Dissertations / Theses on the topic 'Cell receptors – Physiological effect'
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1
Siwik, Steven Anthony 1963. "Regulation of receptor-mediated phosphatidylinositol hydrolysis in AR42J rat carcinoma cells." Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277180.
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Receptor-activated phosphatidylinositol (PtdIns) hydrolysis was examined in AR42J rat pancreatic acini. Cholecystokinin-octapeptide (CCK₈) and bombesin induced a dose-dependent accumulation of [³H] inositol monophosphate ([³H]InsP₁). Manganese (Mn²⁺), a known calcium channel blocker, did not alter basal PtdIns hydrolysis. In contrast, when added 5 minutes prior to the addition of agonists for 60 minutes, Mn²⁺ markedly inhibited secretagogue-mediated [³H]InsP1 formation. Mn²⁺ also attenuated the CCK₈-mediated increase in biologically active inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate. These inhibitory effects of Mn²⁺ were mimicked by lanthanum and by EGTA. Addition of calcium to EGTA-treated cells abolished the inhibitory effects of extracellular calcium depletion. Mn²⁺, La³⁺ and EGTA exerted similar inhibitory effects on PtdIns hydrolysis in pancreatic acini. These findings suggest that receptor-activated calcium influx is required for full activation of the CCK₈-mediated signal transduction pathway that is coupled to PtdIns hydrolysis.
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游燕珍 and Yin-chun Mabel Yau. "Studies on melatonin receptors in guinea pig platelets and melatonin actions on human leukemic megakaryoblast MEG-01 cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242613.
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吳毅賢 and Samuel Ng. "Extracellular calcium in dopamine D1-receptor mediated growth hormone release from Chinese grass carp pituitary cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31219755.
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Bose, Diptiman Dipen. "Role of ryanodine receptors in neuronal calcium signalling and growth control." Scholarly Commons, 2002. https://scholarlycommons.pacific.edu/uop_etds/566.
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The versatility of Ca2+ as a messenger regulating a myriad of signalling events requires that the concentration of Ca2+ ions in the cytoplasm be highly regulated. Capacitative Ca2+ entry (CCE) or store-operated Ca2+ (SOC) entry, whereby the depletion of intracellular Ca2+ stores induces the influx of Ca2+ across the plasma membrane, plays a crucial role in Ca2+ signalling. Despite the recent advances in elucidating the entry pathway, its molecular identity, biophysical properties and store-depletion signal remains undefined. Thapsigargin (TG), a sarcoplasmic/endoplasmic reticulum Ca2+ A TPase pump (SERCA), inhibitor induces passive depletion of the internal Ca2+ stores and triggers CCE. The universality of this signal has been widely accepted and TG has proven to be a valuable tool in studying CCE. The neuronal cell line NG 115 -401 L lacks the TG activated Ca2+ influx pathway. Agonists of the ryanodine receptor (RyR); chlorom- cresol (CMC), polychlorinated biphenyl 95 (PCB), ryanodine, caffeine, and that of the inositol-1 ,4 ,5-trisphosphate receptor (IP3R), bradykinin, effectively couple to the activation of Ca2+ influx in these cells. The Ca2+ influx signal due to these agonists can be inhibited by SOC blockers such as La3+, Zn2+, Ni2+ and SF&F 96365. Thapsigargin, CMC and PCB95 share the same Ca2+ releasable pools in the 401 L cells. Our data thus suggests that the channels present in the 401 L cells are likely to be receptor-activated channels rather than the store-depletion activated channels. Cell viability studies show that thapsigargin (25 nM) can decrease viability by 75% within 24 hrs and the RyR agonist caffeine decreased viability to <60% within 24hrs. CMC, PCB95 and ryanodine also were cytotoxic at higher doses. Nuclear fragmentation patterns and activation of caspase-3 in thapsigargin and caffeine-treated cells suggest the induction of apoptosis within 12 hrs of treatment. The treated cells were shown to generate nitric oxide, a potential apoptosis inducing agent.
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Korpelainen, Eija. "Interleukin -3 receptor expression and function in now-hemopoietic cells /." Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phk84.pdf.
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Fundytus, Marian Elaine. "Contribution of metabotropic glutamate receptors to opioid dependence." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42034.
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We investigated the role of metabotropic glutamate receptors (mGluRs), and related intracellular second messengers, in the development of morphine tolerance and dependence. The mGluRs are divided into three groups: group I mGluRs are positively coupled to phosphatidylinositol (PI) hydrolysis, while group II and III mGluRs are negatively coupled to cyclic adensoine-3$ sp prime$,5$ sp prime$-monophosphate (cAMP) production. Opioid receptors are also coupled to these same systems, and have been shown to elicit changes in these messenger systems during chronic treatment.We showed that chronic intracerebroventricular (i.c.v.) administration of selective group II and III mGluR antagonists concurrently with subcutaneous (s.c.) morphine significantly reduced the severity of precipitated withdrawal symptoms. Conversely, acute i.c.v. injection of a selective group II mGluR antagonist just prior to the precipitation of withdrawal significantly exacerbated the severity of abstinence symptoms. In addition, acute i.c.v. injection of a selective group II mGluR agonist just prior to the precipitation of withdrawal significantly reduced abstinence symptoms. From these results we hypothesized that chronic opioid treatment may induce a desensitization of group II mGluRs.
We also demonstrated that chronic i.c.v. infusion of a selective group I mGluR antagonist concurrently with s.c. morphine significantly attenuated the precipitated withdrawal syndrome. In addition, we showed that chronic i.c.v. antagonism of $ delta$-opioid receptors with a highly selective antagonist also decreased the development of morphine dependence, as well as tolerance. Since both group I mGluRs and $ delta$-opioid receptors are positively coupled to PI hydrolysis, further evidence for a role of products of PI hydrolysis in the development of morphine dependence was obtained when we showed that selective chronic inhibition of protein kinase C (PKC) activation, as well as selective chronic inhibition of intracellular Ca$ sp{2+}$ release, concurrently with morphine treatment significantly reduced the severity of abstinence symptoms. Thus, compensatory changes usually elicited by chronic opioid treatment may be counteracted by antagonizing receptors positively coupled to PI hydrolysis, as well as by inhibiting products of PI hydrolysis.
In the General Discussion, we propose a model based on the possible interaction of mGluRs and opioid receptors, via related intracellular second messengers, to explain the development of morphine dependence.
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Mendelson, Scott Douglas. "Differential roles of serotonin receptor subtypes in the modulation of lordosis behaviour in the female rat." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29021.
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In 1985, Mendelson and Gorzalka proposed the dual role hypothesis of serotonergic modulation of lordosis behaviour. In this hypothesis it was proposed that serotonergic activity can either inhibit or facilitate lordosis behaviour. Specifically it was suggested that the lordosis-inhibiting effects of serotonin are mediated by activity at 5-HT₁ receptors, whereas lordosis-facilitating effects of serotonin are mediated by activity at 5-HT₂ receptors. The purpose of the following series of studies was both to confirm and to extend the dual role hypothesis. The intraperitoneal administration of the 5-HT2 antagonists pizotefin (1 mg/kg), cyproheptadine (1 mg/kg), metitepine (1 mg/kg), and ketanserin (1 mg/kg) were found to inhibit lordosis behavior in ovariectomized rats that had been primed with estradiol benzoate (EB) and progesterone (P). Pipamperone was ineffective. The 5-HT₂ agonist guipazine (3 mg/kg) was ineffective alone, but it reversed the inhibitory effects of pizotefin, cyproheptadine, and ketanserin. It did not reverse the effects of metitepine. The highly selective 5-HT₂ antagonist LY53857 (0.3 mg/kg) was also found to inhibit lordosis behaviour in female rats that had been primed with EB and P. The lordosis-inhibiting effect of LY53857 (1 mg/kg) in females primed with EB and P was reversed by quipazine (3 mg/kg). The nonselective 5-HT antagonist methysergide (7 mg/kg) was found to inhibit lordosis behavior 30 min after intraperitoneal administration to females treated chronically with EB, or with EB and P. However, methysergide was found to facilitate lordosis behavior 200 and 300 min after administration to female rats treated acutely with EB. In an analysis of dose response it was found that methysergide (0.02 - 7 mg/kg) administered 30 min prior to behavioural testing produced no facilitation of lordosis in females primed with EB. However, when administered 200 min prior to testing, methysergide (1 mg/kg) produced a significant facilitation of lordosis.
The administration of the 5-HT₁ A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH DPAT) inhibited lordosis behavior in ovariectomized rats primed with EB. 8-OH DPAT was ineffective at 0.01 mg/kg, whereas inhibition occurred at the 0.03, 0.1, 0.3, 1.0, and 3.0 mg/kg doses. In an evaluation of the effects of 8-OH DPAT on the expression of male sexual behaviour by females treated chronically with testosterone, 8-OH DPAT ( 1 mg/kg) increased the number of females mounting and significantly increased mount frequency. The 5-HT₁ A agonists ipsapirone (0.1 mg/kg) and gepirone (0.3 mg/kg) facilitated lordosis in females treated with EB. When administered at higher doses, ipsapirone (3.0 mg/kg) and buspirone (3.0 mg/kg) inhibited lordosis in rats treated with EB. In females treated with EB and P, ipsapirone (> 1.0 mg/kg), gepirone (> 0.3), and buspirone (> 0.3) inhibited lordosis behaviour. The newly developed 5-HT₁ A antagonist BMY 7378 (0.2 mg/kg) facilitated lordosis behaviour in females treated with EB. However, this facilitation was no longer apparent at the 5 mg/kg dose. BMY 7378 (0.04 - 5 mg/kg) was ineffective in females primed with EB and P. The 5-HTTB agonist 1 -(3-trifluoromethylphenyl)piperazine (TFMPP, 0.2 -5 mg/kg) was found to facilitate lordosis in females treated with EB. In females primed with EB and P, TFMPP (5 mg/kg) produced a significant inhibition of lordosis. The 5-HT₁ B agonist m-chlorophenylpiperazine (MCPP, 0.04 - 5 mg/kg) was ineffective in females primed either with EB or with EB and P.
The 5-HT₃ Antagonist ICS 205-930 (5 mg/kg) was found to facilitate lordosis behaviour, whereas the 5-HT₃ Antagonist MDL 72222 (0.05 - 5 mg/kg ) was found to be ineffective in females primed with EB.
The results of these studies tend to confirm that serotonergic activity can either inhibit or facilitate lordosis behaviour. It is suggested that the lordosis-inhibiting effects of serotonin are mediated by activity at postsynaptic 5-HTTA and possibly 5-HT₃ Receptors. The lordosis-facilitating effects of serotonin are mediated by activity at 5-HT₂ and possibly presynaptic 5-HT₁ B receptors. Finally, it is suggested that activity at somato-dendritic 5-HT₁ A autoreceptors may mediate facilitatory effects of low doses of 5-HT₁ A agonists. In closing, there is a discussion of the implications these results might hold for the understanding of the effects of serotonergic drugs on human behaviour.Arts, Faculty of
Psychology, Department of
Graduate
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Marsicano, Giovanni. "Physiological role of the cannabinoid receptor 1 (CB1) in the murine central nervous system." n.p, 2000. http://ethos.bl.uk/.
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Herrera, Yelenis. "Modulation of ASIC1a Function by Sigma-1 Receptors: Physiological and Pathophysiological Implications." [Tampa, Fla.] : University of South Florida, 2009. http://digital.lib.usf.edu/?e14.2855.
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Trout, Amanda L. "SEX DIFFERENCES IN CELL DEATH AND STEROID HORMONE RECEPTORS IN CORTICAL EXPLANTS." UKnowledge, 2013. http://uknowledge.uky.edu/physiology_etds/6.
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Estrogens, such as the biologically active 17-b estradiol (E2) have many actions in the male and female brain. Not only does E2 regulate reproductive behavior in adults, it organizes and activates the brains of younger animals in a sex-specific manner. In addition, many human studies have shown E2 to provide protection against a variety of neurological disorders, including stoke. These studies have been controversial and depend largely on the type and timing of hormone replacement. Animal studies are much less controversial and clearly demonstrate a neuroprotective role for E2 following ischemic brain injury. Because much of E2 neuroprotection requires sex steroid hormone receptors, it is essential to understand expression patterns of these receptors. For the current studies, I evaluated estrogen receptor alpha (ER α), estrogen receptor beta (ER β) and androgen receptor (AR) expression in the cortex. It is known that these receptors change in expression at several times in an animal’s life span including during early postnatal development and following ischemic brain injury. Here I used an in vitro cortical explant model to further examine how these receptors change both during development and following injury. This in vitro model is important because it provides a way to investigate changes in receptor expression pattern in the cortex without input from other brain regions. In addition to characterizing this model, I also evaluated the contribution of E2 to changes in receptor expression and on cell death following injury in the explants. To begin to decipher mechanisms for E2 mediated neuroprotection, I added antagonist for each of the receptors before and after injury. In each these experiments, I also examined potential sex differences by separating the female and male brains before I cultured the explants. Overall, these experiments showed that cortical explants are a good in vitro model. Here we found that E2 was protective in female, but not male cortical explants following injury. However, the exact mechanisms of E2-mediated neuroprotection are still to be deciphered.
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Beauglehole, Anthony Robert, and anthony@adenrx com. "N3-substituted xanthines as irreversible adenosine receptor antagonists." Deakin University. School of Biological and Chemical Sciences, 2000. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20080612.084330.
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8-Cyclopentyl-3-(3-(4-fluorosulfonylbenzoyl)oxy)propyl-propylxanthine (44, FSCPX) has been reported to exhibit potent and selective irreversible antagonism of the A1 adenosine receptor when using in vitro biological preparations. However, FSCPX (44) suffers from cleavage of the ester linkage separating the reactive 4-(fluorosulfonyl)phenyl moiety from the xanthine pharmacophore when used in in vivo biological preparations or preparations containing significant enzyme activity, presumably by esterases. Cleavage of the ester linkage renders FSCPX (44) inactive in terms of irreversible receptor binding. In order to obtain an irreversible A1 adenosine receptor antagonist with improved stability, and to further elucidate the effects of linker structure on pharmacological characteristics, several FSCPX (44) analogues incorporating the chemoreactive 4-(fluorosulfonyl)phenyl moiety were targeted, where the labile ester linkage has been replaced by more stable functionalites. In particular, ether, alkyl, amide and ketone linkers were targeted, where the length of the alkyl chain was varied from between one to five atoms.
Synthesis of the target compounds was achieved via direct attachment of the N-3 substituent to the xanthine. These compounds were then tested for their biological activity at the A1 adenosine receptor via their ability to irreversibly antagonise the binding of [3H]-8-cyclopentyl-1,3-dipropylxanthine ([3H]DPCPX, ( 9) to the A1 adenosine receptor of DDT1 MF-2 cells. For comparison, the xanthines were also tested for their ability to inhibit the binding of [3H]-4-(2-[7-amino-2-{furyl} {1,2,4}- triazolo{2,3-a} {1,3,5}triazin-5-ylamino-ethyl)]phenol ([3H]ZM241385, 36) to the A2A adenosine receptor of PC-12 cells. The results suggest that the length and chemical composition of the linker separating the reactive 4-(fluorosulfonyl)phenyl moiety from the xanthine ring contribute to the potency and efficacy of the irreversible A1 adenosine receptor ligands. Like FSCPX (44, IC50 A1 = 11.8 nM), all derivatives possessed IC50 values in the low nM range under in vitro conditions. Compounds 94 (IC50 A1 = 165 nM), 95 (IC50 A1 = 112 nM) and 96 (IC50 A1 = 101 nM) possessing one, three and five methylene spacers within the linkage respectively, exhibited potent and selective binding to the A1 adenosine receptor versus the A2A adenosine receptor. Compound 94 did not exhibit any irreversible binding at A1 adenosine receptors, while 95 and 96 exhibit only weak irreversible binding at A1 adenosine receptors. Those compounds containing a benzylic carbonyl separating the 4-(fluorosulfonyl)phenyl moiety from the xanthine ring in the form of an amide (119, IC50 A1 = 24.9 nM, and 120, IC50 A1 = 21 nM) or ketone (151, IC50 A1 = 14 nM) proved to be the most potent, with compound 120 exhibiting the highest selectivity of 132-fold for the A receptor over the A2A receptor. compounds 119, 120 and 151 also strongly inhibited the binding of [3H]DPCPX irreversibly (82%, 83% and 78% loss of [3H]DPCPX binding at 100 nM respectively). compounds 120 and 151 are currently being evaluated for use in in vivo studies.
Structure-activity studies suggest that altering the 8-cycloalkyl group of A1 selective xanthines for a 3-substituted or 2,3-disubstituted styryl, combined with N-7 methyl substitution will produce a compound with high affinity and selectivity for the A2A adenosine receptor over the A1 adenosine receptor. Compound 167 (IC50 A2A = 264 nM) possessing 8-(m-chloro)styryl substitution and the reactive 4-(fluorosulfonyl)phenyl moiety separated from the xanthine ring via an amide linker in the 3-position (as for 119 and 120), exhibited relatively potent binding to the A2A adenosine receptor of PC-12 cells, with a 16-fold selectivity for that receptor over the A1 adenosine receptor. However, compound 167 exhibited only very weak irreversible binding at A2A adenosine receptors.
Overall, at this stage of biological testing, compound 120 appears to possess the most advantageous characteristics as an irreversible antagonist for the A1 adenosine receptor. This can be attributed to its high selectivity for the A1 adenosine receptor as compared to the A2A adenosine receptor. It also has relatively high potency for the A1 adenosine receptor, a concentration-dependent and selective inactivation of A1 adenosine receptors, and unbound ligand is easily removed (washed out) from biological membranes. These characteristics mean compound 151 has the potential to be a useful tool for the further study of the structure and function of the A1 adenosine receptor.
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Woo, Man-man Michelle, and 胡文文. "The effect of melatonin on human luteal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223746.
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Sadideen, Doraid, and Doraid Sadideen. "Exploring G-Protein-Coupled Receptors Regulation, Specificity and Controllability of Exosomes Release in the Neuronal Cell Line SH-SY5Y." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/621166.
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Parkinson's disease is a neurodegenerative disease characterized by the buildup of aggregated and spread of misfolded alpha-synuclein. How the misfolded alpha-synuclein contributing to the toxicity and death of neuronal cells has been the focal point of research. The spread of alpha-synuclein has been attributed to many mechanisms, one of which is via cell-derived vesicles called exosomes. This project aims to examine the controllability of exosome release. SH-SY5Y, MCF-7 and CHO-K1 cells were transfected with dopamine receptor 3-green fluorescent protein, G-protein receptor 143 or green fluorescent protein and treated with either dopamine or L-DOPA. Medium was harvested and subjected to ultracentrifugation and a silver stain and western blot were performed. There was no significant difference in the total protein in the exosome fraction lanes between the treatment groups or within them. Another aim was to test the specificity of exosomes. Exosomes isolated from SH-SY5Y or MCF-7 were labeled with Exo-Red dye and introduced to wells containing SH-SY5Y, MCF-7 and CHO-K1 cells at room temperature and -4C. At room temperature, exosomes were observed intercellular in all of the cell lines, however, they did not deliver their content. At -4C exosome uptake was halted and they remained on the surface of the cells. Exo-Red labeled SH-SY5Y exosomes were treated with proteinase K and were introduced to CHO-K1 cells at -4C and room temperature. CHO-K1 did not take up exosomes, suggesting exosomes contain one or more necessary proteins needed to interact with the cellular membrane to initiate internalization. CHO-K1 cells were treated with versene to examine the involvement of integrin proteins. Exo-Red labeled SH-SY5Y exosomes were trapped on the surface of CHO-K1 after versene treatment. Lastly, Exo-Red labeled SH-SY5Y exosomes were biotinylated and magnetically captured then introduced to SH-SY5Y and MCF-7 cells and a silver stain and a biotinylated blot were performed. MCF-7 bound more Exo-Red labeled SH-SY5Y exosomes.
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Yamamura, Soichiro. "Mechanism of physiological function of sphingosine-1-phosphate : extracellular action and demonstration of alleged receptor /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/9278.
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Kasten, Chelsea Rae. "Intra-nucleus accumbens shell injections of R(+)- and S(-)- baclofen bidirectionally alter binge-like ethanol, but not saccharin, intake in C57Bl/6J mice." Thesis, Behavioural Brain Research (Elsevier), 2014. http://hdl.handle.net/1805/6453.
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Indiana University-Purdue University Indianapolis (IUPUI)It has been proposed that the GABAB receptor subtype plays a role in alcoholism and alcohol use disorders (AUDs) (Cousins et al., 2002; Agabio et al., 2012). Specifically, the GABAB agonist baclofen has been looked at extensively in clinical and pre-clinical studies. In various animal models of chronic and intermittent consumption, baclofen has been shown to both increase (Petry, 1997; Smith et al., 1999; Czachowski et al., 2006; Moore et al., 2007) and decrease (Colombo et al., 2000; 2002; 2005; Stromberg, 2004; Moore et al., 2009) drinking. A critical issue in determining pharmacological effects of a drug is using the appropriate animal model. The drinking-in-the-dark (DID) model, developed by Rhodes et al. (2005, 2007), produces high levels of drinking in a binge-like paradigm and has been used to assess many pharmacological targets (e.g. Kamdar et al., 2007; Gupta et al., 2008; Moore et al., 2007; 2009). While DID produces high-levels of binge drinking, it is unclear what areas of the brain are involved in this behavior. A direct way to target areas that are believed to be involved in the circuitry of particular behaviors is through microinjection of drugs (Kiianmaa et al., 2003). Of particular recent interest involving motivated behaviors and addiction is the nucleus accumbens (Acb) (Everitt & Robbins, 2005); specifically the accumbens shell (AcbSh) (e.g. Rewal et al., 2009, 2012; Nie et al., 2011; Leriche et al., 2008). The current study aimed to investigate the role of GABAB receptors in the AcbSh by examining the ability of two different enantiomers of baclofen to alter ethanol and saccharin intake in male C57BL/6J (B6) mice. B6 mice underwent bilateral cannulation surgery targeting the AcbSh. After 48 hours of recovery time, animals began a five day Drinking-in-the-Dark (DID) procedure where they received 20% ethanol or 0.2% saccharin for two hours, three hours into the dark cycle, each day. Throughout the five drinking sessions, animals were kept in home-cage locomotor activity chambers to monitor activity throughout the drinking cycle. Day 4 drinking was immediately preceded by a mock microinjection, whereas Day 5 drinking was immediately preceded by a drug microinjection. Microinjection of one of five doses of baclofen was given in ng/side dissolved in 200 µl of aCSF (aCSF alone, 0.02 R(+)-, 0.04 R(+)-, 0.08 S(-)-, or 0,16 S(-)-). Intake was recorded every twenty minutes on Days 4 and 5. Retro-orbital sinus blood samples were taken from ethanol animals immediately following the Day 5 drinking period to determine blood ethanol concentrations (BECs). A one-way ANOVA on total Day 4 ethanol consumption revealed no baseline differences between dose groups. A one-way ANOVA on total Day 5 ethanol consumption revealed that the 0.04 R(+)- baclofen dose reduced total drinking, but the 0.16 S(-)- baclofen dose increased total drinking (p’s<0.05). This pattern was reflected in the BECs; 0.04 R(+)- baclofen reduced BECs, whereas 0.16 S(-)- baclofen increased BECs (p’s<0.05). These results were also time-dependent, with R(+)-baclofen reducing drinking in the first 20 minutes of the session and S(-)- increasing drinking in the last 40 minutes of the session. There were no effects on saccharin intake. An issue with the locomotor activity boxes led to unreliable locomotor activity counts. However, because there were no drug effects on saccharin consumption, it was concluded that locomotor effects did not contribute to the decreases or increases in ethanol consumption. These results further implicate the role of GABAB receptors in modulating ethanol intake. The bidirectional effects shown highlight the importance of considering enantioselective drug effects when interpreting data. Finally, these results also support previous conclusions that the AcbSh plays an important role in modulating use of drugs of abuse, but not other reinforcers.
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Amend, Diane Lisa 1964. "The effect of pentylenetetrazol kindling on the somatostatin cell population in the rat hippocampus." Thesis, The University of Arizona, 1990. http://hdl.handle.net/10150/278383.
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The kindling model of epilepsy in animals has become a widely used tool in the study of convulsive mechanisms. A recent interest in the role of somatostatin (SS) in epileptic brains has produced a small body of literature, but few insights into the function of SS in seizures. Two experiments utilizing a chemical model of kindling were used. Experiment 1 using a high dose of pentylenetetrazol (PTZ) (30mg/kg) and experiment 2 using a subseizure dose of PTZ (20mg/kg). Behavioral results of experiment 1 showed an increase in seizure sensitivity over the 2 month course of the study but failed immunostaining confounded any anatomical localization of SS. Behavioral results of experiment 2 yielded no significant difference between control and experimental animals but showed both qualitative differences and a decreased number of SS cells in the experimental group. The results of these studies make few predictions about the role of SS in seizure activity or in the kindling model of epilepsy and it is painfully obvious that more work needs to be done in this realm.
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Idrus, Nirelia, and n/a. "Investigation of cerebellar cell death after ethanol exposure during development." University of Otago. Department of Anatomy & Structural Biology, 2007. http://adt.otago.ac.nz./public/adt-NZDU20071127.162052.
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Binge-like ethanol exposure of the rat during the developmental period, equivalent to the human third trimester, results in a permanent loss of cerebellar Purkinje and granule cells. This study presents data that defines the temporal and lobular windows of acute cell death in specific layers of the developing cerebellar vermis following a single ethanol binge. Any resulting permanent effects on Purkinje cell number following ethanol exposure prior to postnatal day (PD) 4 are also presented.
Sprague-Dawley pups were randomly assigned to either alcohol-exposed (AE) (4.5g/kg/day; two feedings via intragastric intubation) or sham-intubation control (IC) groups, and treated on a single day during PD0-10. 10-12 hours after treatment, active caspase-3 immunohistochemistry detected cells that had entered the apoptotic cell death pathway. The total number of caspase-3-positive cells in the developing layers of the vermis (Purkinje cells [Pcells]; external granular [eGL]; internal granular [iGL]) were counted using the physical disector/fractionator method. Ethanol induced significantly more cell death - its acute neurotoxic effect was observed on Pcells from PD0-8; on eGL cells on PD0-3, PD7 and PD9; and on cells in the iGL on PD3 and PD6-10. Regional variability was also demonstrated on a lobular basis in each cell population.
A second cohort of pups was treated on either PD0, PD2 or PD4. The total number of Pcells in the adult vermis, Lobule III and Lobule IX were determined using the optical disector/Cavalieri technique. Significantly fewer Pcells were counted in the vermis of PD4-treated AE animals, and a significant deficit in Pcells within Lobule III was observed in PD2-treated AE animals. Ethanol exposure on PD2 or PD4 showed a tendency towards there being a significant deficit in Pcell number within Lobule IX, but a 10-20% Pcell loss is certainly biologically and clinically relevant.
No significant differences in Pcell numbers were observed in the adult rat following ethanol treatment on PD0, either on a vermal or lobular basis, despite the significant acute cell death observed. Whether the rate of naturally occurring cell death decreased following early ethanol exposure on PD0 was subsequently investigated.
This thesis is the first to demonstrate acute apoptosis induced by ethanol prior to PD4, which may result in permanent Pcell loss. Activated caspase-3 was detected in cells throughout the developing cerebellar cortex, indicating many cell types are acutely vulnerable to ethanol over longer timeperiods than previously recognised. This thesis also showed significant cell loss could occur in discrete cerebellar sub-regions, which may have consequences for cerebellar function. This is important to the human condition, as a single ethanol episode is all that is required to delete neurons rapidly and permanently from the developing brain.
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Holdcraft, Robert Wesley. "Regulation of spermatogenesis by androgen receptor : effect of hypomorphic and cell-specific mutations /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/10249.
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Luk, Hui Ying. "Effect of the Resistance Exercise-Induced Hormonal Changes on Satellite Cell Myogenic State." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1157528/.
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Skeletal muscle satellite cells are important for muscle repairing and muscle mass growth. For a successful muscle regenerative process, satellite cells have to sequentially undergoing different stages of myogenic process, i.e. proliferative state and differentiation state. To support this process, the presence of different circulating factors, such as immune cells, cytokines, and hormones, at the appropriate time course is critical. Among these factors, hormones, such as testosterone, cortisol, and IGF-1, have shown to play an important role in satellite cell proliferation and differentiation. Studies investigated the effect of testosterone on satellite cell using a supraphysiological dose in human or in cell culture demonstrated that testosterone is critical in satellite cell myogenic process. Due to the anabolic effect of testosterone on muscle, studies had been focused on the physiological means to increase the circulating testosterone concentration in the body to maximize the muscle mass growth from resistance exercise. The acute and transient increase in testosterone has shown to be beneficial to muscle mass growth and strength gain; however, this change in physiological testosterone concentration on satellite cell myogenesis is not known. Therefore the purpose of this dissertation is to first determine the effect of acute change in exercise-induced hormones on satellite cell myogenic state, then to determine if testosterone promotes satellite cell proliferation.
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Li, Yiming. "Ryanodine receptors in calcium signaling pathways." Scholarly Commons, 2008. https://scholarlycommons.pacific.edu/uop_etds/710.
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Calcium (Ca2+) plays an important role as a second messenger, transmitting the message of arrival of stimuli such as hormones and neurotransmitters to the intracellular system that carries out the cellular response to the stimulus. The universality of Ca2+ as an intracellular messenger depends on its enormous versatility. This versatility is exploited to control processes as diverse as fertilization, proliferation, development, learning and memory, contraction and secretion, and must be accomplished within the context of Ca2+ being highly toxic.
Ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs) are Ca2+ -release channels located on intracellular membranes of the endoplasmic reticulum (ER)/sarcoplasmic reticulum (SR) that perform essential functions as key targets of hormone/neurotransmitter action to initiate intracellular Ca2+ signals. The purpose of this project was to study the role of RyR2 in Ca2+ signaling in the NG115-401L neuronal cell line. siRNA transfection methods were employed to knockdown RyR2 expression levels in NG115-401L cells. We used reverse transcription and real-time PCR to evaluate RyR2 gene expression in transfected/untransfected cells. We also evaluated cytosolic Ca2+ changes induced by RyR activators or regulators, using fura-2 AM as the Ca2+ indicator. Successful RyR2 gene knockdown allowed us to carry out some initial experiments to characterize the specific roles played by the RyR2 receptor isoform. We examined cell responses to FK-506 under the condition of RyR2 knockdown, finding that RyR2 appears to confer selectivity to this response. Finally, the effects of siRNA transfection and FK-506 treatment on NG115-401L cell growth were evaluated. These experimental results may contribute to future studies of RyR2, and help develop novel treatments for RyR2-base d dysfunctional diseases.
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Cui, Rui. "The role of Ryanodine receptors in neuronal calcium signaling." Scholarly Commons, 2008. https://scholarlycommons.pacific.edu/uop_etds/705.
Full textAbstract:
Calcium (Ca2+) is a universal second messenger controlling a wide variety of cellular reactions and adaptive responses. All the versatility of a Ca2+ signaling requires that the concentration of Ca2+ ions in the cytoplasm be highly regulated. Generation of Ca2+ mobilizing signals in cells involves regulation by multiple components controlling Ca2+ release from the internal stores, Ca2+ influx across the plasma membrane, elicitation of Ca2+ sensitive processes and finally the removal of Ca2+ from the cells.
Inositol-1, 4, 5-trisphosphate receptors (IP3Rs) and ryandine receptors (RyRs) are the most studied Ca2+ release channels located on the internal stores. Previous studies have shown ryanodine receptors (RyRs) play a key role in the process of Ca2+ signaling participating in the oscillatory patterns of controlling the release of Ca2+ from ER and regulating the influx of Ca2+ by coupling with plasma Ca2+ channels. Although recent progress deciphered the behavior and function of RyRs in regulation of Ca2+ signal, it still remains mysterious in understanding the molecular mechanism of its regulation and its connection with plasma membrane Ca2+ channels in neuronal cells. Here this study aimed to utilized the most cutting-edge RNA interference techniques, along with well-characterized pharmacological regulators of RyRs, to better characterized the role of RyRs is our neuronal cell line model NG115-401L.
Our first main goal of this project was to develop an effective protocol that could selectively knockout or knockdown expression levels of the RyR1 gene in NG115-401L cells. After testing different siRNA primers including their combination with different transfection reagent, the result shows a significant silencing effect to the RyR1 mRNA expression levels. In the second part of this study, we used a group of pharmacological agents with well-known regulatory actions on RyRs to characterize the functional roles of the RyRs expressed in NG115-401L cells. All four agonists which are ryanodine, caffeine, CMC and PCB 95 show their abilities to activate the RyRs, increase [Ca2+]iand induce the influx of Ca2+ via SOC. After transfected NG115-401L cells by siRNA, the Ca2+ release and influx signals were highly diminished suggesting RyR1 gene was successfully knocked down and the successfully knocked down and the Ca2+ mobilization mediated by RyR1 was decreased greatly. Finally in order to study the effects of the regulation of Ca2+ by RyR modulators and RyR gene knockdown on cell growth patterns and cell viability, the NG115-401L cells were exposed to various concentrations of RyR regulators and siRyR1 primer for different time periods. The siRNA transfection showed the least effect on cell growth, as compared with pharmacological agents that modulate RyR function. Considering we achieved high levels of gene knockdown and its low cytotoxity, our result suggests that siRNA silencing for RyRs may become a promising gene therapeutic target in the future.
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Mattern, Janet. "Muscarinic Receptor Modulation of the Phospholipid Effect in Cardiac Myocytes." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc500469/.
Full textAbstract:
The muscarinic agonist carbachol stimulates a rapid increase in ^32Pi incorporation into phosphatidic acid (PA) and phosphatidylinositol (PI) in calcium tolerant myocytes prepared from heart tissue. The density of muscarinic receptors, determined by [^3H]-QNB binding, is greater in the atria than in the ventricles. 250 uM carbachol decreased specific [^3H]-QNB binding to muscarinic receptors on myocyte membranes by fifty percent. Trifluoperazine, also a phospholipase C inhibitor, inhibited the carbachol stimulated increase in ^32Pi incorporation into PA and PI and did not interfere with muscarinic receptor binding. Therefore, isolated canine myocytes provide a suitable model system to further study the muscarinic receptor stimulated phospholipid effect, and its role in mediating biochemical processes and physiological function in the heart.
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Deering, Susan. "The effect of overexpressing prolactin receptors on cell proliferation and milk protein synthesis in a bovine mammary epithelial cell line." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ50752.pdf.
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Deering, Susan. "The effect of overexpressing prolactin receptors on cell proliferation and milk protein synthesis in a bovine mammary epithelial cell line /." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21538.
Full textAbstract:
The Mac-T cell system was used to investigate the role of the prolactin (PRL) receptor in cell proliferation and the regulation of milk protein synthesis. This study was designed to investigate whether overexpressing the PRLR in the Mac-T cell line resulted in a change in its growth rate and an enhancement of its ability to produce milk proteins. To accomplish these goals, Mac-T cells were stably transfected with the rabbit prolactin receptor gene. Fifteen clones and a pool of transfectants were obtained. Of these, one clone and the pool were positive for the PRL receptor expression. The clone (S15) and pool (SP) cells were sorted into high (H), medium (M), and low (L) expressors, of the PRLR. The high expressors were used for all subsequent experiments. The presence of high levels of the PRLR on the surface of S15 and SP cells was further confirmed by receptor binding assay and Western Blot. Following the establishment of these cell lines, the cells were used to investigate the effect of increased levels of PRLR on cell proliferation and milk protein synthesis.It was found that the growth rate of parental cells was depressed in the presence of 5 mug/ml of PRL. In contrast, the growth rate of the transfectants was enhanced by the addition of 5 mug/ml PRL to the culture medium. In addition, both "SP" and "S15" cells produced higher levels of STAT5 upon long-term (48 h) PRL stimulation. No effect on the synthesis of alpha S1- and beta-caseins was noted. It is likely that no differences in protein synthesis were observed because the cells have lost the ability to differentiate, even when cultured on collagen gels in the presence of lactogenic hormones.
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Klipp, Robert Carl. "Catecholamine Interactions with the Cardiac Ryanodine Receptor." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/1439.
Full textAbstract:
The cardiac ryanodine receptor (RyR2) is a Ca2+ ion channel found in the sarcoplasmic reticulum (SR), an intracellular membranous Ca2+ storage system. It is well known that a destabilization of RyR2 can lead to a Ca2+ flux out of the SR, which results in an overload of intracellular Ca2+; this can also lead to arrhythmias and heart failure. The catecholamines play a large role in the regulation of RyR2; stimulation of the Beta-adrenergic receptor on the cell membrane can lead to a hyperphosphorylation of RyR2, making it more leaky to Ca2+. We have previously shown that strong electron donors will inhibit RyR2. It is hypothesized that the catecholamines, sharing a similar structure with other proven inhibitors of RyR2, will also inhibit RyR2. Here we confirm this hypothesis and show for the first time that the catecholamines, isoproterenol and epinephrine, act as strong electron donors and inhibit RyR2 activity at the single channel level. This data suggests that the catecholamines can influence RyR2 activity at two levels. This offers promising insight into the potential development of a new class of drugs to treat heart failure and arrhythmia; ones that can both prevent the hyperphosphorylation of RyR2 by blocking the Beta;-adrenergic receptor, but can also directly inhibit the release of Ca2+ from RyR2.
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Shanmugam, Vijayalakshmi. "Characterization of osteopontin in RSV transformed rat-1 cells and its role in cell transformation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0005/NQ37025.pdf.
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Ong, Jennifer. "GABA and GABA-receptors in the enteric nervous system /." Title page, contents and summary only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09pho582.pdf.
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Eager, Blenerhassit Edward. "The modulating effect of sildenafil on cell viability and on the function of selected pharmacological receptors in cell cultures / B.E. Eagar." Thesis, North-West University, 2004. http://hdl.handle.net/10394/611.
Full textAbstract:
Since sildenafil's (Viagra®), a phospodiesterase type 5 (PDE5) inhibitor, approval for the
treatment of male erectile dysfunction (MED) in the United States early 1998, 274
adverse event reports were filed by the Food and Drug Administration (FDA) between 4
Jan. 1998 and 21 Feb. 2001 with sildenafil as the primary suspect of various
neurological disturbances, including amnesia and aggressive behaviour (Milman and
Arnold, 2002). These and other research findings have prompted investigations into the
possible central effects of sildenafil.
The G protein-coupled muscarinic adetylcholine receptors (mAChRs) and serotonergic
receptors (5HT-Rs), have been linked to antidepressant action (Brink et al. 2004).
GPCRs signal through the phosphatidylinositol signal transduction pathway known to
activate protein kinases (PKs). Since the nitric oxide (NO)-guanylyl cyclase signal
transduction pathway is also known to involve the activation of PKs (via cyclic guanosine
monophosphate (cGMP)), the scope is opened for sildenafil to possibly modulate the
action of antidepressants by elevating cGMP levels.
It is generally assumed that excitotoxic delayed cell death is pathologically linked to an
increase in the release of excitatory neurotransmitters e.g. glutamate. Glutamate
antagonists, especially those that block the define NMDA-receptors, are neuroprotective,
showing the importance of the NMDA-NO-cGMP pathway in neuroprotection (Brandt et
al., 2003). Sildenafil may play a role in neuroprotection by elevating cGMP levels.
Aims: The aims of the study were to investigate any neuroprotective properties of
sildenafil, as well as modulating effects of sildenafil pre-treatment on mAChR function.
Methods: Human neuroblastoma SH-SY5Y or human epithelial HeLa cells were seeded
in 24-well plates and pre-treated for 24 hours in serum-free medium with no drug
(control), PDE5 inhibitors sildenafil (100nM and 450 nM), dipiridamole (20 µM) or
zaprinast (20 µM), non-selective PDE inhibitor 3-isobutyl-I-methylxanthine (IBMX -
ImM), cGMP analogue N2,2'-0-dibutyrylguanosine 3'5'-cyclic monophosphate sodium
salt (500 µM), guanylcyclase inhibitor 1H-[1 ,2,4]oxadiazolo[4,3-a]quinoxalin-I-one (ODQ
- 3 µM) or sildenafil + ODQ (450 nM and 3 µM respectively). Thereafter cells were used
to determine mAChR function by constructing dose-response curves of methacholine or
to determine cell viability utilising the Trypan blue, propidium iodide and MTT tests for
cell viability.
Results: Sildenafil pre-treatments induced a 2.5-fold increase in ,the Emax value of
methacholine in neuronal cells but did not show a significant increase in epithelial cells
The Trypan blue test suggests that neither the PDE5 inhibitors nor a cGMP analogue
show any neuroprotection. Rather, sildenafil 450 nM, dipiridamole and IBMX displayed
a neurodegenerative effect. The MTT test was not suitable, since pre-treatment with the
abovementioned drugs inhibited the formation of forrnazan. The propidium iodide assay
could also not be used, due to severe cell loss.
Conclusion: Sildenafil upregulates mAChR function in SH-SY5Y cells and displays a
neurodegenerative, and not a protective property, in neuronal cells. This is not likely to
be associated with its PDE5 inhibitory action, but may possibly be linked to an increase
in cGMP levels via the NO-cGMP pathway.Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.
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Stein, Melissa Marie. "Humoral and T cell immune responses to model antigen delivered with biomaterials used in tissue engineering." Thesis, Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/20175.
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Wang, Hongying, and 汪紅英. "Studies on the mechanisms of cigarette smoke-induced apoptosis and cell proliferation in gastric epithelial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B3124113X.
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BECKMANN, M. PATRICIA. "SYNTHESIS AND OLIGOSACCHARIDE PROCESSING OF NORMAL AND ALTERED IMMUNOGLOBULIN M DURING B-CELL DIFFERENTIATION (GLYCOPROTEIN, GLYCOPEPTIDE, MUTANT, CARBOHYDRATE, ASPARAGINE-LINKED)." Diss., The University of Arizona, 1985. http://hdl.handle.net/10150/187906.
Full textAbstract:
Glycoproteins play a key role in cellular growth and differentiation. In order to study glycoprotein biosynthesis and processing, we have chosen the murine Immunoglobulin M (IgM) system as a model. Our system utilizes hybridoma, lymphoma and plasmacytoma cell lines which synthesize intracellular, membrane-bound and secreted IgM. Each type of IgM is synthesized during a specific phase of B-cell differentiation. We have examined the kinetics of IgM synthesis and processing in cells at each developmental stage. The rate of synthesis of membrane-bound and soluble IgM are different. Characteristic rates for membrane versus soluble IgM may be dependent on the extent of oligosaccharide processing. The membrane-bound IgM contains more high-mannose oligosaccharide than does the secreted product. In addition, we have begun to determine how protein structural requirements can affect final glycosylation patterns on the glycoprotein. Two cell lines were studied which secreted smaller than normal IgM heavy chains in tissue culture. One cell line studied (208) contains one glycosylation site, while another (562) retains three sites on the molecule synthesized in tissue culture. Studies performed on these cell lines in tissue culture indicate greater processing of the oligosaccharides on these mutant IgM molecules when compared to the parental cell line (PC700). Studies on the 208 IgM molecules synthesized in the mouse and purified from ascites fluid confirm these results. Upon injection into the mouse, the 562 cell line reverts to produce protein and carbohydrate structures characteristic of the parental cell line. Studies on the 562 protein purified from ascites fluid illustrate the need for more precisely defined cell lines and genetic engineering for the study of altered protein structures.
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Hoong, Isabelle Yoke Yien. "Expression of 11β-hydroxysteroid dehydrogenases in mice and the role of glucocorticoids in adipocyte function." Monash University, Dept. of Biochemistry and Molecular Biology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9473.
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Wong, Tin Lok. "Mechanism of action of silicon in cell signalling." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709339.
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Whittington, John. "Physiological effects of salinity on chara corallina /." Title page, contents and summary only, 1990. http://web4.library.adelaide.edu.au/theses/09PH/09phw6258.pdf.
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Chen, Jianping. "The Effects of Chronic Ethanol Intake on the Allosteric Interaction Between GABA and Benzodiazepine at the GABAA Receptor." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc501231/.
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This study examined the effects of chronic ethanol intake on the density, affinity, and allosteric modulation of rat brain GABAA receptor subtypes. In the presence of GABA, the apparent affinity for the benzodiazepine agonist flunitrazepam was increased and for the inverse agonist R015-4513 was decreased. No alteration in the capacity of GABA to modulate flunitrazepam and R015-4513 binding was observed in membranes prepared from cortex, hippocampus or cerebellum following chronic ethanol intake or withdrawal. The results also demonstrate two different binding sites for [3H]RO 15-4513 in rat cerebellum that differ in their affinities for diazepam. Chronic ethanol treatment and withdrawal did not significantly change the apparent affinity or density of these two receptor subtypes.
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Shao, Zuoyi. "The effect of polyamine amide toxins and polyamines in nicotinic acetylcholine receptors of the TE671 cell line." Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338532.
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Judkins, Courtney Peta. "Pharmacological characterisation of relaxin and the relaxin receptor." Monash University, Dept. of Pharmacology, 2004. http://arrow.monash.edu.au/hdl/1959.1/9497.
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Deo, P. "Effect of Food-Derived Advanced Glycation Endproducts on Receptors and Markers of Oxidative Stress in Human Cell Lines." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501257.
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Schroeder, Jan-Hendrik. "Adherence of microfilariae of the filarial nematode Brugia malayi to human endothelial cells and their effect on human endothelial cell mediated immune responses." Thesis, Royal Veterinary College (University of London), 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558986.
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Rider, Mark Sterling. "Effect of Cell-Specific, Music-Mediated Mental Imagery on Secretory Immunoglobulin A (sIgA)." Thesis, University of North Texas, 1988. https://digital.library.unt.edu/ark:/67531/metadc331777/.
Full textAbstract:
This study was an investigation of the effects of physiologically-oriented mental imagery on immune functioning. College students with normal medical histories were randomly selected to one of three groups. Subjects in Group 1 participated in short educational training on the production of secretory immunoglobulin A. They were then tested on salivary IgA, skin temperature and the Profile of Mood States (POMS) before and after listening to a 17-minute tape of imagery instructions with specially-composed background "entrainment" music, designed to enhance imagery. Subjects in Group 2 (placebo controls) listened to the same music but received no formal training on the immune system. Group 3 acted as a control and subjects were tested before and after 17 minutes of no activity. Treatment groups listened to their tapes at home on a bi-daily basis for six weeks. All groups were again tested at Weeks 3 and 6. Secretory IgA was analyzed using standard radial immuno-diffusion techniques. Repeated measures analyses of variance with planned orthogonal contrasts were used to evaluate the data. Significant overall increases (p < .05) were found between pre- and posttests for all three trials. Groups 1 and 2 combined (treatment groups) yielded significantly greater increases in slgA over Group 3 (control) for all three trials. Group 1 (imagery) was significantly higher than Group 2 (music) in antibody production for Trials 2 and 3. No group differences were noted in saliva volume or skin temperature, indicating that autonomic physiological mechanisms were not responsible for differences in antibody production. POMS changes more often favored Group 1. Symptomatology, recorded by subjects at weeks three and six, was significantly lower for three symptoms (rapid heartbeat, breathing difficulty, and jaw clenching), again favoring both treatment groups over the control group. Conclusions were that CNS-mediated immunoenhancement through mental imagery is possible.
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Chow, Ka-man. "The antioxidant effect of lycium fruit extract on hyperglycemia-induced oxidative stress in human liver and rat muscle cell lines." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36186132.
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Vingren, Jakob L. "Effect of Chronic Alcohol Abuse and Resistance Training on the Skeletal Muscle Androgen Receptor Concentration of Rats." Thesis, University of North Texas, 2004. https://digital.library.unt.edu/ark:/67531/metadc4540/.
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The purpose was to examine the effect of chronic alcohol abuse on the androgen receptor content (AR) in skeletal muscle, and to determine if this effect was influenced by resistance training. Thirty-four male rats (456 ± 1 g; mean ± SE) were divided into 4 groups: Sham exercise-Ethanol, Sham exercise-Normal diet, Exercise-Ethanol, and Exercise-Normal diet. Both Exercise groups underwent a 6-week "squat" resistance training protocol and both Ethanol groups received an alcohol-rich diet throughout the 6-week period. Western blot analysis showed no effect of alcohol or resistance training on the AR of the extensor digitorum longus. For the rectus femoris, alcohol caused a decline in the AR (p=0.01). This reduction was not attenuated by resistance training. The AR of the soleus was not affected by chronic alcohol abuse alone; however, the resistance training induced increase in the AR was prevented by chronic alcohol abuse (p=0.03).
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黃卓睿 and Cheuk-yui Max Wong. "Role of k-opioid receptor in cardioprotection against stress with coldexposure and restraint or against morphine." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31971283.
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Xia, Yun. "Neuronal Network Analyses in vitro of Acute Individual and Combined Responses to Fluoxetine and Ethanol." Thesis, University of North Texas, 2002. https://digital.library.unt.edu/ark:/67531/metadc3191/.
Full textAbstract:
Embryonic murine neuronal networks cultured on microelectrode arrays were used to quantify acute electrophysiological effects of fluoxetine and ethanol. Spontaneously active frontal cortex cultures showed highly repeatable, dose-dependent sensitivities to both compounds. Cultures began to respond to fluoxetine at 3 µM and were shut off at 10-16 µM. EC50s mean ± S.D. for spike and burst rates were 4.1 ± 1.5 µM and 4.5 ± 1.1 µM (n=14). The fluoxetine inhibition was reversible and without effect on action potential wave shapes. Ethanol showed initial inhibition at 20 mM, with spike and burst rate EC50s at 52.0 ± 17.4 mM and 56.0 ± 17.0 mM (n=15). Ethanol concentrations above 100 -140 mM led to cessation of activity. Although ethanol did not change the shape and amplitude of action potentials, unit specific effects were found. The combined application of ethanol and fluoxetine was additive. Ethanol did not potentiate the effect of fluoxetine.
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Lee, Sherman. "The effect of acute cigarette smoke exposure on regional pulmonary blood flow, volume, red cell transit and polymorphonuclear leukocyte retention in the rabbit lung." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24840.
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Regional pulmonary blood flow and volume was measured in ten rabbits
anesthetized with pentobarbital (30 mg/kg). Tracheostomy was performed and
catheters were placed into the jugular vein and carotid artery. The cardiac
⁹⁹mtc output was measured using the indicator-dilution technique using Tc labelled RBC followed by an injection of radiolabelled macroaggregates (MAA) to mark regional blood flow. Measurements were made both before and after either exposure to cigarette smoke (3 cigarettes for ten minutes at 4 puffs/minute) or sham exposure to air. The animals were sacrificed and the lungs were removed with the vessels tied. The lungs were then inflated and rapidly frozen over liquid nitrogen. The lungs were sampled into slices by vertical height, each slice was further sampled and then gamma counted for the injected isotopes. Regional pulmonary blood flow was calculated by setting the total lung MAA counts for each MAA equal to the cardiac output so that the sample flow was calculated as the fraction of sample counts to total counts times the cardiac output. The blood volume was marked by the labelled RBC and RBC transit was calculated as blood volume (ml) divided by blood flow (ml/sec).
In a second series of experiments (N=10) , ⁵¹Cr PMN were injected as a bolus along with ⁹⁹mtc RBC in an indicator-dilution run. Following the injection of the cells, the blood flow was marked with MAAs and then the same sham or smoke treatments were given as in the previous experiments. At the end of ten minutes, the animals were sacrificed and the lungs were processed the same as before. Regional PMN retention was calculated as the [formula omitted]. The data show that smoke exposure increased pulmonary blood volume (p<.01), pulmonary transit time (pPathology and Laboratory Medicine, Department of
Graduate
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Franco, Rohini-Ann. "Effect of Estrogen on LPS-induced human endothelial cell adhesion moledule expression and calcium signaling." Scholarly Commons, 2005. https://scholarlycommons.pacific.edu/uop_etds/627.
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Winter, Lara. "Characterisation of the neurosteroid analgesic alphadolone." Monash University, Dept. of Anaesthesia, 2004. http://arrow.monash.edu.au/hdl/1959.1/9669.
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Karhu, T. (Toni). "Isolation of novel ligands for MAS-related G protein-coupled receptors X1 and X2, and their effect on mast cell degranulation." Doctoral thesis, Oulun yliopisto, 2017. http://urn.fi/urn:isbn:9789526216331.
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Abstract The mast cells are an integral part of the human immune system. They are important modulators of inflammatory and physiological processes. Mast cells exert their functions through degranulation and release of inflammatory mediators, such as histamine, proteases and cytokines. There are two main pathways leading to the mast cell activation, the immunoglobulin-dependent and the immunoglobulin-independent pathway. The latter pathway can be triggered by several non-immunological stimuli, and two novel receptors responsible for the activation have been identified, the MAS-related G protein-coupled receptor X1 (MRGPRX1) and X2. The MRGPRX1 and MRGPRX2 have two established functions: i) they trigger the degranulation of mast cells and ii) they are involved in pain perception and itch on a specific subset of sensory neurons. These receptors are not expressed in all of the populations of mast cells, only in the tryptase and chymase containing mast cells, contributing to the mast cell heterogeneity. Unlike most G protein-coupled receptors, the MRGPRX1 and MRGPRX2 are quite non-selective, binding an ever growing list of different ligands. Their ligands include endogenous neuropeptides, host defense peptides and protein fragments, as well as synthetic compounds such as different antibiotics. Their endogenous ligands could be a triggering signal in some mast cell-related diseases by degranulating mast cells and thereby inducing inflammation. Due to the non-selectivity of MRGPRX1 and MRGPRX2, they probably still have many hitherto unknown ligands. The aim of this study was to isolate novel endogenous ligands for the MRGPRX1 and MRGPRX2 from human tissues with the “reverse pharmacology approach” and to determine their potential to degranulate mast cells. The starting materials for the isolation, human platelets and plasma, contained MRGPRX1 and MRGPRX2 activating compounds. From the human plasma, three fragments of albumin able to activate the MRGPRX2 were isolated and sequenced. These fragments were dose-dependently activating the MRGPRX2 and degranulating mast cells. Two MRGPRX1 activating hemoglobin β-chain fragments were isolated from human platelets. These fragments were dose-dependently activating the MRGPRX1, but had no effect on mast cell degranulationTiivistelmä Syöttösolut on tärkeä osa ihmisen immuunijärjestelmää. Ne ovat tärkeitä tulehdus- ja fysiologistenprosessien säätelijöitä. Syöttösolujen vaikutus välittyy degranulaation ja siinä vapautuvien tulehdusvälittäjäaineiden kautta. Vapautuviin aineisiin lukeutuu esim. histamiini ja lukuisia sytokiinejä, sekä proteaaseja. Syöttösolujen aktivaatio voi tapahtua immunoglobuliineista riippuvaa tai immunoglobuliineista riippumatonta reittiä pitkin. Monet ei-immunologiset tekijät voivat laukaista jälkimmäisen reitin ja kaksi uutta tähän vaikuttavaa G-proteiinikytkentäistä reseptoria on löydetty, MAS-related G protein-coupled receptor X1 (MRGPRX1) ja X2. MRGPRX1:llä ja MRGPRX2:lla on kaksi tunnettua tehtävää: i) ne laukaisevat syöttösolujen degranulaation ja ii) ne osallistuvat kivun ja kutinan aistimiseen tietyissä tuntohermoissa. Näitä reseptoreita ei ilmennetä kaikissa syöttösoluissa, vaan ainoastaa tryptaasia ja kymaasia sisältävissä syöttösoluissa, ja täten osaltaan selittävät syöttösolujen monimuotoisuutta. Useimmista G-proteiinikytkentäisistä reseptoreista poiketen MRGPRX1 ja MRGPRX2 ovat laajakirjoisia, sitoen monia erilaisia ligandeja. Ligandeihin kuuluu endogeenisia neuropeptidejä, antimikrobiaalisia peptidejä ja proteiinin fragmentteja, sekä synteettisiä yhdisteitä kuten erilaisia antibiootteja. Reseptoreiden endogeeniset ligandit voivat toimia laukaisijana jossain syöttösoluihin liittyvissä sairauksissa, degranuloidessaan syöttösoluja ja aiheuttaen paikallisen tulehdustilan. Reseptoreiden laajakirjoisuudesta johtuen niillä on oletettavasti monia vielä tuntemattomia ligandeja. Tämän tutkimuksen tarkoitus oli eristää uusia endogeenisiä ligandeja MRGPRX1:lle ja MRGPRX2:lle ihmisen kudoksista ”kääteisfarmakologista lähestymistapaa” hyödyntäen ja selvittää ligandien kyky syöttösolujen degranulaatioon. Lähtömateriaalina käytetyt ihmisen verihiutaleet ja plasma sisälsivät MRGPRX1:ta ja MRGPRX2:ta aktivoivia yhdisteitä. Plasmasta eristettiin ja sekvensoitiin kolme albumiinin fragmenttia, jotka aktivoivat MRGPRX2:ta. Nämä fragmentit aktivoivat MRGPRX2:ta ja degranuloivat syöttösoluja annosriippuvaisesti. Kaksi MRGPRX1:tä aktivoivaa hemoglobiinin β-ketjun fragmenttia eristettiin ihmisen verihiutaleista. Nämä fragmentit tunnistettiin hemorfiineiksi ja ne aktivoivat MRGPRX1:tä annosriippuvaisesti, mutta eivät vaikuttaneet syöttösolujen degranulaatioon
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McKendrick, Joseph James. "Epithelial ovarian cancer cell adhesion to extracellular matrix proteins and the effect on adhesion of peptide inhibitors of adhesion receptors." Thesis, University of Southampton, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316401.
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Thomas, William James. "60 Hz magnetic field exposure inhibits protein Kinase C dependent induction of Neuropeptide Y mRNA in PC-12 cells." CSUSB ScholarWorks, 1994. https://scholarworks.lib.csusb.edu/etd-project/907.
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