bluuebunny/crossref_metadata_2025_split huggingface dataset:
Safety and efficacy of the use of lumen-apposing metal stents in the management of postoperative fluid collections: a large, international, multicenter study
Authors: Yang Juliana , Kaplan Jeremy H. , Sethi Amrita , Dawod Enad , Sharaiha Reem Z. , Chiang Austin , Kowalski Thomas , Nieto Jose , Law Ryan , Hammad Hazem , Wani Sachin , Wagh Mihir S. , Yang Dennis , Draganov Peter V. , Messallam Ahmed , Cai Qiang , Kushnir Vladimir , Cosgrove Natalie , Ahmed Ali Mir , Anderloni Andrea , Adler Douglas G. , Kumta Nikhil A. , Nagula Satish , Vleggaar Frank P. , Irani Shayan , Robles-Medranda Carlos , El Chafic Abdul Hamid , Pawa Rishi , Brewer Olaya , Sanaei Omid , Dbouk Mohamad , Singh Vikesh K. , Kumbhari Vivek , Khashab Mouen A. 
Published: June 2019

Abstract
Background Multiple studies have examined the use of lumen-apposing metal stents (LAMSs) for the drainage of peripancreatic fluid collections. Data on the use of LAMSs for postoperative fluid collections (POFCs) are scarce. POFCs may lead to severe complications without appropriate treatment. We aimed to study the outcomes (technical success, clinical success, rate/severity of adverse events, length of stay, recurrence) of the use of LAMSs for the drainage of POFCs.
Methods This international, multicenter, retrospective study involved 19 centers between January 2012 and October 2017. The primary outcome was clinical success. Secondary outcomes included technical success and rate/severity of adverse events using the ASGE lexicon.
Results A total of 62 patients were included during the study period. The most common etiology of the POFCs was distal pancreatectomy (46.8 %). The mean (standard deviation) diameter was 84.5 mm (30.7 mm). The most common indication for drainage was infection (48.4 %) and transgastric drainage was the most common approach (82.3 %). Technical success was achieved in 60/62 patients (96.8 %) and clinical success in 57/62 patients (91.9 %) during a median (interquartile range) follow-up of 231 days (90 – 300 days). Percutaneous drainage was needed in 8.1 % of patients. Adverse events occurred intraoperatively in 1/62 patients (1.6 %) and postoperatively in 7/62 (11.3 %). There was no procedure-related mortality.
Conclusion This is the largest study on the use of LAMSs for POFCs. It suggests good clinical efficacy and safety of this approach. The use of LAMSs in the management of POFCs is a feasible alternative to percutaneous and surgical drainage.
HAEMOPHILIC ARTHROPATHY: IMMUNOLOGICAL MECHANISMS AND SYNOVITIS
Authors: Störkel F , Scharrer I , Hovy L , Rüdigier J , Störkel S 
Published: June 2019

Up to now questions of pathogenisis in hemophilic arthropathy are still remaining, i.e. humoral mediated imnunological mechanisms (type II/III reactions) are supposed to play an important role (Arnold and Hilgartner (1977), Rippjey (1978)). Therefore we investigated synovial tissue by imnunohistologic technique using antibodies against IgG, IgA, IgM, C1q, C3, fibrinogen ando61-ACT. First we examined synovial membrane biopsies (n=7; non-haemo-philic) following acute traumatic joint bleeding, to study the first and acute bleeding/absorption pahase. Light microscopy showed typical changes as described before by Roy et al. 1967. Iirrnunohistological results revealed negativity for immunoglobulins and complement components in general, whereas fibrinogen and α1-ACT showed marked intensity of fluorescence.Secondly synovial membrane biopsies (n=7) of haemophiliacs who have had recurrent joint bleedings were examined, in the same way. In light microscopy we found typical synovial alterations as described by Mohr (1984) . Immunohistology shewed negativity for immunoglobulins and complement components and the intensity of fluorescence of fibrinogen and α1 -ACT was lower as in patients with acute traumatic joint bleeding.At last synovial tissue specimens (n=2) of patients with pigmented villonodular synovitis were investigated. Light microscopy was in aquaintance with findings of FaBbender (1976) . The imnuno-histological results were similar to those aforementioned. Conclusions: 1) There is no evidence that acute or chronic joint bleeding causes a humoral mediated immune reaction in synovial membrane. 2) In the contrary the inflammatory reaction leeds to detritus-synovialitis, supported by recurrent bleeding episodes. Concequences for clinical management: a) prevention of joint bleeding b) joint-pxinction in cause of bleeding, to reduce the intraarticular haematcma c) synovectomy to prevent the progress of arthropathy.
VON WILLEBRAND FACTOR (VWF) ANTIGENS IN URINE
Authors: Silveira A M V , Hessel B , Blombäck B 
Published: June 2019

Human urine was analyzed using a sensitive enzyme linked immunosorbent assay (ELISA) for von Willebrand factor (VWF) antigen. Urine of healthy persons contained VWF immunoreactivity. In the urine of a patient with severe von Willebrand disease, the VWF antigen was only detectable after intravenous infusion of VWF-Factor VIII concentrate. The VWF antigen in normal urine was analyzed by gel permeation high performance liquid chromatography (HPLC) and gel electrophoresis combined with immunoblotting. These analyses revealed three immunoreactive components of Mr 350 kDa, 60 kDa, and 20 kDa, respectively, the 60 kDa being the major component. Monoclonal antibodies of known specificity to VWF molecule were used in ELISA and immunoblotting to analyze urinary VWF. The three components reacted with an antibody to the central part of VWF, which is called fragment I, and contains the binding site for collagen. No significant immunoreac-tion was observed with monoclonal antibodies to the Nor C-terminal portions of VWF.VWF derivatives of molecular size similar to the largest urinary antigens were also observed in normal plasma. However, there is not an obvious relationship between these plasma forms and the products in urine since reduction of plasma and urine yields different products.These results indicate that VWF antigens excreted in normal urine are most likely fragments of VWF produced by limited degradation in vivo. This degradation preserves the central part of VWF molecule, the one which reacts with the antibody that blocks the binding of VWF to collagen.
TREATMENT OF PLASMA DERIVATIVES WITH UNSATURATED FATTY ACIDS TO INACTIVATE VIRUSES
Authors: Horowitz B , Piët M , Prince A M 
Published: June 2019

Virus sterilization of blood plasma derivatives by addition of several naturally occurring fatty acids was evaluated using VSV and Sindbis virus as markers for lipid enveloped virus inactivation. Complete inactivation >4 log10) of virus added to an AHF concentrate with 60-101)% retention of AHF activity was achieved with oleic, 11-eicosenoic, linoleic, linolenic, palmitoleic and arachidonic acids. Elaidic, gamma-linolenic, palmitic, and arachidic acids. Another fat-soluble compound previously reported to inactivate virus, butylated hydroxytoluene, was less effective. A long chain mono- but not a di- or tri-glyceride also displayed virucidal properties.The degree of virus inactivation depended on the sample composition. A favorable balance was achieved between degree of virus inactivation and retention of protein function for AHF concentrate, prothrombin complex concentrate, antithrombin-III concentrate, and immune globulin solution on incubation with 0.033% (w/v) sodium oleateat 24°C for 4-6 hours. Virus inactivation in whole plasma and plasma cryoprecipitate was not complete despite use of higher concentrations of sodiumleate and/or incubation at 37°C.Utilization of fatty acids for thepreparation of blood derivatives has the advantage that they are naturallyoccurring and have low toxicity, thussimplifying the production process. This simplicity encourages the sequential use of fatty acids with other procedures designed to inactivate or remove viruses and which operate by a distinct mechanism.
THE DILUTE PH0SPH0LIPID-APTT:EVALUATION OFSPECIFICITY FOR ANTIBODIES AGAINST CARDIOLIPIN AND PHOSPHATIDYLSERINE
Authors: Alving B M , Barr C F 
Published: June 2019

The dilute phospholipid-APTT (PL-APTT) has been used to detect lupus anticoagulants, but its specificity for antibodies to negatively-charged phospholipids has not been assessed. The current study determined what percent of plasmas with a positive PL-APTT contained antibodies (IgG or IgM) to cardiolipin (CL) and phosphatidylserine (PS). The PL-APTT was performed by mixing patient plasma with normal plasma and measuring the clotting time in an APTT that contained increasing dilutions of Thrombofax (Alving et al. , Thromb. Haemostas. 54:709, 1985). A positive test gave a negative slope at least twice that of a normal plasma-buffer control. Sera were tested for anti-CL and anti-PS antibodies at a 1:100 dilution in a solid-phase ELISA that contained PS or CL in microtiter plates and antiserum to human IgG or IgM. A result that was >2 S. D. above mean values obtained for sera from 64 normal individuals was considered positive. Sera were studied from 25 patients with a positive PL-APTT; plasma from one patient had a normal APTT and correction studies for prolonged APTTs were normal in 3 plasmas. The patients' illnesses included systemic lupus erythematosus, bacterial infections, or use of procainamide; only one had a history of thrombosis. The table lists the percent of patient sera having the indicated antibodies.The one plasma with the normal APTT and positive PL-APTT had elevated levels of IgM directed against CL and PS. The correlation coefficient between levels of IgM against CL and PS, or between levels of IgG against CL and PS, was >0.95. There was no correlation between the extent of prolongation of the APTT and the class or potency of antibodies to CL and PS. The data indicate that the dilute PL-APTT, which may be positive in plasmas with a minimal or no prolongation of the APTT, has high specificity in detection of anti-CL and anti-PS antibodies.
LUPUS ANTICOAGULANT (LA) COEXISTENT WITH TRANSIENT PROTHROMBIN (FII) INHIBITOR: FTI DEFICIENCY DUE TO CLEARANCE OF THE B/MUNOCOMPLEX
Authors: Redaelli R , Baudo F , Busnach B , Caimi T M , Perrino L , Pezzetti L , deCataldo F 
Published: June 2019

23 y.o. man with acute nephritis and bleeding (epistaxis, ecchymosis) at presen-taticn. Family and personal past history negative for bleeding. Laboratory data consistent with SLE. Coagulation tests: FT Ratio (R) 1.8, aPTT R 2.4, FII:C <1%, FIIR:Ag 996, other coagulation factors normal. Tissue thromboplastin inhibition test (TTIT) R 2.8, congenital FII deficiency (696) R 1.6.1. FII survival time (Fll-ccncentrate infusion - 60 U/kg) t1/2: 9 hours.2. FII neutralizing activity (FTI:C normal plasma (NP) + buffer 5996; NP + patient plasna {PtP) 5096): absent.3. Irmunoccrplex formaticn4. FII inhibitor characterization (purified FII coupled to CNBr-activatedSepharose →PtP incubation with Fll-Sepharose→specific antiFII irrrrunoglobulins (Ig)* elution at acid pH→identification by double iimunodifftision): precipitin line with anti IgA, anti IgG2, anti k, anti 1.5. LA characterization (after FII inhibitor disappearance): TTTT on mixtures NP + PtP or N Ig in equal volumes.Diagnosis: SIE, LA (IgG); polyclonal (IgA, IgG2, k, 1) not neutralizing FII inhibitor; hypoprothrxmbinemia due to clearance of the irrrrunocorrplex.FII inhibitor was transient. Bleeding was rapidly controlled by replacement therapy. LA persits after FII inhibitor disappearance.
Inhibitors Interfering with the Quantitative Estimation of Tissue Plasminogen Activator
Authors: Wijngaards G. , Potjer A. T. 
Published: June 2019

The commonly used quantitative assay for plasminogen activator in tissues by Astrup and Albrechtsen (1957) was re-evaluated with special reference to the presence of inhibitors in tissue extracts at different stages of the procedure.Human lung, liver, and placenta tissues were chosen for their different activator and inhibitor content. Samples of the extracts were tested for inhibitory capacity against purified human tissue plasminogen activator, urokinase, and plasmin on different kinds of fibrin plates.The procedure for preparing the samples according to Astrup and Albrechtsen did not completely eliminate the inhibitory action against the plasminogen activators added. The presence of inhibitors was partly obscured by 2M KCNS in the sample. In order to quantitate the plasminogen activator content in tissues, the method should be revised with respect to the elimination of inhibiting material.Some interesting aspects of the inhibitory components extracted from liver and placenta were revealed by comparing urokinase inhibition to tissue activator inhibition as to the degree of denaturation during the procedure. It was suggested that, although they have much in common, urokinase and tissue activator inhibitors are separate entities.
The Rapid Fibrin Plate – a Method for Streptokinase Assay
Authors: Marsh N. A. , Gaffney P. J. 
Published: June 2019

The fibrin plate has become established as a convenient method for studying components of the fibrinolytic enzyme system, in particular, urokinase. However for streptokinase estimations, a clot lysis method is more frequently favoured. This study reports on the use of the fibrin plate to assay streptokinase.In order to overcome the disadvantages of some twenty hours incubation for the conventional plate, the method was modified by the addition of comparatively large amounts of the intermediate substrate, plasminogen. For each plate 2.5 units of plasminogen were added to the fibrinogen-calcium-thrombin mixture, and the plates allowed to clot for one hour. Three dilutions of standard and unknown streptokinase solutions were tested on each of four to six plates. Incubation was carried out for three hours only and measurement of lysis areas facilitated by magnification on an overhead projector. Mean potency ratio, fiducial limits and information on linearity and parallelism of the dose response curves, was obtained by means of an analysis of variance program.The technique compares favourably with the conventional clot lysis method and has the advantage of requiring less bench working time, an entire assay being completed in under five hours.
Coagulation Inhibitors in Plasma and Serum
Authors: Ødegård O. R. , Abildgaard U. 
Published: June 2019

Heparin cofactor activity and antithrombin III (At-III) activity measured with amidolytic methods; antifactor Xa by a clotting method (Biggs et al., Brit. J. Haemat. 19, 287, 1970) and immunoassay of At-III (Fagerhol & Abildgaard, Scand. J. Haemat. 7, 10, 1970) in plasma and serum showed:1) There was a close correlation between the plasma values as measured by all these methods (r = 0.84–0.93).2) The difference between plasma and serum values (“consumption”) was lower in warfarin treated and in haemophiliacs than in the other groups.3) The difference between plasma and serum was greater when measured by the heparin cofactor activity method than by the other methods. The reason for this discrepancy will be discussed. The results in different patient groups will be reported.4) As the heparin cofactor activity assay can be completed within 10 minutes after blood sampling, and has a higher precision than clotting assay and immuno assay, it is preferable for clinical use.
Animal Experiments of a New Synthetic Thrombin-Inhibitor, Dansyl-Arginine-Methyl-Piperidine Amide
Authors: Hijikata A. , Okamoto S. , Ikezawa K. , Kikumoto R. , Tonomura S. , Tamao Y. 
Published: June 2019

A noticeable effect of dansyl-arginine-methyl-piperidine amide in animal experiments is described, which is one of the representative compounds of a new series of potent thrombin-inhibitors synthetized by the authors very recently. The inhibitor solution was intravenously administered to rabbits by means of the infusion pump to maintain the inhibitor in the circulatory blood at a concentration intended. When bovine thrombin was intravenously administered (5 NIH units/Kg/min) for 75 minutes, a remarkable decrease of plasma fibrinogen content was observed in control, while any decrease of fibrinogen content was hardly observed at the inhibitor concentration of 10 ~ 20 μMin plasma. Further, the decrease of plateletes in number due to thrombin infusion (7.5 ~ 9NIH units/Kg/min) for 5 minutes was suppressed satisfactorily at the inhibitor concentration of 1 ~ 2 μM in plasma.These results indicate that the new synthetic thrombin-inhibitor is effective enough at a very low concentration to control the hazard due to thrombin given in vivo, encouraging the authors to extend the studies further toward the application.
Platelet Studies During Vascular Surgery
Authors: Gjesdal K. , Sørlie D. 
Published: June 2019

Platelet counts, in vivo aggregates and platelet factor 4 (PF-4) were studied in 5 patients during femoro-popliteal revascularization. Blood samples were taken from radial artery, superior vena cava and the popliteal vein before clamping of the common femoral artery, at the end of the ischaemic period, 5 minutes after release of the clamps and just before wound closure.Platelet counts fell transiently to 80%. Reversible platelet aggregates were more frequent on the venous side. The initial and final values from v. poplitea approximated to those from the v. cava. Both during ischaemia and after onset of flow, the popliteal vein samples had a higher aggregation percentage then arterial and central venous blood. Extremely high values (60%) were found in 2 cases with prolonged arterial clamping (3 h). The highest arterial values (27%) were found during maximal ischaemia, followed by gradual normalization. Plasma PF-4 immunoassay revealed that the popliteal vein had the highest levels. The profile was similar in all vessels, there were no significant changes until the end of the operation, when a marked increase occurred.The results suggest that ischaemia may be a more potent stimulus for aggregation than endothelial damage is. There may be a delay of some minutes before aggregated platelets release PF-4.
α, ω-Diadenosine Polyphosphates, a New Class of Substances, and ADP-Methylester Inhibit Platelet Aggregation and the Release Reaction
Authors: Brossmer R. , Harrison M. J. , Goody R. S. 
Published: June 2019

A series of α, ω-diadenosine polyphosphates, which may be represented by the formula, where A = adenosine and n = the number of phosphate groups, were studied for their effect on the aggregation and release reaction of human platelets. The adenosine derivatives inhibit ADP-induced aggregation in the same order of efficiency as they inhibit the enzyme activity of adenylate kinase i. e. up to n = 5 the more phosphate groups, the more inhibitory the activity. Double reciprocal plots suggest that these adenosine derivatives act competitively with ADP. AP5A and AP4A inhibit the release reaction in washed platelets but AP3A and AP2A do so only in high concentrations. In platelet-rich plasma the APnA derivatives inhibit the ADP release reaction with diminished strength as n decreases from 5(55 ± 13% inhibition) to 2 (4±4% inhibition). The adenosine polyphosphates also inhibit the aggregation of washed platelets by thrombin and dextran sulphate but do not affect DEAE-Dextran aggregation.The ADP-methylester does not cause aggregation of platelets but inhibits ADP-induced aggregation and release in a manner suggestive of competitive inhibition.(Supported by “Deutsche Forschungsgemeinschaft, Bonn”, Sonderforschungsbereich 90, “Cardiovasculares System”.)
Reduction of Platelet Survival: Development of a Thrombosis Model
Authors: Meuleman D. G. 
Published: June 2019

In male Wistar rats a PT 46 cannula was inserted in the carotid artery via the aortic arch into the abdominal aorta and fixed in that position. Twenty-four hours later 51Cr-labelled blood platelets were injected into these animals and into sham operated animals.The survival time of the 51Cr-labelled platelets in the cannulated group was significantly reduced as compared to the sham operated group. The mean half lives and s.e. mean were 15.5±1.3 hours and 30.3±0.5 hours respectively.The distribution of radioactivity deposited in various organs three days after administration of the label was determined. In the cannulated group the kidney contained twice as much radioactivity as in the sham operated animals, the spleen contained approximately 30% less.The number of free, single platelets was decreased in the cannulated group.These results and the relevance of aortic cannulation for the development of a model for thrombo-embolism will be discussed.
Thrombogenicity of Human Factor IX Concentrates. In vitro Studies
Authors: Sas G. , Owen R. , Smith J. K. , Middleton S. , Cash J. D. 
Published: June 2019

A series of in vitro studies, designed to ascertain the potential in vivo thrombogenicity of human factor IX containing concentrates, is described. Using concentrates obtained from several different centres the fibrinogen clotting time with some preparations was less than 6 hours and/or the recalcification time of normal plasma was shortened. In some preparations however, the plasma recalcification time was lengthened.Further studies revealed that all diluted factor IX concentrates generated thrombin after recalcification, and that the rate of thrombin generation appeared to be characteristic of a particular preparation. This characteristic we have expressed as the TGt50 which is the incubation period in minutes required, after recalcification, to obtain a 50 second clotting time of a fibrinogen substrate. The TGt50 was found to correlate most strongly with recalcification time of celite exhausted plasma (p < 0.001), but no correlation was observed between it and the immunological factor VIII or antithrombin III levels. However some factor IX concentrates contained antithrombin III in a free (biologically active) and in a complexed (inactive) form.Evidence is presented which suggests that the thrombin generation test and recalcification time of celite exhausted plasma may represent suitable in vitro quality control assays for the potential thrombogenicity of factor IX concentrates.
Factor IX Concentrates and Thrombosis: Amplification of Thrombotic Potential by Interaction between Material Infused and the Host
Authors: Lundblad R. L. , Kingdon H. S. 
Published: June 2019

Therapeutic infusion of Factor IX concentrates have occasionally been accompanied by episodes of thrombosis, some of them fatal (Blatt et al., Ann. Int. Med. 81, 766, 1974). On this occasion there were diffuse arterial and venous thrombi; in other cases pulmonary emboli or thrombosis of the vein being infused were observed (Kasper, N. Eng. J. Med., 289, 160, 1973). Disseminated intravascular coagulation has also been reported (Ceder-baum and Roberts, Clin. Res. 21, 92, 1973). When the concentrates were dissolved according to the manufacturer’s directions, diluted serially in buffered saline, and assayed for their ability to shorten the non-activated partial thromboplastin time (PTT) of normal plasma in plastic tubes, marked shortening of the PTT was observed, demonstrating the presence of clot-promoting enzymes. When reconstituted concentrates were incubated with calcium chloride prior to assay, much more thrombogenic enzyme was detected. The untreated concentrates contained no thrombin, and much of our data now suggest that the major thrombogenic enzyme is activated Factor IX. However, the concentrate after treatment with calcium contained large amounts of thrombin, up to 350 NIH units per ml of concentrate. This demonstrated interaction between concentrates and calcium ion suggests a mechanism whereby the thrombogenic potential of the material infused could be amplified by interaction with the calcium ion in the bloodstream of the patient beino-treated.Other experiments have shown that antithrombin III plus heparin can inhibit either the thrombogenic materials found in concentrates, or the enzymes generated de novo by prior incubation with calcium.