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Introduction: Hemorheology is the study of the flow properties of the blood and its elements, which, together with natural anticoagulants, are important determinants of cardiovascular events. This study aimed to assess hemorheological and natural anticoagulant profiles of patients with celiac disease (CeD) comprehensively., Methods: Our study is a case-control study (registered under ISRCTN49677481) comparing patients with CeD with age- and sex-matched control subjects (1:1). We measured erythrocyte deformability (ED) at high (3-30 Pa) and low shears (0.3-3 Pa), erythrocyte aggregation, whole blood viscosity, plasma viscosity, and natural anticoagulants (protein C, protein S, and antithrombin activity). Adherence to gluten-free diet was estimated through dietary interview and urine gluten immunogenic peptide (urine GIP) detection., Results: After matching, we analyzed the data of 100 study participants. ED at high shears was impaired in CeD (P < 0.05 for all shears, confirmed by random forest analysis) independently of findings on CeD-specific serological assessment and urine GIP detection but slightly dependently on dietary adherence (P = 0.025 for 30 Pa shear). ED at low shears seemed to be impaired only in urine GIP+ CeD patients (P < 0.05 for all comparisons with urine GIP- CeD patients and control subjects). All parameters describing erythrocyte aggregation and whole blood viscosity were shifted toward a prothrombotic direction in patients with CeD with poor dietary adherence compared with those with good dietary adherence. Plasma viscosity and activity of natural anticoagulants did not differ across groups., Discussion: We observed diet-dependent and diet-independent prothrombotic hemorheological alterations in CeD, which can contribute to the elevated cardiovascular risk. The untoward metabolic changes during gluten-free diet, which can further aggravate hemorheological status, may indicate the implementation of prevention strategies.(Equation is included in full-text article.).

Introduction: Cytokeratin-18 (CK-18) is releasing into the blood during systemic cell death due to ischemia-reperfusion injury after cardiac arrest. Its caspase-cleaved form is specific to apoptosis. Previous investigations proved their prognostic value in different conditions. We firstly investigated the prognostic value of these markers after cardiac arrest. Method: Plasma samples of 40 resuscitated patients were collected 6, 24, and 72 hours after successful resuscitation to determine the marker concentrations. We investigated the association of the markers with the 30-day mortality, neurological outcome, circumstances of the cardiac arrest, laboratory and physical parameters. Results: Resuscitated patients had highly elevated CK-18 levels (3842 vs. 242; 559; 1644 ng/L) and decreased caspase-cleaved CK-18/CK-18 ratio (0.14 vs. 0.58; 0.22; 0.24) compared to healthy subjects, septic and postoperative patients suggesting severe grade of cell death, mainly necrosis. Neither the marker concentrations nor their kinetics showed difference between survivors and non-survivors. They did not show association with the length of the resuscitation, the initial rhythm or the neurological outcome either. CK-18 decreased in patients with good renal function in contrast to patients with renal failure. Significant negative correlation was observed between the 6-hour cytokeratin-18 and hemoglobin concentrations (r = -0.400, p<0.01), while the 30-day survival was associated with lower hemoglobin levels. Conclusion: Surprisingly the biomarkers did not show prognostic value among resuscitated population. The outcome is probably not determined by the complete cell damage, but the loss of a small group of cells with critical role and the reserve capacity of the patient. Orv Hetil. 2020; 161(1): 26-32.

Introduction: Haemorheological and haemostatic changes predispose to the development of arterial and venous thrombotic events; however, limited information is available on the status of these changes in coeliac disease (CeD) and inflammatory bowel disease (IBD). In this study, we aim to describe the haemorheological and haemostatic profiles of CeD and IBD patients in a Hungarian cohort of patients to investigate whether any alterations contribute to elevated thrombotic risk., Methods and Analysis: This is a case-control study involving newly diagnosed and followed CeD and IBD patients with age-matched and sex-matched non-CeD, non-IBD subjects with an allocation ratio of 1:1:1.After informed consent is obtained, a detailed medical history will be collected, including venous and arterial thrombotic risk factors and medications. Symptoms in CeD patients will be assessed with the Gastrointestinal Symptoms Rating Scale, and disease activity in IBD patients will be determined by disease-specific scores. Dietary adherence will be assessed among CeD patients with a thorough interview together with a measurement of self-reported adherence, dietary knowledge and urine analysis (detection of gluten immunogenic peptides). In addition to routine laboratory parameters, haemorheological (ie, erythrocyte deformability and aggregation, viscosity of whole blood and plasma) and haemostatic parameters (eg, protein C, protein S and antithrombin) with immunological indicators (ie, coeliac-specific serology and antiphospholipid antibodies) will be measured from venous blood for every participant.Primary and secondary outcomes will be haemorheological and haemostatic parameters, respectively. Univariate and multivariate statistics will be used to compare CeD and IBD patients to control subjects. Subgroup analysis will be performed by disease type in IBD, (Crohn's disease and ulcerose colitis), dietary adherence in CeD, and disease activity in IBD and CeD., Ethics and Dissemination: The study was approved by the Regional and Local Research Ethics Committee, University of Pécs (Ref. No. 6917). Findings will be disseminated at research conferences and in peer-reviewed journals., Trial Registration Number: ISRCTN49677481., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Endothelial cells of brain capillaries forming the blood-brain barrier play an important role in the pathogenesis and therapy of Alzheimer's disease. Amyloid-β (Aβ) peptides are key pathological elements in the development of the disease. A blood-brain barrier model, based on primary rat brain endothelial cells was used in which the barrier properties were induced by glial cells. The effects of amyloid peptides have been tested on cell viability and barrier functions. Aβ showed toxic effects on primary rat brain endothelial cells measured by MTT dye conversion and the lactate dehydrogenase release. Morphologically cytoplasmic vacuolization, disruption of the structure of cytoplasmic organelles and tight junctions could be observed in brain endothelial cells. Treatment with Aβ1-42 decreased the electrical resistance, and increased the permeability of brain endothelial cell monolayers for both fluorescein and albumin. Serum amyloid P component which stabilizes Aβ fibrils in cortical amyloid plaques and cerebrovascular amyloid deposits significantly potentiated the barrier-weakening effect of Aβ1-42. Sulfated polysaccharide pentosan could decrease the toxic effects of Aβ peptides in brain endothelial cells. It could also significantly protect the barrier integrity of monolayers from damaging actions of peptides. Pentosan modified the size, and significantly decreased the number of amyloid aggregates demonstrated by atomic force microscopy. The present data further support the toxic effects of amyloid peptides on brain endothelial cells, and can contribute to the development of molecules protecting the blood-brain barrier in Alzheimer's disease.