bluuebunny/crossref_metadata_2025_split huggingface dataset:
NSAID und langkettige maritime ω-3-Fettsäuren
Authors: Gröber Uwe 
Published: June 2018

ZusammenfassungBei der rheumatoiden Arthritis greifen langkettige maritime ω-3-Fettsäuren auf mehreren Wegen in das Entzündungsgeschehen ein. Die regelmäßige Einnahme von EPA und DHA senkt den Bedarf an nichtsteroidalen Antirheumatika und die Nebenwirkungsrate.
Familiäre Kardiomyopathien – von der Phänomenologie zur zielgerichteten Therapie
Authors: Amr Ali , Katus Hugo , Meder Benjamin 
Published: June 2018

ZusammenfassungKardiomyopathien stellen eine heterogene Gruppe von Herzmuskelerkrankungen dar, die häufig durch genetische Mechanismen bedingt sind oder in ihrem Verlauf durch solche beeinflusst werden. Im Bereich der genetischen Diagnostik spielen insbesondere die monogenen und syndromalen Formen eine wichtige Rolle, da durch die Identifikation einer pathogenen genetischen Variante nicht nur eine Bestätigung der Diagnose, sondern auch eine Abklärung auf Anlageträgerschaft und damit Erkrankungsrisiko bei Angehörigen möglich ist, sowie in bestimmten Fällen eine Vorhersage des zu erwartenden Krankheitsverlaufs erfolgen kann. Schon heute ergeben sich durch Nachweis von bestimmten Genvarianten therapeutische Konsequenzen, was durch die zunehmende Anzahl an molekularen Therapieentwicklungen in Zukunft deutlich zunehmen wird. Die genetische Diagnostik von Patienten und Angehörigen ist dabei eingebettet in ein strukturiertes Kardiomyopathie-Management und folgt 3 Hauptkonzepten: 1) Identifizierung und, falls möglich, Behandlung der Krankheitsursache, 2) Erkennung und Verringerung des Risikos für den plötzlichen Herztod und 3) Prävention oder Behandlung von Herzinsuffizienz und deren Folgen. In dem vorliegenden Übersichtsartikel sollen aktuelle Entwicklungen zu den überwiegend genetischen, strukturellen Kardiomyopathien reflektiert werden.
High Serum Fractalkine is Associated with Lower Trabecular Bone Score in Premenopausal Women with Graves’ Disease
Authors: Kužma Martin , Vaňuga Peter , Binkley Neil , Ságová Ivana , Pávai Dušan , Blažíček Pavel , Kužmová Zuzana , Jackuliak Peter , Vaňuga Anton , Killinger Zdenko , Payer Juraj 
Published: June 2018

AbstractChemokine CX3CL1 (fractalkine) may be an important factor linking thyroid status and bone remodeling, through tetrac, a derivative of thyroxine. This study explores the relationship between serum fractalkine levels and parameters of thyroid status and bone in premenopausal women with Graves’ disease (GD) in comparison to healthy controls. This cross-sectional study included three premenopausal female groups: active GD; cured GD, and healthy age-, gender-, and BMI-matched controls. Measurement of serum fractalkine levels (Quantikine® ELISA), total amino-terminal peptide of procollagen type 1 (P1NP), CTx, thyroid hormones, BMD and trabecular bone score (TBS) were performed in all study subjects. Sixty women (21, 16, and 23 in active GD, cured GD, and healthy control groups, respectively) were included. Serum fractalkine levels were higher (p<0.05) in active and cured GD subjects compared to healthy controls (mean 0.7±0.14; 0.93±0.15, and 0.48±0.13 ng/ml, respectively). Lumbar spine BMD was lowest in the cured GD group in comparison to active GD and control group subjects (0.926±0.03; 1.016±0.03; 1.051±0.03 g/cm2; p<0.05, respectively). TBS was lower (p<0.05) in both GD groups than controls being lowest in those with active GD (1.395±0.02; 1.402±0.02, 1.469±0.02, respectively). Serum fractalkine concentration was positively correlated with fT4, and negatively correlated with TBS values. GD in pre-menopausal females is associated with increased serum fractalkine concentration and decreased TBS. Fractalkine may be a currently unappreciated link between hyperthyroidism and bone; further research into this possibility is needed.
ω-3-Fettsäuren bei Migräne
Authors: Schmiedel Volker 
Published: June 2018

ZusammenfassungEin 50-jähriger Migränepatient konnte durch regelmäßige Einnahme von Fischöl von seinen Beschwerden befreit werden. Die Therapie sollte sich am AA / EPA-Quotienten des Patienten orientieren und bei der Dosierung sind die unterschiedlichen DHA- und EPA-Gehalte der Öle bzw. Kapseln zu beachten.
Fusarihexins A and B: Novel Cyclic Hexadepsipeptides from the Mangrove Endophytic Fungus Fusarium sp. R5 with Antifungal Activities
Authors: Zhu Xinwei , Zhong Yu , Xie Zihui , Wu Manlin , Hu Zhibo , Ding Weijia , Li Chunyuan 
Published: June 2018

AbstractTwo novel cyclic hexadepsipeptides, fusarihexin A (1) and fusarihexin B (2), and two known compounds, cyclo-(L-Leu–L-Leu–D-Leu–L-Leu–L-Val) (3) and cyclo-(L-Leu–L-Leu–D-Leu–L-Leu–L-Ile) (4), were isolated from the marine mangrove endophytic fungus Fusarium sp. R5. Their chemical structures were elucidated on the basis of spectroscopic data and Marfeyʼs analysis. In an in vitro bioassay, fusarihexin A (1) remarkably inhibited three plant pathogenic fungi: Colletotrichum gloeosporioides (Penz.) Sacc., which causes anthracnose in many fruits and vegetables, Colletotrichum musae (Berk. and M. A. Curtis) Arx, which causes crown rot and anthracnose in bananas, and Fusarium oxysporum Schlecht. f. sp. lycopersici (Sacc.) W. C. Snyder et H. N. Hansen, which causes Fusarium wilt and fruit rot in tomatoes. Fusarihexin B (2) strongly inhibited C. gloeosporioides and C. musae. The compounds were more potent than carbendazim, which is widely used as an agricultural and horticultural fungicide worldwide.
On the Mechanism of Thrombolytic Action of Thromboxane Synthetase Inhibitors
Authors: Korbut R , Dembińska-Kieć A , Świȩs J , Źmuda A , Gryglewski R J 
Published: June 2018

SummaryUsing our in vivo model for studying drugs which prevent deposition of thrombi or dissipate thrombi formed in extracorporeal circulation over a collagen strip superfused with arterial blood of anaesthetized and heparinized cats, we have found that dazoxiben - a thromboxane synthetase inhibitor - possesses not only antithrombotic but also thrombolytic potency in vivo (ED50 = 3.8 mg/kg i.v.). The thrombolytic potency of dazoxiben was antagonized by aspirin at a dose of 50 mg/kg i.v. Moreover, dazoxiben stimulated the generation of prostacyclin in isolated rat aortic slices incubated in platelet rich plasma, but not in platelet poor plasma. It is suggested that the thrombolytic potency of thromboxane synthetase inhibitors after their systemic administration is associated with the release of prostacyclin and/or prostacyclin-stable metabolites by the vascular endothelium owing to feeding of prostacyclin synthetase with prostaglandin endoperoxides acumulated in platelets following the inhibition of thromboxane synthetase.
Contact Thermography, 99mTc-Plasmin Scintimetry and 99mTc-Plasmin Scintigraphy as Screening Methods for Deep Venous Thrombosis Following Major Hip Surgery
Authors: Christensen S Winter , Wille-Jørgensen P , Kjær L , Stadeager C , Widding A , Vestergaard Aa , Bjerg-Nielsen A 
Published: June 2018

SummaryFifty-six patients scheduled for total hip alloplasty were screened for deep venous thrombosis by means of 99mTc-plasmin scintimetry, 99mTc-plasmin scintigraphy and contact thermography. Investigations were performed on the seventh postoperative day, and a total of 112 legs were examined. Bilateral ascending phlebography was used as reference procedure, and the criteria for deep venous thrombosis were intraluminal filling defects at phlebography. Six patients developed unilateral deep venous thrombosis. All three screening procedures revealed many false positive and several false negative results. The nosographic sensitivity/specificity was 33%/75% for scintimetry, 50%/91% for scintigraphy and 33%/87% for contact thermography, respectively. It is concluded that all three tests are of no value as screening methods for deep venous thrombosis following major elective hip surgery.
Release Pattern of the Vascular Plasminogen Activator and Its Inbibitor in Human Postvenous Occlusion Plasma as Assessed by a Spectrophotometric Solid-Phase Fibrin-tPA Activity Assay
Authors: Anglés-Cano E , Boutière B , Arnoux D , Masson C , Contant G , Benchimol P , Sampol J 
Published: June 2018

SummaryVascular or tissue-type plasminogen activatbr(plasma t-PA) is the circulating physiological fibrinolytic enzyme of endothelial cell origin which function is regulated by fibrin and a specific inhibitor (PAI). To study the pattern of release of t-PA and the behavior of t-PA-PAI complexes in plasma. we determined t-PA activity in 44 healthy subjects before and after 10 min offorearm venous occlusion using a new spectrophotmnetrio solid-phase fibrin-tPA activity assay. The assay is based on 1) the high affinity binding of t-PA tofibrin, and 2) the detection of fibrin-bound t-PA by measuring the release of pNA from a chromogenic substrate in the presence of plasminogeu. Values at.rest were rather undetectable in plasma (0.05 ± 0.03 IU/ml, in 23 out of 44 samples) but were positively detected in all the euglobulins: 0.88 ± 0.68 IU/ml. After venous occlusion the majority ofplasmas (36 out of 44) shoWed a slight increase in t-PA activity (0.65 ± 0.63 IU/ml) as compared to the important level observed in all the euglobulins (9.78 ± 9.58 IU/ml). So, the ratio plasma/euglobulin t-PA activity was very low (0.06) and remained identical in both pre- and postocclusion samples. However, when diluted plasmas were tested the inhibitory effect disappeared and t-PA activity increased indicating that although t-PA circulates in a neutralized state it can be available for fibrinolysis. Since 1) no binding of α2 antiplasmin to fibrin in solid-phase could be demonstrated, 2) there was no correlation between α2 antiplasmin and t-PA activity, and 3) a PAI-depleted plasma with a normal content of α2 antiplasmin did not suppress the activity of t-PA, the inhibitory effect was attributed to PAL Our findings suggest that both t-PA and PAI are released. by venous occlusion and circulates in plasma as a t-PA-PAI complex.
Plasma Thrombospondin as an Indicator of Intravascular Platelet Activation in Patients with Vasculitis
Authors: McCrohan M B , Huang S W , Sleasman J W , Klein P A , Kao K J 
Published: June 2018

SummaryThe use of plasma thrombospondin (TSP) concentration was investigated as an indicator of intravascular platelet activation. Patients (n = 20) with diseases that have known vasculitis were included in the study. The range and the mean of plasma TSP concentrations of patients with vasculitis were 117 ng/ml to 6500 ng/ml and 791±1412 ng/ml (mean ± SD); the range and the mean of plasma TSP concentrations of control individuals (n = 33) were 13 ng/ml to 137 ng/ml and 59±29 ng/ml. When plasma TSP concentrations were correlated with plasma concentrations of another platelet activation marker, β-thromboglobulin (P-TG), it was found that the TSP concentration inei eased exponentially as the plasma β-TG level rose. A positive correlation between plasma levels of plasma TSP and serum fibrin degradation products was also observed. The results suggest that platelets are the primary source of plasma TSP in patients with various vasculitis and that plasma TSP can be a better indicator than β-TG to assess intravascular platelet activation due to its longer circulation half life.
Plasminogen Activator Inhibitor-1 Is the Primary Inhibitor of Tissue-Type Plasminogen Activator in Pregnancy Plasma
Authors: Jørgensen Maja , Philips Malou , Thorsen Sixtus , Selmer Johan , Zeuthen Jesper 
Published: June 2018

SummaryThe aim of the present work was to clarify to what extent plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) contribute to the increase in plasma inhibition of tissue-type plasminogen activator (t-PA) observed during pregnancy. It was demonstrated that a monoclonal antibody against PAI-1 almost completely quenched inhibition of single-chain t-PA and most of the inhibition of two-chain t-PA in plasma during the third trimester of piegnancy. The remaining inhibition of two-chain t-PA was to a great extent abolished by a PAI-2 antibody. The second order rate constant (k1) for inhibition of single-chain t-PA by the inhibitor neutralized by the PAI-1 antibody was about 4.8 · 106 M-1 · s-1. The conversion of singlechain t-PA to the two-ehain form increased the reaction rate with the inhibitor about 3-fold. These kinetic data are compaiable with those obtained with TAI-l in non-pregnancy plasma oi with purified PAI-1. From the above results it is concluded that PAI-1 is the primary inhibitor of both single-chain and two chain t PA and that PAI-2 is the secondary inhibitor of two-chain t-PA in pregnancy plasma. The concentration of reactive PAI-1 versus gestation age was assayed in plasma from 6 women by binding of PAI-1 to 125I-labelled single-chain t-PA followed by quantitation of the labelled t-PA-PAI-1 complex after separation by SDS- polyacrylamide gel electrophoresis. It was found that the concentration of PAI-1 increased 4 to 8-fold during the gestation period reaching a level of about 1.4 nM at term. Post partum the plasma concentration declined abruptly within 24 h to the level observed in age-matched non-pregnant women.
Comparison of Specific Antibody, D-Phe-Pro-Arg-CH2Cl and Aprotinin for Prevention of In Vitro Effects of Recombinant Tissue-Type Plasminogen Activator on Haemostasis Parameters
Authors: Seifried E , Tanswell P 
Published: June 2018

SummaryIn vitro, concentration-dependent effects of rt-PA on a range of coagulation and fibrinolytic assays in thawed plasma samples were investigated. In absence of a fibrinolytic inhibitor, 2 μg rt-PA/ml blood (3.4 μg/ml plasma) caused prolongation of clotting time assays and decreases of plasminogen (to 44% of the control value), fibrinogen (to 27%), α2-antiplasmin (to 5%), FV (to 67%), FVIII (to 41%) and FXIII (to 16%).Of three inhibitors tested, a specific polyclonal anti-rt-PA antibody prevented interferences in all fibrinolytic and most clotting assays. D-Phe-Pro-Arg-CH2Cl (PPACK) enabled correct assays of fibrinogen and fibrinolytic parameters but interfered with coagulometric assays dependent on endogenous thrombin generation. Aprotinin was suitable only for a restricted range of both assay types.Most in vitro effects were observed only with rt-PA plasma concentrations in excess of therapeutic values. Nevertheless it is concluded that for clinical application, collection of blood samples on either specific antibody or PPACK is essential for a correct assessment of in vivo effects of rt-PA on the haemostatic system in patients undergoing fibrinolytic therapy.
Synergistic Effect on Thrombolysis of Sequential Infusion of Tissue-Type Plasminogen Activator (t-PA) Single-Chain Urokinase-Type Plasminogen Activator (scu-PA) and Urokinase in the Rabbit Jugular Vein Thrombosis Model
Authors: Collen D , Stassen J M , De Cock F 
Published: June 2018

SummaryIn a quantitative model of thrombolysis, consisting of rabbits with a 125T-fibrin labeled blood clot in the jugular vein, simultaneous intravenous infusion over 4 hours of t-PA and scu-PA or of t-PA and urokinase had a significantly greater (p <0.01) thrombolytic effect than could be anticipated on the basis of the added effects of each agent alone. In order to further investigate the mechanism of this in vivo synergism, recombinant t-PA (rt-PA) and scu-PA in synergistic amounts were infused: 1) simultaneously over 4 hours, 2) rt-PA over 1 hour, then 15 min later scu-PA over 2 hours and 3) scu-PA over 1 hour, then 15 min later rt-PA over 2 hours. Simultaneous infusion of 0.1 mg/kg rt-PA and 0.2 mg/kg scu-PA gave 48°2 percent thrombolysis (mean ° SEM, n = 5) and of 0.2 mg/kg rt-PA and 0.4 mg/kg scu-PA 67°5 percent (n = 5). When these infusions were given sequentially, rt-PA followed by scu-PA gave 32 °5 (n = 4) and 49 °8 (n = 4) percent lysis, but scu-PA followed by rt-PA yielded only 14° 1 (n = 4) and 21 ° 1 (n = 4) percent lysis, indicating that synergism occurs when rt-PA is followed by scu-PA but not when scu-PA is followed by rt-PA. In order to investigate the hypothesis that rt-PA predigests the clot resulting in more efficient plasminogen activation by scu-PA at the clot surface, partial thrombolysis was induced by injection of urokinase. Subsequent infusion of 0.4 mg/ kg of scu-PA did however not result in more thrombolysis than expected for additive effects. Infusion of 0.5 mg/kg of urokinase followed by 0.1 mg/kg rt-PA was not synergistic (24 °3 percent lysis, n = 3) whereas lysis by rt-PA followed by urokinase was 34°3 percent (p <0.1, n = 3).Sequential therapy with rt-PA followed by scu-PA might constitute an alternative to simultaneous infusion of synergistic thrombolytic agents.
Potentiation by Heparin Fragments of Thrombolysis Induced with Human Tissue-Type Plasminogen Activator or Human Single-Chain Urokinase-Type Plasminogen Activator
Authors: Stassen J M , Juhan-Vague I , Alessi M C , De Cock F , Collen D 
Published: June 2018

SummaryThe effect of heparin and of two low molecular weight (low M
r) fractions of heparin on thrombolysis with recombinant human tissue-type plasminogen activator (rt-PA, Genentech Inc., So. San Francisco, CA) or human single chain urokinase-type plasminogen activator (scu-PA, Sandoz AG, Basle, Switzerland) was measured in a rabbit jugular vein thrombosis model. Four bolus injections of 200 anti-Factor Xa units/kg body weight of heparin (Liquemine, Hoffmann-La Roche, Basle, Switzerland), of 90 units/kg of CY 216 (Choay, Paris, France) or of 90 units/kg of CY 222 (Choay, Paris, France) were given intravenously, immediately after the start of the infusion of rt-PA or scu-PA and at hourly intervals during their intravenous infusion over 4 hours. The bolus injections resulted in anti-Factor Xa levels in plasma of 5.7 ± 1.2 units/ml just before the repeat bolus injections of heparin with corresponding values of 3.9 ± 0.2 units/ml for CY 216 and 1.6 ± 0.2 units/ml for CY 222.Thrombolysis with 0.25 mg/kg rt-PA was 36 ± 1 percent (n = 9) in the absence of anticoagulant, 40 ± 1 percent (n = 7, p <0.05) in the presence of heparin, 49 ± 5 percent (n = 7, p <0.02) with CY 216 and 62 ± 5 percent (n = 7, p <0.01) with CY 222. Thrombolysis with 0.5 mg/kg scu-PA was 23 ± 1 percent (n = 4) without heparin, and increased to 24 ± 1 percent (n = 4, p >0.1) with heparin, to 32 ± 2 percent (n = 4, p <0.01) with CY 216 and to 33 ± 3 percent (n = 4, p <0.01) with CY 222.It is concluded that, at these high doses, the two low M
r heparin fractions CY 216 and CY 222, potentiate thrombolysis by rt-PA and scu-PA in this animal model.
Plasma and Urinary Heparin Cofactor II Levels in Patients with Nephrotic Syndrome
Authors: Grau E , Oliver A , Félez J , Barceló P , Fernandez C , Ballarin J A , Fontcuberta J , Rutilant M L I 
Published: June 2018

SummaryHeparin cofactor II (HC II) levels were measured by electroimmunoassay in plasmas and urines from 68 patients with nephrotic syndrome. In addition, antithrombin III (AT III) and protein C (PC) activities and antigens were measured also in the same group of patients. Seven of these patients had histories of thrombosis. Plasma HC II levels (mean ± SD 105 ± 43) were not different from levels in healthy subjects (94 ± 17). Only 5 patients had low plasma levels of HC II. None of the patients with thrombosis had low HC II levels. Even though measurable amounts of HC II were found in 25 urines from 50 patients. There was a relationship in the urinary excretion between HC II and AT III and their urinary clearances were quite similar. However, no correlation was found between plasma HC II and AT III levels, and levels of AT III activity and antigen were significantly lower than in healthy subjects. Three patients with hystories of thrombosis had low AT III levels. Most patients (including those with thrombosis histories) had high plasma PC levels and increased urinary loss.It is suggested that HC II does not play an important role in the pathogenesis of thrombosis in nephrotic syndrome.
Immunochemical Characterization of Crosslinked Derivatives Isolated from Alpha Chain Oligomers Formed During Early Stages of Fibrin Crosslinking
Authors: Sobel Joan H , Thibodeau Christiane A , Ann Gawinowicz Kolks Mary , Canfield Robert E 
Published: June 2018

SummaryEarly crosslinked α chain oligomers (EαXL) that formed within ½ h of in vitro clot formation were isolated from preparations of reduced, carboxymethylated fibrin by gel filtration on Sepharose CL-4B. Cyanogen bromide (CNBr) digestion of EaXL released a mixture of fragments which could be partially separated by Sephadex G-150 chromatography. Crosslinked ahd noncrosslinked forms of the Aα chain peptides, CNBr VIII (Aα #241-476) and CNBr X (Aα #518-584) were identified in the column effluent both by radioimmunoassay (RIA) and by immunoblotting using polyclonal antisera (anti-CNBr VIII, anti-CNBr X) and monoclonal antibodies (F-103, binds to Aα #259-276; F-102, binds to Aα #540-554), respectively. Immunoaffinity chromatography of the crosslinked material, on F-103, followed by F-102 Sepharose, resulted in the separation of two types of fragments, each of which contained an early a chain crosslink. One of these (35-37K) exhibited coincident CNBr VIII and CNBr X immunoreactivities, while the other (54-59K) exhibited only CNBr VIII immunoreactivity, based on immunoblotting and RIA findings. NH2-terminal sequencing and cyanoethylation data provided biochemical evidence for the occurrence of covalent CNBr VIII-X as well as covalent CNBr VIII-VIII interactions during early a chain crosslinking. These findings indicate, for the first time, that both glutamine acceptor and lysine donor activities may be localized within CNBr VIII. This information should facilitate the chemical identification of a chain residues that partner during factor XIIIa-catalyzed crosslinking and thus enable development of reagents for the generation of fibrin-specific antibodies.
Glucose Inhibits Prostacyclin Production by Cultured Aortic Endothelial Cells
Authors: Ono Hiroshi , Umeda Fumio , Inoguchi Toyoshi , Ibayashi Hiroshi 
Published: June 2018

SummaryA reduction in production of prostacyclin (PGI2) by the cells in the vascular wall may play a role in the pathogenesis of atherosclerosis in diabetic patients. The present study was undertaken to evaluate the effect of glucose on PGI2 production by endothelial cells in vitro. It was shown that PGI2 production by cultured bovine aortic endothelial cells was significantly reduced in the presence of a high concentration of glucose (300 mg/dl) compared with physiological concentrations of glucose (100 mg/ dl). In contrast, no reduction in PGI2 production was observed in cells cultured with equimolar mannitol, suggesting that glucose itself, rather than the effect of osmolality, inhibited PGI2 production by cultured endothelial cells.In addition, a high concentration of glucose also inhibited the proliferation of cultured endothelial cells.