Journal of pharmacological sciences最新文献

{"title":"Diurnal variations of neurokinin-1 receptor defines dosing time-dependent differences in antitumor effects of aprepitant in mice","authors":"Yoshihiro Seto ,&nbsp;Shun Tokeshi ,&nbsp;Daisuke Inoue ,&nbsp;Fumiyasu Okazaki ,&nbsp;Hideto To","doi":"10.1016/j.jphs.2025.04.007","DOIUrl":"10.1016/j.jphs.2025.04.007","url":null,"abstract":"<div><div>Aprepitant, a neurokinin-1 receptor (NK1R) antagonist, has the potential as a novel anticancer agent. This study explored the impact of chronotherapy on the antitumor effect of aprepitant in a mouse model of colorectal carcinoma. Aprepitant inhibited the proliferation of Colon-26 cells <em>in vitro</em> in a concentration-dependent manner and reduced the expression of cell cycle-related genes. Diurnal variations in NK1R mRNA and protein levels were observed in Colon-26 tumors, peaking at zeitgeber time (ZT) 2 and ZT 10, respectively. Administration of aprepitant at ZT 6, achieving peak plasma concentration at ZT 10, significantly reduced the tumor volume compared with administration at ZT 18. Despite the lower plasma concentrations and AUC_0–12 h in the ZT 6 group, superior antitumor effect suggests a dosing time-dependent efficacy due to variations in NK1R expression rather than its pharmacokinetics. These findings indicate that the antitumor activity of aprepitant against colorectal cancer can be enhanced by aligning its administration with NK1R expression rhythms, warranting further exploration of aprepitant chronotherapy in cancer chemotherapy.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 193-198"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rosamultin attenuates cerebral ischemia/reperfusion injury by inhibiting autophagy via the PI3K/Akt/mTOR pathway","authors":"Hailin Zhang ,&nbsp;Baoyuan Zhou ,&nbsp;Jixing Liu ,&nbsp;Bo Tang ,&nbsp;Zongzhi Xie ,&nbsp;Jianxiong Li","doi":"10.1016/j.jphs.2025.04.001","DOIUrl":"10.1016/j.jphs.2025.04.001","url":null,"abstract":"<div><div>Rosamultin (Rosa), a natural small-molecule compound, is known for its protective activity against hypoxia-induced injury, but its role in cerebral ischemic stroke injury remains unclear. To assess Rosa's effects on cerebral ischemic stroke, the intraluminal filament method was used to construct the middle cerebral artery occlusion and reperfusion (MCAO) in vivo model with 1 h occlusion and 48 h reperfusion. In addition, an oxygen-glucose deprivation and reoxygenation (OGD/R) in vitro model was constructed using HT22 cells. The protective role and underlying mechanism of Rosa on cell injury was also determined in vivo and in vitro. Rosa notably inhibited neurological deficits and diminished infarct volume and neuronal apoptosis in mice exposed to MCAO. Rosa also exerted neuroprotection in the OGD/R model by improving cell viability, decreasing apoptosis, and enhancing the p-Akt and p-mTOR levels. However, <span>LY294002</span>, a PI3K inhibitor, restored the beneficial influences of Rosa after OGD/R. Moreover, Rosa treatment inhibited autophagy levels, and <span>LY294002</span> partially restored the inhibition of autophagy levels caused by Rosa in the OGD/R model. In addition, Rosa enhanced the p-Akt and p-mTOR levels and inhibited autophagy levels in mice after MCAO. Rosa could attenuate autophagy via activating the PI3K/Akt/mTOR axis, thereby alleviating cerebral ischemia stroke injury.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 182-192"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginkgolide B inhibits ferroptosis in PC12 cells and ameliorates the oxidative stress in spinal cord injury through activating Nrf2 signaling pathway","authors":"Wei She ,&nbsp;Wenji Ma ,&nbsp;Tongtong Zhang ,&nbsp;Xunian Wu ,&nbsp;Jianfu Li ,&nbsp;Xingyong Li","doi":"10.1016/j.jphs.2025.05.004","DOIUrl":"10.1016/j.jphs.2025.05.004","url":null,"abstract":"<div><div>Spinal cord injury (SCI) commonly leads to loss of motor and sensory function and results in huge socioeconomic burden, and it triggers numerous secondary pathological events, including oxidative stress and ferroptosis. This study investigates the therapeutic potential of Ginkgolide B (GB), a neuroprotective compound derived from <em>Ginkgo biloba</em>, in mitigating SCI by targeting on ferroptosis. By using Erastin-induced ferroptosis in PC12 cells and a rat contusion SCI model, the present study demonstrated that GB significantly improved locomotor recovery, reduced neuronal loss, and attenuated histopathological damage. Mechanistically, GB suppressed ferroptosis markers, including elevated iron content, lipid peroxidation, and ACSL4, while restoring the expression of GPX4 and xCT. Crucially, GB enhanced nuclear translocation of Nrf2, upregulating downstream antioxidants and ferroptosis-related genes (HO-1 and NQO1). Notably, the functions of GB were abolished after utilization of Nrf2 signaling inhibitor ML385 which revealed the role of GB on recovery of SCI was highly related to the activation of Nrf2 signaling. These findings reveal that GB alleviates SCI by inhibiting ferroptosis through Nrf2 activation, positioning it as a promising therapeutic agent. This study elucidates a novel mechanism linking Nrf2 signaling to ferroptosis suppression in SCI and provides a translational framework for repurposing GB in SCI treatment.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 199-206"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-peptidic natural products that target and modulate oxytocin and arginine vasopressin receptors: Opportunities and challenges","authors":"Dane Tregeagle ,&nbsp;Catherine Doherty ,&nbsp;Timothy Callis,&nbsp;Michael Kassiou","doi":"10.1016/j.jphs.2025.04.004","DOIUrl":"10.1016/j.jphs.2025.04.004","url":null,"abstract":"<div><div>The ability to target the oxytocin and vasopressin receptors is of high therapeutic value due to their clinical relevance in wide range of neuropsychiatric conditions spanning from anxiety to schizophrenia. Despite the massive therapeutic potential in modulating this system, the only clinically approved small molecule-based therapeutics (Mozavaptan, Conivaptan and Tolvaptan) are for use in the periphery. Cyclotide mimetics of the native neuropeptides are well explored in the literature although these scaffolds are unsuitable for application to the central nervous system. This work highlights non-peptidic natural products that are active within the neurohypophysial system that may be used to inspire future drug discovery endeavours.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 238-258"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A selective eukaryotic elongation factor 2 kinase inhibitor, A484954 lowered blood glucose in Zucker fatty diabetes mellitus rat","authors":"Ko Adachi,&nbsp;Tomoko Kodama,&nbsp;Kosuke Otani,&nbsp;Keito Sano,&nbsp;Asuka Sugiyama,&nbsp;Muneyoshi Okada,&nbsp;Hideyuki Yamawaki","doi":"10.1016/j.jphs.2025.05.006","DOIUrl":"10.1016/j.jphs.2025.05.006","url":null,"abstract":"<div><div>Eukaryotic elongation factor 2 kinase (eEF2K) is a protein kinase, regulating peptide translation. Zucker fatty diabetes mellitus (ZFDM) rat is a recently developed obesity and type 2 diabetes animal model with a missense mutation (<em>fa</em>) in leptin receptor gene (<em>Lepr</em>). ZFDM-<em>Lepr</em>^{<em>fa/fa</em>} rats (Homo) develop obesity and type 2 diabetes, while ZFDM-<em>Lepr</em>^{<em>fa/+</em>} rats (Hetero) are normal. The aim of this study was to determine effects of A484954 on glucose metabolism in ZFDM rats. A484954 (2.5 mg/kg) or carboxymethyl cellulose (CMC; 0.5 %), a vehicle was injected intraperitoneally for 15 days in 17–19-week-old rats. Compared with Hetero CMC, in Homo CMC; 1) blood and urine glucose levels were significantly elevated, 2) Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was significantly elevated, 3) mRNA expression of sodium-glucose cotransporter (SGLT)2 in kidney tended to be elevated, while that of glucose transporter (GLUT)4 in vastus lateralis muscle decreased. Compared with Homo CMC, in Homo A484954; 1) blood glucose was significantly reduced, while urine glucose did not change, 2) HOMA-IR tended to decrease, 3) mRNA expression of SGLT2 in the kidney and GLUT4 in the muscle did not change. This study demonstrates for the first time that A484954 induces hypoglycemic effects in Homo partly via preventing insulin resistance.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 270-275"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143935791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel role of celecoxib in the inhibition of calcium-activated chloride channel ANO1","authors":"Ping Zhou ,&nbsp;Qinqin Li ,&nbsp;Xiangyu Li ,&nbsp;Yani Liu","doi":"10.1016/j.jphs.2025.05.003","DOIUrl":"10.1016/j.jphs.2025.05.003","url":null,"abstract":"<div><div>Celecoxib, a non-steroidal anti-inflammatory drug, is widely used in the clinic for its analgesic and anti-inflammatory effects by inhibiting COX-2. Celecoxib also modulates many ion channels including Nav1.5, Kv7 and Kv2.1 channels. Here we show a novel role of celecoxib in inhibiting calcium-activated chloride channel ANO1 that is involved in pain sensation. Celecoxib results in a concentration-dependent inhibition of ANO1 current with an IC₅₀ value of 20.3 ± 1.9 μM, and the residue P701 in the S7 is important for celecoxib-mediated ANO1 inhibition. These results suggest that ANO1 inhibition may contribute to celecoxib's analgesic and anti-inflammatory effects.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 207-211"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143912560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effects of ferulic acid on the contraction responses of porcine coronary arteries: a comparison with diltiazem","authors":"Kento Yoshioka ,&nbsp;Keisuke Obara ,&nbsp;Yilin Luo,&nbsp;Qianghaodi Hong,&nbsp;Ayaka Fujiwara,&nbsp;Wakaba Kinami,&nbsp;Hideaki Ozawa,&nbsp;Yoshio Tanaka","doi":"10.1016/j.jphs.2025.04.006","DOIUrl":"10.1016/j.jphs.2025.04.006","url":null,"abstract":"<div><div>Ferulic acid (FA) exerts protective effects against cardiovascular-related diseases; however, its role in coronary artery dilation is unclear. Here, we examined the effects and underlying mechanisms of FA in response to contractions induced by spasmogenic candidates in porcine coronary arteries (PCAs). FA (3 × 10⁻⁴–3 × 10⁻³ M) inhibited high-KCl-induced contractions in a concentration-dependent manner, and FA (3 × 10⁻⁴–10⁻³ M) inhibited high-KCl-induced increases in intracellular Ca²⁺ concentrations in A7r5 cells. FA (3 × 10⁻³ M) showed greater inhibition than diltiazem (3 × 10⁻⁵ M) against chemical-induced contractions but weaker inhibition against high-KCl-induced contractions. FA (3 × 10⁻⁴–3 × 10⁻³ M) inhibited contractions induced by endothelin-1 (10⁻⁸ M) and NaF (10⁻² M) under Ca²⁺-free conditions in a concentration-dependent manner; these contractions were fully suppressed by ML-7 (10⁻⁴ M, a myosin light chain kinase inhibitor). FA (3 × 10⁻³ M) also inhibited myosin light chain phosphorylation induced by NaF (10⁻² M) in A7r5 cells regardless of extracellular Ca²⁺ conditions. These findings indicate that FA inhibits PCA contractions induced by coronary spasmogens by inhibiting L-type Ca²⁺ channels and intracellular routes responsible for extracellular Ca²⁺ influx-independent contractions. The latter mechanism may involve the inhibition of myosin light chain phosphorylation-related processes.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 172-181"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effects of γ-linolenic acid on contractile responses in pig coronary arteries: Possible involvement of prostanoid TP receptor inhibition","authors":"Keisuke Obara ,&nbsp;Kento Yoshioka ,&nbsp;Mikoto Ozawa,&nbsp;Haruki Kimura,&nbsp;Mayu Kiguchi,&nbsp;Yuri Nakao,&nbsp;Hinako Miyaji,&nbsp;Toma Yamashita,&nbsp;Noboru Saitoh,&nbsp;Yutaka Nakagome,&nbsp;Sakika Ichihara,&nbsp;Yoshio Tanaka","doi":"10.1016/j.jphs.2025.05.009","DOIUrl":"10.1016/j.jphs.2025.05.009","url":null,"abstract":"<div><div>We examined whether γ-linolenic acid (GLA), an n−6 polyunsaturated fatty acid (PUFA) and a structural isomer of α-linolenic acid (an n−3 PUFA), inhibited contractions of isolated pig coronary arteries. GLA potently inhibited the contractions elicited by U46619/prostaglandin F_2α, while showing marginal effects against other contractions. Schild plot analysis of GLA versus U46619 showed a competitive antagonistic effect. GLA also inhibited the intracellular Ca²⁺ concentration increases caused by prostanoid TP but not by FP receptor stimulation. These results suggest that TP receptor antagonistic activity can be exhibited by non-n−3 PUFAs in coronary arteries.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 283-287"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144071367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nerol enhances lipid synthesis in human sebocytes via cannabinoid receptor-2-mediated MAPK signaling","authors":"Qi Zhao ,&nbsp;Zhiwei Liu ,&nbsp;Yong Wang ,&nbsp;Tan Li ,&nbsp;Juan Wang ,&nbsp;Yaozhao Li ,&nbsp;Chengliang Li ,&nbsp;Chuntao Zhai ,&nbsp;Christos C. Zouboulis ,&nbsp;Xiaolei Ding ,&nbsp;Qiang Ju ,&nbsp;Zhenlin Hu","doi":"10.1016/j.jphs.2025.04.008","DOIUrl":"10.1016/j.jphs.2025.04.008","url":null,"abstract":"<div><h3>Purpose</h3><div>Nerol, a natural monoterpene, is commonly used as a fragrance additive in perfumes and cosmetics due to its pleasant rose-like aromas. Nerol application possesses diverse pharmacological properties, including anti-microbial, antioxidant, antinociceptive and anti-inflammatory activities, but its effects on sebum production and the consequent skin barrier function remain elusive. Here, we explored the effect of nerol on the lipogenesis of sebocytes.</div></div><div><h3>Patients and methods</h3><div>Immortalized human SZ95 sebocytes were used. The intracellular lipids were quantitatively measured by western blotting or fluorescent Nile Red staining followed by fluorometric analysis, semiquantitative detection or flow cytometry. The cell proliferation and differentiation were detected with CCK8 and flow cytometry, respectively. Moreover, RT-qPCR and immunocytochemistry were used to determine the expression levels of olfactory receptor OR2W3 and cannabinoid receptor-2 (CB2) receptors in SZ95 sebocytes.The mechanism was investigated by RNA interference and Western blotting.</div></div><div><h3>Results</h3><div>Our findings revealed that nerol induced lipid production in SZ95 sebocytes, together with the upregulation of multiple genes related to lipid synthesis, including PPARγ, SREBP-1, and FAS. Nerol also induced sebocyte differentiation, as evidenced by elevated cellular granulation and upregulated differentiation marker genes. Mechanistically, the lipogenic effect of nerol was mediated via CB2, rather than OR2W3 and TRP channels. Moreover, MAPK signaling was involved in neurol's effect.</div></div><div><h3>Conclusion</h3><div>Collectively, our findings show that nerol exerts a lipogenic effect on human sebocytes in a CB2-dependent manner through the activation of MAPK pathway, suggesting the therapeutic potential of this monoterpene in controlling cutaneous disorders involving sebaceous gland dysfunction and reduced sebum production, such as atopic dermatitis, skin dryness and aging.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 219-230"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143929574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clarifying the mechanism of astaxanthin in the treatment of inflammation in ischemic stroke using integrated network analysis","authors":"Jinwen Yao ,&nbsp;Xu Wang ,&nbsp;Dexi Zhao","doi":"10.1016/j.jphs.2025.04.003","DOIUrl":"10.1016/j.jphs.2025.04.003","url":null,"abstract":"<div><h3>Background and objective</h3><div>Ischemic stroke is a disease with high incidence. Astaxanthin is a functional foods with protective effects against ischemic stroke. However, the integral mechanism of astaxanthin protect ischemic stroke is not clear. The aim of this study was to investigate the mechanism of astaxanthin protect ischemic stroke by integrated network analysis.</div></div><div><h3>Methods</h3><div>Middle cerebral artery occlusion model was used to establish ischemic stroke model, and ischemic stroke models were treated with 25, 45, 65 mg/kg astaxanthin for 7 days. The rats were killed 24 h after successful modeling. Integrated network analysis, molecular docking, molecular dynamics (MD) simulation, and Western blot were used to explore the astaxanthin and potential proteins related to inflammation and cell death.</div></div><div><h3>Results</h3><div>The results of integrated network analysis indicate that astaxanthin may protect ischemic stroke through Toll like receptor signaling pathway and apoptosis pathway. The main targets involved MMP9, IL1B, IL10, Bcl2 and among others. astaxanthin has a low binding score and compact complex with PARP1, AIF, Bax, IL10, MMP9, Bcl2. In addition, astaxanthin has reduced inflammation and cell death-related proteins such as PARP1, AIF, Bax, TLR4, MMP9, IL1β and increased anti-inflammation and anti-cell death-related proteins by Bcl2 and IL10.</div></div><div><h3>Conclusions</h3><div>Astaxanthin can improve anti-inflammatory, anti-cell death ability after ischemic stroke. Our study provides a theoretical basis for the subsequent experimental and clinical application of astaxanthin in the treatment of ischemic stroke.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 3","pages":"Pages 155-165"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}