Relevant bibliographies by topics / Rats – Anatomy

Academic literature on the topic 'Rats – Anatomy'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Rats – Anatomy"

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Xiang, Xian-Hong, He-Ping Li, Wei Chen, Jia-Ping Li, Yu Wang, Guo-Sheng Tan, Lei Yu, and Jian-Yong Yang. "Anatomy research of coeliac trunk of Wistar rats." World Chinese Journal of Digestology 16, no. 26 (2008): 2988. http://dx.doi.org/10.11569/wcjd.v16.i26.2988.

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Sato, Karina Laurenti, Jussara Márcia do Carmo, and Valéria Paula Sassoli Fazan. "Ultrastructural anatomy of the renal nerves in rats." Brain Research 1119, no. 1 (November 2006): 94–100. http://dx.doi.org/10.1016/j.brainres.2006.08.044.

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Olivares, Ricardo, Carlos Morgan, Hernán Pérez, Alejandro Hernández, Francisco Aboitiz, Rubén Soto-Moyano, Julio Gil, et al. "Anatomy of corpus callosum in prenatally malnourished rats." Biological Research 45, no. 1 (2012): 87–92. http://dx.doi.org/10.4067/s0716-97602012000100012.

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Niyomchan, Apichaya, Sirinush Sricharoenvej, Passara Lanlua, and Sani Baimai. "Cerebellar Synaptopathy in Streptozotocin-Induced Diabetic Rats." International Journal of Morphology 37, no. 1 (2019): 28–35. http://dx.doi.org/10.4067/s0717-95022019000100028.

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Ortug, G., S. Ignak, and A. Ortug. "Characteristics of lingual papillae in diabetic rats." Morphologie 102, no. 339 (December 2018): 250–54. http://dx.doi.org/10.1016/j.morpho.2018.08.003.

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Moravec, Steven J., and John F. Cleall. "An assessment of posture in bipedal rats." American Journal of Anatomy 180, no. 4 (December 1987): 357–64. http://dx.doi.org/10.1002/aja.1001800406.

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Orlinskaya, N. Yu, and A. B. Elkanova. "Pathological anatomy of thyrotoxic liver." Medical alphabet, no. 17 (September 23, 2020): 36–38. http://dx.doi.org/10.33667/2078-5631-2020-17-36-38.

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The work was performed on experimental material. An experimental model of thyrotoxicosis in laboratory animals, white male rats, was obtained by daily administration оf l-thyroxine at a dose of 1.6 mg per 1 kg of body weight. The duration of the experiment was 45 days. 67 mature rats weighing 250–300 g were selected for the experiment. Rats were removed from the experiment after 7, 14, 21, 28, 35 and 45 days. As a control, we used 22 rats that were not injected with L-thyroxine. The level of thyroid hormones in the blood of rats was determined by enzyme immunoassay. A macroscopic study was performed and the size and mass of the rat liver were determined. For histological examination, pieces of liver tissue were taken, and they were fixed in 10 % buffered formalin for 10 days. Histological preparations were prepared by the standard method, using histological, histochemical and immunohistochemical studies. The results of the study showed that in experimental thyrotoxicosis, the level of thyroid hormones increases: T3 (triiodothyronine) equals 21.37 ± 0.03 mmol/l, 4.75 ± 0.02 mmol/l in the control; T4 (thyroxine) equals 2.55 ± 0.03 mmol/l, 1.80 ± 0.03 mmol/l in the control. Macroscopic examination revealed a 2-fold increase in the size and weight of the liver. Histological examination revealed widespread interstitial edema of the liver stroma, dystrophic and destructive changes, necrosis of hepatocytes, formation of cavities, thinning and atrophy of the liver beams, lymphocytic infiltration. The immunohistochemical study shows a decrease in Ki-67 expression level to 1.8 % compared to the control (5.0 %), which indicates a decrease in reparative processes in the liver.
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Shi, Ji-Hua, Sheng-Xing Zhu, and Shui-Jun Zhang. "Applied anatomy of liver and partial hepatectomy in rats." World Chinese Journal of Digestology 16, no. 22 (2008): 2516. http://dx.doi.org/10.11569/wcjd.v16.i22.2516.

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Pasierbek, Michal. "Functional Anatomy of the Mediastinal Lymph Nodes in Rats." Lymphatic Research and Biology 12, no. 3 (September 2014): 157–63. http://dx.doi.org/10.1089/lrb.2013.0044.

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Santos, Ana Paula, Carla Adelino Suaid, Valéria Paula Sassoli Fazan, and Amilton Antunes Barreira. "Microscopic anatomy of brachial plexus branches in Wistar rats." Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology 290, no. 5 (2007): 477–85. http://dx.doi.org/10.1002/ar.20519.

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Dissertations / Theses on the topic "Rats – Anatomy"

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Buhrmann, Kristin. "A behavioral and anatomical examination of the intramodal and intramodal effects of early stimulation history and selective posterior cortical lesions in the rat." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29348.

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The aim of this study was to investigate the intra- and intermodal impact of different kinds of early sensory experience on the development of specific neural/perceptual systems. The manipulations of the rats' early experience involved a combination of early binocular deprivation through dark-rearing, somatosensory restriction through cauterization of mystacial vibrissae, and multimodal enrichment through rearing in a complex environment. Specific lesions to somatosensory (Parl) and visual (Oc2M) cortex in differentially reared animals were included in an attempt to gain further insight into the plasticity surrounding manipulations of early stimulation history. Five tasks were used to assess these effects of early rearing condition in combination with later cortical lesions. Behavioral assessment focused on the ability of the animals to encode, abstract, and remember specific relationships between stimuli within the deprived modality itself, their ability to do so with information presented in other modalities, and on the basic species specific behavior. The only effect found was a main effect for rearing condition. Basically, complex-reared rats were more competent on several of the behavioral tasks than were dark-reared rats. However, this result provided little behavioral support for ideas of modality interdependence. Dendritic proliferation is considered to be a general mechanism supporting behavioral change. The subsequent neuroanatomical assessment focused on dendritic branching of neurons in specific cortical areas thought to be most affected by early environmental manipulations. Animals that were raised in a complex environment, but had experienced early tactile restriction through cauterization of vibrissae, showed significantly more dendritic branching than animals from all other rearing conditions in all cortical areas measured. This finding is consistent with ideas of both intra- and intermodal compensation following damage to an early developing modality, as well as behavioral demand acting as a significant factor in determining the impact of early somatosensory restriction. It is reasonable to assume that anatomical changes should be manifested behaviorally. Suggestions for smaller, more restricted studies, that would be more effective in describing the behavioral impact of early manipulations of the environment, were outlined.
Arts, Faculty of
Psychology, Department of
Graduate
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Todd, Dorothy A. "A study of pyretics in rats and mice." Thesis, University of Aberdeen, 1986. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU004772.

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In this study, the suitability of rodents for the detection and assay of microbial pyrogens was investigated and the pathophysiology of the 'yeast rat' model, currently used for screening antipyretic drugs, was documented. Mice do not consistently develop pyrexia following systemic injections of bacterial endotoxin (BE). These findings are in contrast to the dose-dependent hyperthermia observed in mice following intrahypothalamic injections of prostaglandin E2 (PGE2), a putative central mediator of pyrexia. Hyperthermia was associated with a decrease in skin temperature or an increase in oxygen consumption depending on the ambient temperature. These results suggest that mice have the ability to co-ordinate thermoregulatory mechanisms to raise their body temperature. Unlike PGE2, BE injected into the preoptic and anterior hypothalamic nuclei did not consistently raise body temperature in mice. This suggests that the failure of systemically administered endotoxin to consistently induce pyrexia is not due to insufficient quantities of pyrogen reaching the central thermoregulatory centres. However, central injections of BE may not mimic the central events occurring during the development of pyrexia as a result of peripheral infection. The inconsistent effect of systemic endotoxin on body temperature in mice in this study suggests that this species is unsuitable for the assay of microbial pyrogens. Unlike mice, rats developed pyrexia following systemic injections of BE; the doses of BE required were at least 100 fold greater than those reported for the rabbit (see General Introduction), rendering rats less sensitive than other species as models for the detection and assay of microbial pyrogens. Yeast also raised body temperature in rats. Pyrexia coincided with the acute phase of a yeast-induced inflammatory response. An abscess was formed at the site of injection; this subsequently developed into a chronic granuloma. The pyrogenic response to yeast was not directly attributable to inflammatory mediators associated with increased vascular permeability, phagocytosis or granuloma formation. It is unlikely therefore, that antipyretic activity displayed by drugs tested in the 'yeast rat' model is due to peripheral anti-inflammatory activity. However, results from this study suggest that BE may be a suitable replacement for yeast as a pyrexic challenge in rats for screening antipyretics. BE would be less emotive than yeast and would not induce a chronic granuloma. No endogenous pyrogenic mediators were detected in yeast-treated rats. No endogenous pyrogen (EP) was obtained from rat blood or peritoneal exudates in vitro. Either rats do not release detectable EP or attempts in this study to activate rat white blood cells in vitro do not mimic events occurring in vivo. Athymic rats injected with yeast developed pyrexia which suggests that Interleukin 1 is not an endogenous pyrogenic mediator unless its release is independent of T-cell derived lymphokines. Changes in thermoregulatory behaviour following pyrogen administration in rats were studied as an alternative method for assaying pyrogens. Detectable changes in thermoregulatory behaviour can precede but do not always accompany changes in body temperature in rats. Therefore, body temperature was considered to be a more reliable measure of thermoregulatory changes than behaviour in this study.
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Huang, Zhigao. "Implication of anti-apoptotic genes in neuronal death following focal cerebral ischemia in rats." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6270.

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Accumulating biochemical and morphological evidence suggests that apoptosis contributes to neuronal cell death following cerebral ischemia. Recent research which has examined changes in expression of proapoptotic proteins has further strengthened the important role of apoptosis in ischemic cell death. In this thesis I first addressed the role of apoptosis in ischemic death by examining p53, which is itself a complex multifunctional tumor suppresser gene, following transient focal ischemia. Of particular note were the alterations of the anti-apoptosic gene, naip, that were observed under stress conditions. The anatomical distribution of naip expression and neuronal survival following middle cerebral artery occlusion (MCA-o) were closely examined. In experiment I, SHR rats were subjected to 90 minute MCA-o followed by 22.5 hr reperfusion (RP) and compared with sham operated controls. In experiment II, sections obtained from fresh frozen or fixed brain tissue of long-Evans hooded rats (n = 3--4) that had been subjected to hippocampal kindling were used for ISHH or immunohistochemistry for naip expression. Neuronal protection against cerebral ischemia by hippocampal kindling was assessed in experiment III. Hippocampal kindled animals were also used to study the time course of naip expression in the frontoparietal cortex, which is mainly supplied by MCA. Both p53 mRNA and protein were elevated in the ischemic penumbra in experiment I. The induction of p53 peaked within 8--12 hr then returned to basal levels within 24 hr after RP. The short duration of p53 induction in ischemic penumbra may suggest that p53 activate downstream genes responsible for growth arrest, DNA repair or/and apoptosis. Experiment II demonstrated a significant elevation in naip mRNA and proteins in piriform cortex and hippocampus, where neuronal populations known to be protected by kindling. The duration of the elevation lasted up to three weeks. In contrast, naip mRNA and protein remained at baseline levels in regions that are not protected, such as endopiriform cortex and medial thalamus. We also demonstrated that hippocampal kindling attenuated cortical infarct induced by MCA-o to 57.7 +/- 4.6mm3 as compared to 156.5 +/- 12.6mm3 in controls. This neuroprotection was associated with a two to three fold elevation of naip expression in the corresponding areas by kindling treatment. (Abstract shortened by UMI.)
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Watson, Charles. "Brain mapping." Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/28840.

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These publications are a summary of work I have completed in brain mapping over many years. The work includes one book (The Rat Brain in Stereotaxic Coordinates, 6th compact edition), ten articles on hindbrain and spinal cord anatomy published in peer reviewed journals between 1975 to 2011, and five published chapters on spinal cord anatomy, including two spinal cord atlases. Over my career I have published 15 books on the anatomy of the brain and spinal cord of experimental animals. I am first author or equal co-author of ten of these books. The most successful of these books, "The Rat Brain in Stereotaxic Coordinates" (Paxinos and Watson, l 982, 1986, 1996, 1998, 2005, 2007), has earned over 50,000 citations since it was first published in 1982. The second edition alone is ranked 32 in the Thomson ISI 50 most cited publications of all time, having been cited 17,093 times up to January 2006. Dr George Paxinos and l are equal contributors to this work; the order of authors was decided on alphabetical precedence.
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Kruszynska, Y. T. "Metabolic effects of portal and peripheral insulin delivery in streptozotocin diabetic rats." Thesis, University of Newcastle Upon Tyne, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356789.

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Rupanagudi, S. R. "Pathogenesis of thyroid enlargement and involution in rats treated with antithyroid compounds." Thesis, University of Surrey, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383301.

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Baker, Gregory Lloyd. "The role of milk-borne epidermal growth factor on hepatic development in artificially reared suckling rats." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/289229.

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Breast milk contains many biologically active substances, including epidermal growth factor (EGF), that are absent from artificial milk formulas. Previous studies have shown dramatic growth and maturation effects of milk-borne EGF on the intestine. This raises the question as to whether artificial milk formulas should be supplemented with biologically active substances, such as EGF. As a result, this dissertation examined whether feeding suckling rats artificial milk formula supplemented with EGF modulates liver development. The normal development of hepatic cells in suckling and weanling rats also was characterized. Additionally, this dissertation examined whether gut-derived endotoxin and tumor necrosis factor alpha (TNFα) play a role in liver development. Dam-fed suckling and weanlings showed increases in the reorganization of hepatocellular plates, numbers of binucleated hepatocytes, and a tendency for sinusoidal endothelial cell fenestrae density and porosity to increase with age. Monocytic derived cells increased at days 8-12 and decreased at day 16. Hepatic stellate cells decreased with age. Colon microbial flora and portal venous endotoxin were present from day 8 onward. Compared to artificial milk formula feeding alone, EGF in the artificial formula elicited increased numbers of binucleated hepatocytes, changes in colon microbial flora, and a tendency for increased numbers of Kupffer cells and portal venous endotoxin. Compared to breast milk, the artificial diet caused decreases in binucleated hepatocytes, increases in monocytic derived cells, Kupffer cells, hepatic stellate cells, portal venous endotoxin and changes in the composition of the colon microbial flora. These increases in cells may be due to colonization of the colon with microbial flora which increased portal venous endotoxin. Increased endotoxin may provide a stimulus for the recruitment of monocytic derived cells to the liver and differentiation into Kupffer cells, which then stimulates hepatic stellate cell proliferation. However, the increases in portal venous endotoxin were not sufficient to elicit hepatic TNFα, mRNA production. In conclusion, milk-borne EGF is involved in differentiation of hepatocytes and changes colon microbial flora that occur in suckling rats. Whether accelerating maturation of hepatocyte is beneficial or detrimental to the suckling rats remains to be determined. Therefore, the supplementation of artificial milk formula with EGF warrants further consideration and research.
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Wan, J. M.-F. "The effect of E. coli endotoxin on the metabolic responses of Wistar rats." Thesis, University of Southampton, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376188.

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Carter, Katharine Christine. "The specificity of the host's immunological response to invasive nematode parasites of rats." Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/13330.

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Britton, Ann Patricia. "A morphological investigation of the effects of pregnant mare serum gonadotrophin on oocyte maturation, fertilization and embryonic development in rats." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30962.

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A delicate balance of steroid and gonadotrophic hormones is essential for intrafollicular oocyte maturation and successful fertilization and embryonic development. Previous studies have demonstrated that a superovulatory dose of pregnant mare serum gonadotrophin (PMSG) has excessive gonadotrophic activity and alters intrafol1icular steroid hormone levels. In a series of four experiments, the morphology of oocytes and embryos retrieved from immature rats, treated with either a low or high dose of PMSG, and mature, cycling rats was compared to determine whether a superovulatory dose of PMSG has an adverse effect on oocyte maturation and subsequent fertilization and embryonic development in immature rats. Morphological criteria for the assessment of intraoviductal oocyte aging were established in the first experiment. During intraoviductal aging, progressive morphological changes directed by the intrinsic developmental program of the oocyte were observed. Further alterations in morphology were attributed to abnormalities of cytoskeletal function. In the second experiment, no difference in morphology was observed between oocytes retrieved from immature rats treated with either 4 or 40 IU PMSG. When compared with mature rats, changes attributable to cytoskeletal instability were observed in aged oocytes from immature rats treated with both doses of PMSG. This was concluded to be a manifestation of altered intrafollicular oocyte maturation as a result of the administration of exogenous gonadotrophin. In the third and fourth experiments, delayed fertilization and a significant reduction in fertilization rate were observed in superovulated, immature rats. The major cause of fertilization failure was determined to be intraoviductal oocyte aging. A significant increase in abnormal embryos was observed as a result of parthenogenetic activation of the aged oocytes. Abnormal, fertilized embryos retrieved from the superovulated group were concluded to be the manifestation of delayed fertilization. In conclusion, the major effect of a superovulatory dose of PMSG on oocyte fertilizability and embryonic development was intraoviductal oocyte aging and delayed fertilization. Changes attributed to altered intrafol1icular maturation were manifested during oocyte aging in immature rats treated with either the low or high dose of PMSG.
Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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Books on the topic "Rats – Anatomy"

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Olds, R. J. A colour atlas of the rat: Dissection guide. London: ELBS with Wolfe Publishing, 1991.

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Outside and inside rats and mice. New York: Atheneum Books for Young Readers, 2001.

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Hebel, Rudolf. Anatomy and embryology of the laboratory rat. Wörthsee: BioMed Verlag, 1986.

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Zilles, Karl. The cortex of the rat: A stereotaxic atlas. Berlin: Springer-Verlag, 1985.

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Laboratory anatomy of the white rat. 5th ed. Boston, Mass: WCB McGraw-Hill, 1994.

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Chiasson, Robert B. Laboratory anatomy of the white rat. 5th ed. Dubuque, Iowa: Wm.C.Brown, 1988.

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Chiasson, Robert B. Laboratory anatomy of the white rat. 5th ed. Dubuque, Iowa: Wm. C. Brown, 1988.

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1940-, Bayer Shirley A., ed. Atlas of prenatal rat brain development. Boca Raton, Fla: CRC Press, 1995.

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Thyagarajan, Subramanian, ed. Atlas of the neonatal rat brain. Boca Raton, FL: CRC Press, 2011.

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1953-, Sakai T., and Kriz Wilhelm 1936-, eds. The vascular pole of the renal glomerulus of rat. Berlin: Springer, 1998.

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Book chapters on the topic "Rats – Anatomy"

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Iaizzo, Paul A. "Cardiac Devices and Technologies: Continued Rapid Rates of Development." In Handbook of Cardiac Anatomy, Physiology, and Devices, 787–93. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19464-6_44.

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"Rats." In Clinical Anatomy and Physiology of Exotic Species, 209–25. Elsevier, 2005. http://dx.doi.org/10.1016/b978-070202782-6.50013-2.

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Wang-Fischer, Yanlin, Ricardo Prado, and Lee Koetzner. "Anatomy and Cerebral Circulation of the Rat." In Manual of Stroke Models in Rats, 13–24. CRC Press, 2008. http://dx.doi.org/10.1201/9781420009521-4.

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Prado, Ricardo, Yanlin Wang-Fischer, and Lee Koetzner. "Anatomy and Cerebral Circulation of the Rat." In Manual of Stroke Models in Rats, 13–23. CRC Press, 2008. http://dx.doi.org/10.1201/9781420009521.ch4.

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Burwell, Rebecca D., and Menno P. Witter. "Basic anatomy of the parahippocampal region in monkeys and rats." In The Parahippocampal RegionOrganization and Role in Cognitive Function, 34–59. Oxford University Press, 2002. http://dx.doi.org/10.1093/acprof:oso/9780198509172.003.0003.

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Komárek, Vladimír. "Gross Anatomy." In The Laboratory Rat, 253–83. Elsevier, 2000. http://dx.doi.org/10.1016/b978-012426400-7.50052-2.

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KOMAREK, V. "Gross Anatomy." In The Laboratory Rat, 253–83. Elsevier, 2000. http://dx.doi.org/10.1016/b978-012426400-7/50052-2.

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Numan, Michael. "Brain Mechanisms Regulating Maternal Behavior in Nonhuman Mammals." In The Parental Brain, 52–98. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190848675.003.0004.

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Chapter 4 examines the roles of oxytocin (OT) and olfaction in the maternal behavior of nonhuman mammals. It also presents an overview of brain anatomy. In concert with pregnancy hormones, the release of OT into the brain, derived from the paraventricular hypothalamic nucleus, stimulates the onset of maternal behavior. Although OT is not required for the maintenance of maternal behavior, it does enhance maternal behavior during the postpartum period in challenging environments by decreasing anxiety and increasing maternal motivation. OT, in the absence of pregnancy hormones, may also enhance maternal responsiveness in alloparents. For many postpartum mammals, maternal motivation is under multisensory control, and olfaction is not required, although it is necessary for maternal selectivity in sheep. In contrast, for laboratory mice, olfaction is essential for maternal motivation. For virgin female rats and rabbits, olfactory input from pups inhibits maternal behavior, but this inhibition is eliminated at parturition.
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Crisler, Robin, Nancy A. Johnston, Christine Sivula, and Carl L. Budelsky. "Functional Anatomy and Physiology." In The Laboratory Rat, 91–132. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-814338-4.00004-0.

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"Normal Respiratory Rate, Heart Rate, and Temperature Reference Ranges." In Comparative Veterinary Anatomy, 1423–24. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91015-6.09996-9.

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Conference papers on the topic "Rats – Anatomy"

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Rai, Rajalakshmi, Latha V Prabhu, and Hema Kini. "Influence of sildenafil mediated nitric oxide and phosphodiesterase on the kidney in rats." In Annual International Conference on Microscopic and Macroscopic Anatomy. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2382-6096_cmma14.20.

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Koyuum Akinloye, Adebayo, and Bankole Olusiji Oke. "Gross, Histological And Ultrastructural Features of The Cervices of African Giant Rat (Cricetomys Gambianus, Waterhouse) During Oestrous Cycle The Anatomy of Cervices of the Female African Giant Rats." In Annual International Conference on Microscopic and Macroscopic Anatomy. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2382-6096_cmma14.11.

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Mess, Griffin, Rasika Thombre, Max Kerensky, Eli Curry, Fariba Abhabaglou, Safwan Alomari, Henry Brem, Nicholas Theodore, Betty Tyler, and Amir Manbachi. "Designing a Murine Model of Human Glioblastoma Brain Tumor: Development of a Platform for Validation Using Ultrasound Elastography." In 2022 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/dmd2022-1025.

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Abstract Glioblastoma Multiforme (GBM) is a malignant brain cancer with low overall survival. Therefore, researchers are looking to augment its current therapeutic regimen, which includes surgical tumor resection, chemotherapy and radiation. A promising treatment modality, focused ultrasound, has been used as a non-invasive treatment for GBM through multiple approaches such as thermal ablation, immunomodulation, and blood brain barrier disruption. In order to develop these treatments for clinical trials, testing in animal models needs to be performed to investigate the efficacy of the treatment in complex biological environments, as well as to evaluate any side-effects. The more biologically relevant the animal model is to human anatomy, the more applicable the results will be for translation to clinical trials. Here, we report a human GBM rat model, which utilizes an IDH-wildtype, EGFRvIII mutant patient-derived xenograft in athymic rats. The in vivo tumor growth rate was assessed over a period of 20 days to evaluate reproducibility and to develop the model for future testing of FUS in the treatment of GBM.
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Xing, Qi, Mark M. Theiss, Wenzhen Yang, Jim X. Chen, and Jihui Li. "Automatic Assessment of Lower Extremity Deformity Based on Patient Specific Computer Models." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53808.

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Lower extremity deformity can cause joint pain and malfunction. Patients with severe deformity usually need a correction surgery or total knee replacement (TKR) surgery to realign the orientation of the femur and tibia. Lower extremity deformity needs to be accurately assessed before any clinical decision can be made. In practice, physicians and radiologists rely mainly on X-ray images to evaluate the deformity, and CT is used in complex cases only. Manual assessment on X-rays is tedious, time consuming and inaccurate [1]. Computer aided diagnosis was proved efficient to understand patients’ anatomy, analyze lower limb deformity and plan the possible surgery [2]. However, notable interactive works were required during the identification of the anatomic features, and the accuracy was unguaranteed when the physician is not familiar with the diagnosis software. In this study we developed an automatic assessment system to identify patients’ anatomic features and quantify lower extremity deformity.
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Giray, Sait Murat. "Anatomy of unmanned aerial vehicle hijacking with signal spoofing." In 2013 6th International Conference on Recent Advances in Space Technologies (RAST). IEEE, 2013. http://dx.doi.org/10.1109/rast.2013.6581320.

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Chen, Lei, Jeremiah Hartner, David Van Dyke, Tianshu Dong, Brendon Watson, and Albert Shih. "Custom Skull Cap With Precision Guides for Deep Insertion of Cellular-Scale Microwire Into Rat Brain." In ASME 2019 14th International Manufacturing Science and Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/msec2019-2967.

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Abstract To understand the brain functioning mechanisms, electrophysiological methods represent the most mature approach for recording brain dynamics at millisecond timescales in either local or large spatial scales. Microwire-based microelectrode arrays (MEAs) are a well-established tool for chronic recording of electrophysiologic signals and furthermore have the advantage of minimal brain damage if constructed from cellular-scale (4–100 μm neuron diameter) microwires. However, such cellular-scale MEAs are not widely used by neuroscientists, especially on deep insertion cases, due to the barrier of implantation. Efforts to reduce the size of microwires bring collateral difficulties due to buckling during penetration through membranes (dura/pia) and consequent inability to implant deeply into the brain or in a manner that leaves intact protective biolayers such as the dura mater. In this paper, we developed a custom skull cap with precision guide holes to stabilize the brain and dura, provide sufficient support to microwire along the insertion path, and minimize the unsupported length of microwire during dura penetration and deeper insertion. A cap matched to individual skull anatomy with offset for brain stabilization was designed based on computed tomography (CT) scan of the rat head and fabricated by stereolithography. Micro-milling and wax molding were conducted to fabricate precision insertion guide inside the cap. Animal surgical studies were conducted to test the performance of skull cap and insertion guide. Rats with skull cap attached had survived for multiple weeks until sacrificed by experimenters. Through a test cube with precision guide, a 25 μm diameter tungsten microwire penetrated through the dura mater and was manually inserted over 10 mm into the brain without buckling. In comparison, without the precision guide, insertion of the same microwire caused over 2 mm dimpling of the dura without penetration and finally led to wire buckling. Results showed that the custom skull cap with precision guide holes enabled the insertion of cellular-scale microwire electrodes deep into the brain through the dura mater without buckling.
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Yu, Li, Qian Liu, Xueling Bai, Yinping Liao, Qingming Luo, and Hui Gong. "A digital rat atlas of sectional anatomy." In Fourth International Conference on Photonics and Imaging in Biology and Medicine, edited by Kexin Xu, Qingming Luo, Da Xing, Alexander V. Priezzhev, and Valery V. Tuchin. SPIE, 2006. http://dx.doi.org/10.1117/12.710690.

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Niiyama, Ryuma, Carine Rognon, and Yasuo Kuniyoshi. "Printable pneumatic artificial muscles for anatomy-based humanoid robots." In 2015 IEEE-RAS 15th International Conference on Humanoid Robots (Humanoids). IEEE, 2015. http://dx.doi.org/10.1109/humanoids.2015.7363565.

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Karargyris, A., S. Antani, and G. Thoma. "Segmenting anatomy in chest x-rays for tuberculosis screening." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091917.

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Tan, X. G., Andrzej J. Przekwas, and Joseph B. Long. "Validations of Virtual Animal Model for Investigation of Shock/Blast Wave TBI." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64587.

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Complementary to animal testing and analysis of clinical data, a validated anatomy and physiology based mathematical models can provide capabilities for a better understanding of blast wave brain injury mechanisms, animal-human injury scaling, assessing and improving protective armor. We developed the 3D “virtual” animal models for multi-scale computational simulations of blast induced injury. A multi-scale modeling tool, CoBi, has been adopted for the analysis of blast wave primary TBI mechanisms and coupled biomechanics events. The shock wave over a rat in a shock tube was modeled by the CFD method. The primary biomechanics FEM study uses anatomic based animal geometry with a high resolution brain model. The virtual rat model has been validated against recently collected data from shock tube tests on rodents, including pressure time history in the free-stream and inside the rat brain. The model has been used to conduct parametric simulations to study the effect of animal placement location in the shock tube, and different loading orientations on the rat response. We also compared the rat brain biomechanical response between simulations of a free-to-move and a protected or constrained rat under the same shock tube loading to identify the role of body protection and head movement and on the rat TBI. The implications of these results suggest that virtual animal model could be used to predict the biomechanical response in the blast TBI event, and help design the protection against the blast TBI.
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Reports on the topic "Rats – Anatomy"

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Manski, Charles, and Francesca Molinari. Estimating the COVID-19 Infection Rate: Anatomy of an Inference Problem. Cambridge, MA: National Bureau of Economic Research, April 2020. http://dx.doi.org/10.3386/w27023.

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Molinari, Francesca, and Charles F. Manski. Estimating the COVID-19 Infection Rate: Anatomy of an Inference Problem. The IFS, May 2020. http://dx.doi.org/10.1920/wp.cem.2020.2020.

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Stall, Nathan M., Kevin A. Brown, Antonina Maltsev, Aaron Jones, Andrew P. Costa, Vanessa Allen, Adalsteinn D. Brown, et al. COVID-19 and Ontario’s Long-Term Care Homes. Ontario COVID-19 Science Advisory Table, January 2021. http://dx.doi.org/10.47326/ocsat.2021.02.07.1.0.

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Key Message Ontario long-term care (LTC) home residents have experienced disproportionately high morbidity and mortality, both from COVID-19 and from the conditions associated with the COVID-19 pandemic. There are several measures that could be effective in preventing COVID-19 outbreaks, hospitalizations, and deaths in Ontario’s LTC homes, if implemented. First, temporary staffing could be minimized by improving staff working conditions. Second, homes could be further decrowded by a continued disallowance of three- and four-resident rooms and additional temporary housing for the most crowded homes. Third, the risk of SARS-CoV-2 infection in staff could be minimized by approaches that reduce the risk of transmission in communities with a high burden of COVID-19. Summary Background The Province of Ontario has 626 licensed LTC homes and 77,257 long-stay beds; 58% of homes are privately owned, 24% are non-profit/charitable, 16% are municipal. LTC homes were strongly affected during Ontario’s first and second waves of the COVID-19 pandemic. Questions What do we know about the first and second waves of COVID-19 in Ontario LTC homes? Which risk factors are associated with COVID-19 outbreaks in Ontario LTC homes and the extent and death rates associated with outbreaks? What has been the impact of the COVID-19 pandemic on the general health and wellbeing of LTC residents? How has the existing Ontario evidence on COVID-19 in LTC settings been used to support public health interventions and policy changes in these settings? What are the further measures that could be effective in preventing COVID-19 outbreaks, hospitalizations, and deaths in Ontario’s LTC homes? Findings As of January 14, 2021, a total of 3,211 Ontario LTC home residents have died of COVID-19, totaling 60.7% of all 5,289 COVID-19 deaths in Ontario to date. There have now been more cumulative LTC home outbreaks during the second wave as compared with the first wave. The infection and death rates among LTC residents have been lower during the second wave, as compared with the first wave, and a greater number of LTC outbreaks have involved only staff infections. The growth rate of SARS-CoV-2 infections among LTC residents was slower during the first two months of the second wave in September and October 2020, as compared with the first wave. However, the growth rate after the two-month mark is comparatively faster during the second wave. The majority of second wave infections and deaths in LTC homes have occurred between December 1, 2020, and January 14, 2021 (most recent date of data extraction prior to publication). This highlights the recent intensification of the COVID-19 pandemic in LTC homes that has mirrored the recent increase in community transmission of SARS-CoV-2 across Ontario. Evidence from Ontario demonstrates that the risk factors for SARS-CoV-2 outbreaks and subsequent deaths in LTC are distinct from the risk factors for outbreaks and deaths in the community (Figure 1). The most important risk factors for whether a LTC home will experience an outbreak is the daily incidence of SARS-CoV-2 infections in the communities surrounding the home and the occurrence of staff infections. The most important risk factors for the magnitude of an outbreak and the number of resulting resident deaths are older design, chain ownership, and crowding. Figure 1. Anatomy of Outbreaks and Spread of COVID-19 in LTC Homes and Among Residents Figure from Peter Hamilton, personal communication. Many Ontario LTC home residents have experienced severe and potentially irreversible physical, cognitive, psychological, and functional declines as a result of precautionary public health interventions imposed on homes, such as limiting access to general visitors and essential caregivers, resident absences, and group activities. There has also been an increase in the prescribing of psychoactive drugs to Ontario LTC residents. The accumulating evidence on COVID-19 in Ontario’s LTC homes has been leveraged in several ways to support public health interventions and policy during the pandemic. Ontario evidence showed that SARS-CoV-2 infections among LTC staff was associated with subsequent COVID-19 deaths among LTC residents, which motivated a public order to restrict LTC staff from working in more than one LTC home in the first wave. Emerging Ontario evidence on risk factors for LTC home outbreaks and deaths has been incorporated into provincial pandemic surveillance tools. Public health directives now attempt to limit crowding in LTC homes by restricting occupancy to two residents per room. The LTC visitor policy was also revised to designate a maximum of two essential caregivers who can visit residents without time limits, including when a home is experiencing an outbreak. Several further measures could be effective in preventing COVID-19 outbreaks, hospitalizations, and deaths in Ontario’s LTC homes. First, temporary staffing could be minimized by improving staff working conditions. Second, the risk of SARS-CoV-2 infection in staff could be minimized by measures that reduce the risk of transmission in communities with a high burden of COVID-19. Third, LTC homes could be further decrowded by a continued disallowance of three- and four-resident rooms and additional temporary housing for the most crowded homes. Other important issues include improved prevention and detection of SARS-CoV-2 infection in LTC staff, enhanced infection prevention and control (IPAC) capacity within the LTC homes, a more balanced and nuanced approach to public health measures and IPAC strategies in LTC homes, strategies to promote vaccine acceptance amongst residents and staff, and further improving data collection on LTC homes, residents, staff, visitors and essential caregivers for the duration of the COVID-19 pandemic. Interpretation Comparisons of the first and second waves of the COVID-19 pandemic in the LTC setting reveal improvement in some but not all epidemiological indicators. Despite this, the second wave is now intensifying within LTC homes and without action we will likely experience a substantial additional loss of life before the widespread administration and time-dependent maximal effectiveness of COVID-19 vaccines. The predictors of outbreaks, the spread of infection, and deaths in Ontario’s LTC homes are well documented and have remained unchanged between the first and the second wave. Some of the evidence on COVID-19 in Ontario’s LTC homes has been effectively leveraged to support public health interventions and policies. Several further measures, if implemented, have the potential to prevent additional LTC home COVID-19 outbreaks and deaths.
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