Fig. 1. Loss of circadian rhythms in iKO mice.

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Fig. 1. Loss of circadian rhythms in iKO mice.

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Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

Fig. 5. Circulating PPi concentration does not correlate with severity of calcification phenotype in mice. Circulating PPi concentration does not correlate.

Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 1. APP/PS1;C3 KO mice show improved cognitive flexibility (reversal) compared to APP/PS1 mice at 16 months of age. APP/PS1;C3 KO mice show improved.

Fig. 3. A circadian rhythm in fibroblast wound-healing response.

Fig. 5. In vivo characterization of adipogenesis by CT.

Fig. 3 Fbln4E57K/E57K mice develop large artery stiffness and systolic hypertension. Fbln4E57K/E57K mice develop large artery stiffness and systolic hypertension.

Expression of NCoR1∆ID in PAX8−/− mice does not reverse repression of T3-positive target genes. qPCR on the indicated pituitary (A) and neuronal (B) genes.

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Volume 30, Issue 2, Pages (May 2001)

In Vivo Monitoring of Circadian Timing in Freely Moving Mice

Fig. 5 Early and modest immune response at day 3 after exposure in Delayed animals. Early and modest immune response at day 3 after exposure in Delayed.

Human cells produce type I and III IFNs upon Af stimulation.

Fig. 6 Transmissibility of adiposity from humanized mice to germ-free recipients. Transmissibility of adiposity from humanized mice to germ-free recipients.

Fig. 7 Correlation of NHP and human ISGs.

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Fig. 5. In vivo characterization of adipogenesis by CT.

Fig. 2. Deficiency of neuronal HS leads to reduced neuroinflammation.

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Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

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Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing.

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Fig. 2 PK dosing results. PK dosing results. (A) Plasma concentration of hPTH(1–34) versus time after release of 40-μg dose from implanted microchip device.

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Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

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Fig. 1. APP/PS1;C3 KO mice show improved cognitive flexibility (reversal) compared to APP/PS1 mice at 16 months of age. APP/PS1;C3 KO mice show improved.

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Circadian gene expression in ILC3s is associated with rhythmic cytokine expression. Circadian gene expression in ILC3s is associated with rhythmic cytokine.

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Fig. 1. Loss of circadian rhythms in iKO mice. Loss of circadian rhythms in iKO mice. (A) Representative double-plotted actograms of wheel-running activity of 3-month-old Bmal1f/f and Bmal1f/f-EsrCre mice (red dots, tamoxifen treatment). Similar results were obtained in n = 8 to 9 mice per group. (B) Counts of wheel revolutions per hour from control mice (Ctrls) and iKO mice under conditions of DD (n = 8 to 9, Student’s t test; ns, no significant difference). (C) Representative double-plotted actograms of wheel-running activity from 18-month-old Ctrl and iKO mice under DD. Similar results were obtained in n = 6 to 7 mice per group. (D) Counts of wheel revolutions from 18-month-old Ctrls and iKOs under DD (n = 6 to 7; Student’s t test). (E) Representative radiotelemetry results of locomotor activity, systolic BP (SBP), and HR in Bmal1f/f and Bmal1f/f-EsrCre mice (red inverted triangles, tamoxifen treatment). Similar results were obtained in n = 3 mice per group. (F) Hepatic mRNA levels of canonical clock genes and clock-controlled gene Dbp were determined by qRT-PCR [n = 4 per genotype per time point; x axis, circadian time (CT); y axis, relative mRNA levels; *P < 0.05; **P < 0.01; ***P < 0.001, two-way analysis of variance (ANOVA)]. Guangrui Yang et al., Sci Transl Med 2016;8:324ra16 Copyright © 2016, American Association for the Advancement of Science