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Academic literature on the topic 'Puketa Camp (N. Z.)'
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Journal articles on the topic "Puketa Camp (N. Z.)"
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Ay, Binnaz, Adeyemi Iyanoye, Gary C. Sieck, Y. S. Prakash, and Christina M. Pabelick. "Cyclic nucleotide regulation of store-operated Ca2+ influx in airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 2 (February 2006): L278—L283. http://dx.doi.org/10.1152/ajplung.00188.2005.
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Sarcoplasmic reticulum (SR) Ca2+ release and plasma membrane Ca2+ influx are key to intracellular Ca2+ ([Ca2+]i) regulation in airway smooth muscle (ASM). SR Ca2+ depletion triggers influx via store-operated Ca2+ channels (SOCC) for SR replenishment. Several clinically relevant bronchodilators mediate their effect via cyclic nucleotides (cAMP, cGMP). We examined the effect of cyclic nucleotides on SOCC-mediated Ca2+ influx in enzymatically dissociated porcine ASM cells. SR Ca2+ was depleted by 1 μM cyclopiazonic acid in 0 extracellular Ca2+ ([Ca2+]o), nifedipine, and KCl (preventing Ca2+ influx through L-type and SOCC channels). SOCC was then activated by reintroduction of [Ca2+]o and characterized by several techniques. We examined cAMP effects on SOCC by activating SOCC in the presence of 1 μM isoproterenol or 100 μM dibutryl cAMP (cell-permeant cAMP analog), whereas we examined cGMP effects using 1 μM (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO nitric oxide donor) or 100 μM 8-bromoguanosine 3',5'-cyclic monophosphate (cell-permeant cGMP analog). The role of protein kinases A and G was examined by preexposure to 100 nM KT-5720 and 500 nM KT-5823, respectively. SOCC-mediated Ca2+ influx was dependent on the extent of SR Ca2+ depletion, sensitive to Ni2+ and La3+, but not inhibitors of voltage-gated influx channels. cAMP as well as cGMP potently inhibited Ca2+ influx, predominantly via their respective protein kinases. Additionally, cAMP cross-activation of protein kinase G contributed to SOCC inhibition. These data demonstrate that a Ni2+/La3+-sensitive Ca2+ influx in ASM triggered by SR Ca2+ depletion is inhibited by cAMP and cGMP via a protein kinase mechanism. Such inhibition may play a role in the bronchodilatory response of ASM to clinically relevant drugs (e.g., β-agonists vs. nitric oxide).
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Li, Fuying, Theresa A. Kopajtic, Jonathan L. Katz, Dan Luo, Thomas E. Prisinzano, Gregory H. Imler, Jeffrey R. Deschamps, Arthur E. Jacobson, and Kenner C. Rice. "Synthesis and Pharmacological Evaluation of Enantiopure N-Substituted Ortho-c Oxide-Bridged 5-Phenylmorphans." Molecules 27, no. 24 (December 12, 2022): 8808. http://dx.doi.org/10.3390/molecules27248808.
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The design of enantiopure stereoisomers of N-2-phenylcyclopropylmethyl-substituted ortho-c oxide-bridged phenylmorphans, the E and Z isomers of an N-cinnamyl moiety, and N-propyl enantiomers were based on combining the most potent oxide-bridged phenylmorphan (the ortho-c isomer) with the most potent N-substituent that we previously found with a 5-(3-hydroxy)phenylmorphan (i.e., N-2-phenylcyclopropyl methyl moieties, N-cinnamyl, and N-propyl substituents). The synthesis of the eight enantiopure N-2-phenylcyclopropylmethyl ortho-c oxide-bridged phenylmorphans and six additional enantiomers of the N-substituted ortho-c oxide-bridged phenylmorphans (N-E and Z-cinnamyl compounds, and N-propyl compounds) was accomplished. The synthesis started from common intermediates (3R,6aS,11aS)-10-methoxy-1,3,4,5,6,11a-hexahydro-2H-3,6a-methano-benzofuro[2,3-c]azocine (+)-6 and its enantiomer, (3S, 6aR, 11aR)-(-)-6, respectively. The enantiomers of ±-6 were obtained through salt formation with (S)-(+)- and (R)-(-)-p-methylmandelic acid, and the absolute configuration of the (R)-(-)-p-methylmandelate salt of (3S, 6aR, 11aR)-(-)-6 was determined by single-crystal X-ray analysis. The enantiomeric secondary amines were reacted with N-(2-phenylcyclopropyl)methyl derivatives, 2-(E)-cinnamyl bromide, and (Z)-3-phenylacrylic acid. These products led to all of the desired N-derivatives of the ortho-c oxide-bridged phenylmorphans. Their opioid receptor binding affinity was measured. The compounds with MOR affinity < 50 nM were examined for their functional activity in the forskolin-induced cAMP accumulation assay. Only the enantiomer of the N-phenethyl ortho-c oxide-bridged phenylmorphan ((-)-1), and only the (3S,6aR,11aR)-2-(((1S,2S)-2-phenylcyclopropyl)methyl)-1,3,4,5,6,11a-hexahydro-2H-3,6a-methanobenzofuro[2,3-c]azocin-10-ol isomer ((+)-17), and the N-phenylpropyl derivative ((-)-25) had opioid binding affinity < 50 nM. Both (-)-1 and (-)-25 were partial agonists in the cAMP assay, with the former showing high potency and low efficacy, and the latter with lower potency and less efficacy. Most interesting was the N-2-phenylcyclopropylmethyl (3S,6aR,11aR)-2-(1S,2S)-enantiomer ((+)-17). That compound had good MOR binding affinity (Ki = 11.9 nM) and was found to have naltrexone-like potency as a MOR antagonist (IC50 = 6.92 nM).
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Pearse, David B., and Patrice M. Becker. "Effect of time and vascular pressure on permeability and cyclic nucleotides in ischemic lungs." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 5 (November 1, 2000): H2077—H2084. http://dx.doi.org/10.1152/ajpheart.2000.279.5.h2077.
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We previously found that increased intravascular pressure decreased ischemic lung injury by a nitric oxide (NO)-dependent mechanism (Becker PM, Buchanan W, and Sylvester JT. J Appl Physiol 84: 803–808, 1998). To determine the role of cyclic nucleotides in this response, we measured the reflection coefficient for albumin (ςalb), fluid flux ( J˙), cGMP, and cAMP in ferret lungs subjected to either 45 min (“short”; n = 7) or 180 min (“long”) of ventilated ischemia. Long ischemic lungs had “low” (1–2 mmHg, n = 8) or “high” (7–8 mmHg, n = 6) vascular pressure. Other long low lungs were treated with the NO donor ( Z)-1-[ N-(3-ammoniopropyl)- N-( n-propyl)amino]diazen-1-ium-1,2-diolate (PAPA-NONOate; 5 × 10−4 M, n = 6) or 8-bromo-cGMP (5 × 10−4 M, n = 6). Compared with short ischemia, long low ischemia decreased ςalb (0.23 ± 0.04 vs. 0.73 ± 0.08; P < 0.05) and increased J˙ (1.93 ± 0.26 vs. 0.58 ± 0.22 ml · min−1 · 100 g−1; P < 0.05). High pressure prevented these changes. Lung cGMP decreased by 66% in long compared with short ischemia. Lung cAMP did not change. PAPA-NONOate and 8-bromo-cGMP increased lung cGMP, but only 8-bromo-cGMP decreased permeability. These results suggest that ischemic vascular injury was, in part, mediated by a decrease in cGMP. Increased vascular pressure prevented injury by a cGMP-independent mechanism that could not be mimicked by administration of exogenous NO.
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Guan, Win, Susan Thompson, and Jeanne Hurlburt. "Bright Line Eating: Efficacy Across Age in a Commercial Weight Loss Program Using a Food Addiction Model." Current Developments in Nutrition 5, Supplement_2 (June 2021): 410. http://dx.doi.org/10.1093/cdn/nzab038_022.
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Abstract Objectives As individuals age, they become more susceptible to developing weight-related obesity comorbidities–which makes weight loss and weight maintenance key issues in older age groups. Prior research on the efficacy of weight loss programs across age groups has yielded inconsistent results. The Bright Line Eating (BLE) program, which follows a food addiction model that emphasizes abstinence from added sugars and processed flours, has been shown to be effective for weight loss and weight maintenance. This study builds on that research to assess age-related differences in the efficacy of the BLE program. Methods Participants in this study (n = 4509; 93.9% white; 95.6% female; 29.6% overweight, 58.2% obese at baseline) attended an 8-week BLE Boot Camp program and completed pre- and post-program surveys that measured demographic characteristics, anthropometrics, and psychosocial factors. We used two-way ANOVA to assess the effect of age on % weight loss from baseline (%WL) while accounting for race, gender, and program adherence. Logistic regression was used to estimate the effect of age on improvement in quality of life, energy level, and life satisfaction. Results Participants experienced 6.5%WL (SD = 5.2) with no significant difference across age groups (F = 1.5, P = 0.15). After completing the BLE Boot Camp program, 54.3% reported improved quality of life, 46.6% reported higher energy levels, and 60.4% described increased life satisfaction. Percent weight loss was associated with improvements in all of psychosocial factors that we examined (z = 13.8, P < .000; z = 13.5, P < .000; z = 12.4, P < .000). Older study participants were more likely than younger to see an increase in energy level (z = 2.8, P = 0.01). Conclusions This evaluation of the BLE Boot Camp program demonstrated its success across all adult age groups. These results are particularly encouraging, given the need for feasible and scalable weight loss interventions that have been shown to be effective across all demographic groups. Funding Sources None to report.
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Larsen, Kristian Traberg, Tao Huang, Niels Christian Møller, Lars Bo Andersen, and Jan Sørensen. "Cost-effectiveness of a day-camp weight-loss intervention programme for children: Results based on a randomised controlled trial with one-year follow-up." Scandinavian Journal of Public Health 45, no. 6 (July 30, 2017): 666–74. http://dx.doi.org/10.1177/1403494816688374.
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Aims: The aim was to analyse the cost-effectiveness of an intensive weight-loss intervention for children compared with a low-intensity intervention. Methods: One hundred and fifteen overweight children (mean age 12.0 ± 0.4) were randomised to either the camp group (CG) ( N=59) or the standard group (SG) ( N=56). Participants in the CG were offered a six-week day-camp weight-loss programme followed by a family-based supportive programme containing four meetings during the succeeding 46 weeks. Participants in the SG were offered a weekly two-hour exercise session for six weeks. Changes in body mass index (BMI) and BMI z-score 12 months after inclusion were used to compare the effects of the two interventions. Incremental cost-effectiveness ratios (ICER) were estimated from the perspective of a Danish municipality. To achieve the required number of participants, an additional intervention was initiated one year later. Results: In comparison with the SG, the CG changed their mean BMI by −1.2 (95% CI −1.8 to −0.5). Compared with the SG children, the CG children changed their BMI z-score by −0.20 (95% CI −0.35 to −0.05). The ICER per decreased BMI point in the CG compared with the SG was DDK 24,928. Conclusions: Compared with the SG, the CG showed favourable effects after 12 months. However, the CG was more costly. The results observed in the present study may be helpful in guiding decision makers to take more informed decisions when choosing different types of intervention.
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Hopkins, Laura C., Christopher Holloman, Bernadette Melnyk, Mary Fristad, Jacqueline D. Goodway, Julie A. Kennel, Ihuoma Eneli, and Carolyn Gunther. "Participation in structured programming may prevent unhealthy weight gain during the summer in school-aged children from low-income neighbourhoods: feasibility, fidelity and preliminary efficacy findings from the Camp NERF study." Public Health Nutrition 22, no. 06 (January 3, 2019): 1100–1112. http://dx.doi.org/10.1017/s1368980018003403.
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AbstractObjectiveEvaluate the feasibility, fidelity and preliminary efficacy of Camp NERF to prevent unhealthy weight gain and promote healthy behaviours in children during the summer.DesignCamp NERF was an 8-week, multicomponent, theory-based programme coupled with the US Department of Agriculture’s Summer Food Service Program. Twelve eligible elementary-school sites were randomized to one of three treatment groups: (i) Active Control (non-nutrition, -physical activity (PA), -mental health); (ii) Standard Care (nutrition and PA); or (iii) Enhanced Care (nutrition and PA, plus cognitive behavioural techniques) programming. Efficacy was determined by assessing mean change by group in child outcomes using hierarchical linear regression models.SettingLow-income, urban neighbourhoods in Columbus, OH, USA.ParticipantsEconomically disadvantaged, racial minority children of elementary school age (kindergarten–5th grade).ResultsEighty-seven child–caregiver dyads consented; eighty-one completed pre- and post-intervention assessments resulting in a 93·10 % retention rate. Delivery of the intended lesson occurred 79–90 % of the time. Of the children, 56·98 % (n 49) were female; 89·53 % (n 77) were Black. Overall mean change in BMI Z-score from baseline to post-intervention was −0·03 (se 0·05); change in BMI Z-score did not differ significantly between treatment group. Change in nutrition, PA, mental health or psychosocial outcomes did not differ between groups.ConclusionsResults from the current study demonstrate feasibility and fidelity, yet no intervention effect of Camp NERF. Instead, findings suggest that participation in structured programming of any type (health behaviour-related or not) may prevent unhealthy summer weight gain. Additional studies are needed to confirm findings. Results have implications for child nutrition policy addressing the issue of summer health.
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Ishimaru, RS, K. Leung, L. Hong, and PS LaPolt. "Inhibitory effects of nitric oxide on estrogen production and cAMP levels in rat granulosa cell cultures." Journal of Endocrinology 168, no. 2 (February 1, 2001): 249–55. http://dx.doi.org/10.1677/joe.0.1680249.
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Previous studies demonstrated inhibitory effects of nitric oxide (NO) and cGMP on ovarian steroidogenesis. This study examined the effects of NO on estrogen levels and cAMP accumulation from immature cultured rat granulosa cells. Granulosa cells were incubated with media alone (control), FSH or FSH plus increasing concentrations of the NO generator, (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA/NO). While FSH increased estrogen levels 15-fold compared with controls, DETA/NO inhibited FSH-stimulated aromatase activity in a dose-dependent manner. Time-course studies revealed that the inhibitory effects of DETA/NO on aromatase activity persisted throughout the 72 h culture period. Treatment with DETA/NO also inhibited the stimulatory effects of forskolin on estrogen production, indicating that NO can influence steroidogenesis by actions downstream of the FSH receptor. Incubation of cells with FSH plus DETA/NO increased cGMP accumulation over 100-fold, compared with cells treated with media or FSH alone. In this regard, a cGMP analog mimicked the inhibitory effects of NO on FSH- and forskolin-stimulated estrogen production, indicating a potential mechanism of NO action. NO also decreased FSH-stimulated (cAMP) accumulation from cultured cells, indicating an antagonistic effect of NO on the second messenger mediating FSH actions. These findings demonstrate that NO inhibits estrogen production from rat granulosa cells, potentially reflecting actions on the second messengers cGMP and cAMP.
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Perkins, William J., Miwa Taniguchi, David O. Warner, Eduardo N. Chini, and Keith A. Jones. "Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 1 (July 2007): L84—L95. http://dx.doi.org/10.1152/ajplung.00368.2006.
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In a newly characterized cultured porcine pulmonary artery (PA) preparation, 24-h treatment with the nitric oxide (NO) donor ( Z)-1-[ N-(2-aminoethyl)- N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) decreased the response to acutely applied DETA-NO compared with 24-h control (−log EC50 6.55 ± 0.12 and 5.02 ± 0.21, respectively). Treatment of PA with the cell-permeable superoxide dismutase mimetic, Mn(III) tetra(4-benzoic acid) porphyrin chloride, did not change NO responsiveness in either freshly prepared or 24-h DETA-NO-treated PA. cGMP and cAMP phosphodiesterase activities were approximately equal in PA. Twenty-four-hour DETA-NO treatment did not change either cGMP or cAMP phosphodiesterase activities. Twenty-four hours in culture had no significant effect on soluble guanylyl cyclase (sGC) subunit mRNA expression, but 24-h DETA-NO treatment significantly decreased the expression of both sGCα1 and sGCβ1. sGCβ1 protein expression was 42 ± 4 ng/mg soluble protein. Twenty-four hours in culture without and with DETA-NO reduced sGCβ1 protein expression (36 ± 3 and 31 ± 3 ng/mg soluble protein, respectively, P < 0.025). Basal tissue cGMP [(cGMP)i] was significantly increased, and NO-induced (cGMP)i was significantly decreased by 24-h DETA-NO treatment. (cGMP)i normalized to the amount of sGC protein expressed in PA was significantly lower in PA treated for 24 h with DETA-NO compared with both freshly isolated and 24-h cultured PA. We conclude that prolonged NO treatment induces decreased acute NO responsiveness in part by decreasing both sGC expression and sGC-specific activity.
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Yokoshiki, H., Y. Katsube, and N. Sperelakis. "Regulation of Ca2+ channel currents by intracellular ATP in smooth muscle cells of rat mesenteric artery." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (February 1, 1997): H814—H819. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h814.
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Regulation of L-type Ca2+ channels of vascular smooth muscle (VSM) cells by adenosine 3',5'-cyclic monophosphate (cAMP)-dependent and guanosine 3',5'-cyclic monophosphate (cGMP)-dependent phosphorylation, which requires Mg2+ATP as a phosphate donor, has been reported (T. Ishikawa, J. R. Hume, and K. D. Keef. Circ. Res. 73: 1128-1137, 1993; Z. Xiong, N. Sperelakis, and C. Fenoglio-Preiser. J. Vasc. Res. 31: 271-279, 1994), and regulation by ATP has been demonstrated (Y. Ohya and N. Sperelakis. Circ. Res. 64: 145-154, 1989). However, it has not been elucidated whether the regulation by ATP is mediated by a mechanism that is distinct from phosphorylation. In the present study, we examined the effects of intracellularly perfused ATP on Ca2+ channel currents of VSM cells isolated from rat mesenteric arteries using a whole cell voltage clamp combined with an intracellular perfusion technique. Ba2+ currents (I(Ba)) through Ca2+ channels were evoked by depolarizing pulses from a holding potential of -80 mV with 130 mM Cs+ in the pipette and 100 mM Ba2+ in the bath. The decrease in the ATP concentration (from 5 to 0.1 mM) in the pipette caused a 45 +/- 5% (n = 8) reduction of maximal I(Ba) obtained at +40 mV within 10 min. The dose-response relation between I(Ba) and ATP showed a dissociation constant of 0.53 mM ATP. This concentration is much higher than that usually required for phosphorylation (e.g., few micromolar). Increase in the ATP (from 0.1 to 5 mM) caused an enhancement of maximal I(Ba) by 57 +/- 10% (n = 6), and this enhancement was not prevented in the presence of 30 microM H-7, a nonspecific inhibitor of protein kinases, or 1 microM protein kinase inhibitor, an inhibitor protein of cAMP-dependent protein kinase. These results indicate that slow Ca2+ channels in VSM cells are regulated by intracellular ATP, independently of phosphorylation, implying a direct regulatory action, such as a requirement for ATP binding to the inner surface of the channel, to exhibit activity.
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Erdemli, G., Y. Z. Xu, and K. Krnjevic. "Potassium Conductance Causing Hyperpolarization of CA1 Hippocampal Neurons During Hypoxia." Journal of Neurophysiology 80, no. 5 (November 1, 1998): 2378–90. http://dx.doi.org/10.1152/jn.1998.80.5.2378.
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Erdemli, G., Y. Z. Xu, and K. Krnjević. Potassium conductance causing hyperpolarization of CA1 hippocampal neurons during hypoxia. J. Neurophysiol. 80: 2378–2390, 1998. In experiments on slices (from 100- to 150-g Sprague-Dawley rats) kept at 33°C, we studied the effects of brief hypoxia (2–3 min) on CA1 neurons. In whole cell recordings from submerged slices, with electrodes containing only KMeSO4 and N-2-hydroxyethylpiperazine- N′-2-ethanesulfonic acid, and in the presence of kynurenate and bicuculline (to minimize transmitter actions), hypoxia produced the following changes: under current clamp, 36 cells were hyperpolarized by 2.7 ± 0.5 (SE) mV and their input resistance ( R in) fell by 23 ± 2.7%; in 30 cells under voltage clamp, membrane current increased by 114 ± 22.3 pA and input conductance ( G in) by 4.9 ± 0.9 nS. These effects are much greater than those seen previously with K gluconate whole cell electrodes, but only half those seen with “sharp” electrodes. The hypoxic hyperpolarizations (or outward currents) were not reduced by intracellular ATP (1–5 mM) or bath-applied glyburide (10 μM): therefore they are unlikely to be mediated by conventional ATP-sensitive K channels. On the other hand, their depression by internally applied ethylene glycol-bis-(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid (1.1 and 11 mM) and especially 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid (11–33 mM) indicated a significant involvement of Ca-dependent K (KCa) channels. The β-adrenergic agonist isoprenaline (10 μM) reduced hypoxic hyperpolarizations and decreases in R in ( n = 4) (and in another 11 cells corresponding changes in G in); and comparable but more variable effects were produced by internally applied 3′:5′-adenosine cyclic monophosphate (cAMP, 1 mM, n = 6) and bath-applied 8-bromo-cAMP ( n = 8). Thus afterhyperpolarization-type KCa channels probably take part in the hypoxic response. A major involvement of G proteins is indicated by the near total suppression of the hypoxic response by guanosine 5′- O-(3-thiotriphosphate) (0.1–0.3 mM, n = 23) and especially guanosine 5′- O-(2-thiodiphosphate) (0.3 mM, n = 26), both applied internally. The adenosine antagonist 8-( p-sulfophenyl)theophylline (10–50 μM) significantly reduced hypoxic hyperpolarizations and outward currents in whole cell recordings (with KMeSO4 electrodes) from submerged slices but not in intracellular recordings (with KCl electrodes) from slices kept at gas/saline interface. In further intracellular recordings, antagonists of γ-aminobutyric acid-B or serotonin receptors also had no clear effect. In conclusion, these G-protein-dependent hyperpolarizing changes produced in CA1 neurons by hypoxia are probably initiated by Ca2+ release from internal stores stimulated by enhanced glycolysis and a variable synergistic action of adenosine.
Books on the topic "Puketa Camp (N. Z.)"
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dkova, Ludmila Chla. Litome r ice, Terezi n: Places of suffering and braveness. Praha, Czech Republic: Published for the Terezi n Memorial by Jitka Kejr ova , V RA JI Pub., 2003.
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