bluuebunny/crossref_metadata_2025_split huggingface dataset:
CHANGES IN PLATELET HALF-LIFE, SENSITIVITY TO PROSTANOIDS AND AGGREGATION INDUCED IN THE DOG BY BODY HYPOTHERMIA
Authors: Cunha-Ribeiro L M , Cunha S , Brandão T , Goncalves F S , Almeida-Dias A , Pina-Cabral J M 
Published: August 2018

During body cooling, there is a progressive thrombocytopenia, which is reversible after rewarming and is not prevented by previous treatement with aspirin, ticlopidine or prostacyclin.In this work, in order to evaluate if hypothermia induces alterations of platelet function we studied, in the dog, the platelet aggregation (PA) and the inhibitory action of PGE1 and of a stable prostacyclin analog, l loprost, before hypothermia(37°C.) and after rewarming(37°C.).Platelet half-life was also studied in another group of dogs before induction of hypothermia and after rewarming and recuperation of the animals. PA has been evaluated by platelet counting in whole blood.P1atelet half-life was estimated by serial determinations of MDA following administration of aspirin.PA induced by ADP (30μM) decreased 40% after rewarming(n=8). Platelet sensitivity to PGE1 (35 nM -1.4 μM f.c.) and Iloprost (7nM-172nM f.c.) was also decreased after rewarming: inhibition index 2.08±1.082 versus 1.19±0.362 (n=8; p<0.01) and 2.48<1.250 versus 1.10±0.227 (n=8; p<0.005) respectively.Platelet half-life increased after hypothermia from 3.99±0.730 days to 4.48±0.846 days(n=8 p<0.05).In the control group(n=6) platelet half-life determined twice with one week interval, did not change significantly.We conclude that body hypothermia decreases platelet reactivity to ADP; renders platelets less sensitive to the inibitory effect of prostanoids and increases platelet half-1 ife.These results are probably due to alterations in platelet membrane induced by cooling and rewarming the animals.
GLANZMANN'S THROMBASTHENIA IN PREGNANCY: CLINICAL FEATURES AND PLATELET SEROLOGY
Authors: Picó M , Ribera A , Martin C , Zuazu J , Monasterio J 
Published: August 2018

A 24-year-old woman with a diagnosis of Glanzmann's Thrombasthenia (GT) type I (confirmed in our Hemostasis Section by sodium dodecyl sulphate-polyacrylamide gel electrophoresis) and with a history of several transfusions, was seen in our Service since the second month of her first pregnancy.In the first visit a strong anti-Rh(D) antibody was found in her serum. In 28th week an ammiocentesis was done. Seventy two hours later, she was hospitalized because of disminution of foetal movements. Then, a platelet-allo-antibody, IgG+IgM type (title IgG 1/512, IgM 1/2) was detected in her scrum by immunofluorescence test, as well as an anti-HLA antibody (by lymphocytotoxicity test) which reacted with her husband lyin-phocites.The platelet antibody wasn't EDTA or Paraformaldehide (PFA) dependent and reacted with all normal platelets of a panel of known platelet phenotypes and, also although significantly weakly, with GT type II platelets. The negative results were only observed with GT type I platelets. Therefore, it seemed to recognize an antigenic site located in GP IIb-IIIa. Besides, this antibody inhibited the normal platelet aggregation.A caesarian was advised because of foetal suffering an was performed without immediate complications. The patient was protected by our hemotherapy established support and delivered a boy with a severe hemolytic disease (Hematocrit: 6%, bilirrubine: 1,9 mgs./lOCimls., platelets: 40.000/ mm3), who died 48h. later. His platelets had a direct positive test IgG type and in his serum the platelet antibody as in his mother's was detected.We discuss the specificity of the antibody detected and also, its possible implication in the neonatal thrombocytopenia.
GRAY PLATELET SYNDROME AND IDIOPATHIC PULMONARY FIBROSIS OCCURRING IN THE SAME PATIENT : A FORTUITOUS ASSOCIATION?
Authors: FACON T , GOUPEMAND J , CARON C , ZANDECKI M , ESTIENNE M H , COSSON A 
Published: August 2018

A 46 yr old Caucasian woman has been diagnosed as having a congenital deficiency of platelet a-granules (gray platelet syndrome - GPS) associated with an extensive idiopathic pulmonary fibrosis (IPF). The patient had a life long history of bleeding tendency including dental bleedings in childhood, intraperitoneal bleeding, metrorrhagias which led to hysterectomy, and post-operative hemorrhages. When aged 16, splenectomy was performed because of a mild thrombocytopenia but did not result in a subsequent improvement of the platelet count. The spleen was enlarged and showed an excess of fibrous tissue.Evaluation of hemostasis (July 1986) revealed a moderate thrombocytopenia of 120 × 109/1 constrasting with a markedly prolonged Simplate bleeding time (>30 min.). When examined on stained blood films, the platelets presented a "ghost-like" gray appearance. The mean platelet volume (coulter S + IV) was increased to 14 μ3 (N : 6.5-9.5 μ3). Ultrastructural studies confirmed the lack of a-granules and showed normal presence of dense-bodies, mitochondria and peroxisomes. Platelet aggregation was decreased when induced by thrombin, ADP and collagen but normal in response to arachidonic acid and ristocetin. A severely decreased content of platelet proteins such as fibrinogen, vWF:Ag, BTG and PF4. was further demonstrated. A bone marrow biopsy performed on March 1986 gave no evidence of myelofibrosis (occasionally recorded in GPS) but the patient developed for these last 6 years a severe IPF requiring a permanent oxygen-therapy. Although the association GPS-IPF might be only considered as a fortuitous one, we hypothesize that these two events might be related to each other, possibly through the presence of megakaryocytes in pulmonary capillaries, in the same way as bone marrow fibrosis has been suggested as a possible consequence of the lack of a-granules in GPS (DR0UET et al. - Nouv. Rev. Fr. Hematol., 1981, 23 : 95).
ELECTRONMICROSCOPIC STUDIES ON PLATELETS AND MEGAKARYOCYTES IN GIANT PLATELET SYNDROME
Authors: Suzuki Sozo , Mori Kazuo , Sugai Koji , Akutsu Yasuyuki , Ishikawa Masaaki , Sakai Hideaki , Hiwatashi Katsuhide 
Published: August 2018

Giant platelet syndrome are characterized morphologically by many giant platelets associated with several functional abnormalities in the peripheral blood. However, the mechanism of large platelet production has not yet been clarified. In 1981, we reported acase with Bernard-Soulier syndrome(BSS) in whom giant platelets were considered to be formed by fusion of two or three platelets in the circulating blood. We examined the ultrastructure of platelets and megakaryocytes in another case with BSS (29 year-old female) and a case with May-Hegglin anomaly (31 year-old male). Whole blood and bone marrow specimens were fixed with glutaraldehyde-osmium solution. Thin sections were prepared and stained with uranyl acetate and lead cytrate. Membrane systems of platelets and megakaryocytes in a case with BSS was investigated by staining of surface coating with ruthenium red.In a case with BSS, most platelets were very large and similar in morphology to those in formerly reported case. Giant platelets contained several-fold increased number of α-granules and mitochondria. Typical dense bodies were also observed. Contents of ATP/ADP, platelet factor-4(PF-4), B-thromboglobulin(B-TG) and platelet factor-3 availability(PF-3) were increased. Disorganization of microtubules was recognized. Some giant platelet contained membrane systems similar to demarcation membranes(DM) in megakaryocytes, characteristically. In mature megakaryocytes, areas divided by DM similar in size to those in normal megakaryocytes were observed. Several of these areas appeared to fuse together to form the giant platelets containing many granules and remnants of DM. In a case with May-Hegglin anomaly, typical Dohle’s bodies were shown in neutrophilic granulocytes. Giant platelets in this case also contained large number of α-granules and some of them contained membrane systems similar to DM. Areas similar in morphology to these giant platelets were clearly noted in the cytoplasm of mature megakaryocytes.In these cases, most giant platelets in the peripheral blood may be formed in the cytoplasm of megakaryocytes by fusion of several areas divided by DM, each of which may become normal sized platelets in normal megakaryocytes.
THE BLEEDING TENDENCY OF PROGRESSIVE RENAL FAILURE IS NOT ASSOCIATED WITH DEFECTIVE PLATELET AGGREGATION
Authors: Gordge M P , Faint R W , Rylance P B , Neild G H 
Published: August 2018

The bleeding tendency of uraemia may be related to reduction by anaemia of erythrocyte/platelet interaction, toxic inhibition of platelet aggregation and abnormal von Willebrand Factor (vWF) mediated platelet adhesion. Our aim in this study was to determine at what stage of renal failure bleeding time becomes prolonged and to investigate the mechanisms involved.We have measured bleeding time (Simplate II), plasma levels of fibrinogen and vWF, and ex-vivo platelet responsiveness in 31 patients with chronic renal failure (CRF) of various degrees of severity and compared them with values obtained in 22 healthy controls. No patient was dialysed, nephrotic or suffering from immunological renal disease. Patients were divided into mild (plasma creatinine <300 umol/1), n=10, moderate (300-600 umol/1), n=14, or severe (>600 umol/1), n=7, CRF.Bleeding time became significantly prolonged only in severe CRF (p<0.005). Haematocrit fell as renal failure advanced, and correlated with bleeding time (r=0.40, p<0.05). Platelet counts were normal. Platelet aggregation in response to ristocetin (mediated by vWF) and ADP increased progressively (p<0.005 in severe CRF), as did spontaneous aggregation (p<0.005 in severe CRF). This was associated with an increase in plasma vWF and fibrinogen (p<0.005 in severe CRF). Collagen induced aggregation was slightly, but not significantly increased. Thromboxane (TxB2) generation in clotting blood was the only measurement that showed a reduced platelet response (p<0.025 in severe CRF).In summary, a bleeding tendency develops late in the course of progressive CRF when plasma creatinine has risen to at least 600 umol/1. Platelet aggregation is enhanced rather than reduced and platelet interaction with vWF is not defective. Anaemia appears more important than abnormal platelet aggregation in mediating uraemic bleeding, although reduced serum TxB2 generation suggests a defect in platelet response to endogenous thrombin which may also contribute. Increased platelet aggregation and fibrinogen concentrations might promote glomerular thrombosis and contribute to the progression of CRF.
INCIDENCE AND CHARACTERISTICS OF MACROTHROMBOCYTOPENIA IN A MEDITERRANEAN AREA
Authors: Casals F J , Moreno R , Alfonso L , Alonso A , Guerrero R 
Published: August 2018

Idiopathic Thrombocytopenia Purpura (ITP) is diagnosed by exclusion in presence of a chronic thrombocytopenia, with evidence of bone marrow megakaryocytes and exclusion of associated diseases shortened platelet survival (PS), increased platelet volume (PV) and platelet associated immunoglobulin G (PAIgG) support this diagnosis. In subjects from mediterranean area, the idiopathic macrothrombocytopenia (IM) has been reported. This entity could be erroneously considered as a moderate type of ITP.To evaluate the incidence and characteristics of the IM we studied in 147 patients with not secondary megakaryocytic chronic thrombocytopenia, the PS by the 111-Indium-Oxine method, the PV distribution in citrated blood with the Coulter ZBI- Channelyzer C1000 and the PAIgG by the antiglobulin consumption assay.In 20 cases we found a macrothrombocytopenia, along with normal PS in 12 (Group A) or a near normal PS but marked facts of idiopathic hyperesplenism in the other eight (Group B ).25 % patients in the Group A and 57%in the Group B had increased PAIgG , more marked in the latter.Out of 147 patients studied, we found 40 with moderate thrombocytopenia (>40×10 plts/l) and 20 subjects were studied in remission (>100×10 plts/l), in all cases the PS was shortened.In conclusion we think that idiopathic macrothrombocytopenia and the idiopathic hypersplenic thrombocytopenia could be the broad spectrum of the same entity, with a high prevalence inthe mediterranean area. 14% of the patients studied had this alteration and this incidence increase to 35% when considering exclusively the moderate thrombocytopenias.
QUININE CAN INHIBIT OR ENHANCE PRODUCTION OF MURINE ANTI-HUMAN PLATELET ANTIBODIES
Authors: Christie D J , Lennon S S , Wischnack L L 
Published: August 2018

Quinine (Qn) can provoke potent antibodies capable of destroying platelets and inducing life-threatening immunologic thrombocytopenia (DITP). A question critical to understanding the mechanism of DITP is why do platelets from all normal individuals express Qn-induced antigens while only relatively few individuals make the destructive drug-dependent antibodies? This problem was investigated in a murine animal model. BALB/c mice (6-12wk) were injected intraperitoneally, every other week, with saline or lOOOpg of Qn (this dose of drug gave serum levels comparable to human therapeutic serum levels). Two wk after the second injection, mice were immunized with a single dose of 108 human platelets and either 0 or 1000μg of Qn. One wk later, mouse serum was screened in the presence and absence of drug for anti-platelet activity by a complement-dependent 51Cr release assay. Results are shown in the table and represent data from at least 2 groups of five mice each.Antibody titers were more than 10-fold lower in mice receiving 1000 |lg Qn than in mice injected with platelets alone. In contrast, mice repeatedly immunized (3-6 injections) with platelets and low doses of Qn (20μg) developed enhanced antibody activity (drug-dependent and nondrug-dependent) that consistently titered two-to four-fold higher than mice injected with platelets alone. Results were confirmed by an enzyme-linked immunosorbent assay which showed that the murine antibodies were IgG. These findings demonstrate that by varying the dose, Qn can either inhibit or enhance production of anti-human platelet antibodies in mice. This suggests the possibility that most individuals fail to respond to Qn because therapeutic doses of the drug inhibit antibody formation; yet in individuals capable of responding, even low doses of Qn (as found in tonic water) can enhance production of antibodies that provoke DITP.
ANALYSIS OF PLATELET ANTIGENS FOR ANTI-PLATELET ANTIBODIES IN ITP USING FLOW CYTOMETRY
Authors: Nomura S , Nagata H , Sone N , Oda K , Kokawa T , Yasunaga K 
Published: August 2018

Idiopathic thrombocytopenic purpura (ITP) is a syndrome caused by circulating antibodies reactive with the platelet membrane. The antigenic specificity of these antibodies is unknown. We have characterized new monoclonal antibodies that react with a determinant specific to GP Ib and GP Ib- Ia complex, and used flow cytometry to investigate platelets in ITP for antigenic determinants to which autoantibodies are directed. Forty cases of ITP were analyzed in detail by the platelet suspension immunofluorescence test(PSIFT) of von dem Borne et al. The monoclonal antibodies used were 5 against GP Ib-Ia complex (NNKY1-32, NNKY2-5, NNKY2-6, NNKY2-11, NNKY2-18) and 2 against GP lb (NNKY5-4, NNKY5-5). The reactivity of monoclonal antibodies was inhibited by the presence of autoantibody on platelets in some ITP patients. Differences in inhibition were found not only between monoclonal antibodies but also between cases.These results suggest that some ITP patients have circulating antibodies to GP Ib or GP II b - Ia, and that heterogeneous antibodies are present on platelets. Moreover, the presence of these autoantibodies may aggravate or initiate a bleeding tendency.
THE EFFECT OF INTRAVENOUS IMMUNOGLOBULIN ON PLATELET KINETICS IN CHRONIC IMMUNE THROMBOCYTOPAENIC PURPURA (ITP)
Authors: Badenhorst P N , Kotze H F , duP Heyns A , Lotter M G , Wessels P , Roodt J P 
Published: August 2018

Most patients with ITP respond to high doses of intravenous immunoglobulin (IVIg) with a transient increase in platelet count. The effect of IVIg on platelet kinetics was studied in 5 patients with chronic ITP. Autologous platelets were labelled with In-111 and mean platelet lifespan (MPLS) calculated; in vivo distribution and sites of platelet sequestration were determined with a scintillation camera and computer assisted image analysis. The studies were performed before and after treatment with 2 g/kg Sandoglobulin. Two groups of patients were identified: those with a splenic platelet sequestration pattern (spleen-liver In-111-activity ratio >1.4) and those with diffuse sequestration of platelets in the reticuloendothelial system (RES).There was a significant difference in mean platelet counts before and after treatment (p<0.05). Patients with a splenic sequestration pattern responded better to IVIg: the MPLS lengthened and the high spleen-liver ratio decreased. In the diffuse RES sequestration pattern group, IVIg had almost no effect on platelet kinetics. We conclude that platelet kinetic studies identify a subgroup of patients with ITP who will respond to IVIg therapy.
VASOCONSTRICTION IN RESPONSE TO HUMAN PLATELET-VESSEL WALL INTERACTIONS
Authors: Van Nueten J M , Janssens W J , De Clerck F 
Published: August 2018

Human blood platelets, stimulated with thrombin, induced contractions of isolated basilar artery segments of the dog. These platelet-mediated vascular contractions were inhibited in a concentration-dependent way by flunarizine, a Ca2+-entry blocker, selective for vascular tissues. This inhibition increased gradually as a function of time after contact with flunarizine to reach its maximum after 60-90 min. Biochemical and pharmacological analyses, using the 5-HT2-serotonergic antagonist ritanserin, the thromboxane A2/prostaglandin endo-peroxide antagonist BM 13.177 and the fatty acid cyclo-oxygenase inhibitor suprofen, showed that 5-hydroxytryptamine and prostanoids (thromboxane A2, prostaglandine endoperoxides) were the main mediators involved. They further suggested amplification between 5-hydroxytryptamine and prostanoids at the vascular level.(1) Incubation period; (2) Inhibition of platelet-mediated vascular contractions.This study demonstrates that 5-hydroxytryptamine, acting in concert with thromboxane A2 and/or prostaglandine-endoper-oxides, is responsible for the vasoconstrictor effects of aggregating platelets. It further indicates that influx of calcium ions is involved in these vasoconstrictor responses.
ENDOTHELIUM-INDEPENDENT PARTIAL AGONISTIC ACTIVITY OF VASOPRESSIN IN THE RAT COMMON CAROTID ARTERY
Authors: Katušić Z S , Krstić M K 
Published: August 2018

It has been shown that vasopressin causes endothelium-dependent relaxations of the canine basilar artery, suggesting that_increased circulating concentrations of vasopressin can produce redistribution of the blood from the peripheral to the cerebral circulation (Katušić et al., 1984). The present experiments were done to examine effect of vasopressin on the rat peripheral arteries* The experiments were performed on rings (4 mm long) of aorta, common carotid and renal arteries* The arteries were placed in Krebs-Ringer-bicarbonate solution gassed with 95%O2-5%co2 gas mixture and kept at 37°c. In certain rings the endothelium was removed mechanically by gentle rubbing of the intimal surface. Isometric tension was continously recorded (IPM electronic).Vasopressin (10-11 to 3×10-8 M) caused concentration-dependent contraction being full agonist in aorta and renal artery, but partial agonist in common carotid artery. After removal of endothelium vasopressin-induced contractions were not significantlly afected in any of the tested arteries. Gyclooxygenase inhibitor indomethacin (10-5 M; contact time = 40 min) did not affect partial agonistic activity of vasopressin in common carotid artery. This results indicate that partial agonistic activity of vasopressin in common carotid artery is not related to increased production of "EDRF" or prostacyclin from endothelium. In addition, our findings are consistent with the hypothesis that vasopressin may contribute to redistribution of the blood flow from the peripheral to the cerbral circulation.Z.S. Katušić, J.T. Shepherd and P.M. Vanhoutte. Circ. Res., 55: 575-579, 1984
ENDOTHELIAL CELL INJURIES AND SMOOTH MUSCLE CELL PROLIFERATION INDUCED BY MATERIALS RELEASED FROM PLATELET-RICH THROMBUS IN VIVO
Authors: Asada Y , Hayashi T , Sumiyoshi A 
Published: August 2018

It is widely held that the disturbance in the integrity of the arterial endothelium may lead to the development of arteriosclerosis and many factors have been postulated to cause the endothelial injury, such as hemodynamic stress, anoxia, platelet-releasing materials, and so on. However, whether any of these is important for endothelial injury is unclear. We studied whether the released products from activated platelets and/or thrombi could cause endothelial damage and proliferation of smooth muscle cells in large vessels in vivo.Polyethylene tubing was inserted into the ascending aorta of rabbits via the common carotid artery and placed for one, 4, and 24 weeks continuously to induce vessel wall injury and thrombotic events. Then the direct non-injured segments from the descending thoracic and abdominal aorta was morphologically examined, and 3H-thymidine incorporation into the arterial wall was also examined. The descending aortas of experimental rabbits showed endothelial damage and increased mitoses of endothelial cells. Modified smooth muscle cells were noted in the subendothelial layer, and 3H-thymidine incorporation into the intima and media significantly increased in the experimental group at one week(Fig.). At 24 weeks, the intimal thickening with smooth muscle cell proliferation was also found.This experiment indicates that materials released from the activated platelets and/or thrombi into the circulation can cause endothelial damage and smooth muscle cell proliferation and intimal thickening at downstream and remote aortic segments.
BIOSYNTHESIS AND SECRETION OF β-THROMBOGLOBULIN BY A HUMAN MEGAKARYOBLASTIC CELL LINE ( MEG-01 )
Authors: Ogura M , Tanabe N , Hamaguchi M , Hotta T , Saito H 
Published: August 2018

β-Thromboglobulin ( βTG ) is a well known platelet specific a-granular protein, but synthesis of βTG by human megakaryocytes has not been fully proved. A human megakaryoblastic cell line ( MEG-01 ) was investigated for the presence of βJG in the culture medium and cell lysates using a specific radioimmunoassay ( RIA ). The concentration of βTG increased with time in the serum-free culture medium as well as in the cell lysates as shown in the following table.By an indirect immunofluorescent technique using a monospesific rabbit anti serum against human βTG, βTG antigen was detected in MEG-01 cells. Immunoblot analysis of culture medium revealed a single band ( mol wt 8,900 ) that is identical to the band of human plasma βTG. De novo synthesis of βTG was demonstrated by the presence of specific immunoprecipitable radioactivity in the medium after 5 h of labeling of the cells with [35S]-methionine as a 8,900 mol wt protein. These results indicate that human megakaryocytes produce βTG, The production of βTG by MEG-01 cells may be useful for the study of megakaryocyte maturation and differentiation.