Ji-Kui Wang, Di Zhang, Jin-Feng Wang, Wan-Lin Lu, Jing-Yuan Wang, Shi-Feng Liang, Ran Liu, Jing-Xin Jiang, Hong-Tao Li, Xuan Yang
{"title":"Clinical study on the effect of jejunoileal side-to-side anastomosis on metabolic parameters in patients with type 2 diabetes.","authors":"Ji-Kui Wang, Di Zhang, Jin-Feng Wang, Wan-Lin Lu, Jing-Yuan Wang, Shi-Feng Liang, Ran Liu, Jing-Xin Jiang, Hong-Tao Li, Xuan Yang","doi":"10.4239/wjd.v16.i1.99526","DOIUrl":"https://doi.org/10.4239/wjd.v16.i1.99526","url":null,"abstract":"<p><strong>Background: </strong>At present, the existing internal medicine drug treatment can alleviate the high glucose toxicity of patients to a certain extent, to explore the efficacy of laparoscopic jejunoileal side to side anastomosis in the treatment of type 2 diabetes, the report is as follows.</p><p><strong>Aim: </strong>To investigate the effect of jejunoileal side-to-side anastomosis on metabolic parameters in patients with type 2 diabetes mellitus (T2DM).</p><p><strong>Methods: </strong>We retrospectively analyzed the clinical data of 78 patients with T2DM who were treated <i>via</i> jejunoileal lateral anastomosis. Metabolic indicators were collected preoperatively, as well as at 3 and 6 months postoperative. The metabolic indicators analyzed included body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), 2-hour blood glucose (PBG), glycated hemoglobin (HbA1c), fasting C-peptide, 2-hour C-peptide (PCP), fasting insulin (Fins), 2-hour insulin (Pins), insulin resistance index (HOMA-IR), β Cellular function index (HOMA-β), alanine aminotransferase, aspartate aminotransferase, serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), high-density lipoprotein, and uric acid (UA) levels.</p><p><strong>Results: </strong>SBP, DBP, PBG, HbA1c, LDL-C, and TG were all significantly lower 3 months postoperative <i>vs</i> preoperative values; body weight, BMI, SBP, DBP, FBG, PBG, HbA1c, TC, TG, UA, and HOMA-IR values were all significantly lower 6 months postoperative <i>vs</i> at 3 months; and PCP, Fins, Pins, and HOMA-β were all significantly higher 6 months postoperative <i>vs</i> at 3 months (all <i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>Side-to-side anastomosis of the jejunum and ileum can effectively treat T2DM and improve the metabolic index levels associated with it.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 1","pages":"99526"},"PeriodicalIF":4.2,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143014557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"COVID-19 infection and inactivated vaccination: Impacts on clinical and immunological profiles in Chinese children with type 1 diabetes.","authors":"Zhen-Ran Xu, Li Xi, Jing Wu, Jin-Wen Ni, Fei-Hong Luo, Miao-Ying Zhang","doi":"10.4239/wjd.v15.i12.2276","DOIUrl":"10.4239/wjd.v15.i12.2276","url":null,"abstract":"<p><strong>Background: </strong>The coronavirus disease 2019 (COVID-19) pandemic has been linked to an increased incidence of diabetes and diabetic ketoacidosis (DKA). However, the relationship between COVID-19 infection and progression to type 1 diabetes (T1D) in children has not been well defined.</p><p><strong>Aim: </strong>To evaluate the influence of COVID-19 infection and inactivated vaccine administration on the progression of T1D among Chinese children.</p><p><strong>Methods: </strong>A total of 197 newly diagnosed patients with T1D were retrospectively enrolled from Children's Hospital of Fudan University between September 2020 and December 2023. The patients were divided into three groups based on their history of COVID-19 infection and vaccination: the infection group, the vaccination-only group, and the non-infection/non-vaccination group. Comprehensive clinical assessments and detailed immunological evaluations were performed to delineate the characteristics and immune responses of these groups.</p><p><strong>Results: </strong>The incidence of DKA was significantly higher in the COVID-19 infection group (70.2%) compared to the non-infection/non-vaccination group (62.5%) and vacscination-only group (45.6%; <i>P</i> = 0.015). Prior COVID-19 infection was correlated with increased DKA risk (OR: 1.981, 95%CI: 1.026-3.825, <i>P</i> = 0.042), while vaccination was associated with a reduced risk (OR: 0.558, 95%CI: 0.312-0.998, <i>P</i> = 0.049). COVID-19 infection mildly altered immune profiles, with modest differences in autoantibody positivity, lymphocyte distribution, and immunoglobulin levels. Notably, <i>HLA-DR3</i> positive children with a history of COVID-19 infection had an earlier T1D onset and lower fasting C-peptide levels than the <i>HLA-DR3</i> negative children with a history of infection (both <i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>COVID-19 infection predisposes children to severe T1D, characterized by enhanced DKA risk. Inactivated vaccination significantly lowers DKA incidence at T1D onset. These findings are valuable for guiding future vaccination and T1D risk surveillance strategies in epidemic scenarios in the general pediatric population.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2276-2284"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anne Christine Jugnet, Tatiana Benard, Corinne Lequint, Elise Bobony, Anna-Rosiana Pieheiro, Thomas Winther, Alfred Penfornis, Dured Dardari
{"title":"Intact fish skin graft a new hope for the treatment of diabetic foot ulcers: A case report.","authors":"Anne Christine Jugnet, Tatiana Benard, Corinne Lequint, Elise Bobony, Anna-Rosiana Pieheiro, Thomas Winther, Alfred Penfornis, Dured Dardari","doi":"10.4239/wjd.v15.i12.2353","DOIUrl":"10.4239/wjd.v15.i12.2353","url":null,"abstract":"<p><strong>Background: </strong>Diabetic foot ulcers (DFUs) are a real public health problem which carry a high risk of amputation. The treatment of DFUs is based on general management such as the treatment of infection, arterial disease, and offloading, but recent studies have shown that the quality of the local covering can impact the healing rate.</p><p><strong>Case summary: </strong>We report the case of a 39-year-old man, living with diabetes since the age of 15, who developed DFU on the dorsum of his left foot, with muscle and tendon involvement. Conventional management with intensive diabetes control, surgery, treatment of infection and negative pressure therapy gave only limited results. The patient benefited from the application of an intact fish skin graft with complete epithelialisation of the ulcer after 10 weeks of treatment.</p><p><strong>Conclusion: </strong>The use of intact fish skin graft appears to be a promising option for deep DFUs.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2353-2359"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ke-Xin Zhang, Cheng-Xia Kan, Yu-Qun Wang, Ning-Ning Hou, Xiao-Dong Sun
{"title":"Intestinal glucagon-like peptide-1 in hypoglycemic counterregulation for type 1 diabetes management.","authors":"Ke-Xin Zhang, Cheng-Xia Kan, Yu-Qun Wang, Ning-Ning Hou, Xiao-Dong Sun","doi":"10.4239/wjd.v15.i12.2380","DOIUrl":"10.4239/wjd.v15.i12.2380","url":null,"abstract":"<p><p>Type 1 diabetes (T1D) is characterized by the autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency and the need for exogenous insulin. A significant concern in T1D management is hypoglycemia, which is worsened by impaired counterregulatory mechanisms. Effective counterregulation involves hormones such as glucagon and adrenaline, which work to restore normal blood glucose levels. However, in T1D, these mechanisms often fail, particularly after recurrent hypoglycemia, resulting in hypoglycemia-associated autonomic failure. Recent research indicates that elevated levels of intestinal glucagon-like peptide-1 (GLP-1) impair counterregulatory responses by reducing the secretion of glucagon and adrenaline. This editorial underscores GLP-1's role beyond its incretin effects, contributing to impaired hypoglycemic counterregulation. This understanding necessitates a nuanced approach to GLP-1-based therapies in T1D, balancing the benefits of glycemic control with potential risks. Future research should delve into the mechanisms behind GLP-1's effects and explore potential interventions to improve hypoglycemic counterregulation. The goal is to enhance the safety and quality of life for T1D patients.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2380-2383"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Teneligliptin mitigates diabetic cardiomyopathy through inflammasome inhibition: Insights from experimental studies.","authors":"Chun-Yao Cheng, Wen-Rui Hao, Ju-Chi Liu, Tzu-Hurng Cheng","doi":"10.4239/wjd.v15.i12.2370","DOIUrl":"10.4239/wjd.v15.i12.2370","url":null,"abstract":"<p><p>This article provides commentary on the article by Zhang <i>et al</i>. In this original research, Zhang <i>et al</i> investigated the therapeutic potential of teneligliptin for diabetic cardiomyopathy (DCM), which was mediated by targeting the NOD-like receptor protein 3 (NLRP3) inflammasome. Through the use of both <i>in vivo</i> and <i>in vitro</i> models, the study demonstrated that teneligliptin alleviates cardiac hypertrophy, reduces myocardial injury, and mitigates the inflammatory responses associated with DCM. These findings suggest that teneligliptin's cardioprotective effects are mediated through the inhibition of NLRP3 inflammasome activation, positioning it as a promising therapeutic option for managing DCM in diabetic patients.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2370-2375"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of intestinal glucagon-like peptide-1 in impaired counter-regulatory responses to hypoglycemia.","authors":"Manjunath Havalappa Dodamani, Juniali Hatwal, Akash Batta","doi":"10.4239/wjd.v15.i12.2394","DOIUrl":"10.4239/wjd.v15.i12.2394","url":null,"abstract":"<p><p>Patients with type 1 diabetes mellitus (T1DM) experience multiple episodes of hypoglycemia, resulting in dysfunctional counter-regulatory responses with time. The recent experimental study by Jin <i>et al</i> explored the role of intestinal glucagon-like peptide-1 (GLP-1) in impaired counter-regulatory responses to hypoglycemia. They identified intestinal GLP-1 along with GLP-1 receptor (GLP-1R) as the new key players linked with impaired counter-regulatory responses to hypoglycemia in type 1 diabetic mice. They also demonstrated that excessive expression of GLP-1 and GLP-1R was associated with attenuated sympathoadrenal responses and decreased glucagon secretion. The study has enormous clinical relevance as defective counter regulation and hypoglycemia unawareness negatively impacts the intensive glycemic management approach in this group of patients. However, the physiological processes must be validated in dedicated human studies to comprehensively understand the pathophysiology of this complex relationship, and to clarify the true extent of impaired hypoglycemia counter regulation by intestinal GLP-1. For now, following the results of the index study and other similar studies, GLP-1 analogues usage in T1DM must be carefully monitored, as there is an inherent risk of worsening the already impaired counter-regulatory responses in these patients. Further studies in the future could identify other key players involved in this clinically relevant interaction.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2394-2398"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mesenchymal stem cell-derived extracellular vesicles: A promising therapeutic strategy in diabetic osteoporosis.","authors":"Ya-Jing Yang, Xi-Er Chen, Xu-Chang Zhou, Feng-Xia Liang","doi":"10.4239/wjd.v15.i12.2399","DOIUrl":"10.4239/wjd.v15.i12.2399","url":null,"abstract":"<p><p>Diabetic osteoporosis (DOP) is a serious complication of diabetes mellitus. It is urgent to explore efficient clinical treatment strategies for DOP. It has been found that mesenchymal stem cell-derived extracellular vesicles (MSC-EVs), as an emerging cell-free therapy, show great potential in DOP treatment. MSC-EVs can effectively promote bone formation, inhibit bone resorption, and modulate the inflammatory microenvironment by delivering cargoes of microRNAs, long non-coding RNAs, and proteins to target cells, thereby ameliorating bone loss in DOP. However, there are limited reports on the treatment of DOP with MSC-EVs. To evoke more attention to this potential strategy, this article summarised the extant literature on MSC-EVs for DOP to provide new directions for further research and to promote the application of MSC-EVs in the clinical management of DOP.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2399-2403"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Intersection of the glymphatic system and diabetes: Navigating a new frontier.","authors":"Asad Gul Rao, Abdulqadir J Nashwan","doi":"10.4239/wjd.v15.i12.2376","DOIUrl":"10.4239/wjd.v15.i12.2376","url":null,"abstract":"<p><p>Diabetes is one of the most devastating medical dilemmas impacting every region of the world severely. The study by Tian <i>et al</i> investigates glymphatic system dysfunction in the context of glucose metabolism and diabetes, using diffusion tensor imaging along the perivascular space. The study evaluated individuals with type 2 diabetes mellitus (T2DM), prediabetes, and normal glucose metabolism. It found that prediabetic and T2DM groups had significantly impaired glymphatic function. Glymphatic dysfunction may serve as an early indicator of cognitive deterioration in diabetes due to the correlations shown between these abnormalities and clinical factors as well as cognitive performance. The study has some positives, such as thorough evaluations and novel imaging methods, but its cross-sectional design and limited sample size restrict its applicability. More extensive, long-term research is required to verify these results. Furthermore, there are significant clinical implications. Patients with diabetes may benefit from immediate therapies to prevent microvascular and macrovascular damage if glymphatic dysfunction is identified early. The study promotes comprehensive diabetes care with a focus on maintaining cognitive function. In conclusion, the work of Tian <i>et al</i> is crucial because it opens the door to better treatment and diagnostic strategies for diabetes-related cognitive deterioration.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2376-2379"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"What is the optimal dialysis method for diabetic patients with end stage kidney disease?","authors":"Nirmal Noor Kheber, Abdulqadir J Nashwan","doi":"10.4239/wjd.v15.i12.2272","DOIUrl":"10.4239/wjd.v15.i12.2272","url":null,"abstract":"<p><p>Diabetes is one of the most catastrophic diseases ruling every corner of the world, and this has led to elevated incidents of end-stage kidney disease (ESKD). The standard treatment for ESKD is kidney transplantation/replacement, which is limited due to a deficiency of donors. Hence, dialysis has become the second-best option for treating patients with ESKD. Patients with ESKD with underlying diabetes have an additional risk of complications and infections over non-diabetic ESKD patients. Furthermore, these patients also experience variations in blood glucose levels and are more liable to develop malnutrition. This article elaborates on the different dialysis methods for ESKD patients. This editorial highlights the evidence-based studies that include randomized clinical trials, cohort studies, retrospective studies and case-control studies and suggests the most suitable type of dialysis under the following components.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2272-2275"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"β-Arrestin-2 enhances endoplasmic reticulum stress-induced glomerular endothelial cell injury by activating transcription factor 6 in diabetic nephropathy.","authors":"Jiang Liu, Xiao-Yun Song, Xiu-Ting Li, Mu Yang, Fang Wang, Ying Han, Ying Jiang, Yu-Xin Lei, Miao Jiang, Wen Zhang, Dong-Qi Tang","doi":"10.4239/wjd.v15.i12.2322","DOIUrl":"10.4239/wjd.v15.i12.2322","url":null,"abstract":"<p><strong>Background: </strong>Glomerular endothelial cell (GENC) injury is a characteristic of early-stage diabetic nephropathy (DN), and the investigation of potential therapeutic targets for preventing GENC injury is of clinical importance.</p><p><strong>Aim: </strong>To investigate the role of β-arrestin-2 in GENCs under DN conditions.</p><p><strong>Methods: </strong>Eight-week-old C57BL/6J mice were intraperitoneally injected with streptozotocin to induce DN. GENCs were transfected with plasmids containing siRNA-β-arrestin-2, shRNA-activating transcription factor 6 (ATF6), pCDNA-β-arrestin-2, or pCDNA-ATF6. Additionally, adeno-associated virus (AAV) containing shRNA-β-arrestin-2 was administered <i>via</i> a tail vein injection in DN mice.</p><p><strong>Results: </strong>The upregulation of β-arrestin-2 was observed in patients with DN as well as in GENCs from DN mice. Knockdown of β-arrestin-2 reduced apoptosis in high glucose-treated GENCs, which was reversed by the overexpression of ATF6. Moreover, overexpression of β-arrestin-2 Led to the activation of endoplasmic reticulum (ER) stress and the apoptosis of GENCs which could be mitigated by silencing of ATF6. Furthermore, knockdown of β-arrestin-2 by the administration of AAV-shRNA-β-arrestin-2 alleviated renal injury in DN mice.</p><p><strong>Conclusion: </strong>Knockdown of β-arrestin-2 prevents GENC apoptosis by inhibiting ATF6-mediated ER stress <i>in vivo</i> and <i>in vitro</i>. Consequently, β-arrestin-2 may represent a promising therapeutic target for the clinical management of patients with DN.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 12","pages":"2322-2337"},"PeriodicalIF":4.2,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}