Relevant bibliographies by topics / C56BL/6 mice

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'C56BL/6 mice'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "C56BL/6 mice"

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Martins, Frederico Severino, Sherwin K. B. Sy, Edemilson Cardoso da Conceição, Maria José Vieira Fonseca, and Osvaldo de Freitas. "Pharmacokinetic-Pharmacodynamic Characterization of a Topical Photochemotherapy Using Brosimum gaudichaudii in C56BL/6 Mice." Revista Brasileira de Farmacognosia 31, no. 2 (2021): 184–92. http://dx.doi.org/10.1007/s43450-021-00139-4.

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Hernández, Lya G., and John A. Heddle. "A carcinogenic western diet does not induce somatic mutations in various target tissues of transgenic C56BL/6 mice." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 570, no. 2 (2005): 185–96. http://dx.doi.org/10.1016/j.mrfmmm.2004.11.001.

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Lee, Yeonju, Sergiy Oliynyk, Jae-Chul Jung, Jeong Jun Han, and Seikwan Oh. "Administration of Glucosylceramide Ameliorated the Memory Impairment in Aged Mice." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/824120.

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The function and the role of glucosylceramide have not been well studied in the central nervous system. This study was aimed to investigate the possible roles of glucosylceramide in memory function in aged mice. Glucosylceramide (50 mg/kg, p.o.) showed memory enhancing activity after 3-month treatment in the aged mice (C56BL/6, 18–20 months old) through Y-maze, novel objective test, and Morris water maze test. Long-term treatment of glucosylceramide decreased the expression of iNOS and COX-2 in the brain of aged mice. The LPS-induced mRNA level of iNOS, COX-2, IL-1β, and TNF-αwas reduced by the acute treatment with glucosylceramide in adult mice. These results suggest that glucosylceramide plays an important role in anti-inflammatory and memory enhancement, and it could be a potential new therapeutic agent for the treatment of neurodegenerative diseases such as Alzheimer’s disease.
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Sarpong, S. B., E. Asamoa-Odei, V. Kamendi, and J. Okomo-Awich. "Genetic Variability in Pulmonary Physiological Responses to Cockroach and Dust Mite Allergen in A/J and C56BL/6 Mice." Journal of Allergy and Clinical Immunology 117, no. 2 (2006): S141. http://dx.doi.org/10.1016/j.jaci.2005.12.561.

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Naghshin, Jahan, Rosa H. Rodriguez, Eric M. Davis, Lia C. Romano, Kenneth R. McGaffin, and Christopher P. O'Donnell. "Chronic intermittent hypoxia exposure improves left ventricular contractility in transgenic mice with heart failure." Journal of Applied Physiology 113, no. 5 (2012): 791–98. http://dx.doi.org/10.1152/japplphysiol.00185.2012.

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We previously reported the unexpected finding that 4 wk of exposure to intermittent hypoxia (IH), which simulates the hypoxic stress of obstructive sleep apnea, improved LV cardiac function in healthy, lean C57BL/6J mice. The purpose of the present study was to assess the impact of 4 wk of IH on cardiac function in a transgenic murine model that exhibits a natural history of heart failure. We hypothesized that IH exposure would exacerbate cardiac decompensation in heart failure. Adult male FVB (wild type) and transgenic mice with cardiac overexpression of tumor necrosis factor α (TNF-αTG) at 10–12 wk of age were exposed to 4 wk of IH (nadir inspired oxygen 5–6% at 60 cycles/h for 12 h during light period) or intermittent air (IA) as control. Cardiac function was assessed by echocardiography and pressure-volume loop analyses, and mRNA and protein expression were performed on ventricular homogenates. TNF-αTG mice exposed to IA exhibited impaired LV contractility and increased LV dilation associated with markedly elevated cardiac expression of atrial natriuretic peptide and brain natriuretic peptide compared with wild-type mice. When wild-type FVB mice were exposed to IH, they exhibited increases in arterial pressure and dP/d tmax, consistent with our previous report in C57BL/6J mice. Surprisingly, we found that TNF-αTG mice exposed to IH showed a reduction in end-diastolic volume (38.7 ± 3.8 to 22.2 ± 2.1 ul; P < 0.01) and an increase in ejection fraction (29.4 ± 2.5 to 41.9 ± 3.1%; P < 0.05). In contrast to our previous study in C56Bl/6J mice, neither FVB nor TNF-αTG mice exhibited an upregulation in β-adrenergic expression or cAMP in response to IH exposure. We conclude that 4 wk of exposure to IH in mice induces adaptive responses that improve cardiac function in not only healthy animals but also in animals with underlying heart failure.
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Harlan, Shannon M., Robert A. Ostroski, Tamer Coskun, Loudon D. Yantis, Matthew D. Breyer, and Josef G. Heuer. "Viral transduction of renin rapidly establishes persistent hypertension in diverse murine strains." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 5 (2015): R467—R474. http://dx.doi.org/10.1152/ajpregu.00106.2015.

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Mice provide a unique platform to dissect disease pathogenesis, with the availability of recombinant inbred strains and diverse genetically modified strains. Leveraging these reagents to elucidate the mechanisms of hypertensive tissue injury has been hindered by difficulty establishing persistent hypertension in these inbred lines. ANG II infusion provides relatively short-term activation of the renin-angiotensinogen system (RAS) with concomitant elevated arterial pressure. Longer-duration studies using renin transgenic mice are powerful models of chronic hypertension, yet are limited by the genetic background on which the transgene exists and the exposure throughout development. The present studies characterized hypertension produced by transduction with a renin-coding adeno-associated virus (ReninAAV). ReninAAV mice experienced elevated circulating renin with concurrent elevations in arterial pressure. Following a single injection of ReninAAV, arterial pressure increased on average +56 mmHg, an increase that persisted for at least 12 wk in three distinct and widely used strains of adult mice: 129/S6, C56BL/6, and DBA/2J. This was accomplished without surgical implantation of pumps or complex breeding and backcrossing. In addition, ReninAAV mice developed pathophysiological changes associated with chronic hypertension, including increased heart weight and albuminuria. Thus ReninAAV provides a unique tool to study the onset of and effects of persistent hypertension in diverse murine models. This model should facilitate our understanding of the pathogenesis of hypertensive injury.
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Kim, Hyun-Ju, Eun-Young Park, Mi-Jeong Oh, et al. "Central administration of metformin into the third ventricle of C57BL/6 mice decreases meal size and number and activates hypothalamic S6 kinase." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 5 (2013): R499—R505. http://dx.doi.org/10.1152/ajpregu.00099.2013.

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Administration of metformin is known to reduce both body weight and food intake. Although the hypothalamus is recognized as a critical regulator of energy balance and body weight, there is currently no evidence for an effect of metformin in the hypothalamus. Therefore, we sought to determine the central action of metformin on energy balance and body weight, as well as its potential involvement with key hypothalamic energy sensors, including adenosine monophosphate-activated protein kinase (AMPK) and S6 kinase (S6K). We used meal pattern analysis and a conditioned taste aversion (CTA) test and measured energy expenditure in C56BL/6 mice administered metformin (0, 7.5, 15, or 30 μg) into the third ventricle (I3V). Furthermore, we I3V-administered either control or metformin (30 μg) and compared the phosphorylation of AMPK and S6K in the mouse mediobasal hypothalamus. Compared with the control, I3V administration of metformin decreased body weight and food intake in a dose-dependent manner and did not result in CTA. Furthermore, the reduction in food intake induced by I3V administration of metformin was accomplished by decreases in both nocturnal meal size and number. Compared with the control, I3V administration of metformin significantly increased phosphorylation of S6K at Thr389 and AMPK at Ser485/491 in the mediobasal hypothalamus, while AMPK phosphorylation at Thr172 was not significantly altered. Moreover, I3V rapamycin pretreatment restored the metformin-induced anorexia and weight loss. These results suggest that the reduction in food intake induced by the central administration of metformin in the mice may be mediated by activation of S6K pathway.
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Chun, Rene F., Ivan Hernandez, Renata Pereira, et al. "Differential Responses to Vitamin D2 and Vitamin D3 Are Associated With Variations in Free 25-Hydroxyvitamin D." Endocrinology 157, no. 9 (2016): 3420–30. http://dx.doi.org/10.1210/en.2016-1139.

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25-Hydroxyvitamin D (25D) circulates bound primarily to serum vitamin D binding protein (DBP), with DBP showing higher binding affinity for 25D3 than 25D2. We therefore hypothesized that vitamin D2 (D2) promotes higher serum levels of unbound 25D (free 25D), with different functional responses, relative to vitamin D3 (D3). Week 3 C56BL/6 mice were placed on diets containing either D2 or D3 alone (both 1000 IU/kg). At week 8 and week 16, D2 mice had only 25D2 in circulation (26.6 ± 1.9 and 33.3 ± 4.4 ng/mL), and D3 mice had only 25D3 (28.3 ± 2.0 and 31.7 ± 2.1 ng/mL). At week 8 (44.5 ± 6.4 vs 62.4 ± 11.6 pg/mL, P < .05) and week 16 (78.4 ± 12.6 vs 95.5 ± 11.6), D2 mice had lower serum 1,25-dihydroxyvitamin D relative to D3 mice. By contrast, measured free 25D was significantly higher in D2 mice at week 8 (16.8 ± 0.65 vs 8.4 ± 0.63 pg/mL, P < .001) and week 16 (17.4 ± 0.43 vs 8.4 ± 0.44, P < .001). A two-way ANOVA of bone histomorphometry showed that week 8 D2 mice had significantly higher osteoclast surface/bone surface, eroded surface/bone surface, and mineral apposition rate compared with D3 mice. Osteoblast surface/bone surface was higher in week 8 D2 females but not week 8 D2 males. At week 16, D2 mice had significantly higher bone volume/total volume and trabecular number compared with D3 mice. Differences in bone phenotype were observed despite D2 mice reaching similar serum 25D levels and lower 1,25D levels compared with D3 mice. These data indicate that 25D2 binds less well to DBP than 25D3, with resulting higher levels of free 25D promoting differential effects on bone in mice exposed to D2 alone.
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Margos, Maxi, and Bruno Gottstein. "Gerbu adjuvant modulates the immune response and thus the course of infection in C56BL/6 mice immunised with Echinococcus multilocularis rec14-3-3 protein." Parasitology Research 107, no. 3 (2010): 623–29. http://dx.doi.org/10.1007/s00436-010-1907-x.

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Nascimento, Emmani B. M., Michiel P. B. Moonen, Carlijn M. E. Remie, et al. "Nicotinamide Riboside Enhances In Vitro Beta-adrenergic Brown Adipose Tissue Activity in Humans." Journal of Clinical Endocrinology & Metabolism 106, no. 5 (2021): 1437–47. http://dx.doi.org/10.1210/clinem/dgaa960.

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Abstract Context Elevating nicotinamide adenine dinucleotide (NAD+) levels systemically improves metabolic health, which can be accomplished via nicotinamide riboside (NR). Previously, it was demonstrated that NR supplementation in high-fat-diet (HFD)-fed mice decreased weight gain, normalized glucose metabolism, and enhanced cold tolerance. Objective Because brown adipose tissue (BAT) is a major source of thermogenesis, we hypothesize that NR stimulates BAT in mice and humans. Design and intervention HFD-fed C56BL/6J mice were supplemented with 400 mg/kg/day NR for 4 weeks and subsequently exposed to cold. In vitro primary adipocytes derived from human BAT biopsies were pretreated with 50 µM or 500 µM NR before measuring mitochondrial uncoupling. Human volunteers (45-65 years; body mass index, 27-35 kg/m2) were supplemented with 1000 mg/day NR for 6 weeks to determine whether BAT activity increased, as measured by [18F]FDG uptake via positron emission tomography-computed tomography (randomized, double blinded, placebo-controlled, crossover study with NR supplementation). Results NR supplementation in HFD-fed mice decreased adipocyte cell size in BAT. Cold exposure further decreased adipocyte cell size on top of that achieved by NR alone independent of ex vivo lipolysis. In adipocytes derived from human BAT, NR enhanced in vitro norepinephrine-stimulated mitochondrial uncoupling. However, NR supplementation in human volunteers did not alter BAT activity or cold-induced thermogenesis. Conclusions NR stimulates in vitro human BAT but not in vivo BAT in humans. Our research demonstrates the need for further translational research to better understand the differences in NAD+ metabolism in mouse and human.
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Dissertations / Theses on the topic "C56BL/6 mice"

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Donahue, Timothy J. "CHARACTERIZATION OF THE DISCRIMINATIVE STIMULUS PROPERTIES OF THE ATYPICAL ANTIPSYCHOTIC AMISULPRIDE IN C57BL/6 MICE." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3607.

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Amisulpride, a benzamide derivative, is an atypical antipsychotic drug used to treat both schizophrenia and depression. Amisulpride is a selective antagonist at dopamine D2 and D3 receptors and at serotonin 5-HT2B and 5-HT7 receptors and displays an atypical clinical profile with reduced extrapyramidal motor effects. The drug has a chiral center and is a mixture of two optical isomers: (S)-amisulpride and (R)-amisulpride. The present study used a two-lever drug discrimination assay to allow a direct comparison between amisulpride and its two isomers. Additionally, substitution testing was conducted with the typical antipsychotics, atypical antipsychotics, antidepressants, the anxiolytic chlordiazepoxide, several benzamide derivatives, and selective ligands with receptor mechanisms relevant to amisulpride. C57BL/6 mice were trained to discriminate 10 mg/kg rac-amisulpride from vehicle in a two-lever drug discrimination task for food reinforcement in an average of 35.7 sessions (range 6-89). The amisulpride dose-response curve (0.078 – 10.0 mg/kg) yielded an ED50 = 0.64 mg/kg, 95% CI [.47, 0.84 mg/kg]. The isomers fully substituted for amisulpride with a significant left-ward shift in the dose-response curve for (S)-amisulpride as compared to rac-amisulpride and (R)-amisulpride. The benzamide derivatives sulpiride and the (S)-sulpiride isomer fully substituted for amisulpride; tiapride produced partial substitution (76.4% DLR); none of the other tested drugs substituted for rac-amisulpride’s discriminative stimulus. These results showed that the rac-amisulpride stimulus was readily acquired in C57BL/6 mice, and that it has a unique and robust discriminative stimulus that is dose-dependent, time-dependent and stereoselective and is not shared with other antipsychotic or antidepressant drugs.
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Johnson, Joshua Edward Newland M. Christopher. "The opportunity for alternative reinforcement shortens bout length in BALB/c C57BL/6 mice." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SUMMER/Psychology/Thesis/Johnson_Joshua_56.pdf.

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Edgar, Nicole M. "Mechanisms of Compass Orientation in C57BL/6 Laboratory Mice." Thesis, Virginia Tech, 2004. http://hdl.handle.net/10919/32850.

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Compass orientation or menotaxis is defined as the ability to orient at a specific angle relative to a directional cue. Cues used for compass orientation include the sun, stars, moon, geomagnetic field and polarized light. While there is evidence in a variety of organisms for compass orientation, the ability of mammals to use cues for compass orientation has been relatively unexplored. The goal of this research was to explore whether laboratory mice could use either magnetic or auditory cues for compass orientation. The results indicate that mice are able to learn to position their nest using a magnetic compass. The development of a magnetic compass assay in laboratory mice will allow the investigation of the mechanism of magnetic compass orientation in mammals, a goal that has been unattainable to this point.In addition, this research has provided preliminary evidence that mice are able to learn to position their nests using an auditory compass. While there is evidence in several organisms for place navigation using auditory cues (i.e. the ability to locate a specific spatial position using auditory cues), this is the first evidence in any organism for an auditory compass (i.e. the ability to calculate a directional heading relative to an auditory cue).In conclusion, both experiments provide evidence for specialized compass systems in mice and suggest that further research is necessary to fully understand the role of these systems in the behavioral ecology of mice.<br>Master of Science
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OBAFEMI, TOLULOPE FESAYO. "THE EFFECTS OF INTERLEUKIN 6 AND INTERLEUKIN 10 ON FRAILTY IN C57BL/6 MICE." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/613394.

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Studies have shown that pro-inflammatory IL-6 and anti-inflammatory IL-10 interleukins may correlate to frailty and aging. This frailty can be defined in the context of clinical symptoms which include sarcopenia and osteoporosis, decreased activity level; or in the context of increased susceptibility to adverse health outcomes from a deficient immune system. In this experiment we tested a cohort of conditionally regulated IL-6 and IL-10 mice with controls (IL-6tg+.rtTA(r/r) (n=8), IL-10(-/-). IL-10tg+ rtTA(r/r) (n=10) and rtTA(r/r) (n=5)) under frailty assessments and immunological cell analysis. We were unable to successfully induce expression in the conditionally regulated mice. Subsequently, there was no difference in the frailty scores, weight, or temperature fluctuation between all three genotypes. As a preliminary study, there arose essential learning points of improvement that can be applied to future experiments concerning frailty in transgenic mice.
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Araghi-Niknam, Moshen 1960. "Effects of dehydroepiandrosterone supplementation in aged humans and C57BL/6 mice." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282417.

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DHEA (dehydroepiandrosterone) is a major adrenal hormone, with known accepted function. In both animals and humans low DHEA and DHEA-sulfate levels are associated with a number of problems in the aging: immunosenescence, increased mortality, increased incidence of several cancers, loss of sleep, decreased feelings of well-being, osteoporosis, atherosclerosis and premature death. DHEA hormone replacement in aged mice significantly normalized immunosenescence suggesting that this hormone plays a key role in aging and stimulating immune regulation in mice. Similarly osteoclasts and lymphoid cells, were stimulated by DHEA replacement which should delay osteoporosis. Recent studies do not support the original suggestion that low serum DHEA levels were associated with Alzheimer's and other losses of mental function in aged people. As DHEA modulates energy metabolism low levels should affect lipogenesis and gluconeogenesis, increasing the risk of diabetes and heart disease. Most of the actions of DHEA restoration are hypothesized from epidemiological or animal model studies and need to be tested in human trials. Those conducted in humans show essentially no toxicity of DHEA treatment at levels restoring serum DHEAS levels without evidence of altering some aging physiological systems. Thus DHEA is a steroid whose deficiency could facilitate development of some diseases common to the aged. Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) are steroids, synthesized from cholesterol (Fig. 1.1). While DHEA is secreted primarily by the adrenal gland in larger quantities than any other adrenal steroid including cortisol, the precise functions of DHEA and DHEAS in humans are not known (1-5). The decline of DHEAS levels during aging is parallel to development of immunosensecence, an inability to conserve protein, a physical frailty, decreased muscle mass, an increased fat mass, decreased ability to cope, disrupted sleep patterns and increased incidence of disease. Thus DHEAS serves as a marker of aging in humans. While the precise biological functions of DHEA and DHEAS are not known, both animal and human studies suggest some hypotheses while dispelling others. Therefore key physiological dysfunctions are investigated here to determine biological relationships which participate in the declining blood levels of DHEA with age.
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Romao, P. L. "Mapping ENU-induced thymic lymphoma susceptibility loci in C57BL/6 mice." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/47379/.

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Tumour development is a complex process involving susceptibility loci (oncogenes) and the accumulation of spontaneous somatic mutations in tumour suppressor genes that interact to result in cancer. Tumours may require the accumulation of a variety of mutations before developing but the general principle is that the mutations result in an imbalance between the oncogene and tumour suppressor gene function (Berger et al., 2011). This multi-hit process can be tested by subjecting strains of mice susceptible to certain types of tumours to chemical mutagens, thereby inducing further mutations. This technique is used in this study to identify loci resulting in the susceptibility to thymic lymphoma in the C57BL/6J strain in order to further our understanding of the processes involved in the development of such tumours.
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Iñiguez, Sergio Diaz. "The effects of acute posttraining injections of cocaine on spatial memory in C57BL/6 mice." CSUSB ScholarWorks, 2007. https://scholarworks.lib.csusb.edu/etd-project/3244.

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The purpose of this study was to investigate the effects of cocaine on spatial memory consolidation using the Morris water maze. Specifically, male and female C57BL/6 mice were trained on a spatial water task, and then administered a single posttraining injection of saline or cocaine (1.25, 2.5, 5.0, or 20.0 mg/kg).
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Philibin, Scott D. "The Discriminative Stimulus Properties of the Atypical Antipsychotic Clozapine in C57BL/6 Mice." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/1318.

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Serotonin and α1 adrenergic receptor antagonism may contribute to atypical antipsychotic drug effects. Clozapine (2.5 mg/kg) drug discrimination in C57BL/6 mice may selectively screen atypical antipsychotic drugs. Previous data show that the atypical antipsychotics olanzapine, risperidone, ziprasidone but not the typical antipsychotic haloperidol fully substitutes for clozapine. The present study demonstrated that the atypical antipsychotics quetiapine, sertindole, zotepine, iloperidone, melperone fully substituted for clozapine but aripiprazole did not. The typical antipsychotics fluphenazine and perphenazine failed to fully substitute for clozapine but chlorpromazine and thioridazine fully substituted for clozapine. This model does not differentiate between atypical and typical antipsychotic drugs but it may be useful in the detection of antipsychotics with potent serotonin and α1 adrenergic receptor antagonist actions.
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Sahin, Ebru Karpuzoglu. "Estrogen Regulates Interferon-gamma (IFN-g) and IFN-g-Inducible iNOS Gene Expression: Implications to Immunity and Autoimmunity." Diss., Virginia Tech, 2005. http://hdl.handle.net/10919/27129.

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It is now clear that estrogen not only modulates the differentiation and function of reproductive systems, but it also profoundly regulates the immune system of normal and autoimmune individuals. An important mechanism by which estrogen regulates the immune system is by altering the secretion and/or response to cytokines. We hypothesized that estrogen may alter the levels and/or response to IFN-g, a prototype Th1 cytokine, that plays a pivotal role in immunity against intracellular infections and in many autoimmune and inflammatory disorders. We found that estrogen treatment tended to upregulate the secretion of IFN-g protein and mRNA expression from Concanavalin-A (Con-A)-activated splenic lymphocytes. Impressively, we found that splenocytes from estrogen-treated mice when activated with Con-A also resulted in increased release of nitric oxide compared to placebo-treated mice. Furthermore, Con-A-activated splenocytes from estrogen-treated mice also had upregulated iNOS mRNA, iNOS protein, and nitric oxide-regulated COX-2 protein when compared to control mice. Blocking co-stimulatory signals mediated through interactions of CD28 and B7 molecules by using CTLA-4Ig markedly decreased not only IFN-g, but also nitric oxide, thereby implying an important role for CD28/B7 interactions in IFN-g/nitric oxide. Estrogen-induced upregulation of iNOS/nitric oxide is mediated through IFN-g since: (i) Estrogen alone did not upregulate iNOS/nitric oxide in IFN-g knockout mice; (ii) addition of rIFN-g to activated splenocytes from estrogen-treated mice further upregulated nitric oxide levels. We next investigated whether estrogen also upregulated IFN-g-inducing cytokines and select IFN-g-inducing transcription factors. Estrogen treatment resulted in increased mRNA and/or protein expression of IFN-g inducing cytokines and their receptors, including: IL-18, IL-15, IL-27, IL-12Rb2, and IL-18Rb. We also found that T-bet, a critical Th1 transcription factor, and STAT-4 phosphorylation, a key molecule in IL-12 signaling were both increased, while IRF-4, an important player in Th2 differentiation, was diminished in Con-A-activated splenocytes from mice treated with estrogen. Altogether, these studies are the first to demonstrate that estrogen regulates IFN-g-dependent iNOS and describes the potential mechanisms of how estrogen alters IFN-g-inducible genes, IFN-g inducing cytokines, and transcription factors in normal C57BL/6 mice. These studies may have profound implications to many autoimmune and inflammatory disorders, where estrogen is known to regulate the course of these diseases. Since estrogen may promote inflammatory disorders by upregulating pro-inflammatory biomolecules including IFN-g, nitric oxide, and COX-2, these studies may help in the design of therapeutic agents that regulate or block secretion and/or response to these inflammatory molecules.<br>Ph. D.
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YATES, JONATHAN WAYNE. "DIFFERENTIAL INVOLVEMENT OF OPIOID RECEPTORS IN REGULATING THE BEHAVIORAL RESPONSE TO AMPHETAMINE IN C57BL/6 MICE." University of Cincinnati / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1047070637.

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Books on the topic "C56BL/6 mice"

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Penner, Mark Douglas. NK cell mediated cellular cytotoxicity in C57BL/6 mice transgenic for antisene natural killer cell tumour recognition molecule p150. National Library of Canada, 1993.

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(Editor), P. R. Hof, W. G. Young (Editor), F. E. Bloom (Editor), P. V. Belichenko (Editor), and M. R. Celio (Editor), eds. Comparative Cytoarchitectonic Atlas of the C57BL/6 and 129/Sv Mouse Brains. Elsevier, 2000.

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Book chapters on the topic "C56BL/6 mice"

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Rimbach, S., D. Wallwiener, D. Pollmann, et al. "Experimental CO2 Laser Surgery on the Lewis Lung Carcinoma Tumor Model in C56BL/6 Mice." In Lasers in Gynecology. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-45683-1_63.

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Sprecher, Eli, Leonard D. Shultz, and Yechiel Becker. "Epidermal Dendritic Cells in Aged C57BL/6 J MICE." In Skin Langerhans (Dendritic) Cells in Virus Infections and AIDS. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3942-1_6.

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Contarini, Gabriella, Pietro Giusti, and Stephen D. Skaper. "Active Induction of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice." In Neurotrophic Factors. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_26.

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Gonsalvez, David G., SangWon Yoo, Georgina A. Craig, et al. "Myelin Protein Zero180–199 Peptide Induced Experimental Autoimmune Neuritis in C57BL/6 Mice." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7862-5_19.

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Perlman, S., R. Schelper, and D. Ries. "Maternal Antibody-Modulated MHV-JHM Infection in C57BL/6 and BALB/c Mice." In Coronaviruses. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_39.

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Spongr, Vlasta P., Joseph P. Walton, Robert D. Frisina, Ann Marie Kazee, Dorothy G. Flood, and Richard J. Salvi. "Hair Cell Loss and Synaptic Loss in Inferior Colliculus of C57BL/6 MICE." In Acoustical Signal Processing in the Central Auditory System. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4419-8712-9_49.

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Gagne, S., L. Thibodeau, and L. Lamontagne. "Clonal Deletion of Some Vβ+ T Cells in Peripheral Lymphocytes from C57BL/6 Mice Infected with MHV3." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_62.

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Pyo, Hyun Mi, Jie Yun Park, Sue Nie Park, Hyun Su Kim, Kee Sun Shin, and Har Young Poo. "Immunization with Virus-Like Particle of Human Papillomavirus Type 16 L1 Elicits CTL Immune Response in C57BL/6 Mice." In Key Engineering Materials. Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-958-x.119.

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Solares, G., R. Zamenhof, S. Saris, et al. "Biodistribution and Pharmacokinetics of p-Boronophenylalanine in C57BL/6 Mice with GL261 Intracerebral Tumors, and Survival Following Neutron Capture Therapy." In Progress in Neutron Capture Therapy for Cancer. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3384-9_105.

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Habálek, F. "Induction of Hepatoma in Seven-Day-Old C57BL/6 Mice with a Single dose of Aflatoxin and the Influence of Diethyldithiocarbamate." In Biochemistry of Chemical Carcinogenesis. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0539-2_19.

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Conference papers on the topic "C56BL/6 mice"

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Turner, Charles H., and Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal genetics: C57BL/6, DBA/2, and C3H/He. The C57BL/6 strain is characterized by low BMD and large total cross-sectional area (CSA) in the midshaft femur; the C3H/He strain exhibits very high femoral BMD and a smaller femoral CSA than the C57BL/6 mice; and DBA/2 mice have moderately high femoral BMD and a very small midshaft femur CSA. Mechanical loading of the skeleton during growth can substantially enhance periosteal bone apposition, and ultimately produce a diaphyseal cross section with enlarged area. Therefore we hypothesized that the mouse strain with greater femoral cross-sectional area (C57BL/6) might have a genetic predisposition for greater mechanosensitivity than mice with smaller cross sections (C3H/He and DBA/2).
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Neumann, U., F. Derwenskus, A. Gille, S. Louis, and SC Bischoff. "BIOAVAILABILITY AND SAFETY OF THREE MICROALGAE IN C57BL/6 MICE." In Nutrition 2017 – Ernährung: eine multiprofessionelle Herausforderung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1603260.

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Nishio, Naomi, Sachiko Ito, Yuriko Tanaka, and Ken-ichi Isobe. "Establishment of neutrophil-lineage stem cells from C57BL/6 mice." In 2012 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2012. http://dx.doi.org/10.1109/mhs.2012.6492412.

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Zin, Walter, Gaudio Sena, Giovanna Carvalho, et al. "Pulmonary burden in C57Bl/6 mice infected withplasmodiumbergheistrains NK65 or ANKA." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2311.

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Zhu, Hui, Jessica Shih, David S. Long, John R. Hagaman, Nobuyo Maeda, and Morton H. Friedman. "Different Strains of Mice Exhibit Different Aortic Arch Geometry and Plaque Distribution: A Fluid Dynamic Effect." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175844.

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In earlier work, we observed different patterns of disease distribution in the aortic arches of apolipoprotien E (apoE)-deficient C57BL/6 (B6) and 129/SvEv (129) mouse strains [1]. In the relatively young mice (6 mo old), fatty plaques are seen mainly in the aortic root area, extending into the right innominate artery (RIA), with very little plaque in the more distal aortic arch in the B6 strain. However, in the 129 strain, plaques are found more in the inner curvature of the aortic arch but less in the sinus area than in B6 strain (Fig. 1).
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Jiang, Dingyuan, Xiaoxi Huang, Jing Geng, Shuhong Li, Chen Wang, and Huaping Dai. "Repeated boost withpropionibacterium acnesinduce pulmonary fibrosis following sarcoidosis in C57BL/6 mice." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3313.

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Carvalho, Jorge Luis, Ana Karolina Sá, Aurileia Britto, et al. "Bifidobacterium breve significantly reduces cigarette smoke-induced COPD in C57Bl/6 mice." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4244.

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Nikolskaya, Kira, and Marina Kondashevskaya. "AGING PROBLEM: PSYCHOPHYSIOLOGICAL AND NEUROIMMUNO-HORMONAL EFFECTS IN MICE F1 (C57BL/6×DBA/2)." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1179.sudak.ns2020-16/348-349.

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Silva, C. R., C. F. M. Camargo, D. P. Aureliano, L. R. De Pretto, A. Z. Freitas, and M. S. Ribeiro. "Attenuation coefficient of the light in skin of BALB/c and C57BL/6 mice." In SPIE Biophotonics South America, edited by Cristina Kurachi, Katarina Svanberg, Bruce J. Tromberg, and Vanderlei S. Bagnato. SPIE, 2015. http://dx.doi.org/10.1117/12.2181015.

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Zangerolamo, Lucas, Helena Cristina De Lima Barbosa Sampaio, GABRIELA MOREIRA SOARES, Sara Olalla Saad, and Antonio Carlos Boschiero. "ARHGAP21 modulates the secretion of VLDL vesicles in the liver of C57BL/6 mice." In XXV Congresso de Iniciação Cientifica da Unicamp. Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78719.

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