bluuebunny/crossref_metadata_2025_split huggingface dataset:
Circulating levels of inflammatory cytokines (IL-1β and TNF-α), resistance to activated protein C, thrombin and fibrin generation in uncomplicated pregnancies
Authors: Arkel Yale , Paidas Michael , Lockwood Charles , Ku De-Hui 
Published: November 2003

SummaryWe studied 33 women during normal uneventful pregnancies and with no history of previous adverse pregnancy events for markers of activated coagulation and thrombin activity including prothrombin fragment 1.2(PF1.2), thrombin- antithrombin (TAT), and soluble fibrin polymer (SFP). In addition, we measured potential thrombin generation through the addition of thromboplastin to patient plasma in the presence of a throm-bin-specific chromogenic substrate determined serially over a period of time - Endogenous Thrombin Potential assay (ETP). This assay was performed with plasma treated and untreated with activated protein C (APC). The fibrinolytic system was assessed by measurement of thrombin activatable fibrinolysis inhibitor (TAFI). These findings were correlated with the levels of pro-inflammatory cytokines, interleukine-1β and tumor necrosis factor-α. Our data supports previous reports that indicate that resistance to activated protein C and coagulation activation markers are commonly increased in the later 2/3rds of pregnancy. There are no differences in thrombin generation potential, as determined by the ETP assay without the addition of APC, in the three trimesters. However, the thrombin reserve (TR), the ETP result without APC divided by the ETP result with the addition of APC, is increased above the reference range in the 2nd and 3rd trimesters. Patients with increased TR and resistance to APC had increased levels of TNF-α. Increased proinflammatory cytokines are reportedly associated with changes in the APC system with a decrease in the ability to generate APC. A sub-group of pregnancies with APC resistance had increased levels of TNF-α and may be important in the risk for adverse pregnancy outcomes.
Syndecan-4-dependent signaling in the inhibition of endotoxin-induced endothelial adherence of neutrophils by antithrombin
Authors: Kaneider Nicole , Förster Ellen , Mosheimer Birgit , Sturn Daniel , Wiedermann Christian 
Published: November 2003

SummaryCirculating endotoxin is elevated in sepsis and plays a role in endothelial dysfunction whereas antithrombin is decreased by virtue of its consumption during complex formation with clotting factors and by proteolytic degradation by granulocyte elastase. Dysfunction of endothelium results in enhanced leukocyte rolling and diapedesis into tissues leading to edema formation and injury. Antithrombin exerts beneficial effects on endothelial function in sepsis. A direct anti-inflammatory action of anti-thrombin in inflammatory cells is exerted via heparan sulfate proteoglycans. In this study, we investigated whether antithrom-bin affects endotoxin-induced adhesion of neutrophils to human endothelial cells in vitro and whether glycosaminoglycans are involved in its signaling. Adhesion of human neutrophils to monolayers of umbilical vein endothelial cells was tested under static conditions. Endothelial cells were pretreated with endotoxin, interleukin-1, heparinase-I, chondroitinase-ABC or anti-syndecan-4-antibody. Endotoxin and interleukin-1 increased neutrophil adherence to human umbilical vein endothelial cells which was inhibited by antithrombin. Concomitant incubation with pentasaccharide abolished this effect of antithrombin. Treatment of endothelial cells with heparinase or chondroitinase led to higher adhesion and prevented effects of antithrom-bin. With antibodies to syndecan-4, enhanced adhesion of neutrophils was observed. As studied by Western blotting, endo-toxin-induced signaling was diminished by antithrombin and the effect was reversible by chondroitinase or heparinase. From our results, we can conclude that endotoxin-induced adhesion of leukocytes to endothelium can be reversed by ligation of syndecan-4 with antithrombin´s heparin-binding site and interferences with stress response signaling events in endothelium.
The angiotensin-converting-enzyme insertion/deletion polymorphism is not related to venous thrombosis
Authors: Renner Wilfried , Gugl Alexander , Cichocki Lisa , Gasser Robert , C.Wascher Thomas , Pilger Ernst , Köppel Herwig 
Published: November 2003

SummaryThe insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting-enzyme (ACE) is associated with ACE plasma levels and activity. Conflicting results have been reported about the relevance of this polymorphism for venous thrombosis. The aim of the present study was to analyze the role of this polymorphism for deep venous thrombosis. The study was designed as a case-control study, including 330 patients with documented deep venous thrombosis and 354 controls. ACE genotype was determined by size-analysis of polymerase chain reaction products. Results showed that, ACE genotype frequencies were similar between patients (II: 24.8%; ID: 43.3%; DD: 31.8%) and controls (II: 22.9%; ID: 50.6%; DD: 26.6%, P = 0.15).The adjusted odds ratio of carriers of the DD genotype for venous thrombosis was 1.24 (95% confidence interval 0.90–1.80).The polymorphism was furthermore not associated with age at first thromboembolic event or the occurrence of pulmonary embolism. From these results, we can conclude that the ACE I/D polymorphism is not a significant risk factor for deep venous thrombosis.
Antithrombotic role of nitric oxide in rats under physiological conditions
Authors: Okudaira Mariko , Ontachi Yasuo , Mizutani Tomoe , Omote Mika , Yoshida Tomotaka , Kaneda Minori , Yamazaki Masahide , Morishita Eriko , Takami Akiyoshi , Miyamoto Ken-ichi , Nakao Shinji , Asakura Hidesaku 
Published: November 2003

SummaryAlthough sepsis-induced release of nitric oxide (NO) is known to have an antithrombotic effect, it is unknown if NO exerts this same effect under physiological conditions. We have therefore attempted to determine whether or not NO protects against thrombus formation in normal Wistar rats injected with various amounts (0.8, 4.0, 20.0 and 100mg/kg/4hr) of L-NAME (N (omega)-nitro-l-arginine methyl ester), an NO synthase inhibitor, via the tail vein. Plasma levels of D-dimer fragments of fibrin were significantly increased in rats receiving L-NAME (0.21±0.04, 0.22±0.05, 0.26±0.07, 0.59±0.17µg/mL, means±SE; p<0.05, 0.05, 0.05, 0.01: L-NAME 0.8, 4, 20, 100, respectively, compared with control levels: <0.06 µg/mL), and thrombin-antithrombin complex (TAT) levels were significantly increased in rats receiving 20mg/kg/4hr or greater doses of L-NAME (4.5±1.1, 4.7±1.4, 18.7±4.9, 42.5±4.0ng/mL, NS, NS, p<0.05, 0.01, respectively, compared with control levels: 3.8±1.2 ng/mL). Glomerular fibrin deposition was increased in a dose-dependent manner in rats receiving L-NAME (6.8±1.5, 13.9±1.6, 32.4±2.6, 49.2±5.2%, p<0.05, 0.05, 0.01, 0.01, respectively, compared with control levels: 0.0±0.0%). Renal dysfunction and hepatic dysfunction were observed in rats receiving 20mg/kg/4hr or greater, or 100mg/kg/4hr, doses of L-NAME, respectively. Mean blood pressure was also elevated in rats receiving L-NAME in a dose-dependent manner. These findings suggest that NO, in addition to regulating blood pressure, is involved in prevention of thrombus formation under physiological circumstances.
Cell-matrix and cell-cell contacts of myofibroblasts: role in connective tissue remodeling
Authors: Gabbiani Giulio , Hinz Boris 
Published: November 2003

SummaryIt is presently accepted that fibroblast/myofibroblast modulation represents a crucial step in granulation tissue contraction and in the production of the connective tissue deformations typical of fibrocontractive diseases. In addition to synthesizing extracellular matrix (ECM) components, myofibroblasts can develop tensile force through the neoformation of α-smooth muscle actin (α-SMA) containing cytoplasmic stress fibers. Tension has been shown to be a crucial regulator of connective tissue remodeling. In order to coordinate tension distribution within connective tissue, cell-matrix and cell-cell contacts appear essential. This review addresses the formation, molecular structure and function of such structures that are characterized by their association with intracytoplasmic actin filaments. Actin associated cell-matrix adhesions appear to provide the interface between ECM components and intracellular stress fibers, thus contributing to the transmission of force to the substrate and to the detection of stress level in the matrix. Cell-cell adherens junctions appear to synchronize myofibro-blast contractile activity. Further studies investigating the functions of these structures will be important for the understanding of the mechanisms of granulation tissue evolution and for the planification of strategies in view of influencing connective tissue deformations.
Effects of a snake venom metalloproteinase, triflamp, on platelet aggregation, platelet-neutrophil and neutrophilneutrophil interactions: involvement of platelet GPIbα. and neutrophil PSGL-1
Authors: Tseng Yu-Lun , Lee Chia-Jung , Huang Tur-Fu 
Published: November 2003

SummaryThe biologically active components fromViperidae venoms specifically affect cell-matrix interactions, and have been utilized for developing anti-adhesive therapy as anti-thrombotic and antiangiogenic agents. Utilizing platelet aggregometry coupled with flow cytometry, we found that a metalloproteinase isolated from Trimeresurus flavoviridis, termed triflamp, inhibited heterotypic adhesion between platelets and neutrophils in whole blood samples. Triflamp is a monomeric glycoprotein with a molecular weight of ∼28 kDa. Triflamp has a N-terminal amino acid sequence homologous to other venom metalloproteinases isolated from T. flavoviridis. The enzymatic activity of triflamp was inhibited by EDTA and phenanthroline but not by PMSF. Moreover, triflamp is a pure α-fibrinogenase. Studies aimed at determining the nature of triflamp in affecting platelets or neutrophils revealed a selective inhibitory activity to glycoprotein (GP) Ibα.-dependent platelet aggregation and PSGL-1-dependent neutrophil homotypic aggregation, indicating that its effects are rather specific. As judged by Western blotting, GPIbα. on platelets and PSGL-1 on neutrophils are the substrates of triflamp. In conclusion, we suggest the novel role of venom metalloproteinase from Viperidae affecting the blood cell-cell interactions, thus offering a potential approach for further exploration of anti-inflammatory agents.
Titre of anti-heparin/PF4-antibodies and extent of in vivo activation of the coagulation and fibrinolytic systems
Authors: Chilver-Stainer Lara , Lämmle Bernhard , Alberio Lorenzo 
Published: November 2003

SummaryHeparin-induced thrombocytopenia (HIT) is mediated by antibodies directed against the heparin/platelet factor 4 (PF4) complex. Our aim was to investigate whether the antibody titre is associated with the degree of in vivo thrombin generation. We measured the anti-heparin/PF4-antibody titre, prothrombin fragments F1+2, thrombin-antithrombin (TAT) complexes and D-dimers in plasma samples from 225 patients with suspected HIT. Antibody titres as detected by a particle gel immunoassay strongly correlated with optical density values measured by ELISA (r=0.84, p<0.0001). Patients with titres ≥ 4 (n=44) had significantly higher median levels of F1+2 (2.49 nmol/l), TAT (13.01 µg/l) and D-dimers (3340 µg/l) compared to patients with undetectable antibodies (n=148; F1+2 1.61 nmol/l, TAT 4.95 µg/l, D-dimers 1911 µg/l; p<0.0001 for all comparisons) or patients with titres of 1-2 (n=33; F1+2 1.44 nmol/l, p=0.0014; TAT 4.37 µg/l, p=0.0018; D-dimers 2231 µg/l, p=0.0016). Multivariate analysis indicated the anti-heparin/PF4-antibody titre as an independent predictor for F1+2 (p=0.0036), TAT (p=0.0176) and D-dimer (p=0.0003) levels. This relationship remained statistically significant after exclusion of patients with concomitant prothrombotic conditions and/or thromboembolic complications during heparin treatment. These data demonstrate that high anti-heparin/PF4-antibody titres are independently associated with an increased in vivo thrombin generation. Rapid determination of the anti-heparin/PF4-antibody titre could help guide clinical management, identifying a subset of HIT-patients who are at high risk of developing thromboembolic complications and possibly require alternative anticoagulation in therapeutic dosage even in the context of isolated HIT.
THE "JURIDICAL DIALOGUE": A LITERARY-JUDICIAL PATTERN
Authors: Bartor Asnat 
Published: November 2003

AbstractSeveral passages in the Bible explicitly describe "institutional" judicial proceedings. This study, however, focuses on eight passages which were not "declared" to be trials by their authors; nonetheless, their content, language, and apparent intentions indicate an attempt to convey the character of a juridical criminal proceeding. Close examination of the texts reveals a recurrent literary pattern, and as these texts are dialogues, this pattern is termed the "juridical dialogue". The first part of the study presents the characteristics of the juridical dialogue, by drawing a parallel between the phases of the juridical criminal proceedings, on the one hand, and the linguistic formulations used in the literary pattern, on the other. The second part focuses on the link between human dialogue and juridical proceedings; the features of a specific human discourse, the nature of which is judicial, are examined by applying sociolinguistic criteria.
TREADING THE BOW
Authors:   Emerton
Published: November 2003

Abstract"To tread a bow" (dārak qešet) is often thought to mean bending or drawing it, but some believe that it denotes stringing a bow. The former interpretation is generally supported by the ancient versions, and also by medieval Jewish scholars; and Rashi says that, when a bow was "strong", the archer needed to use his foot to bend it. Some Greek writers tell of peoples who had exceptionally long bows and needed to use their feet to bend them. Egyptian pictures show archers using their feet to bend bows when stringing them. It is argued that a choice must be made between translating "to bend" and "to string", that Israelite bows do not seem to have been unusually long, and that some biblical references are best interpreted to imply that treading a bow means stringing it.
HEBRAISMS IN THE OLD LATIN VERSION OF THE BIBLE
Authors: Kraus Matthew 
Published: November 2003

AbstractRecent work on the Old Latin version of the Bible attributes Hebraisms to a hebraized Greek Vorlage. The results of this work question previous claims that the Hebraisms of the Old Latin derive from Jewish attempts to revise the Old Latin towards the Hebrew directly through Hebrew texts and Jewish exegetical traditions. This study reconsiders the evidence in favor of Hebraizations of the Old Latin from a Hebrew source and concludes that: 1. There was no translation of the Bible directly from the Hebrew into Latin prior to Jerome. 2. There was no editorial reworking of the Old Latin directly from the Hebrew. 3. Hebraisms in the Old Latin must be attributed to the Greek tradition or Jerome and his influence. 4. Since Jerome's time, interest in the Hebrew text behind the Latin also accounts for the Hebraisms found in the Old Latin. 5. Jewish communities utilized a Latin Bible borrowed from Christians after Jerome.
THE PROPHET AS INCOMPETENT DRAMATIST
Authors: Wilks John 
Published: November 2003

AbstractScholars have recently shown a fascination with the idea that Deutero-Isaiah is the text of a drama. Allied with this is a deepened interest in the cult and the Psalter as source texts, and a possible role for the Annual Enthronement Festival. Investigation of these proposals fail to convince. First, the idea that Deutero-Isaiah draws its inspiration from the cult cannot be substantiated from the way it utilizes the Psalms. They were undoubtedly influential, but there is insufficient evidence that this was due to any imitation of the Annual Enthronement Festival. Second, consideration of the practical demands of the sort of staging proposed, and an awareness of the difference between dramatic and poetic writing, argues against the idea of a drama. It would demand a changed perception of the prophet from his traditional status as "master poet" to that of "incompetent dramatist".
Is it Possible to Dispense with Q?
Authors: Foster Paul 
Published: November 2003

AbstractSolutions to the Synoptic Problem that argue for Markan priority, but the non-existence of Q as the basis of the double tradition material continue to attract scholars. The best known of these theories, the Farrer-Goulder hypothesis arguing for Luke's direct use of Matthew, has been championed most recently by Mark Goodacre. He reworks some of the previous arguments in favour of that hypothesis as well as offering a number of new arguments. This paper assesses the validity of such arguments and the claim that it is now possible to finally dispense with Q.
Son of Man, Stone of Blood (John 1:51)
Authors: O'Neill J.C. 
Published: November 2003

AbstractThe plural "you will see" in John 1:51 shows that the saying was not originally part of the Nathanael story. "You will see" also makes it unlikely that the Son of Man was the new Jacob. Joachim Jeremias's defence of the view that the Son of Man was the stone Jacob set up and anointed at Bethel is likely to be right. The stone became the altar in the Temple. Out of the stone came manna. "Ben Adam" was "Eben Dam".
Estradiol Supplementation Enhances Submaximal Feed-Forward Drive of Growth Hormone (GH) Secretion by Recombinant Human GH-Releasing Hormone-1,44-Amide in a Putatively Somatostatin-Withdrawn Milieu
Authors: Veldhuis Johannes D. , Evans William S. , Bowers Cyril Y. 
Published: November 2003

Abstract
To test the clinical hypothesis that an estrogen-enriched milieu enhances GHRH action, we administered placebo (Pl) and estradiol-17β (E2) orally for 23 d to six postmenopausal women in a prospectively randomized, double-masked, within-subject crossover design with 6 wk intervening. The GHRH stimulation protocol entailed consecutive iv infusion of l-arginine and a single iv pulse of saline or one of five randomly ordered doses of recombinant human GHRH-1,44-amide (0.03, 0.1, 0.3, 1.0, or 3.0 μg/kg) in a total of 12 separate morning, fasting sessions. GH secretion was monitored by sampling blood every 10 min for 6 h; chemiluminescence assay of GH concentrations; deconvolution analysis of stimulated GH release; and nonlinear dose-response reconstruction. Supplementation with E2, compared with Pl: 1) increased (mean ± sem) E2 concentrations from 18 ± 3 (Pl) to 164 ± 12 pg/ml (to convert to picomoles per liter, multiply by 3.57) (P &lt; 0.001); 2) decreased IGF-I concentrations from 181 ± 14 to 120 ± 11 μg/liter (P &lt; 0.01); 3) elevated mean GH concentrations from 0.27 ± 0.06 to 0.59 ± 0.08 μg/liter (P = 0.014); 4) potentiated GH secretion stimulated by l-arginine alone by 1.43-fold (P = 0.012); 5) reduced the ED50 of GHRH from 0.27 ± 0.02 to 0.13 ± 0.01 μg/kg (P &lt; 0.01), denoting enhanced GHRH potency; and 6) heightened the maximal slope of the dose-response function from 1.1 ± 0.1 to 1.4 ± 0.05 [(μg/liter) (μg/kg)−1] (P &lt; 0.05), signifying augmented pituitary sensitivity. The foregoing facilitative mechanisms were specific because E2 replacement did alter maximal l-arginine/GHRH-induced GH secretion, indicating unchanged secretagogue efficacy. In conclusion, inasmuch as E2 also attenuates inhibition of GH secretion by infused somatostatin and potentiates stimulation of GH secretion by GH-releasing peptide-2, we postulate that estrogenic steroids drive pulsatile GH production in part via mechanisms that include all three of GHRH, somatostatin, and putatively GH-releasing peptide/ghrelin signaling.
Increased Soluble Leptin Receptor in Children with Nephrotic Syndrome
Authors: Schroth Michael , Kratzsch Jürgen , Gröschl Michael , Rauh Manfred , Rascher Wolfgang , Dötsch Jörg 
Published: November 2003

Abstract
In patients with nephrotic syndrome, severe proteinuria is related to significant leptinuria; serum leptin levels remain unchanged. The goal of this study was to elucidate the role of the soluble leptin receptor (sOB-R) in maintaining serum leptin levels in nephrotic patients. Patients with proteinuria were compared with patients in remission of nephrotic syndrome. In this group proteinuria did not exceed 100 mg/m2 of body surface area per day. The period of remission was at least 6 months and was equal in all patients included. The sOB-R level (mean ± sd) in serum of patients with nephrotic syndrome was significantly higher during proteinuria (61.0 ± 17.8 ng/ml) than those in remission or in control patients (36.7 ± 7.0 ng/ml, 36.6 ± 12.0 ng/ml, respectively, P &lt; 0.0001). The ratio between serum leptin levels and the sOB-R (free leptin index) was significantly lower in the proteinuric group (0.012 ± 0.005 vs. 0.06 ± 0.03 and 0.07 ± 0.03 in remission and control group, respectively) (P &lt; 0.001). Urinary sOB-R excretion was similar in all groups. Our data suggest that the counteracting pathway in case of leptin loss in parallel to severe proteinuria in nephrotic syndrome is the up-regulation of its soluble binding protein in serum, which can keep total serum leptin levels constant.
Gender Differences in Large Artery Stiffness Pre- and Post Puberty
Authors: Ahimastos Anna A. , Formosa Melissa , Dart Anthony M. , Kingwell Bronwyn A. 
Published: November 2003

Abstract
Age-related large artery stiffening is more pronounced in women compared with men and is an important cause of isolated systolic hypertension. This study aimed to investigate whether such gender differences are inherent or the result of sex steroid influences. Healthy children prepuberty [26 female (10.3 ± 0.1 yr), 32 male (10.3 ± 0.1 yr), mean age ± sd] and post puberty [30 female (15.9 ± 0.2 yr), 22 male (15.9 ± 0.4 yr)] were studied. Large artery stiffness was assessed globally via systemic arterial compliance and regionally via pulse wave velocity. Prepubertal males and females did not differ in body size, cardiac output, or heart rate. Prepubertal females had stiffer large arteries and higher pulse pressure than age-matched males (P &lt; 0.05). Postpubertal males were taller and heavier and had a greater cardiac output and lower heart rate compared with similarly aged females. In relation to pubertal status, females developed more distensible large arteries post puberty whereas males developed stiffer large vessels (P &lt; 0.05). These changes where such that central large artery stiffness was similar between genders in the postpubertal group. Together these data suggest that large artery stiffness varies intrinsically between genders but is also modulated by both male and female sex steroids.