Fig. 5. SUS treatment reduces Aβ in a second cohort of AD mice.

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Scanning ultrasound removes amyloid-β and restores memory in an Alzheimer’s disease mouse model by Gerhard Leinenga, and Jürgen Götz Sci Transl Med Volume.
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2D PAGE/Western blotting analysis for the identification of possible post-translation modification of Hsp27 from the spinal cord tissue of the SCI rat.
Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
Fig. 4 TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV release in murine MSCs. TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV.
Fig. 1. Establishing SUS in an AD mouse model.
Fig. 4. Dabrafenib and trametinib changed the cellular components of the tumor microenvironment. Dabrafenib and trametinib changed the cellular components.
Fig. 2. CD treatment facilitates regression of murine atherosclerosis.
Fig. 6 Transmissibility of adiposity from humanized mice to germ-free recipients. Transmissibility of adiposity from humanized mice to germ-free recipients.
Differentiation of AZD4785 from MAPK pathway inhibitors in vitro
Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.
Murine gingival MSCs and skin MSCs produce and secrete IL-1RA–EV
Consolidated Standards of Reporting Trials flow diagram of VRC trial
Fig. 1. Loss of circadian rhythms in iKO mice.
Fig. 2 AcPGP induces IL-8 and G-CSF release from human bronchial epithelial cells. AcPGP induces IL-8 and G-CSF release from human bronchial epithelial.
Fig. 2. Clinically actionable somatic genomic alterations in various tumor types. Clinically actionable somatic genomic alterations in various tumor types.
Filipin staining of marginal gyrus of cerebral cortex in NPC cats
Fig. 5. Microarray analysis of tumors treated by dabrafenib, trametinib, or the combination of dabrafenib and trametinib with pmel-1 ACT or mock ACT. Microarray.
Fig. 1. Schematic showing the shedding of tumor DNA from head and neck cancers into the saliva or plasma. Schematic showing the shedding of tumor DNA from.
Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.
Fig. 3 M7824 inhibits tumor growth and metastasis and provides long-term antitumor immunity. M7824 inhibits tumor growth and metastasis and provides long-term.
Fig. 4. The effect of combined inhibition of BCL-2 and BCR-ABL on leukemia LT-HSC frequency. The effect of combined inhibition of BCL-2 and BCR-ABL on.
Fig. 5 A competent Fc is required for the antitumor immune response.
Fig. 1. Iontophoretic devices used for the delivery of cytotoxic agents to solid tumors. Iontophoretic devices used for the delivery of cytotoxic agents.
Fig. 6. Nontaxane chemotherapies induce TMEM-dependent prometastatic changes in the breast cancer microenvironment. Nontaxane chemotherapies induce TMEM-dependent.
Fig. 2. Deficiency of neuronal HS leads to reduced neuroinflammation.
Fig. 5 Cell-free membrane cyclase assay confirms that candidate compounds are specific antagonists of hNPR1. Cell-free membrane cyclase assay confirms.
Fig. 3 NK cells are enriched in ICB-sensitive tumors in mouse models and patients and are required for response. NK cells are enriched in ICB-sensitive.
Fig. 3 Biological function of TG2 and the interaction with MT-2.
Fig. 2. Bacterial/viral score in COCONUT-conormalized whole-blood validation data sets. Bacterial/viral score in COCONUT-conormalized whole-blood validation.
Fig. 5. Col IV–Ac2-26 NPs decrease lesion area, necrotic area, and oxidative stress in brachiocephalic arterial plaques. Col IV–Ac2-26 NPs decrease lesion.
Colonization in tumor models and different modes of administration
CD mediates metabolism and efflux of crystal-derived cholesterol
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. 4 Rational therapeutic modulation of the tumor microenvironment sensitizes tumors to ICB. Rational therapeutic modulation of the tumor microenvironment.
Fig. 2 In situ vaccination of CpG in combination with anti-OX40 antibody cures established local and distant tumors. In situ vaccination of CpG in combination.
Fig. 1. Detection of circulating tumor DNA in CRPC patients.
Fig. 5 Treatment with BMS (PO BID) protects from wasting and colitis in two SCID mouse models. Treatment with BMS (PO BID) protects from.
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TOMA does not affect NFTs in posterior hypothalamus or cortex.
Fig. 2. LUM015 fluorescently labels tumor cells in mouse models of STS and breast cancer. LUM015 fluorescently labels tumor cells in mouse models of STS.
Fig. 5. Octet BLI competition assay using D25 and motavizumab.
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. 6. Prolonged miR overexpression in the adult heart reduces fibrotic scar size but compromises cardiac function after MI. Prolonged miR
Fig. 5. miR p inhibits the translational initiation of CACNA1A IRES–driven α1ACT by eIF4AII and eIF4GII. miR p inhibits the translational initiation.
Western blot analysis of skin tissue from CJD and non-CJD patients
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.
Fig. 3 Local Maraba treatment of TNBC tumors provides long-term systemic protection. Local Maraba treatment of TNBC tumors provides long-term systemic.
Fig. 6. Sh-lantibiotics are commonly found on healthy human skin and synergize with a host AMP. Sh-lantibiotics are commonly found on healthy human skin.
Fig. 6. Microglial phagocytosis and lysosomal uptake of Aβ induced by SUS treatment. Microglial phagocytosis and lysosomal uptake of Aβ induced by SUS.
Fig. 4. SUS treatment rescues memory deficits in an AD mouse model.
Fig. 8. Purkinje cell quantification and hearing threshold in NPC cats administered IC HPβCD. Purkinje cell quantification and hearing threshold in NPC.
Fig. 2. Overexpression of miR cluster in the developing heart results in increased cardiomyocyte proliferation and cardiomegaly. Overexpression.
Ketogenic diets combined with fractionated radiation treatment results in decreased immunoreactive PCNA in tumor tissue. Ketogenic diets combined with.
Fig. 3 Mmp-2−/− mice are protected from obesity and leptin resistance.
Fig. 4. Plaque-associated microglia and astrocytes and brain cytokines were altered in APP/PS1;C3 KO mice compared to APP/PS1 mice. Plaque-associated microglia.
Fig. 6. Confocal image series at 10-μm intervals through the full retinal thickness at P48 in WT and vldlr-null mice. Confocal image series at 10-μm intervals.
Fig. 2 In vitro and preclinical study with 18F-MPG.
Fig. 3. HERV-K–induced neuronal toxicity in vivo.
Fig. 7 Heart-specific OMA1 down-regulation protects from hypertrophy induced by TAC. Heart-specific OMA1 down-regulation protects from hypertrophy induced.
Fig. 2 Increasing KLF17, CDH1, and LASS2 expression reduced malignant progression and promoted apoptosis of tumor cells. Increasing KLF17, CDH1, and LASS2.
Fig. 1. Establishing SUS in an AD mouse model.
Fig. 1 ZMAb improves survival of EBOV-challenged NHPs
Fig. 5 Clustering of the distal gut microbiome, the C
Fig. 2. Col IV–Ac2-26 NPs increase subendothelial collagen in Ldlr−/− mice with established atherosclerosis. Col IV–Ac2-26 NPs increase subendothelial.
Fig. 7. Altered morphology after ultrasound but unaltered numbers of microglia in SUS-treated mice. Altered morphology after ultrasound but unaltered numbers.
Fig. 3. Association between peak CTL019 expansion and response.
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. SUS treatment reduces different Aβ species.
Fig. 3 Postnatal assembly of the humanized gut microbiota.
Fig. 2. SUS reduces Aβ plaques in an AD mouse model.
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Fig. 5. SUS treatment reduces Aβ in a second cohort of AD mice. SUS treatment reduces Aβ in a second cohort of AD mice. (A) A second cohort of APP23 mice was analyzed by Western blot with the anti-Aβ antibody W0-2; gel and transfer conditions were optimized to reveal the monomer and trimer specifically. The monomer was efficiently captured by using two sandwiched membranes. (B) The blots showed significant reduction of the monomer (fivefold reduction) and trimer (twofold reduction) in the extracellular fraction (unpaired t tests, P < 0.05). (C) ELISA for Aβ42 in the guanidine-insoluble fraction revealed a twofold reduction in SUS-treated compared to sham-treated mice (unpaired t test, P < 0.008; n = 10 per group). Gerhard Leinenga and Jürgen Götz Sci Transl Med 2015;7:278ra33 Copyright © 2015, American Association for the Advancement of Science