The Journal of community and supportive oncology最新文献

{"title":"Expanded approval for daratumumab in multiple myeloma","authors":"J. Abraham","doi":"10.12788/JCSO.0332","DOIUrl":"https://doi.org/10.12788/JCSO.0332","url":null,"abstract":"THE JOURNAL OF COMMUNITY AND SUPPORTIVE ONCOLOGY 65 Volume 15/Number 2 In November 2016, the US Food and Drug Administration expanded the approval of daratumumab for patients with multiple myeloma. The monoclonal antibody, which targets CD38, a protein that is highly expressed on the surface of multiple myeloma cells, was previously granted approval by the agency as a single agent for the treatment of patients who had received at least three previous therapies. The current approval was for the use of daratumumab in two different combination regimens for the treatment of patients who have received one previous line of treatment. On the basis of improved progression-free survival (PFS), demonstrated in two randomized, open-label, phase 3 trials, daratumumab can now be used in combination with the immunomodulatory agent lenalidomide and dexamethasone, or the proteasome inhibitor bortezomib and dexamethasone, both standard therapies for the treatment of multiple myeloma. In the POLLUX trial, 569 patients with relapsed/refractory multiple myeloma were randomized 1:1 to receive daratumumab in combination with lenalidomide-dexamethasone or lenalidomide-dexamethasone alone. The CASTOR trial randomized 498 patients with relapsed/ refractory multiple myeloma 1:1 to daratumumab in combination with bortezomib-dexamethasone, or bortezomibdexamethasone alone. The eligibility and exclusion criteria for both trials were similar; patients had received at least one previous line of therapy, had documented progressive disease according to International Myeloma Working Group criteria, and had measurable disease on the basis of urine and/or serum assessments or serum-free, light-chain assay. Patients with a neutrophil count of ≤1,000 cells/mm3, hemoglobin level of ≤7.5 g/dL, platelet count of <75,000 cells/mm3, creatinine clearance of ≤20 mL/min per 1.73m2 body surface area (or <30 mL/min in the POLLUX trial), alanine aminotransferase or aspartate aminotransferase level ≥2.5 times the upper limit of normal (ULN) range, bilirubin level of ≥1.5 or more times the ULN range, disease refractory to bortezomib or lenalidomide, and unacceptable side effects from bortezomib or lenalidomide, were ineligible for these studies. In addition, patients with grade 2 or higher peripheral neuropathy or neuropathic pain, were excluded from the CASTOR study. Randomization was stratified according to International Staging System disease stage at the time of screening (stage I, II or III, with higher stage indicating more severe disease), number of previous lines of therapy (1 vs 2, or 3 vs >3), and previous receipt of lenalidomide or bortezomib. In the CASTOR trial, patients received up to eight 21-day cycles of bortezomib, administered subcutaneously at a dose of 1.3 mg/m2 on days 1, 4, 8, and 11 of cycles 1-8, and dexamethasone, administered orally or intravenously at a dose of 20 mg on days 1, 2, 4, 5, 8, 9, 11, and 12 for a total Expanded approval for daratumumab in multiple myeloma","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"65-67"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48791954","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":"Rucaparib - Second PARP inhibitor hits the market for ovarian cancer","authors":"J. D. Lartigue","doi":"10.12788/JCSO.0333","DOIUrl":"https://doi.org/10.12788/JCSO.0333","url":null,"abstract":"March-April 2017 www.jcso-online.com Rucaparib was granted accelerated approval by the US Food and Drug Administration for the treatment of patients with BRCA1/2 mutant advanced ovarian cancer in January this year, making it the second drug in its class for this indication. It is a poly(ADPribose) polymerase inhibitor that works by blocking the repair of damaged DNA in cancer cells and triggering cell death. The approval was based on findings from 2 single-arm clinical trials in which rucaparib led to complete or partial tumor shrinkage in more than half of the patients enrolled. A pooled analysis included 106 patients from the phase 2 trials, Study 10 (NCT01482715; N = 42) and ARIEL2 (NCT01891344; N = 64), in which patients with BRCA1/2 mutation-positive ovarian cancer who had progressed on 2 or more previous chemotherapy regimens, received 600 mg rucaparib twice daily. Study 10 included only patients with platinum-sensitive disease and eligible patients were aged 18 years or older, with a known deleterious BRCA mutation, evidence of measurable disease as defined by Response Evaluation Criteria in Solid Tumors (version 1.1), sufficient archival tumor tissue, histologically confirmed high-grade epithelial ovarian, fallopian tube or primary peritoneal cancer and relapsed disease confirmed by radiologic assessment. Meanwhile, ARIEL2 had similar eligibility criteria, except that patients with platinum-sensitive, resistant, and refractory disease were included. Both studies excluded patients with active second malignancies, and for those with a history of prior cancer that had been curatively treated, no evidence of current disease was required and chemotherapy should have been completed more than 6 months or bone marrow transplant more than 2 years before the first dose of rucaparib. Patients who had previously been treated with a PARP inhibitor, with symptomatic and/or untreated central nervous system metastases, or who had been hospitalized for bowel obstruction within the previous 3 months, were also ineligible. Across the 2 trials, the median age of trial participants was 59 years, 78% were white, and all had an Eastern Cooperative Oncology Group performance status of 0 (fully active, able to carry on all pre-disease performance without restriction) or 1 (restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature). Both trials used a surrogate endpoint for approval, measuring the percentage of patients who experienced complete or partial tumor shrinkage, the overall response rate (ORR), while taking rucaparib. In Study 10, the ORR was 60%, including a complete response (CR) rate of 10% and a partial response (PR) rate of 50%, over a median duration of response (DoR) of 7.9 months, while in ARIEL2, the ORR was 50%, including a CR of 8% and a PR of 42%, over a median DoR of Rucaparib – second PARP inhibitor hits the market for ovarian cancer","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"62-64"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45551500","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":"Emergency department use by recently diagnosed cancer patients in California.","authors":"Rebecca S Lash, Janice F Bell, Richard J Bold, Jill G Joseph, Rosemary D Cress, Ted Wun, Ann M Brunson, Patrick S Romano","doi":"10.12788/jcso.0334","DOIUrl":"10.12788/jcso.0334","url":null,"abstract":"<p><strong>Background: </strong>Improving the quality of cancer care and reducing preventable health system use are goals of increasing importance to health practitioners and policy makers. Emergency department (ED) visits are often cited as a source of preventable health system use, however, few studies have described the incidence of ED use by recently diagnosed cancer patients in population-based samples, and no study has addressed the full spectrum of cancer types.</p><p><strong>Objective: </strong>To describe ED use by recently diagnosed cancer patients.</p><p><strong>Methods: </strong>California Office of Statewide Health Planning and Development data and the California Cancer Registry were used to describe ED use in the year after a cancer diagnosis (2009-2010). The incidence of ED use was tabulated by cancer type. Logistic regression and recycled predictions were used to examine ED use adjusting for confounding factors.</p><p><strong>Results: </strong>Most ED visits (68%) occurred within 180 days of diagnosis. The incidence of ED use for all cancer types examined was 17% within 30 days, 35% within 180 days and 44% within 365 days of diagnosis. ED use varied by cancer type (5%-39% within 30 days of diagnosis; 14% -62% within 180 days; and 22%-69% within 365 days). Patterns of ED use by cancer type remained similar after accounting for demographic and socioeconomic factors.</p><p><strong>Limitations: </strong>Those common to administrative and registry datasets. Specifically, we were unable to account for ED visits in relation to cancer treatment dates and comorbid conditions.</p><p><strong>Conclusions: </strong>Cancer patients use EDs at higher rates than previously reported, with considerable variability by cancer type. Future research should examine reasons for ED visits by cancer type and identify predictors of ED use, including treatment and comorbid conditions.</p>","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 2","pages":"95-102"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673305/pdf/nihms-1637432.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10189267","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":"An unusual case of primary cardiac prosthetic valve-Associated lymphoma","authors":"Sagila George, B. Gehrs, S. Srour","doi":"10.12788/JCSO.0260","DOIUrl":"https://doi.org/10.12788/JCSO.0260","url":null,"abstract":"Primary cardiac tumors are extremely rare neoplasms with an incidence of less than 0.4%.1-3 Primary cardiac lymphoma (PCL), the majority of which is non-Hodgkin lymphoma, accounts for around 2% of cardiac tumors and less than 0.5% of extranodal lymphomas.1,4-6 Primary lymphoma involving cardiac valves has been described in few case reports and small case series owing to its rarity.7-10 Most cases of PCL present with manifestations of congestive heart failure or cardiac arrhythmias,11 whereas primary valve-associated lymphoma (PV-AL) is usually diagnosed incidentally during valve repair or replacement. The pathophysiology remains unclear, but a few cases have been associated with Epstein Barr virus (EBV).7 Cases previously described in the literature carried an overall poor prognosis and to date there is no standardized treatment approach. We provide here an unusual case of primary prosthetic valve-associated cardiac large B-cell lymphoma, which was successfully treated with adjuvant chemotherapy after valve repair and which resulted in an excellent long-term outcome.","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"109-112"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45538178","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":"Prevention and treatment options for mTOR inhibitor-associated stomatitis","authors":"Kelly Staves, K. Ramchandran","doi":"10.12788/JCSO.0335","DOIUrl":"https://doi.org/10.12788/JCSO.0335","url":null,"abstract":"Mammalian target of rapamycin (mTOR), a serine–threonine protein kinase, operates in the phosphoinositide 3-kinase (PI3K)–protein kinase B (AKT)–mTOR signal transduction pathway regulating both normal and cancer cellular processes, including cell growth, proliferation, motility, survival, and protein and lipid synthesis.1 Genetic alterations affecting this pathway, including mutations in receptor tyrosine kinases PI3K and AKT, occur frequently in human cancers,2 supporting the rationale to develop drugs that target pathway components, such as mTOR inhibitors. Two mTOR inhibitors are currently approved by the US Food and Drug Administration for cancer treatment: temsirolimus, for advanced renal cell carcinoma (RCC; approved 2007)3 and everolimus, for advanced RCC (approved 2009), advanced pancreatic neuroendocrine tumors (pNET; approved 2011), and hormone receptor-positive (HR-positive), human epidermal growth factor receptor-2 (HER2)-negative advanced breast cancer (approved 2012).4 Another mTOR inhibitor, sirolimus, is approved for use as an immunosuppressive agent and prophylactic against organ rejection after kidney transplant.5 Stomatitis, inflammation of the oral mucosa with contributing factors of genetic predisposition, nutritional deficiencies, infections, and immunological or hematologic dysfunction,6 occurs frequently as a side effect associated with mTOR inhibitor treatment.7-9 Left untreated or managed unsatisfactorily, mTOR inhibitor-associated stomatitis (mIAS) may cause patients discomfort and trouble with maintaining adequate nutritional intake and proper oral hygiene, as well as strict adherence to cancer treatment. It is therefore important for health care providers of cancer patients receiving mTOR inhibitor treatment to be knowledgeable about this side effect. The purpose of the present systematic review of published literature is to provide a better understanding of the differential diagnosis of mIAS, the pathophysiology of mIAS, preventive strategies for patients initiating mTOR inhibitor treatment, and treatment options available to manage mIAS.","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"74-81"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45797780","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":"Repeal and replace? How about retain, review, and refine?","authors":"David H. Henry","doi":"10.12788/JCSO.0337","DOIUrl":"https://doi.org/10.12788/JCSO.0337","url":null,"abstract":"","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"59-61"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42413815","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":"Meeting the potential of immunotherapy: new targets provide rational combinations","authors":"J. D. Lartigue","doi":"10.12788/JCSO.0336","DOIUrl":"https://doi.org/10.12788/JCSO.0336","url":null,"abstract":"The anti-tumor immune response Cancer is a disease of genomic instability, whereby genetic alterations ranging from a single nucleotide to the whole chromosome level frequently occur. Although cancers derive from a patient’s own tissues, these genetic differences can mark the cancer cell as non-self, triggering an immune response to eliminate these cells. The first hints of this anti-tumor immunity date back more than a century and a half and sparked the concept of mobilizing the immune system to treat patients.1-3 Although early pioneers achieved little progress in this regard, their efforts provided invaluable insights into the complex and dynamic relationship between a tumor and the immune system that are now translating into real clinical successes. We now understand that the immune system has a dual role in both restraining and promoting cancer development and have translated this understanding into the theory of cancer immunoediting. Immunoediting has three stages: elimination, wherein the tumor is seemingly destroyed by the innate and adaptive immune response; equilibrium, in which cancer cells that were able to escape elimination are selected for growth; and escape, whereby these resistant cancer cells overwhelm the immune system and develop into a symptomatic lesion.4,5 Immuno-oncologists have also described the cancer immunity cycle to capture the steps that are required for an effective anti-tumor immune response and defects in this cycle form the basis of the most common mechanisms used by cancer cells to subvert the anti-tumor immune response. Much like the cancer hallmarks did for molecularly targeted cancer drugs, the cancer immunity cycle serves as the intellectual framework for cancer immunotherapy.6,7","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"116-121"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41385474","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":"Distress management in cancer patients in Puerto Rico","authors":"Maricarmen Ramírez-Sola","doi":"10.12788/JCSO.0321","DOIUrl":"https://doi.org/10.12788/JCSO.0321","url":null,"abstract":"A comprehensive, patient-centered approach is required to accomplish cancer best standards of care.1 This approach reflects the holistic conceptualization of health in which the physical, emotional, and social dimensions of the human being are considered when providing medical care. As a result, to look after all patient needs, interdisciplinary and well-coordinated interventions are recommended. Cancer patients should be provided not only with diagnostic, treatment, and follow-up clinical service, but also with the supportive assistance that may positively influence all aspects of their health. To appraise physical, social, emotional and spiritual issues and to develop supportive interventional action plans, the National Comprehensive Cancer Network (NCCN) recommends screening all cancer patients for distress.2 In particular, screening the emotional component of distress occupies a prominent place in this process because it is now recognized as the sixth vital sign in oncology.3 Even though the influence of emotional distress over cancer mortality rates and disease progression is still under scrutiny,4 its plausible implications over treatment compliance have been pointed out. Patients with higher levels of emotional distress show lower adherence to treatment and poorer health outcomes.5 Furthermore, prevalence rates of emotional distress in cancer patients from ambulatory settings6 and oncology surgical units have been studied and have provided justification for distress management.7 Studies have shown low ability among oncologists to identify patients in distress and oncologists’ tendency to judge distress higher than the patients themselves.8 As a consequence, to achieve systematic distress evaluations and appropriate referrals for care, guidelines for distress management should be implemented in clinical settings. It is recommended that tests are conducted to find brief screening instruments and procedures to assure accurate interventions according to patient specific needs. This article presents the process of implementing a distress management program at HIMA-San Pablo Oncologic Hospital in Caguas, Puerto Rico, with particular emphasis on the management of emotional distress, which has been defined as the feeling of suffering that cancer patients may experience after diagnosis. In addition, we have included data from a pilot study that was completed for content validation of the Patient Health Questionnaire (PHQ-9) to estimate depression levels in Puerto Rican cancer patients.","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"68-73"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49469692","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":"Multispecies coalescent delimits structure, not species.","authors":"Jeet Sukumaran, L Lacey Knowles","doi":"10.1073/pnas.1607921114","DOIUrl":"10.1073/pnas.1607921114","url":null,"abstract":"<p><p>The multispecies coalescent model underlies many approaches used for species delimitation. In previous work assessing the performance of species delimitation under this model, speciation was treated as an instantaneous event rather than as an extended process involving distinct phases of speciation initiation (structuring) and completion. Here, we use data under simulations that explicitly model speciation as an extended process rather than an instantaneous event and carry out species delimitation inference on these data under the multispecies coalescent. We show that the multispecies coalescent diagnoses genetic structure, not species, and that it does not statistically distinguish structure associated with population isolation vs. species boundaries. Because of the misidentification of population structure as putative species, our work raises questions about the practice of genome-based species discovery, with cascading consequences in other fields. Specifically, all fields that rely on species as units of analysis, from conservation biology to studies of macroevolutionary dynamics, will be impacted by inflated estimates of the number of species, especially as genomic resources provide unprecedented power for detecting increasingly finer-scaled genetic structure under the multispecies coalescent. As such, our work also represents a general call for systematic study to reconsider a reliance on genomic data alone. Until new methods are developed that can discriminate between structure due to population-level processes and that due to species boundaries, genomic-based results should only be considered a hypothesis that requires validation of delimited species with multiple data types, such as phenotypic and ecological information.</p>","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"12 1","pages":"1607-1612"},"PeriodicalIF":0.0,"publicationDate":"2017-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5320999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88920895","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":"Liquid gold: Blood-based biopsies make headway","authors":"J. D. Lartigue","doi":"10.12788/jcso.0318","DOIUrl":"https://doi.org/10.12788/jcso.0318","url":null,"abstract":"Liquid biopsy gaining traction Biopsies enable oncologists to gather information about a potential or established tumor, including confirmation of the presence of cancerous tissue and determination of its histological characteristics, such as tumor grade and stage, as well as its molecular features, such as the presence of certain gene mutations. Ultimately, this information can be put to use in determining the most appropriate course of treatment. The current gold standard is a tissue biopsy that typically involves an invasive procedure to permit the collection of a piece of tumor tissue. Yet, tissue biopsies are not always feasible because of the location of the tumor or the poor performance status of many patients with advanced disease. They also provide only a snapshot of the disease at the time at which they were taken and don’t necessarily reflect the genetic heterogeneity or evolution of a tumor over time. The detection of components that are derived from the tumor circulating in the blood of cancer patients had fueled the idea of blood-based diagnostics in oncology – so-called liquid biopsies. These have rapidly gained traction in the past several decades as a less expensive (the cost of performing genomic analyses on blood samples is at least an order of magnitude less than on tissue samples), less invasive (requiring only a simple blood draw) alternative source of information about tumors. As researchers have refined the ability to exploit liquid biopsies, commercial interest has been piqued. More than 35 companies within the United States alone are developing liquid biopsies, and it’s easy to see why with a market projected to be in the many billions of dollars.","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":"15 1","pages":"49-54"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66811344","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}