bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accuracy of compression ultrasound in screening for deep venous thrombosis in acutely ill medical patients
Authors: Davidson Bruce , Wisniewska Joanna , Malek Grzegorz , Kober Jaroslaw , Kuca Pawel , Burakowska Barbara , Oniszh Karina , Gallus Alexander , Lensing Anthonie , Tomkowski Witold 
Published: June 2007

SummaryThe value of vein ultrasonography for diagnosis of symptomatic deep vein thrombosis (DVT) is widely accepted. We are unaware of published data comparing ultrasonography with the “gold standard” of venography for DVT diagnosis in asymptomatic persons in the patient group of acutely ill medical patients. It was the objective of this study to evaluate sensitivity and specificity of compression ultrasound (CUS) examinations in the diagnosis of proximal and distal DVT in acutely ill medical patients [with congestive heart failure (NYHA class III and IV), exacerbations of respiratory disease, infectious disease, and inflammatory diseases] considered to be at moderate risk of venous thromboembolism (VTE). CUS examination was performed prior to ascending venography on day 6–15 of the hospital stay. Both investigations were done on the same day, each interpreted without knowledge of the other’s result. Proximal and calf veins were separately evaluated. Technically satisfactory venography was obtained in 160 patients. In 12 of 160 patients (7.5%, 95% CI = [4.0%-12.7%]), venography confirmed the presence of DVT, all of which was asymptomatic. Proximal DVT was detected in five patients (3.1%, 95% CI = [1.0%- 7.1%]) and distal DVT in seven patients (4.4%, 95% CI = [1.8% – 8.8%]). CUS of proximal veins was technically satisfactory in all 160 patients and CUS of distal veins in 150 patients. In three of five patients with veongraphically proven proximal DVT, the diagnosis was confirmed by CUS (sensitivity 60%, 95%CI = [23%-88%]). In one patient, the CUS was false positive (specificity 99.4%, 95%CI = [96%-99%]). Positive and negative predictive values (PPV and NPV) of CUS in the diagnosis of proximal DVT were 75% (95%CI = [30%-95%]) and 98% (95% CI = [95%-99%]), respectively. In two of seven patients with venographically proven calf DVT, the diagnosis was confirmed by CUS (sensitivity 28.6%, 95%CI = [8%-64%]) and in two patients, CUS was false positive (specificity 98.6, 95%CI = [95%-99%]). PPV and NPV of CUS in diagnosis of distal DVT were 50% (95%CI = [15–85%]) and 96% (95% CI = [92%-98%]), respectively. In conclusion, CUS underestimates the incidence of proximal and distal DVT compared to contrast venography in acutely ill medical patients without thrombosis symptoms.
Regulation by DDAH/ADMA pathway of lipopolysaccharideinduced tissue factor expression in endothelial cells
Authors: Jia Su-Jie , Song Kui , Wang Guang-Ping , Li Yuan-Jian , Xin Hong-Ya , Jiang De-Jian , Chen Fang-Ping 
Published: June 2007

SummaryPrevious studies have shown the regulatory effect of nitric oxide (NO) on endotoxin-induced tissue factor (TF) in endothelial cells. Asymmetric dimethylarginine (ADMA), a major endogenous NO synthase (NOS) inhibitor, could inhibit NO production in vivo and in vitro. ADMA and its major hydrolase dimethylarginine dimethylaminohydrolase (DDAH) have recently been thought of as a novel regulatory system of endogenous NO production. The aim of the present study was to determine whether the DDAH/ADMA pathway is involved in the effect of lipopolysaccharide (LPS) on TF expression in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were treated with LPS (1 µ g/ml) to induce TF expression. Exogenous ADMA significantly enhanced the increase in both TF mRNA level and activity induced by LPS, whereas L-arginine, the NOS substrate, markedly attenuated the LPS-induced TF increment. LPS markedly increased the level of ADMA in cultured medium and decreased DDAH activity in endothelial cells, and overexpression of DDAH2 could significantly suppress LPS-induced TF increment in endothelial cells. LPS could increase intracellular reactive oxygen species (ROS) production and activate nuclear factor-κ B, which were enhanced by exogenous ADMA and attenuated by either L-arginine or overexpression of DDAH2. Therefore, our present results for the first time suggest that the DDAH/ADMA pathway can regulate LPS-inducedTF expression via ROS-nuclear factor- κ B-dependent pathway in endothelial cells.
Multicentre ISI assignment and calibration of the INR measuring range of a new point-of-care system designed for home monitoring of oral anticoagulation therapy
Authors: Leichsenring Ingrid , Plesch Winfried , Unkrig Volker , Kitchen Steve , Kitchen Dianne , Maclean Rhona , Dikkeschei Bert , van den Besselaar Anton 
Published: June 2007

SummaryThe new CoaguChek XS system is designed for use in patient selftesting. It is the successor of the current CoaguChek S system. The detection principle is based on the amperometric measurement of the thrombin activity initiated by starting the coagulation cascade using a human recombinant thromboplastin. This study was performed to assign the International SEnsitivity Index (ISI) to the new test according to the WHO guidelines for thromboplastins and plasmas used to control anticoagulant therapy, and to establish the measuring range of the new system. At four study sites a total of 90 samples of normal donors and 291 samples of warfarin-, phenprocoumon- or acenocoumarol-treated patients were included in the study.The ISI value of the new test was assigned against the human recombinant reference thromboplastin rTF/95 at each site using the samples from stabilized patients in the International Normalized Ratio (INR) range between 1.5 and 4.5 only. The new point-of-care system’s measuring range between 0.8 and 8 INR was calibrated against the mean INR of rTF/95 and AD149 using polynomial regression. ISIs were (CV of the slope): Site 1: ISI 0.99 (1.1%); Site 2: ISI 1.02 (2.0%); Site 3: ISI 1.03 (1.1%); Site 4: ISI 1.00 (1.4%). All regression lines calculated from patient-only data pass through the normal donor data points.All CVs of the slopes of the orthogonal regression lines are well below 3%,thus fulfilling the requirements of the WHO guidelines. The mean ISI for the new CoaguChek XS PT Test is 1.01.
Vasa vasorum and atherosclerosis – Quid novi?
Authors: Kampschulte Marian , Buch Thomas , Bohle Rainer , Langheinrich Alexander 
Published: June 2007

SummaryThe role of vasa vasorum (VV) in atherosclerosis is hotly debated, and new experimental techniques have recently opened an opportunity to take a fresh look at this important topic. Although the proliferation of VV due to atherogenic stimuli is controversial, experimental and clinical evidence strongly suggest the potential of VV in vascular proliferative disorders. In the past, paradigms of atherosclerosis and restenosis have excluded the adventitia and VV in the artery wall due, in part, to a lack of i) appropriate animal models featuring adventitial VV neovascularization, ii) imaging technologies to quantitate adventitial VV and plaque neovascularization and iii) its consequences, concerning information on detectable plaque substrate in vulnerable lesions. VV proliferation is associated with increasing plaque burden and is linked to cellular processes which are critical during the development of atherosclerotic plaques such as inflammation, plaque perfusion and concomitant intraplaque hemorrhage – but the regulation and induction of VV based on pathological settings are poorly understood. This review discusses the current scientific status and its controversies and identifies open research questions.
Cellular and molecular mechanisms of hypoxia-inducible factor driven vascular remodeling
Authors: Weissmann Norbert , Grimminger Friedrich , Seeger Werner , Rose Frank , Hänze Jörg 
Published: June 2007

SummaryHypoxia-inducible factor (HIF) is an oxygen-dependent transcription factor that activates a diverse set of target genes, the products of which are involved in adaptive processes to hypoxia. Employing genetic manipulation of HIF expression, in-vivo and cellular studies have focused on HIF as a crucial factor affecting hypoxia-induced vascular remodeling.Vascular remodeling comprises processes which establish and improve blood vessel supply such as vasculogenesis, angiogenesis and arteriogenesis. These processes are observed during ontogenesis, tumor progression, ischemic disease or physical training. Furthermore, under hypoxic conditions, a pulmonary-specific type of vascular remodeling called pulmonary arterial remodeling occurs that is characterized by thickening of the vessel wall with a concomitant reduction in the vessel lumen area, thereby limiting blood flow.This response results in pulmonary hypertension with right ventricular hypertrophy, a lethal disease. In this review, we summarize and discuss mechanisms by which HIF interferes with the different vascular remodeling processes.
Association between the plasminogen activator inhibitor-1 4G/5G polymorphism and venous thrombosis
Authors: Tsantes Argirios , Bagos Pantelis , Rapti Evdoxia , Mantzios Georgios , Kapsimali Violeta , Travlou Anthi , Nikolopoulos Georgios 
Published: June 2007

SummaryThe effect of the 675 insertion/deletion (4G/5G) polymorphism of plasminogen activator inhibitor-1 (PAI-1) gene on the risk of venous thromboembolism (VTE) remains controversial. In this study, we performed a meta-analysis of published data regarding this issue. A comprehensive electronic search was carried out up until September 2006. A total of 22 articles were included in the analysis that was performed using random effects models. Eighteen papers, concerning patients without another known risk factor, comprised 2,644 cases and 3,739 controls. The alleles contrast (4G vs. 5G allele) yielded a statistically significant odds ratio (OR) of 1.153 (95% confidence interval [CI]: 1.068–1.246). In a sub-analysis of five studies that included 256 cases with another genetic risk factor and 147 controls, the combined per-allele OR was still significant (OR:1.833,95% CI:1.325–2.536). On the contrary, the analysis of five studies regarding cases with a non-genetic risk factor for VTE (antiphospholipid antibody syndrome, Behcet disease) provided insignificant results in all aspects. There was no evidence for heterogeneity and publication bias in all analyses. Based on our findings, the 4G allele appears to increase the risk of venous thrombosis, particularly in subjects with other genetic thrombophilic defects. Recommendation for detection of this polymorphism in evaluating thrombophilia in such patients might be considered.
Transmembrane chemokines: Versatile ‘special agents’ in vascular inflammation
Authors: Weber Christian , Ludwig Andreas 
Published: June 2007

SummaryWithin the chemokine family of small chemotactic polypeptides CX3CL1 (fractalkine) and CXCL16 (SR-PSOX) are exceptional in that they are synthesized as transmembrane molecules and can be cleaved from the cell surface to produce a soluble chemoattractant. As transmembrane molecules on the surface of endothelial cells, CX3CL1 and CXCL16 can interact with their receptors CX3CR1 and CXCR6, respectively, which are expressed on leukocyte subtypes.This interaction leads to cell-cell adhesion that is resistant to shear forces. Transmembrane CX3CL1 and CXCL16 are constitutively shed from the cell surface by the activity of a disintegrin and metalloproteinase (ADAM) 10, and cleavage can be rapidly enhanced by activation of the closely related enzyme ADAM17. This cleavage leads to the downregulation of adhesive properties and may even result in the detachment of bound cells. Functionally, both chemokines appear to exert homeostatic and inflammatory activities. Basal expression of CX3CL1 or CXCL16 may be relevant for positioning and survival of tissue-homing leukocytes. Upregulated expression is found under inflammatory conditions such as atherosclerosis where CXCL16 may have a dual function by acting as an adhesion molecule and by promoting uptake of oxidized LDL as a scavenger receptor. Accumulating evidence from knockout mice and genetic polymorphisms in humans points towards a differential contribution of CX3CL1 and CXCL16 in atherosclerosis, where shedding may serve to further regulate their biological functions. Small molecules that block either the receptors or the shedding enzymes of transmembrane chemokines need to be tested in animal models of vascular inflammation.
The specific role of chemokines in atherosclerosis
Authors: Braunersreuther Vincent , Mach François , Steffens Sabine 
Published: June 2007

SummaryAtherosclerosis is a chronic inflammatory disease that represents the primary cause of heart disease and stroke.The recruitment of inflammatory cells in the intima is an essential step in the development and progression of atherosclerosis.This process is triggered by local production of chemokines and chemokine receptors from activated endothelial cells and inflammatory cells. Various members of the CC chemokine family (e.g. MCP- 1/CCL2) as well as CXC family (e.g. IL-8/CCL8, IP-10/CXCL10, SDF-1/CXCL12) and, more recently, fractalkine/CX3CL1 have been implicated in atherosclerosis development. Latest findings in animal models suggest that blocking chemokine/chemokine receptor interactions may serve as a suitable approach to treat atherosclerosis. Likewise, chemokine antagonists that inhibit leukocyte recruitment could particularly be interesting to treat inflammation in response to myocardial infarction, the major consequence of atherosclerosis.
Nuclear factor of activated T cells and early growth response-1 cooperate to mediate tissue factor gene induction by vascular endothelial growth factor in endothelial cells
Authors: Schabbauer Gernot , Schweighofer Bernhard , Mechtcheriakova Diana , Lucerna Markus , Binder Bernd , Hofer Erhard 
Published: June 2007

SummaryBased on the finding that tissue factor belongs to a group of genes upregulated in endothelial cells by VEGF, but not by EGF, we investigated signals selectively triggered by VEGF. Whereas the transcription factor early growth response (EGR)-1, which has previously been shown by us to be essentially involved in tissue factor gene regulation, was similarly induced by both factors, one major difference between VEGF and EGF signaling was the activation of the Ca++-mediated calcineurin/nuclear factor of activated T cells (NFAT) pathway by VEGF. Consistent with the importance of this pathway for tissue factor induction, treatment of endothelial cells with the Ca++ chelator BAPTA-AM, as well as the calcineurin inhibitor cyclosporin A, partially inhibited VEGF induced tissue factor upregulation. Furthermore, tissue factor reporter gene assays revealed a synergistic cooperation of NFAT and EGR-1 in the induction of the TF promoter, and a physical interaction between the two factors was indicated by co-immunoprecipitation assays. Another gene upregulated by VEGF predominantly via NFAT, which is not induced by EGF, is the DSCR-1 gene. The calcineurin inhibitor DSCR-1 seems to be induced by VEGF in a negative feed-back loop to limit NFAT activation. When we tested adenoviral overexpression of DSCR-1, VEGF-mediated induction of tissue factor mRNA was reduced, and complete suppression could be achieved by a combination of viruses expressing DSCR-1 and NAB2, a corepressor of EGR-1. These findings support that both, NFAT and EGR-1, are required for tissue factor upregulation in response to VEGF.
Chemokines and thrombogenicity
Authors: Lambert Michele , Sachais Bruce , Kowalska M. 
Published: June 2007

SummaryThrombosis is an important clinical entity, and pathologic thrombosis, in the form of atherosclerosis, is a major cause of morbidity and mortality. Recent research points to the role of chemokines, normally key factors in inflammation, in thrombogenesis. Many recent studies in murine transgenic and knockout models show that chemokines and their receptors are important modulators of the process of thrombus formation, particularly in atherosclerosis. Platelet-released chemokines can potentiate or inhibit thrombosis and inflammation.This review focuses on the role of chemokines in platelet activation and thrombosis, particularly as it relates to atherosclerosis. Further studies to define this complex interaction are underway.
Platelet-derived chemokines in vascular biology
Authors: Hundelshausen Philipp , Petersen Frank , Brandt Ernst 
Published: June 2007

SummaryUndoubtedly, platelets are key elements in the regulation of thrombosis and haemostasis. Along with their primary task to prevent blood loss from injured vessels, platelets have emerged as regulators of a variety of processes in the vasculature. Multiple challenges, from the contact and adhesion to subendothelial matrix after injury of the vessel wall, to interactions with blood cells in inflammatory conditions, result in platelet activation with concomitant shape change and release of numerous substances. Among these, chemokines have been found to modulate several processes in the vasculature, such as atherosclerosis and angiogenesis. In particular, the chemokines connective tissue activating protein III (CTAP-III) and its precursors, or truncation products (CXCL7), platelet factor 4, (PF4, CXCL4) and its variant PF4alt (CXCL4L1) or regulated upon activation and normal T cell expressed and secreted (RANTES, CCL5), have been investigated thoroughly. Defined common properties as their aptitude to bind glycosaminoglycans or their predisposition to associate and form homooligomers are prerequisites for their role in the vasculature and function in vivo. The current review summarizes the development of these single chemokines, and their cooperative effects that may in part be dependent on their physical interactions.
Chemokines in vascular remodeling
Authors: Zernecke Alma , Schober Andreas 
Published: June 2007

SummaryThe arterial vessel wall response to a variety of injuries consists in structural changes, which can result in luminal narrowing and aggravation of the underlying disease.This arterial remodeling is characterized by neointima formation and medial thickening, inflammatory cell recruitment and endothelial dysfunction. Chemokines and the corresponding receptors have been shown to participate at every step of the remodeling process.The monocyte chemotactic protein (MCP)-1/CC motif receptor 2 (CCR2) axis induces monocyte infiltration of the injured vessel wall and can stimulate proliferation of smooth muscle cells (SMCs) in models of restenosis, cardiac allograft vasculopathy (CAV), pulmonary hypertension, and systemic hypertension. In contrast, stromal cell-derived factor (SDF)-1α and its receptor CXC motif receptor 4 (CXCR4) are centrally involved in the neointimal recruitment of SMC progenitor cells (SPCs), presumably in response to SMC apoptosis, in restenosis and CAV.The RANTES (Regulated upon activation, normally T-cell expressed,and presumably secreted) receptors CC motif receptor 1 (CCR1) and CC motif receptor 5 (CCR5) affect intimal monocyte infiltration and neointimal growth, which could be due to the deposition of platelet-derived RANTES on activated endothelial cells. Fractalkine is expressed on neointimal SMCs and thus mediates the arrest of monocytes. Interestingly, reendothelialization of injured vessels appears to primarily depend on CXC motif ligand 1 (CXCL1).These chemokine effects form a complex network, which operates in all mechanisms of vascular remodeling.The detailed understanding of the function of the chemokine network in the remodeling process may allow specific disease intervention.
Acquired muscle contractures in the dog and cat. A review of the literature and case report
Authors: Tangner C. H. , Taylor J. 
Published: June 2007

SummaryCanine and feline muscle contracture is reported to affect several different muscles, is associated with a number of predisposing factors, and a varying prognosis depending upon which muscle is affected. Most patients suffer some form of trauma weeks to months before the contracture is present. The clinical signs include: lameness, pain, weakness, decreased range of motion, a firmness noted throughout the entire muscle, and usually a characteristic gait. Pre-disposing factors for muscle contracture include: compartment syndrome, infection, trauma, repetitive strains, fractures, infectious diseases, immune-mediated diseases, neoplasia, and ischaemia . There does appear to be some breed and age predilection, however, the sex of the animal does not have an appreciable influence. In general, muscle contractures of the forelimb respond better to treatment and carry a better prognosis than muscle contractures of the hindlimb.
Evaluation of three approaches to meniscal release
Authors: Montgomery R. D. , Wright J. , Bellah J. R. , Tonks C. , Austin B. 
Published: June 2007

SummaryThree approaches to medial meniscal release (MMR) were compared using 48 canine cadaver stifles. The approaches included a caudomedial arthrotomy approach, a blind stab incision based on anatomic landmarks, and an arthroscopic guided approach. The cranial cruciate ligament was intact in all specimens. The time required to perform the meniscal release and joint capsule closure was recorded, as well as completeness and location of the meniscal transection. Damage to the caudal cruciate ligament, femoral cartilage, and medial collateral ligament were recorded. The mini-arthrotomy was 81% successful in accomplishment of MMR with a 4% rate of iatrogenic damage. The blind technique was 56% successful in the accomplishment of MMR with a 4% rate of iatrogenic damage. The arthroscopic guided approach was 62.5% successful in accomplishment of MMR, with a 10% rate of iatrogenic damage. Accomplishment and iatrogenic damage rates were not significantly different among procedures (p>0.05). Significantly less time was required to perform the blind technique, and significantly greater time was required to perform the arthroscopic guided technique (p>0.05). Significant differences were not noted among the procedures regarding the ability to accomplish the meniscal release or damage surrounding structures. None of the evaluated approaches for meniscal release resulted in a complete and accurate meniscal release for over 81% of the time.
Treatment of a shoulder luxation in a forelimb amputee dog
Authors: Owen M. R. , Burton N. J. 
Published: June 2007

SummaryAn eight-year-old, male, thoracic limb amputee Whippet presented with a traumatic lateral luxation of the scapulohumeral joint. Surgical reduction and stabilisation of the shoulder joint by means of a modified Campbell scapulohumeral prosthesis and capsulorrhaphy was unsuccessful and reluxation of the shoulder joint occurred. Subsequent surgical stabilisation using bicipital tendon transposition and a modified Campbell scapulohumeral encircling prosthesis in combination with a novel body cast / Spica splint resulted in a return to satisfactory function of this limb.
Carpal laxity syndrome in forty-three puppies
Authors: Yardimci C. , Sağlam M. , Çetinkaya M. A. 
Published: June 2007

SummaryForty-three dogs with carpal laxity syndrome were included in the study. The cases were assessed with clinical and radiographical examinations. The case histories were obtained from patient owners. We recommended exercise and commercially available balanced diets for the treatment. In all cases, the clinical recovery period varied between one to four weeks. Healing occured by the second week in the majority of cases (65.11%). The deformity was observed more frequently in male dogs (n=30) than in female dogs (n=13), and in six- to eight-week-old dogs.Carpal Laxity Syndrome is a more general term, used for both hyperextension and hyperflexion deformity. Malnutrition or over-nutrition of rapidly growing large breed puppies causes weakness and irregular tension between extensor and flexor muscle groups, which leads to laxity of the carpal joint. Exercise and commercially available balanced diets without any other treatment is usually enough to achieve physical and functional recovery.