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Journal articles on the topic "History.#x1E; 0"
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Zakarija, Anaadriana, Hau C. Kwaan, Nicholas Banderanko, Dilip K. Pandey, John F. Cursio, Ivy M. Weiss, Thanh Ha Luu, et al. "Distinct Clinical Syndromes Are Defined by ADAMTS13 Activity in Idiopathic TTP: Results of the SERF-TTP Study." Blood 110, no. 11 (November 16, 2007): 1320. http://dx.doi.org/10.1182/blood.v110.11.1320.1320.
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Abstract Background: The Surveillance, Epidemiology & Risk Factors for TTP (SERF-TTP) study is the largest prospective cohort of idiopathic TTP cases to date. Methods: Patients with first episode of idiopathic TTP were enrolled at 11 sites in the US. Exclusion criteria include solid organ or allogeneic stem cell transplant, anti-neoplastic therapy or malignancy. All patients underwent therapeutic plasma exchange (TPE). Remission is defined as platelet count >150,000/mm3. ADAMTS13 activity was measured by fluorescence resonance energy transfer assay (FRETS-vWF73, Peptides Int.). ADAMTS13 inhibitor was assessed by ELISA (Technozym ADAMTS13 INH ELISA, Technoclone) and functional inhibition of normal ADAMTS13 activity (modified FRETS). Differences between the groups was evaluated by Chi-square test, t-test or Fisher’s exact test. Results: Complete data is available for 57 cases. 84% were female & median age was 42. ADAMTS13 was severely deficient (<10%) in 53%, moderate (10–50%) in 8%, & normal (>50%) in 39%. Adverse events were frequent & most commonly include citrate toxicity and allergic reactions. Long-term followup was available for 56 patients, and overall relapse rate was 25% with median time to relapse of 11 months. The relapse rate was 41% in patients with severe ADAMST13 deficiency & 0% in patients with normal ADAMTS13 activity (p=0.0077). Conclusions: Severe ADAMTS13 deficiency does not define all cases of idiopathic TTP, yet is associated with a unique syndrome characterized by severe thrombocytopenia, normal renal function, presence of ADAMTS13 neutralizing autoantibodies & high risk of relapse. Non-ADAMTS13 deficient idiopathic TTP has clinical features similar to thrombotic microangiopathies associated with stem cell transplant or drugs such as quinine, yet has a better than expected overall survival after TPE. There is likely an alternate disease mechanism for this cohort, possibly immunologic, which may be responsive to TPE and warrants further study. ADAMTS13 < 10% n=30 ADAMTS13 > 50% n=22 p-value * t-test, ** Fisher’s Exact Test, # Chi-Square Test Presenting Labs Hemoglobin (mean) 8.5 9.2 0.22* Platelet count (mean x10^9/L) 19 57 <0.0005* Serum creatinine (mean) 1.33 3.9 0.0012* ADAMTS13 antibody (neutralizing & non-neutralizing) % 100 63.6 0.0004** ADAMTS13 neutralizing antibody % 83 35 .0003# Presenting Symptoms Neurologic symptoms present 45 52.4 0.23# Diarrhea 23 30.4 0.79# Infection 40 43.5 0.79# Past Medical History Connective Tissue Disease % 10 8.5 0.28# Family history of TTP % 0 4.6 0.11# Remission Labs Hemoglobin (mean) 12.2 8.5 0.16* Platelet count (mean x10^9/L)) 169 152 0.15* Serum creatinine (mean) 1.02 3.7 0.0009* Outcomes Therapy-related Adverse events % 71 55 0.24# Time (days) to remission (plt > 150,000) 9.7 9.2 0.89* Early remission (< 8 days) % 73 57 0.20# 30 day Exacerbation rate % 35 28 0.63# 30 day Survival % 96.6 90.0 0.56** Long-term Relapse % 41 0 0.0077**
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Maltese, Adam V. "Is American Science in Decline? by Yu Xie and Alexandra A. Killewald. Harvard University Press, Cambridge, MA, USA, 2012. x + 230 pp. ISBN 978-067-405-242-0." Science Education 97, no. 3 (April 15, 2013): 494–96. http://dx.doi.org/10.1002/sce.21053.
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Kosaka, Yumi, Tomoki Kimura, Tomokazu Kawaoka, Yutaro Ogawa, Kei Amioka, Kensuke Naruto, Yuki Yoshikawa, et al. "Hepatic Arterial Infusion Chemotherapy Combined with Radiation Therapy for Advanced Hepatocellular Carcinoma with Tumor Thrombosis of the Main Trunk or Bilobar of the Portal Vein." Liver Cancer 10, no. 2 (2021): 151–60. http://dx.doi.org/10.1159/000513706.
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<b><i>Background:</i></b> Overall survival of patients with advanced hepatocellular carcinoma (HCC) with Vp4 (tumor thrombosis of the main trunk or bilobar of the portal vein) is extremely poor. <b><i>Purpose:</i></b> The purpose of this study is to clarify the prognosis of hepatic arterial infusion chemotherapy (HAIC) combined with radiation therapy (RT) for advanced HCC with Vp4 and to analyze the factors that contribute to the prognosis. <b><i>Methods:</i></b> In this retrospective cohort study, 51 HCC patients who were treated with HAIC and RT for portal vein tumor thrombosis and met the following criteria were enrolled: (i) with Vp4; (ii) Child-Pugh score of 5–7; (iii) Eastern Cooperative Oncology Group performance status of 0 or 1; (iv) no history of systemic therapy; and (v) from September 2004 to April 2019. <b><i>Results:</i></b> Median overall survival and median progression-free survival were 12.1 and 4.2 months, respectively. Multivariate analysis showed >50% of relative tumor volume in the liver (HR, 3.027; <i>p</i> = 0.008) and extrahepatic spread with (HR, 3.773; <i>p</i> = 0.040) as significant and independent factors of OS. The total overall response rate (ORR) was 19.6%; ORR in main tumor was 13.7%; and ORR in Vp4 was 51.0%. None of the patients who received HAIC combined with RT for advanced HCC with Vp4 developed hepatic failure. This combination therapy of HAIC with RT was safe and well tolerated in all cases. <b><i>Conclusion:</i></b> Combination therapies of HAIC and RT might be good therapy for advanced HCC with Vp4.
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Roberts, Edward. "Évêques entre Bourgogne et Provence. La province ecclésiastique de Vienne au haut Moyen Âge (Ve-XIe siècle). By NathanaëlNimmegeers. Rennes: Presses universitaires de Rennes. 2014. 402 pp. + 11 colour plates. €24. ISBN 978 2 7535 2884 0." Early Medieval Europe 25, no. 1 (January 6, 2017): 130–33. http://dx.doi.org/10.1111/emed.12196.
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Passamonti, Francesco, Vannucchi Alessandro, Caramazza Domenica, Rambaldi Alessandro, Morra Enrica, Kiladjian Jean Jacques, Rami S. Komrokji, et al. "A New International Multicenter-Based Model to Predict Survival in Myelofibrosis Secondary to Polycythemia and Thrombocythemia: The Mysec Prognostic Model (MYSEC-PM)." Blood 124, no. 21 (December 6, 2014): 1826. http://dx.doi.org/10.1182/blood.v124.21.1826.1826.
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Abstract Background. Polycythemia vera (PV) and essential thrombocythemia (ET) are chronic myeloproliferative neoplasms that can progress to secondary myelofibrosis (MF), named post-PV (PPV) MF and post-ET (PET) MF. While outcome of primary myelofibrosis is defined on the basis of the IPSS models, information on outcome of secondary myelofibrosis (SMF) is scant. The objective of this study is to develop a prognostic model to predict survival of SMF. Patients and Methods.A total of 718 patients from 16 international Centers were included in this study. Diagnosis of PPV-MF and PET-MF was according to the IWGMRT criteria. Since survival varied among centers, statistical analyses took into account this cluster effect. Survival was calculated utilizing Kaplan-Meier estimates for univariate categorical risk factors and Cox proportional hazard regression, when performing multivariate analysis. The log-rank test was applied to compare Kaplan-Meier curves. Survival was censored at date of stem cell transplant, splenectomy or trial enrollment. Results. Among 718 SMF, 364 (51%) were PET-MF and 354 (49%) PPV-MF. The median follow-up was 2.4 years (range, 0.6-20.1). Median age was 64 years (range, 25-96), 370 were males (52%). Median time from PV/ET diagnosis to SMF diagnosis was 10.6 years (range, 2.5-41). Median values of hemoglobin, white blood cell count and platelet count were 11.2 g/dL (range, 5-17), 10.2 x10(9)/L (range, 1.1-98.4) and 343 x10(9)/L (range, 16-1908), respectively. Splenomegaly was present in 606 patients (87%) and constitutional symptoms in 329 (47%). Cytogenetic profile (N= 338) was normal in 222 (66%), unfavorable in 40 (12%), abnormal but favorable in 76 (22%), and the JAK2 (V617F) mutation (N=679) in 73%. Anemia, leukocytosis, thrombocytopenia, advanced age, circulating blasts, JAK2(V617F), constitutional symptoms, time to SMF, history of thrombosis negatively affected survival in univariate analysis (maximum P values, 0.043), while type of diagnosis (PPV, PET), splenomegaly, spleen size, cytogenetics, and cardiovascular risk did not. Since survival did not differ between PPV and PET, multivariable analysis was carried out on a subset of 493 SMF patients randomly selected and stratified by diagnosis from the original cohort of 718 patients to generate the MYSEC-PM. The remaining 225 were used as validation cohort. By multivariable analysis, age over 65 years (Hazard Ratio –HR- 2.6, 95%CI: 1.5-4.4; p<0.0001), time from PV/ET to SMF exceeding 15 years (HR 1.7, 95%CI: 1.3-2.2, p<0.0001), history of thrombosis (HR 2.1, 95%CI: 1.2-3.6, p=0.01), presence of constitutional symptoms (HR 1.8, 95%CI: 1.3-2.6; p=0.001), hemoglobin level less than 10 g/dl (HR 1.5, 95%CI: 1.1-2.0, p=0.004) and circulating blast cells equal to or higher than 1% (HR 2.1, 95% CI: 1.5-2.8, p< 0.0001) retained their significant impact of survival. To develop the prognostic model, we assigned each factor an integer weight closest to the corresponding HR in 421 patients with all available data: age >65 years (3 points), time to SMF >15 years (2 points), history of thrombosis (2 points), constitutional symptoms (2 points), hemoglobin <10 g/dL (1 point) and circulating blast >= 1% (2 points). To facilitate the use in clinical practice, the MYSEC-PM was recoded into three broader categories: low-risk (score, 0 to 2), intermediate-risk (score, 3 to 6), high-risk (score >6). Survival was significantly different among the risk groups (Figure 1, p< 0.0001): median survival and its 95% CI was not reached in low-risk, 7.9 years (95% CI: 6.7-9.3) in intermediate and 3.8 (95% CI: 2.2-5) in high-risk. The predictive value of MYSEC-PM was confirmed in the validation cohort (N=190) with the maximum p value in pairwise comparisons of 0.01. In the validation cohort, by Akaike information criterion, MYSEC-PM model better predicted survival than the IPSS/DIPSS models (N=190, AIC, 330.5 vs. 336.5 vs. 334.3, respectively) and also compared to the DIPSS-plus (N=91, 103.8 vs. 106.5, respectively): lower score implies better prediction. Conclusions. The MYSEC prognostic model, based on age >65 years, time to SMF >15 years, previous thrombosis, constitutional symptoms, hemoglobin <10 g/dL and circulating blast equal or >1%, clearly distinguishes outcome of patients with SMF and outperforms PMF risk models among those patients. This model can be considered for tailoring treatment according to disease risk in SMF. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Baddam, Sujatha, Jose Cavo, and Jorge Diaz Castro. "Cytomegalovirus Induced Thrombocytopenia with No Platelets in an Immunocompetent Young Male." Blood 134, Supplement_1 (November 13, 2019): 4904. http://dx.doi.org/10.1182/blood-2019-132257.
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Introduction Immune thrombocytopenic purpura (ITP) is a common cause of acquired thrombocytopenia in an otherwise asymptomatic adult. It is generally believed to be caused by auto- antibodies against platelet antigens that destroy platelets peripherally and autoreactive cytotoxic T cells, as well as humoral and cellular autoimmunity directed at megakaryocytes, causing impaired platelet production. Cytomegalovirus (CMV) is a known cause of cause of morbidity and mortality in patients with immunosuppressed states, whereas in immunocompetent patients, it commonly manifest as asymptomatic or mononucleosis like syndrome. We are presenting a case of CMV induced thrombocytopenia with severe epistaxis and platelet count of 0 x10 9 in an otherwise healthy immunocompetent male who failed to improve after standard treatments with high dose steroids and intra venous immune globulin (IVIG). Case Description A 36-year-old Caucasian male without any past medical history presented to emergency room (ER) with flu like symptoms for five days associated with subjective fevers, anorexia, nausea, cough and weight loss of 15 lb. in two weeks. He also reported possible tick bite while working in the yard two days prior to admission. No dizziness, vomiting, diarrhea or any bleeding were reported. Denied any smoking, alcohol use or any illicit drug use. No significant family history was reported. On evaluation he was afebrile, normotensive with normal heart rate and respiratory rate. Physical examination was unremarkable. Initial laboratory data revealed hemoglobin of 11.2, platelet count 4 x109, white cell count of 13,100 with 4.5% atypical lymphocytes, aspartate aminotransferase of 41, alanine aminotransferase of 49, and creatinine of 1.4. He tested positive for Influenza A, CMV Immune globulin (Ig)M and IgG antibody. Serological tests for tick panel including anaplasma, babesia, Lyme disease and ehrlichia were negative. Epstein-Barr virus (EBV) antibody, parvo virus antibody, hepatitis screen, HIV screen, auto antibodies including anti-nuclear antibody and anti-double stranded DNA were negative. Coombs test was negative. Further work up includes ADAMTS13 activity was normal. No laboratory evidence of ADAMTS13 deficiency. After excluding all other causes, diagnosis of ITP was made. He was started on Tamiflu for Influenza A and high dose intra venous (IV) methyl prednisone for ITP. After platelet transfusion and two days of IV steroids platelet count improved 43 x 109 and he was discharged home with prolonged prednisone taper. Five days later, he presented to ER with severe epistaxis. Laboratory data revealed platelet count of 0 x109. Serum CMV-DNA was determined by PCR showed viral load of 8,790 copies/ml. Ultrasound abdomen showed mild splenomegaly. He received three doses of IVIG (1g/kg). Platelet count failed to improve after administration of IVIG. Bone marrow biopsy revealed hyper cellular marrow with trilineage hematopoiesis with no increase in CD 34 blasts. Per infectious disease and hematology recommendations, he was started on valganciclovir (900 mg PO BID). One month later, platelet count improved to 150 x 109 and CMV viral load dropped to 413 with subsequent resolution of patient's symptoms. Discussion Secondary ITP is an acquired thrombocytopenia caused by autoantibodies against platelets. Many patients with ITP are asymptomatic. For those who do have symptoms, initial presentations of ITP are petechiae, purpura and epistaxis, with a more severe progression to intracranial hemorrhage or gastrointestinal bleeding leading to a fatal outcome, if treatment is not started on a promptly manner. CMV induced thrombocytopenia in immunocompetent adults seems to be rare. we are presenting a case of CMV induced ITP which failed to improve after standard treatment with high dose steroids and IVIG but responded to anti-viral therapy with valganciclovir. In conclusion, it may be worthwhile to test for CMV infection in patients presenting with ITP. Further research is needed in order to establish treatment guidelines for CMV induced ITP in immunocompetent adults. Disclosures No relevant conflicts of interest to declare.
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Ajzenberg, Nadine, Dorothee Faille, Marie-Genevieve Huisse, Anh Hong Cung, Lamia Lamrani, Nicolas Dumontier, Martine Jandrot-Perrus, Bruno Cassinat, Christine Chomienne, and Christine Dosquet. "Aspirin in Philadelphia-Negative Myeloproliferative Neoplasms: What Is the Optimal Dose ?" Blood 124, no. 21 (December 6, 2014): 3200. http://dx.doi.org/10.1182/blood.v124.21.3200.3200.
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Abstract Background: Myeloproliferative neoplasms (MPN) are associated with an increased risk of arterial and venous thrombosis with an annual incidence varying from 1.1% to 6.6% (Patrono, Blood 2013). Comparable to that recommended in non-MPN high-risk patients, low-dose aspirin (81-100 mg/day) is recommended in primary and secondary prophylaxis of thrombosis in polycythemia vera and essential thrombocytemia (Tefferi, Am J Hematol 2012). However, the daily dose of aspirin to optimize efficacy and safety for MPN patients has never been challenged. Aim of the study: Determine the optimal dose of aspirin to achieve biological efficacy in Philadelphia-negative MPN patients. Methods: Patients with Philadelphia-negative MPN who were treated with low-dose aspirin 75 or 100 mg/day were enrolled in this observational study. Patients without any cytostatic drug and patients treated with either pegylated interferon alpha or hydroxyurea were eligible. Major exclusion criteria included inability to adhere to aspirin therapy and chronic oral anticoagulation. Biological efficacy to aspirin was evaluated by platelet aggregation induced by arachidonic acid 1.33 mM on platelet rich plasma and tested at trough level and 24 hours after last aspirin intake. Resistance to aspirin was defined as a maximal platelet aggregation over 20%. According to the results of platelet aggregation, aspirin dose and dosing regimen were modified as follows: from 100 mg/day to 160 mg/day or 75 mg x2/day. Patients enrolled in this have a median follow up of at least 6 months after the analysis. Results: Between January 2012 and February 2014, 77 patients with Philadelphia-negative MPN were included. 53 were treated with aspirin 75 mg/day (69%) and 24 with aspirin 100 mg/day (31%). Out of the 53 patients treated with aspirin 75 mg/day, 12 patients (23%) were resistant to aspirin. Resistance to aspirin was not correlated to sex, age, presentation, JAK2 status, treatment, history of thrombotic or bleeding and hematologic values (see following table). Table 1:The MPN Grade 1 Fibrosis PhenotypePMF (N:33)PV/ET (N:58)Total (N:91)Median age63 yrs55 yrs58 yrsSex1:31:11:2JAK V617F +16/33: (49%)40/58: (69%)56/91: (62%)Median Hgb(g/dL)11.9 (range 7.9-16.4)12.5 (range 8.0-19.8)12.2 (range 7.9-19.8)Median WBC(X10 (9))26.9 (range 1.3-188)8.9 (range 3.5-51.3)10.8 (range 1.3-188 )Median Platelet(X10 (9))179 (range 18.0-1194)505 (range 67-2286)370 (range 18-2286)Leukoerythroblastic Blood Smear15/33 (45%)PV: 17 ET: 5 Total: 22/58 (38%)37/91 (41%)Splenomegaly(cm below costal margin)18/33: (55%) Median: 1025/58: (43%) Median: 643/91(48%) Median: 4Transfusion dependence6/33: (18%)2/58: (4%)8/91: (9%)Presence Of ³ 1 symptom 17/33: (52%)33/58: (57%)50/91: (55%)DIPSS risk intermediate 2 or higher13/33: (39%)17/58: (29%)30/91: (33%)2 or more prior therapies9/33: (27%)36/58: (62%)45/91: (49%)Vital Status (Alive)25/33: (76%)53/58: (91%)78/90: (86%)Median follow up time (yrs)1.9 (range 0.1-9.8)5.7 (range 0-34.5)3.1 (range 0-34.5) An increased dose of 100 mg/day for at least 7 days overcame this biological resistance in 8 out of 8 re-tested patients. The 2 remaining 75mg resistant patients received an increased dose of aspirin but were not retested. Out of the 24 patients under 100 mg/day, only two (8%) were resistant to aspirin. In these patients, increasing the dose to 160 mg/day did not modify their biological response. However a 75 mgx2 /day was effective to overcome biological resistance. No thrombotic or bleeding event was observed during the 6-month follow-up regardless of the aspirin dose. Conclusions: This is the first study to measure in standardized conditions the biological resistance of aspirin in 77 well-characterized Philadelphia-negative MPN patients. Although this does not reach statistical significance a higher proportion of patients treated with aspirin 75mg/day was resistant to anti-platelet therapy compared to patients treated with aspirin 100 mg/day. Increasing the dose of aspirin from 75 to 100 mg once daily overcomes this biological resistance without increasing bleeding side effects and seems the best compromise. Interestingly in rare cases of extreme resistance to 100mg doubling the dose twice daily (75mgX2) was better than an increase of 160mg in one take. This pilot study on a small number of patients with a limited 6-month follow up compared to the low annual incidence of thromboses in these MPNs will be followed by a prospective study on a larger number of patients with an extended follow-up period to determine if biological resistance to aspirin is correlated to the occurrence of thrombotic events. Disclosures No relevant conflicts of interest to declare.
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Impey, Edward. "La Ville de Cluny et ses Maisons: Xle-XVe siècles. By Pierre Garrigou Grandchamp, Michael Jones, Gwyn Meirion-Jones and Jean-Denis Salveque, with the participation of Susan Content, Philip Dixon, Frederic Guibal, Georges Lambert, Catherine Lambert, Catherine Lavier, Roger Leech and Brigitte Maurice. 320mm. Pp 247, ills. Paris: Picard, 1997. ISBN 2-7084-0516-0. FFr. 390.00." Antiquaries Journal 79 (September 1999): 422–23. http://dx.doi.org/10.1017/s000358150004484x.
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Ogawa, Chitose, Atsushi Manabe, Hiroaki Goto, Katsuyoshi Koh, Daisuke Tomizawa, Keitaro Fukushima, Ken-ichiro Watanabe, et al. "Phase I/II Clinical Trial of Erwinia Asparaginase (ErwinaseR) in Combination with Prednisolone, Vincristine and Pirarubicin in Children and Young Adults with Acute Lymphoblastic Leukemia (ALL) or Lymphoblastic Lymphoma (LBL)." Blood 124, no. 21 (December 6, 2014): 3657. http://dx.doi.org/10.1182/blood.v124.21.3657.3657.
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Abstract Introduction: L-asparaginase is an important component of multi-agent chemotherapy for children and young adults with ALL. In Japan, only one asparaginase preparation, native-E-coli-asparaginase (LeunaseR), has been approved so far by the Health, Labour and Welfare Ministry. The incidence of clinical allergy to native-E-coli -asparaginase can be more than 30% with repeated administration. To continue treatment with asparaginase, Erwinia asparaginase (ErwinaseR), deriving from Erwinia chrysanthemi, is recommended for patients who develop clinical allergy to native-E-coli-asparaginase, because the drug has no cross reactivity. We planned phase I/II trial OP-01-001 to investigate the safety and efficacy of Erwinase in combination chemotherapy consist of prednisolone, vincristine and pirarubicin. Patients and Methods: Eligible patients on this study were children and young adults with ALL/ LBL in remission, >=1 to =<25 years of age, and had developed allergy to E-coli-asparaginase. Patients with a history of pancreatitis or previous administration of Erwinase were excluded. The study was approved by IRB at each institution and patients/guardians provided informed consent/assent. In this trial regimen OP-01-001, level 1 (25,000) or level 0 (20,000 IU/m2) x 6 doses of Erwinase were planned to administer intramuscularly (IM) on day 2, 5, 7, 9, 11 and 13 with 40 mg/m2/day x15 days of prednisolone, 1.5mg/m2 x 3 doses of vincristine and 20 mg/m2x 2 doses of pirarubicin. In phase I, we determined the maximum tolerated dose, dose limiting toxicity (DLT), and the recommended phase II dose (RP2D) of Erwinase. Safety, efficacy and pharmacokinetic/dynamic study were evaluated in all patients. Blood samples were obtained at scheduled time points during Erwinase therapy and assayed for asparaginase activity and asparagine concentration in plasma. Primary endpoint was asparaginase activity in plasma at 48h after the first dosing. Results: A total of 24 eligible patients were enrolled to phase I/II study from February 2012 to January 2014. In phase I study, 6 eligible/evaluable patients were enrolled to level 1, starting at 25,000 IU/m2. Since all patients completed the scheduled treatments without DLT in level 1, RP2D was determined 25,000 IU/m2and 18 patients were enrolled in phase II study. PK, PD, safety and efficacy were evaluated as phase I/II study. The median age of 24 evaluated patients was 7.5 years (range 2-16) and 15 patients (62.5%) were male. In PK/PD study, one patient was excluded because essential clinical dataset was not obtained. After the first dosing, serum asparaginase activity exceeded 0.1 IU/mL in 23/23 patients (100%) at 48 hours and it did in 18/23 patients (78.3%) at 72 hours. After the sixth dosing, the activity at 72 hours was higher than 0.1 IU/mL in 19/23 (82.6%). Plasma asparagine was significantly depleted (<1.0 μM) in 22/23 (95.7%) 48 hours after the first dosing and it was also depleted in 22/23 (95.7%) 72 hours after the last dosing in all but one patients. All patients maintained remission status during the trial. No allergic reaction related to Erwinase was reported. Hypertriglyceridemia or blood triglycerides increased was reported in 12/24 (50%), 4 cases in grade 3 and 1 in grade 4. Increase in blood sugar was observed in 3 patients (12.5%), 2 in grade 1 and 1 in grade 2. In addition, 23 (95.8%) and 1 (4.2%) developed decrease in fibrinogen and increase in ammonia at grade 2-4. Grade 3 febrile neutropenia and bacteremia were reported in 8 patients (33.3%) and in 1 patient (4.2%), respectively. There were no reports of hemorrhage, thrombosis, pancreatitis, or death. Conclusion: Erwinase as administered using the OP-01-001 regimen was well tolerated without unexpected toxicities and achieved good serum asparaginase activity at both 48 and 72 hours after dosing. In previous reports, a much lower dose of Erwinase at 10,000 IU/m2/dose was used in the study of EORTC (Duval M. Blood 2002;99:2734), which was subsequently assessed as suboptimal and the identical dose of erwinase at 25,000 IU/m2/dose was used in the study of COG (Salzer WL. Blood 2013;122:507). We herein showed that following allergy to E-coli native-asparaginase, erwinase 25,000 IU/m2 x 6 doses IM in 2 or 3 days interval in 2 weeks was effective and safe in children and young adults in Japan. Disclosures Ogawa: OHARA Pharmaceutical Co., Ltd.: Honoraria. Manabe:OHARA Pharmaceutical Co., Ltd.: Honoraria. Fukushima:OHARA Pharmaceutical Co., Ltd.: Honoraria. Horibe:OHARA Pharmaceutical Co., Ltd.: Honoraria. Hamada:OHARA Pharmaceutical Co., Ltd.: Employment. Ohara:OHARA Pharmaceutical Co., Ltd.: Honoraria.
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Gazal, Stav, Eyal Lebel, Yosef Kalish, Chen Makranz, Moshe E. Gatt, Neta Goldschmidt, and Boaz Nachmias. "Venous Thromboembolism Prophylaxis with Low-Molecular-Weight Heparin in Primary Central Nervous System Lymphoma." Oncology Research and Treatment, December 9, 2020, 1–6. http://dx.doi.org/10.1159/000512241.
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<b><i>Background:</i></b> Venous thromboembolism (VTE) is a frequent, potentially lethal complication in individuals with cancer. Patients with brain tumors are at particularly high risk for VTE. Primary central nervous system lymphoma (PCNSL) is a rare subtype of diffuse large B cell lymphoma, involving the craniospinal axis. The incidence of VTE in patients with PCNSL was reported as very high, occurring mostly in the early period of therapy. <b><i>Objectives:</i></b> We aimed to evaluate the efficacy and safety of prophylactic low-molecular-weight heparin (LMWH) throughout the treatment of PCNSL. <b><i>Patients:</i></b> All patients >18 years of age diagnosed and treated for PCNSL at our institution in 2005–2017 were included. <b><i>Results:</i></b> There were 44 patients; mean age at diagnosis was 61.5 years. Three patients (6.8%) had a personal history of thrombosis, 11 (25%) had a history of diabetes or smoking, and 32 (72%) had an Eastern Cooperative Oncology Group performance status of 0–1 at diagnosis. During treatment with LMWH, no VTE events were recorded; 2 (4.5%) patients experienced a minor bleeding event and 1 (2.3%) a major bleeding event. <b><i>Conclusions:</i></b> Among our 44 patients with PCNSL treated with prophylactic LMWH, no VTE events were recorded, and only 1 (asymptomatic) intracranial bleed was recorded. Within the limitations of a retrospective nonrandomized study, our findings suggest that VTE prophylaxis may be beneficial for individuals with PCNSL.
Dissertations / Theses on the topic "History.#x1E; 0"
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Boutaghou, Maya. "Roman historique, novation littéraire et identité culturelle à l'aube du XXe siècle : autour de quatre romans historiques : Australie, Bengale, Egypte, Mexique." Limoges, 2007. http://aurore.unilim.fr/theses/nxfile/default/597f4f07-3169-4922-857f-2dfa5fd2ca4a/blobholder:0/2006LIMO2021.pdf.
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A la fin du XIXe siècle, les empires coloniaux connaissent une modernisation culturelle et sociale en réponse au choc des cultures, et un éveil des consciences politiques stimulées par les idées des Lumières et les révolutions européennes. Le roman historique apparaît tel un outil de modélisation d'une conscience historique et de création d'une identité culturelle moderne. A partir de quatre romans historiques principaux : "El Cerro de las campanas" de Juan Antonio Mareos (Mexique, 1868) ; "His natural life" de Marcus Clarke (Australie, 1874) ; "Anandamath" de Bankin Chatterjee (Bengale, 1882) ; "Al Abbassa" de Jurji Zaydan (Egypte, 1906), nous analysons l'émergence du roman, dans des traditions diverses, selon trois approches : structurale, intertextuelle et esthétique, lesquelles révèlent les stratégies rhétoriques de ces écrivains réformateurs et, depuis le discours esthétisé du roman historique postcolonial, interrogent le rapport entre Histoire, littérature et politique.
Books on the topic "History.#x1E; 0"
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F, Cunha Stephen, ed. Our fifty states. Washington, D.C: National Geographic Society, 2004.
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F, Cunha Stephen, and Smith Whitney, eds. Our fifty states. Washington, DC: National Geographic, 2004.
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Fernand, Braudel. Hylikos politismos, kapitalismos, kai oikonomia: XVe-XVIIIe aiōnas. Athēna: Morphōtiko Institouto Agrotikēs Trapezas, 1995.
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(Editor), Oliver Jensen, ed. Bruce Catton's America: Selections from his Greatest Works. Promontory Press, 1993.
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Emily Makes a Difference: A Time of Progress and Problems (1893) (Sisters in Time #16). Barbour Publishing, Incorporated, 2004.
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McFarland, Ben. "Unfolding the Periodic Table." In A World From Dust. Oxford University Press, 2016. http://dx.doi.org/10.1093/oso/9780190275013.003.0007.
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Our starting point is not hidden, nor is it far off. It is not an extreme place like Mono Lake or Freswick Castle, but it is a central concept expressed on a single page. The periodic table is the center of chemistry, and therefore of this book. You can spot it at a distance from its vaguely cathedral-like shape. You can see the chemical symbols that it contains on magnets and T-shirts and restaurant signs. Its regular columns are not quite symmetric, but that is because it has been twisted out of its natural shape by the contingencies of history. Rearrange it just a little and a simple mathematical pattern appears. To see this pattern, imagine that the periodic table is made out of beads on an abacus, arranged in the familiar U shape. Then push all the beads to the left: … Row 1 = H- He Row 2 = Li- Be- B- C- N- O- F- Ne Row 3 = Na- Mg- Al- Si- P- S- Cl- Ar Row 4 = K- Ca- Sc- Ti- V- Cr- Mn- Fe- Co- Ni- Cu- Zn- Ga- Ge- As- Se- Br- Kr Row 5 = Rb- Sr- Y- Zr- Nb- Mo- Tc- Ru- Rh- Pd- Ag- Cd- In- Sn- Sb- Te- I- Xe … By row, there are 2, 8, 8, 18, and 18 elements. The pattern continues in the rows below, but it is obscured by the fact that on most tables 14 elements have been moved out of the sixth and seventh rows. On the table here I have put them where they belong. These rows have 32 elements each. This can be simplified even more. The rows increase, first by 2, then by 6 more (2 + 6 = 8), then by 10 more (2 + 6 + 10 = 18), then by 14 (2 + 6 + 10 + 18 = 32). The series 2, 6, 10, 14 is the doubles of counting up by odd numbers: 1, 3, 5, 7. Put another way, each row is equal to 2n + 1 with n = integers from 0.