bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predictors of mortality in mechanically ventilated patients
Authors: Sudarsanam T D , Jeyaseelan L , Thomas K , John G 
Published: December 2005

Abstract

Objectives
There are scarce data from India validating scoring systems used to predict outcome in patients requiring mechanical ventilation. This study prospectively compared the organ system failure (OSF), the acute physiology and chronic health evaluation (APACHE) II, and the APACHE III, scores on patients requiring mechanical ventilation in the medical intensive care unit, to predict outcome.

Methods
200 consecutive patients requiring mechanical ventilation in a medical intensive care unit were recruited. OSF, APACHE II, and APCHE III scores were calculated at admission and daily for one week or until discharge in all patients. Other variables recorded include age, sex, diagnosis, oxygen therapy before ventilation, complications on ventilation, duration in hospital before ventilation, duration of ventilation, type of respiratory failure, alveolar arterial oxygen gradient, P/F ratio, use of tracheostomy, time on ventilator before tracheostomy, muscle relaxant used, fluid balance, inotrope support. Logistic regression analysis and area under the curve were computed to determine which variables independently predict outcome.

Results
Of the 200 patients, at discharge 143 patients (71.5%) had died. The factors that independently predicted outcome among these patients on mechanical ventilation were the type of respiratory failure (type I) OR = 2.7 (p = 0.02), the use of inotropes OR 2.4 (p = 0.04), and the APACHE II score OR = 1.8 (p = 0.008) for every five point increase in APACHE II score.

Conclusions
Type 1 respiratory failure, the use of inotropes, and the APACHE II score measured at admission are significant independent predictors of mortality in the patients on mechanical ventilation.
Diagnosis and treatment of caecal volvulus
Authors: Consorti E T , Liu T H 
Published: December 2005

Abstract
Caecal volvulus is an infrequently encountered clinical condition and an uncommon cause of intestinal obstruction. Patients with this condition may present with highly variable clinical presentations ranging from intermittent, self limiting abdominal pain to acute abdominal pain associated with intestinal strangulation and sepsis. Lack of familiarity with this condition is a factor contributing to diagnostic and treatment delays. The objective of this review is to promote clinicians’ awareness of this disease through patient case illustration, discussion of disease pathogenesis, clinical features, and management strategies.
SOFT-THRESHOLDING FOR DENOISING OF MEDICAL IMAGES — A MULTIRESOLUTION APPROACH
Authors: KHARE ASHISH , TIWARY UMA SHANKER 
Published: December 2005

Medical images generally have low contrast and they get complex type of noise due to the use of various devices and applications of various algorithms. However, most of the denoising methods consider only additive noise or some special noise model dependent on their systems and conditions only. Such methods when applied to real medical images yield poor results.The present work proposes a method for denoising of medical images using soft-thresholding in wavelet domain on multiple levels. We have developed a method to compute the threshold values for denoising of medical images, which depend on the median as well as the contrast ratio of the wavelet coefficients and also on the level number. We have performed experiments by adding various proportions of Gaussian, Salt-and-Pepper and Speckle noise, and found that the proposed method performs better for these cases. The method is efficient because the threshold values can be calculated directly and it is adaptive as these values depend on mean, median and standard deviation of wavelet coefficients of the particular image. The proposed method also gives a criterion for level-dependent thresholding. Application of the proposed method to Ultrasound, X-ray and MRI images is demonstrated in experiments. In the present work, we have also done studies on how to select the mother wavelet for a particular problem.
Megakaryocytic cells synthesize and platelets secrete α5-laminins, and the endothelial laminin isoform laminin 10 (α5β1γ1) strongly promotes adhesion but not activation of platelets
Authors: Nigatu Ayele , Sime Wondossen , Gorfu Gezahegn , Geberhiwot Tarekegn , Andurén Ingegerd , Ingerpuu Sulev , Doi Masayuki , Tryggvason Karl , Hjemdahl Paul , Patarroyo Manuel 
Published: December 2005

SummaryFollowing vascular injury, basement membrane (BM) components of the blood vessels are exposed to circulating cells and may contribute to hemostasis and/or thrombosis. Laminins 8 (LN-8) (α4β1γ1) and 10 (LN-10) (α5β1γ1) are major laminin isoforms of the endothelial BM, and LN-8 is also secreted by activated platelets. In the present study, we demonstrate synthesis of α5-laminins LN-10 and LN-11 (α5β2γ1) by megakaryocytic cells, and intracellular expression of these laminin isoforms in blood platelets. In contrast to platelet LNα4 chain that had an apparent molecular weight of 180 kDa and associated mostly to LNβ1 chain, platelet LNα5 consisted of 300/350 kDa polypeptides and associated mainly to LNβ2. Both α4– and α5-laminins were secreted by platelets following stimulation. When compared to recombinant human (rh) LN-8, rhLN-10 was much more adhesive to platelets, though adhesion to both proteins was largely mediated via α6β1 integrin. In spite of their adhesive properties, rhLN-8 and rhLN-10 induced neither P-selectin expression nor cell aggregation, two signs of platelet activation. This study demonstrates synthesis/expression of heterotrimeric α5-laminins in hematopoietic/blood cells, and provides evidence for the adhesive, but not activating, role of endothelial laminin isoforms in platelet biology.
Circulating platelet-derived microparticles in systemic lupus erythematosus
Authors: Alfaro Gino , Goycoolea Manuela , Quiroga Teresa , Ocqueteau Mauricio , Massardo Loreto , Pérez Carol , Sáez Claudia , Panes Olga , Matus Valeria , Mezzano Diego , Pereira Jaime 
Published: December 2005

SummaryThe risk for thrombosis is significantly increased in systemic lupus erythematosus (SLE), affecting both venous and arterial vessels. Activated platelets are known to participate in thrombus formation and growth. A general feature of activated cells is the shedding of microparticles (MP) which support coagulation by exposure of negatively charged phospholipids and possibly tissue factor (TF). In this work we characterized circulating MP in patients with SLE and their relationship with a procoagulant state. Thirty patients with SLE (aged 15–72 years, mean age 38 years) and 20 healthy controls (aged 22–54 years, mean age 34 years) were studied; patients fulfilled 4 revised criteria for SLE. The number and cellular source of circulating MP were determined by flow cytometry using double labeling with specific monoclonal antibodies and annexin V. Thrombin generation was measured as the endogenous thrombin potential (ETP) without the addition of exogenous phospholipids and TF; under these conditions the generation of thrombin depended directly on the number of MP present in plasma. Thrombin anti-thrombin (TAT) and plasmin-antiplasmin (PAP) complexes were measured by ELISA. Compared to the controls, circulating MP were significantly elevated in the patient group (1218 ± 136 vs 653 ± 74 x103/ml plasma, p: 0.0007). In both groups, most of these MP were of platelet origin (927± 131 vs 517 ± 72 x103/ml plasma, p:0.009 ). ETP was higher among patients as compared to the controls (804± 64 vs 631 ± 37 nM thrombin, p: 0.025). Plasma levels of TAT in patients and controls were 3.4 ± 0.8 and 1.4 ± 0.5 µg/L, respectively (p:0.04), and of PAP complexes were 62.5 ± 14 and 24.05± 2.5 µg/ml, respectively (p: 0.014).The number of platelet-derived MP correlated significantly with thrombin generation (r: 0.42; p: 0.038) and TAT levels (r: 0.40; p: 0.035).We did not find an association of circulating MP with disease activity nor with the presence of antiphospholipid antibodies. The increased number of circulating platelet-derived microparticles and their association with high ETP and activation of the coagulation system suggest that these microparticles play an important role in the pathogenesis of the prothrombotic state in SLE patients.
The estrogen metabolite 17β-dihydroequilenin counteracts interleukin-1α induced expression of inflammatory mediators in human endothelial cells in vitro via NF-κB pathway
Authors: Kaun Christoph , Rega Gersina , Speidl Walter , Kastl Stefan , Weiss Thomas , Hohensinner Philipp , Dietrich Wolf , Tschugguel Walter , Bochkov Valery , Awad Ezzat , Maurer Gerald , Huber Kurt , Demyanets Svitlana , Pfaffenberger Stefan , Wojta Johann 
Published: December 2005

SummaryIn most studies showing cardio- and vasculoprotective effects of estrogens, 17β-estradiol was used and little information on possible effects of different estrogen metabolites is yet available. We investigated whether particular estrogen metabolites are effective in counteracting inflammatory activation of human endothelium. Human endothelial cells were incubated with 17α-dihydroequilenin, 17β-dihydroequilenin, δ-8,9-dehydroestrone, estrone and 17β-estradiol and stimulated with interleukin (IL)-1α.The expression of IL-6, IL-8 and monocyte chemoattractant protein-1 (MCP-1) was determined. 17β-dihydroequilenin and 17β-estradiol at a concentration of 1µM reduced IL-1α-induced up regulation of IL-6, IL-8 and MCP-1 close to control levels. When both compounds were used in combination an additive effect was observed. 17α-dihydroequilenin and δ-8,9-dehydroestrone showed a similar anti-inflammatory effect only when used at 10µM whereas estrone had no effect. The effect of 17β-dihydroequilenin on IL-1α-induced production of IL-6, IL-8 and MCP-1 was reversed by the estrogen receptor antagonist ICI 182,780. 17β-dihydroequilenin also inhibited IL-1α-induced translocation of p50 and p65 to the nucleus of the cells. We have identified the estrogen metabolite 17β-dihydroequilenin, as an inhibitor of inflammatory activation of human endothelial cells. Characterization of specific estrogens – as shown in our study – could provide the basis for tailored therapies, which might be able to achieve vasoprotection without adverse side effects.
Improved coagulation in bleeding disorders by Non-Anticoagulant Sulfated Polysaccharides (NASP)
Authors: Liu Tongyao , Scallan Ciaran , Broze George , Patarroyo-White Susanna , Pierce Glenn , Johnson Kirk 
Published: December 2005

SummaryAdditional therapeutic options are needed for patients with bleeding disorders such as hemophilia A, hemophilia B, severe von Willebrand disease, and other rare factor deficiencies. A novel approach to improve coagulation in such clotting disorders has been identified that, parodoxically, involves heparinlike sulfated polysaccharides.Select molecules of this broad class are largely devoid of anticoagulant activity and are here denoted Non-Anticoagulant Sulfated Polysaccharides (NASPs).A mechanism involving blockade of the extrinsic pathway downregulator,Tissue Factor Pathway Inhibitor (TFPI) by NASPs, was conceived as an approach for improving procoagulant behavior in hemophilic settings.A subset of NASPs, including pentosan polysulfate (PPS) and fucoidan inhibited both full-length and Kunitz 1 and 2 (K1K2) TFPI and, at concentrations from 4-500 nM, improved (i.e. accelerated) the clotting time of human hemophilia A and hemophilia B plasmas or plasma with reduced factor VII levels when tested in dilute prothrombin time (dPT) assays. Fucoidan did not reduce normal plasma APTT times implying specificity for extrinsic pathway control. Improved hemostasis in vivo was observed in mice with hemophilias A orB following low dose subcutaneous administration of PPS or fucoidan, or a combination of NASP plus factor supplement. Increased survival of factor deficient mice following a bleeding challenge was observed. Accordingly, administration of select NASP(s), via mechanism(s) not fully understood, represents a unique means of improving coagulation in bleeding disorders.
The death of human platelets during incubation in citrated plasma involves shedding of CD42b and aggregation of dead platelets
Authors: Savill John , Brown Simon , Hartley Paul 
Published: December 2005

SummaryThe ability to readily identify dead platelets is invaluable to studies examining the means of their death, factors affecting their lifespan and their means of clearance by phagocytes. The aim of the present work was to develop a vital staining procedure for the rapid and objective discrimination of live from dead platelets that accrued in citrated platelet rich plasma (cPRP) incubated at 37°C for several days. By transmission electron microscopy it was noted that platelet death was morphologically similar to necrosis and associated with aggregate formation. The vital dyes calcein-AM and FM 4–64 were found to robustly report the death of platelets and indicated that the aggregates which formed during incubation were populated exclusively by dead platelets. Additionally, platelet death was associated with the shedding of CD42b. Microscopic and cytometric analyses of incubated cPRP indicated that shedding of CD42b and aggregate formation by dead platelets were completely inhibited by the metalloproteinase inhibitor GM6001. Automated counting of platelets incubated in the presence of GM6001 revealed that death did not lead to a loss in cellularity. It is proposed that calcein-AM and FM4–64 are effective as vital stains for the reliable assessment of platelet viability and that platelet aggregation can occur by a novel mechanism dependent upon platelet death and metalloproteinase activity.
Regulation by cannabinoid receptors of anandamide transport across the blood-brain barrier and through other endothelial cells
Authors: Fiori Anna , Bari Monica , Granata Filippo , Gasperi Valeria , De Stefano M. , Finazzi-Agrò Alessandro , Strom Roberto , Maccarrone Mauro 
Published: December 2005

SummaryThe endocannabinoid anandamide (AEA) has many neurovascular activities. However, it is not yet clear how AEA can be metabolized at the neurovascular interface, and how it can move through the vascular and the cerebral compartments. The results reported in this article show that isolated bovine brain microvessels, an ex vivo model of the blood-brain barrier, have detectable levels of endogenous AEA and possess the biochemical machinery to bind and metabolize it, i. e. type-1 and type-2 cannabinoid receptors (CB1R and CB2R), a selective AEA membrane transporter (AMT), an AEA-degrading fatty acid amide hydrolase, and the AEA-synthesizing enzymes N-acyltransferase and N-acyl-phosphatidylethanolamines-specific phospholipase D. We also show that activation of CB1R enhances AMT activity through increased nitric oxide synthase (NOS) activity and subsequent increase of NO production. AMT activity is instead reduced by activation of CB2R, which inhibits NOS and NO release. In addition, binding experiments and immunoelectronmicroscopy demonstrate that different endothelial cells vary in the expression of CB1R and CB2R on the luminal and/or abluminal sides. The different localization of CBRs can lead to a diverse effect on AMT activity on the luminal and abluminal membranes, suggesting that the distribution of these receptors may drive AEA directional transport through the blood-brain barrier and other endothelial cells.
Impairment of adipose tissue development by hypoxia is not mediated by plasminogen activator inhibitor-1
Authors: Semeraro Fabrizio , Voros Gabor , Collen Désiré , Lijnen H. 
Published: December 2005

SummaryHypoxia in rodents and humans is associated with a reduction of body fat on the one hand, and with enhanced expression of plasminogen activator inhibitor-1 (PAI-1), the main inhibitor of the fibrinolytic system, on the other hand. It was the objective of this study to investigate whether impairment of adipose tissue development by hypoxia may be mediated by PAI-1. Five week old male wild-type (WT) C57Bl/6 mice were fed a standard (SFD) or high fat (HFD) diet and kept under normoxic or hypoxic (10% O2) conditions. In addition, PAI-1 deficient mice and WT littermates were kept on HFD under normoxia or hypoxia. In vitro, the effect of hypoxia (2% O2) was investigated on differentiation of 3T3-L1 cells into adipocytes. Hypoxia induced a significant reduction of weight gain in WT mice on either SFD or HFD, accompanied by lower weights of subcutaneous (SC) and gonadal (GON) fat. Under hypoxic conditions, adipocytes in the adipose tissues were significantly smaller, whereas blood vessel size and density were larger. Serum PAI-1 levels were enhanced in hypoxic mice on SFD but not on HFD, and overall did not correlate with the observed changes in adipose tissue composition. Furthermore, the effects of hypoxia on adipose tissue in mice on HFD were not affected by deficiency of PAI-1. The inhibiting effect of hypoxia on in vitro preadipocyte differentiation was not mediated by PAI-1 activity. In conclusion, impairment of in vivo adipose tissue development and in vitro differentiation of preadipocytes by hypoxia is not mediated by PAI-1.
Right on the spot
Authors: Laudanna Carlo , Alon Ronen 
Published: December 2005

SummaryThe arrest of rolling leukocytes on various target vascular beds is crucial for their recruitment at inflammatory sites and secondary lymphoid tissues. Leukocyte arrest is predominantly mediated by integrins interacting with either constitutive or inducible endothelial ligands. Integrins are cytoskeletally regulated heterodimers maintained in largely low affinity conformational states on circulating leukocytes. For arrest to occur, the affinity of integrin heterodimers must be enhanced in situ upon leukocyte encounter with proper endothelial-displayed chemokines or chemoattractants which bind and signal through specific G-protein coupled receptors (GPCRs) on the leukocyte surface. Recent studies suggest that this integrin activation involves rapid conformational alterations locally induced at confined leukocyte-endothelial contact sites. Following binding, integrin microclustering reinforced by associations with the cortical actin cytoskeleton further enhances integrin-mediated adhesiveness under shear stress. These events are controlled by complex signaling events, involving a series of small GTPases, as well as protein and lipid kinases which are triggered by chemokine bound GPCRs. To rapidly mediate this specialized function, subsets of signaling proteins and their specific targets are thought to preexist in pre-assembled multi-molecular complexes or signalosomes. Recent in vitro dissection of chemokine-triggered integrin activation on lymphocytes and neutrophils suggests that these signalosomes may vary both in composition and mode of activity between different immune cell types and distinct integrins. We review in this article recent findings on key elements implicated in chemokine triggering of integrin activation on rolling leukocytes, and discuss the possible existence of preformed proadhesive signaling networks in different subsets of leukocytes.
Endothelial tight junctions: permeable barriers of the vessel wall
Authors: Bazzoni Gianfranco 
Published: December 2005

SummaryThe endothelial lining of the vessel wall is a permeable barrier, which is located at the interface between the vascular and the perivascular compartments. Although the endothelium acts as an efficient barrier that strictly separates the two compartments,it may also act as a permeable filter which allows selective exchange of solutes and water between the luminal and abluminal sides of the barrier. Similarly to epithelia, also in the endothelium permeability follows two distinct routes, which have been termed transcellular pathway (across the apical and basolateral membranes of individual cells) and paracellular pathway (through the intercellular junctions and the lateral spaces between contacting cells). After an initial description of the two pathways, the review focuses on the cellular and molecular basis of the paracellular pathway, with emphasis on the role of intercellular tight junctions and tight junction-associated claudins. Finally, the signaling events that regulate paracellular permeability are discussed.
Dual effect of apolipoprotein(a) on plasmin(ogen)-induced apoptosis through modulation of cell detachment of adherent cells
Authors: Ho-Tin-Noé Benoît , Meilhac Olivier , Rossignol Patrick , Lijnen H. , Anglés-Cano Eduardo 
Published: December 2005

SummaryBecause of its structural homology with plasminogen, the apolipoprotein(a) [apo(a)] component of the athero-thrombogenic lipoprotein(a) [Lp(a)] particle inhibits plasminogen binding and activation onto fibrin as well as the subsequent fibrinolysis. In a similar manner, apo(a) may also interfere with plasmin(ogen)-induced cell detachment and apoptosis of adherent cells. To investigate this hypothesis, we studied the effect of a recombinant apo(a) [r-apo(a)] on plasminogen activation-induced apoptosis of vascular smooth muscle cells (VSMCs) and fibroblasts-like CHO-K1 cells. We demonstrate for the first time that apo(a) displays a concentration-dependent biphasic, enhancing/preventing effect on plasmin(ogen) induced cell detachment of VSMCs and CHO-K1 cells. Our results show that r-apo(a) binds to these cells with higher affinity than plasminogen [Kd = 0.9 ± 0.2 µM for plasminogen, Kd = 1.77 ± 0.34 nM for r-apo(a)] in a lysine-dependent manner. At high r-apo(a)/plasminogen ratios, their competitive interaction results in a partial inhibition of plasminogen activation by cell-bound t-PA. As a consequence, r-apo(a) prevents plasmin(ogen)-induced cell detachment and apoptosis. Surprisingly,at low r-apo(a)/plasminogen ratios,an enhancement in plasmin(ogen)-induced cell detachment and apoptosis was observed. This effect was shown to be “plasmin-selective” as r-apo(a) was unable to potentiate cell detachment induced by human neutrophil elastase and trypsin. Altogether these data are consistent with a new mechanism of apo(a)/plasmin(ogen) interactions that may contribute to the atherothrombogenic potential of Lp(a).
Association of cardiovascular risk factors with markers of endothelial dysfunction in middle-aged men and women
Authors: Thorand Barbara , Baumert Jens , Döring Angela , Schneider Andrea , Chambless Lloyd , Löwel Hannelore , Kolb Hubert , Koenig Wolfgang 
Published: December 2005

SummaryEndothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases and diabetes mellitus. However, the causes underlying endothelial dysfunction are not fully understood. Therefore, the aim of the present study was to investigate associations of cardiovascular risk factors with soluble adhesion molecules (sE-Selectin, sICAM-1), soluble thrombomodulin (sTM) and von Willebrand factor (vWF) as markers of endothelial dysfunction. The study population consisted of a subcohort of 2,168 men and women aged 35 to 74 years randomly drawn from three cross-sectional population-based MONICA/ KORA Augsburg surveys conducted between 1984 and 1995. In multivariable linear regression analysis, current smoking, high (versus moderate) alcohol consumption, ratio of total cholesterol/HDL-cholesterol (TC/HDL-C) and C-reactive protein (CRP) were significantly associated with elevated levels of sEselectin and sICAM-1. Increased levels of sE-selectin were also found in subjects with actual hypertension, high body mass index and prevalent diabetes mellitus. In addition, low physical activity and no (versus moderate) alcohol consumption were significantly associated with elevated concentrations of sICAM-1. Levels of sTM were higher in subjects with actual hypertension, no or high amounts of alcohol intake and a high ratio of TC/ HDL-C, but were lower in subjects witha history of myocardial infarction. VWF was significantly associated with CRP only. In conclusion, sE-selectin and sICAM-1 are more strongly associated with traditional cardiovascular risk factors than sTM and vWF.