deficiência de Proteína C/genética Proteína S/genética Deficiência de Proteína S/complicações Deficiência de Proteína S/diagnóstico Deficiência de Proteína S/genética República da Coreia Estudos Retrospectivos Análise de Sequência de DNA Dermatopatias Genéticas/complicações Dermatopatias Genéticas/diagnóstico Dermatopatias Genéticas/genética Trombofilia/diagnóstico Trombofilia/etiologia Trombofilia/genética Tromboembolia Venosa/diagnóstico Tromboembolia Venosa/etiologia Tromboembolia Venosa/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Protein C); 0 (Protein S); 9000-94-6 (Antithrombin III); 9001-91-6 (Plasminogen) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171031 [Lr] Data última revisão: 171031 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171018 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0185785

2 / 2012

MEDLINE

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[PMID]: 28686706 [Au] Autor: Tashima Y; Banno F; Kita T; Matsuda Y; Yanamoto H; Miyata T [Ad] Endereço: Department of Molecular Pathogenesis, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan. [Ti] Título: Plasminogen Tochigi mice exhibit phenotypes similar to wild-type mice under experimental thrombotic conditions. [So] Source: PLoS One;12(7):e0180981, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Plasminogen (Plg) is a precursor of plasmin that degrades fibrin. A race-specific A620T mutation in Plg, also known as Plg-Tochigi, originally identified in a patient with recurrent venous thromboembolism, causes dysplasminogenemia with reduced plasmin activity. The Plg-A620T mutation is present in 3-4% of individuals in East Asian populations, and as many as 50,000 Japanese are estimated to be homozygous for the mutant 620T allele. In the present study, to understand the changes of thrombotic phenotypes in individuals with the mutant 620T allele, we generated knock-in mice carrying the homozygous Plg-A622T mutation (PlgT/T), an equivalent to the A620T mutation in human Plg. PlgT/T mice grew normally but showed severely reduced plasmin activity activated by urokinase, equivalent to ~8% of that in wild-type mice. In vitro fibrin clot lysis in plasma was significantly slower in PlgT/T mice than in wild-type mice. However, all experimental models of electrolytic deep vein thrombosis, tissue factor-induced pulmonary embolism, transient focal brain ischaemic stroke, or skin-wound healing showed largely similar phenotypes between PlgT/T mice and wild-type mice. Protein S-K196E mutation (Pros1E/E) is a race-specific genetic risk factor for venous thromboembolism. Coexistence in mice of PlgT/T and Pros1E/E did not affect pulmonary embolism symptoms, compared with those in Pros1E/E mice. Hence, the present study showed that the Plg-A622T mutation, which confers ~8% plasmin activity, does not increase the risk of thrombotic diseases in mice under experimental thrombotic conditions and does not modify the thrombotic phenotype observed in Pros1E/E mice. PlgT/T mice can be used to investigate the potential pathophysiological impact of the Plg-A620T mutation. [Mh] Termos MeSH primário: Conjuntivite/genética Técnicas de Introdução de Genes Mutação Fenótipo Plasminogênio/deficiência Plasminogênio/genética Dermatopatias Genéticas/genética Tromboembolia Venosa/genética [Mh] Termos MeSH secundário: Substituição de Aminoácidos Animais Isquemia Encefálica/sangue Isquemia Encefálica/genética Isquemia Encefálica/patologia Conjuntivite/sangue Conjuntivite/patologia Modelos Animais de Doenças Feminino Fibrina/genética Fibrina/metabolismo Fibrinolisina/genética Fibrinolisina/metabolismo Expressão Gênica Seres Humanos Masculino Camundongos Camundongos Transgênicos Plasminogênio/metabolismo Proteína S/genética Proteína S/metabolismo Embolia Pulmonar/sangue Embolia Pulmonar/genética Embolia Pulmonar/patologia Dermatopatias Genéticas/sangue Dermatopatias Genéticas/patologia Acidente Vascular Cerebral/sangue Acidente Vascular Cerebral/genética Acidente Vascular Cerebral/patologia Tromboembolia Venosa/sangue Tromboembolia Venosa/patologia Trombose Venosa/sangue Trombose Venosa/genética Trombose Venosa/patologia Cicatrização/fisiologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Protein S); 9001-31-4 (Fibrin); 9001-91-6 (Plasminogen); EC 3.4.21.7 (Fibrinolysin) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170922 [Lr] Data última revisão: 170922 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170708 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0180981

3 / 2012

MEDLINE

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[PMID]: 28668213 [Au] Autor: Ochodnicky P; Lattenist L; Ahdi M; Kers J; Uil M; Claessen N; Leemans JC; Florquin S; Meijers JCM; Gerdes VEA; Roelofs JJTH [Ad] Endereço: Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. [Ti] Título: Increased Circulating and Urinary Levels of Soluble TAM Receptors in Diabetic Nephropathy. [So] Source: Am J Pathol;187(9):1971-1983, 2017 Sep. [Is] ISSN: 1525-2191 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: TAM receptors (Tyro3, Axl, and Mer) have been implicated in innate immunity. Circulating TAM receptor soluble forms (sTyro3, sAxl, sMer) are related to autoimmune disorders. We investigated TAM and their ligand protein S in patients with diabetes. Urinary and plasma levels of protein S, sTyro3, sAxl, and sMer were determined in 126 patients with diabetes assigned to a normoalbuminuric or macroalbuminuric (urinary albumin excretion <30 mg/24 hours and >300 mg/24 hours, respectively) study group and 18 healthy volunteers. TAM and protein S immunostaining was performed on kidney biopsy specimens from patients with diabetic nephropathy (n = 9) and controls (n = 6). TAM expression and shedding by tubular epithelial cells were investigated by PCR and enzyme-linked immunosorbent assay in an in vitro diabetes model. Patients with macroalbuminuria diabetes had higher circulating levels of sMer and more urinary sTyro3 and sMer than normoalbuminuric diabetics. Increased clearance of sTyro3 and sMer was associated with loss of tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions of protein S. During in vitro diabetes, human kidney cells had down-regulation of Tyro3 and Mer mRNA and increased shedding of sTyro3 and sMer. Renal injury in diabetes is associated with elevated systemic and urine levels of sMer and sTyro3. This is the first study reporting excretion of sTAM receptors in urine, identifying the kidney as a source of sTAM. [Mh] Termos MeSH primário: Nefropatias Diabéticas/metabolismo Proteína S/metabolismo Proteínas Proto-Oncogênicas/metabolismo Receptores Proteína Tirosina Quinases/metabolismo [Mh] Termos MeSH secundário: Adulto Idoso Idoso de 80 Anos ou mais Linhagem Celular Nefropatias Diabéticas/sangue Nefropatias Diabéticas/urina Feminino Seres Humanos Glomérulos Renais/metabolismo Masculino Meia-Idade Proteína S/urina Proteínas Proto-Oncogênicas/sangue Proteínas Proto-Oncogênicas/urina Receptores Proteína Tirosina Quinases/sangue Receptores Proteína Tirosina Quinases/urina c-Mer Tirosina Quinase [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Protein S); 0 (Proto-Oncogene Proteins); EC 2.7.10.1 (MERTK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (TYRO3 protein, human); EC 2.7.10.1 (axl receptor tyrosine kinase); EC 2.7.10.1 (c-Mer Tyrosine Kinase) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170703 [St] Status: MEDLINE

4 / 2012

MEDLINE

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[PMID]: 28662047 [Au] Autor: Weng SL; Kao HJ; Huang CH; Lee TY [Ad] Endereço: Department of Medicine, Mackay Medical College, New Taipei City, Taiwan. [Ti] Título: MDD-Palm: Identification of protein S-palmitoylation sites with substrate motifs based on maximal dependence decomposition. [So] Source: PLoS One;12(6):e0179529, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: S-palmitoylation, the covalent attachment of 16-carbon palmitic acids to a cysteine residue via a thioester linkage, is an important reversible lipid modification that plays a regulatory role in a variety of physiological and biological processes. As the number of experimentally identified S-palmitoylated peptides increases, it is imperative to investigate substrate motifs to facilitate the study of protein S-palmitoylation. Based on 710 non-homologous S-palmitoylation sites obtained from published databases and the literature, we carried out a bioinformatics investigation of S-palmitoylation sites based on amino acid composition. Two Sample Logo indicates that positively charged and polar amino acids surrounding S-palmitoylated sites may be associated with the substrate site specificity of protein S-palmitoylation. Additionally, maximal dependence decomposition (MDD) was applied to explore the motif signatures of S-palmitoylation sites by categorizing a large-scale dataset into subgroups with statistically significant conservation of amino acids. Single features such as amino acid composition (AAC), amino acid pair composition (AAPC), position specific scoring matrix (PSSM), position weight matrix (PWM), amino acid substitution matrix (BLOSUM62), and accessible surface area (ASA) were considered, along with the effectiveness of incorporating MDD-identified substrate motifs into a two-layered prediction model. Evaluation by five-fold cross-validation showed that a hybrid of AAC and PSSM performs best at discriminating between S-palmitoylation and non-S-palmitoylation sites, according to the support vector machine (SVM). The two-layered SVM model integrating MDD-identified substrate motifs performed well, with a sensitivity of 0.79, specificity of 0.80, accuracy of 0.80, and Matthews Correlation Coefficient (MCC) value of 0.45. Using an independent testing dataset (613 S-palmitoylated and 5412 non-S-palmitoylated sites) obtained from the literature, we demonstrated that the two-layered SVM model could outperform other prediction tools, yielding a balanced sensitivity and specificity of 0.690 and 0.694, respectively. This two-layered SVM model has been implemented as a web-based system (MDD-Palm), which is now freely available at http://csb.cse.yzu.edu.tw/MDDPalm/. [Mh] Termos MeSH primário: Ácido Palmítico/metabolismo Proteína S/metabolismo [Mh] Termos MeSH secundário: Aminoácidos/metabolismo Especificidade por Substrato [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Amino Acids); 0 (Protein S); 2V16EO95H1 (Palmitic Acid) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170928 [Lr] Data última revisão: 170928 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170630 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0179529

5 / 2012

MEDLINE

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[PMID]: 28420729 [Au] Autor: Santamaria S; Reglinska-Matveyev N; Gierula M; Camire RM; Crawley JTB; Lane DA; Ahnström J [Ad] Endereço: From the Centre for Haematology, Faculty of Medicine, Imperial College London, London W12 0NN, United Kingdom. [Ti] Título: Factor V has an anticoagulant cofactor activity that targets the early phase of coagulation. [So] Source: J Biol Chem;292(22):9335-9344, 2017 Jun 02. [Is] ISSN: 1083-351X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Tissue factor pathway inhibitor (TFPI), the main inhibitor of initiation of coagulation, exerts an important anticoagulant role through the factor Xa (FXa)-dependent inhibition of tissue factor/factor VIIa. Protein S is a TFPI cofactor, enhancing the efficiency of FXa inhibition. TFPI can also inhibit prothrombinase assembly by directly interacting with coagulation factor V (FV), which has been activated by FXa. Because full-length TFPI associates with FV in plasma, we hypothesized that FV may influence TFPI inhibitory function. Using pure component FXa inhibition assays, we found that although FV alone did not influence TFPI-mediated FXa inhibition, it further enhanced TFPI in the presence of protein S, resulting in an ∼8-fold reduction in compared with TFPI alone. A FV variant (R709Q/R1018Q/R1545Q, FV ) that cannot be cleaved/activated by thrombin or FXa also enhanced TFPI-mediated inhibition of FXa ∼12-fold in the presence of protein S. In contrast, neither activated FV nor recombinant B-domain-deleted FV could enhance TFPI-mediated inhibition of FXa in the presence of protein S, suggesting a functional contribution of the B domain. Using TFPI and protein S variants, we show further that the enhancement of TFPI-mediated FXa inhibition by protein S and FV depends on a direct protein S/TFPI interaction and that the TFPI C-terminal tail is not essential for this enhancement. In FXa-catalyzed prothrombin activation assays, both FV and FV (but not activated FV) enhanced TFPI function in the presence of protein S. These results demonstrate a new anticoagulant (cofactor) function of FV that targets the early phase of coagulation before prothrombinase assembly. [Mh] Termos MeSH primário: Anticoagulantes/metabolismo Coagulação Sanguínea/fisiologia Fator V/metabolismo [Mh] Termos MeSH secundário: Substituição de Aminoácidos Fator V/genética Fator Xa/genética Fator Xa/metabolismo Seres Humanos Lipoproteínas/genética Lipoproteínas/metabolismo Mutação de Sentido Incorreto Domínios Proteicos Proteína S/genética Proteína S/metabolismo Protrombina/genética Protrombina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Anticoagulants); 0 (Lipoproteins); 0 (Protein S); 0 (lipoprotein-associated coagulation inhibitor); 9001-24-5 (Factor V); 9001-26-7 (Prothrombin); EC 3.4.21.6 (Factor Xa) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 170609 [Lr] Data última revisão: 170609 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170420 [St] Status: MEDLINE [do] DOI: 10.1074/jbc.M116.769570

6 / 2012

MEDLINE

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[PMID]: 28222624 [Au] Autor: Yang N; Hao J; Zhang D [Ad] Endereço: 1 Department of Endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. [Ti] Título: Antithrombin III and D-dimer levels as indicators of disease severity in patients with hyperlipidaemic or biliary acute pancreatitis. [So] Source: J Int Med Res;45(1):147-158, 2017 Feb. [Is] ISSN: 1473-2300 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Objective To assess changes in anticoagulation and fibrinolytic systems between biliary and hyperlipidaemic acute pancreatitis (AP). Methods Patients with biliary or hyperlipidaemic AP were enrolled. Demographic and clinical data were collected, and antithrombin III (ATIII), protein C, protein S, and D-dimer levels were investigated. Results A total of 45 patients with biliary AP and 50 patients with hyperlipidaemic AP were included (68 with mild AP and 27 with moderately-severe AP). ATIII and protein C levels in the mild AP group were significantly higher, but prothrombin time and D-dimer were significantly lower, versus the moderately-severe AP group. ATIII and D-dimer were found to be risk factors for moderately-severe AP. ATIII could predict AP severity, particularly in patients with biliary AP. D-dimer was a sensitive and specific predictor for disease severity in patients with AP, particularly in patients with hyperlipidaemic AP. Conclusion ATIII and protein C levels decreased as severity of AP increased, particularly in cases of biliary AP. D-dimer levels increased with severity of AP, particularly in hyperlipidaemic AP. ATIII and D-dimer may be useful biomarkers for assessing AP severity in patients with biliary and hyperlipidaemic AP, respectively. [Mh] Termos MeSH primário: Antitrombina III/metabolismo Doenças dos Ductos Biliares/diagnóstico Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo Hiperlipidemias/diagnóstico Pancreatite/diagnóstico [Mh] Termos MeSH secundário: Doença Aguda Adulto Idoso Idoso de 80 Anos ou mais Doenças dos Ductos Biliares/sangue Doenças dos Ductos Biliares/patologia Biomarcadores/sangue Coagulação Sanguínea China HDL-Colesterol/sangue LDL-Colesterol/sangue Estudos de Coortes Feminino Seres Humanos Hiperlipidemias/sangue Hiperlipidemias/patologia Masculino Meia-Idade Pancreatite/sangue Pancreatite/patologia Proteína C/metabolismo Proteína S/metabolismo Índice de Gravidade de Doença Triglicerídeos/sangue [Pt] Tipo de publicação: JOURNAL ARTICLE; OBSERVATIONAL STUDY [Nm] Nome de substância: 0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 0 (Fibrin Fibrinogen Degradation Products); 0 (Protein C); 0 (Protein S); 0 (Triglycerides); 0 (fibrin fragment D); 9000-94-6 (Antithrombin III) [Em] Mês de entrada: 1705 [Cu] Atualização por classe: 171004 [Lr] Data última revisão: 171004 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170223 [St] Status: MEDLINE [do] DOI: 10.1177/0300060516677929

7 / 2012

MEDLINE

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[PMID]: 28214760 [Au] Autor: Matsukawa Y; Asano E; Tsuda T; Kuma H; Kitaori T; Katano K; Ozaki Y; Sugiura-Ogasawara M [Ad] Endereço: Department of Obstetrics and Gynecology, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Japan. [Ti] Título: Genotyping analysis of protein S-Tokushima (K196E) and the involvement of protein S antigen and activity in patients with recurrent pregnancy loss. [So] Source: Eur J Obstet Gynecol Reprod Biol;211:90-97, 2017 Apr. [Is] ISSN: 1872-7654 [Cp] País de publicação: Ireland [La] Idioma: eng [Ab] Resumo: OBJECTIVE: Preston et al. indicated that Protein S (PS) deficiency was associated with stillbirths but not miscarriages. The PS-Tokushima missense variant was reported to serve as a genetic risk factor for deep vein thrombosis in the Japanese population. A previous cross-sectional study showed no increase in the prevalence of PS-Tokushima in patients with recurrent early pregnancy loss or in patients with intra uterine fetal death and/or fetal growth restriction. There has been limited number of prospective studies examining the pregnancy outcome in patients with both a PS deficiency and recurrent pregnancy loss (RPL). We examined the association between PS deficiency, PS-Tokushima and RPL. STUDY DESIGN: The study group consisted of 355 Japanese women with two or more consecutive pregnancy losses and 101 parous women. The frequency of PS-Tokushima and the subsequent live birth rate in relation to a PS deficiency defined as low PS-specific activity (total PS activity/total PS antigen) and the carriage of PS-Tokushima were examined. RESULTS AND CONCLUSIONS: There was no significant difference in the frequency of PS-Tokushima between patients and controls. The 8 patients carriers of PS-Tokushima variant were capable of a subsequent live birth without the use of heparin. There was no significant difference in subsequent live birth rates between patients with low or normal PS-specific activity/PS activity without heparin prophylaxis after excluding miscarriages caused by an abnormal embryonic karyotype using multivariate logistic regression analysis. There was no association between PS-Tokushima and RPL and a PS deficiency or low PS activity was shown not to serve as a reliable clinical predictor of subsequent miscarriage. [Mh] Termos MeSH primário: Aborto Habitual/etiologia Genótipo Deficiência de Proteína S/complicações Proteína S/genética [Mh] Termos MeSH secundário: Aborto Habitual/genética Adulto Alelos Coeficiente de Natalidade Estudos Transversais Feminino Frequência do Gene Estudos de Associação Genética Predisposição Genética para Doença Seres Humanos Gravidez Resultado da Gravidez Deficiência de Proteína S/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Protein S); 0 (protein S Tokushima) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170926 [Lr] Data última revisão: 170926 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170220 [St] Status: MEDLINE

8 / 2012

MEDLINE

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[PMID]: 28196919 [Au] Autor: Kristoffersen AH; Petersen PH; Røraas T; Sandberg S [Ad] Endereço: Laboratory of Clinical Biochemistry, Haukeland University Hospital, Bergen, Norway; ann.kristoffersen@helse-bergen.no. [Ti] Título: Estimates of Within-Subject Biological Variation of Protein C, Antithrombin, Protein S Free, Protein S Activity, and Activated Protein C Resistance in Pregnant Women. [So] Source: Clin Chem;63(4):898-907, 2017 Apr. [Is] ISSN: 1530-8561 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: In pregnancy, interpretation of results from coagulation parameters can be difficult because of the procoagulant physiological changes. The aim of this study was to describe the course of 5 coagulation parameters (thrombophilia markers) in healthy pregnancies, and to estimate and compare the within-subject biological variation (CV ) of these parameters in healthy pregnant and nonpregnant women. METHODS: Blood samples were obtained every 4th week during pregnancy and 3 samples after delivery in 20 healthy women and every 4th week during 40 weeks in 19 healthy nonpregnant women. Protein C (PC), antithrombin (AT), protein S free (PS free), protein S activity (PS activity), and activated protein C resistance (with factor V-depleted plasma) (APCR) were analyzed. Before the calculation of CV , results were transformed into multiples of the median (MoM) and natural logarithm of MoM (lnMoM) to adjust for the physiological changes during pregnancy. RESULTS: During pregnancy, PC results showed large variability, AT decreased slightly, and PS free and PS activity decreased significantly. Both activated partial thromboplastin time tests used to calculate APCR decreased, and the APCR ratio was constant. The CV (lnMoM) in pregnancy were for PC 8.4%, for AT 3.8%, for PS free 11.5%, for PS activity 9.3%, and for APCR 0.5%, and similar to corresponding results in nonpregnant women. CONCLUSIONS: Transformation of coagulation parameters in healthy pregnancies to lnMoM is a tool to establish a kind of steady state. Although there is a physiological change in PC, AT, and PS free and PS activity during pregnancy, the CV was comparable with the CV of nonpregnant women. [Mh] Termos MeSH primário: Resistência à Proteína C Ativada/sangue Antitrombinas/sangue Proteína C/análise Proteína S/análise [Mh] Termos MeSH secundário: Adulto Feminino Seres Humanos Gravidez Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antithrombins); 0 (Protein C); 0 (Protein S) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 170601 [Lr] Data última revisão: 170601 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170216 [St] Status: MEDLINE [do] DOI: 10.1373/clinchem.2016.265900

9 / 2012

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[PMID]: 28092096 [Au] Autor: Okoye HC; Eweputanna LI; Okpani AO; Ejele OA [Ad] Endereço: Department of Hematology and Immunology, University of Nigeria Teaching Hospital, Ituku-Ozalla, Enugu, Nigeria. [Ti] Título: Associations between pre-eclampsia and protein C and protein S levels among pregnant Nigerian women. [So] Source: Int J Gynaecol Obstet;137(1):26-30, 2017 Apr. [Is] ISSN: 1879-3479 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: OBJECTIVE: To evaluate levels of protein C and free protein S among women with pre-eclampsia, and determine whether there is a relationship between deficiencies and pre-eclampsia. METHODS: A cross-sectional study was conducted at a hospital in Nigeria from July 2013 to March 2014 among 90 pregnant women with pre-eclampsia (blood pressure ≥140/90 mm Hg, proteinuria ≥300 mg in 24 hours) and 90 normotensive pregnant women (control group). Plasma levels of protein C and free protein S were analyzed by enzyme-linked immunosorbent assay, and protein C activity by a chromogenic method. RESULTS: Mean protein C antigen and activity levels did not differ between groups (P=0.639 and P=0.444, respectively). The incidence of protein C antigen and activity deficiency also did not differ (P=0.288 and P>0.99, respectively). The mean free protein S antigen level was higher among women with pre-eclampsia (54.48%±19.58%) than in the control group (47.23%±10.27%; P=0.004). No woman in the control group had protein S deficiency, as compared with 2 (2%) of the women with pre-eclampsia (P=0.497). No association was found between deficiencies of these proteins and pre-eclampsia. CONCLUSION: Deficiencies of protein C and free protein S are unlikely to be etiopathogenetic for pre-eclampsia; therefore, therapeutic intervention should focus on other potential pathogenetic pathways. [Mh] Termos MeSH primário: Pré-Eclâmpsia/sangue Proteína C/análise Proteína S/análise [Mh] Termos MeSH secundário: Adulto Estudos de Casos e Controles Estudos Transversais Ensaio de Imunoadsorção Enzimática Feminino Seres Humanos Nigéria Gravidez Fatores de Risco Inquéritos e Questionários [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Protein C); 0 (Protein S) [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: 170117 [St] Status: MEDLINE [do] DOI: 10.1002/ijgo.12085

10 / 2012

MEDLINE

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[PMID]: 28088608 [Au] Autor: Taniguchi F; Morishita E; Sekiya A; Nomoto H; Katsu S; Kaneko S; Asakura H; Ohtake S [Ad] Endereço: Department of Clinical Laboratory Science, Kanazawa University, Graduate School of Medical Science, 5-11-80 Kodatsuno Kanazawa, Ishikawa 920-0942, Japan; Department of Central Clinical Laboratory, Kanazawa Medical University Hospital, 1-1 Daigaku Uchinada Kahoku, Ishikawa 920-0293, Japan. [Ti] Título: Gene analysis of six cases of congenital protein S deficiency and functional analysis of protein S mutations (A139V, C449F, R451Q, C475F, A525V and D599TfsTer13). [So] Source: Thromb Res;151:8-16, 2017 Mar. [Is] ISSN: 1879-2472 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Congenital deficiency of protein S (PS), an anticoagulant factor, leads to venous thrombosis, with onset predominantly beginning in adolescence. In the present study, gene analysis of six unrelated Japanese families diagnosed with congenital PS deficiency identified five missense mutations in the PROS1 gene - c.757C>T (Ala139Val; A139V), c.1346 G>T (Cys449Phe; C449F), c.1352G>A (Arg451Gln; R451Q), c.1424G>T (Cys475Phe; C475F) and c.1574C>T (Ala525Val; A525V) - and one frameshift mutation, c.2135delA (Asp599ThrfsTer13; D599TfsTer13). C449F, R451Q, A525V and D599TfsTer13 are novel mutations. Results from ELISA to measure PS antigen levels in culture supernatant showed that the A139V variant was similar to wild-type, but other variants showed reductions when compared with wild-type. Results from pulse-chase analysis confirmed that the A139V variant exhibited secretion equivalent to wild-type, but for the other variants, there was no extracellular secretion, and it had nearly all been degraded inside the cell within six hours. Results from pulse-chase analysis using proteasome inhibitors also showed that intracellular degradation of mutant protein was inhibited. Activity of the A139V variant was decreased to 71% of wild-type, and the phospholipid binding capacity fell to as low as 45%. These results suggest that although the A139V variant has normal secretion, it has abnormal phospholipid binding capacity, and therefore causes type II PS deficiency, in which PS activity is decreased. It is also thought that with the other variants, misfolding due to amino acid mutations causes nearly all PS to be degraded intracellularly, therefore leading to type I PS deficiency. [Mh] Termos MeSH primário: Proteínas Sanguíneas/genética Mutação da Fase de Leitura Mutação de Sentido Incorreto Deficiência de Proteína S/genética Proteína S/genética [Mh] Termos MeSH secundário: Adolescente Adulto Grupo com Ancestrais do Continente Asiático/genética Proteínas Sanguíneas/metabolismo Feminino Genótipo Seres Humanos Japão/epidemiologia Masculino Fosfolipídeos/metabolismo Ligação Proteica Proteína S/metabolismo Deficiência de Proteína S/epidemiologia Deficiência de Proteína S/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Blood Proteins); 0 (PROS1 protein, human); 0 (Phospholipids); 0 (Protein S) [Em] Mês de entrada: 1704 [Cu] Atualização por classe: 170428 [Lr] Data última revisão: 170428 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170116 [St] Status: MEDLINE

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