Open journal of hematology最新文献

{"title":"Protective Role of Human Intravenous Immunoglobulin from Influenza AVirus Infection in Mice","authors":"K. Hagiwara, S. Kawami, Yuuko Kato-Mori, Ritsuko Kubota-Koketsu, M. Tsujikawa, T. Urayama, M. Yunoki, Kazuo Takahashi, K. Ikuta","doi":"10.2174/1874276901206010008","DOIUrl":"https://doi.org/10.2174/1874276901206010008","url":null,"abstract":"Intravenous immunoglobulin (IVIG) has been manufactured from pooled plasma of 10,000 or more units from healthy donors. Recently, we reported that the IVIG manufactured even before the 2009 influenza pandemic contained antibodies reactive to seasonal H1N1 and pandemic H1N1 2009 (H1N1 pdm) viruses. In this study, we used an animal model to evaluate the efficacy of IVIG against influenza infections. A seasonal influenza H1N1 strain (New Caledonia, A/NC/20/99) and an H1N1 pdm strain (A/Osaka/168/2009) were used. The BALB/c and severe combined immuno- deficiency mice (SCID; C.B-17/lcr-scid/scid) were also used. Mice inoculated with A/NC/20/99 or A/Osaka/168/2009 were administrated IVIG and monitored for 3 weeks. The administration of IVIG 48 h before and after inoculation with a mouse-adapted seasonal H1N1 virus, resulted in survival rates of 80 and 88%, respectively. The rate among control mice was 30%. In addition, infectivity in lungs from IVIG-treated mice also decreased significantly. Similar effects of IVIG on the survival rate were obtained with H1N1 pdm. Thus, IVIG was shown to be effective against both viruses in mice.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"10 1","pages":"8-11"},"PeriodicalIF":0.0,"publicationDate":"2012-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88860533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Role of Ras-GTPase Activating Protein SH3 Domain-Binding ProteinG3BP in Adhesion and Migration of 32D Myeloid Progenitor Cells","authors":"K. Schwarz, Frank Aschenbrenner, B. Rüster, M. Kampfmann, M. Komor, W. Hofmann, M. Ruthardt, R. Henschler, G. Bug","doi":"10.2174/1874276901206010001","DOIUrl":"https://doi.org/10.2174/1874276901206010001","url":null,"abstract":"Rho GTPases are involved in homing and mobilization of hematopoietic stem and progenitor cells due to their impact on cytoskeleton remodeling. We have previously shown that inhibition of Rho, Rac and Cdc42 clearly impairs ad- hesion of normal and leukemic hematopoietic progenitor cells (HPC) to fibronectin and migration in a three-dimensional stromal cell model. Here, we identified the Ras GTPase-Activating Protein SH3 Domain-Binding Protein (G3BP) as a target gene of Rho GTPases and analysed its role in regulating HPC motility. Overexpression of G3BP significantly enhanced adhesion of murine 32D HPC to fibronectin and human umbilical vein endothelial cells, increased the proportion of adherent cells in a flow chamber assay and promoted cell migration in a transwell assay and a three-dimensional stromal cell model suggesting a strong impact on the cytoskeleton. Immunofluorescent staining of G3BP-overexpressing fibroblasts revealed a Rho-like phenotype characterized by formation of actin stress fibers in contrast to the Rac-like phenotype of control fibroblasts. This is the first report implicating a role for G3BP in Rho GTPase-mediated signalling towards adhesion and migration of HPC. Our results may be of clinical importance, since G3BP was found overexpressed in human cancers.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"14 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2012-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81988021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell Trafficking in Multiple Myeloma.","authors":"Giada Bianchi,&nbsp;Shaji Kumar,&nbsp;Irene M Ghobrial,&nbsp;Aldo M Roccaro","doi":"10.13055/ojhmt_3_s1_04.120221","DOIUrl":"https://doi.org/10.13055/ojhmt_3_s1_04.120221","url":null,"abstract":"<p><p>Multiple myeloma (MM) is an incurable cancer of terminally differentiated plasma cells (PC) and represents the second most frequent hematologic malignancy in the western world. MM cells localize preferentially to the bone marrow where they interact closely with bone marrow stroma cells (BMSC) and extracellular matrix (ECM) proteins in a reciprocal pro-survival loop. Such a bone marrow niche guarantees a survival advantage for MM cells and has a crucial role in mediating drug resistance to chemotherapy agents. As the name suggests, hallmark characteristic of MM is the ability to localize in multiple, distant bone sites causing disruption of the normal bone architecture and impairment of normal hematopoiesis. The pathogenic mechanisms of MM rely then not only on proliferation of cancerous cells, but also on the ability of myeloma cells to traffic between sites and home to appropriate survival niches. Identifying the mechanisms that regulate the homing of MM cells to the bone marrow, the MM-BMSC interaction and the trafficking of MM cells from the bloodstream to distant bone locations is therefore crucial to design new, more effective therapies capable of overcoming the maladaptive interaction between BMSCs and MM and help in finding a cure for MM.</p>","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"3 Suppl 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677225/pdf/nihms359398.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31502705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell Trafficking in Chronic Lymphocytic Leukemia.","authors":"Matthew S Davids,&nbsp;Jan A Burger","doi":"10.13055/ojhmt_3_s1_03.120221","DOIUrl":"https://doi.org/10.13055/ojhmt_3_s1_03.120221","url":null,"abstract":"<p><p>Chronic lymphocytic leukemia (CLL) is an indolent lymphoproliferative disorder characterized by both circulating peripheral disease as well as involvement of the lymph nodes and bone marrow. Increasing evidence suggests that the stromal microenvironment provides anti-apoptotic and pro-survival signals to CLL cells, and may contribute significantly to resistance to a wide variety of treatments. Our understanding of the complex interactions involved in CLL cell trafficking continues to grow. Chemokines and corresponding chemokine receptors are key factors for organizing CLL cell trafficking and homing and the complex cellular interactions between CLL and accessory cells. Important chemokines include CCL3, CCL4, and CCL22, which are released by CLL cells, and CXCL12, CXCL13, CXCL9, 10, 11, CCL 19, and CCL21, which are constitutively secreted by various stromal cells. Integrins such as VLA-4 (CD49d) as well as selectins and CD44 also likely play a role in directing CLL cell migration within the tissue microenvironments. Data are also emerging that other molecules such as MMP-9 and cytoskeletal proteins also contribute to CLL cell trafficking. Though this interplay is complex, it is critical that we improve our understanding of CLL cell trafficking to facilitate the development of novel therapies that target these pathways. Several drugs in clinical development, such as CXCR4 antagonists and PI3K, Btk, and Syk inhibitors appear to modulate CLL cell trafficking and CLL-stroma interactions. Here, we review the current understanding of the molecular interactions that underlie CLL cell trafficking and we highlight some of the promising approaches underway to target these pathways therapeutically in CLL.</p>","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"3 S1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404599/pdf/nihms-359497.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30798108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the Oligomerization of BCR/ABL by Membrane Permeable Competitive Peptides Inhibits the Proliferation of Philadelphia ChromosomePositive Leukemic Cells","authors":"A. Mian, M. Schull, C. Oancea, Y. Najajreh, J. Mahajna, A. Goldblum, O. Ottmann, T. Beissert, M. Ruthardt","doi":"10.2174/1874276901105010021","DOIUrl":"https://doi.org/10.2174/1874276901105010021","url":null,"abstract":"The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype. Targeted inhibition of BCR/ABL by small molecule inhibitors reverses the transformation potential of BCR/ABL. Recently, we definitively proved that targeting the tetramerization of BCR/ABL mediated by the N-terminal coiled-coil domain (CC) using com- petitive peptides, representing the helix-2 of the CC, represents a valid therapeutic approach for treating Ph+ leukemia. To further develop competitive peptides for targeting BCR/ABL, we created a membrane permeable helix-2 peptide (MPH-2) by fusing the helix-2 peptide with a peptide transduction tag. In this study, we report that the MPH-2: (i) interacted with BCR/ABL in vivo; (ii) efficiently inhibited the autophosphorylation of BCR/ABL; (iii) suppressed the growth and viability of Ph+ leukemic cells; and (iv) was efficiently transduced into mononuclear cells (MNC) in an in vivo mouse model. This study provides the first evidence that an efficient peptide transduction system facilitates the employment of competitive peptides to target the oligomerization interface of BCR/ABL in vivo.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"16 1","pages":"21-27"},"PeriodicalIF":0.0,"publicationDate":"2011-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85573246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence and Prognostic Value of NPM1 and FLT3 Gene Mutations in AML with Normal Karyotype","authors":"D. Nafea, Mohammed A. Abdel Rahman, D. Boris, C. Pérot, Laporte Jp, F. Isnard, P. Coppo, N. Gorin","doi":"10.2174/1874276901105010014","DOIUrl":"https://doi.org/10.2174/1874276901105010014","url":null,"abstract":"NPM1 belongs to a new category of genes that function both as oncogenes and tumor suppressor genes, depending on gene dosage, expression levels, interacting partners, and compartmentalization. Nucleophosmin mutations within exon 12 have been described as the most frequent acquired molecular abnormalities in adult and pediatric acute myeloid leukaemia (AML), mutation can be observed in nearly half of patients with a normal karyotype and is associated with a favorable outcome. NPM1 mutations are characterized by the aberrant cytoplasmic localization of NPM, the absence of CD34, involvement of several cell lineages myeloid, monocytic, erythroid and megakaryocytic but not lymphoid and a high frequency of FLT3-ITD mutation. We aimed to study the prevalence, association with Flt3 mutations, and prognostic impact of NPM1 exon-12 mutations in 71 AML patients with normal karyotype. We studied NPM1 and FLT3 by RT PCR. NPM1 gene mutation was detected among 34 patients (47.9%) and was associated with a high white blood cell count, involvement of the monocytic lineage, CD34 negativity, and high frequency of FLT3ITD. DFS and OS did not differ between mutated and unmutated NPM patients. Prospective studies are needed to confirm the definitive place of NPM mutation among patients with normal karyotype.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"5 1","pages":"14-20"},"PeriodicalIF":0.0,"publicationDate":"2011-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90765752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cost and indications of blood transfusions in Pediatric Oncology in an African Hospital.","authors":"J. Murray, D. Stefan","doi":"10.2174/1874276901105010010","DOIUrl":"https://doi.org/10.2174/1874276901105010010","url":null,"abstract":"Results: Thirty-nine children with cancer were transfused, between one unit and 34 units of blood products per patient, during their treatment in 2008. The total cost of this therapy in 2008 was ZAR 941,966 = USD 125,595 = EUR 89,711. The maximum cost per patient amounted to ZAR 70,682 = USD 9,424 = EUR 6,731 and the minimum ZAR 914 = USD 121 = EUR 87. The average expenditure per patient was ZAR 24,125 = USD 3,216 = EUR 2,297. The management of leukemia required the highest usage of blood products per patient. Conclusion: The use of blood products is indispensable during the treatment of numerous haematology – oncology diseases. Their indications should be specified in internal protocols and their actual use should be audited frequently due to the considerable costs.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"149 6 1","pages":"10-13"},"PeriodicalIF":0.0,"publicationDate":"2011-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75383193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haematological Malignancies on the Island of Sardinia, 1974-1993: A Geographical Study","authors":"G. Broccia, M. Longinotti, Barbara Giannico, C. Porcu, E. Chessa","doi":"10.2174/1874276901105010004","DOIUrl":"https://doi.org/10.2174/1874276901105010004","url":null,"abstract":"We studied the geographical distribution of all cases of HM that were diagnosed among residents of Sardinia during the 20-year period from 1974 to 1993. Cases, grouped into three categories (lymphoproliferative diseases, myeloproliferative diseases, and total haematological malignancies), were assigned to the 356 municipalities of the island according to the reported residence of each patient. In each municipality, the relative risk (RR) of diagnosis was calculated for the three disease groups, for females, for males, and for the total population. The RR of diagnosis of HM was significantly different from 1 (p<0.05) for a limited number of estimates (5.4%), with almost as many instances of elevated RR as of reduced RR.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"33 1","pages":"4-9"},"PeriodicalIF":0.0,"publicationDate":"2011-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81546721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Features of Chronic Active Epstein-Barr virus Infection and Related Human Diseases","authors":"M. Okano","doi":"10.2174/1874276901105010001","DOIUrl":"https://doi.org/10.2174/1874276901105010001","url":null,"abstract":"A chronic undefined illness characterized by infectious mononucleosis (IM)-like symptoms and signs, possibly associated with Epstein-Barr virus (EBV) infection, designated as so-called chronic active EBV infection (CAEBV), is focused and discussed in this mini-review. Patients with CAEBV often develop T cell lymphoproliferative disorder (LPD)/lymphoma or NK cell LPD/lymphoma. Unique manifestations with generally poor prognosis of the disease prompt us to understand in particular the entity, diagnosis and treatment.","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"32 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2011-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83146088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LETTER TO THE EDITOR: Patients with Hemoglobinopathies Require Continuous Flow Supplemental Oxygen During Commercial Airline Flights","authors":"S. Omoigui, Helen Omoigui","doi":"10.2174/1874276901004010015","DOIUrl":"https://doi.org/10.2174/1874276901004010015","url":null,"abstract":"Patients with hemoglobinopathies are known to experience complications e.g. bone pain [1], splenic infarction [2] and osteonecrosis (avascular necrosis) of the hip (anecdotal report) subsequent to commercial airline flights. These complications are due to prolonged decrease in oxygen delivery at high altitudes. There is no study in the literature that has measured the oxygen saturation in these patients on commercial airline flights where planes ascend to altitudes of 30,000 feet or greater. At these altitudes, there is a low partial pressure of oxygen which is about a quarter of that at sea level. Humans would not be able to breathe without a pressurized environment and modern commercial jets are pressurized to an altitude of 5000-8000 feet. Ideally an airplane would be pressurized to ground level pressure (760 Torr). However this is not practical as the fuselage of a plane would have to be incredibly strong (and hence very heavy and expensive to fly) to withstand the outward force caused by 760 Torr while cruising at altitudes of 30,000 feet or greater [3]. At ground level, the partial pressure of oxygen is about 150 Torr or mm of mercury (20% of atmospheric pressure at 760 Torr). Inside a plane at cruising altitude oxygen partial pressure is reduced to about 125 Torr, In most people, this is a negligible change and their blood will remain fully saturated with oxygen at this pressure. This is not the case in patients with hemoglobinopathies in which tissue oxygen delivery is already compromised. We set out to determine the changes in oxygen saturation in seven patients with and without supplemental oxygen (continuous flow and pulse dose) provided during commercial airline travel. These patients with a mix of Hgb SS and SC were stable and without any underlying conditions. We provided them with a Sequal SmartPulseTM fingertip pulse oximeter to monitor oxygen saturation as well as with a SequalTM Eclipse 3 oxygen concentrator (Sequal Technologies, San Diego, California. Phone 858 202-3100). This oxygen concentrator is one of a few that are approved by the Federal Aviation Administration (FAA) for supplemental oxygen delivery on commercial","PeriodicalId":89702,"journal":{"name":"Open journal of hematology","volume":"1 1","pages":"15-16"},"PeriodicalIF":0.0,"publicationDate":"2010-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76573939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}