bluuebunny/crossref_metadata_2025_split huggingface dataset:
Renal Cortical Fibrinolytic Activity in the Rabbit Following One or Two Doses of Endotoxin
Authors: Bergstein Jerry M. , Michael Alfred F. 
Published: July 2018

SummaryA fibrin slide technique has been utilized to study the effect of endotoxin on renal cortical fibrinolytic activity in the rabbit. Lytic activity was absent in kidney tissue obtained from animals given one injection of endotoxin and after development of the generalized Shwartzman reaction. Cortical lytic activity was not inhibited following in vitro incubation of tissue sections in phosphate-buffered saline solutions containing high concentrations of endotoxin.It is suggested that the initial injection of endotoxin may prepare for the generalized Shwartzman reaction by depletion of cortical fibrinolytic activity. The failure of endotoxin to inhibit tissue plasminogen activator in vitro suggests that endotoxin-induced loss of lytic activity is mediated through humoral factors.
Quantitation of Fibrin Deposition and Elimination in Organs of Rats Injected with Labelled Fibrinogen by Isolation of the Labelled Fibrin from Water Soluble Tracer
Authors: Busch Christer , Rammer Lennart 
Published: July 2018

SummaryA method for direct quantitation of fibrin in organs after intravascular coagulation in rats injected with labelled fibrinogen is described. After homogenization and centrifugation of the tissue the fibrin can be measured in the pellet, while the water soluble tracer largely remains in the supernatant.
In Vitro Effects of Lipids on Fibrinolysis
Authors: Chopin Suzzette F. , Beard E Letitia 
Published: July 2018

SummaryThe effect of suspensions of corn oil, butter, cholesterol, and beta lipoprotein in concentrations in the range of normal blood lipid levels on the ability of lytic agents to digest fibrin clots in vitro has been examined. In one assay, the lipid solutions were incubated with streptokinase, plasminogen activator or plasmin prior to addition of the lytic agent to the clot and its fibrinolytic activity was then assessed. Secondly, the lipids were incorporated into the clots and the three lytic agents were added directly. The lipids used markedly inhibited the lytic effect of plasminogen activator (34% mean) and plasmin (28.9% mean) when they were allowed to interact in solution prior to addition to the clot. Streptokinase was significantly inhibited in this manner but to a much smaller degree (7% mean). Lipids incorporated within the clots actually enhanced the lytic action of plasminogen activator (8.8% mean), mildly inhibited clot dissolution by plasmin (5.9%) and insignificantly altered the action of streptokinase. The effects of the lipids used appeared to be relatively nonspecific.
The Phase II Urokinase-Streptokinase Pulmonary Embolism Trial
Authors: Sasahara Arthur A , Bell William R , Simon Toby L , Stengle James M , Sherry Sol 
Published: July 2018

SummaryThe controlled clinical trials of thrombolytic agents in the United States have been carried out in two phases, under the auspices of the National Heart and Lung Institute. Phase I was devoted to the comparison of 12-hour Urokinase (12h–UK) followed by heparin (H) with heparin alone in patients with acute pulmonary embolism (Walsh et al. 1969). The results showed that patients treated with UK had more rapid and greater resolution of pulmonary thromboemboli in the first twenty-four hours of therapy than patients treated with H alone, as assessed by serial pulmonary angiography, hemodynamics and lung scanning (The Urokinase Pulmonary Embolism Trial, 1970, 1973 ; Hyers et al. 1970). Because of the relatively small size of the Trial and the low mortality of treated pulmonary embolism, mortality differences were not sought - nor was one found. Although there was early difference in amount of clot resolution, patients treated with H alone showed similar improvement by two weeks.The Phase II Urokinase-Streptokinase Pulmonary Embolism Trial (USPET) was begun to assess the comparative results of UK and Streptokinase (SK) therapy. Because of favorable results obtained with SK in other countries, it was deemed necessary to make this comparison (Browse and James, 1964 ; Hirsh et al. 1968 ; Miller et al. 1969, 1971 ; Chesterman et al. 1969). A third group, 12-hour UK, was added to relate this study (24-hour UK and SK) with the Phase I results which employed only a 12-hour infusion of UK. This Phase II Trial represents the first controlled, randomized study of UK and SK in thromboembolic disorders.
Enhancement of ADP-Induced Platelet Aggregation by Cholesterol and Its Prevention by Pyridinolcarbamate
Authors: Sano Tadahiro , Yamazaki Hiroh , Shimamoto Takio 
Published: July 2018

SummaryThe authors reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of cholesterol in rabbits. In such circumstances, platelet aggregability to ADP was examined by 2 methods: 1. measurement of intensity of platelet aggregation induced by ADP using the optical density method and 2. determination of minimum concentration of ADP solution to induce platelet aggregation using a light microscope. Three hours after oral administration of 1 g/kg of cholesterol, the intensity of aggregation in 12 rabbits increased to 106.0 ±2.4% (mean ± S. E.) by 10 ìM, 108.5 ±2.6% by 3 ìM and 110.2 ±3.7% of the value before the administration by 1 ìM of ADP. The differences were statistically significant (P <0.05). At that time, platelet in CPRP collected after cholesterol intake were aggregated by eight-times diluted ADP solution compared to that collected before cholesterol administration in 2 rabbits, four-times in 4 and two-times in 3 among 10 cases. Pyridinolcarbamate, which showed preventive effect against appearance of edematous changes in aortic wall induced by cholesterol and/or adrenaline, prevented these phenomena, when it was given 10 mg/kg orally 3 hours prior to cholesterol administration.
Detection of Platelet Desensitization in Pregnancy-Induced Hypertension Is Dependent on the Agonist Used
Authors: Ahmed Y , Sullivan M H F , Elder M G 
Published: July 2018

SummaryThe aggregation of platelets from women with pregnancy-induced hypertension (P.I.H.), or with normal pregnancies, in response to arachidonic acid, ADP, collagen or platelet activating factor (PAF) was examined. No differences in platelet aggregation between the normotensive and hypertensive women were detected when arachidonic acid or collagen were used to stimulate in vitro platelet aggregation. Higher concentrations of ADP and PAF were required to aggregate platelets from women with P.I.H. compared with platelets from normotensive controls. Platelets from women with normotensive pregnancies (n = 80) aggregated maximally in response to 20 nM PAF without exception. Reversible aggregation by platelets from women with P.I.H. (n = 25) was observed at the same concentration of PAF; again, this was found in all subjects tested. These results indicate that PAF at a concentration of 20 nM can clearly demonstrate differences in aggregation of platelets from women with normotensive pregnancy and women with P.I.H.
Acquired Disorder of Platelet Function Associated with Autoantibodies against Membrane Glycoprotein IIb-IIIa Complex - 1. Glycoprotein Analysis
Authors: Meyer M , Kirchmaier C M , Schirmer A , Spangenberg P , Ströhl Ch , Breddin K 
Published: July 2018

SummaryA patient with idiopathic thrombocytopenic purpura developed after splenectomy a thrombasthenia-like severe haemor-rhagic diathesis characterized by a normal or subnormal platelet count, prolonged bleeding time, strongly reduced platelet adhesion to glass and defective platelet aggregation in response to ADP and collagen. In contrast to hereditary thrombasthenia membrane glycoproteins (GP) lib and Ilia were normally present in the patient’s platelets. Immunoelectrophoretic analysis revealed an abnormal behaviour of the patient’s GP IIb-IIIa complex. Autoantibodies against GP IIb-IIIa were detected in Triton-extracted washed platelets. Incubation of normal platelets with plasma from the patient resulted in a similar immunoelectrophoretic abnormality of the GP IIb-IIIa complex indicating that bound autoantibodies (IgG) are responsible for the abnormal immunoelectrophoretic behaviour of the patient’s GP IIb-IIIa complex. Platelet fibrinogen was severely reduced similar to classical thrombasthenia suggesting that the GP IIb-IIIa complex is involved in platelet fibrinogen storage.
Cellular Localization of Activated Factor X by Xa-Specific Probes
Authors: Zacharski Leo R , Dunwiddie Christopher , Nutt Elka M , Hunt Jane , Memoli Vincent A 
Published: July 2018

SummaryA probe, recombinant antistasin, that reacts specifically with the activated form of factor X (Xa) was used in immunohistochemical procedures to detect cellular sites of Xa generation within intact tissues. Factor Xa was detected on tumor cells in small cell carcinoma of the lung, renal cell carcinoma, and malignant melanoma. Tumor-associated macrophages (but not tumor cells) expressed Xa in adenocarcinoma and squamous cell carcinoma of the lung, and Hodgkin’s disease. Factor Xa in these locations corresponded to evidence reported previously for an intact coagulation pathway and thrombin formation associated with these tumor cells and macrophages. By contrast, only rare connective tissue cells stained for Xa in breast and colon cancer, tumor types shown previously to lack an intratumoral coagulation pathway and thrombin generation, and in normal liver, lung, breast, kidney, and placental tissues. Hepatocytes did not stain. These results suggest that such probes may be useful for studying the activation state of cell-associated factor X in situ within intact tissues.
Baboon Fibrinogen Adsorption and Platelet Adhesion to Polymeric Materials
Authors: Chinn Joseph A , Horbett Thomas A , Ratner Buddy D 
Published: July 2018

SummaryThe role of fibrinogen in mediating platelet adhesion to polymers exposed to blood plasma was studied by comparison of the effect of plasma dilution on fibrinogen adsorption and platelet adhesion, and by the use of coagulation factor deficient plasmas. Polyetherurethane substrates were first preadsorbed with dilute plasma, then contacted with washed platelets suspended in a modified, apyrase containing Tyrode’s buffer. Platelet adhesion was studied under static conditions in Multiwell dishes, and also under shearing conditions using a parallel plate perfusion chamber. Fibrinogen adsorption and platelet adhesion were measured using 125I radiolabeled baboon fibrinogen and min radiolabeled baboon platelets, respectively. Surfaces were characterized by electron spectroscopy for chemical analysis (ESCA).When fibrinogen adsorption to Biomer was measured after 2 h contact with a series of dilute plasma solutions under static conditions, a peak in adsorption was observed from 0.26% plasma, i.e., adsorption was greater from 0.26% plasma than from either more or less dilute plasma. A peak in subsequent platelet adhesion to the plasma preadsorbed surfaces, measured after 2 h static incubation with washed platelets, was also observed but occurred on Biomer preadsorbed with 1.0% plasma.When fibrinogen adsorption was measured after 5 min contact under shearing conditions, the fibrinogen adsorption peak occurred on surfaces that had been exposed to 1.0% plasma. A peak in platelet adhesion to these preadsorbed surfaces, measured after 5 min contact with the platelet suspensions under shearing conditions, was observed on Biomer preadsorbed with 0.1% plasma. Shifts between the positions of the peaks in protein adsorption and platelet adhesion occurred on other polymers tested as well.Platelet adhesion was almost completely inhibited when baboon and human plasmas lacking fibrinogen (i. e., serum, heat defibrinogenated plasma, and congenitally afibrinogénémie plasma) were used. Platelet adhesion was restored to near normal when exogenous fibrinogen was added to fibrinogen deficient plasmas. Adhesion was also inhibited completely when a monoclonal antibody directed against the glycoprotein IIb/IIIa complex was added to the platelet suspension. Platelet adhesion to surfaces preadsorbed to von Willebrand factor deficient plasma was the same as to surfaces preadsorbed with normal plasma.While it appears that surface bound fibrinogen does mediate the initial attachment of platelets to Biomer, the observation that the fibrinogen adsorption and platelet adhesion maxima do not coincide exactly also suggests that the degree of subsequent platelet adhesion is dictated not only by the amount of surface bound fibrinogen but also by its conformation.
Recommendations for the Evaluation and Treatment of Neonatal Autoimmune and Alloimmune Thrombocytopenia
Authors: Bussel J , Kaplan C , McFarland J ,   Working Party on Neonatal Immune Thrombocytopenia of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH
Published: July 2018

SummaryThe following recommendations of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH for the management of neonatal immune thrombocytopenia were prepared by the working party on neonatal immune thrombocytopenia. Evaluation, diagnosis, and treatment of the mother and neonate with alloimmune and autoimmune thrombocytopenia are discussed and current recommendations provided. This document is likely to require frequent future revision(s).
Reconstrucción de pene luego de necrosis de glande por priapismo
Authors: Gaviria Gil Federico , Benavides Johana , Lopera Adrián 
Published: July 2018

Introducción El priapismo se define como una erección parcial o completa que dura más de 4 horas en ausencia de estímulo sexual. Se clasifica en isquémico, no isquémico e intermitente. El primero corresponde a la mayoría de casos y puede producirse por un estímulo sexual o por medicamentos. El manejo inicial consiste en la aspiración de los cuerpos cavernosos y la inyección de simpaticomiméticos. Cuando esas medidas fallan, el manejo quirúrgico está indicado. Entre las complicaciones más frecuentes está la disfunción eréctil, sin embargo, en la literatura, hay muy pocos reportes de necrosis de pene.
Descripción del Caso Clínico Paciente de 60 años de edad que presentó priapismo isquémico luego de la inyección intracavernosa de prostaglandina E. Viene a consulta y le realizan lavado de cuerpos cavernosos con inyección de simpaticomiméticos que no fue exitoso; por lo que le realizan fístula espongio-cavernosa distal (Al-Ghorab) y rafia de uretra por lesión advertida. Consulta nuevamente por persistencia de edema, áreas necróticas y sangrado en glande. Se decidió iniciar manejo médico. Presentó evolución estacionaria y aumento en necrosis por lo que se derivó con cistostomía y se realizó desbridamiento de tejido necrótico inicialmente. Posteriormente se realizó Reconstrucción peneana + Uretroplastia peneana + Lavado desbridamiento de tejidos + Cistoscopia con buena evolución clínica.
Conclusiones Existen diferentes factores de riesgo para presentar priapismo de origen isquémico como es la inyección de medicamentos intracavernosos. La principal complicación que se presenta es la disfunción eréctil. Sin embargo, hay pocos casos descritos de necrosis de glande. En el caso de nuestro paciente se plantean diferentes hipótesis como factores contribuyentes a la necrosis como son el uso de simpaticomiméticos y/o la desvascularización del glande posterior a la cirugía. Al enfocar ese tipo de paciente, es indispensable realizar un adecuado manejo inicial para prevenir ese tipo de complicación que, aunque es poco frecuente, puede resultar catastrófica.
Linfoma tipo Burkitt, un inusual subtipo de linfoma testicular no Hodgkin en el adulto: reporte de un caso y revisión de la literatura
Authors: Cerquera Cleves Diana , Donoso Donoso Wilfredo 
Published: July 2018

Objetivo Realizar el reporte de un caso de linfoma testicular no Hodgkin tipo Burkitt, presentando una revisión de la literatura y documentando las variaciones histológicas típicas, los métodos diagnósticos, el impacto del manejo inicial y el abordaje de las metástasis e infiltraciones tumorales en el pronóstico de esa patología oncológica.
Metodología Se describe el caso de un hombre de 36 años en quien se diagnosticó un linfoma testicular tipo Burkitt, durante el estudio de un síndrome proliferativo, que inició con signos y síntomas neurológicos conllevando a la extensión del estudio y demostrando múltiples lesiones metastásicas asociadas a la infiltración del sistema nervioso central. El tratamiento incluye múltiples modalidades entre las que se encuentra la quimioterapia, radioterapia local, profilaxis intratecal entre otras; sin embargo, el pilar del manejo del compromiso testicular sigue siendo el quirúrgico.
Conclusión El linfoma testicular no hodking es una patología rara, siendo aún más infrecuente el subtipo Burkitt, a pesar del pobre pronóstico, el diagnóstico oportuno y el desarrollo de nuevas terapias aplicadas en combinación, han permitido mejorar la sobrevida y disminuir el riesgo de recaída y progresión.
The Role of Venom Haemorrhagin in Spontaneous Bleeding in Bothrops jararaca Envenoming
Authors: Kamiguti A S , Rugman F P , Theakston R D G , Franca F O S , Ishii H , Hay C R M ,   BIASG
Published: July 2018

SummaryThirty-eight patients bitten by Bothrops jararaca were investigated. Twenty-six had signs of local or systemic haemorrhage. Twenty-two of these had incoagulable blood, and these patients were found to have low fibrinogen levels (mean 0.17 ± 0.03 g/1), thrombocytopenia, very high thrombin-antithrombin III complex (850 ± 184 pg/1) and D-dimer (170 ± 44 μg/ml) antigen levels. Serum venom haemorrhagin levels were significantly higher in patients with clinical signs of haemorrhage (36.4 ± 6.4 ng/ml) than those without (11.7 ± 3.7 ng/ml; p <0.002). Twelve out of 13 patients with thrombocytopenia were bleeding. High levels of thrombomodulin (22.3 ± 1.5 ng/ml) and haemorrhagin (35.7 ± 7.7 ng/ml) were detected in these 12 patients, suggesting vascular endothelial damage. Haemorrhagin levels also correlated inversely with platelet count in these patients. It was concluded that thrombocytopenia is one of the main causes of bleeding inB. jararaca victims, possibly as a result of venom haemorrhagin activity.
Homozygous Antithrombin Deficiency: Report of Two New Cases (99 Leu to Phe) Associated with Arterial and Venous Thrombosis
Authors: Chowdhury V , Lane D A , Mille B , Auberger K , Gandenberger-Bachem S , Pabinger I , Olds R J , Thein S L 
Published: July 2018

SummaryInherited antithrombin deficiency is associated with an increased risk of thrombosis, primarily venous rather than arterial. Most affected individuals have inherited only a single copy of an abnormal antithrombin (AT) gene. Homozygously affected individuals, although rare, have a severe thrombotic history of early onset and often affecting the arteries. We report two new cases of type II HBS (heparin binding site) deficiency in which the propositi are homozygous for the previously reported mutation 99 Leu to Phe, and who have a severe thrombotic history. These cases are considered alongside existing homozygote and compound heterozygote cases.
Hereditary Protein C Deficiency Associated with Mutations in Exon IX of the Protein C Gene
Authors: Doig R G , Begley C G , McGrath K M 
Published: July 2018

SummaryThis report describes five families with symptomatic hereditary protein C deficiency. Using a polymerase chain reaction (PCR)-based method, the entire coding sequence and intron-exon boundaries of the protein C gene was amplified from genomic DNA. In each family a single point mutation in the protein C gene was identified. Two unrelated families were found to share the same mutation, while the other three had different mutations. In the first two families with type I protein C deficiency the normal cytosine residue at nucleotide position 8551 in the protein C gene was replaced by thymidine leading to substitution of the normal proline residue at amino acid position 279 by leucine. In the third family with type I deficiency a previously undescribed mutation was identified. In this family the guanosine residue at position 8559 was replaced by adenosine (glycine 282 substituted by serine). In the fourth family, also with type I deficiency, guanosine 8589 was replaced by adenosine (glycine 292 substituted by serine). The fifth family had type II deficiency and in affected members cytosine 8769 was replaced by thymidine (arginine 352 substituted by tryptophan). All these mutations lead to amino acid substitutions in the serine protease domain of the mature protein. All were able to be confirmed by restriction enzyme analysis of PCR-derived DNA. In addition the novel mutation at nucleotide position 8559 was also demonstrable using single strand conformation polymorphism (SSCP) analysis of PCR-derived DNA. These mutations were likely examples of deamination of methylated cytosine occurring in cytosine-phosphate-guanosine (CpG) dinucleotide sequences. These findings confirm the genetic heterogeneity of hereditary protein C deficiency in these families.
CD4+ Counts before and after Switching to Monoclonal High-Purity Factor VIII Concentrate in HIV-Infected Haemophilic Patients
Authors: Sabin Caroline , Pasi John , Phillips Andrew , Elford Jonathan , Janossy George , Lee Christine 
Published: July 2018

SummaryAllogenic proteins that contaminate intermediate purity clotting factor concentrates may activate the immune system of HIV-infected haemophilic patients. In 37 haemophilic patients infected with HIV who had originally been treated with intermediate purity factor VIII concentrate and then changed to monoclonally-purified high purity factor VIII concentrate the rates of CD4+ decline (109/1 per year) were 0.06 before and 0.02 after a switch to high purity products (p = 0.01). The median follow-up of patients after the switch to high purity products was 1.7 years (range 0.2 to 3 years). This significant change in the rate of CD4 decline was independent of the starting CD4 count, age and antiretroviral therapy. This result is consistent with those from randomised trials of the introduction of high-purity concentrate. Given the strong association between the CD4+ count and survival, treatment with high purity rather than intermediate purity clotting factor concentrate may confer a survival benefit for HIV-infected haemophilic patients.
Displacement of Fibrin-bound Thrombin by r-Hirudin Precludes the Use of 131l-r-Hirudin for Detecting Pulmonary Emboli in the Rabbit
Authors: Rubens Fraser D , Ross-Ouellet Bonnie , Dennie Carole , Coates Geoffrey , Kinlough-Rathbone Raelene L , Hatton Mark W C 
Published: July 2018

SummaryPulmonary emboli are detectable by filling defects in the pulmonary vasculature upon pulmonary angiography. Emboli derived from venous thrombi are rich in fibrin to which thrombin remains bound. Hirudin, a specific thrombin inhibitor, binds to thrombin to yield a 1:1 stoichiometric complex. We examined whether 131I-recombinant hirudin (r-hirudin) could be used to detect pulmonary emboli in rabbits. Clots were formed by re-calcifying rabbit plasma in vitro, and then injected (0.034 ml) into a femoral vein to lodge in the lungs. 131I-r-hirudin (29 ± 4 μCi/kg) was injected intravenously but emboli could not be detected by gamma camera in real time. Post-mortem analysis of lung tissue showed that 131I-r-hirudin did not associate with emboli prepared with 125I-fibrin. Because of these findings, we used different techniques to look at the binding of hirudin to plasma clots. Clots formed in vitro were incubated with 131I-r-hirudin in the presence of equimolar amounts of 125I-albumin; specific binding of 131I-r-hirudin was not observed. Experiments with immobilized fibrin(ogen) showed that 125I-r-hirudin did not bind to and remain with fibrin-bound 131I-thrombin but did lead to the inactivation and displacement of up to 70% of bound thrombin as r-hirudin-thrombin complex; residual thrombin bound to fibrin remained active. Thus, released r-hirudin-thrombin complex is probably cleared rapidly from the region of the embolus in vivo; radioiodinated r-hirudin may not, therefore, be useful as a marker for detecting emboli.