Fig. 7. Altered morphology after ultrasound but unaltered numbers of microglia in SUS-treated mice. Altered morphology after ultrasound but unaltered numbers.

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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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Cell Physiol Biochem 2016;38: DOI: /
Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic mice. Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic.
Effects of GM1 on astroglial and microglial markers
CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.
Fig. 5 Local gel scaffold for T cell memory response.
Fig. 4. Irisin protected against oxidative stress and apoptosis in IR-injured lung tissue. Irisin protected against oxidative stress and apoptosis in IR-injured.
CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.
Fig. 4. Loss of DLK expression is neuroprotective in the SOD1G93A mouse model of ALS. Loss of DLK expression is neuroprotective in the SOD1G93A mouse model.
Fig. 7 CSPG4-high GBMs show more microglia than CSPG4-low GBMs and express TNFα. CSPG4-high GBMs show more microglia than CSPG4-low GBMs and express TNFα.
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
Fig. 1. Establishing SUS in an AD mouse model.
Fig. 3. Morphological changes associated with glial activation were reduced in 16-month-old APP/PS1;C3 KO mice. Morphological changes associated with glial.
Fig. 6 Transmissibility of adiposity from humanized mice to germ-free recipients. Transmissibility of adiposity from humanized mice to germ-free recipients.
Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.
Fig. 5 Hypoxic tumors from obese mice associate with increased production of IL-6 by adipocytes and myeloid cells. Hypoxic tumors from obese mice associate.
Consolidated Standards of Reporting Trials flow diagram of VRC trial
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.
TOR, but not OSP, blocks STx2B transport and alters endosomal dynamics
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.
Microglia activation in distinct sites of the spinal cord from mice with bronchial asthma or atopic dermatitis on the back skin at the thoracic spinal.
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.
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. 3. Increased expression of exhaustion markers and apoptosis markers on CAR8 cells in the presence of TCR antigen. Increased expression of exhaustion.
Fig. 4 Administration of BMS to mice inhibits autoimmune-relevant pharmacodynamic endpoints driven by IL-12 and IFNα. Administration of BMS
Fig. 1. DEL-1 is expressed by human and mouse osteoclasts.
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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Fig. 3. Morphological changes associated with glial activation were reduced in 16-month-old APP/PS1;C3 KO mice. Morphological changes associated with glial.
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. 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 IRF8 is expressed in CD68+ macrophages after SCI.
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. 5. Vascularization of human liver seed grafts.
Tissue architecture affects function of expanded liver seed grafts
Fig. 2. Overexpression of miR cluster in the developing heart results in increased cardiomyocyte proliferation and cardiomegaly. Overexpression.
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.
Candesartan diminishes SynO-mediated morphofunctional responses in microglia. Candesartan diminishes SynO-mediated morphofunctional responses in 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. 6 Antitumor effect on tumor growth and pulmonary metastasis of CSSD-9 in vivo. Antitumor effect on tumor growth and pulmonary metastasis of CSSD-9.
Fig. 4. HERV-K env expression and injury to lower motor neurons.
Fig. 3. HERV-K–induced neuronal toxicity in vivo.
Fig. 3. LPS induces degeneration of DA neurons and microglial activation in the SN in vivo. LPS (5 µg/3 µl) was unilaterally injected into the SN in the.
Fig. 2. Human liver tissue seed grafts expand after host liver injury.
miR can promote cardiomyocyte proliferation in the adult heart
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. Paclitaxel delays tumor growth and promotes infiltration of TIE2hi/VEGFhi macrophages and TMEM assembly. Paclitaxel delays tumor growth and promotes.
Fig. 3. miR overexpression leads to increased cell proliferation as well as altered differentiation and metabolism in cardiomyocytes. miR
Fig. 2. Col IV–Ac2-26 NPs increase subendothelial collagen in Ldlr−/− mice with established atherosclerosis. Col IV–Ac2-26 NPs increase subendothelial.
Fig. 3. Association between peak CTL019 expansion and response.
Fig. 3. Col IV–Ac2-26 NPs suppress lesional superoxide and increase lesional Il10 mRNA in Ldlr−/− mice with established atherosclerosis. Col IV–Ac2-26.
Fig. 5. SUS treatment reduces Aβ in a second cohort of AD mice.
Fig. 3. SUS treatment reduces different Aβ species.
Fig. 1. Schematic description of whole-exome or targeted next-generation sequencing analyses. Schematic description of whole-exome or targeted next-generation.
Fig. 3 Ect2 gene inactivation lowers cardiomyocyte endowment and is lethal in mice. Ect2 gene inactivation lowers cardiomyocyte endowment and is lethal.
Fig. 6 Pharmacologic alterations of β-AR signaling regulate cardiomyocyte abscission and endowment. Pharmacologic alterations of β-AR signaling regulate.
PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model
In vivo function of MeTro sealants using rat incision model of lungs
Fig. 5. Paclitaxel promotes breast cancer cell dissemination and metastasis in a MENA-dependent manner. Paclitaxel promotes breast cancer cell dissemination.
Fig. 2. SUS reduces Aβ plaques in an AD mouse model.
Fig. 2. In vivo local CD25-targeted NIR-PIT induces regression of treated LL/2-luc tumors. In vivo local CD25-targeted NIR-PIT induces regression of treated.
Fig. 2. Ex vivo and in vivo investigation of the mechanism of drug delivery enhancement with ultrasound. Ex vivo and in vivo investigation of the mechanism.
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Fig. 7. Altered morphology after ultrasound but unaltered numbers of microglia in SUS-treated mice. Altered morphology after ultrasound but unaltered numbers of microglia in SUS-treated mice. (A to C) Sections of non-Tg mice (A) and sham-treated (B) and SUS-treated APP23 mice (C) stained with the microglial marker Iba1. (D) The microglial surface area did not differ between the three groups. (E) There was also no difference in the size of microglial cell bodies between the three groups. (F) A skeleton analysis in which both the summed microglial process endpoints and the summed process length were normalized per cell showing that microglia in the SUS-treated group were more activated (one-way ANOVA followed by Dunnett’s posttest, P < 0.05) (D to F: n = 4, non-Tg; n = 10, sham-treated and SUS-treated). (G to I) This is also reflected by the fivefold increase in the surface area of CD68 immuno-reactivity (G), a marker of microglial and macrophage lysosomes, in SUS-treated (I) compared with sham-treated (H) APP23 mice (n = 10, sham-treated and SUS-treated; t test, P = 0.001). Scale bars, 100 μm (A to C, H, and I). Gerhard Leinenga and Jürgen Götz Sci Transl Med 2015;7:278ra33 Copyright © 2015, American Association for the Advancement of Science