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

Slides:

Advertisements

Similar presentations

Date of download: 5/28/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Evidence of Multisystem Disorder in Whole-Brain Map.

Advertisements

I.S. Scott1,2, S.M.L. Paine2 and J.S. Lowe2

Fig. 1. TP is highly expressed in myeloma.

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

Poly-GR and poly-PR co-aggregate with ribosomal proteins in C9orf72 patients. Poly-GR and poly-PR co-aggregate with ribosomal proteins in C9orf72 patients.

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.

Fig. 4 Bacterial taxonomic groups that discriminate among RYGB-, SHAM-, and WMS-derived samples. Bacterial taxonomic groups that discriminate among RYGB-,

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

Cytoplasmic poly-GR/PR inclusions resemble stress granules in vitro.

Neutrophil aggregation is selectively induced by PS+ platelets

Poly-GR mainly co-localizes with nucleolar ribosomes.

Abnormal accumulation of U snRNPs in motor neuron nuclei of ALS patients.A–D.Immunofluorescent staining of TDP‐43 and U snRNPs using an anti‐Sm proteins.

Fig. 3. Frequencies of amino acids at critical PGT121 and contact sites in the SHIV-SF162P3 challenge stock. Frequencies of amino acids at critical.

Fig. 6. N95BA5 biocompatibility beyond intended use frame.

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

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.

Fig. 3 BX795 blocks the synthesis of HSV-1 virions.

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. Specific versus nonspecific NP accumulation.

Fig. 5. Vascularization of human liver seed grafts.

Fig. 4. Antitumor efficacy of ERY974 against various cancer types.

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.

Immunofluorescence staining of virus-infected human placental explants

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. 5. MMP-7 expression in human liver, EHBD, and gallbladder.

Representative CT and PET/CT images of three patients with NSCLCs

Volume 10, Issue 8, Pages (March 2015)

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. mGlu7 expression is reduced in RTT autopsy samples.

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. 4. Irisin protected against oxidative stress and apoptosis in IR-injured lung tissue. Irisin protected against oxidative stress and apoptosis in IR-injured.

Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.

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. 6. Rolling neutrophils extract membranes from fragile remnant PS+ platelets. Rolling neutrophils extract membranes from fragile remnant PS+ platelets.

Fig. 1. β-APP overexpression or exposure to inflammatory mediators induces sIBM-like pathology in cultured rat myocytes that is abrogated by arimoclomol.

Fig. 7. Genetic ablation of UCP2 compromised the protective effect of exogenous irisin on lung IR injury. Genetic ablation of UCP2 compromised the protective.

Fig. 7. Treatment with DLK inhibitors reduces p-c-Jun and protects against neuronal and synaptic loss in vitro and in ALS mouse models. Treatment with.

Fig. 1 CSPG4 is expressed in GBM specimens and GBM-NS and associated with more aggressive disease. CSPG4 is expressed in GBM specimens and GBM-NS and associated.

Fig. 3 CSF1 is expressed in human melanoma.

Fig. 7 Analysis of the bacterial nidus within tissue abscesses by MALDI IMS demonstrates a paucity of calprotectin signal. Analysis of the bacterial nidus.

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

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.

HDAC4N increases with Braak stage in CA2 hippocampal pyramidal cells.

Correlation of reovirus RNA/protein with proliferating tumor cells

Neuronal ATM level is reduced in mouse models of AD

Commissural Wt1+ neurons.

Fig. 6 Combination therapy with LVSOD2 and LVshCTGF preserves flap volume and reduces fibrosis after RT. Combination therapy with LVSOD2 and LVshCTGF preserves.

POLG defects cause degeneration of enhancer‐active regions of CNS

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. 6. Cross-section of the stomach wall and spiral intestine of the embryo, stained with PAS. (A) Surface of the stomach wall (SW) and ingested material.

Colocalization of the palmitoylation-deficient mutants of claudin-14 with the lysosomal membrane protein LAMP-2. Colocalization of the palmitoylation-deficient.

Fig. 5. Annexin A11 mutations disrupt binding to calcyclin.

Filipin staining of marginal gyrus of cerebral cortex in NPC cats

RA signaling in early postnatal PFC

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.

Expression of p130CAS in primary culture neurons

Fig. 5. Vascularization of human liver seed grafts.

Fig. 4. HERV-K env expression and injury to lower motor neurons.

Presentation transcript:

Fig. 2. Annexin A11 immunohistochemical analysis in postmortem spinal cord tissue from a SALS case with the p.D40G mutation. Annexin A11 immunohistochemical analysis in postmortem spinal cord tissue from a SALS case with the p.D40G mutation. (A) Phospho–TDP-43–positive cytoplasmic inclusion from the anterior horn of the spinal cord. (B to E) Annexin A11–positive inclusions in motor neurons of the spinal cord include skein-like structures (B) and filamentous and tubular-shaped structures (C and D). Occasional basket-like inclusions were seen in the spinal cord (E). (F) Abundant annexin A11–positive torpedo-like neuritic structures were present in the neuropil of the motor cortex (red arrows). Representative spinal cord staining for annexin A11 inclusions in a SALS case (n = 15) who is negative for ANXA11 mutations (G) and two C9ORF72 expansion–positive ALS cases (spinal cord and frontal cortex) (H and I). (J) Staining for annexin A11 inclusions was also negative in an ALS case harboring a p.D101G mutation in SOD1 (spinal cord). Similarly, frontotemporal lobar degeneration (FTLD)–TDP-43 cases (spinal cord; n = 3) (K) and Alzheimer’s disease (AD) cases (n = 3) (L) and control individuals (n = 13) (M) were also negative for staining for annexin A11 inclusions. (N and O) Double labeling of spinal cord tissue in the p.D40G SALS case for phospho–TDP-43 (green) and annexin A11 aggregates (red). (P) Costaining for ubiquitinated aggregates (red, annexin A11; green, ubiquitin) showed occasional colocalization (white arrow). Scale bars, 30 μm (A, E, G, and H), 20 μm (B and C), 15 μm (D), 50 μm (F, I, J, K, and L), 25 μm (M and N), and 50 μm (O and P). Bradley N. Smith et al., Sci Transl Med 2017;9:eaad9157 Published by AAAS