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1 osed to BD and its potent carcinogenicity in laboratory mice.
2 VP establishes acute and latent infection in laboratory mice.
3 n minimize a widespread source of anxiety in laboratory mice.
4 pects of severe COVID-19 disease in standard laboratory mice.
5 pansions found in old specific pathogen-free laboratory mice.
6 to establish virus latency in the spleens of laboratory mice.
7 ructure of genetic variation among classical laboratory mice.
8 ng-term protective immunity in a majority of laboratory mice.
9 erences in the general learning abilities of laboratory mice.
10 igen of the HGE agent and was infectious for laboratory mice.
11 havior-->gene) approaches in both humans and laboratory mice.
12 responsible for the xenotropism of X-MLVs in laboratory mice.
13 d strain]), were studied in cell culture and laboratory mice.
14 ose previously identified using conventional laboratory mice.
15 activity, as well as the ability to colonize laboratory mice.
16 well as xenotropic MLV, which do not infect laboratory mice.
17 es between control of sleep in humans and in laboratory mice.
18 RNA virus is thus maintained indefinitely in laboratory mice.
19 al inoculation of the spleen homogenate into laboratory mice.
20 gulatory effect of TNF on T cells in healthy laboratory mice.
21 etween M. castaneus and MCF MuLV-susceptible laboratory mice.
22 a challenge in modeling human diseases using laboratory mice.
23 cking in standard preclinical models such as laboratory mice.
24 patocytes across nine widely used strains of laboratory mice.
25 ence and potential triggers of aggression in laboratory mice.
26 changes in muscle force generation in active laboratory mice.
27 r natural rodent pathogens-are cohoused with laboratory mice.
28 e modulated by locomotion in male and female laboratory mice.
29 and 10 mg/kg) alter sleep in wild-type male laboratory mice.
30 of neuronal activity in the visual system of laboratory mice.
31 responses is difficult to model in standard laboratory mice.
32 wo mA3 alleles found among inbred strains of laboratory mice.
33 ate its detailed function, principally using laboratory mice.
34 greater stability than the gut microbiota of laboratory mice.
35 es observed in the colonic mucus of wild and laboratory mice.
36 ously adapted NrHV to prolonged infection in laboratory mice.
37 g natural gut microbiota from wildlings into laboratory mice.
38 of female social aggression and dominance in laboratory mice.
39 V has been adapted to infect immunocompetent laboratory mice.
40 t physiological parameter in many studies of laboratory mice.
41 ighly activated myeloid cells not present in laboratory mice.
42 al inflammation were not observed in Jackson Laboratory mice.
43 populations (i.e., the aged) using standard laboratory mice.
44 aced mating paradigm, in female but not male laboratory mice.
45 at establishes acute and latent infection in laboratory mice.
46 els after acute injury in several strains of laboratory mice.
47 els is widely used to initiate thrombosis in laboratory mice.
48 vation compared with artificially maintained laboratory mice.
49 (-) mice, which include commonly used inbred laboratory mice.
50 mals except most of the classical strains of laboratory mice.
51 at establishes acute and latent infection in laboratory mice.
52 ria parasite Plasmodium chabaudi evolving in laboratory mice.
54 ne the rodent malaria Plasmodium chabaudi in laboratory mice, a parasite-host system in which virulen
56 ns that are inherited as Mendelian traits in laboratory mice affect susceptibility to spontaneous TGC
57 quenced erp loci of bacteria reisolated from laboratory mice after 1 year of infection and found them
58 se microbial experience, and were induced in laboratory mice after co-housing with pet store mice, su
59 f the range of germline mutations induced in laboratory mice after parental exposure to ionizing radi
61 ects both cutaneous and mucosal epithelia of laboratory mice and can be used to model high-risk human
62 he growing evidence, obtained primarily from laboratory mice and humans, that the ability to sense li
66 ort genome sequences of 17 inbred strains of laboratory mice and identify almost ten times more varia
67 s) are found in the common inbred strains of laboratory mice and in the house mouse subspecies ofMus
69 onstrate that the low recombination rates in laboratory mice and rats reflect a more general reductio
70 esembles WS2 than comparable Mitf alleles in laboratory mice and rats, which are expressed as purely
75 te the study of complex genetic traits using laboratory mice and, if implemented as a "gene drive," t
76 ly shown to contribute to Fv1 restriction in laboratory mice, and 3 codons in a 10-codon segment over
77 e seen in blood from pet store-raised versus laboratory mice, and adult versus cord blood in humans.
78 N) virus causes fatal meningoencephalitis in laboratory mice, and gammadelta T cells are involved in
80 1 resistance alleles have been identified in laboratory mice, and they target virus capsid genes to p
81 ites are common in humans, but are absent in laboratory mice, and thus represent potential contributo
82 eri and the spirochetemia of B. hispanica in laboratory mice, apolipoprotein E (apoE)-deficient and l
83 veral methods to model human Ph+ leukemia in laboratory mice are available, including propagation of
86 t female- and male-directed mounting in male laboratory mice are distinguishable by the presence or a
87 The alpha1-protease inhibitor proteins of laboratory mice are homologous in sequence and function
88 indicate that diverse learning abilities of laboratory mice are influenced by a common source of var
89 e data suggest that the cold stress to which laboratory mice are ubiquitously subjected profoundly af
90 nt research that calls into question the way laboratory mice are used to address questions in basic s
94 comprehensive basis for validating (or not) laboratory mice as a useful and relevant immunological m
95 family are not as numerous in the genomes of laboratory mice as are members of the older A and F subf
97 ed analysis of risk factors for barbering in laboratory mice based on point prevalence of hair loss i
99 ne leukemia viruses cannot infect cells from laboratory mice because of the lack of a functional cell
100 row phenotypes not normally observed in aged laboratory mice but commonly seen in elderly humans.
104 1 hybrid EpiSCs derived from crosses between laboratory mice (C57BL/6J) and four wild-derived inbred
105 ice (genus Peromyscus) and compare them with laboratory mice (C57BL6/J strain) and free-living, wild
107 ypic analysis of immunological parameters in laboratory mice carrying susceptibility genes implicated
108 fferentiation are derived from pathogen-free laboratory mice challenged with a single pathogen or vac
109 sters identified in humans, chimpanzees, and laboratory mice, characterized by differences in Bactero
112 estoring physiological microbial exposure in laboratory mice could provide a relevant tool for modell
118 of the hypothalamus of adult male and female laboratory mice does not merely trigger awakening from s
119 MA10) with the potential to infect wild-type laboratory mice, driving high levels of viral replicatio
120 ion define three MLV host range subgroups in laboratory mice: ecotropic, polytropic, and xenotropic M
121 ing the genetics underlying domestication in laboratory mice, especially in the widely used classical
122 e report that the retinas of some strains of laboratory mice exhibit robust circadian rhythms of mela
124 arameters of wild mice and compare them with laboratory mice, finding that wild mouse cellular immune
125 odentium espB mutant also failed to colonize laboratory mice following experimental inoculation.
127 e experiment using 579 genetically identical laboratory mice from a single animal facility, designed
128 In recent years in silico analysis of common laboratory mice has been introduced and subsequently app
129 iota from wild mice to genetically tractable laboratory mice has been shown to enhance modeling of hu
131 s analysis of the recombination landscape in laboratory mice has revealed that the different subspeci
132 c choriomeningitis virus (LCMV) infection of laboratory mice has served as a powerful model to unders
139 lity and inconsistent fungal colonization of laboratory mice hinders the study of the evolutionary an
143 -thermoneutral housing temperatures used for laboratory mice in research institutes is sufficient to
145 permissive Xpr1(sxv) allele in 7 strains of laboratory mice, including a Bxv1-positive strain, F/St,
147 artially attributed to microbial exposure as laboratory mice infected with pathogens exhibit immune p
148 se results suggest that unlike pathogen-free laboratory mice, infection or immunization of latently i
153 virus 68 (MHV68, MuHV-4, yHV68) infection of laboratory mice is a well-established pathogenesis syste
154 ptor for entry, and the unique resistance of laboratory mice is due to two mutations in different put
155 in both radiation safety and the handling of laboratory mice is required for the successful execution
156 y is based on secretions derived from inbred laboratory mice, it remains uncertain whether such stimu
168 The papillomavirus, MmuPV1, which infects laboratory mice (Mus musculus), can cause infections in
171 in Western Europe, which is unable to infect laboratory mice (Mus sp.) without the aid of powerful im
172 ated wound-induced hair neogenesis (WIHN) in laboratory mice (Mus), the regeneration is limited to th
173 -type Mx1 gene (Mx1+/+) differ from standard laboratory mice (Mx1-/-) in being highly resistant to in
175 We therefore tracked behavior of rewilded laboratory mice of three inbred strains in outdoor enclo
176 ety of cell lines and is also able to infect laboratory mice, offering an ideal model with which to s
177 ablish acute and persistent infection within laboratory mice offers a unique opportunity to investiga
181 tanding of immunology was largely defined in laboratory mice, partly because they are inbred and gene
184 Its adaptation to robust infection also in laboratory mice provides access to a broader set of mous
185 es have acquired novel mutational burdens in laboratory mice, providing an evolutionary rationale for
187 e function, but how well immune responses of laboratory mice reflect those of free-living animals is
188 ckcrossing of wild mice with knockout mutant laboratory mice retrieves behavioural traits exhibited e
189 metaanalysis of data from 54 experiments on laboratory mice reveals that basic ecological rules gove
191 , our study shows that the strain and sex of laboratory mice significantly affect the different indic
192 All inbred strains and outbred stocks of laboratory mice studied to date have been found to be su
193 ur data from wild mice and experiments using laboratory mice suggest estrogen signalling associates w
194 in hamsters and the conventional strains of laboratory mice tested, increases in lung infection were
196 We further find that selection is weaker in laboratory mice than in humans and it does not affect th
197 of superficial secondary lymphoid organs in laboratory mice that are earlier than expected and are c
198 cular, our work focuses on images of wounded laboratory mice that are used widely for translationally
199 imulated a search for IRG alleles unknown in laboratory mice that might confer resistance to virulent
200 of intense study of coat color mutations in laboratory mice, thereby creating an impressive list of
201 N) virus causes fatal meningoencephalitis in laboratory mice, thereby partially mimicking human disea
202 The 12 X-MLV ERVs predate the origins of laboratory mice; they were all traced to Japanese wild m
203 tion, reconstituting microbial experience in laboratory mice through co-housing may better inform pre
205 g et al. (2020) and Lin et al. (2020) expose laboratory mice to a natural environment and use immune
209 te the prospects for using dense SNP maps in laboratory mice to refine previous QTL regions and ident
210 s measured in 1812 genetically heterogeneous laboratory mice to study IGE arising between same-sex, a
211 at captures 90% of the known variation among laboratory mice, to identify the genetic loci controllin
212 alize the environmental experience of inbred laboratory mice-to take them where the wild things are (
213 ed because robust colitis is not observed in laboratory mice treated with checkpoint inhibitors.
214 ise quantitation of bis-N7G-BD in tissues of laboratory mice treated with low ppm and subppm concentr
216 LCMV-MN), which was naturally transmitted to laboratory mice upon cohousing with pet shop mice and sh
217 grade fetal calf serum as well as serum from laboratory mice using HPLC and MS identified the presenc
220 A yeast causing widespread infection of laboratory mice was identified from 26S rRNA gene sequen
221 ty of Bb(DeltaA66)-infected nymphs to infect laboratory mice was significantly impaired compared to t
224 span 90% of the common genetic diversity of laboratory mice, we found that high host mortality was a
225 tivation of the ribosomal protein S6 gene in laboratory mice, we found that reduced ribosomal protein
227 dy, we used a "dirty" mouse model, where SPF laboratory mice were cohoused (CoH) with pet store mice
229 Barbering is a common abnormal behavior in laboratory mice, where mice pluck their own fur and/or t
230 types are found in the classical strains of laboratory mice, which are genetic mosaics of 3 wild mou
231 single nucleotide polymorphisms (SNPs) from laboratory mice, which are largely genetic hybrids betwe
235 tis virus (VEEV) is highly virulent in adult laboratory mice, while Sindbis virus (SINV) is avirulent
241 ablish high-titer hepatotropic infections in laboratory mice with immunological features resembling t
242 the feasibility studies and actual tests on laboratory mice with inoculated hepatocellular carcinoma
249 ding an evolutionary rationale for restoring laboratory mice with wild gut bacterial strain diversity