Y Akiba, N Yamaguchi, H Amano, T Fujii, K Fujimoto, T Suzuki, K Kawashima
{"title":"Role of nitric oxide in the control of blood pressure in young and adult spontaneously hypertensive rats.","authors":"Y Akiba, N Yamaguchi, H Amano, T Fujii, K Fujimoto, T Suzuki, K Kawashima","doi":"10.1111/j.1440-1681.1995.tb02855.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02855.x","url":null,"abstract":"<p><p>1. The depressor response to sodium nitroprusside (SNP) and the pressor response to Nomega-nitro-L-arginine methyl ester (L-NAME) were investigated in anaesthetized and ganglion-blocked 6 week old (young) and 20 week old (adult) spontaneously hypertensive rats (SHR), and the results were compared with those in age-matched normotensive Wistar-Kyoto (WKY) rats. 2. SNP produced a dose-dependent decrease of the mean blood pressure (BP) in both strains, and no differences in vascular sensitivity to SNP were observed between the strains. 3. L-NAME caused dose-dependent pressor responses in both strains. The sensitivity and the maximal response to L-NAME in SHR were significantly greater than those in age-matched WKY (P< 0.05 or 0.01; t-test, 13 d.f. in both ages). However, there were no significant differences in the responses between ages in each strain. 4. Acute reduction of BP induced by 7-O-ethylfangchinoline did not affect the responses to SNP and L-NAME in the adult SHR. 5. These results indicate that a greater amount of NO is tonically released in SHR and that its contribution to BP control is greater in SHR than in WKY, whereas vascular sensitivity to NO does not differ between the strains. In addition, acute changes in BP do not affect the degree of dependency on NO for BP control.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S142-3"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02855.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20027862","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":"Stroke-prone SHR and arteriolipidosis-prone SHR as models for atherosclerosis: their mechanisms and application for nutritional and pharmacological studies.","authors":"Y Yamori, S Murakami, Y Nara, K Ikeda","doi":"10.1111/j.1440-1681.1995.tb02901.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02901.x","url":null,"abstract":"<p><p>1. Peritoneal macrophages (Mphi) were harvested from non-stimulated 2 month old SHRSP and WKY, and incubated with acetyl LDL or [14C]-oleate-albumin complex to check total, free and esterified cholesterol (Cho) accumulation as well as acy coenzyme A-cholesterol acyltransferase (ACAT) activity and its activation by hyperlipidaemic serum. 2. Total and esterified Cho accumulation as well as ACAT activity were enhanced in Mphi from SHRSP compared with those from WKY. 3. To observe the dietary or pharmacological influence on atherogenesis, arteriolipidosis-prone SHR (ALR) were given a high fat cholesterol diet with 3% taurine or a Ca blocker (Nilvadipine, N; 30 mg/kg), both of which significantly decreased serum Cho level and clearly attenuated arterial fat deposition.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S244-5"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02901.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20028034","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}
C P Klett, A Palmer, A M Gallagher, N Rioseco-Camacho, M P Printz
{"title":"Differences in cultured cardiac fibroblast populations isolated from SHR and WKY rats.","authors":"C P Klett, A Palmer, A M Gallagher, N Rioseco-Camacho, M P Printz","doi":"10.1111/j.1440-1681.1995.tb02910.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02910.x","url":null,"abstract":"<p><p>1. The mechanisms whereby angiotensin converting enzyme inhibitors reverse cardiac remodelling appear to involve angiotensin and/or bradykinin receptors. Previously we reported that cultured rat cardiac fibroblasts express angiotensin II (AII) receptors. In the present study we compared AII receptor binding, gene expression of angiotensinogen and the AII, Subtype 1A (AT1A) receptor, as well as morphological changes induced by selected hormonal treatments in cultured fibroblasts derived from SHRLJ or WKYLJ rats. 2. Fibroblasts were isolated from adult rat left ventricle by either collagenase B or collagenase P digestion. Collagenase B yielded cell preparations from SHRLJ which grew slower than cells from WKYLJ rats and expressed nearly two-fold fewer AII receptors (compared to WKYLJ) while collagenase P yielded SHRLJ cells with similar binding and growth properties to WKYLJ. A good correlation was observed between receptor binding and AII receptor, type 1A (AT1A) mRNA concentrations. In the presence of steroids collagenase B cells showed a higher tendency to transform towards a preadipocyte cell type, estimated by the formation of lipid containing vacuoles/cell, while collagenase P cells, mainly the SHRLJ type, start to differentiate toward a myofibroblast-like cell type in the presence of AII, as calculated by the expression of alpha-smooth muscle actin. 3. From the results obtained in this study it is evident that a subset of fibroblasts can be isolated from the SHRLJ heart using collagenase B or P which differ in growth rates, AII receptor binding, AT1A and angiotensinogen mRNA levels, morphology and steroid responsiveness when compared to fibroblasts isolated from cardiac WKYLJ tissue.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S265-7"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02910.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026282","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":"Distinction of endothelial cell growth and fibrinolytic activity between WKY/Izm and SHRSP/Izm in vitro.","authors":"S Ito, Y Nara, Y Yamori","doi":"10.1111/j.1440-1681.1995.tb02913.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02913.x","url":null,"abstract":"<p><p>1. In the present study, endothelial cells (EC) growth and fibrinolytic activity of WKY/Izm and SHRSP/Izm were investigated in vitro. 2. EC were isolated from the thoracic aortas of WKY and SHRSP at the age of 8-9 weeks. Proliferative activities of EC were analysed with doubling time and DNA synthesis. Fibrinolytic activity was determined by tissue type plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1) activities in cultured medium. 3. SHRSP-EC growth rate was significantly greater than WKY-EC growth rate in doubling time. In the assay for DNA synthesis, 5-bromo-2'-deoxy uridine incorporation rate in SHRSP-EC was significantly increased compared with that in WKY-EC. 4. The tPA activity in cultured medium of WKY-EC was 2-fold greater than that of SHRSP-EC, while PAI-1 activities were nearly equal in them. 5. These physiological distinctions of EC of SHRSP/Izm from that of WKY/Izm with close genetic background could be contributory genetic factors to hypertension-related vascular diseases in SHRSP.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S273-4"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02913.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026285","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":"Increased calcium sequestration by sarcoplasmic reticulum in small muscular arteries in young spontaneously hypertensive rats.","authors":"Y Toyoda, H Shima, H Sasajima, I Nishio","doi":"10.1111/j.1440-1681.1995.tb02891.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02891.x","url":null,"abstract":"<p><p>1. Sarcoplasmic reticulum (SR) in small resistance arteries plays a role in the regulation of the cytosolic free calcium concentration by sequestration of calcium from cytoplasm. 2. To examine the contribution of calcium (Ca2+) sequestration by the SHR to both contraction and relaxation in young spontaneously hypertensive rats (SHR), we measured evoked tension before and after depletion of SR Ca2+ stores in the rings of the first branch of superior mesenteric artery in 5 week old SHR and age-matched Wistar-Kyoto (WKY) rats. Contractile responses were induced by 40 mmol/L potassium and 10 mmol/L caffeine before and after the treatment with ryanodine or thapsigargin, which depletes SR calcium stores. 3. The magnitude of potassium-induced contraction was almost the same in both strains. 4. Ryanodine and thapsigargin did not affect the resting tension and almost decreased caffeine-induced contraction in both strains. 5. After the treatment with ryanodine or thapsigargin, the magnitude and the rate of potassium-induced contraction were augmented greatly in SHR, but not in WKY. 6. The relative relaxation rate after exposure of potassium was significantly slowed in SHR by ryanodine or thapsigargin, but only slightly in WKY. 7. These results suggest that Ca2+ sequestration by the SR in SHR was greater than in WKY. Therefore, it is concluded that SR plays an important role in preventing the development of hypertension in SHR via a buffering effect on the elevation of cytosolic free Ca2+.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S223-4"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02891.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026506","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}
K Ohta, S Kim, A Hamaguchi, K Miura, T Yukimura, H Iwao
{"title":"Expression of sarcoplasmic reticulum Ca2+ -ATPase mRNA in the hypertrophied heart of young spontaneously hypertensive rats.","authors":"K Ohta, S Kim, A Hamaguchi, K Miura, T Yukimura, H Iwao","doi":"10.1111/j.1440-1681.1995.tb02893.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02893.x","url":null,"abstract":"<p><p>1. Recent evidence indicates that cardiac hypertrophy induced by pressure overload is associated with a decrease in sarcoplasmic reticulum (SR) Ca2+ -ATPase of myocytes, which may contribute to a diastolic dysfunction of the heart by causing intracellular Ca2+ overload. To elucidate whether or not this is also the case in genetic hypertension, we examined cardiac mRNA levels of SR Ca2+ ATPase in 11 week old spontaneously hypertensive rats (SHR) by northern blot analysis. 2. Furthermore, to test the effects of short-term inhibition of the renin-angiotensin system on its expression, we treated 10 week old SHR with angiotensin-converting enzyme inhibitors (alacepril and imidapril) or an AT1 receptor antagonist (SC-52458) for 7 days. 3. Though the left ventricular weight of SHR was significantly higher than that of Wistar-Kyoto (WKY) rats (277 +/- 6 vs 237 +/- 4 mg/100 g bodyweight, respectively, P < 0.05), the level of SR Ca2+ -ATPase mRNA showed no difference between SHR and WKY at this age. 4. Moreover, the aforementioned three drugs did not at all affect the SR Ca2+ -ATPase expression of SHR. 5. Thus, the expression of SR Ca2+ -ATPase was not down-regulated in the heart of 11 week old SHR, and seemed not to be mediated by angiotensin AT1 receptor at this age. Since some evidence on pressure-overloaded cardiac hypertrophy indicate that the decrease in SR Ca2+ -ATPase expression occur in prominent hypertrophy and in the failured heart, further studies on cardiac SR Ca2+ -ATPase expression in more aged SHR will be required.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S228-9"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02893.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026508","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":"Changes of endothelial functions in the coronary artery after chronic nitroarginine feeding.","authors":"N Kajimoto, H Ogawa, A Suzuki","doi":"10.1111/j.1440-1681.1995.tb02861.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02861.x","url":null,"abstract":"<p><p>1. The effects of chronic NG-nitro-L-arginine (LNA) feeding on the endothelial function in isolated coronary arteries from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto (WKY) rats were studied. 2. A diet containing LNA (0.02%) was given to male SHRSP and WKY at 6 weeks of age and the coronary arteries were dissected on the 10th day of feeding. 3. In the SHRSP and WKY fed the LNA-free diet, acetylcholine (ACh) relaxed the precontracted ring segments of the coronary artery with intact endothelium in a dose-dependent manner. The reactivity was stronger in the WKY than in the SHRSP. However, the ACh-induced relaxation after the LNA-feeding was significantly stronger in the coronary arteries from the WKY than in those from the SHRSP. 4. The relaxation induced by the calcitonin gene-related peptide (CGRP) was endothelium-dependent and endothelium-independent. The degree of the response in the rats fed the LNA-containing diet was not significantly different from that in the rats fed the LNA-free diet. 5. The vasodilator response induced by sodium nitroprusside (SNP) was dose-dependent and similar in the rats fed the LNA containing diet and the LNA-free diet. 6. These findings indicate that chronic LNA feeding markedly impaired the endothelial nitric oxide formation in the coronary artery from young SHRSP.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S154-6"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02861.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026702","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":"Relationship between erythrocytes glutathione peroxidase and incidence of stroke lesion in the stroke-prone spontaneously hypertensive rat.","authors":"T Murakami, K Takemori, T Takeda, H Yoshizumi","doi":"10.1111/j.1440-1681.1995.tb02864.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02864.x","url":null,"abstract":"<p><p>1. To determine biochemically the incipient timing of cerebral stroke in stroke-prone spontaneously hypertensive rats (SHRSP) the relation between the glutathione peroxidase (GSH-Px) activity in erythrocytes and the extent of stroke lesion was investigated. 2. When the blood pressure of SHRSP was maintained over 250 mmHg, the GSH-Px activity was lowered and the body weight also decreased. In the SHRSP where the GSH-Px activity in erythrocytes dropped below 23 units/mL blood, the incidence of cerebral stroke was 98% (n = 88/90). 3. The haemoglobin and haematocrit level were unchanged even after the GSH-Px activity dropped to 23 units/mL blood. 4. Lowering of GSH-Px activity in erythrocytes observed during continued hypertension was found to be due to decreased GSH-Px protein, but not to an inactivation of enzymes, as evidenced from immunochemical titration. 5. Lowering of GSH-Px activity in erythrocytes was found to be closely related with the incidence of cerebral stroke in SHRSP. These findings suggest that tracing of the GSH-Px activity in erythrocytes in SHRSP may serve as an indicator for prediction and prognosis of stroke lesion.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S162-4"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02864.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026705","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}
S Kimura, M Minami, H Saito, T Kobayashi, H Okuyama
{"title":"Dietary docosahexaenoic acid (22: 6n-3) prevents the development of hypertension in SHRSP.","authors":"S Kimura, M Minami, H Saito, T Kobayashi, H Okuyama","doi":"10.1111/j.1440-1681.1995.tb02931.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02931.x","url":null,"abstract":"<p><p>1. We previously reported that hypertension in stroke-prone spontaneously hypertensive rats (SHRSP) caused renal membrane phospholipid degradation. Renal phospholipase A2 activity increased and membranous phospholipids decreased along with age in SHRSP. Membranous abnormalities induced by membrane fluidity and calcium permeability changes may contribute to the elevation of blood pressure in SHRSP. DHA, a major component of fish oil, constitutes a part of membrane phospholipid acylchains. 2. The purpose of this study was to clarify the effect of DHA on the relationship between the renal function and the development of hypertension in SHRSP. 3. Six week old male SHRSP were fed a semi-purified diet supplemented with DHA (0, 1 and 5%) for 14 weeks. 4. The systolic blood pressure of control SHRSP (DHA 0%) significantly increased from 120.2 mmHg to 202.9 mmHg. This increase in systolic blood pressure was significantly inhibited in a dose-dependent manner by 1 and 5% DHA diet to 167.8 to 149.8 mmHg, respectively. 5. Serum creatinine concentration and blood urea nitrogen (BUN) were significantly lower in DHA (5%)-treated SHRSP than in the control SHRSP. 6. These results indicate that DHA prevents the development of hypertension in SHRSP, which is associated with changes in renal function.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S308-9"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02931.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026715","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}
T Rosenthal, Y Erlich, E Rosenmann, E Grossman, A Cohen
{"title":"Enalapril improves glucose tolerance in two rat models: a new hypertensive diabetic strain and a fructose-induced hyperinsulinaemic rat.","authors":"T Rosenthal, Y Erlich, E Rosenmann, E Grossman, A Cohen","doi":"10.1111/j.1440-1681.1995.tb02951.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02951.x","url":null,"abstract":"<p><p>1. The present study was undertaken to examine the effect of the angiotensin converting enzyme (ACE) inhibitor, enalapril, on blood pressure and spontaneous blood glucose levels in two rat models: our new diabetic hypertensive rat in which genetic hypertension and diabetes develop following cross-breeding of Cohen diabetic rat (CDR) and spontaneous hypertensive rats (SHR); and a rat in which hypertension, hyperinsulinaemia and hyperlipidaemia were induced by fructose diet. 2. The new strain of animal was fed the usual copper-poor sucrose diet, and for 4 weeks received enalapril. The fructose-induced hyperinsulinaemic animals were fed a fructose-enriched diet for 3 weeks, and enalapril 20 mg per kg per day was added to the drinking water for 2 more weeks. 3. The new strain of diabetic-hypertensive rats that received enalapril showed a significant decrease in blood pressure level. The fructose-fed animals showed a fall in insulin and blood pressure following the introduction of enalapril to their diet. 4. The present study confirms the advantage of the ACE inhibitor enalapril in improving the metabolic parameters of hypertensive diabetic rats, including insulin sensitivity.</p>","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S353-4"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02951.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20027030","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}