Journal articles: 'Rats; Human'

1

Olsen, Jørn. "Although Some Humans are Rats, not all Rats are Human." European Journal of Epidemiology 20, no. 10 (October 2005): 815. http://dx.doi.org/10.1007/s10654-005-3377-5.

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2

Holland, Norman N. "Tickled Rats and Human Laughter." Neuropsychoanalysis 9, no. 1 (January 2007): 41–57. http://dx.doi.org/10.1080/15294145.2007.10773541.

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3

Garau i Florit, Adriana. "Human Extraversion and Ambulation in Rats." Quaderns de Psicologia, no. 15 (October 17, 2009): 23. http://dx.doi.org/10.5565/rev/qpsicologia.538.

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4

Flynn, PD, RM Lawn, JJ Mullins, and PL Weissberg. "Transgenic Rats Expressing Human Apolipoprotein(a)." Clinical Science 94, s38 (February 1, 1998): 7P. http://dx.doi.org/10.1042/cs094007pa.

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5

Wildner, Gerhild. "Are rats more human than mice?" Immunobiology 224, no. 1 (January 2019): 172–76. http://dx.doi.org/10.1016/j.imbio.2018.09.002.

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6

Bohlender, Jürgen, Joël Ménard, Jürgen Wagner, Friedrich C. Luft, and Detlev Ganten. "Human Renin-Dependent Hypertension in Rats Transgenic for Human Angiotensinogen." Hypertension 27, no. 3 (March 1996): 535–40. http://dx.doi.org/10.1161/01.hyp.27.3.535.

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7

Müller, Dominik N., Karl F. Hilgers, Salima Mathews, Volker Breu, Walter Fischli, Regina Uhlmann, and Friedrich C. Luft. "Effects of Human Prorenin in Rats Transgenic for Human Angiotensinogen." Hypertension 33, no. 1 (January 1999): 312–17. http://dx.doi.org/10.1161/01.hyp.33.1.312.

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8

Yang, Xiao-Xia, Zen-Ping Hu, Eli Chan, Wei Duan, and Shufeng Zhou. "Pharmacokinetics of Recombinant Human Endostatin in Rats." Current Drug Metabolism 7, no. 6 (August 1, 2006): 565–76. http://dx.doi.org/10.2174/138920006778017803.

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9

Coghlan, Andy. "Human brain stem cells transplanted into rats." New Scientist 208, no. 2790 (December 2010): 14. http://dx.doi.org/10.1016/s0262-4079(10)63030-8.

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10

Bohlender, Jürgen, Akiyoshi Fukamizu, Andrea Lippoldt, Tatsuji Nomura, Rainer Dietz, Joel Ménard, Kazuo Murakami, Friedrich C. Luft, and Detlev Ganten. "High Human Renin Hypertension in Transgenic Rats." Hypertension 29, no. 1 (January 1997): 428–34. http://dx.doi.org/10.1161/01.hyp.29.1.428.

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11

THYSMAN, SOPHIE, CECILE HANCHARD, and VERONIQUE PRÉAT. "Human Calcitonin Delivery in Rats by Iontophoresis." Journal of Pharmacy and Pharmacology 46, no. 9 (September 1994): 725–30. http://dx.doi.org/10.1111/j.2042-7158.1994.tb03891.x.

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12

Knight, Kathryn. "Young rats’ calls assembled like human speech." Journal of Experimental Biology 220, no. 5 (March 1, 2017): 733.2–734. http://dx.doi.org/10.1242/jeb.157982.

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13

Burcklé, Céline A., A. H. Jan Danser, Dominik N. Müller, Ingrid M. Garrelds, Jean-Marie Gasc, Elena Popova, Ralph Plehm, Jörg Peters, Michael Bader, and Geneviève Nguyen. "Elevated Blood Pressure and Heart Rate in Human Renin Receptor Transgenic Rats." Hypertension 47, no. 3 (March 2006): 552–56. http://dx.doi.org/10.1161/01.hyp.0000199912.47657.04.

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14

Bohlender, Jürgen, Joel Ménard, Friedrich C. Luft, and Detlev Ganten. "Dose Effects of Human Renin in Rats Transgenic for Human Angiotensinogen." Hypertension 29, no. 4 (April 1997): 1031–38. http://dx.doi.org/10.1161/01.hyp.29.4.1031.

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15

BOHLENDER, JÜRGEN, DETLEV GANTEN, and FRIEDRICH C. LUFT. "Rats Transgenic for Human Renin and Human Angiotensinogen as a Model for Gestational Hypertension." Journal of the American Society of Nephrology 11, no. 11 (November 2000): 2056–61. http://dx.doi.org/10.1681/asn.v11112056.

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Abstract. Animal models of gestational hypertension are problematic. A novel mouse model was described earlier. The dams in that study were transgenic for human angiotensinogen and the sires for human renin; human renin was expressed in and produced by the placenta. This model was adapted to the rat, which has greater utility in terms of chronic instrumentation and physiologic measurements. Female rats transgenic for human angiotensinogen were mated with rats transgenic for human renin. Telemetry BP increased on day 5 of pregnancy from 110/80 mmHg to as high as 180/140 mmHg, while heart rate increased slightly. The renin transgene was expressed in the placenta, which resulted in increased human plasma renin concentration from 0 to 937 ± 800 ng angiotensin I ml/h; the values returned to 0 after delivery. Female rats transgenic for human renin that were mated with male rats transgenic for human angiotensinogen in contrast exhibited a decrease in BP. In these rats, human angiotensinogen in plasma remained undetectable. Double transgenic offspring of these transgenic rats developed hypertension and end-organ damage, regardless of the source of the transgenes. The conclusion is that transgenic rats that bear human renin and angiotensinogen genes make an attractive model for gestational hypertension. The rat model will have greater utility than the mouse model.

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16

Li, Ke, Sheng Ma, Liyan Miao, Songhua Fan, Bin Pan, Weihan Zhang, Weiguo Su, et al. "Absorption, Metabolism and Excretion of Surufatinib in Rats and Humans." Current Drug Metabolism 21, no. 5 (July 29, 2020): 357–67. http://dx.doi.org/10.2174/1389200221666200514131721.

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Background: Surufatinib is a potent small-molecule tyrosine kinase inhibitor and exhibited significant efficacy in the treatment of neuroendocrine tumors in clinical trials. Objective: The absorption, metabolism and excretion of surufatinib were investigated in rats and human volunteers following a single oral dose of [14C] surufatinib. Methods: The radioactivity was measured in plasma, urine, feces and bile by liquid scintillation counting, and the metabolites were characterized by liquid chromatography coupled to mass spectrometry. Results: Surufatinib was orally absorbed similarly in rats and human volunteers, with the median Tmax of 4 hours post-dose. The estimated t1/2 appeared longer in humans than in rats (mean t1/2: 3.12 hour for male rats, 6.48 hours for female rats and 23.3 hours for male human volunteers). The excretion of surufatinib was almost complete in rats and human volunteers in the studies, with the total radioactivity recovery of >90% of the dose. Similarly, in rats and humans, fecal excretion predominated (approximately 87% of the dose recovered in feces and only 5% in urine). The parent drug was the major radioactive component detected in the plasma extracts of rats and humans, and no single circulating metabolite accounted for >10% of the total radioactivity. Unchanged drug was a minor radioactive component in the excreta of rats and humans. Conclusion: Fecal excretion was the predominant way for the elimination of surufatinib and its metabolites in rats and humans. No disproportionate circulating metabolite was observed in humans.

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17

Al-Samawy, Eyhab R., Shaima K. Waad, Wissam S. Hashim, and Ghusoon Alabbas. "Comparative Histology of Human, Rats and Rabbits Liver." Indian Journal of Public Health Research & Development 10, no. 5 (2019): 1441. http://dx.doi.org/10.5958/0976-5506.2019.01134.3.

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18

Pinho-Ribeiro, V., A. C. V. Maia, J. P. S. Werneck-de-Castro, P. F. Oliveira, R. C. S. Goldenberg, and A. C. Campos de Carvalho. "Human umbilical cord blood cells in infarcted rats." Brazilian Journal of Medical and Biological Research 43, no. 3 (March 2010): 290–96. http://dx.doi.org/10.1590/s0100-879x2010007500007.

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19

Tamargo, Rafael J., Jonathan I. Epstein, and Henry Brem. "Heterotransplantation of malignant human gliomas in neonatal rats." Journal of Neurosurgery 69, no. 6 (December 1988): 928–33. http://dx.doi.org/10.3171/jns.1988.69.6.0928.

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✓ Three human glioma cell lines (TE-671 medulloblastoma, U-87 MG glioblastoma, and U-373 MG glioblastoma) were transplanted to the quadrigeminal cistern of the brain in 37 newborn Sprague-Dawley rats and to the subcutaneous space in 30 of their siblings. Two of the three gliomas (the TE-671 medulloblastoma and the U-87 MG glioblastoma) grew both intracranially and subcutaneously. The U-373 MG glioblastoma did not grow in either site. The resulting tumors expressed unique morphological features characteristic of their tissue of origin. The newborn rat represents a model for the heterologous transplantation of human gliomas, providing a biological window for the study of these lesions.

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20

Ables, Erin M., Leslie M. Kay, and Jill M. Mateo. "Rats assess degree of relatedness from human odors." Physiology & Behavior 90, no. 5 (April 2007): 726–32. http://dx.doi.org/10.1016/j.physbeh.2006.12.012.

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21

Sim, M. K., and X. S. Qui. "Angiotensins in plasma of hypertensive rats and human." Regulatory Peptides 111, no. 1-3 (March 2003): 179–82. http://dx.doi.org/10.1016/s0167-0115(02)00289-6.

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22

Delemarre, Friso M. C., and Eric A. P. Steegers. "Dietary sodium restriction in rats and human beings." American Journal of Obstetrics and Gynecology 182, no. 6 (June 2000): 1647. http://dx.doi.org/10.1067/mob.2000.104142.

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23

Lund, Amie K., JoAnn Lucero, Lindsay Herbert, Yushi Liu, and Jay S. Naik. "Human immunodeficiency virus transgenic rats exhibit pulmonary hypertension." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 3 (September 2011): L315—L326. http://dx.doi.org/10.1152/ajplung.00045.2011.

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Human immunodeficiency virus (HIV)-associated pulmonary arterial hypertension (PAH) is a serious noninfectious disease involving an aberrant increase in pressure in the blood vessels of the lung, which leads to right ventricular (RV) heart failure and can eventually result in death. A lack of viable animal models of HIV-PAH has limited the identification of signaling pathways involved in HIV-mediated onset and progression of PAH. To determine whether the HIV-1 transgenic (HIV Tg) rat displays pathophysiological end points associated with PAH, we evaluated peak RV systolic pressure (RVSP), RV hypertrophy, pulmonary vessel remodeling, and alterations in gene expression by real-time PCR and microarray. RVSP was measured by RV catheterization via the right jugular vein in 3- and 9-mo-old HIV Tg and age-matched Fischer 344 (control) male rats while under 2% isoflurane anesthesia. RVSP was elevated in the HIV Tg rats (34.2 ± 2.5 mmHg) compared with the F344 controls (21.2 ± 2.5 mmHg), with more significant elevations in the 9-mo-old HIV Tg rats (42.5 ± 3.7 mmHg). We observed significant increases in RV wall thickness in HIV Tg rats compared with controls, both histologically and by echocardiograph measurement. HIV Tg rats also show increased thickening of the pulmonary artery and remodeling of small pulmonary arteries, as well as altered expression of gene pathways associated with PAH. These data represent the first analysis of PAH in HIV Tg rats and suggest that this model will be useful for investigating pathways and identifying potential therapies for HIV-PAH.

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24

Alink, Gerrit M., Jolanda M. Rijnkels, Harry A. Kuiper, Victor M. H. Hollanders, and Ruud A. Woutersen. "Carcinogenicity testing of complete human diets in rats." Cancer Letters 114, no. 1-2 (March 1997): 271–74. http://dx.doi.org/10.1016/s0304-3835(97)04679-x.

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25

LIU, Ke-Xin, Yukio KATO, Tai-ichi KAKU, and Yuichi SUGIYAMA. "Human Placental Extract Stimulates Liver Regeneration in Rats." Biological & Pharmaceutical Bulletin 21, no. 1 (1998): 44–49. http://dx.doi.org/10.1248/bpb.21.44.

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26

O., Wai-Sum, Subin Liao, June Z. Sun, James C. M. Ho, Philip C. N. Chiu, Ernest H. Y. Ng, William S. B. Yeung, Raymond H. W. Li, and Fai Tang. "Adrenomedullin and Oviduct Function in Human and Rats." Biology of Reproduction 81, Suppl_1 (July 1, 2009): 99. http://dx.doi.org/10.1093/biolreprod/81.s1.99.

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27

Gratze, Petra, Michael Boschmann, Ralf Dechend, Fatimunnisa Qadri, Jeanette Malchow, Sabine Graeske, Stefan Engeli, et al. "Energy Metabolism in Human Renin-Gene Transgenic Rats." Hypertension 53, no. 3 (March 2009): 516–23. http://dx.doi.org/10.1161/hypertensionaha.108.124966.

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28

Cao, Xiaohan, Zhiyong Chen, Zhuoran Yu, Yonghong Ge, and Xianyin Zeng. "Pharmacokinetics of PEGylated Recombinant Human Erythropoietin in Rats." Journal of Analytical Methods in Chemistry 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/918686.

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rHuEPO plays a central role as chemicals for the treatment of many diseases. Due to its short half-life, the main aim for this pharmacokinetic study is to investigate a newly developed PEG-rHuEPO with large molecular weight in SD rats. After a single intramuscular administration of different doses of 125I-PEG-rHuEPO, pharmacokinetic parameters, tissue distribution, and excretion were analyzed. Inin vivohalf-life time measured after 125I-PEG-rHuEPO administration at the doses of 1, 2, and 3 μg/kg,t1/2αwas 1.90, 1.19, and 2.50 hours, respectively, whereast1/2βwas 22.37, 26.21, and 20.92 hours, respectively; at 8, 24, and 48 hours after intramuscular administration, PEG-rHuEPO was distributed to all of the examined tissues, however, with high concentrations of radioactivity, only in plasma, blood, muscle at the administration site, and bone marrow. Following a 2 μg/kg single intramuscular administration, approximately 21% of the radiolabeled dose was recovered after almost seven days of study. Urine was the major route of excretion; 20% of the administered dose was recovered in the urine, while excretion in the feces was less than 1.4%. Therefore, this PEG-rHuEPO has potential to be clinically used and could reduce frequency of injection.

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29

Davies, Sian E. C., Ronald A. Chalmers, Edward W. Randall, and Richard A. Iles. "Betaine metabolism in human neonates and developing rats." Clinica Chimica Acta 178, no. 3 (December 1988): 241–49. http://dx.doi.org/10.1016/0009-8981(88)90232-x.

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30

Asakawa, K., N. Hizuka, K. Takano, R. Horikawa, I. Sukegawa, C. Toyoda, and K. Shizume. "Human growth hormone stimulates liver regeneration in rats." Journal of Endocrinological Investigation 12, no. 5 (May 1989): 343–47. http://dx.doi.org/10.1007/bf03350004.

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31

Dinets, Vladimir, and Keishu Asada. "Noble savages: human-independent Rattus rats in Japan." Journal of Natural History 54, no. 37-38 (October 1, 2020): 2391–414. http://dx.doi.org/10.1080/00222933.2020.1845409.

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32

Herring, Matt J., Lei F. Putney, Gregory Wyatt, Walter E. Finkbeiner, and Dallas M. Hyde. "Growth of alveoli during postnatal development in humans based on stereological estimation." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 4 (August 15, 2014): L338—L344. http://dx.doi.org/10.1152/ajplung.00094.2014.

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Alveolarization in humans and nonhuman primates begins during prenatal development. Advances in stereological counting techniques allow accurate assessment of alveolar number; however, these techniques have not been applied to the developing human lung. Based on the recent American Thoracic Society guidelines for stereology, lungs from human autopsies, ages 2 mo to 15 yr, were fractionated and isometric uniform randomly sampled to count the number of alveoli. The number of alveoli was compared with age, weight, and height as well as growth between right and left lungs. The number of alveoli in the human lung increased exponentially during the first 2 yr of life but continued to increase albeit at a reduced rate through adolescence. Alveolar numbers also correlated with the indirect radial alveolar count technique. Growth curves for human alveolarization were compared using historical data of nonhuman primates and rats. The alveolar growth rate in nonhuman primates was nearly identical to the human growth curve. Rats were significantly different, showing a more pronounced exponential growth during the first 20 days of life. This evidence indicates that the human lung may be more plastic than originally thought, with alveolarization occurring well into adolescence. The first 20 days of life in rats implies a growth curve that may relate more to prenatal growth in humans. The data suggest that nonhuman primates are a better laboratory model for studies of human postnatal lung growth than rats.

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33

Hagobian, Todd. "CLARITY-BPA Program in Rats: Is It Translatable to Humans?" Journal of the Endocrine Society 3, no. 7 (May 20, 2019): 1390–92. http://dx.doi.org/10.1210/js.2019-00126.

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Abstract The Consortium Linking Academic and Regulatory Insights on BPA Toxicity (CLARITY-BPA) program was the most comprehensive study to date examining a full range of health effects of varying bisphenol A (BPA) exposure in rats. The major concern of the CLARITY-BPA program that has not previously been discussed is whether exposing rats to varying doses to BPA is translatable to humans, even at the “typical” exposure ranges for humans. This perspective will provide evidence that the vast majority of pharmaceutical drug development and other trials in animals have not been replicated in human randomized studies. Similarly, to truly understand whether BPA exposure affects human health, clinical trials are needed to examine BPA administration in humans in controlled settings.

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34

Clement, Jan, James LeDuc, Graham Lloyd, Jean-Marc Reynes, Lorraine McElhinney, Marc Van Ranst, and Ho-Wang Lee. "Wild Rats, Laboratory Rats, Pet Rats: Global Seoul Hantavirus Disease Revisited." Viruses 11, no. 7 (July 17, 2019): 652. http://dx.doi.org/10.3390/v11070652.

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Recent reports from Europe and the USA described Seoul orthohantavirus infection in pet rats and their breeders/owners, suggesting the potential emergence of a “new” public health problem. Wild and laboratory rat-induced Seoul infections have, however, been described since the early eighties, due to the omnipresence of the rodent reservoir, the brown rat Rattus norvegicus. Recent studies showed no fundamental differences between the pathogenicity and phylogeny of pet rat-induced Seoul orthohantaviruses and their formerly described wild or laboratory rat counterparts. The paucity of diagnosed Seoul virus-induced disease in the West is in striking contrast to the thousands of cases recorded since the 1980s in the Far East, particularly in China. This review of four continents (Asia, Europe, America, and Africa) puts this “emerging infection” into a historical perspective, concluding there is an urgent need for greater medical awareness of Seoul virus-induced human pathology in many parts of the world. Given the mostly milder and atypical clinical presentation, sometimes even with preserved normal kidney function, the importance of simple but repeated urine examination is stressed, since initial but transient proteinuria and microhematuria are rarely lacking.

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35

Taylor, Alex S. "What Lines, Rats, and Sheep Can Tell Us." Design Issues 33, no. 3 (July 2017): 25–36. http://dx.doi.org/10.1162/desi_a_00449.

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In his 2015 Research Through Design provocation, Tim Ingold invites his audience to think with string, lines, and meshworks. In this article I use Ingold's concepts to explore an orientation to design—one that threads through both Ingold's ideas and Vinciane Despret's vivid and moving accounts of human-animal relations. This is a “thinking and doing” through design that seeks to be expansive to the capacities of humans and non-humans in relation to one another.

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36

Müller, Dominik N., Karl F. Hilgers, Jürgen Bohlender, Andrea Lippoldt, Jürgen Wagner, Walter Fischli, Detlev Ganten, Johannes F. E. Mann, and Friedrich C. Luft. "Effects of Human Renin in the Vasculature of Rats Transgenic for Human Angiotensinogen." Hypertension 26, no. 2 (August 1995): 272–78. http://dx.doi.org/10.1161/01.hyp.26.2.272.

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37

Owen, David R., Jinjiang Fan, Enrico Campioli, Sathvika Venugopal, Andrew Midzak, Edward Daly, Aline Harlay, et al. "TSPO mutations in rats and a human polymorphism impair the rate of steroid synthesis." Biochemical Journal 474, no. 23 (November 21, 2017): 3985–99. http://dx.doi.org/10.1042/bcj20170648.

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The 18 kDa translocator protein (TSPO) is a ubiquitous conserved outer mitochondrial membrane protein implicated in numerous cell and tissue functions, including steroid hormone biosynthesis, respiration, cell proliferation, and apoptosis. TSPO binds with high affinity to cholesterol and numerous compounds, is expressed at high levels in steroid-synthesizing tissues, and mediates cholesterol import into mitochondria, which is the rate-limiting step in steroid formation. In humans, the rs6971 polymorphism on the TSPO gene leads to an amino acid substitution in the fifth transmembrane loop of the protein, which is where the cholesterol-binding domain of TSPO is located, and this polymorphism has been associated with anxiety-related disorders. However, recent knockout mouse models have provided inconsistent conclusions of whether TSPO is directly involved in steroid synthesis. In this report, we show that TSPO deletion mutations in rat and its corresponding rs6971 polymorphism in humans alter adrenocorticotropic hormone-induced plasma corticosteroid concentrations. Rat tissues examined show increased cholesteryl ester accumulation, and neurosteroid formation was undetectable in homozygous rats. These results also support a role for TSPO ligands in diseases with steroid-dependent stress and anxiety elements.

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38

Raafat, Dina, Daniel M. Mrochen, Fawaz Al’Sholui, Elisa Heuser, René Ryll, Kathleen R. Pritchett-Corning, Jens Jacob, et al. "Molecular Epidemiology of Methicillin-Susceptible and Methicillin-Resistant Staphylococcus aureus in Wild, Captive and Laboratory Rats: Effect of Habitat on the Nasal S. aureus Population." Toxins 12, no. 2 (January 24, 2020): 80. http://dx.doi.org/10.3390/toxins12020080.

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Rats are a reservoir of human- and livestock-associated methicillin-resistant Staphylococcus aureus (MRSA). However, the composition of the natural S. aureus population in wild and laboratory rats is largely unknown. Here, 144 nasal S. aureus isolates from free-living wild rats, captive wild rats and laboratory rats were genotyped and profiled for antibiotic resistances and human-specific virulence genes. The nasal S. aureus carriage rate was higher among wild rats (23.4%) than laboratory rats (12.3%). Free-living wild rats were primarily colonized with isolates of clonal complex (CC) 49 and CC130 and maintained these strains even in husbandry. Moreover, upon livestock contact, CC398 isolates were acquired. In contrast, laboratory rats were colonized with many different S. aureus lineages—many of which are commonly found in humans. Five captive wild rats were colonized with CC398-MRSA. Moreover, a single CC30-MRSA and two CC130-MRSA were detected in free-living or captive wild rats. Rat-derived S. aureus isolates rarely harbored the phage-carried immune evasion gene cluster or superantigen genes, suggesting long-term adaptation to their host. Taken together, our study revealed a natural S. aureus population in wild rats, as well as a colonization pressure on wild and laboratory rats by exposure to livestock- and human-associated S. aureus, respectively.

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39

Samuelson, Emma, Carola Hedberg, Staffan Nilsson, and Afrouz Behboudi. "Molecular classification of spontaneous endometrial adenocarcinomas in BDII rats." Endocrine-Related Cancer 16, no. 1 (March 2009): 99–111. http://dx.doi.org/10.1677/erc-08-0185.

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Female rats of the BDII/Han inbred strain are prone to spontaneously develop endometrial carcinomas (EC) that in cell biology and pathogenesis are very similar to those of human. Human EC are classified into two major groups: Type I displays endometroid histology, is hormone-dependent, and characterized by frequent microsatellite instability and PTEN, K-RAS, and CTNNB1 (β-Catenin) mutations; Type II shows non-endometrioid histology, is hormone-unrelated, displays recurrent TP53 mutation, CDKN2A (P16) inactivation, over-expression of ERBB2 (Her2/neu), and reduced CDH1 (Cadherin 1 or E-Cadherin) expression. However, many human EC have overlapping clinical, morphologic, immunohistochemical, and molecular features of types I and II. The EC developed in BDII rats can be related to type I tumors, since they are hormone-related and histologically from endometrioid type. Here, we combined gene sequencing (Pten, Ifr1, and Ctnnb1) and real-time gene expression analysis (Pten, Cdh1, P16, Erbb2, Ctnnb1, Tp53, and Irf1) to further characterize molecular alterations in this tumor model with respect to different subtypes of EC in humans. No mutation in Pten and Ctnnb1 was detected, whereas three tumors displayed sequence aberrations of the Irf1 gene. Significant down regulation of Pten, Cdh1, p16, Erbb2, and Ctnnb1 gene products was found in the tumors. In conclusion, our data suggest that molecular features of spontaneous EC in BDII rats can be related to higher-grade human type I tumors and thus, this model represents an excellent experimental tool for research on this malignancy in human.

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40

Ruiz-Grande, Carmen, José Pintado, Cristina Alarcón, Carlos Castilla, Isabel Valverde, and José M. López-Novoa. "Renal catabolism of human glucagon-like peptides 1 and 2." Canadian Journal of Physiology and Pharmacology 68, no. 12 (December 1, 1990): 1568–73. http://dx.doi.org/10.1139/y90-239.

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The renal catabolism of [125I]glucagon-like peptide 1 (GLP-1) and [125I]glucagon-like peptide 2 (GLP-2) has been studied both in vivo, by the disappearance of these peptides from the plasma of bilaterally nephrectomized (BNX), ureteral-ligated (BUL) or normal rats, and in vitro, analyzing their catabolism by the isolated, perfused rat kidney. Results from in vivo studies demonstrated that half-disappearance time for both peptides was lower in controls than in BUL rats, and this value in BUL rats was not significantly different from that in BNX rats. In addition, metabolic clearance rate of GLP-1 was higher in control rats than in the other two groups of animals. Urinary clearance rate of both peptides was negligible. In isolated kidney experiments, values for organ clearance of both [125I]GLP-1 and [125I]GLP-2 were similar to those of inulin clearance, which represents the glomerular filtration rate. Urinary clearance of trichloroacetic acid precipitable radioactivity represented less than 1% of total clearance. In conclusion, these results demonstrate a significant role for the kidney in the plasma removal of [125I]GLP-1 and [125I]GLP-2 by a mechanism that involves glomerular filtration and tubular catabolism.Key words: protein catabolism, gastrointestinal peptides, isolated kidney, renal failure.

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41

Seow, Kok-Min, Jyun-Lin Lee, Ming-Luen Doong, Seng-Wong Huang, Jiann-Loung Hwang, Wei-Ju Huang, Full-Young Chang, Low-Tone Ho, and Chi-Chang Juan. "Human chorionic gonadotropin regulates gastric emptying in ovariectomized rats." Journal of Endocrinology 216, no. 3 (November 28, 2012): 307–14. http://dx.doi.org/10.1530/joe-12-0421.

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Prolongation of gastrointestinal transit resulting in nausea and vomiting in pregnancy (NVP) is the most common phenomenon during the first trimester of pregnancy. Increased human chorionic gonadotropin (hCG) concentration during the first trimester is the most likely cause of NVP. The aim of this study was to investigate the effect of hCG on gastrointestinal transit and plasma concentrations of cholecystokinin (CCK) in ovariectomized (Ovx) rats. I.p. injection of hCG was used to evaluate the dose effect of hCG on gastrointestinal transit in Ovx rats. The CCK antagonist lorglumide was used to clarify the role of CCK in regulating gastrointestinal transit. Gastrointestinal transit was assessed 15 min after intragastric gavage of a mixture of 10% charcoal and Na251CrO4(0.5 μCi/ml). After i.p. administration of hCG, gastric emptying was inhibited in Ovx rats, but intestinal transit was not affected. Plasma CCK concentrations were increased in a dose-dependent manner after hCG treatment, and gastric emptying showed a significant negative correlation with CCK concentrations (P=0.01,r2=−0.5104). Peripheral administration (i.p.) of lorglumide, a selective CCK1receptor antagonist, attenuated the hCG-induced inhibition of gastric emptying in Ovx rats, whereas central administration via the i.c.v. route did not. hCG treatment of Ovx rats inhibits gastric emptying in a dose-dependent manner via a peripheral mechanism of CCK hypersecretion and activation of CCK1receptors.

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42

Ouyang, Edwin C. "Transplantation of human hepatocytes into tolerized genetically immunocompetent rats." World Journal of Gastroenterology 7, no. 3 (2001): 324. http://dx.doi.org/10.3748/wjg.v7.i3.324.

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43

Promrat, Kittichai, Edwin C. Ouyang, Cherie Walton, Catherine H. Wu, and George Y. Wu. "Establishment of tolerance towards human hepatocytes in immunocompetent rats." Gastroenterology 118, no. 4 (April 2000): A906. http://dx.doi.org/10.1016/s0016-5085(00)85759-5.

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Wuillemin, Walter A., Wim K. Bleeker, Jacques Agterb erg, Gemma Rigter, Hugoten Cate, and C. Erik Hack. "Clearance of human factor XIa–inhibitor complexes in rats." British Journal of Haematology 93, no. 4 (June 1996): 950–54. http://dx.doi.org/10.1046/j.1365-2141.1996.d01-1740.x.

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Edelman, Birgitta. "‘Rats are people, too!’: Rat‐human relations re‐rated." Anthropology Today 18, no. 3 (June 2002): 3–8. http://dx.doi.org/10.1111/1467-8322.00118.

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Bachet, Jean. "Commentary: Fortunately enough, most human beings are not rats." Journal of Thoracic and Cardiovascular Surgery 160, no. 4 (October 2020): e189-e190. http://dx.doi.org/10.1016/j.jtcvs.2020.01.017.

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Herman, Laura, Tyler Hougland, and Rif S. El-Mallakh. "Mimicking human bipolar ion dysregulation models mania in rats." Neuroscience & Biobehavioral Reviews 31, no. 6 (January 2007): 874–81. http://dx.doi.org/10.1016/j.neubiorev.2007.04.001.

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Jantscher-Krenn, Evelyn, Carolin Marx, and Lars Bode. "Human milk oligosaccharides are differentially metabolised in neonatal rats." British Journal of Nutrition 110, no. 4 (January 14, 2013): 640–50. http://dx.doi.org/10.1017/s0007114512005727.

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Human milk oligosaccharides (HMO) are complex glycans that are highly abundant in human milk, but not in infant formula. Accumulating data, mostly from in vitro and animal studies, indicate that HMO benefit the breast-fed infant in multiple ways and in different target organs. In vitro incubation studies suggest that HMO can resist the low pH in the infant's stomach and enzymatic degradation in the small intestine and reach the colon in the same composition as in the mother's milk. The oligosaccharide composition in faeces of breast-fed infants is, however, very different from that in the mother's milk, raising questions on when, where and how HMO are metabolised between ingestion and excretion. To answer some of these questions, we established a pulse-chase model in neonatal rats and analysed HMO profiles to track their composition over time in five consecutive equal-length intestinal segments as well as in serum and urine. The relative abundance of individual HMO changed significantly within the first 2 h after feeding and already in the segments of the small intestine prior to reaching the colon. Only 3′-sialyllactose, the major oligosaccharide in rat milk, and hardly any other HMO appeared in the serum and the urine of HMO-fed rats, indicating a selective absorption of rat milk-specific oligosaccharides. The present results challenge the paradigm that HMO reach the colon and other target organs in the same composition as originally secreted with the mother's milk. The present results also raise questions on whether rats and other animals represent suitable models to study the effects of HMO.

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Goodman, Matthew M., Jerry L. McCullough, Catherine A. Biren, and Ronald J. Barr. "A Model of Human Melanoma in Cyclosporine-Immunosuppressed Rats." Journal of Investigative Dermatology 88, no. 2 (February 1987): 141–44. http://dx.doi.org/10.1111/1523-1747.ep12525289.

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Adzick, Scott. "Human small bowel transplants into athymic mice and rats." Journal of Pediatric Surgery 22, no. 9 (September 1987): 884. http://dx.doi.org/10.1016/s0022-3468(87)80681-4.

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Journal articles on the topic 'Rats; Human'

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