ライフサイエンスコーパス: chow

1 e with high-iron (HI) diets (2 or 20 g Fe/kg chow).

2 undernourished rats were rehabilitated with chow.

3 d nondiabetic Nos3(-/-) mice received normal chow.

4 mpared with those of control mice fed normal chow.

5 ed proteinuria than were animals on standard chow.

6 s of GLUT5 in adult wild-type mice consuming chow.

7 epatic insulin resistance in rats fed normal chow.

8 ) mice, maintained on hard (HC) or soft (SC) chow.

9 ereafter, offspring were fed standard rodent chow.

10 PLA2 activity and MUC2 density compared with chow.

11 known about its essential role under regular chow.

12 rmed in rats fed a high fat diet or standard chow.

13 plemented low-AGE (MG(+)), and regular (Reg) chow.

14 pared with control ASO-treated mice on HTF-C chow.

15 th PN but failed to reach levels measured in chow.

16 hosphorylated JAK-1 and STAT-6 compared with chow.

17 posity when mice were maintained on standard chow.

18 without chow, and controls received standard chow.

19 well as pIgR, and luminal IgA compared with chow.

20 muscle of C57BL/6 mice compared with normal chow.

21 treated with lithium, valproate, or control chow.

22 t alterations in beta-cell mass with control chow.

23 eserve when compared with mice fed on normal chow.

24 the retina as compared with mice fed normal chow.

25 able from wild-type littermates on a regular chow.

26 atic steatosis in mice fed normal laboratory chow.

27 tion in the human population, posits Clement Chow.

28 divided into 2 groups that received chow, or chow + 1.25% HDCA, diets for 15 wk.

29 pared with cohorts fed WSD alone and control chow (14% fat) to distinguish between WSD and resveratro

30 ek-old C57BL/6 virgin female mice were fed a chow (21%) or high-fat (60%) diet and divided into four

31 C57BL/6 female mice were fed a chow (21%) or high-fat (60%) diet and further divided by

32 Rats self-administered 60% high fat or chow 45 mg pellets and were then tested for incubation o

33 islet morphology was evident in 0 of 6 sham-chow, 5 of 8 sham-HF, 4 of 8 IUGR-chow, and 8 of 9 IUGR-

34 re fed a HFD (59% kcal from fat) or standard chow (9% Kcal from fat) for 8 weeks.

35 Female C57BL/6 mice were exposed to normal chow, an HFD, or an HFD with voluntary wheel exercise fo

36 KO mice only to the level in the WT mice fed chow and had no effect on aortic eNOS(Ser1177) phosphory

37 On both standard chow and HFD, SINKO mice were more insulin sensitive tha

38 Finally, incubation of craving for chow and high fat was accompanied by an increase in calc

39 s the hypothesis, behavioral tests including chow and high-fat diet intake, meal patterns, conditione

40 in female G6pc2 knockout (KO) mice on both a chow and high-fat diet, observations that are all consis

41 ite dramatic changes in IMTG content on both chow and high-fat diets, modulation of ATGL-mediated IMT

42 exhibited insulin resistance on both normal chow and high-fat diets.

43 sma glucose levels in mice fed both standard chow and high-fat diets.

44 g, we tested the effects of memantine on the Chow and Palatable food groups' intake.

45 f VTA amylin receptors reduces the intake of chow and palatable sucrose solution in rats.

46 increased with IL-25 treatment compared with chow and PN.

47 macrophages isolated from mice fed standard chow and supplemented with DHA in vitro.

48 re fed an AIN-93G diet with 1000 IU VD/kg of chow and were kept under fluorescent light for 2 months;

49 istration potently reduced food intake (both chow and Western diet) and body weight, whereas HPFv GLP

50 nsity lipoprotein cholesterol levels on both chow and Western diets.

51 ated fat, 30% sucrose solution, and standard chow and whether this was mediated by the Y1R.

52 of 6 sham-chow, 5 of 8 sham-HF, 4 of 8 IUGR-chow, and 8 of 9 IUGR-HF rats (chi-square, P = 0.007).

53 One group received TPN without chow, and controls received standard chow.

54 PY increased intake of fat, but not sugar or chow, and this was mediated by the Y1R.

55 beneficial glucose-lowering effects in both chow- and high-fat-fed mice lacking GLP1R in the CNS or

56 played an adjuvant-free IgE-sensitization to chow antigens that was most pronounced for wheat and soy

57 eived ASK1 inhibitor (GS-444217 delivered in chow) as an early intervention (2-8 weeks after STZ) or

58 besity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of

59 ly associated with high fat was greater than chow at both 1 and 30 days.

60 ce fed with a high-fat diet (HFD) or regular chow at weeks 1, 9, and 18.

61 g the transition from a milk-based diet to a chow-based diet after weaning.

62 ither atorvastatin (15 mg/kg; 7d) or control chow before sacrifice.

63 red glucose and lipid metabolism in mice fed chow but not a high-fat diet, which was paralleled by dy

64 Compared to controls pair-fed normal chow, carbonyl iron-fed rats had elevated serum iron (42

65 tion of the maintenance diet (i.e., standard chow compared with diets high in energy, fat, and sugar

66 tion of LHA (GABA) neurons increased overall chow consumption.

67 old, female mdr2(-/-) mice were fed high-fat chow containing 0.006% SC-435, a minimally absorbed, pot

68 loading and high TGs, Fischer rats were fed chow containing 1% carbonyl iron.

69 tribution of FXa and thrombin, mice were fed chow containing either rivaroxaban or dabigatran, respec

70 When the Tg mice were fed chow containing IC3, plasma prolactin concentrations inc

71 et (Palatable group) or a regular chow diet (Chow control group), for 1 h a day, under a fixed-ratio

72 re(+/0) mice, respectively) were fed regular chow (control) or a high-fat diet supplemented with 30%

73 s were isolated from adult mice fed standard chow, control diets, or DHA supplemented diets.

74 -rich diet (3 mumoles/day SFN versus control chow) decreased the arthritis score in the DMM model of

75 IC3 chow did not affect the WT mice.

76 nes were reared as control group on standard Chow diet (18% fat).

77 kout (WT/KO) dams were fed a control breeder chow diet (25% fat) or a semi-purified HFD (45% fat) 4 w

78 Mice fed either a low-fat chow diet (CD) or high fat and sucrose Western diet (WD)

79 In this work, we fed mice either a chow diet (CD), a 16 week high-fat diet (HFD), or a CR d

80 , sugary diet (Palatable group) or a regular chow diet (Chow control group), for 1 h a day, under a f

81 alatable diet (Palatable group) or a regular chow diet (Chow group) in 1-h daily sessions, under fixe

82 r tissues collected from mice fed a standard chow diet (controls) and 9 mouse models of NAFLD: mice o

83 /SCD: six wild-type (WT) mice fed a standard chow diet (SCD); WT/HFD, six WT mice fed a HFD; NOX2(-/-

84 ine body weights compared with wild types on chow diet and attenuated weight gain when fed cafeteria

85 These mice gain more weight on chow diet and short-term as well as long-term high-fat d

86 protein E-deficient mice were fed a standard chow diet and treated either with IL-17A mAb (n = 15) or

87 ckground (n = 3-5/group) were fed a standard chow diet and water ad libitum.

88 pe diet for 10 wk, after which they received chow diet and were treated with anti-OX40L or PBS for 10

89 male rats fed a low-fat, standard laboratory chow diet did not gain extra weight when fed yogurt diet

90 that Fyn knockout (FynKO) mice on a standard chow diet display increased glucose clearance and whole-

91 adipocyte-specific hRBP4 mice fed a standard chow diet display significantly elevated hepatic triglyc

92 TDAG51(-/-) mice fed a chow diet exhibited greater body and WAT mass, had reduc

93 reatic insulin content, MIP-CreERT mice on a chow diet exhibited normal ambient glycemia, glucose tol

94 ntrol group (143 mice maintained on standard chow diet for 20 weeks).

95 min D-deficient mice to vitamin D-sufficient chow diet for 6 weeks.

96 different CC lines were maintained on rodent chow diet for 8 weeks and were subsequently transferred

97 t loss resulting from conversion to a normal chow diet for 8 weeks resulted in more than a 25% decrea

98 -6J mice were fed a high fat (60%) or normal chow diet for 8-10 weeks followed by analysis of lymphat

99 .05), in the HDCA group as compared with the chow diet group.

100 l efflux ex vivo as compared with HDL of the chow diet group.

101 ty-like behavior and anorexia of the regular chow diet in rats withdrawn from palatable diet cycling,

102 -), and Ldlr(-/-);Gsk3a(-/-) mice were fed a chow diet or a high-fat diet for 10 weeks and then sacri

103 leaved caspase 3 in mice fed either a normal chow diet or a high-fat diet.

104 Mice were fed a standard, iron-balanced chow diet or an iron-deficient diet for 9 days before de

105 nto 4 groups: control (chow diet), MCD diet, chow diet plus G49, and M+G49 (MCD diet plus G49).

106 betaPKD1KO mice under a chow diet presented no significant difference in glucose

107 s end mice received either regular chow or a chow diet supplemented with canola oil for 6 months.

108 liver of mice fed a high cholesterol diet or chow diet supplemented with the HMGCR inhibitor lovastat

109 V1.1 pore gain more body weight and fat on a chow diet than control mice, without changes in food int

110 )ApoE(-/-) and ApoE(-/-) mice fed a standard chow diet were given an oral gavage of Porphyromonas gin

111 ult male C57BL/6 mice maintained on a normal chow diet were subjected to a microbiome depletion/trans

112 Five noninjured rabbits fed a chow diet were used as controls.

113 1 week were divided into 4 groups: control (chow diet), MCD diet, chow diet plus G49, and M+G49 (MCD

114 enic mice were randomized to receive regular chow diet, a diet deficient in folate and B vitamins (Di

115 observed in p55(Deltans/Deltans) mice fed a chow diet, and HFD-induced insulin resistance was no wor

116 ct the response to damage of adult muscle in chow diet, and it determines the maintenance of muscle f

117 With mice on a standard chow diet, body weight and glucose homeostasis were not

118 n mice had normal levels of hepatic fat on a chow diet, but when challenged with a high-sucrose diet

119 ded into groups that were placed on a normal chow diet, fasted for 24 hours, or fasted for 24 hours a

120 Compared with mice on chow diet, HFD-fed mice displayed higher levels of oxalo

121 On a chow diet, plasma levels of leptin are decreased, and ad

122 On chow diet, Sucnr1(-/-) mice had increased energy expendi

123 K-186 did not alter weight gain in mice on a chow diet, suggesting that the obesity-inducing diet enh

124 When fed a chow diet, these mice show an elevation in adipose total

125 ation upon transfer to a standard laboratory chow diet, these results provide strong evidence that di

126 e is seen in CX3CR1(+/GFP)/apoE(-/-) mice on chow diet, with a further 2- to 3-fold increase on Weste

127 aralpha(-/-)mice fed a Wy14,643-supplemented chow diet.

128 iver and serum, compared to mice on a normal chow diet.

129 lammation properties on a high-fat or normal chow diet.

130 and modestly reduced adiposity in mice fed a chow diet.

131 /-) genetic background and fed a high-fat or chow diet.

132 t protein (GFP) and on a high-fat vs. normal chow diet.

133 even more pronounced when the mice were fed chow diet.

134 eriodicity that was longer than animals on a chow diet.

135 f weight gain in mice on an HFD but not on a chow diet.

136 ed on a 45% high-fat diet (HFD) or a regular chow diet.

137 ipid profile in mice fed a standard, low-fat chow diet.

138 or(-/-) mice consuming a high-cholesterol or chow diet.

139 ozygous (Het), and wild type (WT) mice fed a chow diet.

140 e diet was evaluated and compared to mice on chow diet.

141 striction-induced overeating of the standard chow diet.

142 ice fed the HFD and both sexes of mice fed a chow diet.

143 All mice were fed a standard chow diet.

144 ein tolerance and lethal hyperammonemia on a chow diet.

145 signed randomly to the following groups: (1) chow diet; (2) high-fat diet (HFD); (3) HFD and 100 mg C

146 /-) mice were glucose-intolerant even on the chow diet; HFD further increased fasting glucose and ins

147 in the presence of FCCP when compared to the chow-diet fed control mice.

148 Pups were fed either HF or chow diets after weaning.

149 Alcohol Abuse and Alcoholism binge model) or chow diets along with water containing 0.18% DL-homocyst

150 inbred ILSXISS strains were fed high-fat or chow diets and subjected to metabolic phenotyping and me

151 (Lmo4) become rapidly obese when fed regular chow due to hyperphagia rather than to reduced energy ex

152 oduced to HFD, similar to WT mice on regular chow during IU/L.

153 ed with QC inhibitors (PBD155 and PQ529) via chow during the experiment.

154 After return to the same body weight as chow fed control mice, the fasting insulin, glucose, and

155 d obese female C57BL6/J mice were mated with chow fed males.

156 Male offspring were chow fed, sedentary, and studied at 8, 12, 24, 36, and 5

157 , hyperglycemia, and PoG signaling in normal chow-fed (CTR) and HFFD-fed dogs.

158 se oligonucleotide-induced loss of HMGCS2 in chow-fed adult mice caused mild hyperglycemia, increased

159 ltered the whole-body energy balance in both chow-fed and high-fat diet-fed mice.

160 matic changes associated with PoG sensing in chow-fed animals were abolished in HFFD-fed animals, con

161 Absent in chow-fed animals, PI-BMDCs account for 60% of the ATMs i

162 In addition, FFC-fed mice, but not chow-fed animals, underwent significant liver injury and

163 Compared with chow-fed C57BL/6 mice, fasted or ketogenic diet-fed mice

164 Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARalph

165 Offspring from chow-fed dams that trained both before and during gestat

166 glucose tolerance compared with offspring of chow-fed dams throughout their first year of life, an ef

167 Primary quiescent satellite cells (SC) from chow-fed DKO mice, not in Ldlr(-/-)xLcat(+/+) single-kno

168 Ex vivo cholesterol loading of chow-fed DKO SC recapitulated the effect, indicating tha

169 Chow-fed GLP-1RKD(DeltaNkx2.1cre) mice exhibited increas

170 liraglutide treatment reduced body weight in chow-fed GLP-1RKD(DeltaNkx2.1cre) mice, but this effect

171 and diglyceride contents were normalized to chow-fed levels in HF-fed itga1(-/-) mice.

172 atic accumulation of hepatic BMP compared to chow-fed littermates.

173 Hepatic Fas overexpression in chow-fed mice compromises fatty acid oxidation, mitochon

174 In 5 mmol/L glucose, islets from C57BL/6J chow-fed mice cycled approximately 16% of net glucose up

175 Chow-fed mice lacking T39 (T39(-/-)) display increased h

176 sis and causes hepatic insulin resistance in chow-fed mice while selectively conferring protection fr

177 the etiology of muscle insulin resistance in chow-fed mice with skeletal and cardiac muscle VEGF dele

178 In chow-fed mice, acute or chronic intravenous injections o

179 nesis (DNL) was increased in male and female chow-fed mice, compared with GHR-intact littermate contr

180 Compared with chow-fed mice, HFD-fed mice had a rapid increase in body

181 Controls were chow-fed mice, T1 receptor-3 (T1R3)-knockout (KO) mice,

182 D4CD25Foxp3 T regulatory cells compared with chow-fed mice, whereas PN + BBS assimilated chow levels.

183 ectible effect on any measured parameters in chow-fed mice.

184 increased in ALIOS mice compared with normal chow-fed mice.

185 f PEMT in hepatic carbohydrate metabolism in chow-fed mice.

186 levels of Nrp1 in macrophages compared with chow-fed mice.

187 aximal respiration, when compared to control chow-fed mice.

188 aximal respiration, when compared to control chow-fed mice.

189 Cardiac power of control hearts from chow-fed rats recovered to 93%, while insulin-resistant

190 food intake and worsens glucose tolerance in chow-fed rodents and causes excess weight gain during hi

191 Females were bred with chow-fed sedentary C57BL/6 males.

192 the glucose intolerance observed in standard chow-fed SOD1-null mice.

193 GSIS during HG clamps was equal in chow-fed sod2(+/-) and sod2(+/+) but was markedly decrea

194 Chow-fed TG and KO mice had normal liver histologic find

195 versed and renin was suppressed by returning chow-fed vitamin D-deficient mice to vitamin D-sufficien

196 When implanted into normal chow-fed, or into high-fat diet (HFD)-fed, glucose-intol

197 re assessed using a concurrent fixed-ratio 5/chow feeding choice task that is known to be sensitive t

198 nt did not affect performance of the control Chow food group.

199 d to repeated intermittent cycles of regular chow food restriction during which they were also given

200 Pde11a knockout mice (KO) given 0.4% lithium chow for 3+ weeks exhibit greater lithium responsivity r

201 rague-Dawley rats were fed either a standard chow for 4 weeks or a methionine- and choline-deficient

202 high in unsaturated fat (HF) (61%) or normal chow for 5 or 10 weeks.

203 A BA overload, feeding 0.5% cholic acid chow for 6 days, resulted in adaptive responses of alter

204 were fed vitamin D-deficient or -sufficient chow for 6 weeks and then switched to high fat (HF) vita

205 et (Palatable group) or a regular chow diet (Chow group) in 1-h daily sessions, under fixed ratio (FR

206 ption by 76% (P<0.0001) as compared with the chow group.

207 Adipose-Stra6(-/-) mice fed chow had decreased body weight, fat mass, leptin levels,

208 vely suppressed intake in OP and OR rats fed chow; however, during HE/HF-feeding, OP rats suppressed

209 (RH), and high fat diet switched to regular chow (HR).

210 d on excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior.

211 or in Chow/Palatable rats, without affecting chow hypophagia.

212 -4 and IL-13 decreased with PN compared with chow (IL-4: P < 0.0001, IL-13: P < 0.002), whereas IL-25

213 se intake in ad libitum-maintained rats, and chow in food-deprived rats, but only at the 30-ng dose.

214 n both male and female mice fed with regular chow, increased susceptibility to diet-induced obesity (

215 sistance when compared with mice fed regular chow, indicating that the mice developed MetS.

216 Chow intake and meal size were significantly increased f

217 aserin significantly reduced both ad libitum chow intake and PR responding for chocolate pellets and

218 In sham-lesioned rats, Ex4 reduced chow intake within 4 h of injection and sucrose intake w

219 ing neurons significantly reduced ad libitum chow intake, operant responding for chocolate pellets, a

220 ored sucrose pellets without affecting prior chow intake.

221 On chow, JAK2L mice had hepatic steatosis and severe whole-

222 ydrocollidine (DDC) 0.1% (wt/wt) Purina 5015 Chow (LabDiet, St.

223 was not activated in Fx-/- mice fed standard chow, leading to decreased expression of its target Hes1

224 n of IL-25 to PN decreased enteroinvasion to chow levels (P < 0.01).

225 propria) T cells, whereas PN-BBS assimilated chow levels.

226 4 memory B cells, whereas PN-BBS assimilated chow levels.

227 chow-fed mice, whereas PN + BBS assimilated chow levels.

228 (one session) and sedentary rats fed either chow (low-fat diet [LFD]; normal insulin sensitivity) or

229 MCK-Plin5 mice fed high-fat chow manifest lower expression of inflammatory markers i

230 onsisting of either pure rodent chow, rodent chow mixed to yield a content of either 20% glucose or 2

231 e of Cancer Research mice were randomized to chow (n = 11) or PN (n = 9).

232 er Research) mice were randomized to receive chow (n = 12), PN (n = 9), or PN + 0.7 mug of exogenous

233 When the Tg mice were fed normal chow (NC), plasma prolactin concentrations were comparab

234 eceived Ex4 (1 mug/kg) before 24 h home cage chow or 90 min 0.3 M sucrose access tests, and licking m

235 To this end mice received either regular chow or a chow diet supplemented with canola oil for 6 m

236 C57BL/6 mice were placed on chow or a diet high in fat, fructose, and cholesterol to

237 the SCN of mouse offspring exposed to normal chow or a high fat diet during early development and in

238 deficient (ILK(lox/lox)HSAcre) mice were fed chow or a high-fat (HF) diet for 16 weeks.

239 can model retinal disease, we weaned mice to chow or a high-fat diet and tested the hypothesis that d

240 ormed inhalation exposure of mice fed normal chow or a high-fat diet to airborne fine particulate mat

241 Hif-p4h-2-deficient mice, whether fed normal chow or a high-fat diet, had less adipose tissue, smalle

242 weight or food intake in animals fed normal chow or a high-fat diet.

243 atory Ly6C(hi) monocytes in mice fed regular chow or a high-fat diet.

244 full-length Il6 gene (controls), were fed a chow or a high-fat diet; some mice were given injections

245 9 weeks later, mice were fed either regular chow or a high-fat, high-cholesterol (HFC) diet for 3 mo

246 ith normal senescence (n=15) were fed normal chow or a high-fat, high-salt diet (WD).

247 C57Bl/6 mice fed chow or a methionine and choline-deficient (MCD) diet fo

248 mice (12 weeks of age; n=6) were fed regular chow or a Western diet (1.25% cholesterol, 2% fat).

249 onditions: food-deprived rats given standard chow or ad libitum-fed rats given a palatable chocolate

250 metabolic characterization of these mice fed chow or after 6 wk of a high-fat diet.

251 ild-type mice were fed with either a control chow or atherogenic paigen-type diet for 12 weeks.

252 nfusions did not alter the overall intake of chow or chocolate shake.

253 (WT) and Cyp2e1-null mice were fed standard chow or FF for 2, 12, and 24 weeks.

254 C57BL/6 mice were placed on 3-month chow or FFC (high saturated fats, fructose, and choleste

255 Mice were placed on standard chow or fucose-containing diet (equivalent to a control

256 ch were improved in ECIRS1 TG mice on normal chow or HF diet.

257 ous injections of 27HC and placed on regular chow or HFC diets for 3 weeks.

258 HCR and LCR rats were fed a chow or HFD for 3 days and received a single in vivo HT

259 IL-18 receptor (IL-18R(-/-)) fed a standard chow or HFD.

260 protein (RIP) 3(-/-) mice were randomized to chow or HFD.

261 in glucose homeostasis in mice fed either a chow or high fat diet.

262 CXCR3(-/-) and wild type (WT) mice were fed chow or high saturated fat, fructose, and cholesterol (F

263 e in OP and obese-resistant (OR) rats during chow or high-energy/high-fat (HE/HF) feeding.

264 ozygous knockout mice (sod2(+/-)) were fed a chow or high-fat (HF) diet, which accelerates ROS produc

265 ontrol wild-type (WT) mice were fed either a chow or high-fat diet (HFD).

266 ta-cell function of these mice fed a control chow or high-fat diet.

267 pid metabolism in Atf4(-/-) mice fed regular chow or provided with free access to fructose drinking w

268 PBNx rats did not show reduced chow or sucrose intake after Ex4 treatment, indicating t

269 breakpoint for cocaine, but not for regular chow or sucrose, and attenuated cue-, footshock-, and yo

270 out and wild-type mice were fed either mouse chow or WD for 16 weeks.

271 -HDL cholesterol levels in F2 mice on either chow or Western diet.

272 and then divided into 2 groups that received chow, or chow + 1.25% HDCA, diets for 15 wk.

273 ic CES2 causes liver steatosis and damage in chow- or Western diet-fed C57BL/6 mice.

274 invaded the PN-treated tissue compared with chow (P < 0.01), and the addition of IL-25 to PN decreas

275 ive cells in CeA--but not in BlA or BNST--of Chow/Palatable rats, during both withdrawal and renewed

276 ble food intake and anxiety-like behavior in Chow/Palatable rats, without affecting chow hypophagia.

277 : Intravenously cannulated ICR mice received chow, PN, or PN + BBS injections for 5 days.

278 sulting in four experimental groups: regular chow (R), high fat diet (H), regular chow switched to hi

279 dy weight and glucose tolerance on a regular chow (RC) diet.

280 ponse (UPR) was perturbed in control regular-chow (RC)-fed Nrf2(-/-) mouse livers, and this was assoc

281 in adipocytes in adipose-Stra6(-/-) mice fed chow resulted in leanness, which may contribute to their

282 treatments consisting of either pure rodent chow, rodent chow mixed to yield a content of either 20%

283 aving effect than those paired with standard chow (SC) pellets.

284 Four rabbits fed standard chow served as controls.

285 In adult mice fed normal chow, skeletal muscle expression of insulin receptor bet

286 After surgery, animals were fed either a chow (standard) diet or a high-fat diet (HFD), and gluco

287 regular chow (R), high fat diet (H), regular chow switched to high fat diet (RH), and high fat diet s

288 d by feeding rats a novel ketone ester diet: chow that is supplemented with (R)-3-hydroxybutyl (R)-3-

289 up, and these mice were fed the same regular chow throughout the entire carcinogenic period.

290 that inhalation exposure of mice fed normal chow to concentrated ambient PM2.5 repressed hepatic tra

291 , a finding confirmed by feeding Neu5Gc-rich chow to human-like Neu5Gc-deficient mice.

292 s, followed by a period of 2 weeks on normal chow to induce the formation of lesion foci in the foreb

293 n weeks followed by additional five weeks of chow, to identify HFD-mediated changes to the hepatic tr

294 WT) and Gipr(-/-) offspring received control chow until 25 weeks of age followed by 20 weeks of HFD.

295 ntial effectiveness of ShK-186 in mice fed a chow vs. an obesity diet.

296 isolated from the mice provided Ni-deficient chow were statistically lower than those for mice given

297 iang YB, Hosgood HD III, Ji BT, Hu W, Wen C, Chow WH, Cai Q, Yang G, Gao YT, Zheng W, Lan Q.

298 ncreased consumption of the low-fat standard chow when either heterozygous or homozygous mutant anima

299 ignificantly decreased with PN compared with chow, whereas IL-25 significantly increased tissue sPLA2

300 < 0.0001) and MUC2 (P <0.002) compared with chow, whereas the addition of IL-25 to PN increased lumi