{"title":"L-Theanine prevents ulcerative colitis by regulating the CD4+ T cell immune response through the gut microbiota and its metabolites.","authors":"Wei Xu, Aoxiang Liu, Zhihua Gong, Wenjun Xiao","doi":"10.1016/j.jnutbio.2025.109845","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109845","url":null,"abstract":"<p><p>The disturbance of gut microbiota and its metabolites are considered to be the causes of ulcerative colitis (UC), which leads to immune abnormalities. Diet is the most important regulator of gut microbiota; therefore, it has a beneficial impact on UC. A novel food ingredient, L-theanine, alters the gut microbiota, thereby regulating gut immunity. However, whether L-theanine prevents UC by altering the gut microbiota, as well as the underlying mechanisms, remains unknown. Here, L-theanine was used to optimize the gut microbiota and its metabolites. Furthermore, to explore the mechanism by which L-theanine prevents UC, an L-theanine fecal microbiota solution was used to prevent dextran sulfate sodium-induced UC via fecal microbiota transplantation. Improvements in the colonic structure, colon histology scores, immune factors (IL-10), and inflammatory factors (IL-1β) demonstrated the preventive effect of L-theanine on UC. The 16S rDNA and metabolomic results showed that tryptophan-, short chain fatty acid-, and bile acid-related microbiota, such as Muribaculaceae, Lachnospiraceae, Alloprevotella, and Prevotellaceae were the dominant. Flow cytometry results showed that L-theanine decreased helper T (Th)1 and Th17 immune responses, and increased Th2 and T-regulatory immune responses via regulation of antigen-presenting cell responses, such as dendritic cells and macrophages. Therefore, L-theanine regulated the immune response of colon CD4 + T cells to dendritic cell and macrophage antigen presentation via tryptophan-, short chain fatty acid-, and bile acid-related microbiota, thereby preventing dextran sulfate sodium-induced UC.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109845"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yewei Zhong, Junlin Yan, Yi Lei, Rui Zhang, Adalaiti Abudurexiti, Shuwen Qi, Wenhui Hou, Xiaoli Ma
{"title":"Lactucin & Lactucopicrin ameliorate obesity in high-fat diet fed mice by promoting white adipose tissue browning through the activation of the AMPK/SIRT1/PGC-1α pathway.","authors":"Yewei Zhong, Junlin Yan, Yi Lei, Rui Zhang, Adalaiti Abudurexiti, Shuwen Qi, Wenhui Hou, Xiaoli Ma","doi":"10.1016/j.jnutbio.2025.109851","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109851","url":null,"abstract":"<p><p>Lactucin and lactucopicrin are the characteristic lipid-lowering active components found in Cichorium glandulosum. However, their effects and underlying mechanisms in obesity remain unclear. In the present study, C57BL/6J mice were simultaneously subjected to a high-fat diet (HFD) and treated with drugs to investigate the impacts of lactucin and lactucopicrin on HFD-induced obese mice. The results demonstrated that in HFD obese mice, lactucin and lactucopicrin significantly decreased body weight and the weights of adipose tissues, improved serum metabolic parameters, and increased the content of irisin. Regarding the intermediate metabolites of intestinal flora, which are closely associated with white adipose tissue (WAT) browning, lactucin and lactucopicrin treatment led to a reduction in the levels of 12-α-OH/non-12-α-OH bile acids (BAs) and also tended to enhance the levels of short-chain fatty acids (SCFAs). qRT-PCR results indicated that lactucin and lactucopicrin treatment elevated the expression levels of genes related to beige fat markers, thermogenesis, mitochondrial biogenesis, and lipolysis in WAT, as well as those of thermogenesis and lipolysis genes in brown adipose tissue (BAT). Western blot analysis revealed that lactucin and lactucopicrin up-regulated the expression of uncoupling protein 1 (UCP1), the core protein in thermogenesis, in both WAT and BAT. Moreover, they also up-regulated the expression levels of AMP-activated kinase (AMPK), sirtuin 1 (SIRT1), and PPARγ coactivator 1-alpha (PGC-1α), which are key pathway proteins involved in WAT browning. Furthermore, 16S rRNA sequencing results showed that in HFD obese mice, lactucin and lactucopicrin improved the composition and function of the intestinal microbiota. In conclusion, lactucin and lactucopicrin may promote WAT browning by activating the AMPK/SIRT1/PGC-1α pathway, thereby ameliorating obesity in HFD mice.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109851"},"PeriodicalIF":4.8,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Saptarnab Ganguly, Tandrika Chattopadhyay, Rubina Kazi, Souparno Das, Bhavisha Malik, Uthpala Ml, Padmapriya S Iyer, Mohit Kashiv, Anshit Singh, Amita Ghadge, Shyam D Nair, Mahendra S Sonawane, Ullas Kolthur-Seetharam
{"title":"Consumption of sucrose-water rewires macronutrient uptake and utilization mechanisms in a tissue specific manner.","authors":"Saptarnab Ganguly, Tandrika Chattopadhyay, Rubina Kazi, Souparno Das, Bhavisha Malik, Uthpala Ml, Padmapriya S Iyer, Mohit Kashiv, Anshit Singh, Amita Ghadge, Shyam D Nair, Mahendra S Sonawane, Ullas Kolthur-Seetharam","doi":"10.1016/j.jnutbio.2025.109850","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109850","url":null,"abstract":"<p><p>Consumption of sugar-sweetened beverages (SSBs) have been linked to metabolic dysfunction, obesity, diabetes and enhanced risk of cardiovascular diseases across all age-groups globally. Decades of work that have provided insights into pathophysiological manifestations of sucrose overfeeding have employed paradigms that rarely mimic human consumption of SSBs. Thus, our understanding of multi-organ cross-talk and molecular and/or cellular mechanisms, which operate across scales and drive physiological derangement is still poor. By employing a paradigm of sucrose water feeding in mice that closely resembles chronic SSB consumption in humans (10% sucrose in water), we have unraveled hitherto unknown tissue-specific mechanistic underpinnings, which contribute towards perturbed physiology. Our findings illustrate that systemic impaired glucose homeostasis, mediated by hepatic gluconeogenesis and insulin resistance, does not involve altered gene expression programs in the liver. We have discovered the pivotal role of the small intestine, which in conjunction with liver and muscles, drives dyshomeostasis. Importantly, we have uncovered rewiring of molecular mechanisms in the proximal intestine that is either causal or consequential to systemic ill-effects of chronic sucrose water consumption including dysfunction of liver and muscle mitochondria. Tissue-specific molecular signatures, which we have unveiled as the primary outcome, clearly indicate that inefficient utilization of glucose is exacerbated by enhanced uptake by the gut. Besides providing systems-wide mechanistic insights, we propose that consumption of SSBs causes intestinal 'molecular addiction' for deregulated absorption of hexose-sugars, and drives diseases such as diabetes and obesity.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109850"},"PeriodicalIF":4.8,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhenghao Ye, Archana Kini, Qinghai Tan, Sabrina Woltemate, Marius Vital, Katerina Nikolovska, Ursula Seidler
{"title":"Oral Tributyrin Treatment affects Short-Chain Fatty Acid Transport, Mucosal Health, and Microbiome in a Mouse Model of Inflammatory Diarrhea.","authors":"Zhenghao Ye, Archana Kini, Qinghai Tan, Sabrina Woltemate, Marius Vital, Katerina Nikolovska, Ursula Seidler","doi":"10.1016/j.jnutbio.2025.109847","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109847","url":null,"abstract":"<p><p>Butyrate may decrease intestinal inflammation and diarrhea. This study investigates the impact of oral application of sodium butyrate (NaB) and tributyrin (TB) on colonic butyrate concentration, SCFA transporter expression, colonic absorptive function, barrier properties, inflammation, and microbial composition in the colon of slc26a3<sup>-/-</sup> mice, a mouse model for inflammatory diarrhea. In vivo fluid absorption and bicarbonate secretory rates were evaluated in the cecum and mid-colon of slc26a3<sup>+/+</sup> and slc26a3<sup>-/-</sup> mice before and during luminal perfusion of NaB-containing saline and were significantly stimulated in both slc26a3<sup>+/+</sup> and slc26a3<sup>-/-</sup> colon by NaB. Age-matched slc26a3<sup>+/+</sup> and slc26a3<sup>-/-</sup> mice were either fed chow containing 5% NaB or gavaged twice daily with TB for 21 days. Food and water intake, weight, and stool water content were assessed daily. Stool and tissues were collected for further analysis of SCFA production, barrier integrity, mucosal inflammation, and microbiome analysis by 16S rRNA gene sequencing. 5% NaB diet did not exert a significant impact on SCFA levels, mucus barrier, or inflammatory markers, but significantly increased oral water intake. TB gavage treatment increased the expression of SCFA transporters Mct1 and Smct1, mucus content and microbial diversity, and decreased the neutrophil marker Lipocalin 2, Phospholipase A2, and the antimicrobial peptide Reg3b in the slc26a3<sup>-/-</sup> cecum. However, TB treatment also resulted in an increase in inflammatory markers such as TNFα, Il-1β and CD3e in the wildtype mucosa. While there are some benefits with TB ingestion for barrier properties and microbial composition in the diseased cecum, potentially detrimental effects were noted in the healthy colon.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109847"},"PeriodicalIF":4.8,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Milk-derived bioactive peptides in insulin resistance and type 2 diabetes.","authors":"Marjan Ramezan, Pishva Arzhang, Andrew C Shin","doi":"10.1016/j.jnutbio.2025.109849","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109849","url":null,"abstract":"<p><p>Diabetes is a global health issue affecting over 6% of the world and 11 % of the US population. It is closely linked to insulin resistance, a pivotal factor in Type 2 diabetes development. This review explores a promising avenue for addressing insulin resistance through the lens of Milk-Derived Bioactive Peptides (MBAPs). Taken from casein or whey fractions of various milks, MBAPs exhibit diverse health-promoting properties. Specific interactions between these peptides and enzymes involved in glucose digestion and metabolism have been examined, leading to the identification of some key peptides exerting the effects. This review emphasizes the positive impact of MBAPs on glycemic control through various mechanisms. Different cell lines have been used to investigate MBAPs' effects on insulin signaling, inflammation, and oxidative stress. Preclinical in vivo studies have also shown that MBAPs lower glucose, stimulate insulin, and reduce inflammation. Human trials further substantiate these findings and suggest the potential utility of milk protein hydrolysates containing MBAPs in individuals with insulin resistance or T2D to improve insulin action and glucose homeostasis.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109849"},"PeriodicalIF":4.8,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Increased fecal glycocholic acid levels correlate with obesity in conjunction with the depletion of archaea: the DOSANCO Health Study.","authors":"Ryodai Yamamura, Ryo Okubo, Shigekazu Ukawa, Koshi Nakamura, Emiko Okada, Takafumi Nakagawa, Akihiro Imae, Takashi Kimura, Akiko Tamakoshi","doi":"10.1016/j.jnutbio.2025.109846","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109846","url":null,"abstract":"<p><strong>Background: </strong>Recent studies have focused on the relationship between obesity and gut microbiota. This study aims to identify fecal components and gut bacterial species associated with different BMI categories.</p><p><strong>Methods: </strong>In this study, 538 participants aged ≥18 years were categorized into underweight, normal, and obese groups based on BMI (cutoffs: 18.5 and 25.0 kg/m²). We compared 30 fecal components among these groups and calculated correlation coefficients between each component and BMI. Participants were then divided into quartiles based on fecal component levels correlated with BMI, and the prevalence ratio (PR) of obesity was calculated, adjusted for confounding factors. We also analyzed the composition and diversity of gut microbiota and bacterial gene expression among the quartiles for each fecal component.</p><p><strong>Results: </strong>Fecal glycocholic acid (GCA) showed a significant positive correlation with BMI. The PR for obesity in the highest quartile of fecal GCA was 3.30 (95% CI: 1.21-9.54), indicating a significantly higher risk of obesity compared to the lowest quartile. Gut microbiota analysis revealed significant differences in the abundance of Ruminococcaceae Incertae Sedis, Faecalibacterium, and Methanobrevibacter, with Methanobrevibacter being absent in the higher quartiles of fecal GCA. Additionally, gene expression for enzymes involved in the deconjugation of conjugated bile acids, including GCA, was downregulated in the highest quartile.</p><p><strong>Conclusions: </strong>Increased fecal GCA levels are positively correlated with obesity, alongside a depletion of archaea.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109846"},"PeriodicalIF":4.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yingdong Han, Xinxin Han, He Zhao, Menghui Yao, Tiange Xie, Juan Wu, Yun Zhang, Xuejun Zeng
{"title":"The exploration of the relationship between hyperuricemia, gout and Vitamin D deficiency.","authors":"Yingdong Han, Xinxin Han, He Zhao, Menghui Yao, Tiange Xie, Juan Wu, Yun Zhang, Xuejun Zeng","doi":"10.1016/j.jnutbio.2025.109848","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109848","url":null,"abstract":"<p><strong>Background: </strong>Our study aims to provide evidence concerning the relationship between hyperuricemia, gout and Vitamin D deficiency by analyzing data from Peking Union Medical College Hospital (PUMCH), the National Health and Nutrition Examination Survey (NHANES) database, and through Mendelian randomization (MR) analyses.</p><p><strong>Methods: </strong>Sample 1 involved patients from PUMCH (n=13,532), and sample 2 involved participants from NHANES (Unweighted n=22,860; weight n=182,829,142). Logistic regression and restricted cubic spline analyses were applied to assess above relationship. A two-sample MR analysis was performed using the genome-wide association study summary statistics to identify the causal association between gout and 25-hydroxyvitamin D (25(OH)D).</p><p><strong>Results: </strong>The results from both samples confirmed a positive correlation among hyperuricemia, gout and risk of Vitamin D deficiency. The restricted cubic spline showed positive dose-response relationship between uric acid and risk of Vitamin D deficiency and the minimal threshold of uric acid at 307.5 umol/L and 316.1 umol/L, respectively. Mediation analysis in the sample 2 found that about 29.4% of the total effect of gout on Vitamin D deficiency were mediated by serum uric acid, and 37.1% of which were mediated by body mass index.The results of our MR analysis supported a causal association between gout (IVW β(SE), -0.843 (0.337); P = 0.0123) and 25(OH)D. Sensitivity analysis and genetic risk scores approach confirmed the robustness and reliability of the above findings.</p><p><strong>Conclusions: </strong>Hyperuricemia and gout are both strong indicators of increased risk of Vitamin D deficiency. Findings highlight the causal effects of gout-associated genetic variants on 25(OH)D.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109848"},"PeriodicalIF":4.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Oleanolic acid inhibits appetite through the TGR5/cAMP signaling pathway","authors":"Shuang Liu, Xiaoling Chen, Daiwen Chen, Bing Yu, Ping Zheng, Yuheng Luo, Jun He, Zhiqing Huang","doi":"10.1016/j.jnutbio.2025.109844","DOIUrl":"10.1016/j.jnutbio.2025.109844","url":null,"abstract":"<div><div>Inhibition of appetite is an effective approach to fight obesity. Recently, bile acids have been reported to suppress appetite and alleviate obesity via the Takeda G protein-coupled receptor 5 (TGR5). However, whether the downstream signaling molecule cyclic adenosine monophosphate (cAMP) of TGR5 is involved in this process remains unclear. Oleanolic acid (OA) is a plant analogue of bile acids. The study aimed to explore the effect of dietary OA supplementation on appetite and to examine the role of TGR5/cAMP signaling in this process. In our study, mice were divided into four treatment groups: basal diet, 50mg/kg OA-supplemented diet, 100mg/kg OA-supplemented diet, and 30mg/kg tauroursodeoxycholic acid (TUDCA)-supplemented diet. Our results showed that dietary supplementation of OA and TUDCA both suppressed appetite. Additionally, OA and TUDCA downregulated the expression of appetite-stimulating factors while upregulating appetite-suppressing factors in the hypothalamus. Furthermore, OA was found to activate TGR5 signaling in the hypothalamus. Mechanistic studies using N38 cells revealed that OA reduced the expression and secretion of agouti-related peptide (AgRP), while inhibition of TGR5 and cAMP attenuated this effect of OA. In conclusion, our findings suggest that OA may suppress appetite through activation of the TGR5/cAMP signaling pathway in the hypothalamus.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"138 ","pages":"Article 109844"},"PeriodicalIF":4.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lu Ding , Jing Liu , Liyuan Zhou , Qian Zhang , Jieying Liu , Xinhua Xiao
{"title":"Maternal high-fat diet alters the transcriptional rhythm in white adipose tissue of adult offspring","authors":"Lu Ding , Jing Liu , Liyuan Zhou , Qian Zhang , Jieying Liu , Xinhua Xiao","doi":"10.1016/j.jnutbio.2025.109843","DOIUrl":"10.1016/j.jnutbio.2025.109843","url":null,"abstract":"<div><div>A maternal high-fat diet (HFD) deteriorates the long-term metabolic health of offspring. Circadian rhythms are crucial for regulating metabolism. However, the impact of maternal HFD on the circadian clock in white adipose tissue (WAT) remains unexplored. This study aimed to identify transcriptional rhythmic alterations in inguinal WAT of adult male offspring induced by maternal HFD. To this end, female mice were fed an HFD and their male offspring were raised on a standard chow diet until 16 weeks of age. Transcriptome was performed and the data was analyzed using CircaCompare. The results showed that maternal HFD before and throughout pregnancy significantly altered the circadian rhythm of inguinal WAT while slightly modifying the WAT clock in adult male offspring. Specifically, maternal HFD contributed to gaining rhythmicity of <em>Cry2</em>, resulted in the elevated amplitude of <em>Nr1d2</em>, and led to increased midline estimating statistic of rhythm (MESOR) of <em>Clock</em> and <em>Nr1d2</em>. Furthermore, maternal HFD changed the rhythmic pattern of metabolic genes, such as <em>Pparγ, Hacd2</em>, and <em>Acsl1</em>, which are significantly enriched in metabolic regulation pathways. In conclusion, a maternal HFD before and throughout pregnancy altered the circadian rhythm of inguinal WAT in adult offspring. These alterations may play a significant role in disturbing metabolic homeostasis, potentially leading to metabolic dysfunction in adult male offspring.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"138 ","pages":"Article 109843"},"PeriodicalIF":4.8,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143007053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}