Academic literature on the topic 'Rat (wistar'

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Journal articles on the topic "Rat (wistar"

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Li, Yan, and Kenneth E. McMartin. "Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats." American Journal of Physiology-Renal Physiology 296, no. 5 (May 2009): F1080—F1087. http://dx.doi.org/10.1152/ajprenal.90727.2008.

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Ethylene glycol (EG)-induced hyperoxaluria is the most commonly employed experimental regimen as an animal model of calcium oxalate (CaOx) stone formation. The variant sensitivity to CaOx among different rat strains has not been fully explored, although the Wistar rat is known to accumulate more CaOx in kidney tissue after low-dose EG exposure than in the Fischer 344 (F344) rats. Supersaturation of CaOx in tubular fluid contributes to the amount of CaOx crystal formation in the kidney. We hypothesized that the urinary supersaturation of CaOx in Wistar rats is higher than that of F344 rats, thereby allowing for greater CaOx crystal deposition in the Wistar rat. Age-matched male Wistar and F344 rats were treated with 0.75% EG or drinking water for 8 wk. Twenty-four-hour urine was collected at 0, 2, 4, 6, and 8 wk for analysis of key electrolytes to calculate the CaOx supersaturation. Plasma oxalate level was also measured. Our data confirmed the different sensitivity to renal toxicity from EG between the two rat strains (Wistar > F344). After EG treatment, the plasma oxalate level and urine oxalate excretion were markedly greater in the Wistar rats than in the F344 rats, while urine calcium was slightly decreased in Wistars. Thus, the CaOx supersaturation in urine of Wistar rats was higher, which led to a greater crystal deposition in kidney in Wistar rats. These studies suggest that during EG treatment, changes in urine electrolytes and in CaOx supersaturation occur to a greater extent in the Wistar rat, in agreement with its greater sensitivity to EG toxicity.
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Martins, A. R., G. S. S. Matias, V. F. Batista, M. A. Miglino, and P. Fratini. "Wistar rat dermis recellularization." Research in Veterinary Science 131 (August 2020): 222–31. http://dx.doi.org/10.1016/j.rvsc.2020.05.005.

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Kava, R., R. G. Peterson, D. B. West, and M. R. C. Greenwood. "Wistar Diabetic Fatty Rat." ILAR Journal 32, no. 3 (January 1, 1990): 9–13. http://dx.doi.org/10.1093/ilar.32.3.9.

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Wilby, Owen K., Karen Critchell, and Debbie Coulby. "The Wistar rat chondrodystrophy syndrome." Reproductive Toxicology 32, no. 2 (September 2011): 177–78. http://dx.doi.org/10.1016/j.reprotox.2011.06.113.

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FITZGIBBON, WAYNE R., EDDIE L. GREENE, JASJIT S. GREWAL, FLORENCE N. HUTCHISON, SALLY E. SELF, SAJATA Y. LATTEN, and MICHAEL E. ULLIAN. "Resistance to Remnant Nephropathy in the Wistar-Furth Rat." Journal of the American Society of Nephrology 10, no. 4 (April 1999): 814–21. http://dx.doi.org/10.1681/asn.v104814.

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Abstract. The Wistar-Furth rat, an inbred strain resistant to actions of mineralocorticoids, was used to study the concept that mineralocorticoids contribute to progressive renal injury. It was postulated that if chronic nephropathy depends on aldosterone and if Wistar-Furth rats are resistant to aldosterone, remnant nephropathy would be attenuated in Wistar-Furth rats. Wistar-Furth rats and control Wistar rats were subjected to 5/6 nephrectomy or a sham procedure and then followed for 4 wk. Renal ablation resulted in hypertension at 4 wk in both strains (164 ± 5 [Wistar-Furth] versus 184 ± 7 [Wistar] mmHg mean arterial pressure), with sham animals remaining normotensive (134 ± 6 mmHg). Renal damage in response to 5/6 nephrectomy was greatly decreased in Wistar-Furth rats compared with Wistar rats. Albuminuria was markedly less in Wistar-Furth rats (12.7 ± 4.2 [Wistar-Furth] versus 97.4 ± 22.6 [Wistar] mg/d per 100 g body wt, P < 0.01). Glomerular damage, consisting of mesangial proliferation, mesangial lysis, and segmental necrosis, was observed in 42% of glomeruli from Wistar rats but in 0% of glomeruli from Wistar-Furth rats (P < 0.01). To address the possibility that higher BP in partially nephrectomized Wistar rats mediated the greater renal damage, the study was repeated, with Wistar rats (not Wistar-Furth rats) being treated with a hydralazine-reserpine-hydrochlorothiazide regimen. Although this antihypertensive regimen equalized BP (conscious systolic) (144 ± 8 mmHg [Wistar] versus 157 ± 7 mmHg [Wistar-Furth] at 4 wk), albuminuria remained more than 10-fold greater in Wistar rats. In summary, renal damage upon 5/6 nephrectomy was markedly reduced in Wistar-Furth rats, a finding not attributable to reduced systemic BP. Since Wistar-Furth rats have been shown previously to be resistant to the actions of mineralocorticoids, the data from the present study support the hypothesis that aldosterone mediates, at least in part, the renal injury attendant to renal mass reduction.
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Silva, Letícia Maria, Fernanda Bresolin, Jane Prado, Leonardo Grouschekei, Andressa Zanon, Antonio Leis-Filho, Juliana Rozolen, Carlos Fonseca-Alves, and Fabiana Elias. "Primary hepatic fibrosarcoma in a Wistar rat (Rattus norvegicus)." Brazilian Journal of Veterinary Pathology 13, no. 1 (March 31, 2020): 21–25. http://dx.doi.org/10.24070/bjvp.1983-0246.v13i1p21-25.

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Li, Yan, Marie C. McLaren, and Kenneth E. McMartin. "Involvement of urinary proteins in the rat strain difference in sensitivity to ethylene glycol-induced renal toxicity." American Journal of Physiology-Renal Physiology 299, no. 3 (September 2010): F605—F615. http://dx.doi.org/10.1152/ajprenal.00419.2009.

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Ethylene glycol (EG) exposure is a common model for kidney stones, because animals accumulate calcium oxalate monohydrate (COM) in kidneys. Wistar rats are more sensitive to EG than Fischer 344 (F344) rats, with greater COM deposition in kidneys. The mechanisms by which COM accumulates differently among strains are poorly understood. Urinary proteins inhibit COM adhesion to renal cells, which could alter COM deposition in kidneys. We hypothesize that COM accumulates more in Wistar rat kidneys because of lower levels of inhibitory proteins in urine. Wistar and F344 rats were treated with 0.75% EG in drinking water for 8 wk. Twenty-four-hour urine was collected every 2 wk for analysis of urinary proteins. Similar studies were conducted for 2 wk using 2% hydroxyproline (HP) as an alternative oxalate source. Total urinary protein was higher in F344 than Wistar rats at all times. Tamm-Horsfall protein was not different between strains. Osteopontin (OPN) levels in Wistar urine and kidney tissue were higher and were further increased by EG treatment. This increase in OPN occurred before renal COM accumulation. Untreated F344 rats showed greater CD45 and ED-1 staining in kidneys than untreated Wistars; in contrast, EG treatment increased CD45 and ED-1 staining in Wistars more than in F344 rats, indicating macrophage infiltration. This increase occurred in parallel with the increase in OPN and before COM accumulation. Like EG, HP induced markedly greater oxalate concentrations in the plasma and urine of Wistar rats compared with F344 rats. These results suggest that OPN upregulation and macrophage infiltration do not completely protect against COM accumulation and may be a response to crystal retention. Because the two oxalate precursors, EG and HP, produced similar elevations of oxalate, the strain difference in COM accumulation may result more so from metabolic differences between strains than from differences in urinary proteins or inflammatory responses.
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Chen, Tao, Ke Chen, Shaung Qiu, and Peter C. Mann. "Spontaneous Cholangiofibrosis in a Wistar Rat." Toxicologic Pathology 47, no. 4 (April 15, 2019): 556–60. http://dx.doi.org/10.1177/0192623319842549.

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In a 2-year carcinogenicity study, we identified a spontaneous cholangiofibrosis in a control male Wistar rat. This lesion has long been considered as a compound-related change, with no spontaneous cases reported in the Wistar rat. In addition to routine hematoxylin and eosin stains evaluation, we applied Masson’s trichrome staining, Alcian blue-periodic acid–Schiff staining, and OV-6 immunohistochemistry staining. The special staining demonstrated the fibrous component in the interstitium and intestinal metaplasia of the epithelium (presence of goblet cells), while the positive anti-OV-6 reaction indicated the bile duct origin of the epithelium. These results help to confirm the diagnosis of cholangiofibrosis in this case. We report this rare case to alert pathologists that spontaneous cholangiofibrosis does occur in Wistar rats.
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Khosho, F. K., R. C. Kaufmann, and K. S. Amankwah. "Cervical and vaginal surface epithelial changes in persistent estrous, chemically diabetic BB wistar rats observed by scanning electron microscope." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 250–51. http://dx.doi.org/10.1017/s0424820100142876.

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Studies of the effects of diabetes on reproduction in the female BB Wistar rat are not available in the literature. Male reproduction has been studied in these spontaneously-diabetic BB Wistar rats, and abnormalities of the reproductive tract have been found. This investigation, therefore, compared the ultrastructure of the lower reproductive tract of the chemically-diabetic female BB Wistar rat which has developed persistent estrous(PE) to normalcycling controls.
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Teredesai, A., and T. Wohrmann. "Endocardial Schwannomas in the Wistar Rat." Journal of Veterinary Medicine Series A 52, no. 8 (October 2005): 403–6. http://dx.doi.org/10.1111/j.1439-0442.2005.00750.x.

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Dissertations / Theses on the topic "Rat (wistar"

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Wright, James Roscoe. "Characterization of the spontaneously diabetic BB Wistar rat /." The Ohio State University, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487862972134951.

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Carter, Tiffany. "Hemostatic efficiency of amphiphilic peptide solution in Wistar Rat model." Thesis, Kansas State University, 2014. http://hdl.handle.net/2097/35239.

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Master of Science
Department of Grain Science and Industry
X. Susan Sun
One of the leading causes of death following traumatic injury is exsanguination. The body addresses bleeding through the process of hemostasis which includes the formation of a fibrin mesh structure that holds a blood clot together. During traumatic injury, hemostasis may be unable to stop excess bleeding. Fibrin based hemostatic agents have been developed, however, these studies often use fibrin obtained from biological sources, which poses risk of infection. A novel amphiphilic peptide (h9e) has been studied to form three dimensional nanofibers networks. In this research, we studied the ability to form a synthetically produced, fibrin-mimic, hemostatic material from the h9e peptide sequence. The objective of this study was to determine the blood gelation strength of the h9e peptide necessary to arrest bleeding in the Wistar Rat model. Commercial mouse blood was used for blood gelation in vitro studies. Dynamic rheometer was used to determine the gelation kinetics at varied h9e peptide concentrations ranging from 1-5% wt. By directly mixing the h9e peptide with blood, we observed that the blood gelation strength right after mixing increased as the h9e peptide weight % concentration increased, from 67 to 1086 Pascals in the peptide concentration from 1 to 5%, respectively. After 24 hours, final gelation strength of all concentrations with commercial mouse blood was lower than the instantaneous strength but consistent throughout testing. Similar testing was conducted using commercial Wistar Rat blood with weight % concentrations of 1, 3, and 5% of h9e peptide. The gelation strength was 500, 1665, and 1914 Pascals, respectively. We also determined the gelation strength of Wistar Rat blood components, such as red blood cells, serum, and plasma with 1% h9e peptide. We observed the gelation response induced with individual blood components; however, the strength is weaker than whole blood. In vivo, we applied the cut-tail method by dipping the cut-tail of Wistar Rats into the h9e peptide solutions for 10 seconds and then took it out for blood lost collection. We observed that h9e peptide solution at 1, 3, and 5% weight concentrations can all generate hemostatic function. The h9e peptide solution at 5% weight concentration (1914 Pa) was able to outperform a commercial hemostatic material (Moore Medical CELOX* Hemostatic Granules), significantly reducing both bleeding time and blood lost: h9e peptide at 5% had a bleeding time of 94 sec and 0.75 mL blood lost, while the Celox hemostatic granules had a bleeding time of 225 sec and 1.5 mL blood lost. Transmission Electron Microscopy and Spinning Disk Confocal Microscope imaging indicated a blood component reinforced, web-like, h9e nanofiber structure similar to the structure formed by fibrin in a blood clot. This study showed that h9e peptide has the potential to be used to induce hemostasis.
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Benoit, Pascal. "Effets du stigmastérol sur le métabolisme lipidique du rat Wistar." Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37602881w.

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Houti, Imad Eddine. "Chronopharmacocinétique de la cyclosporine A Etude expérimentale chez le rat Wistar." Toulouse 3, 1994. http://www.theses.fr/1994TOU30062.

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La cyclosporine a (csa) est un puissant immunodepresseur largement utilise pour prevenir le rejet des organes transplantes. Son index therapeutique est etroit et sa biodisponibilite est tres variable. Notre etude a eu pour objectif d'analyser l'influence du stade temporel d'administration de la csa sur son devenir, chez le rat wistar. Cette etude chronopharmacocinetique comporte deux volets complementaires, selon la voie d'administration de la csa: intraveineuse i. V. (5 mg/kg) ou orale p. O. (20 mg/kg). 4 groupes de rats sont constitues, different par l'horaire de traitement (exprime en heure apres le debut de la lumiere): 02, 08, 14 ou 20 hadl. La methode de dosage par hplc de la csa a fait l'objet de validations statistiques. Voie iv: un modele tri-exponentiel a permis d'ajuster aux mieux les variations des concentrations en fonction du temps. Une analyse de variance a 2 facteurs a conclu a l'influence tres significative (s0. 0001) de l'horaire d'administration. Le temps de demi-vie d'elimination (22. 5 2. 2 h) est independant de l'heure de traitement, contrairement a l'aire sous la courbe de concentration en fonction du temps asc (35275 1185 g. 1#-#1. H a 08 hadl vs 29087 752 g. 1#-#1. H a 20 hadl) et a la clairance cl (0. 142 0. 005 1/h/kg a 08 hadl vs 0. 172 0. 004 1/h/kg a 20 hadl). Voie orale: l'influence de l'horaire d'administration est dans ce cas encore plus marquee, car elle affecte essentiellement la phase d'absorption. Les asc et la biodisponibilite f varient d'un facteur 4 a 5 selon l'horaire de traitement. 0. 19 0. 03 a 08 ou 20 hadl, 0. 05 0. 009 a 02 ou 14 hadl. Ces variations ultradiennes pourraient etre attribuees en partie a des modifications de la capacite de metabolisation des enzymes des enterocytes. Les profils pharmacocinetiques obtenus pour le sang et les organes evoluent parallelement a ceux du plasma. Les plus fortes concentrations sont obtenues dans le foie, puis le rein, le sang et les plus faibles dans le plasma. Le rapport de concentration sang/plasma depend significativement de l'horaire de traitement, c'est a 08 hadl qu'il est le plus bas. Ce fait est revelateur de variations circadiennes de la liaison de la csa aux erythrocytes. Des pics secondaires decales de 3 a 4 heures ont ete observes dans tous les cas, tres marques apres administration orale, plus tenus mais statistiquement significatifs apres administration iv. Ils pourraient etre attribues a une remise en circulation (voie iv) ou une solubilisation de novo (voie orale) par la bile. Les variations temporelles de la toxicite renale induite par la csa peuvent resulter en partie de ces modifications chronopharmacocinetiques
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Houri, Tarek. "Rôle des caspases au cours de la photodégénérescence rétinienne." Thesis, Clermont-Ferrand 1, 2012. http://www.theses.fr/2012CLF1PP04/document.

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Quelque soit le type de dégénérescences rétiniennes, les cellules photoréceptrices à l'origine de la genèse du signal lumineux, meurent par un mécanisme commun : l'apoptose. Au laboratoire, nous avons mis en évidence que l'inhibition de la caspase-3, une caspase effectrice de l'apoptose, permet de réduire l'apoptose des cellules photoréceptrices (Perche et al. 2007). Dans la continuité de ces résultats, le but de nos travaux de thèse est d'identifier les molécules impliquées en amont de la caspase-3. Pour mener à bien notre projet, nous avons utilisées un modèle expérimentale de dégénérescence rétinienne induite par une exposition à la lumière (modèle de photodégénérescence rétinienne). Les atteintes rétiniennes sont quantifiées par : l'électrorétinographie in-vivo permettant d'évaluer la fonction rétinienne, l'histologie pour l'analyse morphométrique de la rétine aux quelles sont associés des dosages enzymatiques. Ainsi, nous avons montré que l'injection d'un inhibiteur de la caspase-12 à 0,4 ou à 0,8 mM, de la caspase-9 à 0,2 ou à 0,4 mM, ou de la caspase-8 à 0,2 mM, injecté dans le vitré n'a aucun effet toxique sur la rétine et n'a aucun effet protecteur contre l'apoptose des cellules photoréceptrices induites par la lumière. Ces résultats suggèrent que les caspases-8, 9 et 12 ne sont pas impliquées dans l'activation de la caspase-3 et donc dans l'initiation de l'apoptose des photorécepteurs induite par la lumière. Toutefois, après injection dans le vitré, les inhibiteurs inhibent leur cible respective uniquement transitoirement. Par conséquent, pour pouvoir conclure sur le rôle de ces caspases dans le processus dégénératif, il faudrait pouvoir inhiber les caspases de façon plus persistante. Il serait donc intéressant de reproduire des expérimentations similaires en augmentant la concentration de l'inhibiteur injecté ou en réduisant le délai entre l'injection de l'inhibiteur et l'induction du stress. De plus, la caspase-3 peut être activée indépendamment des caspases initiatrices, comme par exemple : les céramides, les cathepsines et les calpaïnes
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McGill, Jetta. "Functional recovery after stroke in the stroke-prone spontaneously hypertensive rat (SHRSP) and Wistar Kyoto rat (WKY)." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422503.

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Pascotto, Viviane Mattos [UNESP]. "Influência da mistura de cinco praguicidas em baixas doses sobre o sistema reprodutor de ratas Aprague-Dawley, Wistar e Lewis." Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/95894.

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Made available in DSpace on 2014-06-11T19:27:56Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-02-22Bitstream added on 2014-06-13T19:36:18Z : No. of bitstreams: 1 pascotto_vm_me_botfm.pdf: 1234125 bytes, checksum: 1d563b2c7f6645fcba3865762f9c46c7 (MD5)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O presente projeto objetivou investigar os efeitos da combinação, em baixas doses, de cinco praguicidas (dieldrin, dicofol, endosulfan, diclorvos e permetrina) sobre o sistema reprodutor de ratas Sprague-Dawley, Wistar e Lewis. Ratas de cada linhagem, com seis semanas de idade, foram randomizadas em três grupos: GI: controle negativo; GII: praguicidas adicionados à ração em doses de NOEL (mg/Kg/dia) - diclorvos (0,23), dicofol (0,5), dieldrin (0,025); endosulfan (0,7), permetrina (5); GIII: praguicidas adicionados à ração em doses de LOEL (mg/Kg/dia) - diclorvos (2,3), dicofol (2,1), dieldrin (0,05), endosulfan (3,8), permetrina (25). A eutanásia foi realizada entre a 10ª e a 12ª semana experimental, na fase de estro. Os parâmetros de avaliação foram: peso de fígado, útero e ovários; análise histológica qualitativa de fígado, útero e ovários; morfometria do endométrio; avaliação do ciclo estral; dosagem de LH, FSH e progesterona; e contagem de folículos ovarianos. Animais das três linhagens tratados com a LOEL apresentaram toxicidade sistêmica, evidenciada pela diminuição de peso corpóreo e aumento de peso de fígado. A análise qualitativa de útero e ovários, assim como a avaliação do ciclo estral e níveis hormonais não indicaram sinais de toxicidade reprodutiva exercida pelas misturas. A contagem de folículos ovarianos indicou ausência de resposta dose dependente e alta variabilidade entre os animais de mesmo grupo experimental. Desta forma concluímos que, embora os resultados tenham mostrado diminuição de algumas populações foliculares nas doses de NOEL e LOEL, este parâmetro não pode ser utilizado isoladamente como indicativo de toxicidade reprodutiva. Estes achados remetem à necessidade de maiores estudos para o esclarecimento dos efeitos destes compostos nas populações foliculares
This project aimed to investigate the effects of the combination, in low doses, of five pesticides (dieldrin, dicofol, endosulfan, dichlorvos and permethrin) on the reproductive system of Sprague- Dawley, Wistar and Lewis rats. Six-weeks-old rats from each strain were randomized into three groups: GI: negative control; GII: pesticides added to the feed at NOEL doses (mg/kg/day) - dichlorvos (0.23), dicofol (0.5), dieldrin (0.025), endosulfan (0.7), permethrin (5), GIII: pesticides added to the feed at LOEL doses (mg / kg / day) – dichlorvos (2.3), dicofol (2.1), dieldrin (0.05), endosulfan (3.8), permethrin (25). Euthanasia was performed between the 10th and 12th experimental week, in the estrous stage. The evaluation parameters were: weight of liver, uterus and ovaries; qualitative histological analysis of liver, uterus and ovaries; endometrium morphometry; estrous cycle assessment; dosage of LH, FSH and progesterone; and counting of ovarian follicles. Animals from all three strains showed systemic LOEL toxicity, as evidenced by decreased body weight and increased liver weight. Qualitative analysis of the uterus and ovaries, as well as estrous cycle and hormone levels evaluations indicated no signs of reproductive toxicity exerted by the mixtures. Counting of ovarian follicles indicated lack of dose-dependent response and high variability among animals from the same experimental group. Hence, we concluded that, although our results have shown a decrease of some follicular populations at the NOEL and LOEL doses, this parameter can not be used alone as an indicator of reproductive toxicity. These findings underscore the need for more studies to clarify the effects of these compounds on follicular populations
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Ahmad, Qadeer. "The behavioral and neurochemical profile of the spontaneously diabetic Wistar B.B. rat." Thesis, University of Ottawa (Canada), 1993. http://hdl.handle.net/10393/7520.

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The Spontaneously Diabetic Wistar B.B. Rat (SDR) is considered to be a genetically determined animal model of human Type-1 diabetes. The overall objective of this thesis was to elucidate the behavioral and neurochemical profile of the SDR. This objective was attained using various pharmacological, behavioral and neurochemical approaches. The course of the changes was followed sequentially, at discretely defined time frames (0-2, 2-8 and 8-12 months duration of diabetes), to explore and characterize the contended dysfunctions. Overall, it was found that the insulin treated SDR exhibited a significantly attenuated locomotor and rearing response to the systemically administered dopamine agonists d-amphetamine and amfonelic acid. In the case of d-amphetamine, it was found that the attenuated response was robust and chronic as it persisted across all three time frames. The attenuated response of the insulin treated SDR to amfonelic acid demonstrated that the behavioral deficit could also be elicited by a dopamine agonist with a different mechanism of action from d-amphetamine. In a nonpharmacological experiment, it was found that the insulin treated SDR manifested a significantly attenuated nocturnal locomotor and rearing response, particularly to transitional photoperiodic cues. This deficit in responding was chronic and robust as it was observed across all three time frames. The possible neurochemical substrates of the aforementioned effects were investigated. A post-mortem neurochemical analysis of the region specific basal levels of CNS catecholamines and metabolites, in the insulin maintained and deprived SDR, was undertaken. There were no significant differences between the insulin maintained SDR and non-diabetic littermates or genetically distinct controls. The cessation of insulin administration to the SDR for four consecutive days resulted in significant increases in the levels of norepinephrine in the cortex and hypothalamus, dopamine in the hippocampus, and homovanillic acid in the striatum. The neurochemical response of the insulin treated SDR was assessed following a pharmacological challenge. The SDR was exposed to a single dose of (1.0 mg/kg, i.p.) amfonelic acid. The SDR exhibited a significantly greater reduction in the post-mortem levels of dopamine in the striatum, midbrain, and olfactory bulbs as well as striatal norepinephrine. The behavioral effects elicited by d-amphetamine and amfonelic acid are believed to be dopamine mediated. Thus, it was hypothesized that one source of the observed neurochemical and behavioral deficits may be related to an impairment of dopaminergic neurotransmission. Therefore, the concomitant measurement of spontaneous nocturnal locomotor activity and levels of interstitial dopamine from the ventral striatum was measured using in vivo microdialysis. No significant differences between the insulin treated SDR and controls were found. The SDR did exhibit significantly lower levels of locomotor activity. In a different vein, the behavioral response of the insulin treated SDR was assessed following exposure to environments varying in degree of novelty. It was found that the SDR exhibited a heightened behavioral response to novelty-stress. The insulin maintained SDR manifested a greater aversion to the anxiogenic regions of the open field and elevated plus maze whilst being treated with chlordiazepoxide. The anxiolytic effects of this drug were significantly attenuated in the SDR when compared to controls. In essence, it would appear that the SDR when treated with insulin and unchallenged by: (1) withdrawal of insulin treatment, (2) pharmacological stimulation or, (3) environmental stimulation, is able to maintain relatively stable baseline levels of brain catecholamines and behavior. (Abstract shortened by UMI.)
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Aguiar, Marcus Vinicius de Almeida. "Estudo da atividade neuroprotetora da Parawixina10, molécula isolada da peçonha da aranha Parawixia bistriata (Araneae: Araneidae), em ratos Wistar submetidos à modelo de glaucoma agudo." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-12042017-155940/.

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Peçonhas de aranhas são uma rica fonte de moléculas, dentre as quais se destacam os peptídeos neuroativos, que atuam no tecido nervoso de insetos e mamíferos, tais como receptores colinérgicos e glutamatérgicos A retina constitui um neuroepitelio, uma das membranas do segmento posterior do olho, é uma extensão do sistema nervoso central. A lesão isquêmica nesse tecido desencadeia um processo de degeneração celular, sendo os neurônios os principais afetados. Várias patologias oculares, como o glaucoma, estão associadas a uma degeneração neuronal secundária à isquemia, na qual o excesso de L-glutamato (L-Glu) extracelular é lesivo aos neurônios. A peçonha da aranha Parawixia bistriata contém componentes com grande potencial neuroprotetor, como a Parawixina10 (Pwx10), que atua potencializando o transporte de L-Glu e glicina para o meio intracelular. Neste contexto, diante da necessidade de se buscar novas terapias para o tratamento de neuropatologias e de se entender a lesão isquêmica, a Pwx10 surge como potencial fármaco neuroprotetor. Portanto, o objetivo deste trabalho foi analisar o potencial neuroprotetor da Pwx10, em um modelo de isquemia retiniana aguda, com e sem reperfusão, em ratos Wistar. Durante os experimentos de isquemia (ISQ), a pressão intra-ocular (PIO) foi aumentada para 120 mmHg, e mantida por 45 minutos. Nos experimentos em que houve reperfusão (ISQ/REP), após a isquemia, a pressão foi reduzida aos níveis normais e mantida por mais 15 minutos, de forma a restaurar o fluxo sanguíneo e os níveis basais da PIO. As drogas utilizadas para tratamento foram injetadas por via intravitrea, 15 minutos antes do início da isquemia. Após a cirurgia foram realizados os processos histológicos que envolvem técnicas de H-E e Fluoro-Jade C. Em seguida, foram analisadas as densidades de células viáveis na camada nuclear interna (CNI) e camada de células ganglionares (CCG). Os resultados mostraram que os tratamentos com a Pwx10 protegeram as células da CNI tanto em ISQ como ISQ/REP. Comparada com o Riluzole, a Pwx10 foi mais eficaz em CCG ISQ em 15% e CNI ISQ/REP em 23%. Portanto, a Pwx10 apresenta efeitos neuroprotetores em ratos Wistar submetidos à isquemia retiniana aguda, seguida por reperfusão ou não.
Spider venoms are a rich source of molecules, among which stand out the neuroactive peptides that act on the nervous tissue of insects and mammals, such as cholinergic and glutamatergic receptors. The retina is a neuroepithelium, a membrane lining the cavity of the eyeball, it being an extension of the central nervous system. Ischemic injury that tissue triggers a cell degeneration process, and the neurons affected major. Various eye diseases such as glaucoma, are associated with neuronal degeneration secondary to ischemia in which excess L-glutamate (L-Glu) extracellular is harmful to neurons. The venom of Parawixia bistriata spider contains components with high neuroprotective potential, as Parawixina10 molecule (Pwx10), which operates enhancing the transport of L-Glu and glycine to the intracellular medium. In this context, on the need to seek new therapies for the treatment of these diseases and to understand the ischemic injury, Pwx10 emerges as potential neuroprotective drug. Therefore the aim of this study was to evaluate the neuroprotective potential of Pwx10 on an acute retinal ischemia model, with and without reperfusion in rats. During the experiments ischemia (ISC), the intraocular pressure (IOP) was increased to 120 mmHg and maintained at this level for 45 minutes. In experiments in which there was reperfusion (I/R) after the period of ischemia, the pressure was reduced to normal levels and maintained there for 15 minutes in order to restore blood flow and baseline IOP. The drugs used for the treatment were intravitreally injected 15 minutes before the onset of ischemia. After surgery were performed histological techniques involving procedures H-E and Fluoro-Jade C. Then, viable cell densities in the inner nuclear layer were analyzed (INL) and ganglion cell layer (GCL). The results showed that the treatments with Pw10 protected the INL cells both in ISC as IR. Compared with Riluzole, the Pwx10 was more effective in GCL ISC 15% and INL I/R 23%. Therefore, Pwx10 shows neuroprotective effects in Wistar rats with acute retinal ischemia followed by reperfusion or not.
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Rizzolo, Lou. "Effets d'une exposition chronique à la musique sur le vieillissement chez le rat Wistar." Thesis, Normandie, 2018. http://www.theses.fr/2018NORMC420/document.

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Le déclin cognitif associé au vieillissement chez l’Homme, impacte fortement la vie quotidienne des personnes âgées. Si la pratique musicale apparait comme une activité de loisir prometteuse pour le maintien d’un bon fonctionnement cognitif au cours du vieillissement, les mécanismes neurobiologiques sous-jacents sont à l’heure actuelle, mal connus. L’objectif de ce travail a donc été d’étudier les effets d’une exposition tardive et chronique à la musique sur les performances comportementales et certains processus neurobiologiques au cours du vieillissement chez le rat Wistar. Si quelques études rapportent qu’une exposition à la musique améliore les performances d’apprentissage et de mémoire, associé à une augmentation de la neurogenèse hippocampique et du BDNF chez le Rongeur jeune adulte, il n’en existe aucune qui se soit intéressée à ces effets chez le Rongeur âgé. Des rats d’âge médian ont été répartis dans 2 groupes, l’un exposé à de la musique et l’autre à du bruit blanc, puis inclus dans une étude longitudinale, au cours de laquelle les performances comportementales ont été évaluées jusqu’à l’âge de 24 mois, suivi d’analyses biologiques. Ainsi, nous avons pu montrer qu’une exposition chronique à la musique démarrant à un âge médian, réduit le déclin cognitif associé au vieillissement. En revanche, la neurogenèse hippocampique et le BDNF n’apparaissent pas comme des mécanismes neurobiologiques potentiels impactés par la musique chez le rat âgé
Cognitive decline associated to aging impacts daily life of elderly. While the music practice appears as promising leisure activity to prevent cognitive decline in elder, little is known about the neurobiological mechanisms involved. The aim of this work was to study the effects of music exposure on behavioral performances and some neurobiological processes across aging in rats. Indeed, improved behavioral performances together with an increased hippocampal neurogenesis and a higher BDNF expression were reported after music exposure in both young and adult animals. Yet, no study has so far investigated these effects in aged rats. After a fine appraisal of the cognitive state in middle-aged Wistar rats (15 months), they were divided in two groups, exposed either to classic music or to white noise. Thereafter, a longitudinal follow up of 9 months was performed. We observed for the first time that chronic music exposure alleviated age-related cognitive decline. However, contrary to what was observed in adult animals, we did not reported any differences in age-related changes of hippocampal neurogenesis and BDNF expression. These promising results of a beneficial effect of music exposure in the field of aging still lay open the question about the underlying mechanisms in the context of aging of the beneficial effect of music exposure
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Books on the topic "Rat (wistar"

1

Tucker, Mary J. Diseases of the Wistar rat. London: Taylor & Francis, 1997.

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Berns, Trevor Aaron. The influence of CYP2D1 in the behavioural pharmacology of amphetamine and hydrocodone in the male wistar rat. Ottawa: National Library of Canada, 1995.

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Yatim, Wildan. Efek anti-fertilitas gosipol dan gula berkhlor terhadap tikus wistar (Rattus narvegicus) dan implikasi prospeknya sebagai kontraseptif pria: Anti-fertility effect of gossypol and chlorinated sugar in wistar rat (Rattus norvegicus) and its prospect implications as male contraceptive. [Bandung]: Universitas Padjadjaran, 1991.

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VandenBoer, Trevor. Development of an analysis for ketamine in wistar rat femoral bone, bone marrow and blood following a single acute administration by enzyme-linked immunosorbent assay and gas chromatography electron capture detection methods. Sudbury, Ont: Laurentian University, 2007.

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tao, Wang zeng. WISTAR da shu jie pou tu pu. Ji nan: Shan dong ke xue ji zhu chu ban she, 2009.

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Johnson, Brooke Leann. Heart rate and behaviour during the presence of an aversive stimuli in wistar rats. Sudbury, Ont: Laurentian University, 2003.

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Potter, Beatrix. Hanes Sami Wisgars: Neu'r pwdin rholi-poli. Llandwrog: Cyhoeddiadau Sain, 1996.

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Potter, Beatrix. Hanes Sami Wisgars: Addasiad o'r gyfres a animeiddiwyd o'r straeon gwreiddiol. Llandwrog: Cyhoeddiadau Sain, 1994.

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L, Snyder David, ed. Dietary restriction and aging: Proceedings of the Symposium on the Effects of Dietary Restriction on Aging and Disease in Germfree and Conventional Lobund-Wistar Rats, held in Notre Dame, Indiana, March 27-29, 1988. New York, NY: A.R. Liss, 1989.

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Restu, I. Wayan. Kajian potensi sumberdaya hayati perairan sebagai salah satu atraksi dan daya tarik wisata dalam pengembangan ekowisata di kawasan Taman Hutan Raya Ngurah Rai, Bali: Laporan penelitian. Denpasar: Universitas Udayana, 2004.

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Book chapters on the topic "Rat (wistar"

1

Kojo, A., H. Hanhijärvi, M. Ylinen, and V. M. Kosma. "Toxicity and Kinetics of Perfluoro-octanoic Acid in the Wistar Rat." In Archives of Toxicology, 465–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71248-7_96.

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Garcia, J. H., K. F. Liu, and X. J. Hu. "Time Course of Leukocyte Influx Following Middle Cerebral Artery Occlusion in the Wistar Rat." In Thrombolytic Therapy in Acute Ischemic Stroke III, 3–9. Tokyo: Springer Japan, 1995. http://dx.doi.org/10.1007/978-4-431-68459-6_1.

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Desor, D., C. Colin, F. Thuillier, J. Mos, and B. Krafft. "Experimental Social Differentiation in the Rat: Behavioural Characteristics in Wistar and Long-Evans Strains." In Animal Models in Psychopharmacology, 339–40. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-6419-0_32.

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Morales-Guerrero, Nelly A., Alfredo Varela-Echavarría, Carlos Lozano-Flores, Francisco G. Vázquez-Cuevas, Esperanza Mata-Martínez, and Hebert Luis Hernández-Montiel. "Determination of the Survival of Recellularized Primary Hepatocytes in a Wistar Rat Liver Extracellular Matrix." In IFMBE Proceedings, 176–79. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-46936-7_19.

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Kumari, Namrata, and Pratibha Mehta Luthra. "Establishment of a 6-OHDA Induced Unilaterally Lesioned Male Wistar Rat Model of Parkinson’s Disease." In Neuroprotection, 491–98. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3662-6_33.

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Cools, Alexander R., and B. Ellenbroek. "Wistar Rats." In Advances in Behavioral Biology, 493–98. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0194-1_59.

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Albanese, R. "4-Dimethylaminoazobenzene (DAB) and 4-Cyanodimethylaniline (CDA): An in vivo Cytogenetic Study in the Alderley Park (Wistar) Rat." In Comparative Genetic Toxicology, 475–81. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07901-8_55.

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Brouwer, Elisabeth, Jan J. Weening, Pieter A. Klok, Minke G. Huitema, Jan Willem Cohen Tervaert, and Cees G. M. Kallenberg. "Induction of an Humoral and Cellular (Auto) Immune Response to Human and Rat Myeloperoxidase(MPO) in Brown-Norway(BN), Lewis and Wistar Kyoto(WKY) Rat Strains." In Advances in Experimental Medicine and Biology, 139–42. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9182-2_24.

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Jackson, C. W., S. A. Steward, and N. K. Hutson. "Characterization of Platelets and Megakaryocytes of the Wistar Furth Rat: An Animal Model with Inherently Large Mean Platelet Volume." In Platelet Heterogeneity, 145–54. London: Springer London, 1990. http://dx.doi.org/10.1007/978-1-4471-1763-6_7.

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Ichrak, Madkour, Madkour Aicha, Taghzouti Khalid, and El Abbadi Jamal. "The Impact of Different Modes of Radiofrequency–Electromagnetic Field Emitted by Cell Phones on Uterine Contractions of Wistar Rat Ex Vivo." In Advances in Science, Technology & Innovation, 159–67. Cham: Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-74470-9_19.

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Conference papers on the topic "Rat (wistar"

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Ghasemi, Masih, M. Nouri, A. Ansari, M. T. Kouhbanani, Arash Dehzangi, S. Nazeri, M. Abbasi, P. Nori, MohammadMahdi Ariannejad, and P. K. Choudhury. "On the healing process of Wistar rat burnt scars implementing micro-encapsulation of reactive oxygen." In Reporters, Contrast Agents, and Molecular Probes for Biomedical Applications XVI, edited by Ramesh Raghavachari and Mikhail Y. Berezin, 26. SPIE, 2025. https://doi.org/10.1117/12.3047119.

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Hu, Dingyu, Qin Li, Bo Li, Rongji Dai, Lina Geng, and Yulin Deng. "Normobaric Hypoxia-induced Brain Damage and Mechanism in Wistar Rat." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2009). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5163120.

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Deshmukh, Sanket, Avinash Lokhande, Ratul Wasnik, and Nitin Singhal. "Vacuole Segmentation and Quantification in Liver Images of Wistar Rat." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176500.

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Jackson, C. W., N. K. Hutson, S. A. Steward, and H. H. Edwards. "THE WISTAR-FURTH RAT: AN ANIMAL MODEL OF HEREDITARY MACRO THROMBOCYTOPENIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643925.

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The mechanisms which determine and regulate platelet size are unknown. By phase microscopy, we serendipitously observed that Wistar/Furth (W/F) rats had macrothrombocytopenia. In this study, we have characterized and compared platelets and megakaryocytes (MK) of W/F rats to those of Wistar (W), Long-Evans hooded (LE) and Sprague-Dawley (SD) rats. In addition, we have examined the mode of inheritance of this W/F rat platelet abnormality. Average platelet count of W/F rats was only 312 ± 57 x 103/mm3 compared to 1086 ± 68, 868 ± 91 and 926 ± 82 x 103/mm3 respectively for W, LE and SD rats. Mean platelet volume (MPV) of W/F rats (8.1 ± 1.4 fl) was twice that of W (4.0 ± 0.2 fl), LE (4.2 ± 0.3 f1) and SD (4.1 ± 0.2 f1) rats. However, average MK diameter and DNA content distribution of W/F rats were not significantly different than those of LE rats. Average MK concentration was somewhat lower (4.5 MK/high power field) in the W/F strain compared to that of LE rats (6.6 MK/HPF). Maze-like membrane formations were observed in W/F MK and platelets by electron microscopy. Reciprocal crosses of W/F and LE rats resulted in offspring with MPVs (4.2 fl) and platelet counts like those of LE rats, indicating that the macrothrombocytopenic trait is recessive in its inheritance. Reciprocal marrow transplants between the W/F and LE strains resulted in MPVs like those of the donor strain indicating that the macrothrombocytopenia is an intrinsic marrow abnormality of the W/F strain. Analysis of W/F platelets by two-dimensional polyacrylamide gel electrophoresis revealed two readily detectable differences from those of W and LE rats: (1) absence of a protein of MW of 41,000 and pi of 6.35 and (2) presence of a protein of MW of 35,000 and pi of 5.9. In summary, the W/F rat has a hereditary macrothrombocytopenia which is recessive in nature and not due to differences in MK size or DNA content. These results suggest that the macrothrombocytopenia of W/F rats results from formation of fewer platelets per MK, possibly due to a qualitative or quantitative defect in some component necessary for proper subdivision of megakaryocyte cytoplasm into platelets.
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Arwini, Ananda Eka, Syahrir A. Pasinringi, and Nurhaedar Jafar. "Okra Powder Effect to Low Density Lipoprotein and Triglycerides in Diabetic Wistar Rat." In the International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3242789.3242831.

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Paramita, Farah, and Hiya Alfi Rahmah. "Effect of Purple Passion Fruit Juice on Total Cholesterol of Atherogenic Wistar Rat." In 3rd International Scientific Meeting on Public Health and Sports (ISMOPHS 2021). Paris, France: Atlantis Press, 2022. http://dx.doi.org/10.2991/ahsr.k.220108.024.

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Gautam, Rohit, Neha Jha, Anuj Kumar Tomar, Jay Prakash Nirala, Taruna Arora, and Paulraj Rajamani. "Effect of 35.5 GHz millimeter waves on reproductive parameters of male Wistar rat." In 6th URSI Regional Conference on Radio Science. Gent, Belgium: URSI – International Union of Radio Science, 2024. https://doi.org/10.46620/ursi_rsrc24/0406txu6365.

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Hu, Dingyu, Qin Li, Bo Li, Rongji Dai, Lina Geng, and Yulin Deng. "Stress Response to Hypoxia in Wistar Rat: LA, MDA, SOD and Na+-K+-ATPase." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2009). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5163429.

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Rajamani, Paulraj. "3G and 4G mobile phone radiation effects on brain and sperm cells of Wistar rat." In 6th URSI Regional Conference on Radio Science. Gent, Belgium: URSI – International Union of Radio Science, 2024. https://doi.org/10.46620/ursi_rsrc24/0121hda2841.

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"SEARCH FOR DRUG PROTOTYPES FOR NMDA- AND AMPA-RECEPTOR ANTAGONISTS AMONG QUINOXALINE AND PYRAZINOBENZIMIDAZOLE DERIVATIVES." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-319.

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The project is dedicated to screening of ionotropic glutamate receptors inhibitors among pyrazinobenzimidazole and quinoxaline derivatives. The pyramidal neurons of the hippocampus of Wistar rat brain were used for the study. With the patch clamp technique, we found the most active compound — this is a representative of the quinoxaline class with the code name ZDM-15.
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Reports on the topic "Rat (wistar"

1

กลันทกานนท์ ทองทรง, สฤณี, บุญฤทธิ์ ทองทรง, and ศิริเพ็ญ โกมลวานิช. The usage of soy bean extracts (Genistein and Daidzein) to modulate anxiety disorder : using wistar rat as a model. คณะสัตวแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2009. https://doi.org/10.58837/chula.res.2009.76.

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ไฟโตเอสโตรเจน เช่น เจนิสเตอีนและไดด์ดีซีน เป็นสารที่สามารถพบได้ในพืชตระกูลถั่ว ทั้งนี้สารดังกล่าวมีลักษณะโครงสร้างคล้ายเอสโตรเจน ซึ่งจากการศึกษาที่ผ่านมาพบว่าภาวะวิตกกังวลเป็นปัญหาด้านสุขภาพจิตที่พบในเพศหญิงมากกว่าเพศชาย และจากรายงานทางคลินิกและการทดลองในสัตว์ พบว่าการขาดฮอร์โมนเอสโตรเจนเป็นปัจจัยที่สำคัญ อย่างไรก็ตาม การให้ฮอร์โมนเอสโตรเจนนั้นมีข้อจำกัดในทางคลินิก ในการศึกษาครั้งนี้มีวัตถุประสงค์เพื่อศึกษาผลของสารไฟโตเอสโตรเจน ได้แก่ เจนิสเตอีน และไดด์ดีซีน ในการลดความกังวลในหนูทดลองที่ถูกเหนี่ยวนำให้เกิดความกังวลด้วยการตัดรังไข่เปรียบเทียบกับเอสโตรเจน และเพื่อศึกษาผลของสารดังกล่าวในการเปลี่ยนแปลงระดับความกังวลในหนูเพศผู้ โดยการทดลองแบ่งออกเป็น 2 ตอน ตอนที่ 1 ทำการศึกษาในหนูเพศเมียโดยการเหนี่ยวนำให้ขาดฮอร์โมนเอสโตรเจนโดยการตัดรังไข่ หาระยะเวลาที่ทำให้หนูเกิดความกังวล และจากนั้นศึกษาว่า เอสโตรเจน เจนิสเตอีน หรือไดด์ดีซีนสามารถแก้ไขความผิดปกติที่เกิดขึ้นได้หรือไม่ ผลการศึกษาพบว่า การตัดรังไข่เป็นระยะเวลาอย่างน้อย 3 สัปดาห์สามารถเหนี่ยวนำให้หนูเกิดความกังวล เมื่อทำการวัดด้วยอุปกรณ์ทดสอบพฤติกรรม elevated T-maze ทั้งนี้หนูที่ตัดรังไขและได้รับเอสโตรเจนทดแทนที่ระยะเวลาต่าง ๆ (7, 14, 21 และ 28 วัน) ไม่พบว่ามีความกังวลแตกต่างกัน เมื่อทำการทดสอบผลของเจนิสเตอีน (0.25 มก./กก.) และไดด์ดีซีน (0.25 มก./กก.) เทียบกับเอสโตรเจน (1 ไมโครกรัม/กก.) ในการลดความกังวลในหนูที่ถูกเหนี่ยวนำให้เกิดความกังวล โดยการให้สารต่าง ๆ เป็นเวลา 28 วัน ภายหลังจากการตัดรังไข่ 21 วัน พบว่าเจนิสเตอีนสามารถระดับความกังวลได้ไม่ต่างจากเอสโตรเจน ในขณะที่ไดด์ดีซีนสามารถลดความกังวลได้ไมต่างจากเจนิสเตอีนและเอสโตรเจน แต่พบว่าค่าความแตกต่างไม่มากพอที่จะทำให้เกิดความแตกต่างทางสถิติจากกลุ่มควบคุม โดยเจนิสเตอีนหรือไดด์ดีซีนไม่มีผลต่อน้ำหนักตัว หรือน้ำหนักมดลูกเมื่อเทียบกับกลุ่มควบคุม ตอนที่ 2 ทำการศึกษาถึงผลของเจนิสเตอีนหรือไดด์ดีซีนที่มีต่อระดับความกังวลในหนูเพศผู้พบว่าการให้เจนิสเตอีน ขนาด 1 มก./กก. เป็นเวลา 5 สัปดาห์ มีแนวโน้มที่จะทำให้หนูมีความกังวลเพิ่มมากขึ้น และทำให้น้ำหนักของหนูเพิ่มขึ้นน้อยกว่าการได้รับเจนิสเตอีนขนาด 0, 0.25 และ 0.50 มก./กก. โดยเจนิสเตอีนขนาดต่าง ๆ ไม่มีผลต่อการเปลี่ยนแปลงน้ำหนักอวัยวะสืบพันธุ์ ได้แก่ อัณฑะ อิพิดิไดมิส พรอสเตทแกลนด์ และเซมินอล เวสซิเคิล สำหรับผลของไดด์ดีซีนนั้นพบว่า การให้ไดด์ดีซีน ขนาด 0.25 มก./กก. เป็นเวลา 5 สัปดาห์ สามารถลดความกังวลในหนูกลุ่มนี้ได้ และถ้าให้ในขนาดที่สูงขึ้น (0.50-1.00 มก./กก.) จะเป็นการเพิ่มระดับความกังวล ทั้งนี้ไดด์ดีซีนไม่มีผลต่อการเปลี่ยนแปลงน้ำหนักตัว หรือน้ำหนักอวัยวะสืบพันธุ์ แต่มีแนวโน้มว่าการใช้ไดด์ดีซีนในระดับสูง (1.00 มก./กก.) อาจมีผลต่อการทำงานของพรอสเตทแกลนด์ เนื่องจากมีแนวโน้มที่จะมีน้ำหนักลดลง จากการทดลองสามารถสรุปได้ว่าการตัดรังไข่ทิ้งไว้เป็นเวลา 3 สัปดาห์ทำให้หนูเกิดความกังวลขึ้นได้ โดยเจนิสเตอีนสามารถแก้ไขความกังวลที่เกิดขึ้นดังกล่าวได้เมื่อให้ติดต่อกันเป็นเวลา อย่างน้อย 4 สัปดาห์ โดยไม่มีผลต่ออวัยวะสืบพันธุ์ ในขณะที่การให้ไดด์ดีซีนนั้นอาจจะต้องให้เป็นระยะเวลาที่นานขึ้น หรือให้ในระดับที่สูงขึ้น สำหรับในเพศผู้นั้นเป็นที่น่าสังเกตว่าสารดังกล่าวมีผลต่อความกังวลที่แตกต่างกันโดยเจนิสเตอีนในระดับสูงทำให้มีความกังวลเพิ่มมากขึ้น ในขณะที่ไดด์ดิซินในระดับต่ำสามารถลดความกังวลได้ จึงเป็นที่น่าสนใจเจนิสเตอิน หรือไดด์ดิซีนอาจมีการทำงานที่แตกต่างกัน เนื่องจากความสามารถในการจับกับตัวรับเอสโตรเจนแตกต่างกัน และการให้ในหนูเพศผู้ปกตินั้นเจนิสเตอีนอาจไปมีผลรบกวนการทำงานของฮอร์โมนเอสโตรเจน และ/หรือเทสโทสเตอโรน และทำให้เกิดความกังวลขึ้นได้
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2

Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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3

Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.sup.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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4

Patumraj, Suthiluk, and Sheepsumon Viboolvorakul. Protective effects of exercise training against vascular and neuronal dysfunction in aging brain. Department of Physiology, Faculty of Medicine, Chulalongkorn University, 2019. https://doi.org/10.58837/chula.res.2019.11.

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During advancing age, reduction of microvessels in the brain contributes insufficiency tissue perfusion. Mounting evidence indicates that microvascular deterioration in aged brain relates to oxidative stress. Nuclear factor erythroid-related factor 2 (Nrf2) plays an important role in cellular antioxidant defense. Regular physical exercise is well known to have beneficial effect to brain health, including promoted blood flow and augmented angiogenesis, in aging individuals. However, the underlying mechanism of regular physical exercise in improvement of brain microvascular density during advancing age has not been fully elucidated. This study aimed to investigate the underlying mechanism of exercise training in improvement of microvascular density associated with PI3K/Akt/Nrf2 pathway in aged rat brain. Male Wistar rats were divided into three groups; sedentary-young (SY), sedentary-age (SA) and trained-age (TA). Exercise program included swimming exercise for eight weeks. Expression of CD31 (as indicator of microvascular density) and Nrf2 were evaluated by immunohistochemistry staining. Activity of Nrf2, protein levels of phosphatidylinositol-4,5-biphosphate 3-kinase (PI3K) and phosphorylated-protein kinase B (p-Akt) in isolated brain microvessels were assessed by immunoassay. Aging (SA) induced significant reduction of brain microvascular density and expression of Nrf2, PI3K and p-Akt proteins, as well as Nrf2 activity, comparing to those of SY group. The eight-week exercise training significantly improved brain microvascular density and upregulated Nrf2, PI3K and p-Akt proteins as well as activated Nrf2 activity, than that of the age group without exercise (SA). In conclusion, exercise training can improve brain microvascular deterioration associated with PI3K/Akt/Nrf2 pathway in aging rats.
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5

Lawanprasert, Somsong, Chaiyo Chaichantipyuth, Supatra Srichairat, Nuansri Niwattisaiwong, and Laddawal Phivthong-ngam. Subchronic exposure of Pueraria mirifica in normal - and high cholesterol diet fed rats : influence on hepatic cytochrome P450, lipid profile and toxicity. Chulalongkorn University, 2004. https://doi.org/10.58837/chula.res.2004.28.

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Pueraria mirifica airy shaw and suvatabandhu, know locally as Kwao Keur, is a plant in family Leguminosae. In this study, effects of P.mirifica on hepatic cytochrome P450 (CYP), serum lipid profile and subchronic toxicity were investigated in male Wistar rats. Rats were randomly divided into four treatment groups as following: normal diet-fed group; normal diet-fed supplemented with P.mirifica group; high cholesterol diet-fed group; high cholesterol diet-fed supplemented with P.mirifica group. Each group comprised 10 rats. P.mirifica was administered orally at a dosage of 100 mg/kg/day for 90 consecutive days. At the end of the treatment, animals were anesthesized. Blood samples were collected by heart puncture and serum sample were prepared for determination of hematology and clinical blood chemistry, respectively. Microsomes were prepared from livers for enzyme assays. The results showed that body weight of rats given P.mirifica in either normal diet or high cholesterol diet conditions were significantly lower than their corresponding control groups. There was no significant difference of these following hematology and clinical blood chemistry: hemoglobin, hemotocrit, WBC count, %differential WBC, platelet count, RBC morphology, glucose, BUN, SCr, total bilirubin, and direct bilirubin in all experimental groups. P.mirifica did not affect serum level of AST, ALT, and ALP in normal diet-fed condition. High cholesterol diet-fed condition caused a significant increase of AST, ALT, and ALP but P.mirifica attenuated these effects. P.mirifica significantly decreased serum total cholesterol and LDL-C in either normal diet-fed or high cholesterol diet-fed rats. Serum triglyceride was increased in normal diet-fed rats but decreased in high cholesterol diet-fed rats. P.mirifica caused a significant decrease of HDL-C in both normal and high cholesterol diet-fed rats whereas its improvement in the LDL-C/HDL-C ratio was shown only in high cholesterol diet-fed rats. Concerning the effects on CYPs, P.mirifica significantly inhibited CYP2B1&B2 in either normal diet or high cholesterol diet-fed rats. Its inhibitory effect of CYP1A2 and CYP2E1 was found only in normal diet-fed rats. No effect of P.mirifica was found on CYP1A1 and CYP3A. Inhibitory effects of P.mirifica on CYP2B1&2B2 and CYP2E1 were also found in the in vitro study. Although, P.mirifica demonstrated a benefit on lipid profile and did not show any toxic effects on liver, kidney, and blood system in this study, an increment of serum triglyceride in normal rat receiving P.mirifica, howerer, is not favorable. Inhibitory effects of P.mirifica on CYP1A2, CYP2B1&2B2 and CYP2E1 indicated a beneficial potential of this plant regarding the chemical-induced carcinogenesis as well as a possible potential of this plant regarding drug-drug interaction with other medicines that are metabolized by these CYPs. Effects of P.mirifica at various doses, long term used as well as mechanism of effects should be further investigated. Effects of P.mirifica on other isoforms of CYP in human should also be explored.
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6

Iheagwam, Franklyn, Shalom Chinedu, Opeyemi Emiloju, Chisom Anichebem, and Ositadinma Okolie. Thaumatococcus daniellii Seed Improves Lipid Profile in Male Wistar Rats. Peeref, July 2022. http://dx.doi.org/10.54985/peeref.2207p8763009.

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7

Ivanova, Natasha, Jana Tchekalarova, Dimitrinka Atanasova, Daniela Pechlivanova, and Nikolai Lazarov. Strain-dependent Effects of AT1 Receptor Antagonist Losartan on Spatial Memory Performance of Wistar and Spontaneously Hypertensive Rats in Kainate Model of Temporal Epilepsy. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2018. http://dx.doi.org/10.7546/crabs.2018.06.15.

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8

NTP Technical Report on the Toxicology and Carcinogenesis Studies of TRIM® VX in Wistar Han [Crl:WI (Han)] Rats and B6C3F1/N Mice (Inhalation Studies). NIEHS, November 2016. http://dx.doi.org/10.22427/ntp-tr-591.

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9

NTP Technical Report on the Toxicology and Carcinogenesis Studies of Antimony Trioxide (CASRN 1309-64-4) in Wistar Han [Crl:WI(Han)] Rats and B6C3F1/N Mice (Inhalation Studies). NIEHS, December 2017. http://dx.doi.org/10.22427/ntp-tr-590.

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10

NTP Technical Report on the Toxicology and Carcinogenesis Studies of 2,3-Butanedione (CAS NO. 431-03-8) in Wistar Han [Crl:WI (Han)] Rats and B6C3F1/N Mice (Inhalation Studies). NIEHS, August 2018. http://dx.doi.org/10.22427/ntp-tr-593.

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