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O J Nielsen

Publications and source records attributed to O J Nielsen.

At least 19 recordsLinked to original sources

Atmospheric chemistry of n-C(x)F(2)(x)(+1)CHO (x = 1, 2, 3, 4): fate of n-C(x)F(2)(x)(+1)C(O) radicals.

Smog chamber/FTIR techniques were used to study the atmospheric fate of n-C(x)F(2)(x)(+1)C(O) (x = 1, 2, 3, 4) radicals in 700 Torr O(2)/N(2) diluent at 298 +/- 3 K. A competition is observed between reaction with O(2) to form n-C(x)()F(2)(x)()(+1)C(O)O(2) radicals and decomposition to form n-C(x)F(2)(x)(+1) radicals and CO. In 700 Torr O(2)/N(2) diluent at 298 +/- 3 K, the rate constant ratio, k(n-C(x)F(2)(x)(+1)C(O) + O(2) --> n-C(x)F(2)(x)(+1)C(O)O(2))/k(n-C(x)F(2)(x)(+1)C(O) --> n-C(x)F(2)(x)(+1) + CO) = (1.30 +/- 0.05) x 10(-17), (1.90 +/- 0.17) x 10(-19), (5.04 +/- 0.40) x 10(-20), and (2.67 +/- 0.42) x 10(-20) cm(3) molecule(-1) for x = 1, 2, 3, 4, respectively. In one atmosphere of air at 298 K, reaction with O(2) accounts for 99%, 50%, 21%, and 12% of the loss of n-C(x)F(2)(x)(+1)C(O) radicals for x = 1, 2, 3, 4, respectively. Results are discussed with respect to the atmospheric chemistry of n-C(x)F(2)(x)(+1)C(O) radicals and their possible role in contributing to the formation of perfluorocarboxylic acids in the environment.

Air Pollutants↗

Atmospheric chemistry of perfluorinated aldehyde hydrates (n-C(x)F(2x+1)CH(OH)2, x = 1, 3, 4): hydration, dehydration, and kinetics and mechanism of Cl atom and OH radical initiated oxidation.

Smog chamber/Fourier transform infrared (FTIR) techniques were used to measure k(Cl+C(x)F(2x+1)CH(OH)(2)) (x = 1, 3, 4) = (5.84 +/- 0.92) x 10(-13) and k(OH+C(x)F(2x+1)CH(OH)(2)) = (1.22 +/- 0.26) x 10(-13) cm(3) molecule(-1) s(-1) in 700 Torr of N(2) or air at 296 +/- 2 K. The Cl initiated oxidation of CF(3)CH(OH)(2) in 700 Torr of air gave CF(3)COOH in a molar yield of 101 +/- 6%. IR spectra of C(x)F(2x+1)CH(OH)(2) (x = 1, 3, 4) were recorded and are presented. An upper limit of k(CF(3)CHO+H(2)O) < 2 x 10(-23) cm(3) molecule(-1) s(-1) was established for the gas-phase hydration of CF(3)CHO. Bubbling CF(3)CHO/air mixtures through liquid water led to >80% conversion of CF(3)CHO into the hydrate within the approximately 2 s taken for passage through the bubbler. These results suggest that OH radical initiated oxidation of C(x)F(2x+1)CH(OH)(2) hydrates could be a significant source of perfluorinated carboxylic acids in the environment.

Journal Article↗

Formation of C7F15COOH (PFOA) and other perfluorocarboxylic acids during the atmospheric oxidation of 8:2 fluorotelomer alcohol.

Calculations using a three-dimensional global atmospheric chemistry model (IMPACT) indicate that n-C8F17CH2CH2OH (widely used in industrial and consumer products) degrades in the atmosphere to give perfluorooctanoic acid (PFOA) and other perfluorocarboxylic acids (PFCAs). PFOA is persistent, bioaccumulative, and potentially toxic. Molar yields of PFOA depend on location and season, are in the range of 1-10%, and are of the correct order of magnitude to explain the observed levels in Arctic fauna. Fluorotelomer alcohols such as n-C8F17CH2CH2OH appear to be a significant global source of persistent bioaccumulative perfluorocarboxylic acid pollution. This is the first modeling study of the atmospheric chemistry of a fluorotelomer alcohol.

Alcohols↗

Acute lymphoblastic leukemia in adolescents between 10 and 19 years of age in Denmark--secondary publication.

INTRODUCTION: Data seem to indicate that young adults with acute lymphoblastic leukemia (ALL) have a better survival when treated with pediatric protocols compared with adult ALL protocols. The purpose of the study was to report the clinical characteristics and outcome of all children and young adults 10-19 years of age diagnosed with ALL in Denmark between 1992 and 2001. MATERIAL: The study includes 99 patients 10-19 years of age with ALL in Denmark during a ten year period found in the complete NOPHO (Nordic Society of Pediatric Hematology and Oncology) registry and through the Danish Cancer Registry and local pathology databases. Data were retrieved by reviewing medical charts of the patients. A total of 61 children (10-14 years) treated on pediatric protocols and 38 young adults (15-19 years) were diagnosed with ALL. Data were reported as of January 1st 2005. RESULTS: There were no difference with respect to the distribution of T-ALL, CNS-leukemia, total white blood count and high risk chromosomal abnormalities between the two groups. There was a statistical significant lower event free survival (p<0.01) and lower overall survival (p<0.01) in young adults compared with 10-14 year-old children (0.38 vs 0.60 and 0.47 vs 0.67). There were more transplant-related deaths in the young adults. Higher treatment intensity in children may be an additional explanatory factor. Children received more prednisone, vincristine and high-dose methotrexate than young adults. CONCLUSION: Young adult patients with ALL might benefit from therapy with pediatric NOPHO ALL protocols.

Adolescent↗

Atmospheric chemistry of CF3OCF2CF2H and CF3OC(CF3)2H: reaction with Cl atoms and OH radicals, degradation mechanism, global warming potentials, and empirical relationship between k(OH) and k(Cl) for organic compounds.

Using FTIR smog chamber techniques, k(Cl + CF3OCF2CF2H) = (2.70 +/- 0.52) x 10(-16), k(OH + CF3OCF2CF2H) = (2.26 +/- 0.18) x 10(-15), k(Cl + CF3OC(CF3)2H) = (1.58 +/- 0.27) x 10(-18) and k(OH + CF3OC(CF3)2H) = (3.26 +/- 0.95) x 10(-16) cm3 molecule(-1) s(-1) were measured. The atmospheric lifetimes of CF3OCF2CF2H and CF3OC(CF3)2H are estimated to be 27 and 216 years, respectively. Chlorine atom initiated oxidation of CF3OCF2CF2H in 700 Torr of air in the presence of NO(x) gives CF3OC(O)F in a molar yield of 36 +/- 5% and COF2 in a molar yield of 174 +/- 9%, whereas oxidation of CF3OC(CF3)2H gives CF3OC(O)CF3 and COF2 in molar yields that are indistinguishable from 100%. Quantitative infrared spectra were recorded and used to estimate global warming potentials of 3690 and 8230 (100 year time horizon, relative to CO2) for CF3OCF2CF2H and CF3OC(CF3)2H, respectively. All experiments were performed in 700 Torr of N2/O2 diluent at 296 +/- 2 K. An empirical relationship can be used to estimate the preexponential factor, which can be combined with k(298 K) to give the temperature dependence of reactions of OH radicals with organic compounds proceeding via H-atom abstraction: log(A/n) = (0.239 +/- 0.027) log(k(OH)/n) - (8.69 +/- 0.372), k(OH) is the rate constant at 298 K and n is the number of H atoms. The rates of H-atom abstraction by OH radicals and Cl atoms at 298 K from organic compounds are related by the expression log(k(OH)) = (0.412 +/- 0.049) log(k(Cl)) - (8.16 +/- 0.72). The utility of these expressions and the atmospheric chemistry of the title hydrofluoroethers are discussed.

Journal Article↗

Atmospheric chemistry of 4:2 fluorotelomer alcohol (n-C4F9CH2CH2OH): products and mechanism of Cl atom initiated oxidation in the presence of NOx.

Smog chamber/FTIR techniques were used to study the Cl atom initiated oxidation of 4:2 fluorotelomer alcohol (C(4)F(9)CH(2)CH(2)OH, 4:2 FTOH) in the presence of NO(x) in 700 Torr of N(2)/O(2) diluent at 296 K. Chemical activation effects play an important role in the atmospheric chemistry of the peroxy, and possibly the alkoxy, radicals derived from 4:2 FTOH. Cl atoms react with C(4)F(9)CH(2)CH(2)OH to give C(4)F(9)CH(2)C(*)HOH radicals which add O(2) to give chemically activated alpha-hydroxyperoxy radicals, [C(4)F(9)CH(2)C(OO(*))HOH]*. In 700 Torr of N(2)/O(2) at 296 K, approximately 50% of the [C(4)F(9)CH(2)C(OO(*))HOH]* radicals decompose "promptly" to give HO(2) radicals and C(4)F(9)CH(2)CHO, the remaining [C(4)F(9)CH(2)C(OO(*))HOH]* radicals undergo collisional deactivation to give thermalized peroxy radicals, C(4)F(9)CH(2)C(OO(*))HOH. Decomposition to HO(2) and C(4)F(9)CH(2)CHO is the dominant atmospheric fate of the thermalized peroxy radicals. In the presence of excess NO, the thermalized peroxy radicals react to give C(4)F(9)CH(2)C(O(*))HOH radicals which then decompose at a rate >2.5 x 10(6) s(-1) to give HC(O)OH and the alkyl radical C(4)F(9)CH(2)(*). The primary products of 4:2 FTOH oxidation in the presence of excess NO(x) are C(4)F(9)CH(2)CHO, C(4)F(9)CHO, and HCOOH. Secondary products include C(4)F(9)CH(2)C(O)O(2)NO(2), C(4)F(9)C(O)O(2)NO(2), and COF(2). In contrast to experiments conducted in the absence of NO(x), there was no evidence (<2% yield) for the formation of the perfluorinated acid C(4)F(9)C(O)OH. The results are discussed with regard to the atmospheric chemistry of fluorotelomer alcohols.

Journal Article↗

Anagrelide treatment in 52 patients with chronic myeloproliferative diseases.

In this retrospective multi-centre study, we report our experience with anagrelide in the treatment of thrombocytosis in patients with chronic myeloproliferative diseases. Our study included 52 patients (age 20-78 years). The initial anagrelide dose was, in general, 0.5 mg once daily and mean maintenance dosage was 1.7 mg/day. The overall response rate was 79% including 75% complete remission and 4% partial remission. Forty-two patients (81%) had adverse effects and in 29% of the study population, the adverse effects necessitated cessation of anagrelide. The most common adverse effect was moderate anaemia (50%). Two patients experienced erectile dysfunction which has been described only once previously in association with anagrelide treatment. One patient progressed to acute leukaemia. However, this patient had been pre-treated with two potentially leukaemogenic drugs and had only been in short-term treatment with anagrelide. Furthermore, a total of 13 events were recorded. More than 25% of these events occurred in patients with platelet counts between 400 and 600 x 10(9)/l and almost 40% of all events occurred in patients with platelet counts above 400 x 10(9)/l. This observation supports the hypothesis that aggressive control of thrombocytosis to a platelet count <400 x 10(9)/l might reduce the number of thrombohaemorrhagic events. Anagrelide is safe and effective in reducing the platelet counts, but a high proportion of the patients discontinue treatment because of the adverse effects of the drug.

Adult↗

Isotopic processes in atmospheric chemistry.

Trace gases are responsible for the atmospheric processes underlying air pollution and global change. Analysis of the distribution of stable isotopes in these gases is a way of gaining additional knowledge that may not otherwise be available. This approach requires knowledge of the isotopic signature of emissions sources and chemical reactions. This review focuses on the chemical physics of the processes underlying the distribution of stable isotopes in atmospheric gases.

Air Pollutants↗

[The chronic Philadelphia chromosome-negative myeloproliferative syndrome I. Pathogenesis and pathophysiology].

In polycythaemia vera (PV) the erythroid progenitors proliferate autonomously independently of the circulating erythropoietin. The progenitors are hypersensitive to various growth factors, including insulin-like growth factor 1, which inhibits apoptosis in erythroid and myeloid progenitor cells. No change has been found in the erythropoietin (EPO) receptor. Thrombopoietin (Tpo) regulates the production of haematopoietic progenitor cells, particularly of platelets. By inhibiting apoptosis, this growth factor may be responsible for the autonomous proliferation of the megakaryocyte cell lineage in PV and idiopathic myelofibrosis (IMF), which are featured by highly elevated circulating Tpo levels. Thrombopoietin may also be involved in the pathogenesis of myelofibrosis and development of extramedullary haematopoiesis. Both fibrogenesis and angiogenesis in the bone marrow, spleen, and liver develop secondary to the release of various growth-promoting factors from the megakaryocyte cell lineage. The lesion of the pluripotent stem cell in PV and IMF seems to imply several defects, including lack of or decreased expression of the Tpo receptor, alterations in the sensitivity of progenitor cells to various growth factors, and alterations in important gene systems (Bcl-2), which govern cell survival. Essential thrombocytosis seems to be a heterogeneous disease entity, as about 50% of the patients have polyclonal haematopoiesis.

Hematopoiesis↗

[The chronic Philadelphia chromosome-negative myeloproliferative syndrome II. Clinical findings, diagnostics and treatment].

Polycythaemia vera (PV) and essential thrombocytosis (ET) are clinically characterised by non-specific neurologic symptoms, peripheral circulatory disturbances (acrocyanosis, wounds, erythromelalgia) or abdominal symptoms. The treatment of PV includes phlebotomy, antiaggregation and cytoreduction. In ET, the primary treatment is also low-dose aspirin except for patients presenting with a haemorrhagic diathesis. Hydroxyurea may be associated with an increased risk of acute leukaemia or myelodysplasia. Therefore alpha-interferon and anagrelide should be considered in younger patients. Early cytoreductive therapy is advocated in patients with idiopathic myelofibrosis (IMF) to inhibit further progression of bone marrow fibrosis and further expansion of myeloid metaplasia in the spleen and liver. Treatment with androgens (danazol) and glucocorticoids may improve severe anaemia and thrombocytopenia. In younger patients, allogeneic bone marrow transplantation should be considered.

Bone Marrow↗

[Acute thrombotic complication at the debute of the Philadelphia chromosome-negative myeloproliferative syndrome].

METHODS: We describe eight patients with a diagnosis of a chronic myeloproliferative disorder, characterised in most patients by severe thrombotic complications at the debut of the disease. RESULTS: The symptoms were life-threatening in seven patients: acute upper gastrointestinal haemorrhage from oesophageal varices in four, an acute abdominal catastrophy owing to mesenteric vein thrombosis with intestinal gangrene in two, and a large cerebral infarction, which was lethal, in one. The same patient also suffered a thrombosis of the axillary and subclavian veins. Neurological symptoms, with headache, visual disturbances, dizziness, and impaired memory, were initial cardinal symptoms. In two patients, explorative laparotomy was performed with intestinal resection owing to gangrene. One patient had a toe amputation. DISCUSSION: The above symptoms are explained by thrombosis in the microcirculation because of thrombocytosis and circulating platelet aggregates. In patients with polycythaemia vera, the elevated haematocrit contributes significantly to the impaired microcirculation. Early diagnosis and management of these disorders are of utmost importance to prevent the potentially life-threatening complications described above.

Acute Disease↗

[Anterior screw fixation of fractures of the dens axis].

INTRODUCTION: The aim of the present study was to evaluate the results of anterior screw fixation in the treatment of odontoid fracture. MATERIALS AND METHODS: The clinical and radiographic records of the first 14 patients treated with anterior screw fixation for odontoid fracture were reviewed retrospectively. RESULTS: Satisfying stabilisation of the fracture was achieved in 10 patients (71%). In four patients, two of whom had severe osteoporosis, additional posterior C1/C2 fusion, owing to failure of screw treatment was needed. Two patients developed small occipital bedsores caused by preoperative treatment, but no further complications were observed. CONCLUSION: Although only a few patients were entered in the study, the results justify the use of anterior screw fixation as the treatment of odontoid fracture in selected patients.

Adolescent↗

Increased circulating platelet-leukocyte aggregates in myeloproliferative disorders is correlated to previous thrombosis, platelet activation and platelet count.

Platelet-leukocyte adhesion may occur as a consequence of platelet activation and possibly plays a key role in the deposition of activated platelets and fibrin in the thrombotic plug. The aim of the present study was to assess by whole blood flow cytometry the presence of circulating platelet-leukocyte aggregates (PLA) and the platelet-leukocyte response to platelet agonist stimulation (ADP and TRAP) in 50 patients with chronic myeloproliferative disorders (MPD) and 30 controls. PLA were identified as platelet-granulocyte/monocyte aggregates (PGMA), platelet-monocyte aggregates (PMA) and defined as the percentage of leukocytes coexpressing the platelet-specific marker glycoprotein Ib. Compared to controls the mean percentage of PGMA and PMA was increased in unstimulated whole blood from patients with MPD (7.98 vs. 1.76%; p<0.001 and 12.34 vs. 3.2%; p<0.001, respectively). The percentage of PGMA was correlated to the platelet count (r=0.46; p<0.001), percentage of P-selectin (r=0.69; p<0.001) and thrombospondin (r=0.58; p<0.001) positive platelets and platelet expression of GPIV (r=0.33; p=0.02). The mean percentage of PGMA and PMA was significantly increased in ADP-stimulated whole blood of patients (57.14 vs. 47.92%; p=0.009 and 54.91 vs. 45.89%; p<0.001, respectively). Compared to patients without a history of thrombosis, patients having experienced microvascular disturbances or a thrombotic event had a higher mean percentage of PGMA and PMA in non-stimulated whole blood (10.07 vs. 6.34%; p=0.025 and 14.81 vs. 10.48%; p=0.021, respectively) and a higher percentage of PGMA in ADP stimulated whole blood (64.32 vs. 51.50%; p<0.01). These data document an increased frequency of PLA in non-stimulated whole blood in MPD associated with a previous history of thrombosis or microvascular disturbances.

Adenosine Diphosphate↗

Sustained remission of platelet counts following monoclonal anti-CD20 antibody therapy in two cases of idiopathic autoimmune thrombocytopenia and neutropenia.

Idiopathic autoimmune thrombocytopenia and neutropenia (ITN) is a primary haemocytopenic disorder clinically characterised by recurrent mucocutaneous bleeding episodes and infections. Unlike in simple idiopathic thrombocytopenic purpura, the platelet deficiency of ITN tends to be chronic and difficult to treat. We describe two patients with ITN who obtained sustained remission of their platelet counts after therapy with the chimeric monoclonal anti-CD20 antibody Rituximab. In one of two cases, Rituximab also induced prolonged normalisation of the neutrophil count and disappearance of auto-antibodies. Our observations indicate that disturbed B-cell function plays a central role in the pathogenesis of ITN. Anti-CD20 antibody therapy seems to constitute a safe and efficient alternative to corticosteroids for the management of ITN patients with chronic thrombocytopenia.

Adult↗

High prevalence of hyperhomocysteinemia due to marginal deficiency of cobalamin or folate in chronic myeloproliferative disorders.

Hyperhomocysteinemia is an established risk factor for thrombosis. In patients with myeloproliferative disorders, thrombotic events are common. Our aim was to investigate whether the increased burden of proliferating cells present in these patients implies a risk of homocysteine (HCY) accumulation secondary to depletion of folate and/or cobalamin. Fifty patients (PV, 25; ET, 10; IMF, 15) and 163 healthy volunteers (HV) participated in the study. The prevalence of hyperhomocysteinemia was 56.0% in PV, 70.0% in ET, 60.0% in IMF, and 34.9% in HV. The mean P-homocysteine (P-HCY) was 13.88 +/- 4.24 micromol/L in PV, 12.78 +/- 3.70 in ET, 11.34 +/- 4.22 in IMF, and 9. 71 +/- 2.76 in HV. In PV and ET, but not in IMF, the mean P-HCY was significantly higher than in the HV group (P < 0.001, P = 0.028, and P = 0.163, respectively). Thirty-three percent of the patients with hyperhomocysteinemia displayed metabolic changes compatible with cobalamin deficiency (P-HCY and P-methylmalonic acid both elevated), while 67% were folate deficient (P-HCY elevated, P-methylmalonic acid normal). Supplementation therapy with the relevant vitamin was implemented in 11 vitamin-deficient patients and led to normalization of metabolite levels in all cases. No correlation between hyperhomocysteinemia and thrombosis was found. Our data indicate that patients with PV, ET, and IMF frequently develop hyperhomocysteinemia due to discrete depletion of cobalamin or folate. Vitamin therapy leads to normalization of P-HCY and should be considered, even though hyperhomocysteinemia does not seem to be of crucial importance for the thrombotic tendency in the myeloproliferative disorders.

Adult↗

Incidence, clinical features and outcome of essential thrombocythaemia in a well defined geographical area.

In an attempt to characterise the clinical features, incidence and outcome of essential thrombocythaemia (ET) we report our experience in a large unselected series of patients from a well defined region. All new cases of ET in the County of Copenhagen were registered during the period 1977-98. We identified 96 cases of ET, yielding an age- and sex-adjusted annual incidence rate of 0.59/100.000 and a point-prevalence at last follow up of 11/100.000. The overall incidence rate was 0.31 and 1.00 per 100.000 population during the consecutive periods 1977-89 and 1990-98, respectively, corresponding to a 3.2-fold increase. Median age at diagnosis was 67 yr (females 68 yr, males 66 yr, range 18-87 yr), and the female to male (F/M) ratio was 2.6:1. At diagnosis, 52% of the patients displayed no ET-related symptoms and were discovered fortuitously by a routine platelet count. Forty-eight percent presented with thrombohaemorrhagic phenomena, of which microvascular disturbances of the central nervous system (CNS), extremities and skin were most frequently observed (23%). Compared to patients diagnosed after 1989, patients diagnosed before 1990 had a significantly higher mean platelet count, white blood cell (WBC) count, lactate dehydrogenase (LDH) value and alkaline phosphatase value. With a median follow up of 70 months, 5-yr survival was 76%, significantly lower than the expected survival of an age- and sex-matched control group (p = 0.0052). Thirty-seven patients experienced a total of 55 thrombohaemorrhagic events during follow-up, corresponding to an incidence of thrombosis and microvascular disturbances or haemorrhage of 8.1% per pt-yr and 2.5% per pt-yr, respectively. The number of patients experiencing thrombosis or microvascular disturbances was significantly higher among the 29 patients who never received acetylsalicylic acid (ASA) compared to the 67 patients who received ASA during follow up (45% vs. 21%; p = 0.017). This study provides population-based data suggesting the benefit of treatment with low-dose ASA in a non-selected population of patients with ET.

Adolescent↗

Increased platelet activation and abnormal membrane glycoprotein content and redistribution in myeloproliferative disorders.

Chronic myeloproliferative disorders (MPDs) are characterized by a high incidence of thrombohaemorrhagic complications, possibly caused by platelet dysfunction. In an attempt to define platelet functional abnormalities, we assessed the expression of activation-dependent membrane proteins in unstimulated and agonist [ADP and thrombin receptor-activating peptide (TRAP)]-stimulated platelets using quantitative whole blood flow cytometry in samples from 50 MPD patients and 30 controls. The receptor densities of activation markers and glycoproteins (GPs) were quantified using standardized fluorescent beads. Compared with controls, the mean percentage of P-selectin-positive (15.3% vs. 7.2%; P < 0.001) and thrombospondin (TSP)-positive (6.6% vs. 3.7%; P = 0.003) platelets was increased in unstimulated platelets from patients. Patients having experienced a thrombotic event had a higher mean percentage of TSP-positive non-stimulated platelets than patients without a history of thrombosis (9.0% vs. 4.6%; P = 0.02) and a higher GPIV molecules of equivalent fluorochrome (MEF) value (33113 vs. 24471 MEF; P = 0.02). Mean MEF values of monoclonal antibodies (mAbs) against GPIb (34055 vs. 38945 MEF; P < 0.001) and GPIIb/IIIa (1416 vs. 1648 MEF; P < 0. 001) were significantly reduced among patients, whereas surface expression of GPIV was increased in patients (28273 vs. 16258 MEF; P < 0.001). In TRAP (10 micromol/l) stimulated whole blood, the MEF of P-selectin (9611 vs. 13293 MEF; P = 0.004) and CD63 (2385 vs. 5177 MEF; P < 0.001) and the ratio of PAC-1/GPIIb/IIIa MEF (0.98 vs. 2. 00; P < 0.001) was reduced in patients, indicating either a reduced granule GP content or an intrinsic cellular defect in receptor-mediated granule secretion and activation of the GPIIb/IIIa complex. Expressed as the relative change of MEF compared with unstimulated platelets, TRAP induced decrease of GPIb (7.8% vs. 45%; P < 0.001) and increase of GPIIb/IIIa (49.1% vs. 95.7%; P < 0.001) and GPIV expression (17.8% vs. 55.2%; P < 0.001) was attenuated in patients.

Adenosine Diphosphate↗