bluuebunny/crossref_metadata_2025_split huggingface dataset:
Factors Influencing the Use of Registered Nurse Overtime in Hospitals, 1995–2000
Authors: Berney Barbara , Needleman Jack , Kovner Christine 
Published: May 2005

Purpose

: To assess nurse overtime in acute care general hospitals and the factors that influence overtime among various hospitals and in the same hospitals from year to year.
Methods

: Staffing data from 1995 to 2000 from 193 acute general hospitals in New York State were used to examine hospital characteristics (size, location, RN unionization, hospital ownership, and teaching status) to determine whether they were associated with nurse overtime.
Results

: The average weekly overtime RNs worked was 4.5% of total hours, varying from almost none to 16.6%. At mean overtime levels, nurses were working less overtime than the mean for manufacturing workers, but, at the extreme, nurses were working more than 6 hours overtime per week. Significant differences were observed in the use of overtime by hospital ownership and by union status. Nurses in government hospitals worked less overtime than did those in nongovernment hospitals. Nurses in unionized hospitals worked slightly more overtime than did nurses in nonunionized hospitals.
Conclusions

: Hospitals varied dramatically in their overtime use. That some categories of hospitals (e.g., government‐owned) used little overtime indicates that hospital management can find substitutes for overtime to meet fluctuating staffing needs. The finding that hospitals with similar characteristics varied greatly in their number of overtime hours also supported this conclusion.
A study of Q‐switched Nd:YAG laser irradiation and paracrine function in human skin cells
Authors: Burd Andrew , Zhu Ningwen , Poon Vincent K. M. 
Published: May 2005

Background and objectives: This preliminary laboratory‐based study looks at the paracrine release from human skin cells subject to sublethal Q‐switched Nd:YAG 532 nm laser irradiation.Study design/Materials and methods: Human dermal fibroblast and keratinocyte cultures were exposed to sublethal energy using the Nd:YAG 532 nm laser. Altered gene expression was then screened using RT‐PCR for a range of paracrine factors known to affect melanogenesis, basic fibroblast growth factor (b‐FGF), hepatocyte growth factor (HGF), stem cell factor (SCF), melanocyte stimulating hormone (MSH), endothelin‐1 (ET‐1), interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α) and protease‐activated receptor‐2 (PAR‐2). Enzyme‐linked immunosorbent assay (ELISA) was used to confirm protein production. Conditioned medium was used to assess altered melanogenesis in a melanoma cell line.Results: Fibroblasts exposed to sublethal radiation showed upregulation of b‐FGF, HGF and SCF. This contrasts with keratinocytes which showed upregulation of IL‐6. Elevated protein levels of b‐FGF and SCF were confirmed by ELISA assay. Conditioned fibroblast medium was shown to stimulate melanogenesis in a melanoma cell line.Conclusions: This preliminary laboratory study reports, for the first time, specific gene upregulation using the Q‐switched Nd:YAG 532 nm laser.
Evaluation of vaseline oil applied prior to UVB TL01 phototherapy in the treatment of psoriasis
Authors: Penven K. , Leroy D. , Verneuil L. , Faguer K. , Dompmartin A. 
Published: May 2005

AbstractBackground: Use of emollient prior to phototherapy could enhance UV transmission through psoriasis plaques on the condition that the emollient is not photoprotective. Emollient pretreatment with narrow‐band phototherapy (313 nm) has not been studied extensively. We conducted a study to assess if vaseline oil prior to UVB TL01, in chronic psoriasis plaques could accelerate psoriasis clearance.Methods: Fifteen patients with chronic psoriasis plaques were enrolled in a prospective, single‐blind, controlled study. For each patient, one to three symmetrical pairs of plaque were selected and scored initially and after every six exposures.Results: On the vaseline oil pretreated side, significantly more plaques were cleared, especially in severe psoriasis. Scaling and infiltration were significantly improved. Application of vaseline oil was more interesting in thick and scaly psoriasis probably because the oil penetrates the intercellular space allowing an optical matching effect which increases the UV transmission.Conclusion: We strongly recommend vaseline oil pretreatment with UVB TL01 phototherapy in psoriasis, especially in severe psoriasis.
Factor VIII efficient and specific non-covalent binding to PEGylated liposomes enables prolongation of its circulation time and haemostatic efficacy
Authors: Carmel-Goren Lea , Barenholz Yechezkel , Dayan Inbal , Ostropolets Savely , Slepoy Igal , Gvirtzer Nira , Fukson Vladimir , Spira Jack , Baru Moshe 
Published: May 2005

SummaryHaemophilia A is a bleeding disorder caused by the lack of factor VIII (FVIII). We report the prolongation of exogenous FVIII circulation time and haemostatic efficacy by its formulation with PEGylated liposomes (PEGLip). FVIII binds non-covalently but with high affinity in a specific mode with the external surface of PEGLip neither losing its activity nor its binding to von Willebrand Factor. Experiments in haemophilic and non-haemophilic mice indicate that the circulation time and clotting efficacy of PEGLip-formulated exogenous FVIII (PEGLip-FVIII) are significantly enhanced over those of free FVIII. The data support the feasibility of using PEGLip-FVIII to extend the duration of haemostatic efficacy in the treatment of haemophilia A.
Activation of coagulation and inhibition of fibrinolysis in the lung after inhalation of lipopolysaccharide by healthy volunteers
Authors: Maris Nico , de Vos Alex , Bresser Paul , van der Zee Jaring , Meijers Joost , Lijnen Roger , Levi Marcel , Jansen Henk , van der Poll Tom 
Published: May 2005

SummaryPneumonia is frequently associated with changes in coagulation and fibrinolysis in the bronchoalveolar space. To determine the effect of lipopolysaccharide (LPS) on the hemostatic balance in the human lung, six healthy subjects inhaled nebulized LPS or saline in a randomized cross-over study and bronchoalveolar lavage fluid was obtained six hours thereafter. LPS induced soluble tissue factor and thrombin-antithrombin complexes and inhibited plasminogen activator activity in BALF. Additionally plasminogen activator inhibitor type 1 production was upregulated after LPS inhalation. LPS also elicited local activation of neutrophils (release of elastase, myeloperoxidase and bactericidal/permeability increasing protein) and secretion of interleukin (IL)-6 and IL-8. Inhalation of LPS by healthy humans reproduces major features of the procoagulant response to inflammatory and infectious lung diseases and may be used as a novel model to evaluate pathogenetic mechanisms and new interventions.
Elevated factor VII as a risk factor for recurrent fetal loss
Authors: De Staercke Christine , Benson Jane , Hooper Craig , Dilley Anne , Evatt Bruce , Benito Carlos , Patterson-Barnett Anne , Eller Daniel , Philipp Claire , Miller Connie 
Published: May 2005

SummaryHaemostatic abnormalities can be detected in a portion of the women who have recurrent fetal loss. We measured factor VII coagulant activity (FVII:C) in 65 women with 3 or more fetal losses (recurrent cases), 31 women with one 2nd or 3rd trimester loss (late loss cases), and 81 women with only live births (controls). FVII:C was greater than 2 standard deviations above the mean for controls in 9 recurrent cases (13.8%) and 2 controls (2.5%) for an odds ratio of 6.35 (95% CI 1.32–30.52, p=0.012). In recurrent cases, mean levels were significantly higher than controls for FVII:C (p=0.003), FVII antigen (p=0.024), and FVIIa (p=0.001). Late loss cases had an odds ratio of 4.23 (95% CI 0.67–26.67, p=0.098) with FVII:C, FVII antigen, and FVIIa not significantly different from the controls. DNA was examined for the presence of mutations or polymorphisms in the promoter region of the FVII gene, using denaturing HPLC. Abnormal patterns were confirmed with direct sequencing. A previously reported polymorphism,–402 G>A, was found to be present in 11/14 subjects with elevated FVII:C (79%) and 43% of those with normal levels (p=0.029). FVII:C, FVII antigen and FVIIa varied significantly with genotype; however, genotype frequencies did not differ between controls and either case group. No other promoter polymorphisms were identified. This is the first report of a significant elevation of FVII in a population with recurrent fetal loss. These data suggest the need for further investigation of this potential risk factor.
Platelet P2Y12 receptors enhance signalling towards procoagulant activity and thrombin generation
Authors: van der Meijden Paola , Feijge Marion , Giesen Peter , Huijberts Maya , van Raak Lisette , Heemskerk Johan 
Published: May 2005

SummaryActivated platelets participate in arterial thrombosis by forming aggregates and potentiating the coagulation through exposure of procoagulant phosphatidylserine. The function of the two receptors for ADP, P2Y1 and P2Y12, is well-established in aggregation, but is incompletely understood in the platelet procoagulant response. We established that, in PRP from healthy subjects, ADP accelerated and potentiated tissue factor-induced throm-bin generation exclusively via stimulation of P2Y12 and not via P2Y1 receptors. The P2Y12 receptors also mediated the potentiating effect of PAR-1 stimulation on thrombin generation. Furthermore, ADP enhanced in a P2Y12-dependent manner the Ca2+ response induced by thrombin, which was either added externally or generated in-situ. This ADP effect was in part dependent of phosphoinositide 3-kinase and was paralleled by increased phosphatidylserine exposure. In PRP from (young) patients with either stroke or type-II diabetes, platelet-dependent thrombin generation was similarly enhanced by ADP or SFLLRN as in healthy subjects. In PRP from stroke patients of older age, the P2Y12-mediated contribution to thrombin generation was variably reduced by two weeks of clopidogrel medication. Remaining P2Y12 activity after medication correlated with remaining P2Y12-dependent P-selectin exposure, i.e. Ca2+-dependent secretion, likely due to incomplete antagonism of P2Y12 receptors. Together, these results indicate that physiological platelet agonists amplify phosphatidylserine exposure and subsequent thrombin generation by release of ADP and P2Y12-receptor stimulation. This P2Y12 response is accomplished by a novel Ca2+ signalling pathway. It is similarly active in platelets from control subjects and patients at thrombotic risk. Finally, the thrombo-gram method is useful for measuring incomplete P2Y12 inhibition with clopidogrel.
High utilization rate of vena cava filters in deep vein thrombosis
Authors: Goldhaber Samuel , Tapson Victor , Jaff Michael 
Published: May 2005

SummaryThe objective was to investigate newly diagnosed patients with deep vein thrombosis (DVT) who received inferior vena cava filters (IVCFs). A prospective registry enrolled 5451 patients from 183 US study sites. In all patients, examination by venous duplex ultrasound confirmed the diagnosis of DVT. We collected and analyzed data on 781 patients who received an IVCF . The most frequently prescribed treatments were low–molecular-weight heparin and unfractionated heparin, which were used as a bridge to warfarin in 39% (n=2143) and 35% (n=1926) of patients, respectively. Of the total population, 781 (14%) (235 outpatients, 546 inpatients) underwent IVCF placement. The most common reasons for IVCF placement were contraindication to anticoagulation (n = 271), prophylaxis (n = 259), major bleeding related to anticoagulation therapy (n = 92), and anticoagulation failure (n = 73). Multivariate analysis revealed that patients were more likely to undergo IVCF insertion with multiple system organ failure (odds ratio [OR], 3.6; 95% CI, 1.48–8.60), previous stroke (OR, 3.2; 95% CI, 2.11–4.74), or history of pulmonary embolism (OR, 2.4; 95% CI, 1.95–2.91). In conclusion, a surprisingly high 14% (781) of patients with confirmed DVT received an IVCF. Many of these patients may have warranted less invasive methods of venous thromboembolism prophylaxis. Improved physician education regarding mechanical and pharmacologic prophylaxis alternatives might reduce the use of IVCFs.
Downregulation of vascular endothelial-cadherin expression is associated with an increase in vascular tumor growth and hemorrhagic complications
Authors: Zanetta Lucia , Corada Monica , Lampugnani Maria , Zanetti Adriana , Breviario Ferruccio , Moons Lieve , Carmeliet Peter , Pepper Michael , Dejana Elisabetta 
Published: May 2005

SummaryThe pathogenesis of vascular tumors such as angiosarcomas is poorly understood. Cadherin expression inversely correlates with tumor malignancy and the endothelial specific VE-cadherin is low or absent in angiosarcomas, suggesting an inhibitory role for this protein in tumor progression. In this paper we report that Pmy T VE-cadherin null (VEC null) endothelial cells form larger vascular tumors in nude mice when injected subcutaneously as compared to isogenic VE-cadherin positive (VEC pos) cells. This effect requires the association of β-catenin to VE-cadherin, since a VE-cadherin mutant lacking the domain responsible for β-catenin binding (Δβcat) cannot rescue the phenotype. In VEC null cells β-catenin is phosphorylated and partly degraded. N-cadherin is increased and detected at junctions. VEC null cells also present an altered fibrinolytic activity with increases in tPA, uPA, uPAR and a strong reduction in PAI-1, which may be correlated to the high incidence of abrupt hemorrhages in VEC null tumors. Overall, these data strongly suggest that downregulation of VE-cadherin in endothelial tumors may have important consequences for tumor growth and bleeding complications.
Angiotensin II enhances thrombosis development in renovascular hypertensive rats
Authors: Mogielnicki Andrzej , Chabielska Ewa , Pawlak Robert , Szemraj Janusz , Buczko Wlodzimierz 
Published: May 2005

SummaryThere is an increased number of in vitro evidence that angioten-sin II (Ang II) may promote thrombosis. However there are no in vivo experiments exploring the effect of Ang II on thrombus formation. In the present study we have investigated the influence of Ang II on venous thrombosis in renovascular hypertensive rats. Furthermore, we examined the role of AT1 receptor and Ang II metabolites: angiotensin III (Ang III) and angioten-sin IV (Ang IV) in the mechanisms of Ang II action. The contribution of coagulation and fibrinolytic systems in the mode of Ang II action was also determined. Venous thrombosis was induced by ligation of vena cava. Ang II infused into rats developing venous thrombosis caused dose-dependent increase in thrombus weight, which was partially reversed by losartan, selective AT1 antagonist. Ang III did not influence the thrombus formation in hypertensive rats, while Ang IV caused a marked increase in thrombus weight only in one of the used doses. Our study shows that Ang II via AT1 receptor enhances thrombosis development. The prothrombotic effect of Ang II may partially depend on enhanced leukocytes adhesion to endothelial cells accompanied by accelerated fibrin formation and increased plasma level of PAI-1. Moreover, Ang II action is partially mediated by one of its metabolites – Ang IV.
Molecular design and characterization of recombinant long half-life mutants of human tissue factor pathway inhibitor
Authors: Bai Hao , Zhang Yu-Gao , Zhang Nong , Kong De-Sheng , Guo Hong-Shen , Mo Wei , Tang Qi-Qun , Song Hou-Yan , Ma Duan 
Published: May 2005

SummaryTissue factor pathway inhibitor (TFPI) is a physiological inhibitor of extrinsic pathway of coagulation and has biological functions of anticoagulation and anti-inflammation. Although TFPI has been proved to be a good therapeutic agent of sepsis, inflammatory shock, and DIC, the clinical application and therapeutic effects of TFPI are impeded because of its short half-life in vivo. In order to prolong the half-life of TFPI, homology modeling and molecule docking were performed on a computer workstation principally in protein structural biology and binding characteristics between TFPI and its receptor LRP (low-density lipoprotein receptor related protein). Two recombinant long half-life human TFPI mutants coined TFPI-Mut1 and TFPI-Mut4 were designed and expressed in E.coli. In comparison with the wild-type TFPI, TFPI-Mut1 and TFPI-Mut4 presented a few of changes in spatial configuration and a decrease in relative Gibbs free energy of docking complex by 17.3% and 21.5%, respectively, as indicated by a computer simulation. After refolding and purification, anticoagulant activities, anti-TF/FVIIa and anti-FXa activities of the mutants were found to be the same as those of wide-type TFPI. The pharmacokinetics research indicated that alpha phase half-life (t1/2α) of TFPI-Mut1 and TFPI-Mut4 were prolonged 1.33-fold and 1.96-fold respectively, beta phase half-life (t1/2 β) of TFPI-Mut1 and TFPI-Mut4 were prolonged 1.62-fold and 4.22-fold respectively. These results suggested that TFPI-Mut1 and TFPI-Mut4 maintained the bioactivities of wild-type TFPI, prolonged half-life in vivo simultaneously and were expected for better clinical value and therapeutic effect.
Deletion of the 60-loop provides new insights into the substrate and inhibitor specificity of thrombin
Authors: Yang Likui , Rezaie Alireza 
Published: May 2005

SummaryStructural data have indicated that the 60-loop of thrombin with 8–9 insertion residues is responsible for the restricted substrate and inhibitor specificity of thrombin. However, previous deletion of 3–4 residues of this loop (des-PPW and des-YPPW) did not widen the specificity of thrombin, but further restricted it. The partial deletion of this loop also dramatically impaired the reactivity of thrombin with antithrombin (AT), protein C and fibrinogen, implicating a role for the productive interaction of the 60-loop with the target macromolecules. To further investigate the role of this loop, a mutant of thrombin was expressed in mammalian cells in which all 8 residues (Tyr-Pro-Pro-Trp-Asp-Lys-Asn-Phe) of the 60-loop were deleted (des-60-loop). In contrast to the partially deleted loop mutants, it was discovered that the des-60-loop mutant cleaved small synthetic substrates, clotted purified fibrinogen, and activated protein C with a near normal catalytic efficiency; however, its activity toward cofactors V and VIII was impaired ~2–4-fold. Direct binding and AT inhibition studies in the presence of heparin revealed that the affinity of heparin for interaction with exosite-2 of des-60-loop thrombin was impaired, though the reactivity of the mutant with AT and other plasma serpins was not impaired, but rather improved ~2-fold. These results suggest that the 60-loop plays a key role in regulating the specificity of thrombin by shielding the active-site pocket, but its productive interaction with the target molecules may not be as critical as has been speculated in previous reports.
Retinal vein occlusion: A form of venous thrombosis or a complication of atherosclerosis?
Authors: den Heijer Martin , Cruysberg Johannes , Wollersheim Hub , Bredie Sebastian , Janssen Mirian 
Published: May 2005

SummaryPrevious studies have shown an increased risk of retinal vein occlusion (RVO) in patients with hypertension, hypercholesterolemia and diabetes mellitus. Literature on the association between thrombophilic factors and RVO consists of small studies and case reports. The objective was to determine the relationship between thrombophilic risk factors and RVO. Thrombophilic risk factors analyzed were hyperhomocysteinemia, MTHFR gene mutation, factor V Leiden mutation, protein C and S deficiency, antithrombin deficiency, prothrombin gene mutation, anticardiolipin antibodies and lupus anticoagulant. For all currently known thrombophilic risk factors odds ratios for RVO were calculated as estimates of relative risk. The odds ratios were 8.9 (95% CI 5.7 –13.7) for hyperhomocysteinemia, 3.9 (95% CI 2.3 – 6.7) for anticardiolipin antibodies, 1.2 (95% CI 0.9 –1.6) for MTHFR, 1.5 (95% CI 1.0 – 2.2) for factor V Leiden mutation and 1.6 (95% CI 0.8 – 3.2) for prothrombin gene mutation. In conclusion, regarding thrombophilic risk factors and RVO there is only evidence for an association with hyperhomocysteinemia and anticardiolipin antibodies, factors that are known as risk factors for venous thrombosis as well as for arterial vascular disease. The minor effect of factor V Leiden mutation and the protrombin gene mutation (risk factors for venous thrombosis only) suggests that atherosclerosis might be an important factor in the development of CRVO.
The role of CD40 in CD40L- and antibody-mediated platelet activation
Authors: Amirkhosravi Ali , Meyer Todd , Siddiqui Farooq , Ahmad Sarfraz , Walker Jamie , Amaya Mildred , Desai Hina , Francis John , Langer Florian , Ingersoll Susan 
Published: May 2005

SummaryOur initial finding that CD40– and CD40 ligand (CD40L)-deficient mice displayed prolonged tail bleeding and platelet function analyzer (PFA-100) closure times prompted us to further investigate the role of the CD40-CD40L dyad in primary hemostasis and platelet function. Recombinant human soluble CD40L (rhs CD40L), chemical cross-linking of which suggested a trimeric structure of the protein in solution, activated platelets in a CD40-dependent manner as evidenced by increased CD62P expression. CD40 monoclonal antibody (mAb) M3, which completely blocked rhs CD40L-induced platelet activation, also prolonged PFA-100 closure times of normal human blood. In contrast, CD40 mAb G28–5 showed less potential in blocking rhs CD40L-induced CD62P expression and did not affect PFA-100 closure times. However, when added to the platelets after rhs CD40L, G28–5 significantly enhanced the platelet response by causing clustering of, and signaling through, FcγRII. Similarly, higher order multimeric immune complexes formed at a 1/3 molar ratio of M90, a CD40L mAb, to rhs CD40L induced strong FcγRII-mediated platelet activation when translocated to the platelet surface in a CD40-dependent manner, including the induction of morphological shape changes, fibrinogen binding, platelet aggregation, dense granule release, microparticle generation and monocyte-platelet-conjugate formation. The results suggest that CD40 may play a role in primary hemostasis and platelet biology by two independent mechanisms: First, by functioning as a primary signaling receptor for CD40L and, second, by serving as a docking molecule for CD40L immune complexes. The latter would also provide a potential mechanistic explanation for the unexpected high incidence of CD40L mAb-associated thrombotic events in recent human and animal studies.Parts of this work have been presented on the 46th Annual Meeting of the American Society of Hematology (San Diego, 2004).