The Korean Journal of Hematology最新文献

{"title":"The premier statistical report of hematologic malignancies in Korea.","authors":"Hee-Je Kim","doi":"10.5045/kjh.2012.47.1.1","DOIUrl":"https://doi.org/10.5045/kjh.2012.47.1.1","url":null,"abstract":"Tada! The current issue of the Korean Journal of Hematology includes a very impressive, surprising report describing, for the first time, the statistics of hematologic malignancies in Korea [1]. In fact, until now, no reliable nationwide cancer statistics describing hematologic malignancies have been published in Korea. While the report presented in this current issue may be somewhat incomplete, it represents an excellent database that can be used both domestically and worldwide as an important source of cancer statistics from Korea. Because the database contains all aspects of population-based, disease-specific statistics, along with survival- and death-related data from 1993 to 2008, we can analyze and compare our own data with that of other countries, allowing high-ranked public officials to shape national policies and health strategies in the field of hematologic malignancy in the future. \u0000 \u0000On the other hand, this statistics presented in the current issue could be representative of the estimated incidence and prevalence since we still do not have a reporting system that enables accurate data collection and creation of a nationwide database for specific regions or specific periods of time. The data from 1993 and prior should differ quite dramatically from data for 2008. However, we recognize that the publication of this statistical report provides us with a beginning from which we can establish a reliable health reporting system in Korea. Undoubtedly, this is the first step toward developing more complementary and up-to-date health statistics in this country. \u0000 \u0000Based on an annually increasing trend, we can say for certain that greater than 8,000 new cases of blood cancer patients were diagnosed in 2008 according to data from the Korea National Cancer Incidence Database (KNCIDB) [1, 2]. In addition, survival and mortality data from 1993 to 2008 were obtained from the Korea National Statistics Office (KNSO) [1, 2]. These data were combined, and the current report calculated, for the first time in Korea, the incidence, mortality, prevalence, limited-duration prevalence, and changes in the annual age-standardized cancer incidence rates. Now, Korean medical students can be taught oncology using Korea's own statistics, rather than the statistics of other countries. Therefore, although it is somewhat shameful to admit that this is the first publication of national data on hematologic malignancies, we should consider this a memorable and historical achievement. \u0000 \u0000To establish further reliable statistics on hematologic malignancies, we anticipate that more aggressive efforts will be made to collect data from every regional database in Korea. Based on a recent report published in the Journal Cancer Research and Treatment in 2011 [2], we found that 2,561 new cases of leukemia were diagnosed in Korea in 2008. In contrast to this report, the most recent report published in our journal showed that 2,262 new cases of lymphoid and myeloid leukemia occurred","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"47 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2012.47.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30554571","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":"Leukemic manifestation of anaplastic lymphoma kinase-negative-type anaplastic large-cell lymphoma.","authors":"Jae Wook Kim, Su-Jin Shin, Chan-Jeoung Park","doi":"10.5045/kjh.2012.47.1.6","DOIUrl":"https://doi.org/10.5045/kjh.2012.47.1.6","url":null,"abstract":"which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. A 53-year-old woman had multiple bilateral axillary and left supraclavicular lymph-node (LN) enlargements for 6 months. LN biopsy revealed anaplastic large-cell lymphoma (ALCL) that was anaplastic lymphoma kinase (ALK)-negative (A. typical \" hallmark \" cell: pleomorphic neoplastic lymphoid cells, hematoxylin & eosin stain, ×400). A bone marrow (BM) study for staging work-up revealed no evidence of neoplastic lymphoid-cell infiltration. Chemotherapy was administered and autologous hematopoietic stem cell transplantation (a-HSCT) was performed. On day 55 post a-HSCT, follow-up complete blood cell count revealed abnormal findings: hemoglobin level, 9.4 g/dL; leukocyte count, 13.8×10 3 /μL; and platelet count, 26×10 3 /μL. Peripheral blood (PB) smear showed small to large pleomorphic neoplastic lymphoid cells (B, Wright stain, ×1,000) comprising 23% of the cells in differential counts. Subsequent BM study disclosed neoplastic lymphoid cells (6% in BM aspirate) in the BM clot, and the cells showed positive results for CD3 and CD30. On day 84 post a-HSCT, the patient's PB smears revealed leukocytosis; ALCL cells comprised over 70-94% of the nucleated cells. Although the small-cell variant of ALK-positive ALCL may be typically associated with involvement of PB, our patient showed a rare manifestation of ALK-negative ALCL involving PB, with a leukemic phase.","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"47 1","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2012.47.1.6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30554573","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":"A patient with acquired hemophilia A induced by clopidogrel.","authors":"Hye Won Hwang,&nbsp;Jee Hyun Kong,&nbsp;Dong Wook Yu,&nbsp;Woo Taek Kim,&nbsp;Hyun Soo Kim,&nbsp;Chong In Lee","doi":"10.5045/kjh.2012.47.1.80","DOIUrl":"https://doi.org/10.5045/kjh.2012.47.1.80","url":null,"abstract":"<p><p>Acquired hemophilia A (AHA) is a rare bleeding disorder caused by autoantibodies against factor VIII (FVIII). Treatment with clopidogrel is a cause of AHA, but its clinical course is unknown. Recently, we treated a 65-year-old man who was hospitalized for cerebellar infarction and had a prolonged activated partial thromboplastin time (aPTT) with soft tissue oozing after 3 weeks of clopidogrel use. We terminated clopidogrel administration and transfused the patient with fresh frozen plasma. However, the aPTT increased up to 98.8 seconds, and the FVIII and FVIII inhibitor levels were <1% and 5.4 Bethesda units/mL, respectively. Clopidogrel-associated AHA was considered, and we began steroid treatment. Two months later, FVIII, FVIII inhibitor, and aPTT values were normalized. No further bleeding or aPTT prolongation has been reported during the 2-year follow-up period. AHA should be considered in patients taking clopidogrel and experiencing bleeding, unless the platelet count and coagulation screen are normal.</p>","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"47 1","pages":"80-2"},"PeriodicalIF":0.0,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2012.47.1.80","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30553686","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":"Treatment strategies for Hodgkin lymphoma recurring following autologous hematopoietic stem cell transplantation.","authors":"Erin-Siobhain R Currin,&nbsp;Ajay K Gopal","doi":"10.5045/kjh.2012.47.1.8","DOIUrl":"https://doi.org/10.5045/kjh.2012.47.1.8","url":null,"abstract":"<p><p>Hodgkin lymphoma (HL) represents one of the great success stories in hematology going from a uniformly fatal disease, to one that is curable in the vast majority of cases. Despite this success, some patients experience relapse. To address this unmet need a variety of agents, classes of drugs, and strategies have demonstrated activity in HL recurring after autologous hematopoietic stem cell transplantation. These include chemotherapeutics (gemcitabine-based combinations, bendamustine), histone deacetylase (HDAC) inhibitors (panobinostat), immunomodulatory agents (lenalidomide), mTOR inhiobitors (everolimus), monoclonal antibodies (rituximab), and antibody-drug conjugates (brentuximab vedotin) as well the potential of long-term disease control via allogeneic transplantation. Such advances reflect our increased understanding of the biology of HL and hold promise for continued improved outcomes for those suffering with this condition.</p>","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"47 1","pages":"8-16"},"PeriodicalIF":0.0,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2012.47.1.8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30554575","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":"Cryoglobulinemic vasculitis and monoclonal gammopathy in end-stage renal disease.","authors":"Dahae Won,&nbsp;Chan Jeoung Park,&nbsp;Jai Won Chang","doi":"10.5045/kjh.2011.46.4.215","DOIUrl":"https://doi.org/10.5045/kjh.2011.46.4.215","url":null,"abstract":"which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. A 75-year-old man with a 2-year history of end-stage renal disease had skin lesions on both feet (A) for 2 weeks. The cause of end-stage renal disease remained to be clarified. Initial laboratory tests showed the following values: extracellular aggregates of pink-tan acellular material (B). We suspected cryoglobulinemia and performed the cryoglobulin test. The sampling was performed using a warmed syringe and a test tube. The patient was positive with a very high cryocrit level (37.02%). Immunofixation showed a monoclonal IgG kappa band in the gamma region. The patient was negative for hepatitis and HIV. Biopsy of the skin lesion showed leukocytoclastic vasculitis with subcorneal bulla. A subsequent bone marrow (BM) examination showed no evidence of clonal plasma cells (＜2%). Flow cytometric analyses showed increased proportion of B cells (PB, 24.4%; BM aspirates, 25.5%) with no clonality. Cytogenetic study revealed normal karyotype of 46,XY. The patient was diagnosed with type I cryoglobulinemia with cryoglobulinemic vasculitis and monoclonal gammopathy. Treatment with methyl prednisolone improved his clinical response. Our data indicate that cryoglobulin could be easily detected by PB smear.","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"46 4","pages":"215"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2011.46.4.215","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30398085","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":"Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.","authors":"Hong-Bum Park,&nbsp;Jeong-Hee Yang,&nbsp;Kwang-Hoe Chung","doi":"10.5045/kjh.2011.46.4.265","DOIUrl":"https://doi.org/10.5045/kjh.2011.46.4.265","url":null,"abstract":"<p><strong>Background: </strong>The underlying rationale of platelet rich plasma (PRP) therapy is that an injection of concentrated PRP at the site of injury may promote tissue repair via cytokine release from platelets. The molecular mechanisms of PRP therapy in the skin wound healing process are not well understood at present, and would benefit from clarification.</p><p><strong>Methods: </strong>PRP was stimulated with angonists for 5 min, and cytokine profile analysis was performed. To investigate the wound healing activity of PRP, cell proliferation and migration analyses were performed in skin cells. The effects of PRP were analyzed on the expression and activity of matrix metalloproteinase (MMP)-1, -2, -9, and the activation of transcription factors.</p><p><strong>Results: </strong>Thrombin was found to be a strong stimulator of PRP activation to release growth factors and chemokines. PRP induced cell proliferation and migration in HUVECs, HaCaT cells, and HDFs, as well as MMP-1and MMP-9 expression in HaCaT cells, but PRP did not have a significant effect on the expression or activity of MMPs in HDFs. The transcription factors, including signal transducer and activator of transcription-3 (STAT-3) were found to be phosphorylated following PRP treatment in HaCaT cells.</p><p><strong>Conclusion: </strong>In this study, we have identified the cytokine profile of activated PRP after agonist stimulation. We have shown that PRP plays an active role in promoting the proliferation and migration of skin cells via the regulation of MMPs, and this may be applicable to the future development of PRP therapeutics to enhance skin wound healing.</p>","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"46 4","pages":"265-73"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2011.46.4.265","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30398596","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":"Splenic infarction in a patient with autoimmune hemolytic anemia and protein C deficiency.","authors":"Min Yong Park,&nbsp;Jung A Kim,&nbsp;Seong Yoon Yi,&nbsp;Sun Hee Chang,&nbsp;Tae Hyun Um,&nbsp;Hye Ran Lee","doi":"10.5045/kjh.2011.46.4.274","DOIUrl":"https://doi.org/10.5045/kjh.2011.46.4.274","url":null,"abstract":"<p><p>Splenic infarction is most commonly caused by cardiovascular thromboembolism; however, splenic infarction can also occur in hematologic diseases, including sickle cell disease, hereditary spherocytosis, chronic myeloproliferative disease, leukemia, and lymphoma. Although 10% of splenic infarction is caused by hematologic diseases, it seldom accompanies autoimmune hemolytic anemia (AIHA). We report a case of a 47-year-old woman with iron deficiency anemia who presented with pain in the left upper abdominal quadrant, and was diagnosed with AIHA and splenic infarction. Protein C activity and antigen decreased to 44.0% (60-140%) and 42.0% (65-140%), respectively. Laboratory testing confirmed no clinical cause for protein C deficiency, such as disseminated intravascular coagulation, sepsis, hepatic dysfunction, or acute respiratory distress syndrome. Protein C deficiency with splenic infarction has been reported in patients with viral infection, hereditary spherocytosis, and leukemia. This is a rare case of splenic infarction and transient protein C deficiency in a patient with AIHA.</p>","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"46 4","pages":"274-8"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2011.46.4.274","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30398597","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":"Lymphoma stem cells: A step toward a new therapeutic target.","authors":"Seok Jin Kim","doi":"10.5045/kjh.2011.46.4.211","DOIUrl":"https://doi.org/10.5045/kjh.2011.46.4.211","url":null,"abstract":"Since lymphoma is a chemosensitive neoplasm, a complete response can be achieved by systemic chemotherapy, even in the metastatic setting. Even so, relapse occurs in a substantial number of patients with an apparently complete clinical response. It is therefore possible that a subset of lymphoma cells that remain viable during treatment causes the relapse. The cancer stem cell hypothesis postulates the presence of this specific cell population in cancers. It suggests that cancers are derived from cancer stem cells, which are a particular subset of cancer cells with stem-like properties, including self-renewal [1]. Since the existence of cancer stem cells was demonstrated in acute myeloid leukemia [2], various surface markers have been identified to isolate cancer stem cells from such solid cancers as breast, brain, and colon. Although a recent publication suggested the probability of lymphoma stem cells in non-Hodgkin lymphoma [3], it did not offer sufficient data to support the presence of cancer stem cells as an origin of lymphoma. However, given the potential role of cancer stem cells in the pathogenesis of cancers, the possibility of lymphoma stem cells deserves attention, for it could improve our understanding of lymphoma biology and lead to the development of a new therapeutic target for lymphomas.","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"46 4","pages":"211-3"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2011.46.4.211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30398083","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":"Hematological manifestations of human immunodeficiency virus infection and the effect of highly active anti-retroviral therapy on cytopenia.","authors":"Se Youn Choi,&nbsp;Inho Kim,&nbsp;Nam Joong Kim,&nbsp;Seung-Ah Lee,&nbsp;Youn-Ak Choi,&nbsp;Ji-Yeon Bae,&nbsp;Ji Hyun Kwon,&nbsp;Pyoeng Gyun Choe,&nbsp;Wan Beom Park,&nbsp;Sung-Soo Yoon,&nbsp;Seonyang Park,&nbsp;Byoung Kook Kim,&nbsp;Myoung-Don Oh","doi":"10.5045/kjh.2011.46.4.253","DOIUrl":"https://doi.org/10.5045/kjh.2011.46.4.253","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study is to investigate the hematological manifestations of human immunodeficiency virus (HIV) infection, the risk factors for cytopenia, and the effect of highly active anti-retroviral therapy (HAART) on cytopenia.</p><p><strong>Methods: </strong>Medical records of patients treated for HIV at the Seoul National University Hospital from January 2005 to March 2010 were retrospectively reviewed. To determine the impact of HIV itself, we excluded HIV patients who had other conditions that could have resulted in hematological manifestations. Multiple logistic regression analyses were performed to identify risk factors for cytopenia.</p><p><strong>Results: </strong>A total of 621 cases were investigated, and after exclusion, data of 472 patients were analyzed. The frequency of cytopenia was anemia, 3.0% (14/472); neutropenia, 10.0% (47/472); thrombocytopenia, 2.4% (12/472); lymphopenia, 25.7% (121/470); isolated cytopenia, 11.2% (53/472); and bicytopenia, 2.1% (10/472). The leading risk factor for cytopenia identified by multivariate logistic regression methods was AIDS status at initial presentation. After HAART, cytopenia was reversed in the majority of patients (thrombocytopenia, 100%; neutropenia, 91.1%; and anemia, 84.6%).</p><p><strong>Conclusion: </strong>This study isolated the impact of HIV infection alone on hematologic manifestations and confirmed that these changes were reversible by HAART. Control of the HIV infection will have the main role in the management of hematological manifestations of the virus.</p>","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"46 4","pages":"253-7"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2011.46.4.253","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30398594","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":"Evans syndrome following long-standing Hashimoto's thyroiditis and successful treatment with rituximab.","authors":"Hye Jin Oh,&nbsp;Myung Jae Yun,&nbsp;Seong Tae Lee,&nbsp;Seung June Lee,&nbsp;So Yeon Oh,&nbsp;In Sohn","doi":"10.5045/kjh.2011.46.4.279","DOIUrl":"https://doi.org/10.5045/kjh.2011.46.4.279","url":null,"abstract":"<p><p>We report a case of a 51-year-old woman with Evans syndrome (autoimmune hemolytic anemia and primary immune thrombocytopenia) and hypothyroidism. She was previously diagnosed with Hashimoto's thyroiditis in 1994 (age, 35) and autoimmune hemolytic anemia (AIHA) 3 years ago. She was treated with oral prednisolone. After a period, in which the anemia waxed and waned, there was an abrupt development of thrombocytopenia (nadir 15×10(9)/L) that coincided with the tapering off of prednisolone after 3 years of administration. Because her thrombocytopenia was refractory to prednisolone, we administered rituximab (375 mg/m(2) weekly) for 4 weeks. Two weeks after the completion of the rituximab treatment, her platelet count was up to 92×10(9)/L. No intermittent peaking of thyroid stimulating hormone occurred after rituximab treatment was initiated. Evans syndrome and autoimmune thyroiditis might share common pathophysiological mechanisms. This notion supports the use of rituximab in a patient suffering from these disorders.</p>","PeriodicalId":23001,"journal":{"name":"The Korean Journal of Hematology","volume":"46 4","pages":"279-82"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5045/kjh.2011.46.4.279","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30398598","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}