5 research outputs found

    The association of bladder myeloid sarcoma and unclassified myelodysplastic/myeloproliferative disease

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    Myeloid sarcoma of the urinary bladder is a rare disorder. We report a 71-year-old man with hematuria who had a diffuse myeloid sarcoma of the bladder. He was also under follow-up for unclassified myeloproliferative/myelodysplastic disorder, diagnosed two months before. Abdominal ultrasonography and computed tomography findings were normal. Diagnostic cystoscopy revealed patchy areas of mucosal swelling with hyperemia. Histopathological examination of biopsies demonstrated a neoplasm composed of blasts showing myeloperoxidase positivity by immunohistochemistry. To our knowledge, the current case is the first case of myeloid sarcoma in the urinary bladder without evidence of a mass lesion, with a concurrent diagnosis of unclassifiable myelodysplastic/myeloproliferative disease

    COST Action CA19114, Network for Optimized Astatine labelled Radiopharmaceuticals

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    Cancer is a major health concerns for European citizens. Thus, the main research aim of this Network for Optimized Astatine labeled Radiopharmaceuticals (NOAR) COST Action is to successfully demonstrate that one of the most promising radionuclides for Targeted Alpha Therapy (TAT), namely astatine-211, can become the European standard for treatment of certain cancerous pathologies. To this end, an efficient networking is essential among all European stakeholders interested in promoting astatine-211 for medical applications. NOAR COST Action brings together European and international excellence labs, astatine-211 production centers, hospitals, industry and patient associations from more than 20 countries, thus covering the whole value chain of innovation: production, chemistry, radiochemistry, biology, preclinical and clinical research and delivery of radiopharmaceuticals to patients. A European web portal will be created containing information for patients, practitioners, researchers, Industry and as a contact point for National and European patient associations. The idea is to gather forces at the European level in order to implement actions to leverage hurdles to the development of this powerful radionuclide and to identify pathologies in which it will be particularly relevant. A special emphasis will be given to train a new generation of young researchers and PhD students, promoting interdisciplinary competencies through international and inter-sectoral mobility. The long-term goal of this project is to make Astatine-211 technology available to all European citizen

    Decreased Myocardial Tl-201 Uptake In Rats: Early Sign Of Doxorubicin Induced Myocardial Damage And The Relation To Inflammation

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    Aim: In the present study, we demonstrated that total cardiac 201Tl uptake changes associated with histological findings in DOX-induced early myocardial injury. Method : Early DOX cardiotoxicity was induced in normal rats by giving 15 mg/kg DOX intraperitoneally. Cardiac uptake studies and the blood sampling for creatine kinase (CK) and lactate dehydrogenase (LDH) assay has been performed on the 3rd (acute phase) and 16th days (subacute phase) after the treatment, respectively. Rats were killed by heart puncture and the hearts removed by dissection at 60 min after the injection of 7.4 MBq 201Tl. The ratio of total cardiac uptake to the injected dose (%ID/g x BW, where ID is injected dose and BW is body weight) was calculated. Result : DOX led to a significant decrease in myocardial uptake of 201Tl in both treatment groups (p< 0.05). There was no significant difference in the %ID/g x BW between acute and subacute phases (p>0.05). DOX induced a significant increase in the levels of CK and LDH in serum, indicating its early cardiotoxicity (p=0.01). DOX treatment produced disorganization of myocardial fibers, vacuolation of the cardiac myocytes and myocardial necrosis (p=0.01). These cardiomyocyte injuries were accompanied by increased numbers of mononuclear cells (p< 0.05). LDH, CK, cardiyomyopathy and mononuclear cell infiltration scores were not found significantly different between acute and subacute phases (p>0.05). Conclusion: The DOX-induced cardiac injury at early stage can be evaluated by 201Tl and the findings may be associated with the myocardial inflammation. Due to the complicated mechanism of DOX injury, we believe that the development process of cardiac injury and the pathological findings should be taken into consideration in interpreting the radiopharmasotic studies to be conducted for the evaluation of the early and late stage cardiac injuries

    Could Pyelonephritic Scarring Be Prevented by Anti-Inflammatory Treatment? An Experimental Model of Acute Pyelonephritis

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    Objectives. This study aimed to demonstrate if the addition of anti-inflammatory treatment to antibiotic therapy shows any superiority to the treatment with antibiotic only. Methods. Forty-nine Wistar rats were divided into 7 groups. Pyelonephritis was performed by E. coli injection to upper pole of kidneys except control group. Group 2 was not treated. Ceftriaxone, ketoprofen, “ceftriaxone + ketoprofen,” methylprednisolone, and “ceftriaxone + methylprednisolone” were given in the groups. The technetium-99m-dimercaptosuccinic acid scintigraphies were performed in 3rd day to detect pyelonephritis and 10th week to detect renal scarring. All kidneys were also histopathologically evaluated. Results. When 3rd day and 10th week scintigraphies were compared, initial 2.00 ± 0.30 point pyelonephritis score resulted in 0.71 ± 0.36 renal scar score in “ceftriaxone + ketoprofen” group (P=0.039). Initial 2.00 ± 0.43 point pyelonephritis score resulted in 0.86 ± 0.26 renal scar score in “ceftriaxone + methylprednisolone” group (P=0.041). Renal scar score was declined in “ceftriaxone + ketoprofen” group and “ceftriaxone + methylprednisolone” group compared with no-treatment group on 10th week of the study (P=0.026, P=0.044). On histopathological evaluation, it was seen that renal scar prevalence and expansion declined significantly in “ceftriaxone + ketoprofen and ceftriaxone + methylprednisolone” (P=0.011, P=0.023). Conclusion. It was evidenced that ceftriaxone treatment in combination with ketoprofen or methylprednisolone declined scar formation in scintigraphic and histopathologic examinations of the kidneys
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