bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prostatectomía paliativa en cáncer de próstata localmente avanzado y metastásico con uropatía obstructiva
Authors: Chavarriaga Soto Julián , Álvarez Villarraga David , Silva Herrera José , Fakih Garcia Nayib , Álvarez Jaramillo Juliana , Quiñones Andrés , Ocampo María , Iregui Juan 
Published: July 2018

Introducción Los pacientes con cáncer de próstata localmente avanzado frecuentemente consultan por síntomas urinarios obstructivos bajos secundarios a la obstrucción del tracto de salida de la vejiga por el efecto obstructivo del adenocarcinoma prostático. El objetivo de este estudio es evaluar la prostatectomía transuretral paliativa en esos pacientes y comparar las características preoperatorias, calidad de vida e IPSS antes de la cirugía y en el postoperatorio.
Métodos y Materiales Estudio retrospectivo multicentrico que mediante el cuestionario WHOQOL-Bref evalúa calidad de vida y compara el IPSS pre y post-quirúrgico en una cohorte de 26 pacientes llevados a Resección transuretral de la próstata paliativa (pRTUP) por Cáncer de próstata localmente avanzado.
Resultados La media de la edad poblacional fue de 73 años, todos fueron llevados a pRTUP entre el 2011 y el 2017, solo un paciente fue dado de alta el mismo día de la cirugía, la media de hospitalización de 2,1 días. Cinco pacientes (26%), tenía antecedente de pRTUP y requirieron una nueva intervención. La media del IPSS inicial fue 23.2 ± 5.4. El Qmax antes de la intervención quirúrgica tuvo una media de 8.3 ± 1, más del 50% de los pacientes eran de alto riesgo dado por el Gleason. Con respecto a la QoL encontramos que en los dominios de salud física y psicológica fue moderada, mientras que en los otros dominios fue adecuada, el IPSS postquirúrgico mejoro considerablemente con una media de 16.5 ± 3.4.
Conclusiones La pRTUP es una buena opción de tratamiento para la desobstrucción al tracto de salida de la vejiga secundaria al adenocarcinoma de próstata localmente avanzado, con mejoría considerable de los síntomas urinarios obstructivos bajos, el IPSS y con buena calidad de vida después de la intervención. Sin evidencia de progresión oncológica de la enfermedad secundaria a la intervención quirúrgica desobstructiva.
Efecto in vitro de los suplementos vitamínicos que se venden como afrodisíacos sobre la movilidad espermática
Authors: Quintero Quinchia Yulieth Catherine , Cardona Maya Walter D. 
Published: July 2018

Objetivo El objetivo de este trabajo es determinar el efecto in vitro de los suplementos vitamínicos que se venden como afrodisíacos sobre la movilidad espermática.
Materiales y métodos Comprimidos de venta libre obtenidos en diferentes centros de venta de productos naturales y sexuales de la ciudad de Medellín fueron evaluados (Sex Bull, Ses-Max, Vigorday, Up12, Furumbao, Canguro, MAGYMas) y diluidos en solución salina. Posteriormente, fueron mezclados en proporciones iguales con las muestras de semen de 22 voluntarios aparentemente sanos y se determinó el efecto sobre la movilidad en función del tiempo (0, 60, 120 y 180 minutos).
Resultados El análisis del efecto de los tratamientos con extractos acuosos de los suplementos vitamínicos sobre los espermatozoides, fueron divididos según la presencia de L-arginina en su composición. No se observaron cambios positivos sobre la movilidad espermática.
Conclusión Los suplementos vitamínicos que se venden en las tiendas naturistas y sexuales de la ciudad, no ejercen ningún efecto sobre la calidad seminal in vitro, seguramente basados en su composición solo sirven como suplementos energéticos.
On The Stimulating Effect Of Bothroxobin Induced Fibrin (Fibrin I) On Tissue Activator Induced Fibrinolysis
Authors: Rånby M , Wallén P , Bergsdorf N 
Published: July 2018

Thrombin induced fibrin is in contrast to fibrinogen a powerful stimulator for the tissue plasminogen activator (TPA) catalysed conversion of plasminogen to plasmin. The aim of the study was to compare fibrin I, obtained from fibrinogen by the release of the fibrinopeptides A with bothroxobin (reptilase), and fibrin II, obtained by release of both fibrinopeptides A and B with thrombin, as for stimulating effect on the plasminogen activation by TPA.The rate of plasmin generation was continuously determined by measuring the absorbancy at 405 nm in reaction mixtures containing a plasmin specific chromogenic substrate. In a solution of 0.1 μM fibrinogen, 0.1 μM Glu-plasminogen in 0.1 M sodium phosphate buffer pH 7.3 containing 0.3 mM D-Val-Leu-Lys-pNA plasmin is generated by one-chain TPA at a turn-over rate of 0.5·10-3 s-1. When thrombin (1 NIH- unit/ml) is added to the solution the turn-over rate is within minutes raised to 40·10-3 s-1. If bothroxobin (0.2 BU/ml) is added the turn-over rate is raised to 200·10-3 s-1. The stimulation noted is 80 and 400 fold for fibrin II and fibrin I respectively.Thus fibrin I seems to be at least as efficient as fibrin II in stimulating the activation of plasminogen. This may be of great physiological importance for removal of soluble fibrin consisting of fibrin I complexes. Nossel et al. have demonstrated that fibrin I may be elevated in prethrombotic states (e.g. in patients after surgery) and have suggested that plasmin digestion of fibrin I may be of importance for the prevention of thrombosis.
Studies Of Factor VIII Inhibitor Bypassing Activity (FEIBA)
Authors: Barrowcliffe T W , Gray E , Kemball-Cook G 
Published: July 2018

The activities of an activated Factor IX concentrate (FEIBA, Immuno AG) were studied by two in vitro assays: a one-stage method using VUI-deficient plasma as substrate, and a two-stage assay based on the thrombin generation test. The nature of the active principle was explored by measuring the reduction in activity when FEIBA was incubated with specific antibodies.Incubation of FEIBA with human antibodies to Factor VIII reduced its activity by about 30% in the one-stage assay, and about 50% in the two-stage assay, suggesting that FEIBA contains Factor VIII procoagulant activity. Inactivation of the Factor VIII in FEIBA was somewhat slower than that of normal Factor VIII, indicating partial protection from inhibition. Human antibodies to Factor IX inhibited the one stage activity by about 30%, and incubation with both antibodies also produced a 30% reduction in activity. The remaining procoagulant activity decayed only slowly when incubated with non-inhibitor plasma. In contrast, purified human Factor Xa lost activity rapidly on incubation in normal plasma, as did a purified fraction from a Factor IX concentrate, which had high activity in the one-stage assay.These results suggest that the in vitro activity of FEIBA is due to at least two components. One component appears to be dependent on both Factors VIII and IX and may be a complex of VIII and IXa. The other component acts later than Factors VIII and IX in the coagulation cascade but, unlike purified Factor Xa, is relatively resistant to inactivation by plasma inhibitors such as antithrombin III. FEIBA was also found to contain phospholipid, and it may be that the phospholipid protects both the Factor VIII and activated enzymes from their inhibitors.
Postoperative Hypercoagulability, Detection And Measurement Using A Modified Recalcification Time System, Effects Of Low Dose Heparin And Types Of Surgery
Authors: Lundquist P B , Swedenborg J 
Published: July 2018

The purpose of the study was to demonstrate postoperative hypercoagulability and its possible prevention by low dose heparin (LDH). Healthy volunteers (with LDH), patients undergoing cholecystectomy (with & without LDH) and patients undergoing arterial reconstructive surgery with synthetic grafts (with LDH), were tested. All were tested 1, 3 & 5 hrs after LDH.Overall coagulability was determined by using platelet free plasma and a modified recalcification time system with a nefelometer to detect first fibrin formation. Recalcification times were measured before (T0) and after (TA) plasma activation against glass, in vitro. Heparin levels were determined with the Factor Xa inhibition test using a chromogenic substrate (CoatestR, Kabi).T0 and TA were prolonged after LDH in healthy volunteers. Cholecystectomy caused shortening of T0 and TA. This could be prevented by LDH, raising T0 to level recorded after LDH in normals. Patients receiving synthetic arterial grafts showed no prolongation of T0 and TA after surgery with LDH, but rather a shortening. These patients showed hypercoagulability in spite of LDH.It is concluded that postoperative hypercoagulability can be traced with the presented method and counteracted by LDH in patients undergoing cholecystectomy but not in patients receiving synthetic arterial grafts. All patients on LDH had similar heparin levels, determined with the Factor Xa inhibition test. Vascular surgery with synthetic grafting and Cholecystectomy seem to induce two different kinds of hypercoagulability, where the former is thought to be induced by the foreign surface. Subcutaneous heparin therapy (LDH) results in poor inhibition of surface induced coagulation, in vivo.
Stimulation Of Prostacyclin Production In Aortic Endothelial Cells By A Non-Dialysable Serum Factor
Authors: Hall E R , Rafelson M , Wu K 
Published: July 2018

The production of prostacyclin (PGI2) by vascular endothelial cells is thought to be of primary importance in maintaining normal hemostasis. We have investigated the production of prostacyclin in bovine arterial endothelial cells maintained in Dulbecco’s modified Eagle’s medium (DMEM) containing 30% fetal calf serum. Intact, confluent monolayers of endothelial cells (3x106 cells) in passages 2	through 6 were used. The growth medium was removed and the cells were washed in DMEM that did not contain serum. 3 mls of medium alone or containing normal plasma or serum was then added and incubated at 37°C for 15 min. Then, 1 mg of arachidonic acid was added and the cells incubated for an additional hour. The test medium was removed, centrifuged to remove any loose cells and stored at -70°C. To determine the production of PGI2 by the endothelial cells, the medium was assayed for 6-keto-PGF1α, the stable metabolite of PGI2, by radioimmunoassay. The synthesis of prostacyclin by bovine aortic endothelial cells was significantly increased in a concentration dependent manner by both normal platelet poor plasma and normal serum. This increase in prostacyclin production was inhibited by both aspirin and indomethacin, indicating an increase in synthesis rather than the release of PGI2. Furthermore, this increase could be demonstrated in the presence or absence of added arachidonic acid. The active component in plasma and serum was non-dialysable, eliminating the possibility of a small compound such as bradykinin or angiotensin II. This active factor was present after freezing and thawing the plasma and serum and was heat stable (60°C, 5 min). The presence of an endogenous prostacyclin stimulating factor may be significant in the in vivo regulation of prostacyclin production.
Prostacyclin Release From Ex Vivo Vascular Endothelium: Comparative Studies With Ionophore A23187, Arachidonic Acid, Bradykinin, And Thrombin
Authors: Goldsmith J C , Jafvert C T 
Published: July 2018

Prostacyclin (PGI2) release from systemic bovine, sheep, canine, and fetal lamb arterial segments has been evaluated in a template device and in cultured cell monolayers employing a radioimmunoassay for 6-keto-PGF1α.Canine segments released the greatest concentration of PGI2 and fetal sheep the lowest under unstimulated conditions. After exposure of the various vascular segments to the ionophore A23187, PGI2 release was increased 5-20 fold over baseline. Similar responses were observed following stimulation with arachidonic acid. Bradykinin induced a dose-dependent release of PGI2 from bovine vascular segments. Pulmonary arterial segments were more responsive than aortic. When exposed to thrombin, all tissues examined except canine did not demonstrate an increase in PGI2 release over baseline. After thrombin stimulation, canine segments slightly increased their PGI2 release from 91.4 ± 15.7 pmoles/ml/15 min to 152.7 ± 21.8 pmoles/ml/15 min. The other fetal and adult systemic vascular segments were unresponsive to thrombin as a releasing agent for PGI2 as were cultured monolayers of bovine and sheep systemic endothelium. This feature contrasted to prior studies with cultured human umbilical venous endothelial cell monolayers in which thrombin released PGI2. Cultured bovine endothelial cell monolayers were employed to examine thrombin-cell interactions more extensively. High affinity binding sites for thrombin were demonstrated on cultured bovine aortic and pulmonary endothelium. Examination of vascular tissue from diverse species has confirmed the presence of PGI2 in super- natents obtained from these vessel segments. Studies with the template model suggest that the vasodilator effects of bradykinin could be a consequence of the release of PGI2 from the endothelium. Our results also suggest that either thrombin binding is causally unrelated to PGI2 release from systemic animal endothelium or that this endothelium lacks a mediator required for thrombin to exert its effect.
Single Oral Dose Administration Of A Specific Thromboxane Synthetase Inhibitor To Normal Volunteers - A Double Blind Placebo Controlled Study
Authors: Kakkar V V , Westwick J , Zahavi J , Tyler H 
Published: July 2018

A specific thromboxane synthetase inhibitor (UK-37248-01) is a new imidazole derivative synthesised by Pfizer Central Research. In vitro and animal experiments showed the compound to be a potent, selective and orally active one.Six healthy male volunteers received a single dose of 100mg of a specific thromboxane synthetase inhibitor or a matching placebo in a double blind cross-over study, there being a 2 week interval between treatments. Production of thromboxane B2 in serum was markedly reduced 1 hour after the drug administration, with about 50% inhibition still evident at 6 hours. The drug had no effect no circulating β-thromboglobulin and platelet factor 4 antigen levels, or on platelet aggregation to ADP or collagen, though release of 5HT was reduced. Increase in bleeding time (2-3 minutes) was recorded in 3 volunteers 1 hour after the drug administration.Chemical assay of the compound showed that up to 45% of the oral dose was excreted in the urine within 24 hours; 90% of this was excreted within the first 4 hours. Routine haematology and clinical chemistry tests repeated 24 hours and 4 days after dosing gave no indication of drug related toxicity.
Sulphinpyrazone Does Not Influence Rejection Of Renal Transplants
Authors: Turney J H , Bewick M , Weston M J 
Published: July 2018

Platelet-mediated intravascular fibrin deposition may be the distal arm of the transplant rejection process. There have been reports that anti pi ate let drugs may prevent ameliorate, or even reverse renal transplant rejection. 50 consecutive cadaveric renal transplant recipients were randomly allocated to receive sulphinpyrazone 400 mg twice daily or no treatment additional to conventional immunosuppressive therapy. Patients were followed for 6 months, at which time they were assessed for graft survival and function, and for the number of rejection episodes. Rejection was defined as a rise in serum creatinine for which no other explanation was identified. Results were analysed by the Chi-squared test with Yates’ correction. Results at 6 months: There were no differences between the two groups, neither did the function of the surviving grafts differ.We conclude that, in this study, antiplatelet therapy with sulphinpyrazone does not affect the outcome of cadaveric renal transplantation.
Endotoxin Inhibits Prostacyclin Release From Rabbit Aorta
Authors: Zahavi J , Honey A C , Westwick J , Kakkar V V 
Published: July 2018

Released prostacyclin (PGI2) activity has been studied in aortic rings of 19 New Zealand white female rabbits. These rings produced a potent inhibitor of platelet aggregation, identified as PGI2. All the rabbits were anaesthetized with pentobarbital and thereafter a solution of endotoxin (E. Coli, 0111, B4, Difco Lab.) was injected intravenously to 7 rabbits (304μg/kg every 15 min during 1 hour to achieve an estimated plasma level of 1-2 μg/ml). Another 5 rabbits served as controls and were injected with saline. After 1 hour the aorta was rapidly excised, cleaned, cut into small rings and the released PGI2 activity studied at various time intervals (5-30 min) at 37°C. The mean release of PGI2 (in pg/mg wet tissue) in the control rabbits was 201 (range 50-443). It decreased significantly to 104 (range 0-237) after 30 min. In the endotoxaemic rabbits, the initial PGI2 release was only 73 (range 0-329) (p<0,008 compared to control rabbits). This level did not change with time and was 71.9 (range 0-261) after 30 min suggesting that the “endotoxinemic” vessels were initially relatively exhausted and were not able to release PGI2. In the remaining 7 rabbits the aorta was removed immediately after anaesthesia and aortic rings incubated for 5-30 min Krebs-Henleit buffer or endotoxin 0.2-10 μg/ml and the released PGI2 activity studied. There was a dose dependent inhibition which was more pronounced after 30 min incubation.The decrease in PGI2 release from rabbit aorta following endotoxaemia removes the inhibitory effect on platelet aggregation of the arterial vessel wall and consequently may contribute to the development of a thrombogenic state.
The Effect Of Angiotensin II On PGI2 Production By Endothelial Cells In Culture
Authors: Lonchampt M O , Romquin N , Bonne C , Regnault F 
Published: July 2018

Angiotensin II, a vasoconstrictor peptide, is also a very potent stimulator of PGI2 synthesis in blood vessels. In this study we have investigated its direct effect in endothelial cells in culture. Bovine aorta endothelial cells were used in primary culture. Angiotensin II was added in Tris buffer for 3 min. PGI2 was measured by radioimmunoassay of 6-keto PGF1α , the degradation product of PGI2 in this system. Angiotensin II was shown to stimulate PGI2 synthesis at concentration as low as 0.5nM. At 5nM the PGI2 production was five-fold increased as compared to controls. A synthetic peptide Sar1-Ile 8-Angiotensin II, known as a specific inhibitor of the hormone in other tissues, was a powerful agonist at the doses of 0.2 to 20nM and exhibited an antagonistic activity at higher doses (1μM).These results suggest that endothelial cells are target cells for angiotensin II as well as smooth muscle cells in blood vessels. Since PGI2 is a potent vasodilator, its production induced by angiotensin II could act as a modulator of the vasoconstrictor effect of the peptide.
Gel Chromatographic Amd Electrophoretic Evidence For The Existence Of Soluble 125-I Fibrinogen-131-I-Fibrin-Des AA (AABB) Complexes In Plasma Containing Ca++ At 37°C
Authors: Kierulf P , Brosstad F , Godal H C 
Published: July 2018

Material and methods: Ca++-boosted (2.5 nmol) protrombin adsorbed plasma (=Ca++-plasma) was prepared by adsorbing thrice with Ba(SO4)2 and dialysing against Ca++-containing Ringer-solution. Ca++-plasma showed negligible thrombin generation as evidenced by Fibrinopeptide A apparance (RIA-FPA), even when continously chromatographed at 20°C for 48h (FPA <15 ng/ml). Plasma containing 125-I fibrinogen and/or 131-I-fibrin Des AA (or Des AABB) monomers (Brosstad et al, Hemostasis 6,225,1977) was subjected to either gel chromato-graphy or to enzyme-fixation. Gel chromatography at 37°C was performed on Sepharose CL-6B, freeze-dried, reconstituted in Ca++-plasma, and developed with Ca++-plasma or Ca++- plasma with EDTA Enzyme-fixation was done by adding thrombin-activated (removable, insolubilized thrombin) Factor XIII (XIIIX). Subsequently XIIIX- activity was quenched with EDTA Enzyme-fixed, radiolabelled complexes were either harvested by thrombin-clotting in the presence of EDTA or chromatographed on Sepharose CL-6B (0.15 M Tris-HCl pH 7.0, 0.15 M NaCl, 2.5 M urea, 10mmol EDTA). Harvested clots were mer-captolysed and SDS-gel electrophoresed. Gel chronatographed specimens were radioprofiled and freeze-dried.Results: In Ca++-plasma both Des AA and Des AABB 131-I fibrin eluted in front of the 125-I fibrinogen, whereas in the presence of EDTA 131-I fibrin Des AA eluted ocnpletely within the 125-I fibrinogen peak. SDS-gel elec trophoresed, mercaptolysed, clots, containing enzyme-fixed,radiolabelled, fibrinogen derivatives,demonstrated 125-I and 131-I activity in γ-γ-dimers and to lesser extent in α-oligemers. Gel chromatographed, enzyme-fixed specimens, demonstrated radiolabelled dimerized fibrinogen derivatives (125-I and 131-I activity) . RIA-FPA of such dimers demonstrated approx. 2 moles FPA/mol dimer.Conclusion: Soluble,covalently-linkable largely dimeric fibrinogen fibrin cenplexes exist in Ca++-plasma at 37°C.
Diabetic Retinopathy And Thromboxane Like Substance
Authors: Lazzari M A , Gimeno M , Sutton N M , Lopez J R 
Published: July 2018

Diabetes Mellitus (DM) is a risk factor in the development of vasculopathies and its complications. It produces also its own microangiopathy. Evidence was reported of increased platelet activity in DM in different assays. Platelets aggregation and the arachidonic cycle could play a key role in the increased tendency to thrombosis. A disorder of ratio TXA2/PGI2, two opposing prostaglandin derivatives, could be the initial step. We intended to evaluate a thromboxane like substance (TLS) produced from platelet rich plasma (PRP) and to compare between normals and diabetic retinopathy (DR) patients. TLS was measured in 16 controls and 16 patients. Assay was done with the aggregating activity developed in PRP (considered TLS) after addition of arachidonic acid (f.c. 2 mM). The supernatant of the PRP (100 μl) was taken 40 sec. after the aggregation started and were added to a normal PRP treated with aspirin (f.c. 40 μl/ml) adjusted to 250.000 - 300.000 pl/μl and the degree of platelet aggregation measured in a Chrono Log Aggregometer. TLS was inactivated after its incubation during 2 min. at 37°C. This finding suggests this activity is due to TXA2.The results obtained (expressed in % of platelet aggregation) were: controls x 16.37% ± 6.28 and DR x 36.00% ± 9.72.The increase detected in the DR group supports previous experimental reports suggesting the role of the thromboxane A2 in vaso occlusive complication of diabetes mellitus.
Plasminogen Activator (PA) Activity In Metastatic Cells: An Amidolytic Approach
Authors: Coen D , Bini A , Balconi G , Delaini F , Mussoni L , Donati M B 
Published: July 2018

It has been proposed that fibrinolytic activity can play an important role in the process of metastasis formation. Nevertheless, it is not yet clear in which phase of the tumor growth and dissemination this activity is involved. We measured the fibrinolytic activity of cells from primary tumor and metastatic nodules of 3LL, an i.m. implanted murine tumor which selectively metastasizes to the lungs. Tumor cells have been studied both immediately after mechanical disruption of tumor tissue and after in vitro culturing to confluence. Their P.A. activity was tested by an amidolytic assay in which cells were incubated with purified plasminogen (3CU/ml) and 4mM S-2251 (Kabi Diagnostica, Stockholm, Sweden), a plasmin specific chromogenic substrate. After 3 hour incubation at 37°C, the reaction was stopped with acetic acid and absorbance read at 405 nm.Cells from the primary tumor and metastatic nodules showed a similar fibrinolytic activity, which was in both cases in- increased 3 to 4 fold in cell extracts obtained after preincubation with TRITON X-100. A dose-response curve plotted with increasing urokinase concentrations showed a parallel course. This data suggests that, in the 3LL model, PA activity is not one of the properties characterizing the selection of metastatic cells.On the other hand,cultured cells presented consistently higher levels of PA than their native counterparts, suggesting that adhesion of cells in culture may stimulate PA production or, alternatively, that cultured cells are a selected population in comparison to the overall number of native cells.