Journal of lung cancer最新文献

{"title":"Development of a Multidisciplinary Care System for Lung Cancer Patients","authors":"K. Na, S. Ahn, Y. Kim, H. Bom, Chan Choi, K. S. Kim, I. Oh, Sang‐Yun Song, Song Choi, Y. Choi, S. Jeong, M. Yoon, Sun-Mi Back, Kang-Eun Kong, Young-chul Kim","doi":"10.6058/JLC.2008.7.2.75","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.2.75","url":null,"abstract":"Purpose: Since the year 2000, lung cancer has been the leading cause of cancer death in South Korea and also in many other parts of the world. Materials and Methods: We developed a multidisciplinary (MD) care system for lung cancer patients in 1996. Here, we report the results obtained in the process of development of MD team (MDT). Results: The MDT was launched with including medical doctors, chest surgeons, radiation oncologists, radiologists, nuclear medicine specialists and physician assistants. To facilitate co-operation between the MDT members, a specialized out-patient clinic was located within a sector of the hospital. A common ward was allocated for lung cancer patients regardless of the department of the attending physician. Shared electronic medical record forms that were specialized for lung cancer were developed. The MDT operates weekly lung cancer conferences and multidisciplinary out-patient clinics. To make diagnostic or therapeutic decisions early on, the electronic medical records of the patients were previewed or consulted by the specialists before they meet the individual patients. Conclusion: Despite every effort, we still need to shorten the waiting time from presentation to the first treatment and we need to improve the patients’ satisfaction. We also have a mission to develop our own regulations and guidelines for our lung cancer MD care system. Clinical trials and basic research should also be encouraged along with improving the quality of life of the team members. (J Lung Cancer 2008;7(2):75 �� 80)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"98 1","pages":"75-80"},"PeriodicalIF":0.0,"publicationDate":"2008-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2008.7.2.75","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160003","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":"Esophageal Cancer with Left Main Bronchus Obstruction","authors":"Seung-Ji Kang, I. Oh, K. S. Kim, Young-chul Kim","doi":"10.6058/JLC.2008.7.1.34","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.1.34","url":null,"abstract":"A 66-year-old man with recurrent esophageal cancer was admitted to our health care facility for evaluation of resting dyspnea. He had undergone an esophagectomy with cervical esophagogastrostomy in May 2007 and had undergone radical radiation treatment from June to August 2007. After 6 months, he complained of cough and dyspnea. A metastatic lymphadenopathy, 4 cm in size, was in the para-aortic space and compressed the left main bronchus, resulting in total atelectasis of the left lung, as demonstrated on follow-up chest simple x-ray and CT (Fig. 1, 2). He initially received one cycle of chemotherapy consisting of docetaxel and cisplatin, but there was no change in the lung atelectasis and the dyspnea had worsened. The decision was therefore made to perform a rigid bronchoscopy. Under general anesthesia, an endobronchial obstructive lesion was removed using a mechanical core-out technique with rigid bronchoscopy (Fig. 3). After the procedure, the atelectasis resolved nearly completely, and neither severe bleeding nor other complications were noted (Fig. 4). The dyspnea was relieved from ATS (American thoracic society) grade 4 to grade 2. Following this treatment, chemotherapy for recurrent esophageal cancer was resumed.","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"7 1","pages":"34-35"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2008.7.1.34","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71159520","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":"Molecularly Targeted Therapy for Lung Cancer: Recent Topics","authors":"N. Saijo","doi":"10.6058/JLC.2008.7.1.1","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.1.1","url":null,"abstract":"Many clinical trials of molecular target drugs have been done against advanced lung cancer, however, majority did not meet the primary endpoint. Positive studies of EGFR-TKI such as BR21 and Interest used unselected populations of non-small cell lung cancer. It was quite difficult to explain why they were positive. In the present review, the difficulties of clinical trial design in molecular target drugs were discussed based on the differences of the magnitude of antitumor activity and the target tumor cell population between cytotoxic drugs and molecular target therapy. (J Lung Cancer 2008;7(1):1 �� 8)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"7 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2008.7.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71159424","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":"May-Thurner Syndrome in Lung Cancer.","authors":"S. Chi, I. Oh, K. S. Kim, Young-chul Kim","doi":"10.6058/JLC.2008.7.1.36","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.1.36","url":null,"abstract":"May-Thurner syndrome is deep vein thrombosis (DVT) of the iliofemoral vein due to compression of the left common iliac vein (CIV) by the overlying right common iliac artery (CIA). In contrast to the right CIV, which ascends almost vertically to the inferior vena cava (IVC), the left CIV follows a more transverse course. Along this course, it underlies the right CIA, which may compress it against the lumbar spine. A 69-year-old man with squamous cell lung cancer presented with acute onset painful left leg swelling. He had been undergoing chemotherapy with gemcitabine and cisplatin as a 2nd line treatment after concurrent chemoradiation. Physical examination revealed left leg edema with tenderness and warmth. The D-dimer level was elevated and a lower extremity computed tomographic angiogram (CTA) showed a DVT involving the left infrapopliteal vein to the common iliac vein with collapsed junction between the CIV and IVC. Systemic anticoagulation with low molecular weight heparin (LMWH) and an IVC filter insertion was performed to prevent further thrombosis, such as a PTE. After IVC filter placement, mechanical thrombectomy was performed on the left femoral vein and left CIV. A vascular stent was then deployed in the left CIV. Left leg swelling seemed to be improved after heparinization, but he had a 2nd episode one week later. Therefore, he underwent a 2nd mechanical thrombectomy and stent deployment of the left external iliac vein. His leg swelling was gradually relieved. He has received LMWH for 3 months, and has received 2 cycles of pemetrexed followed by erlotinib.","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"7 1","pages":"36-36"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71159602","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":"Radiation Induced Lung Damage: Mechanisms and Clinical Implications","authors":"Y. Oh","doi":"10.6058/JLC.2008.7.1.9","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.1.9","url":null,"abstract":"Radiation therapy is one of most important therapeutic modalities for thoracic malignancies. However, radiation-induced lung damage, such as radiation pneumonitis or fibrosis, is a main dose-limiting factor when irradiating the thorax. The radiation over threshold dose results in damage to pneumocytes and endothelial cells and the inflammatory changes following the damage lead to necrosis of damaged tissue, which are then replaced by fibrotic tissue. There is diffuse lung damage and edema on histopathologic inspection; however, the tissue damage and edema is not specific for radiation injury and we are far from a reliable pathogenic model. Many parameters have been evaluated for predicting radiation pneumonitis and the most consistent predictor is cumulative radiation dose to normal lung tissue. The combination of chemotherapy probably increases the incidence and severity of radiation pneumonitis; however, this is not clear. Efforts to reduce the radiation dose to normal lung tissue using new radiotherapy techniques can reduce the incidence and severity of radiationinduced lung damage. Many biological agents have been tried to prevent and treat radiation pneumonitis; however, more data is needed.","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"7 1","pages":"9-18"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2008.7.1.9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71159678","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":"Mutational Analysis of the Tumor Suppressor WTX Gene in Non-small Cell Lung Cancer","authors":"S. Moon, Y. Chung, N. Yoo, M. S. Kim, S. Lee","doi":"10.6058/JLC.2008.7.1.22","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.1.22","url":null,"abstract":"Purpose: In a recent study of Wilms' tumors, a new X chromosome gene, Wilms' tumor gene on the X chromosome (WTX), was discovered that was found to harbor small deletions and point mutations. The WTX protein negatively regulates Wnt/ β-catenin signaling, and is considered to be a tumor suppressor gene. One of the questions about the WTX gene is whether the genetic alterations of the WTX gene are specific only to Wilms' tumors. The aim of this study was to explore whether the WTX gene mutation is a characteristic of human non-small cell lung cancer (NSCLC). Materials and Methods: In the current study, we analyzed the part of the WTX gene encoding the N-terminal of WTX, where most of the WTX point mutations have been detected in Wilms' tumors. Forty-eight NSCLC tissues were analyzed by a single-strand conformation polymorphism assay and DNA sequencing. Results: SSCP analysis revealed no evidence of somatic mutations in the DNA sequences encoding the N-terminal of the WTX gene in the 48 NSCLC tissues. Conclusion: The data presented here indicate that the WTX gene may not be somatically-mutated in human NSCLCs, and suggest that NSCLCs may not utilize mutational events of the WTX gene in the process of pathogenesis. (J Lung Cancer 2008;7(1):22�� 24)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"7 1","pages":"22-24"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2008.7.1.22","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71159070","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":"Immunohistochemical Application to the Pathologic Diagnosis of Lung Cancer","authors":"Choong‐Sik Lee","doi":"10.6058/JLC.2008.7.1.19","DOIUrl":"https://doi.org/10.6058/JLC.2008.7.1.19","url":null,"abstract":"Lung cancer is the most common cause of death from neoplasms in Korea. Since the pathologic diagnosis is very important to determine the optimal treatment protocol of the patients, not only pathologists, but also oncologists, have an interest in the diagnosis of cancer. At the present time, immunohistochemical studies do more than play a supplementary role on the biopsied or excised specimens from cancer patients. Thus, I have reviewed the general principles and applications of immunohistochemistry on the histologic diagnosis of lung cancer. (J Lung Cancer 2008;7(1):19�� 21)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"10 1","pages":"19-21"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2008.7.1.19","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71159047","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":"National Survey of Lung Cancer in Korea, 2005","authors":"Young-chul Kim, Yong-Soo Kwon, I. Oh, K. S. Kim, S. Kim, J. Ryu, H. Yum, S. Yong, K. Lee, C. Lee, Sang Yeub Lee, Sung-Yong Lee, M. Jung, E. Jeong, K. In","doi":"10.6058/JLC.2007.6.2.67","DOIUrl":"https://doi.org/10.6058/JLC.2007.6.2.67","url":null,"abstract":"Purpose: Lung Cancer has been the leading cause of cancer deaths in South Korea since the year 2000, and its incidence continues to rise. Here we report the result of national survey of lung cancer conducted by Korean association for the study of lung cancer (KASLC). Materials and Methods: A total of 8,788 lung cancer patients diagnosed in 2005 were registered using a web based case report form issued to hospitals equipped with more than 400 beds. Results: The age distribution ranged from 11 to 105 years (64.7±10.7 years), 75.8% (6,664) of the patients were male and 28.9% of patients were never smokers. Subjective symptoms at the time of diagnosis included coughing (3,350 patients), dyspnea (2,105), chest pain (1,067), hemoptysis (805), weight loss (789), general weakness (498) and hoarseness (190), while 12% (1,015) of patients had no subjective symptoms. Of the carcinomas grouped into non-small cell lung carcinoma (NSCLC), adenocarcinoma including bronchoalveolar cell carcinoma (1.3%) was the most frequent (36.1%) histopathologic type, followed by squamous cell lung carcinoma (32.1%), large cell carcinoma (1.5%), unclassified non-small cell carcinoma (13.2%) and others (3.7%). In addition, 13.5% of all of the patients were afflicted with small cell lung carcinoma (SCLC). The stage at diagnosis was IA (7.3%), IB (10.2%), IIA (1.3%), IIB (6.1%), IIIA (12.8%), IIIB (21.6%), and IV (40.6%) in the NSCLC group. In SCLC group, 44.6% of the patients were in the limited stage, while 55.4% of the patients were in the extensive stage. The initial treatments included surgery (22.1%), radiation therapy (7.8%), chemo-radiation therapy (5.4%) and chemotherapy (38%), however, 26.6% of the patients were transferred or recorded to have supportive care only. Therefore we compared the outcomes of the Treatment Group (TG, 73.4%) and the Supportive Group (SG, 26.6%). The median survival time (MST) in months (m) was 28 (95% confidence interval 26.5~29.5 m). Multivariate analysis indicated that the independent prognostic factors for NSCLC were age, gender, ECOG PS score, stage, histopathologic type, and treatment or supportive care. In the SCLC group, age, PS score, stage, treatment or supportive care were significant prognostic factors. The TG group showed significantly superior survival when compared to the SG group, even in patients with stage IV disease and in patients that were ＞75 years old. Conclusion: Adenocarcinoma was found to be the most frequent histopathologic type, and active treatments were found to improve the survival of patients with lung cancer, even when they were in advanced stages or elderly. (J Lung Cancer 2007;6(2):67�� 73)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"8 1","pages":"67-73"},"PeriodicalIF":0.0,"publicationDate":"2007-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2007.6.2.67","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71158680","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":"Cyclooxygenase-2 (COX-2) Inhibitors Reduce Immune Tolerance through Indoleamine 2,3-dioxygenase (IDO).","authors":"S. Lee, K. Lee, J. Jung, E. Lee, E. Kang, K. Jung, Sang Yeub Lee, J. H. Kim, C. Shin, J. Shim, K. In, K. Kang, S. Yoo","doi":"10.6058/JLC.2007.6.1.15","DOIUrl":"https://doi.org/10.6058/JLC.2007.6.1.15","url":null,"abstract":"Purpose: Cyclooxygenase-2 (COX-2) and its metabolite, PGE2 affect multiple tumorigenesis, including angiogenesis, invasion, and tumor-induced immune suppression. Their overexpression is association with impaired immune cell function in many tumors. Indoleamine 2,3-dioxygenase (IDO) is an emerging immuno-regulatory enzyme that can catalyze the initial rate-limiting step in tryptophan catabolism, by causing tryptophan depletion can block T lymphocyte activation, and thus, enable tumor cells to escape from immune system. Although the potential of immunosuppression associated with tumorproduced COX-2 has been suggested, the mechanism of immunosuppression in tumor immunology is not yet well defined. Thus, we hypothesized that the tumor immunity of COX-2 could be partly due to IDO-dependent immune tolerance. To test this hypothesis, we evaluated IDO expression in cancer cells treated with selective COX-2 inhibitor. Materials and Methods: The A549 human adenocarcinoma cell line, murine Lewis lung carcinoma (LLC) cell line and C57Bl/6 mice were used for in vitro and in vivo studies. In vitro studies, A549 cells were treated with various concentrations of COX-2 inhibitor (PTPBS) or PGE 2. IDO enzyme activity and protein expression were checked by IDO enzyme activity assay and Western blotting. In vivo study, the 20 mice were randomized into normal control, LLC inoculated control, and low and high selective COX-2 inhibitor (celecoxib 25 or 250 mg/kg/day) treated LLL inoculated mice groups (n=5 per group). At one month, mice were sacrificed and tumor mass was isolated for quantification of IDO expression by immunohistochemical stain and western blotting. Results: In vitro studies, PTPBS treated A549 cells showed a significant decreased in IDO enzyme activity and expression but PGE 2 treated A549 cells showed increased in IDO expression. In vivo studies, the tumor mass and lung metastasis were attenuated by celecoxib (respectively, p＜0.05, p＜0.01). Compared with the LLC inoculated control group, mice treated with celecoxib had significant reductions in IDO expression of tumor mass (IDO immunohistochemical stain and western blotting ). Conclusion: The present study reveals that COX-2 inhibitor serves to restore the tumor-induced IDO expression and promotes antitumor reactivity in an immunocompetent murine lung cancer model. These findings further support the suggestion that COX-2 inhibitor is a potential pharmacological immunotherapy in cancer. (J Lung Cancer 2007;6(1):15 �� 23)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"6 1","pages":"15-23"},"PeriodicalIF":0.0,"publicationDate":"2007-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2007.6.1.15","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71158482","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":"A Comparison of Gemcitabine in Two Doses for Stage III or IV Non-small Cell Lung Cancer: a Multi-Institutional Phase II Study","authors":"H. Park, Jinyoung An, Y. Lee, M. Joung, Y. Lee, S. Jung, H. Yun, Ju Ock Kim, K. S. Kim, Young-chul Kim, M. Jung, J. Ryu, S. Kim","doi":"10.6058/JLC.2007.6.1.1","DOIUrl":"https://doi.org/10.6058/JLC.2007.6.1.1","url":null,"abstract":"Purpose: Since the combination of cisplatin plus gemcitabine (CG) had a significant survival advantage for the treatment of patients with chemotherapynaive advanced or metastatic non-small cell lung cancer (NSCLC), CG combination have been evaluated with different schedules. However, the best schedule is still unclear. We designed to compare the efficacy and toxicity of CG combination chemotherapy in two different doses of gemcitabine (1,000 or 1,250 mg/m 2 3-weekly). Materials and Methods: We randomized patients with stage III or IV NSCLC into either gemcitabine 1,250 mg/m 2 or gemcitabine 1,000 mg/m 2 . Patients received cisplatin 60 mg/m 2 intravenously on day1 of each 3-week cycle. Gemcitabine was administered intravenously on days 1 and 8 of each 3-week cycle. Results: From April 2002 until July 2004, 125 patients were enrolled from four university hospitals (55 patients in the gemcitabine 1,000 mg/m2 arm and 70 patients in the gemcitabine 1,250 mg/m 2 arm). Response rates were not significantly different in both arms (56.4% vs. 55.7%). However, grade 3 neutropenia was significantly lower in gemcitabine 1,000 mg/m2 arm compared to gemcitabine 1,250 mg/m 2 arm (11.0% vs. 15.8%). No differences in non-haematologic toxicities in both arms except anorexia were observed. The median survival was 13.4 months for gemcitabine 1,000 mg group compared with 15.8 months for gemcitabine 1,250 mg group. There were no statistically significant differences in survival between the groups. Conclusion: For stage III or IV non-small cell lung cancer, combination chemotherapy with gemcitabine 1,000 mg/m 2 showed equivalent response rate with lesser neutropenia and anorexia compared to treatment with gemcitabine 1,250 mg/m2 . (J Lung Cancer 2007;6(1):1 �� 7)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"6 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2007-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2007.6.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71158212","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}