Дисертації з теми "Muscles Metabolism Animal models"
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Kump, David S. "Physical inactivity induced dysregulation of skeletal muscle and adipose tissue metabolism." Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/4154.
Повний текст джерелаThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2005" Includes bibliographical references.
Andersen, Ditte K. "The role of microRNAs in skeletal muscle insulin resistance." Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701676.
Повний текст джерелаBrenner, Eiliv. "Glutamate related metabolism in animal models of schizophrenia." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for nevromedisin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-13875.
Повний текст джерелаGlutamat-relatert metabolisme i dyremodeller for schizofreni Schizofreni er en alvorlig psykisk lidelse som preges av psykotiske symptomer som vrangforestillinger, hallusinasjoner og andre symptomer som sosial tilbaketrekning og svekket sosial fungering. Epidemiologiske studier har vist at livstidsrisikoen er 0,5-1% i det meste av verdens befolkning. Etiologien og patofysiologien til schizofreni er ikke kjent. De to viktigste patofysiologiske teoriene for schizofreni har vart den såkalte dopaminteorien og glutamatteorien. Disse predikerer henholdsvis økt aktivitet i dopaminerge systemer og redusert aktivitet i visse glutamaterge systemer. Resultater fra studier i den senere tid tyder også på at det finnes forandringer i cytoskjellettet ved schizofreni, for eksempel i mikrotubuliassosierte proteiner. De fleste schizofrenisymptomer er unike for menneskelig atferd. Å kunne reprodusere schizofreni i en dyremodell er derfor vanskelig. Dyremodeller er likevel et viktig verktøy for a identifisere patofysiologiske mekanismener bak schizofreni, og for a komme fram til nye medisiner. Denne avhandlingen inneholder fire publikasjoner hvor vi studerte dyremodeller for schizofreni. I tre av dem ble NMDA-reseptorantagonisten MK-801 brukt til a redusere glutamaterg nevrotransmisjon i rotter. Tre forskjellige forsøksoppsett ble brukt: En enkelt injeksjon av en høy dose MK-801, daglige injeksjoner med høy konsentrasjon i til sammen seks dager, og daglige injeksjoner med en lavere dose MK-801 i seks dager. Den fjerde studien beskriver glutamatrelatert metabolisme ved ustabile mikrotubili. Dette gjorde vi ved å undersøke ”knock out” mus hvor genet for det mikrotubiliassosierte proteinet STOP (Stable Tubule Only Peptide) var satt ut av funksjon. Vi undersøkte glutamatrelatert metabolisme i alle disse modellene. Hjerneekstrakter fra flere hjerneomrader ble analysert med HPLC (High Performance Liquid Chromatography), 13C- og1H-magnetisk resonansspektroskopi. Ved a injisere 1-13 C merket glukose og 1,2- 13 C merket acetat kunne vi se forskjell pa nevron- og astrocyttmetabolisme. En enkelt dose med 0,5 mg/kg kroppsvekt MK-801 skapte flest metabolske forskjeller i temporal lappen. Her var det okte totale mengder av glutamat og glutamin, og dessuten okt innmerkning fra [1-13C]glukose. Vi så liknende forskjeller da vi injiserte 0,1 mg/kg MK-801 i flere påfølgende dager. Da rottene derimot ble injisert med 0,5 mg/ MK-801, fant vi metabolske forskjeller i cingulate-, retrosplenial- og frontalcortex. Her var det ogsa en økt totalmengde av glutamat, men innmerkning fra bade [1-13C]glukose og [1,2-13C]acetat var redusert i flere metabolitter sammenlignet med kontrolldyrene. Reultater i artikkel 4 viser reduserte mengder av bade totalglutamin og glutamin merket fra [1,2-13C]acetat i cerebrum til STOP ”knock out” mus. Når vi sammenligner resultatene våre med data fra studier av pasienter med schizofreni, ser det ut til at repeterte injeksjoner av en høy dose MK-801, kan vare en god dyremodell for schizofreni i et tidlig stadium. STOP ”knock out” modellen viser lignende metabolske forskjeller som hos pasienter med kronisk schizofreni, og derfor kanskje en god dyremodell for mer langtkommen schizofreni. Resultatene fra studiene i denne oppgaven viser at både blokkering av NMDA-reseptoren og ustabile mikrotubili, forstyrrer glutamatglutamin syklus, og det er fristende a påstå at interaksjonen mellom astrocytter og nevroner er undervurdert i schizofreniforskning.
Ling, Zong-Chao. "Islet glucose metabolism and insulin release in two animal models of glucose intolerance /." Stockholm, 1999. http://diss.kib.ki.se/1999/19990517ling/.
Повний текст джерелаChisholm, Jeffrey W. "Abnormal lipoprotein metabolism in animal models of intrahepatic cholestasis induced by Ã-naphthylisothiocyanate." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24769.pdf.
Повний текст джерелаTakemura, Ai. "Effects of exposure to mild hyperbaric oxygen on metabolism-related diseases in animal models." Kyoto University, 2019. http://hdl.handle.net/2433/242722.
Повний текст джерела0048
新制・課程博士
博士(人間・環境学)
甲第21845号
人博第874号
新制||人||210(附属図書館)
2018||人博||874(吉田南総合図書館)
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)教授 石原 昭彦, 教授 久代 恵介, 教授 神﨑 素樹
学位規則第4条第1項該当
Abass, K. M. (Khaled M. ). "Metabolism and interactions of pesticides in human and animal in vitro hepatic models." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514262999.
Повний текст джерелаAbolghasemi, Armita. "Lipid mediators as regulators of lipid and energy metabolism during energy balance derangement in animal models." Doctoral thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/67011.
Повний текст джерелаLes facteurs environnementaux jouent un rôle clé dans le développement du syndrome métabolique et de l'obésité, qui sont maintenant de véritables épidémies soulevant des problèmes de santé publique. Les excès de graisse corporelle dans l'obésité et la perte de masse grasse et maigre dans les conditions de dénutrition ou d'anorexie mentale sont le résultat d'un déséquilibre énergétique. Par conséquent, le maintien de l'équilibre énergétique est crucial à la fois pour la prévention de l'obésité et pour le traitement de l'anorexie mentale et d'autres formes de dénutrition. Les signaux lipidiques tels que ceux médiés par les médiateurs des endocannabinoidomes sont profondément impliqués dans le contrôle du métabolisme énergétique. Dans cette thèse, au sein de deux projets différents, nous avons étudié comment différents facteurs environnementaux, y compris la restriction calorique, l'activité physique, la supplémentation en vitamine D et les médicaments antipsychotiques, peuvent conduire à une modification du métabolisme énergétique par la modulation de la signalisation des endocannabinoïdomes. Les résultats des travaux expérimentaux montrent comment les différentes conditions étudiées provoquent des changements dans les niveaux tissulaires du médiateur lipidique endocannabinoïdome ainsi que dans l'expression de leurs récepteurs et enzymes métaboliques, ce qui peut contribuer aux changements observés de la masse grasse corporelle et du métabolisme énergétique au sein des modèles. Nous concluons que les conditions étudiées peuvent provoquer des changements dans le bilan énergétique par altération de l'endocannabinoidome.
Environmental factors play a key role in the development of obesity-induced metabolic syndrome and obesity, which are now true epidemics raising public health concerns. Both excess body fat in obesity, and fat and lean mass loss in undernutrition conditions or anorexia nervosa, are the result of energy imbalance. Therefore, maintaining energy balance is crucial for both the prevention of obesity and the treatment of anorexia nervosa and other forms of undernutrition. Lipid signals such as those mediated by endocannabinoidome mediators are deeply involved in the control of energy metabolism. In this thesis, within two different projects, we studied how different environmental factors including calorie restriction, physical activity, vitamin D supplementation and antipsychotic drugs, may lead to energy metabolism modification through modulation of the endocannabinoidome signaling. The results of the experimental work show how the different studied conditions cause changes in the tissue levels of endocannabinoidome lipid mediator as well as in the expression of their receptors and metabolic enzymes, which may contribute to the observed changes in body fat mass and energy metabolism within the models. We conclude that the investigated conditions may cause changes in energy balance through alteration of the endocannabinoidome.
Glenn, L. Lee, and Brad G. Samojla. "A Critical Reexamination of the Morphology, Neurovasculature, and Fiber Architecture of Knee Extensor Muscles in Animal Models and Humans." Digital Commons @ East Tennessee State University, 2002. https://dc.etsu.edu/etsu-works/7526.
Повний текст джерелаNg, Kit-ying, and 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.
Повний текст джерелаMullins, Chad Ryan. "Feeding behavior and metabolism of transition dairy cows supplemented with monensin." Diss., Kansas State University, 2011. http://hdl.handle.net/2097/13102.
Повний текст джерелаDepartment of Animal Sciences and Industry
Barry J. Bradford
The mechanisms behind the metabolic changes observed when transition cows are administered monensin, as well as the effects of supplementing mid-lactation cows with two commercial amino acid products were investigated. Traditionally, the effects of monensin are attributed to increased gluconeogenic precursor supply, but recent research indicated that the effects of monensin extend beyond gluconeogenic flux. Thus, the primary objectives of Experiment 1 were to determine if monensin modulates transition cow feeding behavior, ruminal pH, and/or expression of key metabolic genes. Overall, monensin decreased time between meals prepartum (126 vs. 143 ± 5.0 min; P < 0.03) with a trend appearing postpartum (81.4 vs. 88.8 ± 2.9 min; P < 0.08), which could be related to the smaller ruminal pH standard deviation during the first day cows received the lactation ration (0.31 vs. 0.26 ± 0.015; P < 0.02). Monensin also increased liver mRNA abundance of carnitine palmitoyltransferase 1a (0.15 vs. 0.10 ± 0.002 arbitrary units; P < 0.04), which corresponded to a slower rate of liver triglyceride (TG) accumulation from 7 days before calving through 7 days post calving (412 vs. 128 ± 83 mg TG/g protein over this time period; P = 0.03). No significant effects of monensin supplementation were observed on other metabolic parameters or milk production. Overall, these results confirm that the effects of monensin on transition cows extend beyond altered propionate flux. In Experiment 2, mid-lactation cows consuming a control diet containing 26% wet corn gluten feed (dry matter basis) were compared to cows consuming the same diet supplemented with lysine embedded within Ca salts of fatty acids and the isopropyl ester of 2-hydroxy-4-(methylthio) butanoic acid, a methionine precursor. This trial was conducted because the NRC (2001) model indicated a lysine deficiency prior to supplementation; however amino acid supplementation had no effects. This trial was then extended to decrease dietary CP from 17.9% to 17.1%, and further increase lysine and methionine supply in the treatment diet. No production or intake effects were observed during this period, but MUN was decreased in the treated group (10.8 vs. 12.5 ± 0.2 mg/dL; P < 0.001).
Kohn, Tertius A. "Characteristics and adaptation of skeletal muscle to endurance exercise." Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/16517.
Повний текст джерелаENGLISH ABSTRACT: Skeletal muscle adapts to stimuli by modifying structural and metabolic protein expression. Furthermore, a muscle group may vary within itself to accommodate specialisation in regions. Structural and metabolic characteristics of an individual are regulated partly by genotype, but contraction duration and intensity may play a greater role in muscle phenotype. The aims of this dissertation were to investigate: structural and metabolic regionalisation in a muscle group, possible relationships between training volume and intensity and hybrid fibres, muscle characteristics of athletes from two different ethnic groups, and muscle adaptation in already well-trained athletes subjected to high intensity interval training. Myosin heavy chain (MHC) isoform content and citrate synthase (CS) activities were measured in the Quadriceps femoris (QF) muscle of 18 female rats. Muscle was divided into superficial, middle and deep, distal, central and proximal parts. MHC IIb and IIx were more abundant in superficial regions (P < 0.05) with low CS activities compared to deeper parts. Isoform content varied along the length of deep regions. This study showed that the QF has regional specialisation. Therefore, standardisation of sampling site is important. Hybrid fibre proportions in muscle biopsies of 12 middle distance runners and 12 non-runners were investigated. MHC IIa/IIx correlated with training volume/week in runners (r = -0.66, P < 0.05) and MHC IIa/IIx correlated with exercise hours/week in non-runners (r = -0.72, P < 0.01). Average preferred racing distance (PRDA) correlated better with MHC IIa/IIx in runners (r = -0.85, P < 0.001). MHC IIa/IIx may therefore be more closely related to exercise intensity than previously thought. Fibre type characteristics and performance markers were investigated in 13 Xhosa and 13 Caucasian distance runners, matched for performance, training volume and PRDA. Xhosa runners had less MHC I and more MHC IIa fibres in muscle biopsies than Caucasian runners (P < 0.05). Xhosa runners had lower plasma lactate at 80% peak treadmill speed (PTS) (P < 0.05), but higher lactate dehydrogenase (LDH) (P < 0.01) and phosphofructokinase (P = 0.07) activities in homogenate muscle samples. LDH activities in MHC I (P = 0.05) and IIa (P < 0.05) fibre pools were higher in Xhosa runners. Xhosa athletes may thus have a genetic advantage or they may have adapted to running at a higher intensity. Six weeks of individually standardised high intensity interval treadmill training (HIIT) were investigated in 15 well-trained runners. PTS increased after HIIT (P < 0.01), while maximum oxygen consumption (VO2max) only showed a tendency to have increased as a result of HIIT (P = 0.06). Sub-maximal tests showed lower plasma lactate at 64% PTS (P = 0.06), with lower heart rates at workloads from 64% to 80% PTS (P < 0.01) after HIIT. No changes were observed for cross-sectional area, capillary supply and enzyme activities in homogenates muscle samples. LDH activity showed a trend (P = 0.06) to have increased in MHC IIa pools after HIIT. Higher HIIT speed was related to decreases in MHC I fibres, but increases in MHC IIa/IIx fibres (r = -0.70 and r = 0.68, respectively, P < 0.05). Therefore, HIIT may alter muscle fibre composition in well-trained runners, with a concomitant improvement in performance markers.
AFRIKAANSE OPSOMMING: Skeletspier kan adapteer deur strukturele en metaboliese protein ekspressie te verander as gevolg van stimulante. ‘n Spiergroep kan ook intern verskil om spesialisering in spierdele toe te laat. Strukturele en metaboliese karaktereienskappe van ‘n individu word deels gereguleer deur gene, maar kontraksie tydperk en intensiteit mag ‘n groter rol speel in spierfenotipe. Die doelwitte van hierdie tesis was om ondersoek in te stel in: strukturele en metaboliese eienskappe in spiergroepstreke, moontlike verhoudings tussen oefeningsvolume of intensiteit en baster vesels, spier eienskappe in atlete van twee etniese groepe, en spier adaptasie in goed geoefende atlete blootgestel aan hoë intensiteit interval oefening. Miosien swaar ketting (MSK) isovorm inhoud en sitraat sintase (SS) aktiwiteite is gemeet in die Quadriceps femoris (QF) spier van 18 wyfie rotte. Spiere was opgedeel in oppervlakkig, middel en diep, asook distaal, sentraal en proksimale dele. MSK IIb en IIx was meer oorvloedig in oppervlakkige dele (P < 0.05) met lae SS aktiwiteite in vergelyking met dieper dele. Isovorm inhoud het ook verskil oor die lengte van diep dele. Dus bevat die QF gespesialiseerde streke en is die area van monsterneming belangrik. Baster vesel proporsies is ondersoek in spiermonsters van 12 middel afstand hardlopers en 12 niehardlopers. MSK IIa/IIx van hardlopers het met oefeningsvolume/week gekorreleer (r = -0.66, P < 0.05), asook MSK IIa/IIx van nie-hardlopers met oefeningsure/week (r = -0.72, P < 0.01). Gemiddelde voorkeur wedloop afstand (VWAG) het beter met MSK IIa/IIx gekorreleer in hardlopers (r = -0.85, P < 0.001). MSK IIa/IIx mag dus meer verwant wees aan oefeningsintensiteit. Veseltipe eienskappe en prestasie merkers was ondersoek in 13 Xhosa en 13 Caucasian langafstand atlete, geëweknie vir prestasie, oefeningsvolume en VMAG. Xhosa hardlopers het minder tipe I en meer tipe IIA vesels in hul spiermonsters gehad as die Caucasian hardlopers (P < 0.05). Xhosa hardlopers het laer plasma laktaat by 80% van hul maksimale trapmeul spoed (MTS) (P < 0.05), maar hoër laktaat dihidrogenase (LDH) (P < 0.01) en fosfofruktokinase (P = 0.07) aktiwiteite in homogene spiermonsters gehad. LDH aktiwiteite in MSK I (P = 0.05) en IIa (P < 0.05) veselbondels was hoër in Xhosa hardlopers. Xhosa atlete mag dus ‘n genetiese voorsprong geniet, of hulle het geadapteer om by hoër intensiteite te hardloop. Ses weke van geïndividualiseerde gestandardiseerde hoë intensiteit interval trapmeul oefening (HIIT) was ondersoek in 15 goed geoefende hardlopers. MTS het verhoog na HIIT (P < 0.01), en maksimale surrstof verbruik (VO2max) het ‘n neiging getoon om te verhoog het na HIIT (P = 0.07). Submaksimale toetse het laer plasma laktaat by 64% MTS getoon (P = 0.06), met laer harttempos by werkladings 64% tot 80% MTS (P < 0.01). Geen veranderings was gemerk vir deursnit area, kapillêre toevoer en ensiem aktiwiteite in homogene spiermonsters nie. LDH aktiwiteit het ‘n neiging getoon om te verhoog het (P = 0.06) in MSK IIa veselbondels na HIIT. Hoër HIIT snelhede was verwant aan ‘n daling in MSK I vesels, maar ‘n verhoging in MSK IIa/IIx vesels (r = -0.70 en r = 0.68, respektiwelik, P < 0.05). HIIT mag dus spier veseltipe verander in goed geoefende hardlopers, met gevolglike verbetering in prestasie merkers.
Schwartz, Robert A. "In vivo evaluation of the D¦1 agonist PET ligand R-[¹¹C]SKF 82957, metabolism and regional brain distribution in animal models and humans." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0002/MQ45555.pdf.
Повний текст джерелаKitami, Toshimori. "GENETIC, EVOLUTIONARY, AND GENOMIC ANALYSIS OF HOMOCYSTEINE AND FOLATE PATHWAY REGULATION." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1127865525.
Повний текст джерелаClark, Catherine Renee. "Thyroid hormone influence on oxygen consumption rates, body mass, and lipid metabolism in mice with noninsulin dependent diabetes mellitus." CSUSB ScholarWorks, 1995. https://scholarworks.lib.csusb.edu/etd-project/1025.
Повний текст джерелаKalousek, A. Kay. "The effect of intraperitoneally administered thyroxine, thiidothyronine and iopanoic acid on the in vivo and in vitro oxygen consumption rates of normal (C57BL/KsJ DB/M) and diabetic (C57BL/KsJ DB/DB) mice." CSUSB ScholarWorks, 1986. https://scholarworks.lib.csusb.edu/etd-project/363.
Повний текст джерелаOlivares, Morales Andres. "Prediction of oral drug bioavailability : from animal-based extrapolation towards the application of physiologically-based pharmacokinetic modelling and simulation." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/prediction-of-oral-drug-bioavailability-from-animalbased-extrapolation-towards-the-application-of-physiologicallybased-pharmacokinetic-modelling-and-simulation(9a6e9a95-1727-4f06-829d-a96f763fd8c9).html.
Повний текст джерелаTavares, Leandro Reis. "A ação do digital na fibrose miocárdica em modelo experimental." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-23032011-174637/.
Повний текст джерелаRecent studies on myocardial dysfunction are highlighting the therapeutic potential of the myocardial extracellular matrix management. Its interesting to highlight the importance of the dynamics of the cardiac extracellular matrix, because even the systolic and diastolic functions are implicated on it. Other studies showed that digital compounds may regulates the neuroendocrin misbalance due to myocardial impairment and influencing these systems the digital compounds may regulates the interstitial collagen deposition. Objective: To evaluate the role of the digital on a myocardial fibrosis in an experimental model, examining if the digital is able to prevent the collagen deposition. Methods: The sample was divided in 20 rats from the control group (CG); 20 rats submitted to a fibrosis experimental model in which the rats are uninefrectomized, drink water with 1% NaCl during the protocol and receive aldosterone through an osmotic minipump (AG); and 20 rats submitted to the same experimental model treated with digitoxin in a daily dose of 100 g/Kg (DAG). Results: The interstitial and perivascular collagen volume fraction showed a significant difference between the AG and the other 2 groups (CG and DAG). The myocardial performance index showed a significant difference between the AG (0.49 ± 0.08) and the CG (0.32 ± 0.06) and the DAG (0.40 ± 0.13) (p=0.001). The BNP levels showed a significant difference between the AG (1.07 ± 0.32 ng/ml) and the CG (0.75 ± 0.19 ng/ml) and the DAG (0.84 ± 0.21 ng/ml) (p=0.01). The metalloproteinases levels did not differ among the groups and there was a positive correlation between the shortening fraction and the BNP levels among the GAD animals. Conclusion: These data demonstrate the digitoxin positive effect on the myocardial collagen deposition in this experimental model of interstitial fibrosis and could have a new therapeutic target previously unexplored
Franceschi, Ruben Carvalho. "Avaliação hemodinâmica, metabólica e do transporte de oxigênio durante anestesia com xenônio em cães hipovolêmicos." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-16102014-142317/.
Повний текст джерелаRationale and objectives - Anesthesia induction in subjects with hypovolemic shock may worsen a baseline hemodynamic instability. Xenon (Xe), an inhalation anesthetics, is an inactive gas with properties that, in normal subjects, maintain hemodynamic stability during anesthesia. The aim of this study was to assess Xe effects on hemodynamics, metabolism, and oxygen delivery during anesthesia in dogs with induced hypovolemic shock. Method - Twenty-one hybrid dogs were submitted to hypnosis and muscle relaxation by continuous venous infusion of etomidate and vecuronium and mechanichal controlled ventilation with a 21% FiO2 (oxigen + compressed air). Under local anesthesia, catheters were introduced into the pulmonary artery for hemodynamic monitoring, and in the left and right femoral arteries for mean arterial blood pressure measurements and hypovolemic shock induction. After induction of an hemorrhagic shock until a mean arterial blood pressure of 40mmHg for 2 minutes was reached, the animals were randomized into the Xenon or the control group. Dogs from the Xenon group received controlled mechanichal ventilation with a 21% FiO2 + 79% Xe for 20 minutes. Blood samples were collected for arterial e mixed venous gas analyses; hemodynamic data were also collected, with further hemodynamic calculation of O2 delivery before shock induction, immediately after the artificial bleeding, 5 min and 20 minutes after starting Xe administration, and 20 minutes after stopping Xe. The control group was submitted to the same procedures, without Xe administration. Both groups were compared using variance analysis for repeated measurements, considering statistical significance where a p<0,05 was reached. Results: Both groups were comparable in terms of mean body weight values and bleeding volume. Hemodynamic and metabolic variables and oxygen delviery had no significant differences between both groups, control and Xenon. In the Xenon group, after shock was induced, heart rate changed from 130.22 ± 20.57 to 131.89 ± 24.34 after 5 minutes, and to 138.44 ± 33.66 after 20 minutes. In the control group, heart rate varied from 144.33 ± 21.03 to 143.75 ± 22.58 after 5 minutes (p=0.82), and to 149.50 ± 23.52 after 20 minutes (p=0.16). Conclusion: Xenon administration does not cause changes in hemodynamics, metabolism, and oxygen delivery in dogs with induced hypovolemic shock, supporting its recommendation as a safe anesthetic in such conditions
Ways, Justin Andrew. "An Inbred Rat Model of Exercise Capacity: The Path to Identifying Alleles Regulating Variation in Treadmill Running Performance and Associated Phenotypes." Connect to full text in OhioLINK ETD Center, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1201562803.
Повний текст джерела"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. 142-183.
Pereira, Adriano José. "Gradientes de oxigênio, glicose, dióxido de carbono e lactato em diferentes compartimentos vasculares." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-27102011-160323/.
Повний текст джерелаINTRODUCTION: Despite of the widespread use of the central venous oxygen saturation measurement as a therapeutic goal in critically ill patients, absolute differences between this measurement and the mixed venous oxygen exist. Causes of these differences, as well the behavior of these gradients in critical illness, are not completely understood. Considering current therapeutic interventions aimed to reverse tissue oxygenation impairment are mediated by increases in cardiac output; the particular scenario in which the heart is not physiologically able to further increase oxygen extraction and the absence of tools to monitoring the myocardium impact of those interventions, the present study, facing the theoretical possibility of the coronary sinus effluent participation in those central to mixed venous differences, has analyzed the oxygen saturation (SO2), carbon dioxide partial pressure (PCO2), lactate and glucose concentrations behaviors over time, in different models of tissue hypoxia and in different vascular sites. Emphasis on the myocardial energetic metabolism and its impact over central to mixed venous gradients was placed. METHODS: 37 pigs, males, weighting about 35 Kg, sedated and mechanically ventilated, were studied after induction of four different hypoxic injury models (sepsis, and anemic, stagnant, hypoxic hypoxia), eight for group and five controls. In addition to hemodynamic and oxygen variables, SO2, PCO2, lactate and glucose were measured in different phases, in 9 distinct vascular sites, including coronary sinus (femoral artery, inferior and superior vena cava, right atria, right ventricle, pulmonary artery, right suprahepatic vein and portal vein). MAIN RESULTS: Concentrations of O2, lactate and glucose in the coronary sinus effluent presented distinctive patterns among groups: shift from lactate to glucose consumption in hypoxic hypoxia and anemic hypoxia groups, increase in both glucose and lactate consumption in sepsis and absence of clear trend in stagnant hypoxia group. PCO2 gradients from systemic artery to coronary sinus presented late enlargement trend in all groups. In the regional gradients analysis comparisons, coronary sinus presented the lowest SO2, the lowest lactate concentrations, the highest PCO2 levels, and these patterns changed over time. Similar evolution trends were observed between central to mixed venous O2, PCO2, lactate and glucose gradients and the same parameters measured in coronary sinus. CONCLUSIONS: Different concentrations of O2, PCO2, lactate and glucose in coronary sinus are related to the type of hypoxic injury and not only to energetic substrate availability. Severity-related patterns, common to all groups in late phases, were identified: any reduction of coronary SO2, shift to glucose consumption, net lactate myocardial production and equality or inferiority of PCO2 levels related to other vascular compartments (independently of trend). Trends in transmyocardial PCO2 gradients followed cardiac output ones and, certainly, should mirror coronary blood flow. Regional gradients analysis showed suitable to explore specific regional metabolic settings, as in the described example of liver metabolism, in which production of glucose were maintained in all phases by this organ in hypoxic hypoxia groups, differently from the impaired production described in literature for sepsis. At last, data from sepsis group have showed: a) as to the previously known central to mixed venous SO2 and lactate gradients, PCO2 and glucose gradients also exist; b) coronary sinus has participated significantly in formation of central to mixed venous lactate, PCO2 and glucose gradients
Tavares, Neuziane Kloos Amorim. "Avaliação das consequências da limitação do tamanho da prole de ratos Wistar ao nascimento sobre seu desenvolvimento ponderal e características morfofuncionais na idade adulta." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-27092013-155436/.
Повний текст джерелаDuring intrauterine life, the developing fetus is susceptible to environmental changes that can alter the phenotype of the individual in postnatal life. This phenomenon is called fetal programming. Events that occur during critical periods of rapid cell division may alter the structure and function of organ systems, resulting in consequences both early (low birth weight) and late (diseases in adulthood) in life. The experimental protocols of most of the studies on fetal programming involve a reduction in litter size soon after birth. This approach hampers the interpretation and reproducibility of the observed results. The purpose of this investigation was to determine if blood pressure, carbohydrate metabolism and energy expenditure in adult offspring are influenced by litter size. Female Wistar rats were fed standard rat chow ad libitum and were mated with male rats at 12 weeks of age. After birth, the offspring were divided into three groups: unchanged litter size (GU), culled to eight neonates (G8) and culled to four neonates (G4). At 12 weeks of age, the body weight; blood pressure; food intake; glucose, insulin, cholesterol and triacylglycerol levels; brown adipose tissue mass; adiposity index; renal mass; and cardiac mass were determined. The body weight, adiposity index, glucose level, insulin level and HOMA index were higher in males and females in the G4 group than in the G8 and GU groups. However, food consumption was lower in G4 males. The blood pressure was higher in the GU group. In summary, a small litter size is related to obesity, possible alterations in energy expenditure and insulin resistance in adult offspring
Roux, Candice Rene. "β-cell response to high fat diet induced metabolic demands in the obese Wistar rat". Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/6454.
Повний текст джерелаENGLISH ABSTRACT: Introduction: A westernized diet rich in saturated fats and sugars, together with a sedentary lifestyle, has contributed to the dramatic increase in obesity during the last decade (Zimmett et al, 2001; Wild et al, 2004). Obesity is associated with dyslipidemia and insulin resistance which are major risk factors for the development of type 2 diabetes (T2D) (Zimmet et al, 2001, Kahn et al, 2006; Schröder et al, 2007). High-fat feeding in rodents induces symptoms similar to the human metabolic syndrome without progression to T2D (Woods et al, 2002; Weir and Bonner-Weir, 2007). The addition of fructose to a high-fat diet exacerbates the insulin resistance and leads to impaired pancreatic function of insulin secretion and glucose intolerance (Basciano et al, 2005; Stanhope et al, 2009). Aims: The aim of this study was to establish the effect of a high-fat and sucrose/fructose diet on glucose metabolism, the development of insulin resistance and β-cell dynamics. Methods: Weanling Wistar rats were randomized into two study groups; study one over an experimental period for three months and study two for twelve months. Each study consisted of a control group that received standard rat chow and water; and two experimental groups receiving either a high-fat diet and water (HFD) or a café diet consisting of HFD with the addition of 15% sucrose/fructose (CFD). Fasting glucose and insulin concentrations, intravenous glucose tolerance test (IVGTT), glucose stimulated insulin secretion rates and 2-deoxy-[3H]-D-glucose uptake in muscle, liver and fat were measured. The pancreata were harvested for immunohistochemical labeling of β-cells (insulin), α-cells (glucagon), GLUT2 (glucose transport) and MIB5 (proliferation). Samples of the pancreata were also collected for electron microscopy. Results and discussion: Feeding Wistar rats a CFD induced obesity, insulin resistance and glucose intolerance. By twelve months the rats had an impaired glucose response with increased IVGTT peak values, area under the curve (AUC) values and glucose clearance rates. Concomitantly, the glucose stimulated insulin secretion rate (GS-ISR) was attenuated. Stimulated glucose disposal as measured by 2-deoxy-[3H]-D-glucose uptake was reduced in muscle and adipose tissue at three months. By twelve months, due to the age of the rats, stimulated glucose uptake declined compared to three months with no difference between groups. After three months the diets had no observable effect on the islets using light microscopy. However, by twelve months morphological changes were observed in both the HFD and CFD groups. In the HFD group large hypertrophied irregular islets with fibrous changes were observed. In the CFD group these morphological changes were more prominent with fibrous segregation and disruption of the normal endocrine arrangement. In addition, the presence of inflammatory cells within the affected islets is consistent with T2D. Conclusion: High-fat diet fed to Wistar rats induced obesity, abdominal adiposity and insulin resistance. The addition of sucrose/fructose to a high-fat diet exacerbated the insulin resistance and resulted in glucose intolerance and mild hyperglycemia. Morphological changes in the large islets were observed which are consistent with the development of T2D.
AFRIKAANSE OPSOMMING: Inleiding: ‘n Verwesterde dieët, ryk aan versadigde vette en suikers tesame met 'n passiewe lewenstyl, het bygedra tot die dramatiese verhoging in vetsug gedurende die laaste dekade (Zimmett et al, 2001; Wild et al, 2004). Vetsug word met dislipidemie en insulienweerstandigheid geassosieer wat hoof risikofaktore is vir die ontwikkeling van tipe 2 diabetes (T2D) (Zimmet et al, 2001; Kahn et al, 2006; Schröder et al, 2007). Hoë-vet voeding in knaagdiere induseer simptome soortgelyk aan menslike metaboliese sindroom sonder die ontwikkeling van T2D (Woods et al, 2002; Weir and Bonner-Weir, 2007). Die byvoeging van fruktose tot 'n hoë-vet dieët vererger insulienweerstandigheid en lei tot verswakte pankreas funksie, insuliensekresie en glukoseintoleransie (Basciano et al, 2005; Stanhope et al, 2009). Doelwitte: Die doelwitte van die studie was om die effek van hoë-vet en sukrose/fruktose voeding op glukosemetabolisme, die ontwikkeling van insulienweerstandigheid en β-sel dinamika te bepaal. Metodes: Gespeende Wistar rotte was in twee groepe gerandomiseer; studie een oor ʼn tydperk van drie maande en studie twee oor ʼn tydperk van twaalf maande onderskeidelik. Elke studie het 'n kontrole groep met standaard rot kos en water (control); en twee experimentele diëte wat of ʼn hoë-vet dieët en water (HFD) of 'n kafeedieët groep wat die HFD met die byvoeging van 15% sukrose/fruktose in hul drink water (CFD) ontvang. Fastende glukose en insulien, binneaarse glukose toleransie toets (IVGTT), glukose gestimuleerde insulien sekresie tempo en 2-deoxi-[3H]-D-glukose opname in spier, lewer en vet is gebruik om die effek van die dieët op glukosemetabolisme te bepaal. Die pankreata is uitgehaal vir immunohistochemiese identifisering van β-selle (insulien), α-selle (glukagoon), GLUT2 (glukose transport) en MIB5 (proliferasie). Monsters van die pankreata was ook vir elektronmikroskopie versamel. Resultate en bespreking: Voeding van ʼn CFD aan Wistar rotte induseer vetsug, insulienweerstandigheid en glukose-intoleransie Teen twaalf maande toon die rotte 'n verswakte respons tot glukose met verhoogde IVGTT piekwaardes, AUC waardes en glukose opruimingswaardes. Terselfdetyd is die glukose gestimuleerde insuliensekresie tempo (GS-ISR) ook verswak. Gestimuleerde glukose opruiming, soos deur 2-deoxi-[3H]-D-glukose opname bepaal, was verlaag in spier en vetweefsel teen drie maande. Teen twaalf maande, weens die ouderdom van die rotte, is die gestimuleerde glukose opname verlaag in vergelyking met drie maande sonder 'n verskil tussen groepe. Na drie maande kon geen sigbare morfologiese verskille met ligmikroskopie tussen die diëte waargeneem word nie. Teen twaalf maande is morfologiese verskille waargeneem in beide die HFD en die CFD groepe. In die HFD groep is groot hipertrofiese onreëlmatige eilande met fibrotiese verandering waargeneem. In die CFD groep was die morfologiese verandering meer gevorder met fibrotiese onderverdeling en ontwrigting van die normale endokriene rangskikking. Die teenwoordigheid van inflammatoriese selle in die geaffekteerde eilande is verenigbaar met T2D. Afleiding: Die voer van 'n hoë-vet dieët aan Wistar rotte veroorsaak vetsug, abdominale adipositeit en insulienweerstandigheid. Die byvoeging van sukrose/ fruktose tot die hoë-vet dieët vererger die insulienweerstandigheid en veroorsaak glukoseintoleransie en matige hiperglukemie. Morfologiese veranderings in die groter eilande was verenigbaar met T2D.
Salmon, Benjamin. "ASARM et biominéralisation de progéniteurs pulpaires." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T072.
Повний текст джерелаIn X-linked familial hypophosphatemic rickets (XLH), MEPE (Matrix Extracellular PhosphoglycoprotEin) is cleaved, releasing phosphorylated ASARM (acidic serine- and aspartate- rich motif) peptides that inhibit mineralization of bone extracellular matrix (ECM), and renal tubular phosphate reabsorption. We recently identified high levels of MEPE-derived ASARM peptides in human XLH dentin. The present study was aimed to investigate their effects on dentin mineralization in order to better understand their role in the etiology of tooth abnormalities observed in XLH patients. Dental pulp stem cells derived from deciduous teeth (SHEDs) were seeded in a collagen scaffold, cultured in human tooth slices under mineralizing conditions as a control, and with 20 µM of either phosphorylated (p-ASARM) or non-phosphorylated (np-ASARM) MEPE-derived ASARM peptides. Mineralization was assessed by scanning electron microscopy and von Kossa staining. Odontogenic markers (DSPP, osteocalcin, MEPE) were assessed by immunohistochemistry, RT-PCR and Western blot. In parallel, agarose beads soaked with recombinant ASARM peptides were implanted in a rat pulp injury model where a reparative dentin bridge is spontaneously formed; the repair process was evaluated by micro-CT and IHC. In the tooth slice culture model, p-ASARM inhibited SHED differentiation, with 1) no formation of mineralization nodule, 2) decreased odontogenic marker expression, and 3) up-regulation of MEPE expression, in contrast with np-ASARM and control. In the rat pulp injury model, p-ASARM impaired the formation of the reparative dentin bridge and increased MEPE expression. The present data support our hypothesis that p-ASARM impairs odontogenic differentiation process and the resulting mineralization of dentin. Moreover, the identification of a stimulating effect of p-ASARM on MEPE expression suggests a positive feedback loop in the pathogenicity of XLH disease. Accordingly, the mineralized defects in XLH tooth dentin may be a direct consequence of the release of ASARM peptides in the ECM
Abad, César Cavinato Cal. "Efeitos do treinamento físico contínuo ou intervalado em um modelo experimental de dislipidemia e isquemia miocárdica." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16092013-161614/.
Повний текст джерелаMyocardial infarction (MI) is a major cause of death and disability worldwide. The use of experimental animals has supported to better understand the pathophysiology and treatment forms of myocardial infarction (MI). Knowing that the dyslipidemia associated with IM and that physical training can be prescribed for prevention and treatment of cardiovascular diseases, the present study investigated the effects of two types of physical training on an experimental model of dyslipidemia and myocardial ischemia. Wild mice (WT) and LDL receptor knockout (LDL-/- ) were divided into eight groups: a) LDLr-/- sedentary (LDL-S), b) LDLr-/- myocardium infarction sedentary (LDL-MI-S), c) LDLr-/- myocardium infarction submitted to continuous training (LDL-MI-C), d) LDLr-/- myocardium infarction submitted to interval training (LDLMI- I), e) sedentary WT (WT-S); f) WT myocardium infarction sedentary (WT-MI-S); g) WT myocardium infarction submitted to continuous training (WT-MI-C), h) WT myocardium infarction submitted to interval training (WT-IM-I). After 60 days of descending coronary artery ligation, the continuous training consisted of running at 60% of maximum, while the interval training consisted of eight sprints of 4 min at 80% of maximum and a 4 min recovery at 40% of maximum. In infarcted WT animals, both training programs increased exercise tolerance and promoted decrease of sympathetic-vagal balance and increase of alpha index in similar magnitudes. Nevertheless, the interval training reduced the number of type II fibers in infarcted WT animals compared to WT-S and WT-MI-C groups, as well as reduced the amount of fiber type II-X compared to WT-S. The cross-sectional area of the fiber type I was higher in the WTMI- I animals than in WT-MI-S and S-WT groups. The reason capillary/fiber was higher in group WT-I than in the WT-S. Ejection fraction and shortening fraction were lower in LDL-MII compared to the others, but with no differences among the WT-S, WT-IMI-C and WT-MI-I groups. About the LDL-/- animals, the LDL was higher and VLDL was lower in the group LDL-MI-C in relation to the others. The HDLtg (%) was higher in LDL-C compared to LDL-S. The HDLc (mg and %) of LDL-MI-I was higher than the LDL-MI-C group, and the HDLc (mg) of LDL-MI-I was even higher than LDL-S group. The total triglycerides was lower in LDL- MIC than in LDL-S animals. Only in LDL-MI-I group the resting HR was decreased in comparison to LDL-MI-S. The diastolic blood pressure was lower in LDL-MI-S in relation to LDL-S, while the LDL-MI-I group presented a higher diastolic BP than the LDL-MI-C group. The pulse interval variance was greater in LDL-S than in LDL-MI-I only. In conclusion, our results demonstrate that LDL animals have important functional and physiological differences compared to WT, especially in relation to muscle morphology, hemodynamic and autonomic cardiovascular control. Furthermore, MI leads to damage in both investigated strains and the two types of physical training attenuate similarly the impairment of most of the analyzed variables
McKenney, Mikaela Lee. "Coronary artery disease progression and calcification in metabolic syndrome." Thesis, 2014. http://hdl.handle.net/1805/6460.
Повний текст джерелаFor years, the leading killer of Americans has been coronary artery disease (CAD), which has a strong correlation to the U.S. obesity epidemic. Obesity, along with the presence of other risk factors including hyperglycemia, hypercholesterolemia, dyslipidemia, and high blood pressure, comprise of the diagnosis of metabolic syndrome (MetS). The presentation of multiple MetS risk factors increases a patients risk for adverse cardiovascular events. CAD is a complex progressive disease. We utilized the superb model of CAD and MetS, the Ossabaw miniature swine, to investigate underlying mechanisms of CAD progression. We studied the influence of coronary epicardial adipose tissue (cEAT) and coronary smooth muscle cell (CSM) intracellular Ca2+ regulation on CAD progression. By surgical excision of cEAT from MetS Ossabaw, we observed an attenuation of CAD progression. This finding provides evidence for a link between local cEAT and CAD progression. Intracellular Ca2+ is a tightly regulated messenger in CSM that initiates contraction, translation, proliferation and migration. When regulation is lost, CSM dedifferentiate from their mature, contractile phenotype found in the healthy vascular wall to a synthetic, proliferative phenotype. Synthetic CSM are found in intimal plaque of CAD patients. We investigated the changes in intracellular Ca2+ signaling in enzymatically isolated CSM from Ossabaw swine with varying stages of CAD using the fluorescent Ca2+ indicator, fura-2. This time course study revealed heightened Ca2+ signaling in early CAD followed by a significant drop off in late stage calcified plaque. Coronary artery calcification (CAC) is a result of dedifferentiation into an osteogenic CSM that secretes hydroxyapatite in the extracellular matrix. CAC is clinically detected by computed tomography (CT). Microcalcifications have been linked to plaque instability/rupture and cannot be detected by CT. We used 18F-NaF positron emission tomography (PET) to detect CAC in Ossabaw swine with early stage CAD shown by mild neointimal thickening. This study validated 18F-NaF PET as a diagnostic tool for early, molecular CAC at a stage prior to lesions detectable by CT. This is the first report showing non-invasive PET resolution of CAC and CSMC Ca2+ dysfunction at an early stage previously only characterized by invasive cellular Ca2+ imaging.
"Glucose and lipid dysmetabolism following renin-angiotensin system activation in unilateral nephrectomized rats." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074583.
Повний текст джерелаConclusions. (1) UNX induces progressive renal impairment and dysregulation of pancreatic and renal RAS in rats. (2) Pancreatic RAS activation leads to intra-islet fibrosis, insulin-secreting beta-cell deficit and insulin secretory deficiency. (3) Renal cortex RAS dysregulation induces ectopic adipocyte differentiation and lipid infiltration, in combination with lipodystrophy and lipid peroxidation, results to insulin resistance. (4) Pancreatic insulin-secretion deficit and insulin resistance contribute to the development of glucose intolerance and hyperglycemia. (5) Kidney impacting on glucose and lipid metabolism by affecting pancreatic islet and adipocyte, suggesting an essential role of the kidney in maintaining the whole-body homeostasis. (6) RAS blockade with ACEI or ARB may prevent the development of chronic renal impairment and glucose and lipid dysmetabolisms in UNX rats. (7) Common pathways modulating blood pressure, glucose and lipid metabolism warrant future studies for the better management of the global epidemic of metabolic syndrome.
Materials and methods. Chronic renal impairment and RAS disturbance were induced by unilateral nephrectomy (UNX) in adult Sprague-Dawley rats undergoing as long as 10 months of observation. Three-month old male rats were randomized into 4 groups: (1) sham operated control rats (n=10), (2) untreated UNX model rats (n=10), (3) ACEI---lisinopril treated UNX rats (n=10), and (4) ARB-olmesartan treated UNX rats (n=10). Blood glucose levels during fasting and oral glucose tolerance test (OGTT) conditions, lipids, insulin and renal function were measured at 3, 6, 8 and 10 months after operation. Histological changes of kidney, pancreas, liver, and adipose tissue were examined at 10 months post-operation.
Objectives. (1) To set up a rat model with persistent chronic renal impairment and RAS activation. (2) To examine changes of fasting blood glucose, glucose tolerance, blood lipids and insulin sensitivity. (3) To examine changes of pancreatic islets and the factors contributing to pancreatic islet damage such as RAS, transforming growth factor (TGF)-beta and alpha-smooth muscle actin (SMA). (4) To examine changes of systemic and renal adipose tissue and the factors contributing to adipopathy such as RAS, peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and hydroxy-3-methylglutary coenzyme A reductase (HMGCR). (5) To investigate preventive effect of RAS blockades by the ACEI-lisinopril (4 mg/kg body weight) and ARB-olmesartan (4 mg/kg body weight) on the rat model of progressive renal deficiency.
Results. (1) UNX rats developed time-dependent progressive renal functional impairment and marked glomerulosclerosis and tubulointerstitial lesions. (2) UNX rats showed fasting hyperglycemia, progressive glucose intolerance, hyperlipidemia and insulin resistance. (3) UNX rats demonstrated insulin secretory deficiency in parallel to pancreatic islet fibrosis, beta-cell deficit, and overexpression of RAS components, TGF-beta, and alpha-SMA. (4) UNX rats displayed adipopathy evidenced by shifts the subcutaneous and visceral fats to the ectopic fat with lipid accumulation, lipofuscin pigmentation and adipocytes transformation. The adipopathy associated with down-regulation of AT1R and over-expression of angiotensin, AT2R, PPAR-gamma and HMGCR in the remnant kidney. (5) Treatment with lisinopril and olmesartan significantly attenuated the development of chronic renal impairment, RAS dysregulation and aberrant proteins expression, islet damage, adipose redistribution, and glucose and lipid dysmetabolism.
Sui, Yi.
Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3422.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2008.
Includes bibliographical references (leaves 195-220).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
Dobečka, Kryštof. "Experimentální přístupy pro studium jaterní enzymatické indukce zprostředkované pregnanovým X receptorem." Master's thesis, 2021. http://www.nusl.cz/ntk/nusl-446103.
Повний текст джерелаHimes, Evan Robert. "The role of STAT3 in osteoclast mediated bone resorption." Thesis, 2014. http://hdl.handle.net/1805/4841.
Повний текст джерелаSignal Transducer and Activator of Transcription 3 (STAT3) is known to be related to bone metabolism. Mutation of STAT3 causes a rare disorder in which serum levels of IgE are elevated. This causes various skeletal problems similar to osteoporosis. To examine the effect of STAT3 in the osteoclast, we obtained two osteoclast specific STAT3 knockout mouse models: one using the CTSK promoter to drive Cre recombinase and another using a TRAP promoter. Examination of these mice at 8 weeks of age revealed a decreased trabecular bone volume in CTSK specific STAT3 knockout mice along with a slight decrease in osteoclast number in both CTSK and TRAP specific STAT3 knockout females. We also noticed changes in bone mineral density and bone mechanical strength in females. These data suggest that STAT3 plays a part in the function of the osteoclast.