Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Authors:Sane; Markus; Sund, Reijo; Mustonen, Pirjo Abstract:Pulmonary embolism is listed as a cause of death in fewer and fewer cases in the twenty-first century. Autopsies reveal undiagnosed pulmonary embolism at a significant rate, but fewer and fewer autopsies are being performed. It could be that deaths from pulmonary embolism are not decreasing, but are increasingly missed because of decreasing autopsy rate. Population-based registry data of all individuals with pulmonary embolism related death from the Finnish death certificate archive from 1996 to 2017 were collected. The pulmonary embolism mortality trend was analysed with linear regression and the association of pulmonary embolism mortality with the number of autopsies was also assessed. Deaths with pulmonary embolism as immediate, underlying and contributory cause of death were not only included, but also analysed separately. In addition, the estimated pulmonary embolism mortality when presumptively missed pulmonary embolisms are taken into account is presented. During 1996–2017, the pulmonary embolism related mortality rate decreased 28% from 25: 100 000 to 18: 100 000, if all pulmonary embolism deaths were analysed, and 51% from 21: 100 000 to 11: 100 000 if contributory pulmonary embolism deaths were excluded. From 1996 to 2009, autopsy rate in the population remained unchanged, but declined thereafter. In 1996, autopsy rate was 31.1% (15 319/49167) and in 2017 20.1% (10830/53 923). Our results suggest that there has been real improvement in the prevention of death from pulmonary embolism in Finland in the twenty-first century. However, due to the decreasing autopsy rate, the pulmonary embolism mortality trend after 2010 should be interpreted more carefully. PubDate: Wed, 01 Jun 2022 00:00:00 GMT-
Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Authors:Arslan; Fatma Demet; Başok, Banu Işbilen; Terzioğlu, Mustafa; Altan, Tuba Kansu; Karaca, Yeşer; Senger, Suheyla Serin; Çolak, Ayfer Abstract:Clinicians experience some challenges due to the lack of standardization of test, although D-dimer is a prognostic marker for COVID-19. We compared the clinical and analytical performances of D-dimer results obtained from different devices, kits and methods in patients with a diagnosis of COVID-19. Thirty-nine patients with a diagnosis of COVID-19 and 24 healthy individuals were included in the study. D-dimer levels were measured with Innovance D-DIMER kit (immunoturbidimetric method) on Sysmex CS-2500 and BCS XP and VIDAS D-Dimer Exclusion II kit (enzyme-linked fluorescence method) on mini VIDAS. The studies of precision, method comparison and clinic performance were performed. The variation coefficients in all systems were within the acceptable imprecision (7.8%). Bias%(12.5%) between BCS XP and Sysmex CS-2500 was lower than the acceptable Bias%(15.5%). Bias% values (19.2% and 33.3%, respectively) between Mini VIDAS with BCS XP and Sysmex CS-2500 were higher than the acceptable Bias%. The correlation coefficients among all systems were 0.89–0.98. For 500 ng/ml FEU, there was almost perfect agreement between BCS XP and Sysmex CS-2500, a moderate agreement between Mini VIDAS and BCS XP and Sysmex CS-2500. The cut-off values for distinguishing between individuals with and withoutCOVID-19 were Mini VIDAS, Sysmex CS-2500 and BCS XP 529, 380 and 390 ng/ml FEU, respectively. The immunoturbidimetric method can be used as an alternative to the enzyme-linked fluorescent method because of satisfactory agreement at the different thresholds proposed for venous thromboembolism. However, it is recommended to follow up COVID-19 with the D-dimer results obtained by the same assay system. PubDate: Wed, 01 Jun 2022 00:00:00 GMT-
Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Authors:Schneider; Sabine; Reißig, Julian; Weisbach, Volker; Achenbach, Susanne; Strobel, Julian; Hackstein, Holger Abstract:The members of a Caucasian family were genetically analyzed on suspicion of hereditary protein S deficiency. A novel mutation, c.1904T>C, associated with severe quantitative protein S deficiency was found. The novel PROS1 mutation was identified by sequencing of the PROS1 gene coding sequence. The identified c.1904T>C point mutation results in p.Phe635Ser amino acid exchange, which is located in the Laminin G-like 2 domain of protein S. Computational analysis indicates that this amino acid exchange affects the correct folding of the protein S antigen. Furthermore, this mutation is located in a region of the Laminin G-like 2 domain where changes in the amino acid sequence often result in decreased secretion. We postulate that the novel p.Phe635Ser mutation might lead to an incorrect folding, and thus, to a strongly impaired secretion of this protein S variant. We named this novel variant protein PubDate: Wed, 01 Jun 2022 00:00:00 GMT-
Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
Authors:Ceznerová; Eliška; Kaufmanová, Jiřina; Stikarová, Jana; Pastva, Ondřej; Loužil, Jan; Chrastinová, Leona; Suttnar, Jiři; Kotlín, Roman; Dyr, Jan Evangelista Abstract:Here, we present the first case of fibrinogen variant FGG c.8G>A. We investigated the behaviour of this mutated fibrinogen in blood coagulation using fibrin polymerization, fibrinolysis, fibrinopeptides release measurement, mass spectrometry (MS), and scanning electron microscopy (SEM). The case was identified by routine coagulation testing of a 34-year-old man diagnosed with thrombosis. Initial genetic analysis revealed a heterozygous mutation in exon 1 of the FGG gene encoding gamma chain signal peptide. Fibrin polymerization by thrombin and reptilase showed the normal formation of the fibrin clot. However, maximal absorbance within polymerization was lower and fibrinolysis had a longer degradation phase than healthy control. SEM revealed a significant difference in clot structure of the patient, and interestingly, MS detected several posttranslational oxidations of fibrinogen. The data suggest that the mutation FGG c.8G>A with the combination of the effect of posttranslational modifications causes a novel case of hypofibrinogenemia associated with thrombosis. PubDate: Wed, 01 Jun 2022 00:00:00 GMT-