Fig. 4 Spinally grafted iPSC-NPCs show long-term survival and neuronal and glial differentiation in syngeneic recipient in the absence of immunosuppression.

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Fig. 2. Expression of Ninj1 in cortices of ischemic hemispheres of rat brains at 1 day post-MCAO. Coronal brain sections were prepared at 1 day post-MCAO.

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Fig. 1. TP is highly expressed in myeloma.

Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.

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.

Neutrophil aggregation is selectively induced by PS+ platelets

Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.

Analysis of brain and spinal cord of treated Gaa−/− mice and controls

Fig. 6. N95BA5 biocompatibility beyond intended use frame.

Fig. 8. In vivo suppression of MM by CMLD

Fig. 3. BET inhibition reduces homologous recombination.

Fig. 2. Annexin A11 immunohistochemical analysis in postmortem spinal cord tissue from a SALS case with the p.D40G mutation. Annexin A11 immunohistochemical.

Fig. 4. Prion infectivity of skin samples from sCJD patients.

Fig. 4. Characterization of human liver seed graft morphology.

Fig. 4 Bone tissue formation within the Ti-mesh channels.

Intravenous delivery of reovirus to primary and secondary brain tumors

Fig. 2. GPC3 expression in normal and tumor tissues.

Expression of CD36 and psap in a TMA of human ovarian cancer patients

Fig. 6. Effects of CD31-NP targeting in perfused human kidneys.

Fig. 4 Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after reovirus treatment. Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after.

Fig. 3. Wisper controls CF behavior and survival.

Fig. 4. Specific versus nonspecific NP accumulation.

Fig. 5. Vascularization of human liver seed grafts.

Fig. 1. CD31 is present throughout the human renal vasculature.

Fig. 1. Aberrant JNK pathway activation in mouse models of ALS and in spinal cord tissue from patients with sporadic ALS. Aberrant JNK pathway activation.

Fig. 5. Remnants of PS+ platelets induce neutrophil macroaggregation.

Fig. 5 Combination intravenous reovirus and checkpoint inhibition in an orthotopic syngeneic brain tumor model. Combination intravenous reovirus and checkpoint.

Fig. 4. MATE1 transcription in RCC.

Fig. 2 In vitro assessment of hESC-RPE cell sheets.

Fig. 2 STED microscopy of isolated cardiomyocytes from mice treated with MP-rhodamine–loaded CaPs. STED microscopy of isolated cardiomyocytes from mice.

Fig. 6. Apoptotic MSCs exert in vivo immunosuppression in a TH2-type inflammation model in the absence of cytotoxic cells. Apoptotic MSCs exert in vivo.

Fig. 2. Circulating VEGF in GCA patients up-regulates microvascular endothelial Jagged1. Circulating VEGF in GCA patients up-regulates microvascular endothelial.

Fig. 5 EGFR mutation status of patients with NSCLC, detected by histological examination and ARMS PCR. EGFR mutation status of patients with NSCLC, detected.

Fig. 1. Neurobehavioral testing in YG8R mice transplanted with wild-type mouse HSPCs. Neurobehavioral testing in YG8R mice transplanted with wild-type.

Fig. 7. NPs accumulate at sites of vascular obstruction.

Fig. 7. Inhibitory mechanisms of C12G6.

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.

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. 3 Histomorphological evaluation of the segmental defect healing.

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.

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Fig. 7 DMN-Tre labeling of Mycobacterium tuberculosis is inhibited by tuberculosis drug cocktail, unlike auramine staining. DMN-Tre labeling of Mycobacterium.

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Bexarotene is neuroprotective in mouse and human HD neurons in vitro

Fig. 4. Dabrafenib and trametinib changed the cellular components of the tumor microenvironment. Dabrafenib and trametinib changed the cellular components.

Fig. 5. Prophylactic and therapeutic efficacy of C12G6 in ferrets.

Fig. 3 CSF1 is expressed in human melanoma.

Fig. 8 Analysis of bone structure within the soft and stiff scaffold.

Fig. 5 DMN-Tre labeling is selective for live mycobacteria.

Fig. 2 LAEs are characterized by vascular dysfunction, loss of endothelial perfusion and permeability, and perivascular hypoxia. LAEs are characterized.

Fig. 6 Photoreceptor cell survival in the RCS rat retina after transplantation with hESC-RPE cell sheets. Photoreceptor cell survival in the RCS rat retina.

Fig. 5 BRD0705 induces differentiation in AML cell lines and primary patient samples through GSK3α-selective inhibition. BRD0705 induces differentiation.

Fig. 7. Scale-up of AAV vector–mediated liver gene transfer of secretable GAA to nonhuman primates. Scale-up of AAV vector–mediated liver gene transfer.

Correlation of reovirus RNA/protein with proliferating tumor cells

Fig. 7 Transient immunosuppression (4 weeks) supports long-term graft survival and is associated with progressive decrease in spinal regional inflammatory.

Fig. 4 Lentiviral transgene expression penetrates tissue and provides durable effects in vivo. Lentiviral transgene expression penetrates tissue and provides.

Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.

Indirect fluorescence assay of N. gruberi cells.

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

Activation of glial cells.

Lack of Ctip2 is associated with impaired proliferation and delayed onset of differentiation during early stages of epidermal development. Lack of Ctip2.

Co-expression of VSVG–Cdc42-CA, but not VSVG–Cdc42-DN with eGFP–gephyrin (green) and Myc–CB2ΔPH (blue) rescues postsynaptic gephyrin clustering, as shown.

Fig. 1. DEL-1 is expressed by human and mouse osteoclasts.

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 IRF8 is expressed in CD68+ macrophages after SCI.

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Fig. 4 Spinally grafted iPSC-NPCs show long-term survival and neuronal and glial differentiation in syngeneic recipient in the absence of immunosuppression. Spinally grafted iPSC-NPCs show long-term survival and neuronal and glial differentiation in syngeneic recipient in the absence of immunosuppression. (A) Immunofluorescence staining showing EGFP fluorescence in the core of the graft. (B and C) Immunofluorescence staining showing NF- and GFAP-stained processes in the same areas as in (A). (D to F) Staining with DCX (D), NeuN (E), and NSE (F) in EGFP+ grafts. (G to I) Immunofluorescence staining showing EGFP/NF+ neurites, in areas cranial and caudal to the borders of the graft. (J and K) Costaining of SYN-EGFP+ grafts with VGAT and gephyrin antibodies in the core of the graft. Scale bars, 30 μm (A), 125 μm (B), 10 μm (C), 40 μm (D), 35 μm (E and F), 50 μm (G to I), and 20 μm (J and K). Jan Strnadel et al., Sci Transl Med 2018;10:eaam6651 Published by AAAS