Дисертації з теми "Substance P Physiological effects"
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Uzubalis, Ranate Ingrid. "A study of the metabolism, pharmacological properties and disposition of substance P /." Title page, table of contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phu99.pdf.
Повний текст джерелаSvensson, Erik. "Modulatory effects and interactions of substance P, dopamine, and 5-HT in a neuronal network /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-524-7/.
Повний текст джерелаBarragan, Adrian Alberto. "ASSESSMENT OF PHYSIOLOGICAL AND BEHAVIORAL RESPONSES IN DAIRY COWS TREATED WITH ASPIRIN FOLLOWING PARTURITION AND IN POSTPARTUM COWS DIAGNOSED WITH METRITIS." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500033085971928.
Повний текст джерелаHalliday, Dale Andrew. "The effects of tachykinins and their metabolites or articular cartilage chondrocyte and synviocyte function /." Title page, contents and introduction only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phh1878.pdf.
Повний текст джерелаVilisaar, Janek. "The induction and effects of Substance P and its receptor in human immune cells and neurons : potential relevance in multiple sclerosis." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12663/.
Повний текст джерелаBackman, Ludvig. "Neuropeptide and catecholamine effects on tenocytes in tendinosis development : studies on two model systems with focus on proliferation and apoptosis." Doctoral thesis, Umeå universitet, Anatomi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-70193.
Повний текст джерелаNichols, Nicole L. "The Effects of Chronic Hypoxia and Substance P on the Chemosensitive Response of Individual Nucleus Tractus Solitarius (NTS) Neurons from Adult Rats." Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1215465852.
Повний текст джерелаSong, Yafeng. "Cross transfer effects after unilateral muscle overuse : an experimental animal study about alterations in the morphology and the tachykinin system of muscles." Doctoral thesis, Umeå universitet, Institutionen för integrativ medicinsk biologi (IMB), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-71242.
Повний текст джерелаHallberg, Mathias. "Anabolic Androgenic Steroids : Effects on Neuropeptide Systems in the Rat Brain." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5745.
Повний текст джерелаAfrah, Abdullahi Warsame. "Neuropeptide release in the rat dorsal horn in models of persistent pain : effects of opioids /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-185-3.
Повний текст джерелаCheung, Chung-yan. "Effects of endocrine manipulation on the peptide levels and the gene expression of [beta]-endorphin, met-enkephalin, somatostatin, substance P and cholecystokinin in the rat hypothalamus and pituitary." Click to view the E-thesis via HKUTO, 1998. http://sunzi.lib.hku.hk/hkuto/record/B31220575.
Повний текст джерелаCheung, Chung-yan. "Effects of endocrine manipulation on the peptide levels and the gene expression of b-endorphin, met-enkephalin, somatostatin, substance P and cholecystokinin in the rat hypothalamus and pituitary /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21038272.
Повний текст джерелаZerabruk, MA. "Repair of sub-lethal damage following single and split-dose irradiation using 60co-gamma and p(66)Be neutrons." Thesis, Cape Peninsula University of Technology, 2005. http://hdl.handle.net/20.500.11838/1504.
Повний текст джерелаIn clinical radiotherapy, experiments are performed to determine optimal conditions of the radiation prior to radiotherapy. These experiments focus on the relative biological effectivness(RBE) determination and are predominantly applied in high linear energy transfer (LET) radiations i.e. fast neutrons, as the RBE values for such radiations vary greatly. In general, the RBE of a certain radiation relative to a given reference radiation flCo gamma) varies widely with the energy, dose, dose rate, fractionation, type of tissue and end-point used. Experience with neutron therapy at iThemba LABS has shown that treatment with more fractions and lower doses per fraction may be beneficial for some patients. To calculate the iso-effective treatment dose needed, an appropriate alp ratio for early effects is needed. In this study, the repair of mouse jejunum was measured for split-dose irradiations to determine if a suitable alP ratio for neutrons could be estimated using the known value for gamma rays and the applicable RBE.. Crypt stem cell survival was measured 3.5 days after split-dose exposures to p(66)/Be neutrons and 6OCo gamma rays. Dose response curves for both treatment modalities and for both acute and fractionated exposures were constructed by counting crypts of Leiberkhiin at the base of the villi in haematoxylin and Eosin-stained sections of mouse jejunum. Using a RBE value of 1.64 and an alP ratio of 7Gy noted for tbe fractionated photon exposures, an alP ratio of 11.5 IV could be estimated for neutrons.
Kumarasinghe, Isuru Ransiri. "DESIGN, SYNTHESIS, NMR CONFORMATIONAL ANALYSIS AND DOCKING ANALYSIS OF NOVEL MULTIFUNCTIONAL MOLECULES FOR PAIN." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/193738.
Повний текст джерелаUzubalis, Ranate Ingrid. "A study of the metabolism, pharmacological properties and disposition of substance P / Renate Ingrid Uzubalis." Thesis, 1995. http://hdl.handle.net/2440/21596.
Повний текст джерелаxvii, 199, [68] leaves, [1] leaf of plates : ill. ; 30 cm.
Primary aim was to determine whether levels of the endogenous peptide substance P (SP) would parallel and reflect the reported increased levels of the trophic agent nerve growth factor which is associated with the development of sympathetic hyperinnervation (and ultimately hypertension) in the genetic animal model for hypertension, the spontaneously hypertensive rat.
Thesis (Ph.D.)--University of Adelaide, Dept. of Clinical and Experimental Pharmacology, 1995
Verplaetse, Terril Lee. "Effects of Prazosin Treatment on Ethanol- and Sucrose-Seeking and Intake in P Rats." Thesis, 2012. http://hdl.handle.net/1805/2970.
Повний текст джерелаBackground: Previous studies show that prazosin, an α1-adrenergic receptor antagonist, decreases alcohol drinking in animal models of alcohol use and dependence and in alcohol-dependent men. These studies extended previous findings by using a paradigm that allows for separate assessment of prazosin on motivation to seek versus consume ethanol or sucrose in selectively bred rats given acute or chronic prazosin treatment. Methods: Alcohol-preferring P rats were trained to complete an operant response that resulted in access to either 2% (Exp. 1) or 1% (Exp.2) sucrose or 10% ethanol. In Experiment 1, a 4-week consummatory testing phase consisted of rats bar-pressing to “pay” a specified amount up front to gain access to unlimited ethanol (or sucrose) for a 20-minute period. A 4-week appetitive testing phase examined how much the rats would bar-press for ethanol in an extinction session when no reinforcer could be obtained. In Experiment 2, during testing, the response requirement was dropped to a 1 and daily session cycles of drug (3 weeks/ 14 sessions from Tues to Fri) or vehicle (2 weeks/ 9 sessions from Tues to Fri) treatment were alternated per drug dose for a total of 3 drug doses (3 cycles) per rat. After each drug cycle, a single non-reinforced extinction session was conducted with no drug ‘on board’ and no reinforcer access. On test days, rats were given IP injections of either vehicle or one of three doses of prazosin (Exp 1: 0.5, 1.0, 1.5 mg/kg; Exp 2: 0.25, 0.5, 1.0 mg/kg; balanced design; -30 min). Results: In Experiment 1, prazosin significantly decreased ethanol-seeking at all doses tested. The highest dose decreased ethanol intake and increased the latency to first lever-press and first lick. Sucrose-seeking and intake were decreased by the same doses of prazosin. In Experiment 2, prazosin significantly decreased reinforcer-seeking at the lowest and highest doses while ethanol intake was not decreased by prazosin. Conversely, sucrose-seeking was decreased at the highest dose of prazosin tested while sucrose consumption was decreased by all doses. Latency to lever-press for sucrose was increased by the lowest dose of prazosin compared to vehicle. Conclusions: These findings extend previous research and indicate that prazosin decreases motivation to seek ethanol and sucrose. The specificity of prazosin on different behaviors and over different reinforcers suggests that these findings are not due to prazosin-induced motor-impairment or malaise. These data suggest that prazosin may work by decreasing the reinforcing properties of reinforcers in general.
Toalston, Jamie E. "Peri-adolescent Alcohol Consumption Enhances the Reinforcing and Stimulatory Properties of Ethanol within the Adult Mesolimbic Dopamine System in Alcohol Preferring P Rats." Thesis, 2012. http://hdl.handle.net/1805/2893.
Повний текст джерелаResearch in the alcohol preferring (P) rat has indicated that peri-adolescent alcohol (EtOH) consumption enhances the acquisition of oral operant EtOH self-administration, inhibits the extinction of responding for EtOH, augments EtOH-seeking behaviors, and increases relative reward value of EtOH during adulthood. Experiment 1 was conducted to determine if these adult effects of peri-adolescent EtOH intake could be observed using an Intracranial Self-Administration (ICSA) model. It was hypothesized that an increased sensitivity to the rewarding actions of EtOH would be manifested in peri-adolescent-EtOH-exposed subjects compared to naive subjects when the opportunity to self-administer EtOH to the posterior ventral tegmental area (pVTA) is available in adulthood. The pVTA is a primary site for EtOH’s reinforcing and rewarding properties in the mesolimbic dopamine (DA) system. Experiment 2 was a dose-response examination of the effects of EtOH administered to the pVTA on downstream DA efflux in the nucleus accumbens shell (AcbSh) via a joint Microinjection-Microdialysis (MicroMicro) procedure. Male P rats were given 24-h free-choice exposure to 15% volume/volume EtOH from postnatal day (PD) 30 to PD 60, or remained experimentally naive, with ad lib food and water. By the end of the periadolescent exposure period, average consumption was 7.3 g/kg/day of EtOH. After PD 75, periadolescent-EtOH-exposed and naïve rats were either implanted with an injector guide cannula aimed at the right pVTA for ICSA (Experiment 1), or two cannulae, one aimed at the right pVTA (injector) and one at the ipsilateral AcbSh (microdialysis) for MicroMicro (Experiment 2). Following one week of recovery from surgery, ICSA subjects were placed in standard two-lever (active and inactive) operant chambers. Test sessions were 60 min in duration and occurred every other day for a total of 7 sessions. Rats were randomly assigned to one of 5 groups (n=4-9/group) that self-infused (FR1 schedule) either aCSF (vehicle, 0 mg%), 50, 75, 100, or 150 mg% EtOH during 4 sessions, aCSF only for sessions 5 and 6 (extinction), and the initial concentration again for session 7 (reinstatement). MicroMicro subjects received six days of recovery from surgery, probe implantation the day before testing, and then continuous microdialysis for DA with 15 min microdialysis samples collected before, during, and then two hrs after 10-min pulse microinjection of either aCSF (vehicle, 0 mg%), 50, 75, 100, or 150 mg% EtOH. Neither EtOH-exposed nor naive groups of P rats self-infused the aCSF or 50 mg% EtOH concentration. While the naive group did not self-infuse the 75 or 100 mg% EtOH concentrations, the peri-adolescent EtOH-exposed group of P rats did readily discriminate the active lever from the inactive lever at these concentrations. Both groups self-infused the 150 mg% EtOH concentration. Pulse microinjections of EtOH during the MicroMicro procedure revealed that 75 and 100 mg% concentrations of EtOH increased downstream DA in the AcbSh of EtOH-exposed, but not naïve, subjects. 150 mg% EtOH increased downstream DA in both adolescent treatment groups. Overall, the results indicate that consumption of EtOH by P rats during peri-adolescence increases the reinforcing properties of EtOH in the pVTA in adulthood. The results also indicate that there were differential effects of peri-adolescent EtOH exposure on DA efflux in the AcbSh. This provides evidence that peri-adolescent EtOH-exposure produces long-lasting alterations in neural circuitry involved in EtOH-reinforcement, during adulthood.
Tang, Fu-In, and 唐褔瑩. "Effects of Substance P and GDNF on Nigrostriatal Dopamine System." Thesis, 1997. http://ndltd.ncl.edu.tw/handle/20089145804598447484.
Повний текст джерелаDonkin, James J. "The effects of the neuropeptide substance P on outcome following experimental traumatic brain injury in rats." 2006. http://hdl.handle.net/2440/37854.
Повний текст джерелаThesis (Ph.D.)--School of Medical Sciences, 2006.
Ruby, Carl E. "Direct effects of 2,3,7,8 tetrachlorodibenzo-p-dioxin on antigen-presenting cells and molecular signaling pathways in dendritic cells." Thesis, 2001. http://hdl.handle.net/1957/32558.
Повний текст джерелаGraduation date: 2002
"The protective effects of Ganoderma extracts from the endocrine disruption of p,p'-DDE on breast cancer cell model." 2009. http://library.cuhk.edu.hk/record=b5896912.
Повний текст джерелаThesis (M.Phil.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references (leaves 162-218).
Abstract also in Chinese.
Acknowledgment --- p.i
Abstract --- p.ii
摘要 --- p.iv
Table of Content --- p.vi
List of Figures --- p.x
List of Tables --- p.xv
Abbreviations --- p.xvii
Chapter Chapter 1 --- Introduction --- p.1
Chapter 1.1 --- Ganoderma spp --- p.1
Chapter 1.1.1 --- Introduction of Ganoderma spp --- p.1
Chapter 1.1.2 --- Bioactivities of Ganoderma spp --- p.3
Chapter 1.1.3 --- Endocrine system and breast cancer --- p.11
Chapter 1.1.3.1 --- Estrogen --- p.11
Chapter 1.1.3.2 --- Estrogen receptors --- p.12
Chapter 1.1.3.3 --- Estrogen responsive genes --- p.15
Chapter 1.1.3.3.1 --- pS2 --- p.15
Chapter 1.1.3.3.2 --- Progesterone receptor --- p.18
Chapter 1.1.3.4 --- Androgen --- p.21
Chapter 1.1.3.5 --- Androgen receptor --- p.23
Chapter 1.1.3.6 --- Androgen responsive gene --- p.24
Chapter 1.1.3.6.1 --- Transmembrane prostate androgen-induced RNA --- p.24
Chapter 1.1.3.6.2 --- Uridine diphosphate glucose dehydrogenase --- p.26
Chapter 1.1.3.7 --- Breast cancer --- p.26
Chapter 1.2 --- "Endocrine Disruption of p,p '-DDE" --- p.28
Chapter 1.2.1 --- Introduction of p´ةp '-DDE --- p.28
Chapter 1.2.2 --- "p,p '-DDE in environments" --- p.29
Chapter 1.2.3 --- "p,p '-DDE in human body" --- p.32
Chapter 1.2.4 --- "p,p '-DDE and reproductive system" --- p.33
Chapter 1.2.5 --- Endocrine disruptor --- p.35
Chapter 1.2.6 --- "Action mechanism of p,p '-DDE on endocrine system" --- p.37
Chapter 1.2.7 --- Apoptosis --- p.39
Chapter 1.3 --- Food therapy against endocrine disruption --- p.41
Chapter 1.3.1 --- Food therapy and functional food --- p.41
Chapter 1.3.2 --- Ganoderma as a Functional food --- p.47
Chapter 1.3.3 --- Cancer prevention by dietary agents --- p.47
Chapter 1.3.4 --- Hormone therapy --- p.48
Chapter 1.3.5 --- Hormone-related properties of Ganoderma spp --- p.50
Chapter 1.4 --- The aim of the study --- p.51
Chapter Chapter 2 --- Materials and Methods --- p.52
Chapter 2.1 --- Ganoderma samples --- p.52
Chapter 2.2 --- Artificial cultivation of Ganoderma spp --- p.54
Chapter 2.3 --- Molecular identification of Ganoderma spp --- p.55
Chapter 2.3.1 --- Extraction of genomic DNA --- p.55
Chapter 2.3.2 --- Gene-specific polymerase chain reaction (PCR) --- p.56
Chapter 2.3.3 --- Gel electrophoresis --- p.56
Chapter 2.3.4 --- Purification of PCR amplified product for sequencing --- p.57
Chapter 2.3.5 --- Cycle-sequencing --- p.57
Chapter 2.3.6 --- Sequencing --- p.58
Chapter 2.3.7 --- Sequence analysis --- p.58
Chapter 2.4 --- Chemical analyses of Ganoderma spp --- p.59
Chapter 2.4.1 --- Polysaccharide preparations --- p.59
Chapter 2.4.2 --- Terpene profile --- p.60
Chapter 2.4.3 --- Fatty acid profile --- p.60
Chapter 2.5 --- Anti-oxidation activities --- p.61
Chapter 2.5.1 --- Superoxide radical scavenging assay --- p.61
Chapter 2.5.2 --- DPPH radical scavenging assay --- p.62
Chapter 2.6 --- Anti-proliferation effect on human breast cancer cells --- p.62
Chapter 2.7 --- Hormone-like effects --- p.63
Chapter 2.7.1 --- E-screen test --- p.63
Chapter 2.7.2 --- In vitro estrogen receptors (ERs) competitor binding assays --- p.64
Chapter 2.7.3 --- "Recombinant yeast cell based ER-, AR- and PGR-responsible promoter assays" --- p.65
Chapter 2.7.3.1 --- Recombinant yeasts --- p.65
Chapter 2.7.3.2 --- Growth medium for recombinant yeasts --- p.66
Chapter 2.7.3.3 --- "ER, AR and PGR assays" --- p.67
Chapter 2.7.3.4 --- β-Galactosidase assay --- p.67
Chapter 2.7.4 --- Real time PCR --- p.68
Chapter 2.8 --- Flow cytometry --- p.71
Chapter 2.9 --- Comet assay --- p.71
Chapter 2.10 --- DNA microarray --- p.73
Chapter 2.10.1 --- Total RNA isolation --- p.73
Chapter 2.10.2 --- cDNA synthesis --- p.73
Chapter 2.10.3 --- Preparation of labelled cDNA --- p.74
Chapter 2.10.4 --- cDNA purification --- p.74
Chapter 2.10.5 --- Oligo GEArray hybridization --- p.75
Chapter 2.10.6 --- Chemiluminescent detection --- p.76
Chapter 2.10.7 --- Data analysis --- p.77
Chapter Chapter 3 --- Results --- p.78
Chapter 3.1 --- Analysis of Ganderma spp --- p.78
Chapter 3.1.1 --- Mycelia and fruiting bodies --- p.78
Chapter 3.1.2 --- Identification of Ganoderma spp --- p.79
Chapter 3.1.3 --- Chemical properties of samples --- p.80
Chapter 3.1.4 --- Anti-oxidation activities --- p.90
Chapter 3.1.5 --- Anti-proliferation effect on human breast cancer cells --- p.90
Chapter 3.1.6 --- Hormone-like bioactivities --- p.93
Chapter 3.1.6.1 --- E-screen test --- p.93
Chapter 3.1.6.2 --- In vitro estrogen receptors (ERs) competitor binding assays --- p.94
Chapter 3.1.6.3 --- "Recombinant yeast cell-based ER-, AR- and PGR-responsible promoter assays" --- p.95
Chapter 3.1.6.4 --- ER- and AR-pathway gene expression by real time PCR --- p.97
Chapter 3.2 --- "Action mechanism of p,p' -DDE" --- p.99
Chapter 3.2.1 --- E-screen --- p.99
Chapter 3.2.2 --- In vitro estrogen receptors (ERs) competitor binding assays --- p.101
Chapter 3.2.3 --- Recombinant yeast cell based ER- and AR-responsible promoter assays --- p.103
Chapter 3.2.4 --- ER- and AR-pathway gene expression by real time PCR --- p.106
Chapter 3.3 --- Ganoderma tsugae mycelia extract against p.p' -DDE --- p.109
Chapter 3.3.1 --- E-screen test --- p.109
Chapter 3.3.2 --- ER- and AR-pathway gene expression by real time PCR --- p.110
Chapter 3.3.3 --- Analysis of cell cycle --- p.112
Chapter 3.3.4 --- Analysis of DNA damage --- p.114
Chapter 3.3.5 --- Analysis of sub-G1 peak --- p.117
Chapter 3.3.6 --- DNA damage and apoptosis relative gene expression by real time PCR --- p.120
Chapter 3.3.7 --- DNA microarray --- p.121
Chapter Chapter 4 --- Discussion --- p.131
Chapter 4.1 --- Analysis of Ganoderma spp --- p.131
Chapter 4.2 --- Effects of p.p´ة-DDE --- p.144
Chapter 4.3 --- Protective effects of G. tsugae against p.p' -DDE --- p.151
Chapter 4.4 --- Further investigation --- p.159
Chapter 4.5 --- Conclusion --- p.160
References --- p.162
Shembe, Zamakhosi Thina. "The effects of whoonga on the learning of affected youth in Kwa-Dabeka township." Diss., 2013. http://hdl.handle.net/10500/13827.
Повний текст джерелаEducational Studies
M. Ed. (Socio-Education)
Han, Xu. "Identification and mechanistic investigation of clinically important myopathic drug-drug interactions." Thesis, 2014. http://hdl.handle.net/1805/5275.
Повний текст джерелаDrug-drug interactions (DDIs) refer to situations where one drug affects the pharmacokinetics or pharmacodynamics of another. DDIs represent a major cause of morbidity and mortality. A common adverse drug reaction (ADR) that can result from, or be exacerbated by DDIs is drug-induced myopathy. Identifying DDIs and understanding their underlying mechanisms is key to the prevention of undesirable effects of DDIs and to efforts to optimize therapeutic outcomes. This dissertation is dedicated to identification of clinically important myopathic DDIs and to elucidation of their underlying mechanisms. Using data mined from the published cytochrome P450 (CYP) drug interaction literature, 13,197 drug pairs were predicted to potentially interact by pairing a substrate and an inhibitor of a major CYP isoform in humans. Prescribing data for these drug pairs and their associations with myopathy were then examined in a large electronic medical record database. The analyses identified fifteen drug pairs as DDIs significantly associated with an increased risk of myopathy. These significant myopathic DDIs involved clinically important drugs including alprazolam, chloroquine, duloxetine, hydroxychloroquine, loratadine, omeprazole, promethazine, quetiapine, risperidone, ropinirole, trazodone and simvastatin. Data from in vitro experiments indicated that the interaction between quetiapine and chloroquine (risk ratio, RR, 2.17, p-value 5.29E-05) may result from the inhibitory effects of quetiapine on chloroquine metabolism by cytochrome P450s (CYPs). The in vitro data also suggested that the interaction between simvastatin and loratadine (RR 1.6, p-value 4.75E-07) may result from synergistic toxicity of simvastatin and desloratadine, the major metabolite of loratadine, to muscle cells, and from the inhibitory effect of simvastatin acid, the active metabolite of simvastatin, on the hepatic uptake of desloratadine via OATP1B1/1B3. Our data not only identified unknown myopathic DDIs of clinical consequence, but also shed light on their underlying pharmacokinetic and pharmacodynamic mechanisms. More importantly, our approach exemplified a new strategy for identification and investigation of DDIs, one that combined literature mining using bioinformatic algorithms, ADR detection using a pharmacoepidemiologic design, and mechanistic studies employing in vitro experimental models.