The Open autoimmunity journal最新文献

{"title":"Laboratory Criteria of Antiphospholipid Syndrome Need to be Updated or Strictly Followed?~!2009-09-24~!2009-09-28~!2010-03-11~!","authors":"M. Martinuzzo","doi":"10.2174/1876894601002020028","DOIUrl":"https://doi.org/10.2174/1876894601002020028","url":null,"abstract":"The antiphospholipid syndrome is a very relevant disease that implicates different clinical features and labora- tory criteria. Regarding laboratory diagnosis, it has been established in the last consensus that tests included are lupus an- ticoagulant (LA), anti cardiolipin (aCL) and anti � 2 glycoprotein I antibodies (anti � 2GPI) of IgG or IgM isotype at me- dium to high titres. There is not one unique or a gold standard test for APS, so laboratory diagnosis is one of the more im- portant problems. Considering LA testing, new guidelines have been recently published. They include not only the selec- tion of coagulation tests, but also important recommendations about preanalytical variables, mixing and confirmatory studies interpretation, and cut off calculations. Taking into account solid phase assays, the major problem is the low re- producibility and the high inter assays variation. This problem has been recognized early with aCL. Despite many efforts such as the introduction of polyclonal and monoclonal standards, laboratory workshops, etc, the situation is still compli- cated. This problem was supposed to be solved when anti � 2GPI were introduced, but many collaborative studies and quality control surveys assessment have also demonstrated a lot of problems in standardization. The need of reference ma- terials for LA and solid phase assays has been recognized many years ago but there is no clear advance in this line. An- other important aspect is the fact that none of these tests are specific for APS, so they can be present in many clinical set- tings. Recent advances have been done by developing assays to detect anti domain I � 2GPI antibodies that could be more specific. It is hoped that in the near future, by worldwide collaborative actions, problems on laboratory diagnosis of APS will be overcome.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"28-37"},"PeriodicalIF":0.0,"publicationDate":"2010-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151907","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":"Clinical Studies Examining Thrombosis Related to Autoimmune Antiphospholipid Antibodies~!2009-09-20~!2009-09-25~!2010-03-11~!","authors":"M. Bertolaccini, M. Khamashta","doi":"10.2174/1876894601002020045","DOIUrl":"https://doi.org/10.2174/1876894601002020045","url":null,"abstract":"Laboratory diagnosis of APS relies on the demonstration of positive antiphospholipid antibodies (aPL), includ- ing anticardiolipin antibody (aCL) and/or anti- 2 glycoprotein I antibody (anti- 2GPI) by an in-house or commercially available enzyme-linked immunosorbent assay (ELISA) or lupus anticoagulant (LA) by a coagulation-based test. The re- lationship between aPL and thrombosis has been abundantly studied. However, the reported results, largely influenced by differences in study design, patient population and antibody assays, have been controversial and the precise serological 'fingerprint' of the patients most at risk of thrombosis remains elusive. The risk of recurrent thrombosis is increased in patients with APS. The type of thrombosis is predictive; retrospective analysis of patients with APS and recurrent thrombosis showed that a venous thrombosis is followed by another ve- nous thrombosis in more than 70% of cases, and an arterial thrombosis is followed by another arterial thrombosis in more than 90% of cases (2-4). Laboratory diagnosis of APS relies on the demonstration of a positive anticardiolipin antibody (aCL) and/or anti- 2 glycoprotein I antibodies (anti- 2GPI) by an in-house or commercially available enzyme-linked immunosorbent assay (ELISA) or on the presence of lupus anticoagulant (LA) by a coagulation-based test. It is important that these tests be per- formed in patients suspected of having APS where persistent positivity must be demonstrated and other causes and under- lying factors considered. aPL are not uncommon. The preva- lence of aPL among healthy donors has been reported to be around 10% (5, 6) whilst they have been found in about 25% of patients with unexplained venous thrombosis, 20% of patients with stroke (7), around 18% of patients with prema- ture coronary artery thrombosis (8, 9) and in about 30% of patients with recurrent foetal loss (10).","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"45-48"},"PeriodicalIF":0.0,"publicationDate":"2010-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151529","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":"Tissue-Dependent Expression of Estrogen Receptor β in 17β-Estradiol-Mediated Attenuation of Autoimmune CNS Inflammation.","authors":"Richard E Jones, Laurie Kaler, Stephanie Murphy, Halina Offner","doi":"10.2174/1876894601002010197","DOIUrl":"10.2174/1876894601002010197","url":null,"abstract":"<p><p>Treatment strategies using therapeutic estrogen are being developed and tested for multiple sclerosis (MS). MS is an autoimmune inflammatory disease that attacks the central nervous system, damages myelin and produces neurode-generative changes associated with periodic and chronic progression of functional neurological deficit. Experimental studies in chimeric bone marrow transplant mice treated with 17β-estradiol (E2) have revealed that the estrogen receptor-1 (Esr-1, or -alpha) expressed exclusively within the non-hematopoietic tissue compartment is sufficient for mediating a beneficial neuroprotective therapeutic response in mice lacking Esr-1 expression on T lymphocytes or other bone marrow-derived cells. Less is known regarding requirements for estrogen receptor-2 (Esr-2, or -beta) expression in E2-mediated therapy. Here, we tested and compared requirements for Esr-2 expression within distinct tissue compartments in bone marrow transplant mice. Our studies support a crucial role for Esr-1 in E2 treatment and demonstrate that Esr-2 expressed by non-bone marrow-derived cells plays a role in sustaining the neuroprotective response mediated through Esr-1.</p>","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 ","pages":"197-204"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4d/18/nihms-220615.PMC3254147.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30383467","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":"Analytical Performance of a New Gliadin-Activated Anti-tTransglutaminase ELISA Test","authors":"X. Galan, M. L. Hoyos, E. Cacho, I. Goirigolzarri, P. Munujos","doi":"10.2174/1876894600901010079","DOIUrl":"https://doi.org/10.2174/1876894600901010079","url":null,"abstract":"Significant progresses on the anti-tissue transglutaminase antibodies (anti-tTG) ELISA tests have been achieved since anti-tTG early development. Our goal was to study the optimization of the antigen immobilization and the antibody reaction conditions in an ELISA test for the detection of anti-tTG. Hence, three variants of an anti-tTG ELISA test were developed: tTG-Gliad-U, tTG-U and tTG-Gliad, according to the coating conditions (presence/absence of gli- adin) and the stringency in the sample buffer (presence/absence of urea). To assess IgA and IgG anti-tTG frequencies we used a group of 117 CD patients, 36 under a gluten-free diet and 14 with a selective IgA deficiency, and a control group of 165 non-celiac patients. Sensitivity of IgA anti-tTG in CD patients with villous atrophy was 95.5% (tTG-Gliad-U), 65.0% (tTG-U) and 92.5% (tTG-Gliad), respectively. Sensitivity of the IgG anti-tTG assay was 79.0%, 21.0% and 79.0%, re- spectively. Specificities ranged between 92.9% and 100%. Significant lower IgA and IgG concentration values were ob- served in GFD CD patients. Sensitivity and specificity of IgG anti-tTG in CD patients with selective IgA deficiency were 64.3 and 100%, respectively. In conclusion, we have developed an ELISA test for IgA anti-tTG based on calcium and gli- adin activated recombinant human transglutaminase. This test is sensitive and specific, and it is useful to ensure the com- pliance with diet of CD patients.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"79-85"},"PeriodicalIF":0.0,"publicationDate":"2009-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150647","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":"Thymic Development of CD4+25hi Foxp3+ T-Regulatory Cells Echoes their Suppressogenic Capacity in Periphery","authors":"Cristina Nazarov-Stoica, Jacqueline Surls, M. Kehl, C. Bona, S. Casares, T. Brumeanu","doi":"10.2174/1876894600901010064","DOIUrl":"https://doi.org/10.2174/1876894600901010064","url":null,"abstract":"The CD4 + 25 hi Foxp3 + T regulatory (T-reg) cells are naturally-born in thymus and they are critical for maintain- ing the tolerance to self and non-self antigens. Foxp3 is the master-regulatory gene of development and function of this cell subset. Using two mouse strains that share the same MHC class II (H-2 d ) haplotype, we found that Foxp3 is early ex- pressed in the CD3 + 4 - 8 - 25 +/- 44 - (DN3/4) double negative thymocytes. Furthermore, Foxp3 showed a differential kinetics of expression in the thymus of these two strains that were controlled through the rates of proliferation and apoptosis of T- reg precursors, but not by epigenetic alterations at the Foxp3 gene promoter. Faster T-reg proliferation and lower apopto- sis were associated with higher Foxp3 + thymic cell output. Also, faster proliferating T-reg precursors showed lower ex- pression of CD3/TCR complex, leptin receptor, Bad, and Caspase3 early in the DN stage of differentiation. Despite a dif- ferential T-reg thymic output in these two mouse strains, the size of peripheral CD4 + 25 hi Foxp3 + T-reg compartment was homeostatically normalized. However, the Foxp3 + T-reg suppression tested in an autoimmune mouse model for diabetes was stronger in mice with a higher T-reg thymic output. These findings demonstrate a differential thymic development and suppressive capacity of Foxp3 + T-reg cells in two genetic backgrounds regardless the MHC II haplotype. This raises the question of whether a differential suppressogenic capacity of the T-reg compartment may affect the susceptibility to autoimmune disorders in individuals from different ethnic groups.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"64-78"},"PeriodicalIF":0.0,"publicationDate":"2009-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150271","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":"Plasma Concentration of Osteopontin (OPN) in Children with Systemic Lupus Erythematosus: Relationship with Disease Activity","authors":"M. Afify, G. B. Mohamed, M. A. El-Maboud, E. Abdel-Latif","doi":"10.2174/1876894600901010059","DOIUrl":"https://doi.org/10.2174/1876894600901010059","url":null,"abstract":"Background: Osteopontin (OPN) is an important bone matrix mediator found to have key roles in inflammation and immunity. OPN is a cytokine which can play a number of roles in promoting activation of T lymphocyte, regulating balance between T-helper 1 and T-helper 2, participating in cell-induced immunologic response and stimulating B lym- phocyte to express multi-clone antibodies. Overexpression of OPN has been associated with the development of the auto- immune/ lymphoproliferative syndrome. Objective: The aim of our present study was to analyze the possible correlation between the plasma concentration of OPN and disease activity in children with systemic lupus erythematosus (SLE). We also investigated the correlation between plasma IL-18 and OPN concentrations to further confirm the association of OPN with disease activity. Methods: We measured the plasma concentration of OPN, and the plasma proinflammatory IL-18 concentration in 40 SLE patients with or without renal disease (RSLE group and SLE group, respectively) and in 30 sex- and age-matched controls using enzyme immunoassay. Results: Plasma OPN concentrations were significantly higher in RSLE and SLE patients than in the controls (p = 0.000 and p = 0.002). Plasma OPN concentrations were significantly higher in RSLE patients than in the SLE patients (p = 0.000). Plasma OPN concentration correlated positively and significantly with SLE disease activity index in combined SLE patient groups (r = 0.34; p = 0.04). In RSLE patients, plasma OPN concentration showed a significant positive corre- lation with proinflammatory cytokine IL-18 concentration (r = 0.48; p = 0.004). Conclusion: The above results suggest that the production of OPN is associated with the inflammatory process and SLE development, and may serve as a potential disease marker of SLE.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"59-63"},"PeriodicalIF":0.0,"publicationDate":"2009-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150787","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":"Blood and Synovial Microparticles as Revealed by Atomic Force and Scanning Electron Microscope","authors":"I. Junkar, V. Šuštar, Mojca Frank, V. Janša, A. B. Zavec, B. Rozman, M. Mozetič, H. Hägerstrand, V. Kralj-Iglič","doi":"10.2174/1876894600901010050","DOIUrl":"https://doi.org/10.2174/1876894600901010050","url":null,"abstract":"Microvesicles which are pinched off the cell membrane can be considered extracellular organelles which medi- ate interaction between distal cells. They were suggested to play an important role in many diseases including autoim- mune disorders, however, standard methods for their assessment have not yet been decided upon while their clinical rele- vance and the underlying mechanisms are yet unclear. We present a pilot study results involving atomic force microscope (AFM) and scanning electron microscope (SEM) images of the material isolated from peripheral blood of healthy donors and from synovial fluid of patients with psoriatic arthritis and rheumatoid arthritis, which is expected to contain microve- sicles. Micrographs reveal in the samples isolated from blood the presence of globular and tubular structures which are most probably microvesicles while the identity of grain-like structures isolated from synovial fluid remains obscure. To the best of our knowledge the AFM and SEM images of the material isolated from synovial fluid are presented for the first time.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"50-58"},"PeriodicalIF":0.0,"publicationDate":"2009-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150773","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":"CD4+/FOXP3+ Regulatory T Cells in End-Stage Kidney Disease: Molecular Pathways Trough Cell-Cycle Arrest and Apoptosis","authors":"P. Meier","doi":"10.2174/1876894600901010037","DOIUrl":"https://doi.org/10.2174/1876894600901010037","url":null,"abstract":"CD4 + /FOXP3 + regulatory T cells (Tregs) are essential for the maintenance of self-tolerance, and Tregs defi- ciency results in spontaneous autoimmunity in both mice and humans. The forkhead box P3 (FOXP3) expression is required for both survival of Tregs precursors as well as their function. This suggests that Tregs may use multiple mecha- nisms to limit autoimmunity, and may reflect functional heterogeneity among Tregs subsets that localize to distinct tissue environments. Both cell contact- and cytokine-based immunosuppressive mechanisms would require that Tregs be in close proximity to their targets. The fundamental regulatory activity that can be consistently demonstrated by Tregs in vivo and in vitro has stimulated great interest in developing novel strategies for treating ongoing inflammatory conditions. Patients with end-stage kidney disease (ESKD) are known to display a cellular immune dysfunction. Uremic solutes that accumulate during ESKD may be involved in these processes. In these patients, oxidative stress induced by oxidized LDL (oxLDL) may increase Tregs sensitivity to Fas-mediated apoptosis in part as a consequence of 26S proteasome activation. The 26S proteasome, an ATP-dependent multisubunit protease complex found in the cytoplasm and in the nucleus of all eukaryotic cells, constitutes the central proteolytic machinery of the ubiquitin/proteasome system. Considering the effect of uremia and oxLDL, Tregs from patients with ESKD exhibit early cell-cycle arrest and become apoptotic. These phe- nomena are the consequence of the oxLDL inhibited proteasome proteolytic activity of p27 Kip1 and Bax proteins in Tregs. This may be one mechanistic explanation of the cellular immune dysfunction in patients with ESKD, and may have im- portant implications in clinics, since this response could contribute to the micro-inflammation and atherogenesis encoun- tered in this population.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"37-44"},"PeriodicalIF":0.0,"publicationDate":"2009-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150764","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":"Oxidative Stress, Altered-Self and Autoimmunity","authors":"I. Gerling","doi":"10.2174/1876894600901010033","DOIUrl":"https://doi.org/10.2174/1876894600901010033","url":null,"abstract":"It is well known that oxidative stress can induce production of free radicals that can modify proteins. The hy- pothesis presented here is that the target antigens in autoimmune diseases, such as type 1 diabetes mellitus, are not normal self proteins but rather self proteins that have been altered by free radicals, produced as a result of oxidative stress in the target cells. The observation that disease often occurs only in a single tissue, even when other tissues contain the same an- tigen, could be explained if both the presence of the antigen and severe oxidative stress is required, before tissue destruc- tion occurs. Furthermore, the cyclic nature of tissue destruction and problems with detecting robust high affinity autoreac- tivity to self antigens may be easier to understand if we presume that pathological autoreactivity is targeting redox- modified self antigens, while assays to unmodified self only measure its cross-reactivity to normal self antigens. BACKGROUND Autoimmune diseases such as type 1 diabetes mellitus (DM1) are believed to result from the failure of immu- nological tolerance to protein self antigens. It has been pro- posed that alterations in self antigens could initiate the proc- ess of autoimmunity (1, 2). According to this hypothesis one does not need to assume that autoimmune diseases are initi- ated exclusively by imperfections in the ability of the im- mune system to tolerize itself to normal cellular components (self antigens). Instead, the self antigens change to a previ- ously unseen form and, therefore, become a natural target of the immune system. The immune response to the altered self antigen then progresses and helps develop immunity to unal- tered self antigens as well. If the mitochondria are dysfunctional or cells are under stress, such as during high metabolic demand, viral infec- tions, or exposure to certain cytokines/toxins, cells may pro- duce a sufficient amount of radical oxygen or radical nitro- gen species (ROS/RNS) to overwhelm the antioxidant sys- tems that normally neutralize these free radicals (3). These ROS/RNS are very short-lived because they react with and modify, lipids and proteins in the cell (4). The field of redox proteomics has been progressing rapidly in the past decade and has developed new methods that allow investigators to study a large number of specific modifications of proteins induced by free radicals (5-7). The reaction of ROS/RNS with proteins can create stable end products such as 3- chlorothyrosine and 3-nitrotyrosine that may not only block natural modifications of the tyrosine by e.g., phosphoryla- tion, but also change the antigenic profile of the protein. The reaction of hydrogen peroxide with the chloride anion can create hypochlorous acid, which deaminates serine and con-","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"33-36"},"PeriodicalIF":0.0,"publicationDate":"2009-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150703","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":"The Gastrointestinal Manifestations of Systemic Lupus Erythematosus: A Survey of the Literature","authors":"S. Schulz, C. Derk","doi":"10.2174/1876894600901010010","DOIUrl":"https://doi.org/10.2174/1876894600901010010","url":null,"abstract":"Systemic Lupus Erythematosus (SLE) is an autoimmune disease associated with auto-antibody production and resulting widespread inflammation that has potential to affect and damage many organ systems. Gastrointestinal manifes- tations of SLE are well documented in the literature but the exact extent and frequency of their presence is likely grossly underestimated. Patients present with vague complaints such as abdominal pain and nausea with non-specific physical exam findings and inconclusive diagnostic tests and serologic analysis. Recent research has helped to better clarify these manifestations of SLE and has demonstrated distinct involvement of almost every portion of the GI tract. This article is based upon an exhaustive review of the literature from 1976 to present date and summarizes the major advances in the identification and differentiation of gastrointestinal incarnations related to systemic lupus erythematosus. The review also encompasses theories of etiology of the various manifestations, summarizes accepted and experimental treatment regi- mens, and highlights the differential diagnosis of each presented topic, including disorders of the oropharynx, esophagus, stomach, small and large intestine, liver and gallbladder and beyond.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"10-26"},"PeriodicalIF":0.0,"publicationDate":"2009-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150631","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}