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

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1 Chapter 50 Molecular Basis of Prion Diseases Copyright © 2012, American Society for Neurochemistry. Published by Elsevier Inc. All rights reserved.

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Fig. 1. TP is highly expressed in myeloma.

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. 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. 2. Increased Aβ plaque load in 16-month-old APP/PS1;C3 KO mice.

Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.

Fig. 3. A dynamic STUB1-TF interaction depends on the uremic status.

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

Fig. 4. Bexarotene promotes PPARδ activation of target genes in mouse brain and muscle. Bexarotene promotes PPARδ activation of target genes in mouse brain.

Fig. 3. Antimicrobial activity is detected in diverse strains of CoNS and not predictable at the species level. Antimicrobial activity is detected in diverse.

Neutrophil aggregation is selectively induced by PS+ platelets

In vivo prophylactic and therapeutic efficacy of C12G6 in mice

Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.

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

Fig. 1 Localized treatment of TNBC cancers kills tumor cells and minimizes the metastatic burden. Localized treatment of TNBC cancers kills tumor cells.

Fig. 1. NASH and fibrosis develop late in mice fed an HFD.

Fig. 4 Topical application of SAAP-148 ointment eradicates acute and established infections of MRSA and A. baumannii from the skin. Topical application.

Intravenous delivery of reovirus to primary and secondary brain tumors

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

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

Fig. 4. Specific versus nonspecific NP accumulation.

Fig. 8. Therapeutic effects of the transplantation of hiPSC-EPO–producing cells on renal anemia in adenine-treated mice. Therapeutic effects of the transplantation.

Fig. 1. IS mediates a hyperthrombotic uremic phenotype in an AHR-dependent manner across CKD stages. IS mediates a hyperthrombotic uremic phenotype in.

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.

Immunofluorescence staining of virus-infected human placental explants

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

Fig. 1. Generation of the ΔEx50 mouse model.

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

Fig. 1. Muscles of LAMA2 MD patients and dyW/dyW mice contain high amounts of laminin-α4 and show deficits in BM. Muscles of LAMA2 MD patients and dyW/dyW.

Fig. 4 Nanocages captured multiple TB-related analytes.

Fig. 2. RT-QuIC testing of sCJD and vCJD brain and skin samples.

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

Fig. 7 BRD0705 impairs colony formation in AML cell lines and patient cells and shows in vivo efficacy in multiple AML mouse models. BRD0705 impairs colony.

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.

Molecular and morphological analysis of Pitrm1+/− mouse brain

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

Fig. 7. Inhibitory mechanisms of C12G6.

Fig. 4. Identification of GRP78 as the target antigen of NMO-rAbs ON and ON Identification of GRP78 as the target antigen of NMO-rAbs.

Fig. 5 Local gel scaffold for T cell memory response.

EPS15L1 is predominantly expressed in neurons and surviving Eps15L1-KO mice have development and neural deficits. EPS15L1 is predominantly expressed in.

Fig. 4. Improved tumor response to docetaxel in TNBC and trastuzumab in HER2-amplified PDX models with the addition of S Improved tumor response.

Fig. 7 Improvement of clinical score and axon pathology by nasal IL-4 treatment during chronic EAE. Improvement of clinical score and axon pathology by.

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.

Volume 134, Issue 5, Pages (September 2008)

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.

Comparison of therapeutic efficacies of C12G6 and other bnAbs in mice

HECTD2 knockdown ameliorates Pseudomonas-induced lung injury in vivo

BDNF expression in the cerebellum and brain stem region.

Fig. 7. NAC in breast cancer patients promotes TMEM assembly and increased MENAINV expression. NAC in breast cancer patients promotes TMEM assembly and.

Fig. 3 Hepatic HBV envelope RNA and protein expression levels in HBVRplRag−/− mice 7 days (1 week) and 8 to 24 weeks after adoptive transfer with WT or.

Fig. 3. HRP2 persists at the plasma membrane and around the cytoplasmic vesicles of once-infected RBCs. HRP2 persists at the plasma membrane and around.

Fig. 4. Acute lung injury in miR-223−/y mice.

Fig. 3 CSF1 is expressed in human melanoma.

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

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. 1 Neutrophils derived from patients with MPNs are associated with an increase in NET formation and a prothrombotic, NET-rich phenotype. Neutrophils.

Non–viral Ag–specific CTLs dampen inflammation in a mouse model of viral meningitis. Non–viral Ag–specific CTLs dampen inflammation in a mouse model of.

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

A: Representative Western blot showing a band migrating at ∼90 kDa corresponding to neprilysin protein. A: Representative Western blot showing a band migrating.

Histone crotonylation in kidney tubular cells.

HECTD2 knockdown ameliorates Pseudomonas-induced lung injury in vivo

Upon challenge with oxazolone, human leukocytes (mainly consisting of T cells) infiltrate the dermis and epidermis. Upon challenge with oxazolone, human.

IKKβ protects adipocytes from HFD-induced cell death.

Expression of human tau in GFAP/tau Tg mice.

Western blot analysis of skin tissue from CJD and non-CJD patients

Averaged kinetics, peak fluorescence, and times to threshold using PQ-CSF and/or IQ-CSF conditions. Averaged kinetics, peak fluorescence, and times to.

Volume 4, Issue 2, Pages (July 2013)

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Fig. 4. Prion infectivity of skin samples from sCJD patients. Prion infectivity of skin samples from sCJD patients. (A) Survival curves of TgNN6h or TgWV humanized Tg mice inoculated with skin homogenate from sCJD or non-CJD patients. Six- to 8-week-old TgNN6h (n = 5) or TgWV (n = 7) mice were intracerebrally inoculated with 30 μl of 5% skin homogenate from patients with sCJDMM2 or sCJDVV1. Five TgNN6h mice were intracerebrally inoculated with skin homogenate from a patient with sCJDMM2 (red diamonds), and seven TgWV mice were intracerebrally inoculated with skin homogenate from a patient with sCJDVV1 (blue squares). Seven TgWV mice were intracerebrally inoculated with skin homogenate from a non-CJD patient as a negative control (green line). (B) Western blot analysis of PrPSc in the brains of TgNN6h humanized Tg mice inoculated with skin homogenate from a sCJDMM2 patient. Lanes 1 and 2 show samples of uninoculated mouse brain (control); lanes 3 to 12 show brain samples from five mice inoculated with a skin homogenate from a sCJDMM2 patient; lanes 13 and 14 show brain samples from two mice inoculated with sCJD brain homogenate (brain) as a positive control; lanes 15 and 16 show brain homogenates from sCJD type 2 (T2) and type 1 (T1) patients treated with PK and PNGase F that were used as a reference for PrPSc banding patterns. Samples in lanes 1, 3, 5, 7, 9, and 11 were not PK treated, whereas samples in the other lanes were treated with PK (50 μg/ml) for 1 hour at 37°C. The immunoblot was probed with the anti-PrP antibody 3F4. (C) Western blot analysis of PrPSc in the brains of TgWV mice inoculated with skin homogenate from a patient with sCJDVV1. Lanes 1 to 10 show brain samples from five humanized Tg mice inoculated with skin homogenate from the sCJDVV1 patient; lanes 11 and 12 show brain samples from a mouse inoculated with brain homogenate from a sCJDVV2 patient (brain); lanes 13 and 14 show brain samples from a mouse inoculated with skin homogenate from a non-CJD patient as a negative control (non-CJD skin); lanes 15 and 16 show brain homogenates from patients with sCJD type 1 or type 2 as a positive control. Samples in lanes 1, 3, 5, 7, 9, 11, and 13 were not treated with PK, whereas samples in the other lanes were treated with PK (50 μg/ml) for 1 hour at 37°C. Because of the lower amounts of PrPSc in the brain samples of mice shown in lanes 2 and 4, more PK-treated mouse brain homogenate was loaded onto the gel for these two mice compared to brain homogenate for the other mice. This could have resulted in the slower migration of the PK-resistant PrPSc in mouse brain samples in lanes 2 and 4 compared to the other lanes. The blot was probed with the anti-PrP antibody 3F4. (D) Hematoxylin and eosin (H&E) staining and PrP immunohistochemistry of the cerebral cortex of TgNN6h humanized Tg mice before and after inoculation with sCJD patient brain homogenate. (a and e) Brain sections from uninoculated mice as a negative control; (b and f) brain sections from mice inoculated with sCJD brain homogenate as a positive control; (c, d, g, and h) brain sections from two mice inoculated with skin homogenate from a patient with sCJDMM2. (E) H&E staining and PrP immunohistochemistry using the anti-PrP 3F4 antibody of the cerebral cortex of TgWV Tg mice inoculated with sCJD or non-CJD patient skin or brain homogenate. (a and e) Brain sections from a Tg mouse inoculated with skin homogenate from a non-CJD patient as a negative control; (b and f) brain sections from a Tg mouse inoculated with brain homogenate from a sCJD patient as a positive control; (c, d, g, and h) brain sections from two mice inoculated with skin homogenate from a sCJDVV1 patient. Scale bars, 50 μm. Christina D. Orrú et al., Sci Transl Med 2017;9:eaam7785 Published by AAAS