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Li, Tong-Tong, Susana Larrucea, Shiloe Souza, Suzanne M. Leal, José A. López, Edward M. Rubin, Bernhard Nieswandt, and Paul F. Bray. "Genetic variation responsible for mouse strain differences in integrin α2 expression is associated with altered platelet responses to collagen." Blood 103, no. 9 (May 1, 2004): 3396–402. http://dx.doi.org/10.1182/blood-2003-10-3721.
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Abstract As mouse models have become commonplace for studying hemostasis and thrombosis, we considered whether the mouse system had utility for assessing genetic alterations in platelet receptors. Platelets from 5 mouse strains (C57BL/6 [C57], FVB/N [FVB], BALB/c, C3H/He, and 129Sv) showed only minor differences in the expression of integrin αIIb, integrin β3, glycoprotein (GP) Ibα, or GPVI across strains. However, FVB platelets expressed approximately 50% the level of integrin α2 as platelets from other strains (P < .0001). We bred FVB mice with C57 and assessed α2 expression in FVB/C57xFVB/C57 (F2) offspring. Linkage analysis demonstrated the gene responsible for α2 levels is tightly linked to the D13mit260 marker (log odds [lod] score 6.7) near the α2 gene. FVB platelets showed reduced aggregation and a longer lag phase to collagen. FVB and C57 platelets aggregated similarly to collagen-related peptide, but FVB platelets showed a reduction in rhodocytin-induced Syk and PLCγ2 tyrosine phosphorylation. Thus, FVB platelets express half the level of α2 as other mouse strains, a trait linked to the α2 gene and seemingly responsible for reduced platelet aggregation to collagen. These strain differences serve as a useful model for the 2-fold difference in human platelet α2β1 expression and demonstrate that α2β1 participates in signaling during platelet activation. (Blood. 2004;103:3396-3402)
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Kim, Na-Won, Sun-Min Seo, Eun-Seon Yoo, Ah-Reum Kang, Ji-Hun Lee, Jae-Hoon Lee, Byeong-Cheol Kang, Han-Woong Lee, and Yang-Kyu Choi. "Short-term carcinogenicity study of N-methyl-N-nitrosourea in FVB-Trp53 heterozygous mice." PLOS ONE 18, no. 1 (January 6, 2023): e0280214. http://dx.doi.org/10.1371/journal.pone.0280214.
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Carcinogenicity tests predict the tumorigenic potential of various substances in the human body by studying tumor induction in experimental animals. There is a need for studies that explore the use of FVB/N-Trp53em2Hwl/Korl (FVB-Trp53+/-) mice, created by TALEN-mediated gene targeting in Korea, in carcinogenicity tests. This study was performed to determine whether FVB-Trp53+/- mice are a suitable model for short-term carcinogenicity studies. To compare the carcinogenicity at different concentrations, 25, 50, and 75 mg/kg of N-methyl-N-nitrosourea (MNU), a known carcinogen, were administered intraperitoneally to FVB-Trp53+/- and wild-type male mice. After 26 weeks, the survival rate was significantly reduced in FVB-Trp53+/- mice compared to the wild-type mice in the 50 and 75 mg/kg groups. The incidence of thymic malignant lymphoma (TML) in the 50 and 75 mg/kg groups was 54.2 and 59.1% in FVB-Trp53+/- male mice, respectively. TML metastasized to the lungs, spleen, lymph nodes, liver, kidney, and heart in FVB-Trp53+/- male mice. Furthermore, the incidence of primary lung tumors, such as adenomas and adenocarcinomas, was 65.4, 62.5, and 45.4% in the FVB-Trp53+/- mice of the 25, 50, and 75 mg/kg groups, respectively. The main tumor types in FVB-Trp53+/- mice were TML and primary lung tumors, regardless of the dose of MNU administered. These results suggest that systemic tumors may result from malfunctions in the p53 gene and pathway, which is an important factor in the pathogenesis of human cancers. Therefore, FVB-Trp53 heterozygous mice are suitable for short-term carcinogenicity tests using positive carcinogens, and that the best result using MNU, a positive carcinogen, might have a single dose of 50 mg/kg.
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Sclafani, Anthony, Steven Zukerman, and Karen Ackroff. "Fructose- and glucose-conditioned preferences in FVB mice: strain differences in post-oral sugar appetition." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 12 (December 15, 2014): R1448—R1457. http://dx.doi.org/10.1152/ajpregu.00312.2014.
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Recent studies indicate that, unlike glucose, fructose has little or no post-oral preference conditioning actions in C57BL/6J (B6) mice. The present study determined whether this is also the case for FVB mice, which overconsume fructose relative to B6 mice. In experiment 1, FVB mice strongly preferred a noncaloric 0.1% sucralose + 0.1% saccharin (S+S) solution to 8% fructose in a 2-day choice test but switched their preference to fructose after separate experience with the two sweeteners. Other FVB mice displayed a stronger preference for 8% glucose over S+S. In a second experiment, ad libitum-fed FVB mice trained 24 h/day acquired a significant preference for a flavor (CS+) paired with intragastric (IG) self-infusions of 16% fructose over a different flavor (CS−) paired with IG water infusions. IG fructose infusions also conditioned flavor preferences in food-restricted FVB mice trained 1 h/day. IG infusions of 16% glucose conditioned stronger preferences in FVB mice trained 24- or 1 h/day. Thus, fructose has post-oral flavor conditioning effects in FVB mice, but these effects are less pronounced than those produced by glucose. Further studies of the differential post-oral conditioning effects of fructose and glucose in B6 and FVB mice should enhance our understanding of the physiological processes involved in sugar reward.
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Hakim, Luthfi, Ragil Widyorini, Widyanto Dwi Nugroho, and Tibertius Agus Prayitno. "Performance of Citric Acid-Bonded Oriented Board from Modified Fibrovascular Bundle of Salacca (Salacca zalacca (Gaertn.) Voss) Frond." Polymers 13, no. 23 (November 24, 2021): 4090. http://dx.doi.org/10.3390/polym13234090.
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The fibrovascular bundle (FVB) in palm plants consists of fiber and vascular tissue. Geometrically, it is a long fiber that can be used as an oriented board raw material. This research aimed to examine the performance of citric acid-bonded orientation boards from modified FVB salacca frond under NaOH + Na2SO3 treatment and the bonding mechanism between the modified FVB frond and citric acid. The results showed that changes in the chemical composition of FVB have a positive effect on the contact angle and increase the cellulose crystallinity index. Furthermore, the mechanical properties of the oriented board showed that 1% NaOH + 0.2% Na2SO3 with 60 min immersion has a higher value compared to other treatments. The best dimension stability was on a board with the modified FVB of 1% NaOH + 0.2% Na2SO3 with 30 and 60 min immersion. The bonding mechanism evaluated by FTIR spectra also showed that there is a reaction between the hydroxyl group in the modified FVB and the carboxyl group in citric acid. This showed that the modified combination treatment of NaOH+Na2SO3 succeeded in increasing the mechanical properties and dimensional stability of the orientation board from the FVB salacca frond.
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Hakim, L., R. Widyorini, W. D. Nugroho, T. A. Prayitno, and Y. S. Lubis. "Contact angle of modified fibrovascular bundle of salacca (Salacca sumatrana Becc.) frond by NaOH+Na2SO3 combination." IOP Conference Series: Earth and Environmental Science 912, no. 1 (November 1, 2021): 012012. http://dx.doi.org/10.1088/1755-1315/912/1/012012.
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Abstract The fibrovascular bundle (FVB) of the salacca frond is one of the potential raw materials in the development of bio-composite technology. The purpose of this study was to investigate the wettability of FVB using the contact angle method after the alkali modification treatment. The method of this research was to use FVB frond of Salacca sumatrana Becc. which was treated with alkaline modification of the combination of NaOH+Na2SO3 at various concentrations. The results showed that the combination of NaOH 1M+Na2SO3 0.4 M had the smallest contact angle, which means that the FVB has a good wettability value compared to the control treatment. Based on the results, it can be concluded that the modification of NaOH+Na2SO3 can increase the wettability of FVB.
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Jung, Jin Hyuk, and Mary R. Loeken. "Diabetic Embryopathy Susceptibility in Mice Is Associated with Differential Dependence on Glucosamine and Modulation of High Glucose-Induced Oxidative Stress." Antioxidants 10, no. 8 (July 21, 2021): 1156. http://dx.doi.org/10.3390/antiox10081156.
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The high KM glucose transporter, GLUT2 (SLC2A2), is expressed by embryos and causes high rates of glucose transport during maternal hyperglycemic episodes in diabetic pregnancies and causes congenital malformations (diabetic embryopathy). GLUT2 is also a low KM transporter of the amino sugar, glucosamine (GlcN), which enters the hexosamine biosynthetic pathway (HBP) and provides substrate for glycosylation reactions. Exogenous GlcN also increases activity of the pentose phosphate pathway (PPP), which increases production of NADPH reducing equivalents. GLUT2-transported GlcN is inhibited by high glucose concentrations. Not all mouse strains are susceptible to diabetic embryopathy. The aim of this study was to test the hypothesis that susceptibility to diabetic embryopathy is related to differential dependence on exogenous GlcN for glycosylation or stimulation of the PPP. We tested this using murine embryonic stem cell (ESC) lines that were derived from embryopathy-susceptible FVB/NJ (FVB), and embryopathy-resistant C57Bl/6J (B6), embryos in the presence of low or high glucose, and in the presence or absence of GlcN. There were no significant differences in Glut2 expression, or of glucose or GlcN transport, between FVB and B6 ESC. GlcN effects on growth and incorporation into glycoproteins indicated that FVB ESC are more dependent on exogenous GlcN than are B6 ESC. GlcN stimulated PPP activity in FVB but not in B6 ESC. High glucose induced oxidative stress in FVB ESC but not in B6 ESC. These results indicate that FVB embryos are more dependent on exogenous GlcN for glycosylation, but also for stimulation of the PPP and NADPH production, than are B6 embryos, thereby rendering FVB embryos more susceptible to high glucose to induce oxidative stress.
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Ayme-Dietrich, Estelle, Sylvia Da Silva, Ghina Alame Bouabout, Alizée Arnoux, Jérôme Guyonnet, Guillaume Becker, and Laurent Monassier. "Characterization of the spontaneous degenerative mitral valve disease in FVB mice." PLOS ONE 16, no. 9 (September 2, 2021): e0257022. http://dx.doi.org/10.1371/journal.pone.0257022.
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Background The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models. Animals We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system. Methods Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography. Results Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium. Conclusion The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.
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Criswell, David S., Frank W. Booth, Franco DeMayo, Robert J. Schwartz, Scott E. Gordon, and Marta L. Fiorotto. "Overexpression of IGF-I in skeletal muscle of transgenic mice does not prevent unloading-induced atrophy." American Journal of Physiology-Endocrinology and Metabolism 275, no. 3 (September 1, 1998): E373—E379. http://dx.doi.org/10.1152/ajpendo.1998.275.3.e373.
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This study examined the association between local insulin-like growth factor I (IGF-I) overexpression and atrophy in skeletal muscle. We hypothesized that endogenous skeletal muscle IGF-I mRNA expression would decrease with hindlimb unloading (HU) in mice, and that transgenic mice overexpressing human IGF-I (hIGF-I) specifically in skeletal muscle would exhibit less atrophy after HU. Male transgenic mice and nontransgenic mice from the parent strain (FVB) were divided into four groups ( n = 10/group): 1) transgenic, weight-bearing (IGF-I/WB); 2) transgenic, hindlimb unloaded (IGF-I/HU); 3) nontransgenic, weight-bearing (FVB/WB); and 4) nontransgenic, hindlimb unloaded (FVB/HU). HU groups were hindlimb unloaded for 14 days. Body mass was reduced ( P < 0.05) after HU in both IGF-I (−9%) and FVB mice (−13%). Contrary to our hypothesis, we found that the relative abundance of mRNA for the endogenous rodent IGF-I (rIGF-I) was unaltered by HU in the gastrocnemius (GAST) muscle of wild-type FVB mice. High-level expression of hIGF-I peptide and mRNA was confirmed in the GAST and tibialis anterior (TA) muscles of the transgenic mice. Nevertheless, masses of the GAST and TA muscles were reduced ( P < 0.05) in both FVB/HU and IGF-I/HU groups compared with FVB/WB and IGF-I/WB groups, respectively, and the percent atrophy in mass of these muscles did not differ between FVB and IGF-I mice. Therefore, skeletal muscle atrophy may not be associated with a reduction of endogenous rIGF-I mRNA level in 14-day HU mice. We conclude that high local expression of hIGF-I mRNA and peptide in skeletal muscle alone cannot attenuate unloading-induced atrophy of fast-twitch muscle in mice.
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Borenshtein, Diana, Prashant R. Nambiar, Elizabeth B. Groff, James G. Fox, and David B. Schauer. "Development of Fatal Colitis in FVB Mice Infected with Citrobacter rodentium." Infection and Immunity 75, no. 7 (April 30, 2007): 3271–81. http://dx.doi.org/10.1128/iai.01810-06.
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ABSTRACT Citrobacter rodentium is the causative agent of transmissible murine colonic hyperplasia. The disease is characterized by severe but temporary epithelial hyperplasia with limited inflammation in the descending colon of adult mice on a variety of genetic backgrounds. The natural history of infection with this murine pathogen has been characterized in outbred Swiss Webster (SW) mice but not in the cognate inbred FVB strain. In contrast to subclinical infection in SW mice, 12-week-old FVB mice developed overt disease with significant weight loss and mortality beginning by 9 days postinoculation (dpi). By 21 dpi, more than 75% of infected FVB mice died or had to be euthanized, whereas no mortality developed in SW mice. Mortality in FVB mice was fully prevented by fluid therapy. Fecal shedding of bacteria was similar in both groups through 9 dpi; however, a slight but significant delay in bacterial clearance was observed in FVB mice by 12 to 18 dpi. SW mice developed hyperplasia with minimal inflammation in the descending colon. FVB mice developed epithelial cell hyperproliferation, severe inflammation with erosions and ulcers, and epithelial atypia by 6 dpi in the descending colon. In the majority of surviving FVB mice, colonic lesions, including epithelial atypia, were reversible, although a small percentage (5 to 7%) exhibited chronic colitis through 7 months postinoculation. The existence of susceptible and resistant lines of mice with similar genetic backgrounds will facilitate the identification of host factors responsible for the outcome of infection and may lead to the development of novel strategies for preventing and treating infectious colitis.
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Hou, Xue-Fei, Ya-Bo Zhao, Yue-Xiong Yang, Chen Ma, Meng Li, Xin Li, Guo-Rui Ma, Li-Su Zhu, Lin Xu, and Qi-Xin Zhou. "High Morphine Use Disorder Susceptibility Is Predicted by Impaired Learning Ability in Mice." Brain Sciences 12, no. 12 (December 1, 2022): 1650. http://dx.doi.org/10.3390/brainsci12121650.
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An obvious reason for substance uses disorders (SUDs) is drug craving and seeking behavior induced by conditioned context, which is an abnormal solid context memory. The relationship between susceptibility to SUD and learning ability remains unclear in humans and animal models. In this study, we found that susceptibility to morphine use disorder (MUD) was negatively correlated with learning ability in conditioned place preference (CPP) in C57 mice. By using behavioral tests, we identified the FVB mouse as learning impaired. In addition, we discovered that learning-relevant proteins, such as the glutamate receptor subunits GluA1, NR1, and NR2A, were decreased in FVB mice. Finally, we assessed the context learning ability of FVB mice using the CPP test and priming. We found that FVB mice had lower learning performance with respect to normal memory but higher performance of morphine-reinstatement memory. Compared to C57 mice, FVB mice are highly sensitive to MUDs. Our results suggest that SUD susceptibility is predicted by impaired learning ability in mice; therefore, learning ability can play a simple and practical role in identifying high-risk SUD groups.
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Massett, Michael P., and Bradford C. Berk. "Strain-dependent differences in responses to exercise training in inbred and hybrid mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 4 (April 2005): R1006—R1013. http://dx.doi.org/10.1152/ajpregu.00476.2004.
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The aim of this study was to characterize the response to exercise training in several mouse strains and estimate the genetic contribution to phenotypic variation in the responses to exercise training. Male mice from three inbred strains [C57Bl/6J (BL6), FVB/NJ (FVB), and Balb/cJ (Balb/c)] and three hybrid F1 strains [CB6F1/J (CB6 = female Balb/c × male BL6), B6F F1 (female BL6 × male FVB), and FB6 F1 (female FVB × male BL6)] completed an exercise performance test before and after a 4-wk treadmill running program. Distance was used as the primary estimate of endurance exercise performance. FVB mice showed the greatest response to training, with five- to sevenfold greater increases in distance run compared with BL6 and Balb/c strains. Specifically, BL6, FVB, and Balb/c strains increased distance by 33, 172, and 23%, respectively. A similar pattern of changes across strains was observed for run time (17, 87, and 11%) and work (99, 287, and 57%). As a group, F1 hybrid mice derived from BL6 and FVB strains showed an intermediate response to training (61%). However, further analysis indicated that training responses in FB6 F1 mice (80%) were ∼2.5-fold greater than responses in B6F F1 mice (33%, P = 0.08). A similar pattern of changes between FB6 and B6F F1 mice was observed for run time (44.5 and 17%) and work (141 and 59%). These data demonstrate that there are large strain-dependent differences in training responses among inbred mouse strains, suggesting that genetic background contributes significantly to adaptation to exercise. Furthermore, the contrasting responses in B6F and FB6 F1 strains show that a maternal component strongly influences strain-dependent differences in training responses.
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Huseby, April M., Pascal A. Atanga, Jeffrey D. Gamez, Luz M. Cumba-Garcia, Slobodan I. Macura, and Aaron J. Johnson. "Transgenic expression of H-2Db class I molecules influences the development of brain atrophy during Picornavirus infection." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 193.12. http://dx.doi.org/10.4049/jimmunol.196.supp.193.12.
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Abstract Brain atrophy is a common feature of numerous neurological diseases in which the role of neuroinflammation remains poorly defined. We have previously demonstrated the development of brain and spinal cord atrophy in the Theiler’s murine encephalomyelitis virus (TMEV) model of multiple sclerosis. However, cellular and molecular mechanisms of brain atrophy remain poorly understood. We therefore evaluated the contribution of major histocompatibility (MHC) class I molecules in atrophy development during TMEV infection. To accomplish this, we created a novel transgenic FVB/NJ mouse by introducing the H-2Db (Db) class I molecule. Expression of Db class I molecule confers resistance to persistent TMEV infection and demyelination in the normally susceptible FVB/NJ strain (H2-Dq class I haplotype). Next, we compared the development of brain atrophy, assessed by volumetric analysis of T2-weighted MRIs, in FVB/Db mice to wild-type FVB/NJ mice following viral infection. FVB/NJ mice did not significant brain develop atrophy over 4 months, whereas significant brain atrophy was observed in the FVB/Db mice. FVB/Db mice also developed a significant increase in the overall number of CNS infiltrating CD8 T cells and a strong CD8 T cell response towards an immunodominant Db TMEV epitope, VP2121-130. A number of CD8 T cells were also observed in close proximity to virus infected neurons. We therefore propose a hypothesis that class I restricted CD8 T cell responses promote the development of brain atrophy. This model provides a unique opportunity to analyze the contribution of immune cells to neuronal loss and brain atrophy in a system where persistent virus infection and demyelination are not confounding variables.
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Alomar, Abdulazeez S. "Impact of Faddeeva–Voigt broadening on line-shape analysis at critical points of dielectric functions." AIP Advances 12, no. 6 (June 1, 2022): 065127. http://dx.doi.org/10.1063/5.0092287.
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Faddeeva–Voigt broadening (FVB) couples the physical characteristics of both Lorentzian and Gaussian profiles as a combined analytic function shaping the dielectric response. Accurate extraction of the Gaussian and Lorentzian broadening contents in line-shape analysis is essential for reliable optical characterization of semiconductors and dielectrics. By adding the Gaussian-broadening width to each Lorentzian width, we investigate how FVB affects critical-point (CP) analysis. We revisit a selection of earlier work based on classical Lorentz broadening in modulation spectroscopy and spectral ellipsometry. To generalize CP analysis, we derive the FVB’s analytical representation in terms of fractional derivatives of the Faddeeva function and apply the twenty-pole Martin–Donoso–Zamudio approximation for its precise and efficient computation of the FVB of model dielectric functions and derivatives. We investigate the FVB of the electroreflectance line shape of HgCdTe for three-dimensional M0 transitions and of the photoreflectance line shape of InP excitonic E0 transitions. Furthermore, we explore how FVB affects the dielectric functions of three-dimensional excitonic and two-dimensional M0 transitions vs Tanguy’s analytical two-dimensional exciton E1 and E1+Δ1 fits of GaAs to the second-order derivatives. We use the Akaike information criterion to quantitatively estimate the goodness of fit that statistically penalizes overfitting due to extraneous parameters. By consolidating both Gaussian and Lorentzian broadenings, the FVB significantly affects the CP analysis of modulation-spectroscopy line shapes and second-order derivatives of the dielectric function.
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Baker, Anne Marie, Maria C. Grekova, and John R. Richert. "EAE susceptibility in FVB mice." Journal of Neuroscience Research 61, no. 2 (2000): 140–45. http://dx.doi.org/10.1002/1097-4547(20000715)61:2<140::aid-jnr4>3.0.co;2-x.
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Menuet, Clément, Nazim Kourdougli, Gérard Hilaire, and Nicolas Voituron. "Differences in serotoninergic metabolism possibly contribute to differences in breathing phenotype of FVB/N and C57BL/6J mice." Journal of Applied Physiology 110, no. 6 (June 2011): 1572–81. http://dx.doi.org/10.1152/japplphysiol.00117.2011.
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Mouse readiness for gene manipulation allowed the production of mutants with breathing defects reminiscent of breathing syndromes. As C57BL/6J and FVB/N inbred strains were often used as background strains for producing mutants, we compared their breathing pattern from birth onwards. At birth, in vivo and in vitro approaches revealed robust respiratory rhythm in FVB/N, but not C57BL/6J, neonates. With aging, rhythm robustness difference persisted, and interstrain differences in tidal volume, minute ventilation, breathing regulations, and blood-gas parameters were observed. As serotonin affected maturation and function of the medullary respiratory network, we examined the serotoninergic metabolism in the medulla of C57BL/6J and FVB/N neonates and aged mice. Interstrain differences in serotoninergic metabolism were observed at both ages. We conclude that differences in serotoninergic metabolism possibly contribute to differences in breathing phenotype of FVB/N and C57BL/6J mice.
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Torrey, Carla E., Henry G. Wall, James A. Campbell, Puntipa Kwanyuen, Debie J. Hoivik, Richard T. Miller, Jane S. Allen, et al. "Evaluation of the Carcinogenic Potential of Clofibrate in FVB/Tg.AC Mouse After Oral Administration—Part I." International Journal of Toxicology 24, no. 5 (September 2005): 313–25. http://dx.doi.org/10.1080/10915810500208264.
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This study was conducted as part of the International Life Sciences Institute (ILSI) program to evaluate the carcinogenic potential of clofibrate, a nongenotoxic, peroxisome proliferator-activated receptor (PPAR) α agonist following oral administration to Tg.AC (transgenic) and wild-type FVB (nontransgenic) mice for a minimum for 6 months. Clofibrate was well tolerated at doses up to 500 (males) and 650 (females) mg/kg/day. Oral administration of clofibrate to Tg.AC or FVB (wild-type) male and female mice for 6 months did not result in the increased formation of neoplastic lesions. Epithelial hyperplasia in the urinary bladder (Tg.AC and FVB) and prostate gland (Tg.AC only), and interstitial-cell hyperplasia in the testes (Tg.AC) were noted at 500 mg/kg/day. Non-neoplastic nonproliferative findings included hepatic hypertrophy and hematopoietic changes (myeloid hyperplasia, myelodysplasia, lymphoid depletion, and erythropoiesis) in Tg.AC and FVB mice of both sexes; reproductive (cystic degeneration and dilatation, hypospermia, spermatocele, dilated inspissated protein) and urogenital (tubular-cell hypertrophy, degenerative/regenerative nephropathy, necrosis/fibrosis) changes in Tg.AC and FVB male mice; congestion in the lung in male Tg.AC mice; gall bladder dilatation in female Tg.AC mice; and adrenal (intracellular lipofuscinosis and atrophy) and heart (eosinophillic myofibers) findings in Tg.AC mice of both sexes and in female FVB mice. The results of this study indicate that the clofibrate is not carcinogenic when administered to Tg.AC mice by oral gavage for 6 months at doses up to 500 (males) and 650 (females) mg/kg/day, which did produce liver hypertrophy.
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Lopez, A., G. Ricco, G. Mascolo, G. Tiravanti, A. C. Di Pinto, and R. Passino. "Biodegradability enhancement of refractory pollutants by ozonation: a laboratory investigation on an azo-dyes intermediate." Water Science and Technology 38, no. 4-5 (August 1, 1998): 239–45. http://dx.doi.org/10.2166/wst.1998.0634.
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The effectiveness of ozone treatment for improving the biodegradability of recalcitrant pollutants has been proved by investigating the ozonation reaction of FAST-VIOLET-B (FVB) a bioresistant chemical intermediate of azo-dyes. Laboratory scale experiments have been carried out, at room temperature, by bubbling, for 90 min, ozonated air (9ppmO3/min) into 0.35 1 of an alkaline (pH=11) aqueous solution (50 ppm) of FVB. The experimental results indicate that during the ozonation, even though complete FVB degradation occurs in 10 min, ozone consumption goes on for a further 20 min after which time most degradation reactions are completed. The main ozonation by-products, identified by HPLC, IC, and GC-MS are formaldehyde, acetaldehyde, glyoxal, acetone, acetic-, formic-, oxalic- and carbonic-acid, plus six FVB derivatives scarcely biodegradable. At the end of the ozonation, i.e. after 30 min., the initial values of TOC (35 mgC/l) and COD (103 mgO2/l) are respectively 27 and 25 and correspond to a relative removal of about 23% and 76%. As for FVB solution biodegradability expressed as (BOD5)/(COD) ratio, during the first 10 min its value regularly increases from zero up to a maximum of 0.75 that corresponds to an ozone consumption of 2.4 mg per each mg of organic carbon initially present in the solution.
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Shusterman, Vladimir, Irmute Usiene, Chivonne Harrigal, Joon Sup Lee, Toru Kubota, Arthur M. Feldman, and Barry London. "Strain-specific patterns of autonomic nervous system activity and heart failure susceptibility in mice." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 6 (June 1, 2002): H2076—H2083. http://dx.doi.org/10.1152/ajpheart.00917.2001.
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Transgenic mice are widely used to study cardiac function, but strain-dependent differences in autonomic nervous system activity (ANSA) have not been explored. We compared 1) short-term pharmacological responses of cardiac rhythm in FVB vs. C57Black6/SV129 wild-type mice and 2) long-term physiological dynamics of cardiac rhythm and survival in tumor necrosis factor (TNF)-α transgenic mice with heart failure (TNF-α mice) on defined backgrounds. Ambulatory telemetry electrocardiographic recordings and response to saline, adrenergic, and cholinergic agents were examined in FVB and C57Black6/SV129 mice. In FVB mice, baseline heart rate (HR) was higher and did not change after injection of isoproterenol or atropine but decreased with propranolol. In C57Black6/SV129 mice, HR did not change with propranolol but increased with isoproterenol or atropine. Mean HR, but not indexes of HR variability, was an excellent predictor of response to autonomic agents. The proportion of surviving animals was higher in TNF-α mice on an FVB background than on a mixed FVB/C57Black6 background. The homeostatic states of ANSA are strain specific, which can explain the interstrain differences in mean HR, pharmacological responses, and survival of animals with congestive heart failure. Strain-specific differences should be considered in selecting the strains of mice used for transgenic and gene targeting experiments.
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KNOTT, M. L., S. P. HOGAN, H. WANG, K. I. MATTHAEI, and L. A. DENT. "FVB/N mice are highly resistant to primary infection withNippostrongylus brasiliensis." Parasitology 136, no. 1 (January 2009): 93–106. http://dx.doi.org/10.1017/s0031182008005192.
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SUMMARYNippostrongylus brasiliensislarvae are particularly susceptible to immunological attack during the pre-lung stage of primary and secondary infections in mice. Whilst most of the common laboratory strains of mice are permissive hosts for the parasite, in this study we report for the first time, the strong resistance of naïve FVB/N mice toN. brasiliensis. Damage to larvae is evident within the first 24 h of infection and this may be critical to later larval development and reproductive success. Inflammatory responses in the skin, and larval escape from this tissue were comparable in susceptible CBA/Ca and resistant FVB/N mice, with most larvae exiting within 4 h of a primary infection. Lung larval burdens were also similar between strains, but larvae recovered from FVB/N mice were smaller and less motile. In FVB/N mice, larval colonization of the gut was impaired and worms produced very few eggs. However FVB/N mice did not show enhanced resistance toHeligmosomoides bakeri(also known asHeligmosomoides polygyrus), a nematode largely restricted to the gut. Damage done in the pre-lung or lung stages of infection withN. brasiliensisis likely to contribute to ongoing developmental and functional abnormalities, which are profoundly evident in the gut phase of infection.
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Shusterman, Vladimir, Charles F. McTiernan, Anna Goldberg, Samir Saba, Guy Salama, and Barry London. "Adrenergic stimulation promotes T-wave alternans and arrhythmia inducibility in a TNF-α genetic mouse model of congestive heart failure." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H440—H450. http://dx.doi.org/10.1152/ajpheart.01024.2008.
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T-wave alternans (TWA) is a proarrhythmic repolarization instability that is common in congestive heart failure (CHF). Although transgenic mice are commonly used to study the mechanisms of arrhythmogenesis in CHF, little is known about the dynamics of TWA in these species. We hypothesized that TWA is present in a TNF-α model of CHF and can be further promoted by adrenergic stimulation. We studied 16 TNF-α mice and 12 FVB controls using 1) in vivo intracardiac electrophysiological testing and 2) ambulatory telemetry during 30 min before and after an intraperitoneal injection of isoproterenol. TWA was examined using both linear and nonlinear filtering applied in the time domain. In addition, changes in the mean amplitude of the T wave and area under the T wave were computed. During intracardiac electrophysiological testing, none of the animals had TWA or inducible arrhythmias before the injection of isoproterenol. After the injection, sustained TWA and inducible ventricular tachyarrhythmias were observed in TNF-α mice but not in FVB mice. In ambulatory telemetry, before the isoproterenol injection, the cardiac cycle length (CL) was longer in TNF-α mice than in FVB mice (98 ± 9 and 88 ± 3 ms, P = 0.04). After the injection of isoproterenol, the CL became 8% and 6% shorter in TNF-α and FVB mice ( P < 10−4); however, the 2% difference between the groups in the magnitude of CL changes was not significant. In TNF-α mice, the magnitude of TWA was 1.5–2 times greater than in FVB mice both before and after the isoproterenol injection. The magnitude of TWA increased significantly after the isoproterenol injection compared with the baseline in TNF-α mice ( P = 0.003) but not in FVB mice. The mean amplitude of the T wave and area under the T wave increased 60% and 80% in FVB mice ( P = 0.006 and 0.009) but not in TNF-α mice. In conclusion, TWA is present in a TNF-α model of CHF and can be further promoted by adrenergic stimulation, along with the enhanced susceptibility for ventricular arrhythmias.
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Ceylan-Isik, Asli F., Karissa H. LaCour, and Jun Ren. "Sex difference in cardiomyocyte function in normal and metallothionein transgenic mice: the effect of diabetes mellitus." Journal of Applied Physiology 100, no. 5 (May 2006): 1638–46. http://dx.doi.org/10.1152/japplphysiol.01273.2005.
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Evidence suggests a sex difference in intrinsic physiological and diabetic myocardial contractile function related to antioxidant properties of female ovarian hormones. This study was designed to examine the effect of cardiac overexpression of antioxidant metallothionein on intrinsic and diabetic cardiomyocyte function. Weight-matched wild-type (FVB) and metallothionein transgenic mice of both sexes were made diabetic with streptozotocin (220 mg/kg). Contractile and intracellular Ca2+ properties were evaluated including peak shortening (PS), time to PS, time to 90% relengthening (TR90), maximal velocity of shortening or relengthening (±d L/d t), fura-2 fluorescence intensity change, and Ca2+ decay rate. Akt and transcription factor c-Jun levels were evaluated by Western blot. Myocytes from female FVB mice exhibited lower PS, ±d L/d t, and fura-2 fluorescence intensity change, prolonged time to PS, TR90, and Ca2+ decay compared with male FVB mice. Interestingly, this sex difference was not present in metallothionein mice. Diabetes depressed PS, ±d L/d t and caffeine-induced Ca2+ release, as well as prolonged TR90 and Ca2+ decay in male FVB mice, whereas it only reduced PS in female FVB mice. These diabetic dysfunctions were nullified by metallothionein in both sexes. Females displayed elevated Akt phosphorylation and reduced c-Jun phosphorylation. Diabetes dampened Akt phosphorylation in male FVB mice and enhanced c-Jun in both sexes. Diabetes-induced alterations in Akt phosphorylation and c-Jun were abolished by metallothionein. The sex difference in Akt phosphorylation but not c-Jun levels was reversed by metallothionein. These data indicate that antioxidant capacity plays an important role in sex differences in both intrinsic and diabetic cardiomyocyte contractile properties possibly related to phosphorylation of Akt and c-Jun.
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Borenshtein, Diana, Katherine A. Schlieper, Barry H. Rickman, Jeannie M. Chapman, Clifford W. Schweinfest, James G. Fox, and David B. Schauer. "Decreased Expression of Colonic Slc26a3 and Carbonic Anhydrase IV as a Cause of Fatal Infectious Diarrhea in Mice." Infection and Immunity 77, no. 9 (June 22, 2009): 3639–50. http://dx.doi.org/10.1128/iai.00225-09.
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ABSTRACT Citrobacter rodentium causes epithelial hyperplasia and colitis and is used as a model for enteropathogenic and enterohemorrhagic Escherichia coli infections. Little or no mortality develops in most inbred strains of mice, but C3H and FVB/N mice exhibit fatal outcomes of infection. Here we test the hypothesis that decreased intestinal transport activity during C. rodentium infection results in fatality in C3H/HeOu and FVB/N mice. Susceptible strains were compared to resistant C57BL/6 mice and to inbred strains SWR and SJL of Swiss origin, which have not been previously characterized for outcomes of C. rodentium infection. Mortality in susceptible strains C3H/HeOu and FVB/N was associated with significant fluid loss in feces, a remarkable downregulation of Slc26a3 and carbonic anhydrase IV (CAIV) message and protein expression, retention of chloride in stool, and hypochloremia, suggesting defects in intestinal chloride absorption. SWR, SJL, and C57BL/6 mice were resistant and survived the infection. Fluid therapy fully prevented mortality in C3H/HeOu and FVB/N mice without affecting clinical disease. Common pathogenic mechanisms, such as decreased levels of expression of Slc26a3 and CAIV, affect intestinal ion transport in C. rodentium-infected FVB and C3H mice, resulting in profound electrolyte loss, dehydration, and mortality. Intestinal chloride absorption pathways are likely a potential target for the treatment of infectious diarrhea.
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Xu, Jianxiang, Yun Huang, Fenge Li, Shirong Zheng, and Paul N. Epstein. "FVB mouse genotype confers susceptibility to OVE26 diabetic albuminuria." American Journal of Physiology-Renal Physiology 299, no. 3 (September 2010): F487—F494. http://dx.doi.org/10.1152/ajprenal.00018.2010.
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OVE26 (OVE) diabetic mice on the inbred strain FVB are a valuable model of diabetic nephropathy that excretes the highest amount of urine albumin of all diabetic mouse models. Crossing of OVE mice to C57BL6 or DBA2 mice reduced albuminuria 17-fold in F1 diabetic offspring without reducing diabetes. When comparing renal histology of OVE mice on the FVB background to F1 C57BL6 crosses, we found that the F1 kidneys had significantly smaller glomeruli, much less albumin accumulation in tubules, reduced mesangial matrix expansion, and less interstitial fibrosis. A genome scan of 108 OVE-positive N2 offspring for albuminuria revealed one significant peak on chromosome 11 and nearly significant peaks on chromosomes 9, 13, and 19. Homozygosity for the FVB genotype for peaks on chromosomes 11, 13, or 19 increased albuminuria. Homozygosity for the chromosome 9 peak reduced albuminuria. Combined homozyogosity for the peaks on chromosomes 11, 13, and 19 increased albuminuria over 12-fold and accounted for >70% of the difference between OVE mice on the FVB vs. the F1 background. These loci contain sequences important to susceptibility to diabetic albuminuria.
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Kerkvliet, Jason, Laurie Zoecklein, Louisa Papke, Aleksandar Denic, Allan J. Bieber, Larry R. Pease, Chella S. David, and Moses Rodriguez. "Transgenic Expression of the 3D Polymerase Inhibits Theiler's Virus Infection and Demyelination." Journal of Virology 83, no. 23 (September 16, 2009): 12279–89. http://dx.doi.org/10.1128/jvi.00664-09.
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ABSTRACT The RNA-dependent RNA polymerase 3Dpol is required for the elongation of positive- and negative-stranded picornavirus RNA. During the course of investigating the effect of the transgenic expression of viral genes on the host immune response, we evaluated the viral load present in the host after infection. To our surprise, we found that 3D transgenic expression in genetically susceptible FVB mice led to substantially lower viral loads after infection with Theiler's murine encephalomyelitis virus (TMEV). As a result, spinal cord damage caused by chronic viral infection in the central nervous system was reduced in FVB mice that expressed 3D. This led to the preservation of large-diameter axons and motor function in these mice. The 3D transgene also lowered early viral loads when expressed in FVB-D b mice resistant to persistent TMEV infection. The protective effect of 3D transgenic expression was not altered in FVB-Rag−/−.3D mice that are deficient in T and B cells, thus ruling out a mechanism by which the overexpression of 3D enhanced the adaptive immune clearance of the virus. Understanding how endogenously overexpressed 3D polymerase inhibits viral replication may lead to new strategies for targeting therapies to all picornaviruses.
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Li, Xiaocui, Yushan Xie, Wei Qu, Xiaojun Ou, Xiaowen Ou, Chuang Wang, Xiaoxiao Qi, Ying Wang, Zhongqiu Liu, and Lijun Zhu. "Breast Cancer Resistance Protein and Multidrug Resistance Protein 2 Mediate the Disposition of Leonurine-10-O-β-glucuronide." Current Drug Metabolism 21, no. 13 (December 30, 2020): 1060–67. http://dx.doi.org/10.2174/1389200221999201116142742.
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Background: Leonurine (Leo), a promising antilipemic agent that has been approved for clinical trials, is extensively metabolized into bioactive Leonurine-10-O-β-glucuronide (L-10-G) vivo. Objective: To explore the effects of breast cancer resistance protein (Bcrp) and multidrug resistance protein 2 (Mrp2) on the disposition of L-10-G. Methods: The pharmacokinetics, tissue distribution and intestinal perfusion of Leo were studied by using efflux transporter gene knockout mouse models. The enzyme kinetics via liver and intestinal microsomes were also examined. Results: After intravenous injection with Leo, the AUC0-∞ values of L-10-G in Bcrp1-/- and Mrp2-/- mice were 1.55-fold and 16.80-fold higher, respectively, than those in wild-type FVB mice (P < 0.05). After oral administration, the AUC0-∞ value of L-10-G showed a 2.82-fold increase in Mrp2-/- mice compared with wild-type FVB mice (P < 0.05). After gavage with Leo for 10 and 25 min, the bile accumulation of L-10-G in Mrp2-/- mice was 3-fold and 22-fold lower, respectively, than that in wild-type FVB mice (P < 0.05). Besides, the intestinal excreted amount of L-10-G showed 2.22-fold and 2.68-fold decrease in Bcrp1-/- and Mrp2-/- mice, respectively, compared with that in wild-type FVB mice (P < 0.05). The clearance of L-10-G decreased in liver microsomes and increased in intestinal microsomes of Bcrp1-/- and Mrp2-/- mice compared to the wild-type FVB mice (P < 0.05). Conclusion: Both Bcrp and Mrp2 are involved in the disposition of L-10-G, and Mrp2 exhibits a superior influence.
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Lee, So-Young, Markus Hörbelt, Henry E. Mang, Nicole L. Knipe, Robert L. Bacallao, Yoshikazu Sado, and Timothy A. Sutton. "MMP-9 gene deletion mitigates microvascular loss in a model of ischemic acute kidney injury." American Journal of Physiology-Renal Physiology 301, no. 1 (July 2011): F101—F109. http://dx.doi.org/10.1152/ajprenal.00445.2010.
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Microvascular rarefaction following an episode of acute kidney injury (AKI) is associated with renal hypoxia and progression toward chronic kidney disease. The mechanisms contributing to microvascular rarefaction are not well-understood, although disruption in local angioregulatory substances is thought to contribute. Matrix metalloproteinase (MMP)-9 is an endopeptidase important in modifying the extracellular matrix (ECM) and remodeling the vasculature. We examined the role of MMP-9 gene deletion on microvascular rarefaction in a rodent model of ischemic AKI. MMP-9-null mice and background control (FVB/NJ) mice were subjected to bilateral renal artery clamping for 20 min followed by reperfusion for 14, 28, or 56 days. Serum creatinine level in MMP-9-null mice 24 h after injury [1.4 (SD 0.8) mg/dl] was not significantly different from FVB/NJ mice [1.5 (SD 0.6) mg/dl]. Four weeks after ischemic injury, FVB/NJ mice demonstrated a 30–40% loss of microvascular density compared with sham-operated (SO) mice. In contrast, microvascular density was not significantly different in the MMP-9-null mice at this time following injury compared with SO mice. FVB/NJ mice had a 50% decrease in tissue vascular endothelial growth factor (VEGF) 2 wk after ischemic insult compared with SO mice. A significant difference in VEGF was not observed in MMP-9-null mice compared with SO mice. There was no significant difference in the liberation of angioinhibitory fragments from the ECM between MMP-9-null mice and FVB/NJ mice following ischemic injury. In conclusion, MMP-9 deletion stabilizes microvascular density following ischemic AKI in part by preserving tissue VEGF levels.
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Aguilar, Roberto, Carl Tinghao Zhang, Tengchuan Ma, and Chongyu Feng. "Tumor growth following genetic modifications of mouse prostate tumor cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 242.9. http://dx.doi.org/10.4049/jimmunol.204.supp.242.9.
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Abstract Objectives 1) To determine the growth features of MyC-CaP mouse prostate tumors induced in immunodeficient nude mice and in immunocompetent FVB mice; and 2) To assess growth characteristics of MyC-CaP-p53 null tumor cells in vitro. Methods MyC-CaP cells were transfected with enhanced green fluorescent protein (eGFP), and the MyC-CaP-eGFP cells were injected intraperitoneally into naive immunodeficient nude recipients and into naive immunocompetetent FVB recipients. The transplanted tumor cells were subsequently tracked by fluorescent stereo microscopy. MyC-CaP-p53 null tumor cells were generated by inducible CRISPR/Caspase-9 gene deletion targeted to the native mutated p53 tumor suppressor gene. Results 1) Increased growth of MyC-CaP-eGFP tumors occurred in immunodeficient nude mice compared to growth in immunocompetent FVB mice; 2) decreased metastasis of MyC-CaP-eGFP tumors compared to MyC-CaP tumors occurred following injection into immunocompetent FVB mice; and 3) MyC-CaP-p53 null cells showed reduced proliferation and growth in vitro compared to non-modified MyC-CaP tumor cells. Conclusions Three conclusions can be drawn from these studies: 1) Injection of MyC-CaP-eGFP tumor cells into naive immunodeficient nude recipients allowed for adequate examination of initial tumor viability and subsequent tumor growth and metastasis; 2) Decreased MyC-CaP-eGFP tumor growth in immunocompetent FVB mice compared to immunodeficient nude mice indicates that an immune response to the eGFP protein inhibited growth of the MyC-CaP-eGFP tumor; and 3) The growth inhibition following deletion of the mutated p53 tumor suppressor gene in MyC-CaP tumor cells indicates that the mutated allele helps drive the malignancy.
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Chen, Ching-Hao, Chun-Hou Liao, Kuo-Chiang Chen, Kuan-Lin Wang, Xiao-Wen Tseng, Wei-Kung Tsai, Han-Sun Chiang, and Yi-No Wu. "B6 Mouse Strain: The Best Fit for LPS-Induced Interstitial Cystitis Model." International Journal of Molecular Sciences 22, no. 21 (November 8, 2021): 12053. http://dx.doi.org/10.3390/ijms222112053.
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Interstitial cystitis (IC) is a chronic inflammatory disease characterized by bladder pain and increased urinary frequency. Although the C57BL/6J (B6) and FVB/NJ (FVB) mouse strains are commonly used as animal models for studies involving the urinary system, few reports have compared their lower urinary tract anatomy, despite the importance of such data. Our study aimed to characterize bladder function changes in FVB and B6 mouse strains with lipopolysaccharide (LPS)-induced IC, to understand mouse model-based bladder research. The bladder function parameters were measured by cystometrogram. Histological assay was examined by hematoxylin and eosin stain, Masson’s trichrome stain, and immunofluorescence staining. Results indicated that the two strains in the control group exhibited different bladder structures and functions, with significant anatomical differences, including a larger bladder size in the FVB than in the B6 strain. Furthermore, cystometry tests revealed differences in bladder function pressure. LPS-treated B6 mice presented significant changes in peak pressure, with decreased intercontraction intervals; these results were similar to symptoms of IC in humans. Each strain displayed distinct characteristics, emphasizing the care required in choosing the appropriate strain for bladder-model studies. The results suggested that the B6 mouse strain is more suitable for IC models.
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Christen, Urs, Martin Holdener, Edith Hintermann, Eric Johnson, Michael Manns, and Matthias von Herrath. "The CYP450 mouse model for autoimmune hepatitis: Breaking of self-tolerance in transgenic CYP2D6 and wildtype FVB-mice by viral infection (130.1)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S227. http://dx.doi.org/10.4049/jimmunol.178.supp.130.1.
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Abstract The etiology of autoimmune hepatitis (AIH) is poorly understood although the major autoantigen, cytochrome P450 2D6 (CYP2D6), has been identified. We generated an animal model for human AIH using the natural autoantigen CYP2D6. We infected transgenic mice expressing human CYP2D6 in the liver with an Adenovirus-CYP2D6 vector (Ad-2D6) to break self-tolerance. Upon infection with Ad-2D6 not only transgenic CYP2D6 mice but also wildtype FVB mice showed persistent features of severe liver damage associated with AIH (hepatic fibrosis, fused liver lobules, cellular infiltrations, elevated serum ALT levels, confluent necrosis). Ad-2D6-infected mice (CYP2D6 and FVB) generated high titers of anti-CYP2D6 antibodies. Epitope mapping revealed that anti-CYP2D6 antibodies predominantly recognized the same immunodominant linear epitope recognized by sera of AIH patients (AQPPRD aa265-270). In contrast, mice infected with a control Adenovirus expressing green fluorescence protein did neither develop liver damage nor generated anti-CYP2D6 antibodies. The severity of liver damage as well as antibody formation was enhanced in FVB mice compared to transgenic CYP2D6 mice indicating a stronger tolerance to human CYP2D6 in CYP2D6 mice. In FVB mice, due to the homology of the mouse isoenzymes of the CYP superfamily to human CYP2D6, autoimmune liver damage by Ad-2D6-infection was possibly induced via true molecular mimicry.
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Barkley-Levenson, Amanda M., Amy Lee, and Abraham A. Palmer. "Genetic and Pharmacological Manipulations of Glyoxalase 1 Mediate Ethanol Withdrawal Seizure Susceptibility in Mice." Brain Sciences 11, no. 1 (January 19, 2021): 127. http://dx.doi.org/10.3390/brainsci11010127.
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Central nervous system (CNS) hyperexcitability is a clinically significant feature of acute ethanol withdrawal. There is evidence for a genetic contribution to withdrawal severity, but specific genetic risk factors have not been identified. The gene glyoxalase 1 (Glo1) has been previously implicated in ethanol consumption in mice, and GLO1 inhibition can attenuate drinking in mice and rats. Here, we investigated whether genetic and pharmacological manipulations of GLO1 activity can also mediate ethanol withdrawal seizure severity in mice. Mice from two transgenic lines overexpressing Glo1 on different genetic backgrounds (C57BL/6J (B6) and FVB/NJ (FVB)) were tested for handling-induced convulsions (HICs) as a measure of acute ethanol withdrawal. Following an injection of 4 g/kg alcohol, both B6 and FVB mice overexpressing Glo1 showed increases in HICs compared to wild-type littermates, though only the FVB line showed a statistically significant difference. We also administered daily ethanol injections (2 g/kg + 9 mg/kg 4-methylpyrazole) to wild-type B6 mice for 10 days and tested them for HICs on the 10th day following treatment with either a vehicle or a GLO1 inhibitor (S-bromobenzylglutathione cyclopentyl diester (pBBG)). Treatment with pBBG reduced HICs, although this effect was only statistically significant following two 10-day cycles of ethanol exposure and withdrawal. These results provide converging genetic and pharmacological evidence that GLO1 can mediate ethanol withdrawal seizure susceptibility.
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Burgess, Shawn C., F. Mark H. Jeffrey, Charles Storey, Angela Milde, Natasha Hausler, Matthew E. Merritt, Hindrik Mulder, Cecilia Holm, A. Dean Sherry, and Craig R. Malloy. "Effect of murine strain on metabolic pathways of glucose production after brief or prolonged fasting." American Journal of Physiology-Endocrinology and Metabolism 289, no. 1 (July 2005): E53—E61. http://dx.doi.org/10.1152/ajpendo.00601.2004.
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Background strain is known to influence the way a genetic manipulation affects mouse phenotypes. Despite data that demonstrate variations in the primary phenotype of basic inbred strains of mice, there is limited data available about specific metabolic fluxes in vivo that may be responsible for the differences in strain phenotypes. In this study, a simple stable isotope tracer/NMR spectroscopic protocol has been used to compare metabolic fluxes in ICR, FVB/N (FVB), C57BL/6J (B6), and 129S1/SvImJ (129) mouse strains. After a short-term fast in these mice, there were no detectable differences in the pathway fluxes that contribute to glucose synthesis. However, after a 24-h fast, B6 mice retain some residual glycogenolysis compared with other strains. FVB mice also had a 30% higher in vivo phospho enolpyruvate carboxykinase flux and total glucose production from the level of the TCA cycle compared with B6 and 129 strains, while total body glucose production in the 129 strain was ∼30% lower than in either FVB or B6 mice. These data indicate that there are inherent differences in several pathways involving glucose metabolism of inbred strains of mice that may contribute to a phenotype after genetic manipulation in these animals. The techniques used here are amenable to use as a secondary or tertiary tool for studying mouse models with disruptions of intermediary metabolism.
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Duan, Jinhong, Grant E. McFadden, Anthony J. Borgerding, Faye L. Norby, Bonnie H. Ren, Gang Ye, Paul N. Epstein, and Jun Ren. "Overexpression of alcohol dehydrogenase exacerbates ethanol-induced contractile defect in cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 4 (April 1, 2002): H1216—H1222. http://dx.doi.org/10.1152/ajpheart.00780.2001.
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Alcoholic cardiomyopathy is characterized by impaired ventricular function although its toxic mechanism is unclear. This study examined the impact of cardiac overexpression of alcohol dehydrogenase (ADH), which oxidizes ethanol into acetaldehyde (ACA), on ethanol-induced cardiac contractile defect. Mechanical and intracellular Ca2+properties were evaluated in ventricular myocytes from ADH transgenic and wild-type (FVB) mice. ACA production was assessed by gas chromatography. ADH myocytes exhibited similar mechanical properties but a higher efficiency to convert ACA compared with FVB myocytes. Acute exposure to ethanol depressed cell shortening and intracellular Ca2+ in the FVB group with maximal inhibitions of 23.3% and 23.4%, respectively. Strikingly, the ethanol-induced depression on cell shortening and intracellular Ca2+ was significantly augmented in the ADH group, with maximal inhibitions of 43.7% and 40.6%, respectively. Pretreatment with the ADH inhibitor 4-methylpyrazole (4-MP) or the aldehyde dehydrogenase inhibitor cyanamide prevented or augmented the ethanol-induced inhibition, respectively, in the ADH but not the FVB group. The ADH transgene also substantiated the ethanol-induced inhibition of maximal velocity of shortening/relengthening and unmasked an ethanol-induced prolongation of the duration of shortening/relengthening, which was abolished by 4-MP. These data suggest that elevated cardiac ACA exposure due to enhanced ADH expression may play an important role in the development of alcoholic cardiomyopathy.
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Weerasinghe, Sujith V. W., Min-Jung Park, Daniel A. Portney, and M. Bishr Omary. "Mouse genetic background contributes to hepatocyte susceptibility to Fas-mediated apoptosis." Molecular Biology of the Cell 27, no. 20 (October 15, 2016): 3005–12. http://dx.doi.org/10.1091/mbc.e15-06-0423.
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Liver disease progression is modulated by genetic modifiers in mouse strains and across human races and ethnicities. We hypothesized that hepatocyte culture duration and genetic background regulate hepatocyte susceptibility to apoptosis. Hepatocytes were isolated from FVB/N, C57BL/6, and C3H/He mice and cultured or treated with Fas ligand or acetaminophen after different culture times. Protein and mRNA expressions of Fas receptor, caspases-3/7/8, and Bak/Bax/Bid proteins were determined. FVB/N hepatocytes manifested rapid decreases of caspases-3/7 but not caspase-8 as culture time increased, which paralleled decreased susceptibility to apoptosis. Some changes were also found in Fas-receptor and Bak, Bax, and Bid proteins; caspase mRNA decreases were also noted. Caspase protein degradation was partially reversed by lysosomal protease but not proteasome or autophagy inhibitors. C57BL/6 and FVB/N hepatocytes behaved similarly in their limited susceptibility to apoptosis, whereas C3H/He hepatocytes show limited alterations in caspases, with consequent increased susceptibility to apoptosis. Similarly, C3H/He mice were more susceptible than C57BL/6 and FVB/N mice to Fas-mediated liver injury. Therefore there are significant mouse strain–dependent differences in susceptibility to apoptosis and selective loss of caspases upon short-term hepatocyte culture, with consequent decrease in susceptibility to apoptosis. These differences likely reflect genetic modifiers that provide resistance or predisposition to hepatocyte death.
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Hänni, Miriam, Irene Kriesi, and Jörg Neumann. "Entry into and Completion of Vocational Baccalaureate School in Switzerland: Do Differences in Regional Admission Regulations Matter?" Education Sciences 12, no. 3 (March 8, 2022): 188. http://dx.doi.org/10.3390/educsci12030188.
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Upper secondary education in Switzerland is divided into a general and a vocational path. Approximately two thirds of adolescents attend the vocational path. The initial vocational education and training (IVET) can be combined with a federal vocational baccalaureate (FVB), which enables graduates to enter universities of applied sciences. The proportion of FVB holders varies considerably between Swiss regions. We study how admission regulations affect regional entry and graduation rates and how they interact with individual characteristics. We use longitudinal register data from the Federal Statistical Office to study individuals’ chances of pursuing and obtaining a vocational baccalaureate in combination with data about cantonal admission criteria to vocational baccalaureate schools. We find that higher admission barriers reduce individuals’ chances of pursuing a vocational baccalaureate, particularly among apprentices with low socio-economic status and those who pursue an FVB after their VET diploma. Against our expectations, high admission barriers are associated not only with lower entry rates but also with lower graduation rates.
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Mahler, Joel F., William Stokes, Peter C. Mann, Masaya Takaoka, and Robert R. Maronpot. "Spontaneous Lesions in Aging FVB/N Mice." Toxicologic Pathology 24, no. 6 (November 1996): 710–16. http://dx.doi.org/10.1177/019262339602400606.
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Davidson, Courtney E., Qian Li, Gary A. Churchill, Lucy R. Osborne, and Heather E. McDermid. "Modifier locus for exencephaly in Cecr2 mutant mice is syntenic to the 10q25.3 region associated with neural tube defects in humans." Physiological Genomics 31, no. 2 (October 2007): 244–51. http://dx.doi.org/10.1152/physiolgenomics.00062.2007.
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Neural tube defects (NTDs), the second most common birth defect in humans, are multifactorial with complex genetic and environmental causes, although the genetic factors are almost completely unknown. In mice, >100 single gene mutations cause NTDs; however, the penetrance in many of these single gene mutant lines is highly dependent on the genetic background. We previously reported that a homozygous Cecr2 mutation on a BALB/c background causes exencephaly at a frequency of 74% compared with 0% on an FVB/N background. We now report that a major genetic modifier on chromosome 19, mapped using whole genome linkage analysis, increases the relative risk of exencephaly by 3.74 times in homozygous BALB embryos vs. BALB/FVB heterozygotes. Scanning electron microscopy revealed that the modifier does not affect the location of neural tube closure site 2, a known murine susceptibility factor for exencephaly. Crossing the Sp ( Splotch) mutation in the Pax3 gene onto the FVB/N background for two generations indicated that this resistant strain also decreases the penetrance of spina bifida. The chromosome 19 modifier region corresponds to a linkage region on human chromosome 10q25.3 mapped in a whole genome scan of human NTD families. Since the FVB/N genetic background affects susceptibility to both exencephaly and spina bifida, the human homolog of the chromosome 19 modifier locus may be a better candidate for human NTD susceptibility factors than genes that when mutated actually cause NTDs in mice.
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Laval, Marie, Graham S. Baldwin, Arthur Shulkes, and Kathryn M. Marshall. "Increased gastrin gene expression provides a physiological advantage to mice under hypoxic conditions." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 2 (January 15, 2015): G76—G84. http://dx.doi.org/10.1152/ajpgi.00344.2014.
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Hypoxia, or a low concentration of O2, is encountered in humans undertaking activities such as mountain climbing and scuba diving and is important pathophysiologically as a limiting factor in tumor growth. Although data on the interplay between hypoxia and gastrins are limited, gastrin expression is upregulated by hypoxia in gastrointestinal cancer cell lines, and gastrins counterbalance hypoxia by stimulating angiogenesis in vitro and in vivo. The aim of this study was to determine if higher concentrations of the gastrin precursor progastrin are protective against hypoxia in vivo. hGAS mice, which overexpress progastrin in the liver, and mice of the corresponding wild-type FVB/N strain were exposed to normoxia or hypoxia. Iron status was assessed by measurement of serum iron parameters, real-time PCR for mRNAs encoding critical iron regulatory proteins, and Perls' stain and atomic absorption spectrometry for tissue iron concentrations. FVB/N mice lost weight at a faster rate and had higher sickness scores than hGAS mice exposed to hypoxia. Serum iron levels were lower in hGAS than FVB/N mice and decreased further when the animals were exposed to hypoxia. The concentration of iron in the liver was strikingly lower in hGAS than FVB/N mice. We conclude that increased circulating concentrations of progastrin provide a physiological advantage against systemic hypoxia in mice, possibly by increasing the availability of iron stores. This is the first report of an association between progastrin overexpression, hypoxia, and iron homeostasis.
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Louahed, Jamila, Yuhong Zhou, W. Lee Maloy, Pyapalli U. Rani, Christine Weiss, Yaniv Tomer, Anne Vink, et al. "Interleukin 9 promotes influx and local maturation of eosinophils." Blood 97, no. 4 (February 15, 2001): 1035–42. http://dx.doi.org/10.1182/blood.v97.4.1035.
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Abstract The interleukin 9 (IL-9) pathway has recently been associated with the asthmatic phenotype including an eosinophilic tissue inflammation. The mechanism by which IL-9 affects eosinophils (eos) is not known. To investigate whether this cytokine has a direct activity on the development of eos and eosinophilic inflammation, a model of thioglycolate-induced peritoneal inflammation was used in IL-9 transgenic (TG5) and background strain (FVB) mice. In this model, a transient eosinophilic infiltration in the peritoneal cavity was observed in FVB mice 12 to 24 hours after thioglycolate injection that coincided with peak IL-5 and IL-9 release. In contrast, TG5 mice developed a massive eosinophilia that persisted at high levels (81% of total cells) even 72 hours after thioglycolate injection. Release of eosinophilic major basic protein (MBP), IL-4, and IL-5 to the peritoneal cavity of these mice was significantly increased when compared with the control FVB strain. To study the mechanism by which IL-9 exerts its effect on eos, bone marrow or peritoneal cells were cultured in the presence of IL-5, IL-9, or their combination in vitro. IL-5 alone was able to generate significant numbers of eos in TG5 but not FVB mice, whereas a combination of IL-5 and IL-9 induced marked eosinophilia in both strains indicating a synergism between these 2 cytokines. These data suggest that IL-9 may promote and sustain eosinophilic inflammation via IL-5–driven eos maturation of precursors.
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Schnell, Fred, Dan Mourich, and Patrick Iversen. "A novel mouse model for arenavirus hemorrhagic fever (67.20)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 67.20. http://dx.doi.org/10.4049/jimmunol.186.supp.67.20.
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Abstract The viral family Arenaviridae includes a number of viruses that can cause hemorrhagic fever. Arenavirus infection often involves multiple organs and can lead to capillary instability, impaired hemostasis, and death. There is a lack of treatment options available to those suffering from arenaviral hemorrhagic fever and a well established mouse model of arenaviral hemorrhagic fever would benefit preclinical testing for arenavirus antivirals or therapeutics. We have identified the FVB mouse strain, which succumbs to a hemorrhagic fever like illness when infected with lymphocytic choriomeningitis virus (LCMV). FVB mice infected with LCMV demonstrate high mortality associated with thrombocytopenia, hepatocellular and splenic necrosis, and cutaneous hemorrhage whereas C57BL/6 mice survive. Investigation of possible inflammatory mediators revealed increased IFN-g and IL-6, along with increased chemokine production, at early times after LCMV infection as compared to C57BL/6 mice. Removal of CD4+ or CD8+ cells from FVB mice at time of infection prevented mortality in all treated animals and treatment with FK506 early during infection delayed disease onset. This report offers a novel animal model for arenavirus research and pre-clinical therapeutic testing.
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May, C., R. Gunther, and RS McIvor. "Protection of mice from lethal doses of methotrexate by transplantation with transgenic marrow expressing drug-resistant dihydrofolate reductase activity." Blood 86, no. 6 (September 15, 1995): 2439–48. http://dx.doi.org/10.1182/blood.v86.6.2439.bloodjournal8662439.
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Marrow cells from previously established lines of transgenic mice expressing either of two different methotrexate (MTX)-resistant dihydrofolate reductases (DHFRs) were transplanted into recipient animals to determine the resultant in vivo protective effect against toxicity associated with MTX administration. Sublethally irradiated, untransplanted animals were first used to establish conditions of low- dose MTX administration resulting in substantial hematopoietic toxicity with undetectable gastrointestinal toxicity. Under these conditions, low survival rates were observed for normal or transgenic animals not expressing drug-resistant DHFR activity, whereas transgenic animals expressing either the arg22 (line 04) or trp31 (line 03) DHFR variants survived. Transplantation of 10(6) marrow cells from either transgenic lines 03 or 04 rescued normal FVB/N recipient animals from low-dose MTX administration, which was lethal for animals transplanted with 10(6) normal FVB/N marrow cells. Reduced survival of transgenic line 04 marrow recipients was observed when twofold or fourfold doses of MTX were administered. However, when 10(7) transgenic line 04 marrow cells were infused, the recipients were found to be resistant to a MTX dose that was not only lethal for animals transplanted with 10(7) normal FVB/N marrow cells, but also lethal for normal, untransplanted FVB/N mice. Histologic analysis showed protection of both marrow and gastrointestinal tissues from MTX toxicity in transgenic line 04 marrow transplant recipients. Thus, exclusive expression of MTX-resistant DHFR activity in the marrow had a substantial, systemic chemoprotective effect in animals, which could be applied for improved utilization of MTX for antitumor chemotherapy.
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Mo, Yiqun, Jing Chen, Connie F. Schlueter, and Gary W. Hoyle. "Differential susceptibility of inbred mouse strains to chlorine-induced airway fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 2 (January 15, 2013): L92—L102. http://dx.doi.org/10.1152/ajplung.00272.2012.
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Chlorine is a reactive gas that is considered a chemical threat agent. Humans who develop acute lung injury from chlorine inhalation typically recover normal lung function; however, a subset can experience chronic airway disease. To examine pathological changes following chlorine-induced lung injury, mice were exposed to a single high dose of chlorine, and repair of the lung was analyzed at multiple times after exposure. In FVB/NJ mice, chlorine inhalation caused pronounced fibrosis of larger airways that developed by day 7 after exposure and was associated with airway hyperreactivity. In contrast, A/J mice had little or no airway fibrosis and had normal lung function at day 7. Unexposed FVB/NJ mice had less keratin 5 staining (basal cell marker) than A/J mice in large intrapulmonary airways where epithelial repair was poor and fibrosis developed after chlorine exposure. FVB/NJ mice had large areas devoid of epithelium on day 1 after exposure leading to fibroproliferative lesions on days 4 and 7. A/J mice had airways covered by squamous keratin 5-stained cells on day 1 that transitioned to a highly proliferative reparative epithelium by day 4 followed by the reappearance of ciliated and Clara cells by day 7. The data suggest that lack of basal cells in the large intrapulmonary airways and failure to effect epithelial repair at these sites are factors contributing to the development of airway fibrosis in FVB/NJ mice. The observed differences in susceptibility to chlorine-induced airway disease provide a model in which mechanisms and treatment of airway fibrosis can be investigated.
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Radaelli, E., A. Arnold, A. Papanikolaou, R. A. Garcia-Fernandez, S. Mattiello, E. Scanziani, and R. D. Cardiff. "Mammary Tumor Phenotypes in Wild-Type Aging Female FVB/N Mice with Pituitary Prolactinomas." Veterinary Pathology 46, no. 4 (March 9, 2009): 736–45. http://dx.doi.org/10.1354/vp.08-vp-0280-r-fl.
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Prolactin-secreting pituitary adenomas are common spontaneous lesions in aging FVB females. Prolactin-secreting pituitary proliferations play a significant role in mouse mammary tumorigenesis generally producing adenosquamous carcinomas. Since genetically engineered FVB mice are frequently used to study mammary tumor biology, we have examined a cohort of 64 aging wild-type FVB/N females to establish the prevalence and the nature of spontaneous mammary and pituitary tumors. Tissues from mammary and pituitary glands were studied by histopathology and immunohistochemistry. Of the 64 examined mice, 20 had pituitary tumors and 20 had mammary tumors. Mammary and pituitary tumors were associated in 17 mice. All pituitary tumors were prolactin-positive by immunohistochemistry and classified as prolactinomas. Fourteen mammary tumors, including 12 cases with and 2 without concurrent prolactinomas, were adenocarcinomas with different combinations of epithelial growth patterns. Five mice with prolactinomas had mammary tumors characterized by the epithelial-mesenchymal transition (EMT) phenotype. Estrogen receptor alpha (ERα)-positivity was observed for 14 of the 18 mammary tumors tested, including both adenocarcinomas with nuclear immunoreactivity and EMT-phenotype tumors with both nuclear and cytoplasmic immunoreactivity. No immunoreactivity for the progesterone receptor was observed. This study confirms that spontaneous prolactinomas and mammary tumors are both common and significantly associated lesions in FVB mice. Parity and age represented risk factors for the development of these tumors. Compared with previous reports, prolactinoma-associated mammary tumors displayed a broader morphologic spectrum, including cases with the EMT phenotype. The elevated number of prolactinoma-associated and ERα-positive mammary tumors opens intriguing possibilities concerning the role of ERα cytoplasmic localization during EMT tumorigenesis.
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Murph, Mandi M., Shuying Liu, Wei Jia, Ha Nguyen, Megan A. MacFarlane, Susan S. Smyth, Sudeepti S. Kuppa, and Kevin K. Dobbin. "Diet-regulated behavior: FVB/N mice fed a lean diet exhibit increased nocturnal bouts of aggression between littermates." Laboratory Animals 54, no. 2 (March 16, 2019): 159–70. http://dx.doi.org/10.1177/0023677219834582.
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The hyperactive FVB/N inbred mouse strain is widely used for transgenic research applications, although rarely for behavioral studies. These mice have visual impairments via retinal degeneration, but are considered highly intelligent and rely largely on olfaction. While investigating diet-induced obesity in autotaxin transgenic FVB/N mice, we observed an increase in the necessity for male, but not female, cage separations. Based on the observations, we hypothesized that feeding FVB/N mice a lean diet increases nocturnal bouts of aggression between male littermates. The diets of adult littermates were switched from normal chow to either ad libitum high-fat (45% fat) or lean (10% fat) matched diets for 27 weeks, whereby the mice reached an average of 43 g versus 35 g, respectively. Then, cage separations due to nocturnal bouts of aggression became mandatory, even though littermates peacefully cohabitated for 10–16 weeks previously. Since the data was of an unusual nature, it required uncommon statistical methods to be engendered to evaluate whether and where significance existed. Therefore, utilizing the randomization and population models, we established a methodology and postulated that either testosterone, the autotaxin transgene or diet alteration was the causal factor. Statistical evaluation demonstrated a significant correlation between cage separations and aggressive behavior associated with the lean-diet-fed mice, not autotaxin. Biochemical data did not appear to explain the behavior. In contrast, energy metabolism highlighted differences between the groups of normally hyperactive mice by diet. This characteristic makes FVB/N male mice unsuitable subjects for long-term studies with lean-diet modifications.
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Mix, Madison R., Vanessa Y. Ruiz, April M. Huseby Kelcher, Slobodan I. Macura, Prasanna K. Mishra, and Aaron J. Johnson. "Virus antigen-specific CD8 T cells contribute to brain atrophy during Theiler’s murine encephalomyelitis virus (TMEV) infection of the CNS." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 61.2. http://dx.doi.org/10.4049/jimmunol.200.supp.61.2.
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Abstract Brain atrophy is a central feature of numerous neurological diseases for which the contribution of immune cells remains poorly defined. For example, in human multiple sclerosis, clonally expanded CD8 T cells have been observed in proximity to lesions, but their role in mediating brain atrophy has yet to be elucidated. This study aims to define how antigen-specific CD8 T cells contribute to brain atrophy in the TMEV model of neuroinflammation. Specific MHC class I haplotypes have been shown to dictate neuropathology and functional outcomes in mice following intracranial infection with TMEV. In this study, we demonstrate that transgenic FVB mice which express the H-2Db class I molecule rapidly clear picornavirus infection but at the cost of a novel neurodegenerative phenotype consistent with brain atrophy. Following TMEV infection out to four months, FVB mice expressing the Db class I molecule display increased lateral ventricular volume via T2-weighted MRI and hippocampal neuron loss by hematoxylin and eosin staining. Furthermore, these transgenic FVB mice present enhanced brain infiltration of virus-specific CD8 T cells for the immunodominant Db:VP2121–130 epitope. To address these findings mechanistically, we inhibited the Db:VP2121–130 epitope-specific CD8 T cell response and monitored the effect on brain atrophy. This inhibition strategy resulted in a reduction in brain atrophy to levels comparable to wild-type FVB controls. Not confounded by persistent infection or demyelination, these studies are the first to demonstrate antigen-specific CD8 T cells have the capacity to induce brain atrophy in a murine model of neurodegeneration.
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Errijgers, V., D. Van Dam, I. Gantois, C. J. Van Ginneken, A. W. Grossman, R. D?Hooge, P. P. De Deyn, and R. F. Kooy. "FVB.129P2-Pde6b+Tyrc-ch/Ant, a sighted variant of the FVB/N mouse strain suitable for behavioral analysis." Genes, Brain and Behavior 6, no. 6 (August 2007): 552–57. http://dx.doi.org/10.1111/j.1601-183x.2006.00282.x.
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Davis, Michael J., Jorge Rodriguez-Gil, Liz Hoke, Giovana Pinheiro, Yun Chang, Jaspal Khillan, William Paven, and June Kwon-Chung. "Regions of mouse chromosomes 2 and 11 in SJL mice contain critical alleles for resistance to Cryptococcus neoformans." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 82.4. http://dx.doi.org/10.4049/jimmunol.204.supp.82.4.
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Abstract Cryptococcus neoformans (Cn) remains a leading cause of deadly mycosis. While previous studies have elucidated some of the host immune processes, little is known about the fundamental host factors that determine the outcome of Cn infection. Unfortunately, all commonly used inbred mice (including the common C57BL/6) are highly susceptible to virulent Cn strains, whereas humans are resistant to Cn unless immunocompromised. Thus, we sought a murine Cn infection system that more closely models humans. Testing the susceptibility of about 20 inbred strains of mice, we found that the SJL strain is, by far, the most Cn resistant inbred mouse strain in contrast to the closely related FVB strain being completely susceptible. While the early stages of Cn infection seem similar, SJL mice eventually cleared Cn and resolved pulmonary pathology, with little CNS dissemination. In contrast, susceptible mice showed significant and increasing fungal loads in both lungs and brains with associated pathology and death. F1 mice from FVB × SJL crosses were highly resistant to Cn suggesting that the resistant phenotype is dominant. Twenty percent of N2 mice (FVB × SJL F1 mice backcrossed to FVB) survived infection suggesting the involvement of multiple loci. Gene mapping uncovered two areas of genetic linkage to Cn resistance. These areas of interest were in portions of chromosomes 2 and 11. Genomic analysis found several candidate genes which are currently under evaluation. Mapping these cryptococcal resistance gene alleles may illuminate pathways of natural resistance which could be utilized for improved therapeutic options or to identify human populations at risk for cryptococcosis, making SJL mice an important tool for understanding cryptococcosis.
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Kmieciak, Maciej, Jessica L. Kostick, Elizabeth Bolesta, and Masoud H. Manjili. "The status of IFN-gamma receptor on tumor cells will determine the outcome of tumor relapse or tumor-free survival in FVB mice (50.7)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S91. http://dx.doi.org/10.4049/jimmunol.178.supp.50.7.
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Abstract We have previously shown that inoculation of the rat neu-overexpressing mouse mammary carcinoma (MMC), derived from FVBN202 mice, into parental FVB mice resulted in the initial tumor rejection and relapse of the neu antigen negative variant (ANV) in a large fraction of FVB mice. Here, we show that status of IFN-gamma receptor alpha in MMC will determine whether this tumor may or may not relapse in FVB mice. We generated MMC transfectants expressing a dominant negative IFN-gamma receptor (dnIFN-gammaRMMC). Animals were then depleted of CD4+ T cells prior to the tumor challenge in order to omit the contribution of the neu-specific antibody and retard the rejection of MMC. Then, we inoculated FVB mice with MMC or dnIFN-gammaRMMC. Interestingly, animals that were depleted of CD4+ T cells at the priming phase of the immune responses failed to reject MMC and showed tumor relapse of the neu negative variant (ANV), but they managed to reject the dnIFN-gammaRMMC with no relapse until 3 months after the challenge. We also showed that status of IFN-gamma receptor alpha in human carcinoma cells SKBR3 will determine IFN-gamma-mediated down-regulation of HER-2/neu in this human carcinoma line. Treatment of tumor cells with IL-6 or TNF-alpha in order to increase IFN-gamma receptor expression rendered tumors more sensitive to IFN-gamma-mediated downregulation of HER-2/neu. Together, our data suggest that determination of the status of IFN-gamma receptor alpha in tumor lesions of HER-2/neu positive breast cancer patients may be a prognostic factor for relapse of their metastatic tumors.
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Nagpure, S. V., S. V. Deshmane, and K. R. Biyani. "VALIDATION OF PROPOSED RP-HPLC METHOD FOR SIMULTANEOUS ESTIMATION OF FENPIVERINIUM BROMIDE AND PITOFENONE HCL." INDIAN DRUGS 51, no. 07 (July 28, 2014): 39–45. http://dx.doi.org/10.53879/id.51.07.10114.
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A simple, rapid, accurate and precise RP-HPLC method was developed and validated for the determination of fenpiverinium bromide and pitofenone HCl. Separation of the drug was achieved on a reverse phase Thermo Kromasil C18 Column. The method showed a linear response for concentration in the range of 1.2-2.8μg/ml for FVB 6-14 μg/ml for PFH using diammonium hydrogen orthophosphatee buffer pH 7.2: acetonitrile as the mobile phase in the ratio of 55:45, v/v with detection at 220 nm with a flow rate of 1 ml/min and retention time was 3.77min and 7.45 min for FVB and PFH respectively. The method was statistically validated for linearity, accuracy, precision and selectivity.The limit of detection and limit of quantitation was 0.0654 µg/ml and 0.1982 µg/ml for FVB and 0.0927 µg/ml and 0.281 µg/ml for PFH, respectively. In quantitative and recovery studies, % RSD was found less than 2. Due to simplicity, rapidity and accuracy of the method, we believe that the method will be useful for routine quality control analysis of fenpiverinium bromide and pitofenone HCl in pharmaceutical formulations.
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Schnell, Fred, Dan Mourich, and Patrick Iversen. "Immune mediated Arenaviral Hemorrhagic disease in a novel mouse model (P6304)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 182.4. http://dx.doi.org/10.4049/jimmunol.190.supp.182.4.
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Abstract Viral hemorrhagic fever viruses (VHF) are a group of RNA viruses that can cause severe multisystemic illness in humans. Development of efficient countermeasures to this disease has been hampered by the lack of clinically relevant animal models. A better understanding of mechanisms behind disease progression would illuminate therapeutic targets. To this end, we have identified the FVB mouse strain which succumbs to a hemorrhagic fever like illness when infected with lymphocytic choriomeningitis virus (LCMV). Hemorrhagic FVB mice demonstrate increased IFN-gamma, IL-6 and IL-17, along with increased chemokine production, at early times after LCMV infection, which suggests that a viral-induced host immune response is the cause of the pathology. Antisense-targeted reduction of IL-17 cytokine responsiveness provided significant protection from hemorrhagic pathology. F1 mice derived from FVB x C57BL/6 mating were generated to better characterize immune-mediated hemorrhagic disease. LCMV-13 infected F1 mice displayed reduced numbers of LCMV specific T cells compared to both LCMV-Armstrong infected F1 and LCMV-13 infected C57BL/6 mice. This report reveals a possible immune component to Arenaviral Hemorrhagic disease and offers a potential therapeutic target in IL-17.
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Cywińska, A., K. Czumińska, and A. Schollenberger. "Granulomatous inflammation duringHeligmosomoides polygyrusprimary infections in FVB mice." Journal of Helminthology 78, no. 1 (March 2004): 17–24. http://dx.doi.org/10.1079/joh2003205.
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AbstractHost responses to primary infections withHeligmosomoides polygyruswere studied in fast responding FVB mice (H-2q). Pathological changes in the intestinal mucosa, mesenteric lymph nodes and spleen were examined. Features of the fast response were typical: low effectiveness of infection and limiting of parasite survival and egg production, with worm expulsion occurring about 60 days post-infection. The intestinal inflammatory response involved infiltration by different cells into the intestinal mucosa and granulomata formation. As is typical for intestinal nematode infection enteropathy, decreased villus:crypt ratio and hyperplasia of goblet and Paneth cells were also present. Reactions of the intestinal mucosa, mesenteric lymph nodes and spleen increased over time post-infection and after worm expulsion. Enteropathy may help worm expulsion by creating an unfavourable environment forH. polygyrus. The implications of these findings and the potential role of intestinal intraepithelial lymphocytes in the pathogenesis of generated lesions are discussed.