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1

Simmons, Joe H. "Rat respiratory virus (RRV) and other novel rodent diseases /". free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3025651.

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2

Dahlman, Ingrid. "Genetic dissection of experimental autoimmune neuroinflammatory diseases in rats /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3768-0/.

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3

Jacobs, Carvern Denver. "The effect of Cyclopia maculata on AMPK expression in Wistar rats". Thesis, University of the Western Cape, 2012. http://hdl.handle.net/11394/4043.

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>Magister Scientiae - MSc
Being overweight or obese are major factors contributing to the increased morbidity and mortality due to non-communicable diseases such as type 2 diabetes, cardiovascular disease and cancer. The treatment of obesity with pharmaceutical drugs is plagued by side effects. Plants and their phytochemicals possess a number of beneficial health effects including anti-oxidant,anti-mutagenic, anti-inflammatory, anti-obesity and anti-cancer effects, mediated by activation of the adenosine monophosphate protein kinase (AMPK).AMPK controls many metabolic processes including glucose uptake and utilisation, and adipogenesis, and is often referred to as the master regulator establishing cellular homeostasis.Cyclopia maculata, commonly known as honeybush, is an indigenous South Africa plant possessing anti-oxidant, anti-inflammatory and anti-cancer properties. Recently, others in our laboratory have shown that a hot water extract of fermented C. maculata inhibits adipocyte differentiation in 3T3-L1 pre-adipocytes, with some evidence of weight regulatory properties in a Wistar rat model of diet-induced obesity. In the rat study, 21 day old weanlings were fed a high fat, high sugar cafeteria diet for 3 months with (n=10) or without (n=10) C. maculata supplementation. This group of rats was referred to as the lean group (n=20). Another group of rats were fed a cafeteria diet for 4 months to induce obesity (obese group, n=20) and thereafter treated as described for the lean rats. The aim of this MSc study was to determine whether C. maculata induces AMPK activation.Proteins were extracted from the liver and muscle tissue of lean and obese Wistar rats using an optimized extraction method with a commercial lysis buffer and the TissueLyser.Treatment with the C. maculata extract had no effect on the protein yield in lean and obese rats. Interestingly, the protein yield in the liver of obese rats was significantly higher than that observed in lean rats. Although C. maculata treatment slightly increased AMPK activation (calculated as the ratio of phosphorylated AMPK to total AMPK) in the liver of lean and obese rats, the difference was not statistical significant. Conversely, C.maculata treatment decreased AMPK activity in muscle of lean and obese rats, with statistical significance observed in the lean group only (2.3-fold, p<0.05). Differences in AMPK activation between the groups were also noted, a 1.3-fold decreased activity observed in obese groups compared to their lean counterparts, although this was not statistically significant. Expression of PPARα, a downstream protein target affected by AMPK activation was reduced in the liver of lean and obese rats after C. maculata treatment. Moreover, PPARα expression was significantly higher in obese compared to lean rats (2.7-fold, p<0.001). PPARα is a transcription factor mediating fat metabolism (β-oxidation) and its expression is induced by circulating free fatty acids, which are increased in obese compared to lean rats. The expression of PPARα in muscle was too low for Western blot analysis and quantification.Cyclopia maculata treatment did not affect hepatic expression of UCP2, another protein important in establishing energy homeostasis. The expression of UCP2 was 2.9-fold higher in the liver of obese rats compared to their lean counterparts, although the difference was not statistically significant. The opposite results were observed in the muscle where C. maculata treatment decreased UCP2 expression in lean rats (2.8-fold,p<0.0001), and UCP2 expression was decreased 1.4-fold in obese rats compared to lean rats, although the difference was not statistically significant.ELISA results for AMPK activation revealed that C. maculata treatment increased AMPK activity, although not statistically significant. Histological analysis of retroperitoneal fat showed that C. maculata did not affect adipocyte size and number, although a slight decrease in adipocyte size was observed after treatment .This study has demonstrated that treatment of the cafeteria diet fed Wistar rats with 300 mg/kg of a hot water extract of fermented C. maculata does activate AMPK. This study revealed important differences between lean and obese rats. In particular, increased hepatic protein content, PPARα and UCP2 expression was observed in obese rats compared to the lean group. This suggests an adaptive response to the increased circulating free fatty acids during obesity and an increase in β-oxidation in these animals.
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4

Hair-Bejo, Mohd. "Gastrointestinal response to copper excess : studies on copper (and zinc) loaded rats". Thesis, University of Liverpool, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303681.

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5

高加信 i Ka-shun Joshua Ko. "The mechanisms of adaptive cytoprotection against ethanol-induced gastric mucosal damage in rats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31234185.

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6

何美美 i Mai-mai Ho. "A study on the acute and chronic effects of morphine on rat stomachs". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1986. http://hub.hku.hk/bib/B31230611.

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7

Manirafasha, Claudine. "The effects of kolaviron on epididymal and testicular function in streptozotocin induced diabetic wistar rats". Thesis, Cape Peninsula University of Technology, 2014. http://hdl.handle.net/20.500.11838/1508.

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Thesis submitted in fulfilment of the requirements for the degree Master of Technology: Biomedical Technology in the Faculty of Health and Wellness Sciences at the Cape Peninsula University Of Technology 2014
Oxidative stress (OS) plays a central role in the progression of diabetes mellitus (DM). Prevention of DM and its complications is a challenging health problem as it impacts on various organ functions, including reproduction. Diabetes mellitus with hyperglycaemic condition generates high production of reactive oxygen species. An imbalance between antioxidant mechanism and reactive oxygen species generates oxidative stress. OS damages the sperm membrane by oxidation of polyunsaturated fats which in turn reduces the sperm motility and ability to fuse with the oocyte and OS directly damage sperm DNA, compromising the paternal genomic contribution to the embryo development. Recent experimental evidence shows that modulation of oxidative stress and natural antioxidants may determine the outcome of male reproductive function. Previous investigations indicate that the supplementation and treatment with phytomedicine might play role in the prevention and management of DM and its subsequent complications on male reproductive function. This study explored the pharmacological potential of kolaviron (KV) on testicular and epididymal tissue in diabetic and non- diabetic Wistar rats. All experiments were conducted for a period of six weeks. Male Wistar rats (240–290 g) were randomly divided into 5 groups (n=12) where all the rats received a standard diet. Non diabetic rats control group and other four groups injected with different treatments. Non diabetic rat (N) received vehicle: Dimethylsulfoxide. Diabetes rats (D) were induced by a single intraperitoneal injection of freshly prepared streptozotocin (STZ) solution, 50mg/kg body weight. The N and D were treated with kolaviron (100 mg/kg body weight) orally, five times a week .The last group, diabetic rats were given subcutaneously injection of the standard anti-diabetic drug, insulin (0.2 u/kg) every second day. After the feeding period, testicular and epididymal tissues were collected and were analysed. All parameters were determined using appropriate methods in homogenized tissues. Data were expressed as mean ± SD. Plasma glucose as well as malondialdehyde (MDA) was significantly higher, while body, testicular and epididymal weights were lower in the D group compared to the N group and N+KV. Both kolaviron and insulin were able to ameliorate these effects. Testicular and epididymal antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in induced diabetic rats were significantly (p<0.05) low compared to diabetic control group. However, KV treated group shown significantly higher SOD, CAT and GPx activities compared D group. In conclusion, our findings demonstrated that KV could improve antioxidant enzymes and modulate STZ induced diabetic related oxidative stress in the male reproductive system. Kolaviron can potentially be used as an anti-diabetic treatment, however further studies are needed. Key words: Oxidative stress, Diabetes mellitus, antioxidants, kolaviron, epididymal tissue, testicular tissue, superoxide dismutase, catalase, glutathione peroxidase, lipid peroxidation, streptozotocin
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8

Gomes, Débora Aline Silva [UNESP]. "Influência do estado diabético na doença periodontal induzida em ratos. Análise bioquímica, microscópica, radiográfica e dos níveis de mieloperoxidade". Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/96207.

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Made available in DSpace on 2014-06-11T19:28:03Z (GMT). No. of bitstreams: 0 Previous issue date: 2006-02-17Bitstream added on 2014-06-13T19:47:54Z : No. of bitstreams: 1 gomes_das_me_arafo.pdf: 2513950 bytes, checksum: 8cd7796b57e48e98aeb2eb5aa9a87b0d (MD5)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Universidade Estadual Paulista (UNESP)
Evidências sugerem existir correlação positiva entre diabetes mellitus e destruição periodontal. Com intuito de estudar a influência do Diabetes Mellitus sobre a evolução da doença periodontal induzida, o presente estudo apresenta como objetivos, avaliar o peso corporal, os níveis séricos de cálcio, fósforo e fosfatase alcalina, os níveis teciduais de mieloperoxidase, além de, análise macroscópica e radiográfica dos espécimes de cada animal. Foram utilizados 128 ratos machos Wistar divididos em 4 grupos de 32 ratos, sendo: Grupo I controle; Grupo II diabético; Grupo III controle com doença periodontal induzida e Grupo IV diabético com doença periodontal induzida. Após dois dias da confirmação do estado diabético induzido por estreptozotocina, foi realizada a colocação da ligadura. Oito animais de cada grupo foram sacrificados nos períodos experimentais de 3, 7, 15 e 30 dias após colocação da ligadura. Os resultados demonstraram que o estado diabético perdurou até o final do experimento nos grupos II e IV. Dentre os marcadores bioquímicos, somente a ALP apresentou-se estatisticamente maior nos grupos diabéticos (II e IV). Macroscopicamente, houve diferença somente entre os grupos com e sem doença periodontal, independente da presença do diabetes, com maior alteração tecidual nos períodos tardios de periodontite (30 dias). Os níveis gengivais de MPO foram estatisticamente maiores (p<0.05) nos grupos com doença periodontal induzida (III e IV). Radiograficamente, o grupo IV apresentou maior perda óssea estatisticamente significante quando comparada aos demais grupos (p<0,05). Nos limites deste estudo, pode-se concluir que a doença periodontal induzida não alterou o estado hiperglicêmico, no entanto, sugere-se que o diabetes acentue...
Evidences suggest the existence of a positive correlation between diabetes mellitus and periodontal collapse. In order to evaluate the influence of Diabetes Mellitus on the progression of periodontal disease induced in rats, the objective of the present study was to verify glycemic, calcium, phosphorus and alkaline phosphatase serum levels, to evaluate myeloperoxidase (MPO) gingival levels, as well as to carry out macroscopic and radiographic assessment of the animals' hemimandíbulas of experimental periodontitis. A hundred twenty-eight Wistar male rats were used in this study. They were divided into 4 groups of 32 rats each, as follows: Group I - control; Group II - diabetic; Group III - control with periodontal disease induced; and Group IV - diabetic with periodontal disease induced. After streptozotocin diabetic state was confirmed, a ligature was placed on the mandibular first molar teeth of Groups III and IV rats. Eight animals of each group were killed at the experimental periods of 3, 7, 15 and 30 days after the ligature placement. Results demonstrated that the diabetic state lasted up to the end of the experiment at groups II and IV. Significant increases in serum alkaline phosphatase were observed at diabetic groups (II and IV). Macroscopically, in the groups where periodontal disease was induced, it was possible to observe more tissue alterations and it was higher in the 30-day experimental period. The MPO levels were significantly higher in induced periodontitis groups (III and IV) (p<0.05). Radiographically, diabetic with experimental periodontitis group (IV) showed statistically higher bone loss in all the experimental periods (p<0.05). It is possible to conclude that induced periodontal disease did not change the diabetic state... (Complete abstract, click electronic address below)
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9

Lam, Kai-Yee. "A study on the role of probiotic lactobacillus rhamnosus GG on gastric mucosal damages in rats /". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36432891.

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10

Lam, Kai-yee. "A study on the role of probiotic lactobacillus rhamnosus GG on gastric mucosal damages in rats". Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37340050.

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11

Dicks, Dana L. (Dana Lorraine). "The effect of growth hormone treatment on growth in zinc deficient rats /". Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56653.

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The ability of human growth hormone (hGH) to alleviate the effects of zinc deficiency on growth was investigated in the rat. Human GH treatment had no significant effect on food consumption, growth parameters or plasma IGF-I. Food consumption, tail length, liver weight, and tibia weight were significantly lower in the zinc deficient group. Body weight was significantly reduced in the zinc deficient and pair fed groups compared to the control. A significant interaction between zinc and hGH was found for tibial epiphyseal cartilage width but there were no significant differences between the groups receiving hGH and the respective shams. Tissue zinc content and plasma alkaline phosphatase were significantly decreased by the dietary zinc deficiency. Plasma zinc was higher in the groups receiving hGH. Significant interactions between zinc and hGH was found for liver iron, tibial zinc, and tibial copper. Copper and iron showed a competitive interaction with zinc and were lower in the rats receiving the control diet. Both lowered zinc and food intake contributed to the effects of the zinc deficiency; however, these effects were not equally distributed. Food intake had the greater effect on growth and plasma IGF-I while tissue mineral content showed a greater effect for zinc intake.
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12

Waight, Sharma Agnes Phyllis. "The intestinal immune response to Giardia in the rat". Title page, abstract and contents only, 1988. http://web4.library.adelaide.edu.au/theses/09PH/09phw138.pdf.

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13

Williamson, Patricia S. "Regulation of food intake in zinc-deficient rats /". free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3025663.

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14

Lai, Ka-wai, i 黎嘉慧. "An in vitro study of ovarian folliculogenesis in galactosemic rats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B3015134X.

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15

Lam, Kai-yee, i 林佳儀. "A study on the role of probiotic lactobacillus rhamnosus GG on gastricmucosal damages in rats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37340050.

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16

Shafer, Sarah T. "Behavioral and biological effects of housing conditions and stress in male rats -- relevance to heart disease /". Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/Shafer2006.pdf.

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17

Patcharapinyopong, Chaiwut. "The phospholipase B response in rats infected with Fasciola hepatica and demonstration of the enzyme-parasitic interaction". Thesis, University of North Texas, 1999. https://digital.library.unt.edu/ark:/67531/metadc798055/.

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Fasciola hepatica was studied in outbred rats to determine of infection would cause an increase phospholipase B activity and the percentage of periperal blood eosinophilis. A second experiment was performed to investigate eosinophilis.
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18

Zhang, Xiaojun. "Analgesic effect of paeoniflorin in rats with visceral hyperalgesia induced by neonatal maternal separation". HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/919.

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19

Roberts, Jenny Renee. "Soluble metals of residual oil fly ash alter pulmonary host defense in rats". Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4554.

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Thesis (Ph. D.)--West Virginia University, 2006.
Title from document title page. Document formatted into pages; contains xvi, 250 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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20

Garrett, Michael R. "Genetic dissection of hypertension-related renal disease using the Dahl salt-sensitive rat". Connect to Online Resource-OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1175545256.

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Dissertation (Ph.D.)--University of Toledo, 2006.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 89-95, p. 127-131, p. 184-192, p.198-233.
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21

Hum, Susan. "Glutathione metabolism in the rat under varied nutritional conditions". Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59940.

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We developed a methodology to measure plasma hepatic glutathione (GSH) turnover and we tested it in rats treated with an inhibitor of GSH synthesis. Our goal was to determine whether protein intakes above NRC recommendations maximize hepatic GSH stores and turnover in vivo. We also wished to learn if plasma GSH, cysteine, or methionine concentrations or plasma GSH turnover could be used as noninvasive predictors of liver GSH status. Rats were fed purified diets containing 0, 5, 10, 20 or 40% casein for one week. The 0 and 5% casein diets were considered inadequate in protein, 10% marginal, 20% adequate and 40% excessive. Liver GSH content (mmol/liver) of rats fed 0 and 5% casein diets was 12.29 $ pm$ 1.11 and 16.43 $ pm$ 0.95, respectively, and increased to 23.62 $ pm$ 1.82 in the 10% group. Liver GSH content did not differ between the 20 and 40% groups. As dietary casein increased from 0-20%, free plasma GSH and cysteine concentrations and plasma GSH turnover increased, but did not increase further with the 40% diet. A sigmoidal relationship between plasma GSH turnover and hepatic GSH content was demonstrated. The best predictor of liver GSH content was not free plasma GSH concentration nor plasma GSH turnover, but the free plasma cysteine concentration.
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22

Kitto, Michael Ryan. "Biconditional discrimination learning in rats with 192 IgG-saporin lesions of the nucleus basalis magnocellularis". CSUSB ScholarWorks, 2006. https://scholarworks.lib.csusb.edu/etd-project/3002.

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The experiment tested the hypothesis that 192 IgG-saporin lesions of the nucleus basalis magnocellularis (NBM) in rats would impair performance in a biconditional visual discrimination task, which requires configural association learning. Experiment used 22 male Long-Evan rats (Harlan Sprague-Dawley). Behavioral testing was conducted in two identical T-mazes. Rats were randomly assigned to either a bilateral 192 IgG-saporin lesion group (n = 10) or to a control group (n = 12). Results support the hypothesis that NBM is critically involved in configural but not simple association learning and suggest that NBM may be involved more generally in cognitive flexibility.
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23

Dyck, Richard Henry. "Cytochrome oxidase histopathology in the central nervous system of developing rats displaying methylmercury-induced movement and postural disorders". Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27873.

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Sprague-Dawley rats were administered daily, subcutaneous injections of methylmercuric chloride at a dose of 5 mg/Hg/kg beginning on postnatal day 5. By their fourth postnatal week, animals exhibited a constellation of neurological signs of motor impairment which resembled the cerebral palsy syndrome of humans perinatally exposed to methylmercury. Routine histological examination of the brain revealed no gross differences between methylmercury-treated (MeHg), normal control (NC) or weight-matched littermates. The histochemical localization of the mitochondrial enzyme cytochrome oxidase (CO) was utilized in Experiment I to examine possible alterations in the metabolic activity of motor nuclei which might contribute to the observed movement and postural disorders. A population of intensely-staining cytochrome oxidase neurons (ICONs) in the magnocellular portion of the red nucleus (RMC) and interrubral mesencephalon (IRM) were conspicuously present in all MeHg animals at the onset of motor impairment. These morphologically, histochemically, and anatomically distinct neurons did not exhibit intense CO staining in control animals. Conversely, a significant decrease was demonstrated in the oxidative metabolic activity of many neurons in the substantia nigra, zona reticulata of MeHg animals. In Experiment II, the postnatal appearance of ICONs was morphometrically quantified in MeHg animals sacrificed at PND 14, 16, 18, 20, 22, or 25. The histochemically-defined onset of increased metabolic activity in ICONs was first observed on PND 16, at least one week before the onset of clinical signs of neurological impairment. This was the earliest manifestation of methylmercury neurotoxicity yet described in this animal model. A subsequent four-fold increase in the total number of ICONs at PND 18 was followed by a gradual decrease in number to PND 25. Significantly more of the ICONs were found in the IRM than in the RMC at PND 18 & 20. The possibility that the increased activity of ICONs may result from disinhibition of specific afferents to the red nucleus was addressed by introducing either hemidecortication or hemicerebellectomy on PND 10 and then morphometrically determining the deviation from symmetry in the bilateral distribution of the total number of ICONs in the RMC and IRM at PND 22. The distribution of ICONs was symmetrical and not different in either hemidecorticate or unoperated controls. A significant (36%) decrease in the total number of ICONs was observed in both the RMC and IRM contralateral to hemicerebellectomy. The identical ipsilateral regions did not differ from control or hemidecorticate MeHg animals. In Experiment III, the anatomical distribution of major histocompatability complex antigens (MHC) in the brain of MeHg animals was examined using immunohistochemical methods. MHC immunoreactivity was widely distributed throughout the brain of MeHg animals. Areas with low immunoreactivity, or lack of it, stand out and include all of the hippocampus, thalamus, pyriform and entorhinal cortex, and lateral cerebellar hemispheres. Moderate staining intensity was observed in neocortical areas, basal forebrain, caudate-putamen and cerebellar vermis. Strong immunoreactivity was found in red nucleus, substantia nigra, cingulate cortex, retrosplenial cortex, presubiculum, parasubiculum and vestibular nuclei. It was suggested that the increased activity of ICONs likely contributes to the movement and postural disorders resulting from methylmercury intoxication. The increased activity in ICONs was determined to be, at least partially, dependent upon cerebellar input. The results are discussed with reference to the toxic effects of methylmercury and specifically to the susceptibility of GABAergic interneurons in perinatal trauma. Possible analogies are drawn between the mechanisms of methylmercury-induced cerebral palsy syndrome and those of other developmental movement and postural disorders.
Medicine, Faculty of
Graduate
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24

Ricoldi, Milla Sprone Tavares. "Avaliação dos efeitos do probiótico Bifidobacterium animalis subsp. lactis HN019 como terapia adjuvante no tratamento da periodontite experimental em ratos". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/58/58138/tde-21052018-162023/.

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Probióticos do gênero Lactobacillus estão sendo amplamente investigados no tratamento da periodontite. Contudo, os efeitos de microrganismos do gênero Bifidobacterium ainda são pouco conhecidos. Este estudo avaliou os efeitos do probiótico Bifidobacterium animalis subsp. lactis (B. lactis) HN019 como adjuvante à raspagem e alisamento radicular (RAR) no tratamento da periodontite experimental (PE) em ratos. No dia 0 do experimento, 32 ratos foram alocados em 4 grupos: C (controle), PROB (probiótico), PE-RAR e PE-RARPROB. Nos grupos PE-RAR e PE-RAR-PROB, a PE foi induzida pela colocação de ligaduras de seda ao redor dos primeiros molares inferiores dos animais. No 14° dia, as ligaduras foram removidas e realizou-se a RAR. Nos animais dos grupos PROB e PE-RARPROB, o probiótico B. lactis HN019 foi administrado diariamente (10 mL/dia de 109 unidades formadoras de colônia) por 15 dias tendo seu início no 14° dia do experimento. Os animais de todos os grupos foram submetidos à eutanásia 29 dias após o início do experimento. As hemimandíbulas e amostras de intestino delgado foram coletadas. Foram realizadas análises histomorfométricas, microtomográficas e imunohistoquímicas. Foram investigados, também, os efeitos microbiológicos de B. lactis HN019 no biofilme associado às ligaduras durante o desenvolvimento da PE. Todos os dados foram analisados estatisticamente. O Grupo PE-RAR-PROB apresentou menores reabsorção óssea alveolar e perda de inserção conjuntiva quando comparado ao Grupo PE-RAR, bem como menor número de osteoclastos, maior expressão de citocinas anti-inflamatórias e menor expressão de citocinas pró-inflamatórias (p <0,05). No grupo PE-RAR-PROB, os valores médios da profundidade da cripta do jejuno e duodeno foram significativamente maiores que aqueles do grupo PE-RAR. A proporção de bactérias aeróbias/anaeróbias foi maior nas amostras de biofilme de animais tratados com B. lactis HN019 em relação àquelas de animais não tratados (p <0,05). Dentro dos limites deste estudo, pode-se concluir que a utilização de B. lactis HN019 como adjuvante à RAR promove benefícios histológicos, microtomográficos e imunológicos adicionais no tratamento da PE em ratos, bem como melhora a morfologia intestinal.
Lactobacillus probiotics have been investigated in periodontitis. However, the effects of the genus Bifidobacterium on periodontitis are hardly known. This study evaluated the effects of the probiotic Bifidobacterium animalis subsp. lactis (B. lactis) HN019 as an adjunct to scaling and root planing (SRP) in rats with experimental periodontitis (EP). At baseline, 32 rats were assigned to 4 groups: C (control), PROB, EP-SRP and EPSRP- PROB. In groups EP-SRP and EP-SRP-PROB, the mandibular first molars of the animals received a ligature. At day 14, the ligatures were removed and SRP was performed. Animals of groups PROB and EP-SRP-PROB were orally administered with 10 mL/day of 109 colony forming units of B. lactis HN019 for 15 days, starting at day 14. Animals were euthanized at day 29. The jaws and samples of the duodenum, jejunum, and ileum were resected. Histomorphometric, microtomographic and immunohistochemical analyses were performed. Microbiological effects of B. lactis on biofilm were also evaluated. Data were statistically analyzed. Group EP-SRP-PROB presented reduced alveolar bone resorption and attachment loss when compared with Group EP-SRP (p<0.05). Group EP-SRP-PROB showed significantly fewer osteoclasts, increased expression of anti-inflammatory cytokines and reduced expression of proinflammatory cytokines compared with Group EP-SRP (p<0.05). In group EP-SRPPROB, the mean values of crypt depth of the jejunum and dudoenum were significantly higher than the ones from group EP-SRP. B. lactis promoted a higher ratio between aerobic and anaerobic bacteria in biofilm samples (p<0.05). Within the limits of this study it can be concluded that the use of B. lactis HN019 as an adjunct to SRP promotes additional histologic, microtomographic and immunologic benefits in the treatment of EP in rats and improves the intestinal morphology.
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邱博生 i Bosheng Qiu. "A study on the ulcerogenic mechanisms of nicotine in stress-induced gastric glandular ulcers in rats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B3123317X.

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Shelton, Heath W., i Russell W. Brown. "INHIBITION OF TNF-ALPHA DECREASES MICROGLIA ACTIVATION IN RATS NEONATALLY TREATED WITH POLY I:C". Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/166.

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Introduction: Current medical treatment for individuals diagnosed with schizophrenia (SCHZ) primarily relies on the inhibition of the dopamine D2 receptor that has been shown to be supersensitive in these patients. Treatment occurs through the use of antipsychotic medication which leads to a number of debilitating dose-dependent side effects, such as weight gain, agranulocytosis, and seizures. Patients diagnosed with SCHZ have also been shown to have increased inflammation in their central nervous system (CNS), particularly within specific brain regions such as the prefrontal cortex and hippocampus. This is in large part due to the interaction between a pro-inflammatory cytokine called tumor necrosis factor-alpha (TNFa) and microglia, which are resident CNS defense cells. TNFa is a cell-signaling protein, regulates a variety of immune cells, and is involved in the acute phase reaction of inflammation. Upon activation by TNFa secretion, microglial cells switch from being anti-inflammatory (M2) to pro-inflammatory (M1), thereby resulting in neuroinflammation as well as synaptic loss and neuronal death. In this project, we hypothesized oral administration through the diet of a novel TNFa modulator (PD2024) developed by P2D Biosciences, Inc. (Cincinnati, OH) would significantly reduce microglia activation in rats neonatally treated with Polyinosinic:polycytidylic acid (poly I:C). Methods and Results: To test our hypothesis, four groups (Neonatal Poly I:C/TNFa, Neonatal Poly I:C/Control, Neonatal Saline/TNFa, and Neonatal Saline/Control) were intraperitoneally injected with either poly I:C or saline during postnatal days (P)5-7. Poly I:C is an immunostimulant that mimics neonatal infection in humans, which also has been found to be a factor for the development of SCHZ later in life. Between days (P)30-(P)60, the Neonatal Poly I:C/TNFa and Neonatal Saline/TNFa groups were orally administered PD2024 through the diet. After (P)60, brain tissue was evaluated by immunohistochemistry (IHC) and confocal microscopy. Immunohistochemistry was used to label microglial cells in the prefrontal cortex and hippocampus with a green fluorescent dye attached to Iba1, a protein that specifically binds to these cells. Upon completion of IHC, tissue was evaluated using a confocal microscope and then analyzed with NIH ImageJ software. Analysis parameters included cell count, sampled cell body fluorescence, and overall image fluorescence. The results obtained showed a significant decrease in microglia activation for the Poly I:C/TNFa group when compared to the Poly I:C/Control group, as well as similarities in activation levels with the Saline/Control group. These results were demonstrated in both sampled cell body fluorescence and overall image fluorescence measurements. Conclusion: This data supports the hypothesis that PD2024 is successful in reducing microglia activation through the modulation of TNFa. Therefore, treatment with a TNFa modulator such as PD2024 alongside of current antipsychotic medication could mediate neuroinflammation and reduce the dose-dependent side effects. This approach could be a promising therapeutic treatment option for those diagnosed with schizophrenia, as well as potentially for other neurocognitive and behavioral disorders.
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Lucetti, Larisse Tavares. "Efeito da pentoxifilina e da dexametasona na resposta inflamatÃria e nas alteraÃÃes da motilidade digestiva associadas à mucosite intestinal induzida por 5- fluorouracil em ratos". Universidade Federal do CearÃ, 2009. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=7069.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
IntroduÃÃo: A mucosite induzida por antineoplÃsicos à um fator limitante na terapia anticÃncer. Mucosite à um termo clÃnico que descreve uma sÃndrome caracterizada por ulceraÃÃo da mucosa de todo o trato digestivo. O trato gastrintestinal à vulnerÃvel por causa da alta proliferaÃÃo e freqÃÃncia de renovaÃÃo celular. Assim, a mucosite intestinal resulta de eventos inflamatÃrios, que levam as alteraÃÃes de permeabilidade e trÃnsito intestinal e de alteraÃÃes na motilidade intestinal tanto na fase inflamatÃria, como na fase pÃs-inflamatÃria. Pentoxifilina (PTX) à um importante inibidor da sÃntese de citocinas, alÃm de apresentar efeito protetor sobre a mucosite oral por 5-FU em hamster. A dexametasona (DEXA) à um glicocorticÃide cujo principal efeito farmacolÃgico decorre de sua aÃÃo antiinflamatÃria e imunossupressora. Objetivos: Avaliar o efeito do tratamento com pentoxifilina ou dexametasona na resposta inflamatÃria e nas alteraÃÃes da motilidade digestiva associadas a mucosite intestinal experimental induzida por 5-FU. MÃtodos: Ratos Wistar machos (200 â 250g) foram tratados no d0 com 5-FU (150 mg/Kg, i.p. dose Ãnica) ou com 5-FU + PTX (90mg/Kg, s.c.) ou 5-FU + DEXA (2,5mg/Kg, i.p.). A PTX e a DEXA foram administradas meia hora apÃs a administraÃÃo de 5-FU no d0 e diariamente atà o sacrifÃcio. No d3 os animais foram sacrificados, amostras do duodeno, jejuno e Ãleo, foram removidas para avaliar a injÃria epitelial por morfometria, escores histolÃgicos, pela atividade de MPO e pela concentraÃÃo de GSH. Para avaliaÃÃo de citocinas amostras de duodeno foram retiradas e pelo mÃtodo de ELISA foi determinada a concentraÃÃo de TNF- e IL-1 e pela imunohistoquÃmica foi observado a imunomarcaÃÃo. Jà na tÃcnica de esvaziamento gÃstrico os animais receberam o mesmo tratamento descrito anteriormente. Posteriormente, foram deixados em jejum de 18 horas do d2 para o d3. No d3, foram administrados 1,5 ml da soluÃÃo glicosada (5%) contendo vermelho de fenol (VF) a 0,75 mg/ml em cada animal. ApÃs 20 min, os animais foram sacrificados e submetidos a uma laparotomia mediana. O intestino delgado foi exposto e divido em 3 partes iguais: proximal, medial e distal. Com o auxÃlio de uma proveta contendo uma soluÃÃo de NaOH (100ml, 0,1N) o volume do estÃmago e dos segmentos do intestino delgado foram determinados. A absorbÃncia da amostra foi lida sob um comprimento de onda de 540 nm. Resultados: O tratamento com 5-FU foi capaz de induzir uma lesÃo intestinal com um importante comprometimento da barreira epitelial funcional com a presenÃa das seguintes alteraÃÃes: encurtamento acentuado das vilosidades intestinais, necrose parcial de criptas, vacuolizaÃÃo de cÃlulas, presenÃa de infiltrado mono e polimorfonucleares, produÃÃo de radicais livres com consumo de GSH, aumento na concentraÃÃo de TNF- e IL-1 com maior imunomarcaÃÃo (no duodeno) e alteraÃÃes na motilidade digestiva. O tratamento com DEXA e PTX reduziu significativamente as lesÃes intestinais, com recuperaÃÃo da altura dos vilos, recuperaÃÃo da profundidade das criptas, diminuiÃÃo do infiltrado neutrofÃlico, aumento dos nÃveis de glutationa e reduÃÃo da concentraÃÃo de TNF-, IL-1 com uma menor imunomarcaÃÃo. Contudo somente o tratamento com DEXA foi capaz de reverter o retarde do esvaziamento gÃstrico e do transito gastrintestinal. ConclusÃo: 5-FU induz mucosite intestinal em ratos com a participaÃÃo de TNF- e IL-1, a qual se associa com retarde no esvaziamento gÃstrico e no transito gastrintestinal. O tratamento com PTX ou DEXA foram capaz de reverter parte dos achados inflamatÃrios, entretanto, somente o tratamento com DEXA foi capaz de reverter parcialmente Ãs alteraÃÃes na motilidade digestiva associadas a mucosite por 5- FU em ratos.
Introduction: One of the most important limitation of antineoplasic chemotherapy is the intestinal mucositis. Mucositis is a clinical term wich describes a syndrome characterized for ulceration in the digestive tract. Gastrointestinal tract is vulnerable because it have elevated proliferation cellular renovation. Intestinal mucositis results in inflammatory events, that leads the alterations in permeability and gastrointestinal motility in the inflammatory phase, as in the post-inflammatory phase. Pentoxifylline (PTX) is important inhibitor of the cytokines synthesis, with a protective effect against 5-FU- induced oral mucositis in hamster. Dexamethasone (DEXA) is glucorticoide with anti-inflammatory and immunosuppressive effects. Aim: To evaluate the effect of the pentoxifylline or dexamethasone treatments in the inflammatory response and alterations of the gastrointestinal motility associate with 5-FU- induced intestinal mucositis. Methods: Male Wistar rats (200 â 250g) treated in d0 by 5-FU (150 mg/Kg, i.p. only dose) or 5-FU + PTX (90 mg/Kg, s.c.) or 5-FU + DEXA (2.5mg/Kg, i.p.). PTX or DEXA were administrated 30â after 5-FU, and then daily. In d3, animals were sacrificed, samples duodenum, jejunum and ileum were removed for assessment epithelial damage for morphometric, histological scores, MPO activity and GSH concentration. In order to evaluate the concentration of TNF- and IL-1, duodenum samples were removed and ELISA or imunohistoquimic for this cytocines were performed. In order to evaluated the gastrointestinal motility, animals received same treatment described previously, then were fasted for 18h of the d2 to d3. In d3 the animals were gavage-fed with a test meal and sacrificed 20 min later. Stomach and consecutive intestinal segments same (proximal, medial and distal) were obtained. Each segment was placed in a measuring cylinder and the volume measured by adding 100 mL of 0.1 NaOH. The absorbance of the sample was read at a 540 nm. Results: The treatment with 5-FU induced intestinal damage with an important disruption of the functional epithelial barrier and presence of these following alterations: shortening villus, partial necrosis crypts, vacuolated cells, presence of infiltrated mono and polymorphonuclears, production of free radicals with GSH consumption, increase in the concentration of TNF- and IL-1 in the duodenum, and gastrointestinal dismotility. The treatment with DEXA and PTX significantly reduced the intestinal damage, with recovery of the high villus, depth of crypt, reduction of the neutrophil infiltration, increase of the levels of glutathione and reduction in the TNF- and IL-1 concentrations. However, only the treatment with DEXA was able to reverse the delays gastric emptying and gastrointestinal transit induced by intestinal mucositis. Conclusion: 5-FU induces intestinal mucositis in rats with the participation of TNF- and IL-1. It associates with delayed gastric emptying and gastrointestinal transit. We conclude also that PTX or DEXA- treatments decreases the inflammatory response. On the other hand, only DEXA treatment reversed gastrointestinal dismotility associate with 5â FU- induced intestinal mucositis in rats.
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Aquino, Sabrina Garcia de. "Expressão de MMP-13 e ativação de vias de sinalização intracelular em dois modelos de doença periodontal induzida experimentalmente em ratos /". Araraquara : [s.n.], 2008. http://hdl.handle.net/11449/96184.

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Resumo: A progressão da doença periodontal é marcada pela excessiva produção de citocinas que, por sua vez, promove o aumento de outros mediadores inflamatórios, entre os quais, de metaloproteinases de matriz (MMPs). MMP-13 é uma colagenase de regulação complexa que tem sido relacionada à degradação da matriz extracelular (ECM) e à reabsorção óssea em diversas condições inflamatórias, incluindo doença periodontal e artrite reumatóide. A regulação da expressão gênica requer a ativação de várias vias de sinalização através da interação de receptores celulares específicos a estímulos externos, como antígenos bacterianos e citocinas derivadas do hospedeiro. A complexidade da rede de citocinas estabelecida durante a progressão da doença periodontal depende das vias de sinalização ativadas, as quais são influenciadas pela natureza do estímulo extracelular. Considerando o papel fundamental das vias de sinalização no controle da expressão gênica de citocinas e a relevante atividade de MMP-13 na doença periodontal, este estudo avaliou a expressão de MMP-13 e as vias de sinalização ativadas durante o curso de dois modelos de doença periodontal induzida experimentalmente. A expressão de MMP-13 nos níveis de RNA mensageiro (mRNA) e proteína foram avaliados por RT-PCR e Western Blot, respectivamente. A cinética de ativação das vias de sinalização intracelular relacionadas à expressão de mediadores inflamatórios também foi verificada por Western Blot. Estes achados foram relacionados à severidade da reação inflamatória determinada por estereometria. Dois modelos experimentais foram usados: injeção de LPS e colocação de ligadura. Injeções de LPS de Eschericia coli foram realizadas na região palatina de molares superiores 2 vezes por semana (30 μg por aplicação). Ligaduras foram colocadas na região cervical dos primeiros molares inferiores.
Abstract: The hallmark of destructive periodontal disease progression is the overproduction of cytokines which promotes the increased expression of other inflammatory mediators such as, MMPs. MMP-13 is a collagenase of complex gene regulation that has been implicated on ECM degradation and bone resorption in several inflammatory conditions, including periodontal disease and rheumatoid arthritis. Regulation of gene expression requires the activation of several signaling pathways through receptor-ligand binding of external stimuli represented by bacterial antigens and/or host-derived cytokines. The complexity of the cytokine network established during periodontal disease progression results from the signaling pathways activated, which are determined by the nature of external stimuli. Thus, considering the fundamental role of signaling pathways on regulation of cytokine gene expression and the relevant role of MMP-13 in periodontal disease, this study evaluated the expression of MMP-13 and the signaling pathways activated during the course of two experimentallyinduced periodontal disease models. Expression of MMP-13 at mRNA and protein levels was evaluated by reverse transcription polymerase chain reaction (RT-PCR) and Western Blot, respectively. The activation kinetics of some signaling pathways that are related to the expression of inflammatory mediators was also verified by Western Blot. The two experimental models used were: LPS injections and placement of ligatures. Bi-weekly injections of Eschericia coli LPS were done into the palatal aspect of upper molars (30 μg per injection). Ligatures were placed at the cervical portion of both lower first molars. The control animals received injections of PBS vehicle on the palatal gingiva of upper molars, whereas no ligatures were placed on the lower molars.
Orientador: Carlos Rossa Junior
Coorientador: Joni Augusto Cirelli
Banca: Luis Carlos Spolidorio
Banca: Raquel Fernanda Gerlach
Mestre
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29

雷志鵬 i Chi-pang Lui. "Nutritional zinc-deficiency and nitrosamine-induced carcinogenesis in the rat". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1986. http://hub.hku.hk/bib/B31207820.

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Lui, Chi-pang. "Nutritional zinc-deficiency and nitrosamine-induced carcinogenesis in the rat /". [Hong Kong : University of Hong Kong], 1986. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12326550.

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Meyer, Alberto Luiz Monteiro. "Alterações cardíacas na pancreatite aguda experimental". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-01112013-162651/.

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Introdução: Vários são os mecanismos envolvidos no desenvolvimento da resposta local e sistêmico na pancreatite aguda. O sistema cardiovascular pode ser afetado durante todo o curso clínico da pancreatite aguda. O objetivo deste estudo foi avaliar a produção local de citocinas pelo miocárdio, assim como, as alterações funcionais e histológicas do miocárdio na pancreatite aguda grave. Métodos: Os animais foram divididos em três grupos: Grupo 1: controle; Grupo 2: controle operado; Grupo 3: pancreatite aguda grave. Foram medidos os níveis séricos de amilase e de citocinas (TNF-alfa IL-6 e IL-10), expressão de RNAm de TNF-alfa, IL-6 e TGF-beta e ecocardiograma com avaliação da função cardíaca. Alterações do tecido cardíaco foram analisadas pelo exame histológico. Resultados: Os níveis séricos de TNF-alfa e IL-10 foram significativamente maiores no grupo pancreatite aguda 2h. Os níveis de RNAm de IL-6 do grupo pancreatite aguda 2h foram estatisticamente superiores. Os níveis de RNAm do TNF-alfa do grupo controle operado e pancreatite aguda 2h foram estatisticamente menores. Mudanças significativas no diâmetro do ventrículo esquerdo foram encontradas nos grupos pancreatite aguda 2h e 12h. Houve alterações estatísticas para a degeneração vacuolar, picnose e perda de núcleo, e os linfócitos. Conclusão: Encontramos alterações cardíacas e histológicas compatíveis com o processo inflamatório desencadeado por pancreatite aguda grave com o incremento da produção de citocinas pelo miocárdio
Background: Several mechanisms are involved in the development of the local and systemic response in acute pancreatitis. Cardiovascular system may be affected throughout the clinical course of acute pancreatitis. The aim was to evaluate local myocardial cytokine production, as well as, functional and histological myocardial alterations in severe acute pancreatitis. Methods: The animals were divided into three groups: Group 1: control; Group 2: sham; Group 3: severe acute pancreatitis. Echocardiographic assessment of cardiac function, serum levels of amylase and cytokines (TNF-alfa, IL-6 and IL-10), and mRNA expression of TNF-alfa, IL-6 and TGF-beta were measured. Myocardial tissue alterations were analysed by histological examination. Results: The serum TNF-alfa, and IL-10 levels were significant higher in acute pancreatitis 2h group. The mRNA IL-6 levels from acute pancreatitis 2h group were statistically higher. The mRNA TNF-alfa levels from sham group and acute pancreatitis 2h group were statistically lower. Significant changes in the left ventricular diameter were found in acute pancreatitis 2h and 12h groups. There were statistical changes for vacuolar degeneration, picnosis and loss of nucleus, and lymphocytes. Conclusion: We found cardiac and histological changes compatible with the inflammatory process triggered by severe acute pancreatitis with the promotion of local myocardial cytokine production
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Gogo, Arturo R. "The effect of nicotine on liver functions in rats and its modulation of the hepatotoxicity induced by carbon tetrachloride". Thesis, [Hong Kong] : University of Hong Kong, 1992. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13178143.

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Adedeji, Adekunle, Effiong Ottukonyong, Jonathan M. Peterson i W. Andrew Clark. "The Combined Effects of Leptin And Coenzyme Q10 in Ameliorating Obesity-Induced Infertility in Female Rats". Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/2513.

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Infertility is one of the major complications of obesity. Studies have shown that administration of leptin modulated the expression of Β-catenin in the ovary and reversed obesity-induced infertility in rats. Coenzyme Q10 (CoQ10), an antioxidant, supplies the energy used for ovulation, oocyte and embryo development and prevents DNA damage that causes infertility. We hypothesized that leptin when combined with CoQ10 could greatly improve fertility. Twenty-one female Sprague-Dawley rats were used in this study and divided into five treatments groups. Group I rats was fed rat chow diet (RCD) while groups II to V were fed High-fat diet (HFD) for 14 weeks to induce infertility. Group 1 RCD and group II HFD control rats received 1 ml of saline intraperitoneally (i.p.) twice daily for 2 days, group III HFD rats received 1 ml of 100 µg of leptin i.p. twice daily for 2 days, group IV HFD rats received 10 mg/kg of CoQ10 i.p. for 2 weeks plus saline twice daily for 2 days. Group V HFD rats received 1 ml of 100 µg of leptin i.p. twice daily for 2 days plus 10 mg/kg of CoQ1o i.p. for 2 weeks. Estrous cycle was checked daily and food intake and body weight measured twice weekly before and after treatments. Fourteen days post treatment, all the animals were sacrificed. The blood and tissues were collected for analysis. The results show a significant decrease in food intake and body weight and regular estrous cycle restored in groups III and V rats. There was significant (p < 0.05) increase in spleen weight in groups IV and V. FSH level increased significantly (p < 0.05) in the leptin plus CoQ10 treated group while CoQ10 level was increased significantly (p < 0.05) in the leptin-treated group. Β-catenin expression was decreased in group IV and V, suggesting that Β-catenin expression may be downregulated by COQ10 administration. These results indicate that synergistic action of leptin and CoQ10 could delay the onset of obesity-induced infertility exhibited by the reduction of food intake and body weight. In conclusion, combinations of CoQ10 with leptin can improve fertility in obese infertile female rats and could provide a novel therapeutic strategy for the treatment of female infertility.
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Aquino, Sabrina Garcia de [UNESP]. "Expressão de MMP-13 e ativação de vias de sinalização intracelular em dois modelos de doença periodontal induzida experimentalmente em ratos". Universidade Estadual Paulista (UNESP), 2008. http://hdl.handle.net/11449/96184.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
A progressão da doença periodontal é marcada pela excessiva produção de citocinas que, por sua vez, promove o aumento de outros mediadores inflamatórios, entre os quais, de metaloproteinases de matriz (MMPs). MMP-13 é uma colagenase de regulação complexa que tem sido relacionada à degradação da matriz extracelular (ECM) e à reabsorção óssea em diversas condições inflamatórias, incluindo doença periodontal e artrite reumatóide. A regulação da expressão gênica requer a ativação de várias vias de sinalização através da interação de receptores celulares específicos a estímulos externos, como antígenos bacterianos e citocinas derivadas do hospedeiro. A complexidade da rede de citocinas estabelecida durante a progressão da doença periodontal depende das vias de sinalização ativadas, as quais são influenciadas pela natureza do estímulo extracelular. Considerando o papel fundamental das vias de sinalização no controle da expressão gênica de citocinas e a relevante atividade de MMP-13 na doença periodontal, este estudo avaliou a expressão de MMP-13 e as vias de sinalização ativadas durante o curso de dois modelos de doença periodontal induzida experimentalmente. A expressão de MMP-13 nos níveis de RNA mensageiro (mRNA) e proteína foram avaliados por RT-PCR e Western Blot, respectivamente. A cinética de ativação das vias de sinalização intracelular relacionadas à expressão de mediadores inflamatórios também foi verificada por Western Blot. Estes achados foram relacionados à severidade da reação inflamatória determinada por estereometria. Dois modelos experimentais foram usados: injeção de LPS e colocação de ligadura. Injeções de LPS de Eschericia coli foram realizadas na região palatina de molares superiores 2 vezes por semana (30 μg por aplicação). Ligaduras foram colocadas na região cervical dos primeiros molares inferiores.
The hallmark of destructive periodontal disease progression is the overproduction of cytokines which promotes the increased expression of other inflammatory mediators such as, MMPs. MMP-13 is a collagenase of complex gene regulation that has been implicated on ECM degradation and bone resorption in several inflammatory conditions, including periodontal disease and rheumatoid arthritis. Regulation of gene expression requires the activation of several signaling pathways through receptor-ligand binding of external stimuli represented by bacterial antigens and/or host-derived cytokines. The complexity of the cytokine network established during periodontal disease progression results from the signaling pathways activated, which are determined by the nature of external stimuli. Thus, considering the fundamental role of signaling pathways on regulation of cytokine gene expression and the relevant role of MMP-13 in periodontal disease, this study evaluated the expression of MMP-13 and the signaling pathways activated during the course of two experimentallyinduced periodontal disease models. Expression of MMP-13 at mRNA and protein levels was evaluated by reverse transcription polymerase chain reaction (RT-PCR) and Western Blot, respectively. The activation kinetics of some signaling pathways that are related to the expression of inflammatory mediators was also verified by Western Blot. The two experimental models used were: LPS injections and placement of ligatures. Bi-weekly injections of Eschericia coli LPS were done into the palatal aspect of upper molars (30 μg per injection). Ligatures were placed at the cervical portion of both lower first molars. The control animals received injections of PBS vehicle on the palatal gingiva of upper molars, whereas no ligatures were placed on the lower molars.
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35

Jing, Yu, i n/a. "The acute effects of lithium on the rat kidney". University of Otago. Department of Physiology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080930.145652.

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The aim of the experiments reported in the present work was: first, to generate a rat model of lithium-induced nephrogenic diabetes insipidus (NDI), and, second, to use this to test the hypothesis that the effects of lithium were far more reaching than merely the inhibition of vasopressin induced translocation and synthesis of the water channel protein AQP2. Specifically, the effect of lithium on the abundance and distribution of the other water channel proteins, AQP1, AQP3 and AQP4 was investigated. It was found that AQP3 protein abundance was significantly reduced in the renal medulla while AQP4 was not affected. In addition, it was further hypothesized that, given the known effects of lithium on the urea transporter UT-A1 and on sodium channels and transporters, the renal medullary osmotic gradient would be dissipated by lithium. This was examined indirectly by determining the amounts of organic osmolytes in the renal medulla of rats with lithium-induced NDI. Myo-inositol was found to be 85 � 9 mmol kg⁻1 protein in the NDI rats, a reduction of 38% compared with control values, sotbitol fell from 35� 9 mmol kg⁻� in the control rats to 2.5 � 0.5 mmol kg⁻�, and glycerophosphorylcholine levels in the experimental animals were 91 � 18 mmol kg⁻� protein compared with 372 � 72 mmol kg⁻� in the controls. In addition, betaine decreased to 38 � 2 mmol kg⁻� protein from 69 � 10 mmol kg⁻� protein in the control. The urea content of the medulla was found to have fallen from 2868 � 558 mmol kg⁻� protein to 480 � 105 mmol kg⁻� protein. These data indicated that indeed the medullary osmotic gradient, the driving force for AVP-dependent fluid reabsorption in the kidney was greatly reduced during lithium-induced NDI. Thirdly, it was proposed that the sodium-channel blocker, amiloride, by acting to prevent lithium entry into the cells of the collecting duct, should ameliorate or abolish the adverse effects of lithium on the kidney. Treatment of rats with established NDI, with amiloride, reversed to a large extent the reduction in aquaporin protein expression and re-established the medullary osmotic gradient, as assessed by the ability of treated rats to concentrate their urine, and by the rise in amounts of medullary osmolytes. Administration of 0.5 mmol l⁻� amiloride to lithium-treated rats led to medullary AQP2 and AQP3 protein abundance increasing by 82% � 16% and 110% � 4% of the control level respectively. The content of urea in the medulla also increased to 2474 � 557 mmol kg⁻� protein. Finally, since in humans it is known that the chronic effect of lithium on the kidney is to cause cortical fibrosis and renal failure, microarray studies were commenced to look for evidence of early changes in gene activity in response to lithium-administration. The results showed that 77 genes were either up- or down-regulated, in particular, genes that are involved in the apoptosis pathway. In the light of these results it is plausible to suggest that the acute renal effects of lithium to induce NDI can be effectively mitigated, and reversed, by administration of amiloride. Whether this can serve to offset the chronic effects of lithium on the kidney awaits further investigation.
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36

L'Abbé, Mary R. "Role of dietary selenium as an antioxidant during carcinogenesis". Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75681.

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Experiments were conducted to examine the role of dietary selenium (Se) and changes in antioxidant capacity during DMBA-induced mammary carcinogenesis. Weanling rats were fed graded amounts of Se in an AIN-76 diet, modified to approximate the amount and type of dietary fat consumed in Canada. Animals fed 3-4 ppm Se had a reduced tumor incidence but there was evidence of chronic Se toxicity. Low Se did not elevate tumor incidence. Thus, supplemental dietary Se did not offer any protection in reducing the incidence of cancer when rats were fed a diet representative of North American intakes of fat. Blood GSHPx activity was elevated in rats that remained free of tumors (NT group) compared to animals that would eventually develop tumors (WT group). SOD activity was reduced in WT and NT rats, but appeared to be related to carcinogen administration. These differences were observed before tumor development and over a wide range of Se intakes. WT rats excreted more $ sp{75}$Se compared to both control and NT rats. These changes, however, were not reflected in elevated lipid peroxidation. Thus, one of the protective mechanisms during carcinogenesis may be the capacity of the animal to elevate GSHPx activity.
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37

Yip, Siu-leung, i 葉紹亮. "Biocompatibility and efficacy of a new synthetic polymer, crosslinked urethane-doped polyester elastomers (CUPEs), as nerve conduit forreconstruction of segmental peripheral nerve defect using rat model". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45153759.

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38

Ho, Chi-tat, i 何志達. "A study of the effects of (-)-epigallocatechin-3-gallate (EGCG) on a clinically relevant rat model of non-alcoholic fatty liver diseases(NAFLD)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45153036.

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39

Lorigados, Clara Batista. "Estudo da relação entre pressão de perfusão coronariana e função cardíaca em ratos endotoxêmicos". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5167/tde-27082014-142206/.

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Pacientes sépticos com disfunção miocárdica apresentam mortalidade significativamente superior comparados aos sépticos sem alteração cardiovascular. Vários mecanismos contribuem para disfunção orgânica na sepse, como diminuição de perfusão tecidual. A sepse está relacionada a alterações na microcirculação e na permeabilidade capilar que apresentam papel fundamental na fisiopatologia das disfunções orgânicas. O objetivo do estudo foi analisar o papel da pressão de perfusão coronariana como fator determinante do fluxo sanguíneo na microcirculação miocárdica e sua correlação com a função cardíaca sistólica e diastólica em ratos endotoxêmicos. Ratos machos, Wistar, 300g, receberam LPS 10 mg/kg ip. Após uma hora e meia da injeção, um cateter de pressão-volume foi locado no VE e um cateter pressórico na artéria femoral para aquisição dos parâmetros hemodinâmicos cardíacos e sistêmicos respectivamente. Foram estudados os ratos que apresentaram choque endotoxêmico (PAM <= 65 mmHg). Um grupo foi tratado com norepinefrina iv e outro com araminol iv, para atingir PAM de 85 mmHg. Para o estudo do fluxo sanguíneo, microesferas amarelas (15 ?m) foram injetadas no VE para analisar a microcirculação cardíaca. O coração foi analisado em três partes: VD, região epicárdica e região subendocárdica do VE. O estudo demonstrou uma redução de 58% na PPC e de 50% no fluxo miocárdico nos ratos com choque endotoxêmico. Houve queda de 34% na dP/dt max e 15% na dP/dt min comparados ao controle. Os parâmetros de função cardíaca sistólica volume-independentes, Ees e dP/dtmax / EDV, também apresentaram redução. Nos ratos tratados com norepinefrina, observou-se aumento da PPC (38 ± 2 vs. 59 ± 3 mmHg, LPS vs. LPS+NOR) e do fluxo sanguíneo miocárdico (2,0 ± 0,6 vs. 6,2 ± 0,8 mL/min.g tecido, LPS vs. LPS+NOR) e os índices de função cardíaca sistólica e diastólica mostraram recuperação. A PPC apresentou correlação significativa com o fluxo sanguíneo subendocárdico do VE.Os dados demonstraram que os animais em choque endotoxêmico e, portanto com PPC baixa, apresentaram redução no fluxo sanguíneo na microcirculação miocárdica, sobretudo no ventrículo direito e na região subendocárdica de VE. Isto se correlacionou com a disfunção cardíaca sistólica e diastólica. Ao elevar-se a PPC com a utilização de norepinefrina, houve aumento do fluxo sanguíneo miocárdico acompanhado de recuperação dos índices de função cardíaca
Septic patients with myocardial dysfunction have higher mortality compared to patients with no cardiovascular alteration. The aim of the present study was to investigate the role of coronary driving pressure as determinant factor of myocardial microcirculation blood flow and its correlation with the cardiac function in endotoxemic heart. Wistar rats, male, 300g were used. Endotoxemia was induced by the injection of 10 mg / kg ip LPS. After 1.5 h of injection, hemodynamic evaluation was performed. It was studied rats with MAP <= 65 mmHg. Norepinephrine and araminol were used to handle MAP to 85 mmHg. Millar catheter was placed in the left ventricle to the acquisition of cardiac parameters. Microspheres were infused into the left ventricle with a pump and it was collected blood from femoral artery and tissue samples, to measure blood flow in the myocardium (RV, subendocardium LV e epicardium LV) and other organs. Left ventricle parameters demonstrated a reduction (34%) in dP/dt max and (15%) in dP/dt min. Load independent indexes, Ees and dP/dtmax/ EDV showed a reduction after LPS. The coronary driving pressure was (58%) reduced in the endotoxemic rats. We found a reduction in myocardial blood flow (80%) in animals with mean arterial blood pressure below 65 mmHg. Norepinephrine increased coronary driving pressure (38 ± 2 vs. 59 ± 3 mmHg LPS vs. LPS+NOR), and microcirculation perfusion (2.0 ± 0.6 vs. 6.2 ± 0.8 mL/min.g tissue, LPS vs. LPS+NOR). Coronary driving pressure presented a significant correlation with sub endocardium blood flow. These data indicated that myocardial blood flow of left ventricle subendocardial region and right ventricle was decreased in endotoxemic rats in a coronary driving pressure dependent way. The reduced myocardial blood flow was determinant of cardiac dysfunction. Increasing systemic arterial blood pressures and consequently the coronary driving pressure, it succeeded to improve myocardial blood flow and cardiac function
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40

Persson, Kirstin Gracia. "In vivo effects of crinum macowanii on the rat cardiovascular system". Thesis, University of the Western Cape, 2007. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_4721_1222073945.

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Crinum macowanii (C. macowanii) (Amaryllidacea) as authenticated by Mr. F. Weitz at the Herbarium, University of the Western cape, is widely used a traditional remedy and is thought to have therapeutic value (Fennell and van Staden 2001). The objective of this study was to determine the cardiovascular effects of the crude aqueous extract of Crinum macowanii on the rat and to determine the effect of pre-treatment drugs on Crinum macowanii in in vivo, anaesthetized normotensive, male Wistar rats (200-250 g.).

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41

Sonne, James H. "EFFECTS OF INTRANASALLY ADMINISTERED DNSP-11 ON THE CENTRAL DOPAMINE SYSTEM OF NORMAL AND PARKINSONIAN FISCHER 344 RATS". UKnowledge, 2013. http://uknowledge.uky.edu/neurobio_etds/5.

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Due to the blood-brain barrier, delivery of many drugs to the brain has required intracranial surgery which is prone to complication. Here we show that Dopamine Neuron Stimulating Peptide 11 (DNSP-11), following non-invasive intranasal administration, protects dopaminergic neurons from a lesion model of Parkinson’s disease in the rat. A significant and dose-dependent increase in an index of dopamine turnover (the ratio of DOPAC to dopamine) was observed in the striatum of normal young adult Fischer 344 rats by whole-tissue neurochemistry compared to vehicle administered controls. Among animals challenged with a moderate, unilateral 6-hydroxy-dopamine (6-OHDA) lesion of the substantia nigra, those treated repeatedly with intranasally administered DNSP-11 exhibited greater numbers of tyrosine hydroxylase (TH) positive dopaminergic neuronal cell bodies in the substantia nigra and greater TH+ fiber density in the striatum when compared to animals treated intranasally with vehicle only or a scrambled version of the DNSP-11 sequence. Lesioned animals that received intranasal DNSP-11 treatment did not exhibit abnormal, apomorphine-induced rotation behavior, contrasted with animals that received only vehicle or scrambled peptide that did exhibit significantly greater rotation behavior. In addition, the endogenous expression of DNSP-11 from the pro-region of GDNF was investigated by immunohistochemistry with a custom, polyclonal antibody. Signal from the DNSP-11 antibody was found to be differentially localized from the mature GDNF protein both spatially and temporally. While DNSP-11-like immunoreactivity extensively colocalizes with GDNF immunoreactivity at post-natal day 10, the day of maximal GDNF expression, DNSP-11-like signal was found to be present in the 3 month old rat brain with signal in the substantia nigra, ventral thalamic nucleus, dentate gyrus of the hippocampus, with the strongest signal observed in the locus ceruleus where GDNF is not expressed. Results from immunoprecipitation of brain homogenate were not consistent with the synthetic, amidated 11 amino-acid rat DNSP-11 sequence. However, binding patterns in the literature of NPY, the only homologous sequence present in the CNS, do not recapitulate the immunoreactive patterns observed for the DNSP-11 signal. This study provides evidence for a potential easy-to-administer intranasal therapeutic using the DNSP-11 peptide for protection from a 6-OHDA lesion rat model of Parkinson’s disease.
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42

Reynolds, Kathryn A. "The effect of a zinc deficiency and alcohol intake during gestation in the rat". Diss., Virginia Polytechnic Institute and State University, 1987. http://hdl.handle.net/10919/49878.

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The effect of alcohol and/or zinc deficiency was evaluated in seven groups of pregnant rats and their pups. Females which had been acclimated to alcohol before breeding were fed liquid alcohol diets with either 14 or 0.1 ppm Zn. Comparisons were made with animals pair fed isocaloric liquid carbohydrate diets with the same Zn levels. Other comparisons were made by pair feeding a high zinc diet to a low zinc diet, and by feeding a high zinc diet ad lib. A reduced food intake and Zn deficiency affected maternal status by decreasing weight gain, liver Zn and plasma Zn concentration. Litter size, litter weight, and fetal liver and brain weight were decreased only in the alcohol zinc deficient group compared to adequately fed controls. The concentration and total quantity of fetal liver Zn were decreased due to a Zn deficiency. The combination of Zn deficiency and alcohol decreased only total Zn in fetal brain. The concentrations of protein, DNA, and RNA in fetal liver and brain were similar regardless of dietary treatment. The quantities of protein, DNA, and RNA were decreased in fetal liver due to Zn deficiency. ln fetal brain, only the combination of alcohol and Zn deficiency decreased total protein and RNA, while DNA was not affected. Although alcohol by itself had no effect on the above variables, its combination with a Zn deficiency did. In addition, there were 58 resorptions and 15 malformations seen in Zn deficient alcoholic dams compared with no more than 15 and 2, respectively, in any of the other groups. Teratogenesis caused by a Zn deficiency was increased with alcohol consumption.
Ph. D.
incomplete_metadata
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43

Lewandowski, Thomas A. "Toxicokinetic and toxicodynamic modeling of the effects of methyl mercury on development of the embryonic rat midbrain /". Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8450.

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44

Ellis, Rebecca Catherine. "Characterization of cathepsin b mrna and protein expression, enzymatic activity and cellular localization following contusion spinal cord injury in rats". [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0007160.

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Thesis (Ph.D.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 97 pages. Includes Vita. Includes bibliographical references.
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45

Zargham, Emilia Ohsone. "INVESTIGATIONS OF BINDING TARGETS OF THE PRO-MUTAGEN 2-AMINOANTHRACENE IN FISCHER-344 RATS". OpenSIUC, 2011. https://opensiuc.lib.siu.edu/theses/718.

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Environmental exposures causing ingestions of toxic chemicals, such as the polycyclic aromatic hydrocarbon 2-aminoanthracene (2-AA), may increase the risk of developing cancer and other diseases such as diabetes. To understand the mode of action of 2-AA as it relates to diabetogenic processes and pancreatic cancer, 2-AA binding to soluble protein mixtures was investigated using a novel technique called dynamic isoelectric anisotropy ligand binding assay (DIABLA). Twenty four post-weaning 3-4 week old Fischer-344 (F-344) male rats were fed 0 mg/kg (control), 50 mg/kg (low dose), 75 mg/kg (medium dose) and 100 mg/kg (high dose) 2-AA diet for 14 and 28 days. Total proteins extracted from the pancreas and liver were evaluated for their binding potential using DIABLA. This technique utilizes capillary isoelectric focusing and fluorescence anisotropy to separate proteins in their active form as well as evaluate the chemical interactions. Isoelectric point (pI) values for protein binding as well as experimental mass spectra data were determined. Investigation of 2-AA binding through screening a complex mixture of proteins is a step towards understanding the mode of action and the biological activities.
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46

Ye, Xingshen, i 叶星沈. "Studies on effects of coptis extract and berberine against carbon tetrachloride-induced liver damage in rats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38755208.

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47

Huff, Courtney L. "Investigating the binding of streptococcal monoclonal antibody 10F5 in the heart of the Lewis rat". CardinalScholar 1.0, 2009. http://liblink.bsu.edu/uhtbin/catkey/1538086.

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48

Neel, Sarah Elizabeth. "Transplantation of iPS cells reduces apoptosis and fibrosis and improves cardiac function in streptozotocin-induced diabetic rats". Master's thesis, University of Central Florida, 2010. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4686.

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Background: Streptozotocin (STZ) induced diabetes leads to various complications including cardiomyopathy. Recent data suggests transplanted bone marrow stem cells improve cardiac function in diabetic cardiomyopathy. However, whether modified ES, iPS cells, or factors released from these cells can inhibit apoptosis and fibrosis remains completely unknown. The present study was designed to determine the effects of transplanted ES cells overexpressing pancreatic transcription factor 1 a (Ptf1a), a pro-pancreatic endodermal transcription factor, iPS cells, or their respective conditioned media (CM) on diabetic cardiomyopathy. Methods: Experimental diabetes was induced in male Sprague Dawley rats (8-10 weeks old) by intraperitoneal STZ injections (65 mg/kg body weight for 2 consecutive days). Animals were divided into six experimental groups including control, treated with sodium citrate buffer IP, STZ, STZ + ES-Ptf1a cells, STZ + iPS cells, STZ + ES-Ptf1a CM and STZ + iPS CM. Following STZ injections, appropriate cells (1 X 106/mL/injection/day) or CM (2 mL injection/day) were given intravenously for 3 consecutive days. Animals were sacrificed and hearts were harvested at day 28. Histology, TUNEL staining, and Caspase-3 activity were used to assess apoptosis and fibrosis. ERK1/2 phosphorylation was quantified using ELISAs. M-mode echocardiography fractional shortening was used to assess cardiac function. Results: Animals transplanted with ES cells, iPS cells, or both CMs showed a significant (pless than]0.05) reduction in interstitial fibrosis, and apoptosis compared with STZ group. ERK expression was not significantly different compared with STZ. Echocardiography showed a significant (pless than]0.05) improvement in fractional shortening in cell and media transplanted groups compared with STZ. Conclusions: Our data suggest that ES cells, iPS cells, and/or CMs inhibit apoptosis, reduce fibrosis, and improve cardiac function in STZ-treated diabetic rats.
ID: 029049879; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Thesis (M.S.)--University of Central Florida, 2010.; Includes bibliographical references (p. 33-40).
M.S.
Masters
Burnett School of Biomedical Sciences
Medicine
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49

Gomes, Débora Aline Silva. "Influência do estado diabético na doença periodontal induzida em ratos. Análise bioquímica, microscópica, radiográfica e dos níveis de mieloperoxidade /". Araraquara: [s.n.], 2006. http://hdl.handle.net/11449/96207.

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Resumo: Evidências sugerem existir correlação positiva entre diabetes mellitus e destruição periodontal. Com intuito de estudar a influência do Diabetes Mellitus sobre a evolução da doença periodontal induzida, o presente estudo apresenta como objetivos, avaliar o peso corporal, os níveis séricos de cálcio, fósforo e fosfatase alcalina, os níveis teciduais de mieloperoxidase, além de, análise macroscópica e radiográfica dos espécimes de cada animal. Foram utilizados 128 ratos machos Wistar divididos em 4 grupos de 32 ratos, sendo: Grupo I controle; Grupo II diabético; Grupo III controle com doença periodontal induzida e Grupo IV diabético com doença periodontal induzida. Após dois dias da confirmação do estado diabético induzido por estreptozotocina, foi realizada a colocação da ligadura. Oito animais de cada grupo foram sacrificados nos períodos experimentais de 3, 7, 15 e 30 dias após colocação da ligadura. Os resultados demonstraram que o estado diabético perdurou até o final do experimento nos grupos II e IV. Dentre os marcadores bioquímicos, somente a ALP apresentou-se estatisticamente maior nos grupos diabéticos (II e IV). Macroscopicamente, houve diferença somente entre os grupos com e sem doença periodontal, independente da presença do diabetes, com maior alteração tecidual nos períodos tardios de periodontite (30 dias). Os níveis gengivais de MPO foram estatisticamente maiores (p<0.05) nos grupos com doença periodontal induzida (III e IV). Radiograficamente, o grupo IV apresentou maior perda óssea estatisticamente significante quando comparada aos demais grupos (p<0,05). Nos limites deste estudo, pode-se concluir que a doença periodontal induzida não alterou o estado hiperglicêmico, no entanto, sugere-se que o diabetes acentue... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Evidences suggest the existence of a positive correlation between diabetes mellitus and periodontal collapse. In order to evaluate the influence of Diabetes Mellitus on the progression of periodontal disease induced in rats, the objective of the present study was to verify glycemic, calcium, phosphorus and alkaline phosphatase serum levels, to evaluate myeloperoxidase (MPO) gingival levels, as well as to carry out macroscopic and radiographic assessment of the animals' hemimandíbulas of experimental periodontitis. A hundred twenty-eight Wistar male rats were used in this study. They were divided into 4 groups of 32 rats each, as follows: Group I - control; Group II - diabetic; Group III - control with periodontal disease induced; and Group IV - diabetic with periodontal disease induced. After streptozotocin diabetic state was confirmed, a ligature was placed on the mandibular first molar teeth of Groups III and IV rats. Eight animals of each group were killed at the experimental periods of 3, 7, 15 and 30 days after the ligature placement. Results demonstrated that the diabetic state lasted up to the end of the experiment at groups II and IV. Significant increases in serum alkaline phosphatase were observed at diabetic groups (II and IV). Macroscopically, in the groups where periodontal disease was induced, it was possible to observe more tissue alterations and it was higher in the 30-day experimental period. The MPO levels were significantly higher in induced periodontitis groups (III and IV) (p<0.05). Radiographically, diabetic with experimental periodontitis group (IV) showed statistically higher bone loss in all the experimental periods (p<0.05). It is possible to conclude that induced periodontal disease did not change the diabetic state... (Complete abstract, click electronic address below)
Orientador: Denise Madalena Palomari Spolidorio
Coorientador: Andréa Gonçalves
Banca: Benedicto Egbert Correa de Toledo
Banca: Elizabeth Pimentel Roseti
Mestre
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50

Trent, Cassandra Robyn. "Culture independent analysis of greyback canegrub-associated microflora and microbial community comparison using subtractive hybridisation". Thesis, Queensland University of Technology, 2010. https://eprints.qut.edu.au/33289/1/Cassandra_Trent_Thesis.pdf.

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Greyback canegrubs cost the Australian sugarcane industry around $13 million per annum in damage and control. A novel and cost effective biocontrol bacterium could play an important role in the integrated pest management program currently in place to reduce damage and control associated costs. During the course of this project, terminal restriction fragment length polymorphism (TRFLP), 16-S rDNA cloning, suppressive subtractive hybridisation (SSH) and entomopathogen-specific PCR screening were used to investigate the little studied canegrub-associated microflora in an attempt to discover novel pathogens from putatively-diseased specimens. Microflora associated with these soil-dwelling insects was found to be both highly diverse and divergent between individual specimens. Dominant members detected in live specimens were predominantly from taxa of known insect symbionts while dominant sequences amplified from dead grubs were homologous to putativelysaprophytic bacteria and bacteria able to grow during refrigeration. A number of entomopathogenic bacteria were identified such as Photorhabdus luminescens and Pseudomonas fluorescens. Dead canegrubs prior to decomposition need to be analysed if these bacteria are to be isolated. Novel strategies to enrich putative pathogen-associated sequences (SSH and PCR screening) were shown to be promising approaches for pathogen discovery and the investigation of canegrubsassociated microflora. However, due to inter- and intra-grub-associated community diversity, dead grub decomposition and PCR-specific methodological limitations (PCR bias, primer specificity, BLAST database restrictions, 16-S gene copy number and heterogeneity), recommendations have been made to improve the efficiency of such techniques. Improved specimen collection procedures and utilisation of emerging high-throughput sequencing technologies may be required to examine these complex communities in more detail. This is the first study to perform a whole-grub analysis and comparison of greyback canegrub-associated microbial communities. This work also describes the development of a novel V3-PCR based SSH technique. This was the first SSH technique to use V3-PCR products as a starting material and specifically compare bacterial species present in a complex community.
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