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1. Sumariwalla PF, Cao Y, Wu HL, Feldmann M, Paleolog EM: The angiogenesis inhibitor protease-activated kringles 1-5 reduces the severity of murine collagen-induced arthritis. Arthritis Res Ther; 2003;5(1):R32-9
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  • During rheumatoid arthritis there is enlargement and increased cellularity of the synovial lining of joints, before invasion by the synovium of the underlying cartilage and bone.
  • This increased tissue mass requires a network of blood vessels to supply nutrients and oxygen.
  • Disruption of synovial angiogenesis is thus a desirable aim of antiarthritic therapies.
  • The purpose of the present study was to assess the effect on murine arthritis of K1-5.
  • Treatment with K1-5 was commenced on the day of arthritis onset and continued for 10 days, until the end of the experiment.
  • The clinical efficacy of this treatment was reflected by a reduction in joint inflammation and destruction, as assessed histologically.
  • These data suggest that antiangiogenic therapies, which block formation of new blood vessels and hence reduce synovial expansion, might be effective in treating rheumatoid arthritis.
  • [MeSH-major] Angiogenesis Inhibitors / chemistry. Arthritis / drug therapy. Peptide Fragments / chemistry. Plasminogen / chemistry
  • [MeSH-minor] Angiostatins. Animals. Collagen. Joints / pathology. Kringles. Male. Mice. Mice, Inbred DBA. Urokinase-Type Plasminogen Activator / metabolism

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  • (PMID = 12716451.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Peptide Fragments; 86090-08-6 / Angiostatins; 9001-91-6 / Plasminogen; 9007-34-5 / Collagen; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
  • [Other-IDs] NLM/ PMC154428
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2. Klion AD, Robyn J, Akin C, Noel P, Brown M, Law M, Metcalfe DD, Dunbar C, Nutman TB: Molecular remission and reversal of myelofibrosis in response to imatinib mesylate treatment in patients with the myeloproliferative variant of hypereosinophilic syndrome. Blood; 2004 Jan 15;103(2):473-8
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  • [Title] Molecular remission and reversal of myelofibrosis in response to imatinib mesylate treatment in patients with the myeloproliferative variant of hypereosinophilic syndrome.
  • We recently described a subset of patients with a myeloproliferative variant of hypereosinophilic syndrome (MHES) characterized by elevated serum tryptase levels, increased atypical mast cells in the bone marrow, tissue fibrosis, and the presence of the fusion tyrosine kinase, FIP1L1-PDGFRalpha, which is a therapeutic target of imatinib mesylate.
  • Clinical improvement and resolution of eosinophilia was observed in all patients, although cardiac dysfunction, when present, was not altered by therapy.
  • Reversal of bone marrow pathology, including increased cellularity, the presence of spindle-shaped mast cells, and myelofibrosis, was evident in all patients at 4 to 8 weeks following initiation of therapy.
  • Serum tryptase levels declined rapidly to normal levels in all patients and remained in the normal range throughout therapy.
  • The lack of reversal of cardiac abnormalities and persistence of the F/P mutation in some patients suggests that early intervention with higher doses of imatinib mesylate may be desirable in the treatment of patients with MHES.
  • [MeSH-major] Hypereosinophilic Syndrome / drug therapy. Piperazines / therapeutic use. Primary Myelofibrosis / drug therapy. Pyrimidines / therapeutic use

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  • (PMID = 14504092.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Interleukin-2; 8A1O1M485B / Imatinib Mesylate
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3. Campos HS, Xisto DG, Oliveira MB, Teixeira I, Negri EM, Mauad T, Carnielli D, Lima LM, Barreiro EJ, Faffe DS, Zin WA, Lapa e Silva JR, Rocco PR: Protective effects of phosphodiesterase inhibitors on lung function and remodeling in a murine model of chronic asthma. Braz J Med Biol Res; 2006 Feb;39(2):283-7
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  • The aim of the present study was to compare the efficacy of a novel phosphodiesterase 4 and 5 inhibitor, LASSBio596, with that of dexamethasone in a murine model of chronic asthma.
  • Airway resistance, viscoelastic pressure and static elastance increased significantly in the asthma group (77, 56, and 76%, respectively) compared to the control group.
  • Both LASSBio596 and dexamethasone inhibited the changes in lung mechanics, tissue cellularity, bronchoconstriction, as well as airway and lung parenchyma remodeling.

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  • (PMID = 16470317.001).
  • [ISSN] 0100-879X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / LASSBIO596; 0 / Phosphodiesterase Inhibitors; 0 / Phthalic Acids; 0 / Phthalimides; 0 / Sulfonamides; 7S5I7G3JQL / Dexamethasone
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4. Hiçsönmez G, Tunç B, Olcay L, Tuncer MA: Effect of short-course, high-dose steroid therapy in a child with myelodysplastic syndrome. Pediatr Hematol Oncol; 2001 Dec;18(8):525-9
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  • [Title] Effect of short-course, high-dose steroid therapy in a child with myelodysplastic syndrome.
  • Here the beneficial effect of short-course HDMP therapy in a child with myelodysplastic syndrome (MDS) is reported.
  • Oral methylprednisolone sodium succinate (Prednol-L) was administered at a single daily dose of 30 mg/kg for 5 days to a 4-year-old girl with refractory anemia with excess of blasts and hypocellular bone marrow before the initiation of chemotherapy.
  • In addition to dramatic clinical improvement, the patient's white blood cell count increased from 2.3 x 10(9)/L to 5.0 x 10(9)/L, and peripheral blood blast cells disappeared 4 days after HDMP treatment.
  • Repeated bone marrow aspirate 1 week after the initiation of HDMP disclosed increased cellularity with no blasts.
  • Furthermore, short-course HDMP treatment stimulated the increase in the number of peripheral blood lymphocytes and CD3+, CD4+, CD8+, CD19+, CD34+, and NK cells.
  • Results obtained with HDMP from the previous studies and the present case suggest that high-dose methylprednisolone is a promising agent in the treatment of AIDS and it is recommended as an initial treatment especially for MDS children with hypocellular bone marrow at presentation.
  • [MeSH-major] Methylprednisolone Hemisuccinate / administration & dosage. Myelodysplastic Syndromes / drug therapy. Steroids / administration & dosage
  • [MeSH-minor] Anemia, Refractory, with Excess of Blasts / drug therapy. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Blood Cell Count. Bone Marrow / drug effects. Bone Marrow / pathology. Child, Preschool. Female. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Remission Induction. Treatment Outcome


5. Hasserjian RP, Boecklin F, Parker S, Chase A, Dhar S, Zaiac M, Olavarria E, Lampert I, Henry K, Apperley JF, Goldman JM: ST1571 (imatinib mesylate) reduces bone marrow cellularity and normalizes morphologic features irrespective of cytogenetic response. Am J Clin Pathol; 2002 Mar;117(3):360-7
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  • [Title] ST1571 (imatinib mesylate) reduces bone marrow cellularity and normalizes morphologic features irrespective of cytogenetic response.
  • The tyrosine kinase inhibitor STI571 (imatinib mesylate, Gleevec) is an effective treatment for chronic myeloid leukemia (CML).
  • We examined bone marrow samples from 53 patients with CML who were receiving STI571 in 3 multicenter phase 2 trials to assess morphologic changes and cytogenetic response to this drug.
  • In most patients with initially increased blasts, the bone marrow blast count rapidly decreased during STI571 therapy.
  • Reductions in cellularity, the myeloid/erythroid ratio (commonly with relative erythroid hyperplasia), and reticulin fibrosis (if present pretreatment) also were seen in most patients, resulting in an appearance resembling normal marrow in many cases.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • [CommentIn] Am J Clin Pathol. 2002 Mar;117(3):355-7 [11888074.001]
  • (PMID = 11888075.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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6. Hast R, Hellström-Lindberg E, Ohm L, Björkholm M, Celsing F, Dahl IM, Dybedal I, Gahrton G, Lindberg G, Lerner R, Linder O, Löfvenberg E, Nilsson-Ehle H, Paul C, Samuelsson J, Tangen JM, Tidefelt U, Turesson I, Wahlin A, Wallvik J, Winquist I, Oberg G, Bernell P: No benefit from adding GM-CSF to induction chemotherapy in transforming myelodysplastic syndromes: better outcome in patients with less proliferative disease. Leukemia; 2003 Sep;17(9):1827-33
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  • [Title] No benefit from adding GM-CSF to induction chemotherapy in transforming myelodysplastic syndromes: better outcome in patients with less proliferative disease.
  • In this prospective randomized multicenter trial 93 patients, median age 72 years, with RAEB-t (n=25) and myelodysplastic syndrome (MDS)-AML (n=68) were allocated to a standard induction chemotherapy regimen (TAD 2+7) with or without addition of granulocyte-macrophage-CSF (GM-CSF).
  • Median survival times for all patients, CR patients, and non-CR patients were 280, 550, and 100 days, respectively, with no difference between the arms.
  • Response rates were significantly better in patients with serum lactate dehydrogenase (S-LDH) levels </=9.5 microkat/l, bone marrow cellularity </=70%, and WBC counts <4.0 x 10(9)/l, but S-LDH was the only variable independently associated with response by logistic regression analysis.
  • Cox's regression analysis identified four significant prognostic factors for survival: bone marrow cellularity, S-LDH, cytogenetic risk group (International Prognostic Scoring System), and age.
  • Only bone marrow cellularity (P=0.01) and S-LDH (P=0.0003) retained statistical significance in the log-rank test.
  • Thus, addition of GM-CSF to chemotherapy showed no clinical benefit in terms of response but carried an increased risk for side effects.
  • We present a clinically useful tool to predict response to chemotherapy and survival in elderly patients with transforming MDS, favoring patients with features of less proliferative disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid / drug therapy. Thioguanine / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Anemia, Refractory, with Excess of Blasts / drug therapy. Anemia, Refractory, with Excess of Blasts / pathology. Cell Transformation, Neoplastic. Female. Follow-Up Studies. Humans. Male. Middle Aged. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Prospective Studies. Remission Induction. Survival Rate

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  • (PMID = 12970783.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DAT protocol 1
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7. Chatterjee S, Vrolix G, Depoortere I, Peeters T, Van Marck E: The therapeutic effect of the neuropeptide hormone somatostatin on Schistosoma mansoni caused liver fibrosis. BMC Infect Dis; 2005;5:45
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  • [Title] The therapeutic effect of the neuropeptide hormone somatostatin on Schistosoma mansoni caused liver fibrosis.
  • Based on these results this paper explores the therapeutic potential of somatostatin in a mouse model of hepatic fibrosis associated with S. mansoni infections.
  • METHODS: Groups of outbred Swiss mice were infected with 100 S. mansoni cercariae, infection maintained till weeks 10 or 14, and then somatostatin therapy delivered in two regimens -- either a one or a two-day treatment.
  • All animals were sacrificed one week after therapy and controlled for liver, spleen and total body weight.
  • Circulating somatostatin levels in mice plasma were measured at the time of sacrifice by means of a radio-immuno assay.
  • Total liver and spleen weights of S. mansoni infected animals increased over time, with no changes observed due to somatostatin therapy.
  • Total body weights were decreased after infection but were not affected by somatostatin therapy.
  • Snap frozen liver sections were stained with haematoxylin-eosin or Masson's trichrome to study parasite count, hepatocyte status, granuloma size and cellularity.
  • After somatostatin treatment mean egg counts per liver section (43.76 +/- 3.56) were significantly reduced as compared to the egg counts in untreated mice after 10 weeks of infection (56.01 +/- 3.34) (P = 0.03).
  • Similar significant reduction in parasite egg counts were also observed after somatostatin treatment at 14 weeks of infection (56.62 +/- 3.02) as compared to untreated animals (69.82 +/- 2.77)(P = 0.006).
  • Fibrosis was assessed from the spectrophotometric determination of tissue hydroxyproline.
  • Infection with S. mansoni caused increased hydroxyproline levels (9.37 +/- 0.63 micromol at wk 10; 9.65 +/- 0.96 micromol at wk 14) as compared to uninfected animals (1.06 +/- 0.10 micromol).
  • This significant increase in collagen content (P = 0.01; 0.007 respectively) marks the fibrosis observed at these time points.
  • Treatment with somatostatin resulted in a significant decrease in hydroxyproline levels both at wk 10 (4.76 +/- 0.58 micromol) and at wk 14 (5.8 +/- 1.13 micromol) (P = 0.01; 0.03 respectively).
  • Endogenous somatostatin levels were increased at wk 10 (297 +/- 37.24 pg/ml) and wk 14 (206 +/- 13.30 pg/ml) of infection as compared to uninfected mice (119 +/- 11.99 pg/ml) (P = 0.01; 0.008 respectively).
  • Circulating somatostatin levels in infected animals were not significantly affected by somatostatin treatment.
  • Hepatocyte status remained unaltered and granulomas were not remarkably changed in size or cellularity.
  • We have previously shown that the somatostatin receptors SSTR2 and SSTR3 are present on the parasite egg and worms.
  • Our data suggest somatostatin may have therapeutic potential in S. mansoni mediated liver pathology.
  • [MeSH-major] Liver Cirrhosis / drug therapy. Liver Cirrhosis / parasitology. Schistosomiasis mansoni / complications. Somatostatin / pharmacology. Somatostatin / therapeutic use
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drug Administration Routes. Liver / pathology. Male. Mice. Organ Size. Spleen / pathology. Time Factors

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  • (PMID = 15949036.001).
  • [ISSN] 1471-2334
  • [Journal-full-title] BMC infectious diseases
  • [ISO-abbreviation] BMC Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 51110-01-1 / Somatostatin
  • [Other-IDs] NLM/ PMC1166555
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8. Pratheeshkumar P, Kuttan G: Ameliorative action of Vernonia cinerea L. on cyclophosphamide-induced immunosuppression and oxidative stress in mice. Inflammopharmacology; 2010 Aug;18(4):197-207
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  • Cyclophosphamide (CTX) is a widely used antineoplastic drug, which could cause toxicity to normal cells due to its toxic metabolites.
  • The present study reports the protective role of Vernonia cinerea L. against the CTX-induced toxicity in Balb/c mice.
  • Intraperitoneal administration of the extract significantly increased the total WBC Count, bone marrow cellularity, alpha-esterase positive cells, and weights of lymphoid organs in CTX-treated animals, when compared with CTX control mice.
  • Administration of V. cinerea was found to reduce the enhanced level of alkaline phosphatase, glutamate pyruvate transaminase, lipid peroxidation, and also significantly increased the reduced glutathione level in CTX-treated animals.
  • The lowered levels of other cytokines like IFN-gamma, IL-2, GM-CSF, after CTX treatment were also found to be increased by extract administration.
  • Methanolic extract of V. cinerea given intraperitoneally (i.p.) showed a significant chemoprotective activity without compromising the chemotherapeutic efficacy of CTX, indicating its possible use as an adjuvant during chemotherapy.
  • [MeSH-major] Cyclophosphamide / toxicity. Immunosuppression. Oxidative Stress / drug effects. Phytotherapy. Plant Extracts / pharmacology. Protective Agents / pharmacology. Vernonia
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / blood. Antineoplastic Agents, Alkylating / toxicity. Bone Marrow Cells / drug effects. Cytokines / analysis. Drug Evaluation, Preclinical. Mice. Mice, Inbred BALB C. Neoplasms / drug therapy

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  • (PMID = 20473572.001).
  • [ISSN] 1568-5608
  • [Journal-full-title] Inflammopharmacology
  • [ISO-abbreviation] Inflammopharmacology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Cytokines; 0 / Plant Extracts; 0 / Protective Agents; 8N3DW7272P / Cyclophosphamide
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9. Fazzi R, Pacini S, Testi R, Azzarà A, Galimberti S, Testi C, Trombi L, Metelli MR, Petrini M: Carboxy-terminal fragment of osteogenic growth peptide in vitro increases bone marrow cell density in idiopathic myelofibrosis. Br J Haematol; 2003 Apr;121(1):76-85
Genetic Alliance. consumer health - Myelofibrosis.

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  • At present, no efficacious therapy for this disease exists.
  • Synthetic carboxy-terminal pentapeptide of osteogenic growth factor (sOGP10-14) can increase bone marrow cellularity and the number of haematopoietic colonies; this study evaluated the activity of sOGP10-14 in IMF.
  • After 14 d, bone marrow cellularity was significantly increased in samples cultured with the pentapeptide.
  • TPO-primed proliferation of M07-e was reduced by sOGP10-14, and the pentapeptide significantly reduced CFU-Mk on IMF bone-marrow-derived cells. sOGP10-14 increased ex vivo bone marrow cellularity in IMF.
  • [MeSH-minor] Aged. Bone Marrow Cells / drug effects. Bone Marrow Cells / pathology. Bone Marrow Cells / secretion. Cell Count. Cell Division / drug effects. Cells, Cultured. Depression, Chemical. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Image Processing, Computer-Assisted. Megakaryocytes / cytology. Megakaryocytes / drug effects. Middle Aged. Peptide Fragments / pharmacology. Thrombopoietin / pharmacology. Transforming Growth Factor beta / secretion. Tumor Cells, Cultured / drug effects

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  • (PMID = 12670334.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endorphins; 0 / Peptide Fragments; 0 / Transforming Growth Factor beta; 105250-85-9 / historphin; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 9014-42-0 / Thrombopoietin
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10. de Greef GE, van Putten WL, Boogaerts M, Huijgens PC, Verdonck LF, Vellenga E, Theobald M, Jacky E, Löwenberg B, Dutch-Belgian Hemato-Oncology Co-operative Group HOVON, Swiss Group for Clinical Cancer Research SAKK: Criteria for defining a complete remission in acute myeloid leukaemia revisited. An analysis of patients treated in HOVON-SAKK co-operative group studies. Br J Haematol; 2005 Jan;128(2):184-91
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  • Complete remission (CR) in patients with acute myeloid leukaemia (AML) is the primary endpoint for the evaluation of induction treatment and treatment strategies.
  • However, the choice and application of the criteria for a haematological CR can often become a subject of debate because of regeneration more than 5% blasts may be present at the time of response evaluation; platelet and neutrophil recovery may be incomplete and marrow cellularity can vary.
  • This was independent of blast cells present in the peripheral blood or bone marrow (BM) cellularity.
  • In the same patient group, the presence of extramedullary leukaemia, incomplete platelet (<100 x 10(9)/l) or neutrophil (<1.0 x 10(9)/l) recovery caused a reduced OS and increased RR.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy

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  • [CommentIn] Br J Haematol. 2005 Apr;129(1):157-8; author reply 158 [15801968.001]
  • (PMID = 15638852.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Multicenter Study
  • [Publication-country] England
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11. Shukla J, Chatterjee S, Thakur VS, Premachandran S, Checker R, Poduval TB: L-Arginine reverses radiation-induced immune dysfunction: the need for optimum treatment window. Radiat Res; 2009 Feb;171(2):180-7
Hazardous Substances Data Bank. (L)-ARGININE .

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  • [Title] L-Arginine reverses radiation-induced immune dysfunction: the need for optimum treatment window.
  • The aim of the present study was to investigate the protective efficacy of l-arginine in mitigating the injury induced by 2 Gy of total-body gamma radiation (TBI).
  • Mice exposed to radiation (TBI group) had significantly decreased spleen weight, splenocyte numbers and bone marrow cellularity.
  • Administration of l-arginine 2 h after TBI (TBI + l-arginine group) was effective in reducing the radiation-induced depletion of spleen and bone marrow cellularity but was not effective when administered before TBI (l-arginine + TBI group).
  • The radiation-induced increase in serum TNF-alpha levels, serum nitrate/nitrite (NOx) levels, spleen DNA fragmentation, spleen nitric oxide synthase (NOS) activity, spleen inducible NOS (iNOS) activity, and hepatic iNOS activity was reversed in mice in the TBI + l-arginine group. l-Arginine administered before TBI could not reverse these changes.
  • Mice in the TBI + l-arginine group had significantly increased spleen arginase activity compared to mice from either the TBI or l-arginine + TBI group.
  • The results suggest the importance of the time of administration of l-arginine and the l-arginine pathway in mitigating the radiation-induced host immune dysfunction.
  • [MeSH-major] Arginine / therapeutic use. Immune System Diseases / drug therapy. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] Animals. Base Sequence. Cell Proliferation / drug effects. DNA Primers. Male. Mice. Nitric Oxide Synthase Type II / metabolism. Spleen / cytology. Spleen / drug effects. Spleen / enzymology. Spleen / radiation effects. T-Lymphocytes / cytology. T-Lymphocytes / drug effects. T-Lymphocytes / radiation effects. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19267543.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Tumor Necrosis Factor-alpha; 94ZLA3W45F / Arginine; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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12. Smith K, Hamza S, Germain M, Skelton H: Does imiquimod histologically rejuvenate ultraviolet radiation-damaged skin? Dermatol Surg; 2007 Dec;33(12):1419-28; discussion 1428-9
The Lens. Cited by Patents in .

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  • OBJECTIVE: The objective was to determine what histologic and immunohistologic changes were present in actinically damaged skin after treatment with IMI.
  • RESULTS: After IMI therapy there was less compact hyperkeratosis, a more uniform rete ridge pattern with a more ordered proliferation of the epidermis, and a decrease in sun-damaged melanocytes.
  • The papillary dermis showed a more uniform cellularity, and there was increased cellularity within the area of solar elastosis.
  • After therapy, staining for p53, p63, and PCNA was decreased within the epidermis; staining for c-kit was decreased but more uniform in the basal cell; and Factor XIIIa expression was increased within the papillary dermis with a more ordered pattern of staining.
  • CONCLUSION: These morphologic and immunohistochemical patterns may explain some of the improvement in overall skin appearance after IMI therapy and may be related to the spectrum of signaling pathways induced by the imidazoquinolines.
  • [MeSH-major] Aminoquinolines / pharmacology. Dermatologic Agents / pharmacology. Skin / drug effects. Skin / radiation effects. Skin Aging / drug effects. Ultraviolet Rays / adverse effects
  • [MeSH-minor] Biopsy. Female. Humans. Immunohistochemistry. Keratosis / drug therapy. Keratosis / pathology. Male. Middle Aged. Photosensitivity Disorders / drug therapy. Photosensitivity Disorders / pathology. Pilot Projects. Rejuvenation. Signal Transduction. Skin Diseases / drug therapy. Skin Diseases / pathology. Sunlight / adverse effects

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  • (PMID = 18076606.001).
  • [ISSN] 1524-4725
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Dermatologic Agents; 99011-02-6 / imiquimod
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13. Niitsu N, Okamoto M, Tomita N, Aoki S, Tamaru J, Miura I, Hirano M: Multicentre phase II study of the baseline BEACOPP regimen for patients with advanced-stage Hodgkin's lymphoma. Leuk Lymphoma; 2006 Sep;47(9):1908-14
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  • In the BEACOPP regimen, treatment intervals were shortened and the dose-intensity was increased compared with those in the ABVD regimen (doxorubicin, bleomycin, vinblastine and darcarbacine), resulting in a long-term disease-free survival rate of approximately 75-80%.
  • In the present study, we evaluated the safety and efficacy of the BEACOPP regimen.
  • Between April 2001 and February 2004, 20 patients with HL of stage IIB or higher who had received no previous treatment were enrolled.
  • The histologic types were mixed cellularity in four cases and nodular sclerosis in 16 cases.
  • Adverse drug reactions were grade 4 neutropenia in 12 patients, grade 3-4 thrombocytopenia in seven patients, and grade 3 or higher non-hematologic toxicities in two patients (stomatitis in one patient and ALT/AST elevation in one patient).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hodgkin Disease / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Bleomycin / therapeutic use. Cyclophosphamide / therapeutic use. Dacarbazine / therapeutic use. Disease-Free Survival. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Prednisone / therapeutic use. Procarbazine / therapeutic use. Treatment Outcome. Vinblastine / therapeutic use. Vincristine / therapeutic use

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  • (PMID = 17065005.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 5V9KLZ54CY / Vinblastine; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; ABVD protocol; BEACOPP protocol
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14. Edwan JH, Agrawal DK: Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Immunol Res; 2007;37(2):147-59
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  • The present experiments were undertaken to examine the effect of pUMVC3-hFLex in a chronic model of allergic airway inflammation that was established in Balb/c mice by sensitization and challenge with ovalbumin (OVA).
  • Treatment with pUMVC3-hFLex completely reversed established AHR (p < 0.05), and this effect continued even after several exposures to the allergen (p < 0.05).
  • pUMVC3-hFLex treatment prevented the development of goblet cell hyperplasia and subepithelial fibrosis, and significantly reduced serum levels of IL-4 and IL-5, and increased serum IL-10 levels (p < 0.05) with no effect on serum IL-13.
  • Total BALF cellularity and BALF IL-5 levels were reduced (p < 0.05), but there was no significant effect on BALF IL-10 and IL-13.
  • These results suggest that pUMVC3-hFLex treatment can prevent the development of airway remodeling and maintain airway protection in chronic experimental asthma model, and might provide a novel approach for treating chronic asthma.
  • [MeSH-major] Asthma / therapy. Membrane Proteins / genetics
  • [MeSH-minor] Animals. Collagen / metabolism. Cytokines / blood. Cytokines / immunology. Female. Goblet Cells / drug effects. Goblet Cells / immunology. Goblet Cells / pathology. Immunoglobulin E / immunology. Immunoglobulin G / immunology. Immunoglobulin Isotypes / immunology. Immunotherapy / methods. Mice. Mice, Inbred BALB C. Ovalbumin / immunology. Ovalbumin / pharmacology. Plasmids / genetics. Plasmids / immunology

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  • (PMID = 17695249.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01HL070885; United States / NHLBI NIH HHS / HL / R01HL073349
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Immunoglobulin G; 0 / Immunoglobulin Isotypes; 0 / Membrane Proteins; 0 / flt3 ligand protein; 37341-29-0 / Immunoglobulin E; 9006-59-1 / Ovalbumin; 9007-34-5 / Collagen
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15. Arslan E, Milcan A, Unal S, Demirkan F, Polat A, Bagdatoglu O, Aksoy A, Polat G: The effects of carnitine on distally-burned dorsal skin flap: an experimental study in rats. Burns; 2003 May;29(3):221-7
Hazardous Substances Data Bank. MALONALDEHYDE .

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  • OBJECTIVE: In ischemia and burn injuries, there are major alterations threatening tissue survival.
  • Increased energy flow requirements are among the major problems in these disorders.
  • Biochemically, nitric oxide (NO), malondialdehyde (MDA), and acetylcholinesterase levels, and histopathologically tissue examination under light microscope were studied.
  • The most distal 3 cm x 3 cm of the flap was burned to full-thickness.
  • Histopathological examination revealed a full-thickness muscle necrosis in addition to skin tissue in the control group, while healing tissue was present with marked cellularity including mixed inflammatory cells and fibroblast proliferation with an increased vascularity in the form of capillary budding in the study group.
  • [MeSH-major] Burns / drug therapy. Carnitine / therapeutic use
  • [MeSH-minor] Acetylcholinesterase / blood. Animals. Ischemia / drug therapy. Malondialdehyde / blood. Necrosis. Nitric Oxide / blood. Rats. Rats, Sprague-Dawley. Skin / blood supply

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  • (PMID = 12706614.001).
  • [ISSN] 0305-4179
  • [Journal-full-title] Burns : journal of the International Society for Burn Injuries
  • [ISO-abbreviation] Burns
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide; 4Y8F71G49Q / Malondialdehyde; EC 3.1.1.7 / Acetylcholinesterase; S7UI8SM58A / Carnitine
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16. Chenevert TL, Stegman LD, Taylor JM, Robertson PL, Greenberg HS, Rehemtulla A, Ross BD: Diffusion magnetic resonance imaging: an early surrogate marker of therapeutic efficacy in brain tumors. J Natl Cancer Inst; 2000 Dec 20;92(24):2029-36
The Lens. Cited by Patents in .

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  • [Title] Diffusion magnetic resonance imaging: an early surrogate marker of therapeutic efficacy in brain tumors.
  • BACKGROUND: A surrogate marker for treatment response that can be observed earlier than comparison of sequential magnetic resonance imaging (MRI) scans, which depends on relatively slow changes in tumor volume, may improve survival of brain tumor patients by providing more time for secondary therapeutic interventions.
  • Previous studies in animals with the use of diffusion MRI revealed rapid changes in tumor water diffusion values after successful therapeutic intervention.
  • METHODS: The present study examined the sensitivity of diffusion MRI measurements in orthotopic rat brain tumors derived from implanted rat 9L glioma cells.
  • The effectiveness of therapy for individual brain cancer patients was evaluated by measuring changes in tumor volume on neuroimaging studies conducted 6--8 weeks after the conclusion of a treatment cycle.
  • Mean apparent diffusion coefficients in tumors were found to be correlated with and highly sensitive to changes in tumor cellularity (r =.78; two-sided P =.041).
  • Increased diffusion values could be detected in human brain tumors shortly after treatment initiation.
  • CONCLUSIONS: These results suggest that diffusion MRI will provide an early surrogate marker for quantification of treatment response in patients with brain tumors.

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  • (PMID = 11121466.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA086442; United States / NCI NIH HHS / CA / R24 CA083099; United States / NCI NIH HHS / CA / P20CA86442; United States / NCI NIH HHS / CA / R24CA83099
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers, Tumor; 059QF0KO0R / Water; U68WG3173Y / Carmustine
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