tauc3  (Vector Laboratories)


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    Name:
    VECTOR SG Peroxidase HRP Substrate Kit
    Description:
    Vector SG Peroxidase Substrate Kit has greater sensitivity than conventional substrates Consistent and reliableIdeal for IHC ICC ISH and blotsPermanent mountingIdeal for single and multiple labelingStock solutions supplied in convenient dropper bottles promoting ease of handlingNo wait times for mixing and dissolving powders or tabletsOne year expiry dateSufficient reagents to produce 300 ml of working solution Vector SG and ImmPACT SG HRP substrates produce blue gray reaction products that can be used as a single label or as a second color for multiple antigen labeling With the aid of imaging systems and software the spectral profile of both chromogens can be distinguished from other enzyme substrates in applications where antigens are co localized Sections stained with either substrate also can be viewed by darkfield or electron microscopy Vector SG and ImmPACT SG substrates can be used for both manual and automated staining methods Stained sections can be dehydrated cleared and permanently mounted Vector SG Substrate Kit contains stock solutions in convenient dropper bottles The sensitivity of Vector SG subsrate is equivalent to AEC This product can also be used on blots The kit provides all of the necessary reagents to prepare about 300 ml of working solution When stored at 4 °C this kit is stable for one year
    Catalog Number:
    sk-4700
    Price:
    None
    Size:
    1 Kit
    Category:
    Protein chromogenic detection reagents or kits or substrates
    Buy from Supplier


    Structured Review

    Vector Laboratories tauc3
    VECTOR SG Peroxidase HRP Substrate Kit
    Vector SG Peroxidase Substrate Kit has greater sensitivity than conventional substrates Consistent and reliableIdeal for IHC ICC ISH and blotsPermanent mountingIdeal for single and multiple labelingStock solutions supplied in convenient dropper bottles promoting ease of handlingNo wait times for mixing and dissolving powders or tabletsOne year expiry dateSufficient reagents to produce 300 ml of working solution Vector SG and ImmPACT SG HRP substrates produce blue gray reaction products that can be used as a single label or as a second color for multiple antigen labeling With the aid of imaging systems and software the spectral profile of both chromogens can be distinguished from other enzyme substrates in applications where antigens are co localized Sections stained with either substrate also can be viewed by darkfield or electron microscopy Vector SG and ImmPACT SG substrates can be used for both manual and automated staining methods Stained sections can be dehydrated cleared and permanently mounted Vector SG Substrate Kit contains stock solutions in convenient dropper bottles The sensitivity of Vector SG subsrate is equivalent to AEC This product can also be used on blots The kit provides all of the necessary reagents to prepare about 300 ml of working solution When stored at 4 °C this kit is stable for one year
    https://www.bioz.com/result/tauc3/product/Vector Laboratories
    Average 90 stars, based on 4831 article reviews
    Price from $9.99 to $1999.99
    tauc3 - by Bioz Stars, 2021-02
    90/100 stars

    Images

    1) Product Images from "Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer’s disease"

    Article Title: Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer’s disease

    Journal: Neurobiology of disease

    doi: 10.1016/j.nbd.2018.05.021

    The expression of neurotrophin receptor and select downstream signaling molecule gene transcripts is equivalent in pS422+ nbM neurons during the progression of AD. Color-coded heatmap of the relative expression profiles for select transcripts in pS422+ nbM neurons aspirated from NCI, MCI, and AD cases (red to green = increasing mRNA levels). Quantitative analysis revealed no statistical differences in the expression levels of the transcripts examined in pS422+ nbM neurons derived from MCI or AD compared to NCI. This observation suggests that the pathological state of the neuron, not disease status, may drive changes in gene expression. Therefore, in the present analysis, we compared mRNA levels in individual pS422+, pS422+/TauC3+, and TauC3+ nbM neurons independent of clinical diagnosis. Abbreviations: Nrtk1, Nrtk2 , and Nrtk3 , neurotrophin tyrosine kinase receptor type 1 (TrkA), 2 (TrkB), 3 (TrkC); ECD, extracellular domain; TK, intracellular tyrosine kinase domain; Ngfr , nerve growth factor receptor (p75 NTR ); Mapk1 , mitogen-activated protein kinase 1 (extracellular signal-regulated kinase 2); Mapk3 , mitogen-activated protein kinase 3 (extracellular signal-regulated kinase 1); Creb1 , cAMP response element binding protein; Akt1 , Akt serine/threonine kinase 1 (protein kinase B); Prkca, Prkce, Prkci , protein kinase C alpha, epsilon, iota.
    Figure Legend Snippet: The expression of neurotrophin receptor and select downstream signaling molecule gene transcripts is equivalent in pS422+ nbM neurons during the progression of AD. Color-coded heatmap of the relative expression profiles for select transcripts in pS422+ nbM neurons aspirated from NCI, MCI, and AD cases (red to green = increasing mRNA levels). Quantitative analysis revealed no statistical differences in the expression levels of the transcripts examined in pS422+ nbM neurons derived from MCI or AD compared to NCI. This observation suggests that the pathological state of the neuron, not disease status, may drive changes in gene expression. Therefore, in the present analysis, we compared mRNA levels in individual pS422+, pS422+/TauC3+, and TauC3+ nbM neurons independent of clinical diagnosis. Abbreviations: Nrtk1, Nrtk2 , and Nrtk3 , neurotrophin tyrosine kinase receptor type 1 (TrkA), 2 (TrkB), 3 (TrkC); ECD, extracellular domain; TK, intracellular tyrosine kinase domain; Ngfr , nerve growth factor receptor (p75 NTR ); Mapk1 , mitogen-activated protein kinase 1 (extracellular signal-regulated kinase 2); Mapk3 , mitogen-activated protein kinase 3 (extracellular signal-regulated kinase 1); Creb1 , cAMP response element binding protein; Akt1 , Akt serine/threonine kinase 1 (protein kinase B); Prkca, Prkce, Prkci , protein kinase C alpha, epsilon, iota.

    Techniques Used: Expressing, Derivative Assay, Binding Assay

    Phenotypic characterization of NFT evolution with pS422 and TauC3 immunoreactivity in nbM neurons. (A–G) Tissue sections from the nbM of a representative AD case. (A) Cholinergic neurons in the nbM can be identified phenotypically by expression of the pan-neurotrophin (p75 NTR ) receptor. A tissue section from a consecutive series was immunostained with p75 NTR (brown) and pS422 (blue) to confirm the location of the cholinergic nbM. (B) Low magnification view of the nbM subfield immunostained with pS422 (brown) and TauC3 (blue). (C) High magnification of pS422 and TauC3 pathology in boxed area from (B). A Nissl counterstain was used to identify nbM neurons lacking tau pathology (*). (D-G) Confocal microscopy was used to confirm the presence of three discrete populations of nbM neurons. (D) Low magnification view of nbM subfield. (E–G) High magnification of boxed area from (D) identify pS422 (E), TauC3 (F), and overlay (G). Single arrowhead indicates a pS422+ nbM neuron, double arrowheads indicate a TauC3+ nbM neuron, and arrow indicates a pS422+/TauC3+ nbM neuron (colocalization appears yellow). Scale bar in A, 100 μm for A–B; scale bar in C, 50 μm for C; scale bar in D, 100 μm for D; scale bar in G, 50 μm for E–G.
    Figure Legend Snippet: Phenotypic characterization of NFT evolution with pS422 and TauC3 immunoreactivity in nbM neurons. (A–G) Tissue sections from the nbM of a representative AD case. (A) Cholinergic neurons in the nbM can be identified phenotypically by expression of the pan-neurotrophin (p75 NTR ) receptor. A tissue section from a consecutive series was immunostained with p75 NTR (brown) and pS422 (blue) to confirm the location of the cholinergic nbM. (B) Low magnification view of the nbM subfield immunostained with pS422 (brown) and TauC3 (blue). (C) High magnification of pS422 and TauC3 pathology in boxed area from (B). A Nissl counterstain was used to identify nbM neurons lacking tau pathology (*). (D-G) Confocal microscopy was used to confirm the presence of three discrete populations of nbM neurons. (D) Low magnification view of nbM subfield. (E–G) High magnification of boxed area from (D) identify pS422 (E), TauC3 (F), and overlay (G). Single arrowhead indicates a pS422+ nbM neuron, double arrowheads indicate a TauC3+ nbM neuron, and arrow indicates a pS422+/TauC3+ nbM neuron (colocalization appears yellow). Scale bar in A, 100 μm for A–B; scale bar in C, 50 μm for C; scale bar in D, 100 μm for D; scale bar in G, 50 μm for E–G.

    Techniques Used: Expressing, Confocal Microscopy

    Neurotrophin receptor and select downstream signaling molecule mRNAs are dysregulated during the progression of NFT maturation. Heatmap of relative mRNA expression levels of neurotrophin receptors and downstream signaling molecules in pS422+, pS422+/TauC3+, and TauC3+ nbM neurons compared to unlabeled nbM neurons (red to green = increasing mRNA levels). Quantitative analysis revealed downregulated expression of Nrtk1-3 transcripts as well as Akt1 and Prkce in pS422+ nbM neurons as compared to unlabeled control neurons. Appearance of the late stage neoepitope TauC3 was associated with downregulation of the Ngfr transcript and upregulation of the Prkca transcript. a, unlabeled > pS422, p
    Figure Legend Snippet: Neurotrophin receptor and select downstream signaling molecule mRNAs are dysregulated during the progression of NFT maturation. Heatmap of relative mRNA expression levels of neurotrophin receptors and downstream signaling molecules in pS422+, pS422+/TauC3+, and TauC3+ nbM neurons compared to unlabeled nbM neurons (red to green = increasing mRNA levels). Quantitative analysis revealed downregulated expression of Nrtk1-3 transcripts as well as Akt1 and Prkce in pS422+ nbM neurons as compared to unlabeled control neurons. Appearance of the late stage neoepitope TauC3 was associated with downregulation of the Ngfr transcript and upregulation of the Prkca transcript. a, unlabeled > pS422, p

    Techniques Used: Expressing

    Select cholinergic markers are dysregulated during the development of NFTs in nbM neurons. Heatmap of relative expression levels of cholinergic neuronal markers in pS422+, pS422+/TauC3+, and TauC3+ NB neurons compared to unlabeled control neurons (red to green = increasing mRNA levels). Quantitative analysis revealed upregulation of the Chrna7 transcript and downregulation of the Chrnb2 transcript following the appearance of the TauC3 epitope. Abbreviations: Chat choline acetyltransferase; Slcl8a3 , vesicular acetylcholine transporter; Ache , acetylcholinesterase; Bche , butyrylcholinesterase; Chrm1, Chrm2 , cholinergic receptor, muscarinic 1, 2; Chrna7, Chrna4, Chrnb2 , cholinergic receptor, nicotinic, alpha polypeptide 7, alpha polypeptide 4, beta polypeptide 2. a, pS422
    Figure Legend Snippet: Select cholinergic markers are dysregulated during the development of NFTs in nbM neurons. Heatmap of relative expression levels of cholinergic neuronal markers in pS422+, pS422+/TauC3+, and TauC3+ NB neurons compared to unlabeled control neurons (red to green = increasing mRNA levels). Quantitative analysis revealed upregulation of the Chrna7 transcript and downregulation of the Chrnb2 transcript following the appearance of the TauC3 epitope. Abbreviations: Chat choline acetyltransferase; Slcl8a3 , vesicular acetylcholine transporter; Ache , acetylcholinesterase; Bche , butyrylcholinesterase; Chrm1, Chrm2 , cholinergic receptor, muscarinic 1, 2; Chrna7, Chrna4, Chrnb2 , cholinergic receptor, nicotinic, alpha polypeptide 7, alpha polypeptide 4, beta polypeptide 2. a, pS422

    Techniques Used: Expressing

    2) Product Images from "Reactivating the extracellular matrix synthesis of sulfated glycosaminoglycans and proteoglycans to improve the human skin aspect and its mechanical properties"

    Article Title: Reactivating the extracellular matrix synthesis of sulfated glycosaminoglycans and proteoglycans to improve the human skin aspect and its mechanical properties

    Journal: Clinical, Cosmetic and Investigational Dermatology

    doi: 10.2147/CCID.S116548

    ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to CD34 marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values
    Figure Legend Snippet: ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to CD34 marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values

    Techniques Used: Immunostaining, Marker

    3) Product Images from "Endothelial damage, vascular bagging and remodeling of the microvascular bed in human microangiopathy with deep white matter lesions"

    Article Title: Endothelial damage, vascular bagging and remodeling of the microvascular bed in human microangiopathy with deep white matter lesions

    Journal: Acta Neuropathologica Communications

    doi: 10.1186/s40478-018-0632-z

    Double- and triple-label immunohistochemistry (IHC) for UEA-l, COLL4, the plasma proteins fibrinogen (FIBR) or immunoglobulin G fraction (IgG) and the endothelial marker alkaline phosphatase protein (ALPL) in 7 μm thick paraffin sections. a - b The healthy capillary in the control white matter (Co) of a NoSVD case does not have vascular bags ( a ). Vascular bag (short thick arrow) in a SVD case with multiple layers of COLL4-positive membranes around the UEA-l-labeled endothelium (white arrowhead) of a small vessel (
    Figure Legend Snippet: Double- and triple-label immunohistochemistry (IHC) for UEA-l, COLL4, the plasma proteins fibrinogen (FIBR) or immunoglobulin G fraction (IgG) and the endothelial marker alkaline phosphatase protein (ALPL) in 7 μm thick paraffin sections. a - b The healthy capillary in the control white matter (Co) of a NoSVD case does not have vascular bags ( a ). Vascular bag (short thick arrow) in a SVD case with multiple layers of COLL4-positive membranes around the UEA-l-labeled endothelium (white arrowhead) of a small vessel (

    Techniques Used: Immunohistochemistry, Marker, Labeling

    4) Product Images from "Pathological TDP-43 changes in Betz cells differ from those in bulbar and spinal α-motoneurons in sporadic amyotrophic lateral sclerosis"

    Article Title: Pathological TDP-43 changes in Betz cells differ from those in bulbar and spinal α-motoneurons in sporadic amyotrophic lateral sclerosis

    Journal: Acta Neuropathologica

    doi: 10.1007/s00401-016-1633-2

    Schematic diagram summarizing the findings in giant Betz cells ( a , c – e , g , h ) and in α -motoneurons ( b , f ) in the cases of sporadic amyotrophic lateral sclerosis studied. We hypothesize that the pathology may be transferred by means of still soluble but toxic or pathogenic axoplasmic TDP-43 directly (monosynaptically) from involved Betz cells to α -motoneurons. This postulated route is marked by means of the red arrow in the synapse between e and f . Deposits of lipofuscin granules serve as a marker of the cortical cellular type and are represented here by violet shading. a , b Betz cells in controls as well as in non-involved Betz cells and in non-involved α -motoneurons displayed normal, strongly immunoreactive intranuclear TDP-43 staining (here, in brown ). The long axon of the Betz cell projects to, and synapses directly on, the corresponding α -motoneuron in the lower brainstem or in the ventral horn of the spinal cord. c , d Involved Betz cells of the cases examined displayed increasingly weak ( c ) and severe reduction ( d ) of TDP-43 intranuclear immunostaining. e The putative end-point of this development may be reached when the cell nucleus is completely ‘empty’, i.e., TDP-43 immunonegative. Theoretically, the protein could be present (although no longer immunoreactive) in the somatodendritic and/or axonal cytoplasm in a soluble state (here, in pink ), where, for an unknown time interval, it does not convert into insoluble aggregates. f At the same time the above-described abnormalities became visible within the Betz cells (depicted in c – e ), somatic cytoplasmatic pTDP-43 inclusions were found in α -motoneurons (here, as red blasts). It should be emphasized that the aggregates were only found in the somatic and axonal cytoplasm. g Adjacent to the Betz cells that have TDP-43 immunonegative nuclei but lack pTDP-43 cytoplasmic inclusions, one sometimes encountered Betz cells containing discreet (dot-like, granular) aggregates (here, in red ), which could indicate that these cells do not completely forfeit the potential to develop inclusion bodies. h Betz cells containing large aggregates were seldom. The dashed lines in a and e are intended to indicate that the involved axons are much longer than depicted schematically here
    Figure Legend Snippet: Schematic diagram summarizing the findings in giant Betz cells ( a , c – e , g , h ) and in α -motoneurons ( b , f ) in the cases of sporadic amyotrophic lateral sclerosis studied. We hypothesize that the pathology may be transferred by means of still soluble but toxic or pathogenic axoplasmic TDP-43 directly (monosynaptically) from involved Betz cells to α -motoneurons. This postulated route is marked by means of the red arrow in the synapse between e and f . Deposits of lipofuscin granules serve as a marker of the cortical cellular type and are represented here by violet shading. a , b Betz cells in controls as well as in non-involved Betz cells and in non-involved α -motoneurons displayed normal, strongly immunoreactive intranuclear TDP-43 staining (here, in brown ). The long axon of the Betz cell projects to, and synapses directly on, the corresponding α -motoneuron in the lower brainstem or in the ventral horn of the spinal cord. c , d Involved Betz cells of the cases examined displayed increasingly weak ( c ) and severe reduction ( d ) of TDP-43 intranuclear immunostaining. e The putative end-point of this development may be reached when the cell nucleus is completely ‘empty’, i.e., TDP-43 immunonegative. Theoretically, the protein could be present (although no longer immunoreactive) in the somatodendritic and/or axonal cytoplasm in a soluble state (here, in pink ), where, for an unknown time interval, it does not convert into insoluble aggregates. f At the same time the above-described abnormalities became visible within the Betz cells (depicted in c – e ), somatic cytoplasmatic pTDP-43 inclusions were found in α -motoneurons (here, as red blasts). It should be emphasized that the aggregates were only found in the somatic and axonal cytoplasm. g Adjacent to the Betz cells that have TDP-43 immunonegative nuclei but lack pTDP-43 cytoplasmic inclusions, one sometimes encountered Betz cells containing discreet (dot-like, granular) aggregates (here, in red ), which could indicate that these cells do not completely forfeit the potential to develop inclusion bodies. h Betz cells containing large aggregates were seldom. The dashed lines in a and e are intended to indicate that the involved axons are much longer than depicted schematically here

    Techniques Used: Marker, Staining, Immunostaining

    a Overview of the Betz giant pyramidal cells in layer Vb of the primary motor neocortex of a control individual (Table 1 , case #17). Layer V is shown at right angles to the cortical surface ( at left ). The pigment-Nissl staining ( violet - red ) here and the pigment-staining ( violet ) in the remaining micrographs marks the location of the closely packed lipofuscin pigment granules within the cell somata. b – d , f – q Pigment-staining and TDP-43 immunohistochemistry in individuals with sALS. b , f ( at left ), and g Micrographs showing normal Betz cells with strong nuclear TDP-43 immunostaining. c , d A Betz cell with reduced nuclear TDP-43 immunostaining ( d , at left ) alongside of Betz cells in which TDP-43 immunostaining is nearly absent ( d , at right ; see also h , i ) or absent ( f , at right , k and l , at left ; see also m , n , o ). e A pTDP-43-immunopositive α -motoneuron filled with aggregates in the motor nucleus of the hypoglossal nerve (N. XII ) (Table 1 , case #13). In the other micrographs here, the Betz cells that become involved in sALS do not display this kind of lesional profile. h – m These micrographs show the growing reduction and loss of intranuclear TDP-43 immunoreactivity in Betz cells; note also, however, that the cytoplasmic inclusions (aggregates) that do develop are slight. i A Betz cell containing discreet dot-like or granular cytoplasmic inclusions ( arrows ). An exception to this discreet cytoplasmic pathology is seen in p . m A Betz cell with a completely ‘empty’ (i.e., TDP-43 immunonegative) cell nucleus ( at left ) shown next to a Betz cell with normal nuclear TDP-43 immunostaining. In the cell at the left, only the nucleolus is still visible. n , o Subtle TDP inclusions ( arrows ) in Betz cells, including skein-like lesions in o . q Remnants of lipofuscin pigment granules mark the site of a dead Betz cell. Scale bar in d is valid for all micrographs except a . 100 µm polyethylene glycol (PEG) sections. Micrographs b , o (Table 1 , case #1), c , d , f , k – n , p , q (Table 1 , case #3), g – l (Table 1 , case #2). A plan apochromat 40:1 lens was utilized to evaluate and photograph individual Betz cells ( a – d , f – q )
    Figure Legend Snippet: a Overview of the Betz giant pyramidal cells in layer Vb of the primary motor neocortex of a control individual (Table 1 , case #17). Layer V is shown at right angles to the cortical surface ( at left ). The pigment-Nissl staining ( violet - red ) here and the pigment-staining ( violet ) in the remaining micrographs marks the location of the closely packed lipofuscin pigment granules within the cell somata. b – d , f – q Pigment-staining and TDP-43 immunohistochemistry in individuals with sALS. b , f ( at left ), and g Micrographs showing normal Betz cells with strong nuclear TDP-43 immunostaining. c , d A Betz cell with reduced nuclear TDP-43 immunostaining ( d , at left ) alongside of Betz cells in which TDP-43 immunostaining is nearly absent ( d , at right ; see also h , i ) or absent ( f , at right , k and l , at left ; see also m , n , o ). e A pTDP-43-immunopositive α -motoneuron filled with aggregates in the motor nucleus of the hypoglossal nerve (N. XII ) (Table 1 , case #13). In the other micrographs here, the Betz cells that become involved in sALS do not display this kind of lesional profile. h – m These micrographs show the growing reduction and loss of intranuclear TDP-43 immunoreactivity in Betz cells; note also, however, that the cytoplasmic inclusions (aggregates) that do develop are slight. i A Betz cell containing discreet dot-like or granular cytoplasmic inclusions ( arrows ). An exception to this discreet cytoplasmic pathology is seen in p . m A Betz cell with a completely ‘empty’ (i.e., TDP-43 immunonegative) cell nucleus ( at left ) shown next to a Betz cell with normal nuclear TDP-43 immunostaining. In the cell at the left, only the nucleolus is still visible. n , o Subtle TDP inclusions ( arrows ) in Betz cells, including skein-like lesions in o . q Remnants of lipofuscin pigment granules mark the site of a dead Betz cell. Scale bar in d is valid for all micrographs except a . 100 µm polyethylene glycol (PEG) sections. Micrographs b , o (Table 1 , case #1), c , d , f , k – n , p , q (Table 1 , case #3), g – l (Table 1 , case #2). A plan apochromat 40:1 lens was utilized to evaluate and photograph individual Betz cells ( a – d , f – q )

    Techniques Used: Staining, Immunohistochemistry, Immunostaining

    5) Product Images from "Identification of Platelet-Derived Growth Factor D in Human Chronic Allograft Nephropathy"

    Article Title: Identification of Platelet-Derived Growth Factor D in Human Chronic Allograft Nephropathy

    Journal:

    doi: 10.1016/j.humpath.2007.07.008

    PDGF-D, PDGF-Rβ and smooth muscle actin in transplant arteriopathy. A: PDGF-D is expressed by medial smooth muscle cells, neointimal smooth muscle cells and some adventitial cells. B: In a serial section, PDGF-Rβ is expressed in a similar
    Figure Legend Snippet: PDGF-D, PDGF-Rβ and smooth muscle actin in transplant arteriopathy. A: PDGF-D is expressed by medial smooth muscle cells, neointimal smooth muscle cells and some adventitial cells. B: In a serial section, PDGF-Rβ is expressed in a similar

    Techniques Used:

    PDGF-D and PDGF-Rβ expression in glomeruli. PDGF-D is uniformly expressed in visceral epithelial cells and arteriolar wall in A: normal kidneys, B: kidneys with AVR, and C: kidneys with CAN. PDGF-Rβ is expressed weakly in mesangial areas
    Figure Legend Snippet: PDGF-D and PDGF-Rβ expression in glomeruli. PDGF-D is uniformly expressed in visceral epithelial cells and arteriolar wall in A: normal kidneys, B: kidneys with AVR, and C: kidneys with CAN. PDGF-Rβ is expressed weakly in mesangial areas

    Techniques Used: Expressing

    PDGF-D and PDGF-Rβ expression in arteries. A: In normal group, triple immunolabeling shows that PDGF-D (brown) is expressed in arterial medial smooth muscle cells that also express alpha-smooth muscle actin (blue-gray); no monocyte/macrophages
    Figure Legend Snippet: PDGF-D and PDGF-Rβ expression in arteries. A: In normal group, triple immunolabeling shows that PDGF-D (brown) is expressed in arterial medial smooth muscle cells that also express alpha-smooth muscle actin (blue-gray); no monocyte/macrophages

    Techniques Used: Expressing, Immunolabeling

    PDGF-D and PDGF-Rβ expression in tubulointerstitial areas. PDGF-D is expressed uniformly in a few tubuli in A: normal kidneys, B: kidneys with acute vascular rejection (AVR), and C: kidneys with chronic allograft nephropathy (CAN). PDGF-Rβ
    Figure Legend Snippet: PDGF-D and PDGF-Rβ expression in tubulointerstitial areas. PDGF-D is expressed uniformly in a few tubuli in A: normal kidneys, B: kidneys with acute vascular rejection (AVR), and C: kidneys with chronic allograft nephropathy (CAN). PDGF-Rβ

    Techniques Used: Expressing

    PDGF-D colocalization with smooth muscle actin and PDGF-Rβ in the interstitium. A and B: Double IHC showing PDGF-D (brown) and α-smooth muscle actin (purple). PDGF-D is expressed by glomerular podocytes and a subset of interstitial cells
    Figure Legend Snippet: PDGF-D colocalization with smooth muscle actin and PDGF-Rβ in the interstitium. A and B: Double IHC showing PDGF-D (brown) and α-smooth muscle actin (purple). PDGF-D is expressed by glomerular podocytes and a subset of interstitial cells

    Techniques Used: Immunohistochemistry

    3.1 PDGF-D and PDGF-Rβ expression in arteries
    Figure Legend Snippet: 3.1 PDGF-D and PDGF-Rβ expression in arteries

    Techniques Used: Expressing

    6) Product Images from "Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type"

    Article Title: Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type

    Journal: Neuropathology and applied neurobiology

    doi: 10.1111/nan.12362

    Morphology and timeline of glial and neuronal α-syn aggregation in multiple system atrophy of the cerebellar type (MSA-C). Here and in the subsequent two figures we show images of 70-µm-thick sections because they were used to enable to see the histology and pathology in a more three-dimensional manner than conventional 6-µm-thick sections wherein objects have a more two-dimensional appearance. Hence, this figure shows a richer morphology of α-syn aggregation in the inferior olive (IO) ( A – G ) and the pontine nuclei ( H – L ) as depicted by Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry. ( A ) The most frequent pathology in MSA-C consisted of α-syn-positive glial cytoplasmic inclusions (GCIs; arrowheads), whereas α-syn-positive Nis (arrow) were rare. GCIs frequently were seen in oligodendroglial cells with a swollen nucleus and expanded cytoplasm. ( B ) Nis were often seen in association with neurons that showed cytoplasmic and nuclear swelling as well as a loosening of cytoplasmic lipofuscin pigment and the arrow identifies swollen cell of the IO, arrowhead shows enlarged nucleus. ( C ) This may represent changes that are followed by the development of α-syn inclusions (arrow), and, consecutively, by the occurrence of increasingly bulky cytoplasmic neuronal inclusion (NI) ( D ) and the arrow depicts a neuron with both nuclear and cytoplasmic NIs, arrowhead shows GCI). ( E, F ) Cytoplasmic NIs (as shown by arrow in E ) increased to fill most of the neuronal perikarya. In parallel, neurons became surrounded by an increasing numbers of neuritic α-syn inclusions (NRIs), presumablly in dendrites. ( G ) Finally, neuronal loss became apparent by free lipofuscin pigment remnants in the extracellular space. ( H ) Arrowhead depicts neuronal abnormalities as evidenced by cytoplasmic and nuclear swelling of a pontine neuron and the arrow shows an incipient nuclear NI. ( I ) Arrow depicts pontine neuron with nuclear NI. ( J ) Arrow shows pontine neuron including both nuclear and cytoplasmic NI, arrowhead shows GCI. ( K ) Affected neuron (arrow) is increasingly surrounded by GCI. ( L ) After neuronal degeneration, large cytoplasmic NI is observed free in the extracellular space. All scale bars in this figure represent 20 µm.
    Figure Legend Snippet: Morphology and timeline of glial and neuronal α-syn aggregation in multiple system atrophy of the cerebellar type (MSA-C). Here and in the subsequent two figures we show images of 70-µm-thick sections because they were used to enable to see the histology and pathology in a more three-dimensional manner than conventional 6-µm-thick sections wherein objects have a more two-dimensional appearance. Hence, this figure shows a richer morphology of α-syn aggregation in the inferior olive (IO) ( A – G ) and the pontine nuclei ( H – L ) as depicted by Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry. ( A ) The most frequent pathology in MSA-C consisted of α-syn-positive glial cytoplasmic inclusions (GCIs; arrowheads), whereas α-syn-positive Nis (arrow) were rare. GCIs frequently were seen in oligodendroglial cells with a swollen nucleus and expanded cytoplasm. ( B ) Nis were often seen in association with neurons that showed cytoplasmic and nuclear swelling as well as a loosening of cytoplasmic lipofuscin pigment and the arrow identifies swollen cell of the IO, arrowhead shows enlarged nucleus. ( C ) This may represent changes that are followed by the development of α-syn inclusions (arrow), and, consecutively, by the occurrence of increasingly bulky cytoplasmic neuronal inclusion (NI) ( D ) and the arrow depicts a neuron with both nuclear and cytoplasmic NIs, arrowhead shows GCI). ( E, F ) Cytoplasmic NIs (as shown by arrow in E ) increased to fill most of the neuronal perikarya. In parallel, neurons became surrounded by an increasing numbers of neuritic α-syn inclusions (NRIs), presumablly in dendrites. ( G ) Finally, neuronal loss became apparent by free lipofuscin pigment remnants in the extracellular space. ( H ) Arrowhead depicts neuronal abnormalities as evidenced by cytoplasmic and nuclear swelling of a pontine neuron and the arrow shows an incipient nuclear NI. ( I ) Arrow depicts pontine neuron with nuclear NI. ( J ) Arrow shows pontine neuron including both nuclear and cytoplasmic NI, arrowhead shows GCI. ( K ) Affected neuron (arrow) is increasingly surrounded by GCI. ( L ) After neuronal degeneration, large cytoplasmic NI is observed free in the extracellular space. All scale bars in this figure represent 20 µm.

    Techniques Used: Staining, Immunohistochemistry

    α-syn pathology in the cerebellum of multiple system atrophy of the cerebellar type. ( A ) Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry (IHC) [pigment-Nissl (PN) + α-syn] depicts the selective pattern of cerebellar involvement by α-syn pathology and neuronal loss: glial cytoplasmic inclusions (GCIs) most severely affect subcortical white matter (SWM), whereas the deep white matter (DWM) surrounding the dentate nucleus (indicated by arrowheads) is much less affected. Mild GCI pathology can be detected in the granular layer (GL), whereas the molecular layer (MOL) remains free of α-syn inclusions. ( B, C ) PN + α-syn IHC shows more detailed view of GCI (examples shown by arrowheads) in SWM and GL, whereas the ML is unaffected. ( D ) Myelin stain shows severe demyelination of SWM, whereas DWM surrounding dentate nucleus (arrowheads) is well preserved. ( E ) Combined Campbell-Switzer silver staining (CS) and α-syn IHC shows GCI that are argyrophilic (arrow) and not argyrophilic (arrowhead) in SWM of cerebellum. ( F, G ) Combined CS and myelin staining show spatial relation of GCI (arrowhead) to myelinated axons (arrow), and the asterisk in G indicates a Purkinje cell (PC). ( H ) Combined CS and myelin staining shows a GCI (arrowhead) and myelinated axon (arrow) that is ensheathed by argyrophilic processes, most likely oligodendroglial processes. ( I ) Combined CS + PN staining shows loss of PCs in of cerebellar cortex (area indicated by arrowhead). ( J ) Provides more detailed view of i) showing PCs (example depicted by arrow), area with PC loss (arrowhead) and swelling of PC axon (‘torpedo’, indicated by asterisk). ( K ) Combined CS + myelin staining shows multiple torpedoes (asterisks) of proximal PC (arrow) axons; asterisk indicates GCI in subcortical white matter. ( L ) Combined CS + myelin staining shows PC (arrow) with distortion of dendrites (arrowheads) and axonal swelling (asterisk). Scale Bar is equivalent to 1 mm in A and D , 200 µm in B, F, G , and K , 500 µm in I , 100 µm in C, E , and M , and 50 µm in H .
    Figure Legend Snippet: α-syn pathology in the cerebellum of multiple system atrophy of the cerebellar type. ( A ) Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry (IHC) [pigment-Nissl (PN) + α-syn] depicts the selective pattern of cerebellar involvement by α-syn pathology and neuronal loss: glial cytoplasmic inclusions (GCIs) most severely affect subcortical white matter (SWM), whereas the deep white matter (DWM) surrounding the dentate nucleus (indicated by arrowheads) is much less affected. Mild GCI pathology can be detected in the granular layer (GL), whereas the molecular layer (MOL) remains free of α-syn inclusions. ( B, C ) PN + α-syn IHC shows more detailed view of GCI (examples shown by arrowheads) in SWM and GL, whereas the ML is unaffected. ( D ) Myelin stain shows severe demyelination of SWM, whereas DWM surrounding dentate nucleus (arrowheads) is well preserved. ( E ) Combined Campbell-Switzer silver staining (CS) and α-syn IHC shows GCI that are argyrophilic (arrow) and not argyrophilic (arrowhead) in SWM of cerebellum. ( F, G ) Combined CS and myelin staining show spatial relation of GCI (arrowhead) to myelinated axons (arrow), and the asterisk in G indicates a Purkinje cell (PC). ( H ) Combined CS and myelin staining shows a GCI (arrowhead) and myelinated axon (arrow) that is ensheathed by argyrophilic processes, most likely oligodendroglial processes. ( I ) Combined CS + PN staining shows loss of PCs in of cerebellar cortex (area indicated by arrowhead). ( J ) Provides more detailed view of i) showing PCs (example depicted by arrow), area with PC loss (arrowhead) and swelling of PC axon (‘torpedo’, indicated by asterisk). ( K ) Combined CS + myelin staining shows multiple torpedoes (asterisks) of proximal PC (arrow) axons; asterisk indicates GCI in subcortical white matter. ( L ) Combined CS + myelin staining shows PC (arrow) with distortion of dendrites (arrowheads) and axonal swelling (asterisk). Scale Bar is equivalent to 1 mm in A and D , 200 µm in B, F, G , and K , 500 µm in I , 100 µm in C, E , and M , and 50 µm in H .

    Techniques Used: Staining, Immunohistochemistry, Silver Staining

    7) Product Images from "Pyramidal Neurons Are “Neurogenic Hubs” in the Neurovascular Coupling Response to Whisker Stimulation"

    Article Title: Pyramidal Neurons Are “Neurogenic Hubs” in the Neurovascular Coupling Response to Whisker Stimulation

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4943-10.2011

    Distribution of double-immunostained c-Fos nuclei in cells identified with markers of pyramidal cells and interneurons in the stimulated contralateral barrel cortex. A , Distribution of c-Fos-positive COX-2 pyramidal cells in superficial layers of the contralateral somatosensory cortex. B , Higher magnification of c-Fos-positive COX-2 pyramidal cells (black arrows) in layers II/III of the activated barrel cortex. Several COX-2 pyramidal cells are not double stained for c-Fos (open arrow). C , COX-1 immunoreactivity was limited to microglial cells that did not exhibit c-Fos-stained nuclei (open arrows). Among the subsets of interneurons that stained positively for c-Fos (black arrows) were those that colocalized VIP ( D ) and ChAT ( E ), but not SOM or PV (open arrows in F or G ). H , Quantitative analysis of specifically labeled c-Fos-positive COX-2 pyramidal cells and subgroups of GABA interneurons in layers II–IV of the contralateral barrel cortex. * p
    Figure Legend Snippet: Distribution of double-immunostained c-Fos nuclei in cells identified with markers of pyramidal cells and interneurons in the stimulated contralateral barrel cortex. A , Distribution of c-Fos-positive COX-2 pyramidal cells in superficial layers of the contralateral somatosensory cortex. B , Higher magnification of c-Fos-positive COX-2 pyramidal cells (black arrows) in layers II/III of the activated barrel cortex. Several COX-2 pyramidal cells are not double stained for c-Fos (open arrow). C , COX-1 immunoreactivity was limited to microglial cells that did not exhibit c-Fos-stained nuclei (open arrows). Among the subsets of interneurons that stained positively for c-Fos (black arrows) were those that colocalized VIP ( D ) and ChAT ( E ), but not SOM or PV (open arrows in F or G ). H , Quantitative analysis of specifically labeled c-Fos-positive COX-2 pyramidal cells and subgroups of GABA interneurons in layers II–IV of the contralateral barrel cortex. * p

    Techniques Used: Staining, Labeling

    8) Product Images from "Endothelial damage, vascular bagging and remodeling of the microvascular bed in human microangiopathy with deep white matter lesions"

    Article Title: Endothelial damage, vascular bagging and remodeling of the microvascular bed in human microangiopathy with deep white matter lesions

    Journal: Acta Neuropathologica Communications

    doi: 10.1186/s40478-018-0632-z

    Double- and triple-label immunohistochemistry (IHC) for UEA-l, COLL4, the plasma proteins fibrinogen (FIBR) or immunoglobulin G fraction (IgG) and the endothelial marker alkaline phosphatase protein (ALPL) in 7 μm thick paraffin sections. a - b The healthy capillary in the control white matter (Co) of a NoSVD case does not have vascular bags ( a ). Vascular bag (short thick arrow) in a SVD case with multiple layers of COLL4-positive membranes around the UEA-l-labeled endothelium (white arrowhead) of a small vessel (
    Figure Legend Snippet: Double- and triple-label immunohistochemistry (IHC) for UEA-l, COLL4, the plasma proteins fibrinogen (FIBR) or immunoglobulin G fraction (IgG) and the endothelial marker alkaline phosphatase protein (ALPL) in 7 μm thick paraffin sections. a - b The healthy capillary in the control white matter (Co) of a NoSVD case does not have vascular bags ( a ). Vascular bag (short thick arrow) in a SVD case with multiple layers of COLL4-positive membranes around the UEA-l-labeled endothelium (white arrowhead) of a small vessel (

    Techniques Used: Immunohistochemistry, Marker, Labeling

    9) Product Images from "Social isolation alters behavior, the gut-immune-brain axis, and neurochemical circuits in male and female prairie voles"

    Article Title: Social isolation alters behavior, the gut-immune-brain axis, and neurochemical circuits in male and female prairie voles

    Journal: Neurobiology of Stress

    doi: 10.1016/j.ynstr.2020.100278

    Social isolation alters Egr-1 staining in a sex- and brain region-specific manner. Isolated female prairie voles had significantly higher levels of Egr-1 in the NAcc. Social isolation was associated with lower Egr-1 levels in the DR. Females had higher Egr-1 levels in the DR, but lower Egr-1 levels in the DG and in the PVN compared to males. Egr-1, early growth response protein 1, NAcc, nucleus accumbens, DR, dorsal raphe, DG, dentate gyrus of the hippocampus. Bars indicate mean ± SEM. * represents a main effect of sex, p
    Figure Legend Snippet: Social isolation alters Egr-1 staining in a sex- and brain region-specific manner. Isolated female prairie voles had significantly higher levels of Egr-1 in the NAcc. Social isolation was associated with lower Egr-1 levels in the DR. Females had higher Egr-1 levels in the DR, but lower Egr-1 levels in the DG and in the PVN compared to males. Egr-1, early growth response protein 1, NAcc, nucleus accumbens, DR, dorsal raphe, DG, dentate gyrus of the hippocampus. Bars indicate mean ± SEM. * represents a main effect of sex, p

    Techniques Used: Isolation, Staining

    Representative images of immunostaining of Egr-1, OT, and double-labeled Egr-1/OT cells in the PVN ( A-B ). Social isolation alters activation of OT system in a sex-dependent manner. Females had significantly lower levels of Egr-1 in the PVN compared to males (C). Isolated (Iso) females had significantly higher numbers of OT cells compared to cohoused (CH) control females (D) . Isolated females also had a significantly higher percentage of Egr-1 cells co-labeled for OT (E) . There were no significant differences in the percentage of OT cells co-labeled for Egr-1 ( F ). OT, oxytocin, Egr-1, early growth response protein 1, PVN, paraventricular nucleus of the hypothalamus. Bars indicate mean ± SEM. Bars with different letters differ significantly from each other. * represents p
    Figure Legend Snippet: Representative images of immunostaining of Egr-1, OT, and double-labeled Egr-1/OT cells in the PVN ( A-B ). Social isolation alters activation of OT system in a sex-dependent manner. Females had significantly lower levels of Egr-1 in the PVN compared to males (C). Isolated (Iso) females had significantly higher numbers of OT cells compared to cohoused (CH) control females (D) . Isolated females also had a significantly higher percentage of Egr-1 cells co-labeled for OT (E) . There were no significant differences in the percentage of OT cells co-labeled for Egr-1 ( F ). OT, oxytocin, Egr-1, early growth response protein 1, PVN, paraventricular nucleus of the hypothalamus. Bars indicate mean ± SEM. Bars with different letters differ significantly from each other. * represents p

    Techniques Used: Immunostaining, Labeling, Isolation, Activation Assay

    Representative images of immunostaining of Egr-1 in the NAcc, DR, and DG. Treatment and sex are depicted above each image. NAcc, nucleus accumbens, AC, anterior commissure, DR, dorsal raphe, DG, dentate gyrus of the hippocampus. Scale bar = 100 μm.
    Figure Legend Snippet: Representative images of immunostaining of Egr-1 in the NAcc, DR, and DG. Treatment and sex are depicted above each image. NAcc, nucleus accumbens, AC, anterior commissure, DR, dorsal raphe, DG, dentate gyrus of the hippocampus. Scale bar = 100 μm.

    Techniques Used: Immunostaining

    10) Product Images from "Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer’s disease"

    Article Title: Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer’s disease

    Journal: Neurobiology of disease

    doi: 10.1016/j.nbd.2018.05.021

    The expression of neurotrophin receptor and select downstream signaling molecule gene transcripts is equivalent in pS422+ nbM neurons during the progression of AD. Color-coded heatmap of the relative expression profiles for select transcripts in pS422+ nbM neurons aspirated from NCI, MCI, and AD cases (red to green = increasing mRNA levels). Quantitative analysis revealed no statistical differences in the expression levels of the transcripts examined in pS422+ nbM neurons derived from MCI or AD compared to NCI. This observation suggests that the pathological state of the neuron, not disease status, may drive changes in gene expression. Therefore, in the present analysis, we compared mRNA levels in individual pS422+, pS422+/TauC3+, and TauC3+ nbM neurons independent of clinical diagnosis. Abbreviations: Nrtk1, Nrtk2 , and Nrtk3 , neurotrophin tyrosine kinase receptor type 1 (TrkA), 2 (TrkB), 3 (TrkC); ECD, extracellular domain; TK, intracellular tyrosine kinase domain; Ngfr , nerve growth factor receptor (p75 NTR ); Mapk1 , mitogen-activated protein kinase 1 (extracellular signal-regulated kinase 2); Mapk3 , mitogen-activated protein kinase 3 (extracellular signal-regulated kinase 1); Creb1 , cAMP response element binding protein; Akt1 , Akt serine/threonine kinase 1 (protein kinase B); Prkca, Prkce, Prkci , protein kinase C alpha, epsilon, iota.
    Figure Legend Snippet: The expression of neurotrophin receptor and select downstream signaling molecule gene transcripts is equivalent in pS422+ nbM neurons during the progression of AD. Color-coded heatmap of the relative expression profiles for select transcripts in pS422+ nbM neurons aspirated from NCI, MCI, and AD cases (red to green = increasing mRNA levels). Quantitative analysis revealed no statistical differences in the expression levels of the transcripts examined in pS422+ nbM neurons derived from MCI or AD compared to NCI. This observation suggests that the pathological state of the neuron, not disease status, may drive changes in gene expression. Therefore, in the present analysis, we compared mRNA levels in individual pS422+, pS422+/TauC3+, and TauC3+ nbM neurons independent of clinical diagnosis. Abbreviations: Nrtk1, Nrtk2 , and Nrtk3 , neurotrophin tyrosine kinase receptor type 1 (TrkA), 2 (TrkB), 3 (TrkC); ECD, extracellular domain; TK, intracellular tyrosine kinase domain; Ngfr , nerve growth factor receptor (p75 NTR ); Mapk1 , mitogen-activated protein kinase 1 (extracellular signal-regulated kinase 2); Mapk3 , mitogen-activated protein kinase 3 (extracellular signal-regulated kinase 1); Creb1 , cAMP response element binding protein; Akt1 , Akt serine/threonine kinase 1 (protein kinase B); Prkca, Prkce, Prkci , protein kinase C alpha, epsilon, iota.

    Techniques Used: Expressing, Derivative Assay, Binding Assay

    Phenotypic characterization of NFT evolution with pS422 and TauC3 immunoreactivity in nbM neurons. (A–G) Tissue sections from the nbM of a representative AD case. (A) Cholinergic neurons in the nbM can be identified phenotypically by expression of the pan-neurotrophin (p75 NTR ) receptor. A tissue section from a consecutive series was immunostained with p75 NTR (brown) and pS422 (blue) to confirm the location of the cholinergic nbM. (B) Low magnification view of the nbM subfield immunostained with pS422 (brown) and TauC3 (blue). (C) High magnification of pS422 and TauC3 pathology in boxed area from (B). A Nissl counterstain was used to identify nbM neurons lacking tau pathology (*). (D-G) Confocal microscopy was used to confirm the presence of three discrete populations of nbM neurons. (D) Low magnification view of nbM subfield. (E–G) High magnification of boxed area from (D) identify pS422 (E), TauC3 (F), and overlay (G). Single arrowhead indicates a pS422+ nbM neuron, double arrowheads indicate a TauC3+ nbM neuron, and arrow indicates a pS422+/TauC3+ nbM neuron (colocalization appears yellow). Scale bar in A, 100 μm for A–B; scale bar in C, 50 μm for C; scale bar in D, 100 μm for D; scale bar in G, 50 μm for E–G.
    Figure Legend Snippet: Phenotypic characterization of NFT evolution with pS422 and TauC3 immunoreactivity in nbM neurons. (A–G) Tissue sections from the nbM of a representative AD case. (A) Cholinergic neurons in the nbM can be identified phenotypically by expression of the pan-neurotrophin (p75 NTR ) receptor. A tissue section from a consecutive series was immunostained with p75 NTR (brown) and pS422 (blue) to confirm the location of the cholinergic nbM. (B) Low magnification view of the nbM subfield immunostained with pS422 (brown) and TauC3 (blue). (C) High magnification of pS422 and TauC3 pathology in boxed area from (B). A Nissl counterstain was used to identify nbM neurons lacking tau pathology (*). (D-G) Confocal microscopy was used to confirm the presence of three discrete populations of nbM neurons. (D) Low magnification view of nbM subfield. (E–G) High magnification of boxed area from (D) identify pS422 (E), TauC3 (F), and overlay (G). Single arrowhead indicates a pS422+ nbM neuron, double arrowheads indicate a TauC3+ nbM neuron, and arrow indicates a pS422+/TauC3+ nbM neuron (colocalization appears yellow). Scale bar in A, 100 μm for A–B; scale bar in C, 50 μm for C; scale bar in D, 100 μm for D; scale bar in G, 50 μm for E–G.

    Techniques Used: Expressing, Confocal Microscopy

    Neurotrophin receptor and select downstream signaling molecule mRNAs are dysregulated during the progression of NFT maturation. Heatmap of relative mRNA expression levels of neurotrophin receptors and downstream signaling molecules in pS422+, pS422+/TauC3+, and TauC3+ nbM neurons compared to unlabeled nbM neurons (red to green = increasing mRNA levels). Quantitative analysis revealed downregulated expression of Nrtk1-3 transcripts as well as Akt1 and Prkce in pS422+ nbM neurons as compared to unlabeled control neurons. Appearance of the late stage neoepitope TauC3 was associated with downregulation of the Ngfr transcript and upregulation of the Prkca transcript. a, unlabeled > pS422, p
    Figure Legend Snippet: Neurotrophin receptor and select downstream signaling molecule mRNAs are dysregulated during the progression of NFT maturation. Heatmap of relative mRNA expression levels of neurotrophin receptors and downstream signaling molecules in pS422+, pS422+/TauC3+, and TauC3+ nbM neurons compared to unlabeled nbM neurons (red to green = increasing mRNA levels). Quantitative analysis revealed downregulated expression of Nrtk1-3 transcripts as well as Akt1 and Prkce in pS422+ nbM neurons as compared to unlabeled control neurons. Appearance of the late stage neoepitope TauC3 was associated with downregulation of the Ngfr transcript and upregulation of the Prkca transcript. a, unlabeled > pS422, p

    Techniques Used: Expressing

    Select cholinergic markers are dysregulated during the development of NFTs in nbM neurons. Heatmap of relative expression levels of cholinergic neuronal markers in pS422+, pS422+/TauC3+, and TauC3+ NB neurons compared to unlabeled control neurons (red to green = increasing mRNA levels). Quantitative analysis revealed upregulation of the Chrna7 transcript and downregulation of the Chrnb2 transcript following the appearance of the TauC3 epitope. Abbreviations: Chat choline acetyltransferase; Slcl8a3 , vesicular acetylcholine transporter; Ache , acetylcholinesterase; Bche , butyrylcholinesterase; Chrm1, Chrm2 , cholinergic receptor, muscarinic 1, 2; Chrna7, Chrna4, Chrnb2 , cholinergic receptor, nicotinic, alpha polypeptide 7, alpha polypeptide 4, beta polypeptide 2. a, pS422
    Figure Legend Snippet: Select cholinergic markers are dysregulated during the development of NFTs in nbM neurons. Heatmap of relative expression levels of cholinergic neuronal markers in pS422+, pS422+/TauC3+, and TauC3+ NB neurons compared to unlabeled control neurons (red to green = increasing mRNA levels). Quantitative analysis revealed upregulation of the Chrna7 transcript and downregulation of the Chrnb2 transcript following the appearance of the TauC3 epitope. Abbreviations: Chat choline acetyltransferase; Slcl8a3 , vesicular acetylcholine transporter; Ache , acetylcholinesterase; Bche , butyrylcholinesterase; Chrm1, Chrm2 , cholinergic receptor, muscarinic 1, 2; Chrna7, Chrna4, Chrnb2 , cholinergic receptor, nicotinic, alpha polypeptide 7, alpha polypeptide 4, beta polypeptide 2. a, pS422

    Techniques Used: Expressing

    11) Product Images from "Reactivating the extracellular matrix synthesis of sulfated glycosaminoglycans and proteoglycans to improve the human skin aspect and its mechanical properties"

    Article Title: Reactivating the extracellular matrix synthesis of sulfated glycosaminoglycans and proteoglycans to improve the human skin aspect and its mechanical properties

    Journal: Clinical, Cosmetic and Investigational Dermatology

    doi: 10.2147/CCID.S116548

    ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to CD34 marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values
    Figure Legend Snippet: ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to CD34 marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values

    Techniques Used: Immunostaining, Marker

    12) Product Images from "Pyramidal Neurons Are “Neurogenic Hubs” in the Neurovascular Coupling Response to Whisker Stimulation"

    Article Title: Pyramidal Neurons Are “Neurogenic Hubs” in the Neurovascular Coupling Response to Whisker Stimulation

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4943-10.2011

    Distribution of double-immunostained c-Fos nuclei in cells identified with markers of pyramidal cells and interneurons in the stimulated contralateral barrel cortex. A , Distribution of c-Fos-positive COX-2 pyramidal cells in superficial layers of the contralateral somatosensory cortex. B , Higher magnification of c-Fos-positive COX-2 pyramidal cells (black arrows) in layers II/III of the activated barrel cortex. Several COX-2 pyramidal cells are not double stained for c-Fos (open arrow). C , COX-1 immunoreactivity was limited to microglial cells that did not exhibit c-Fos-stained nuclei (open arrows). Among the subsets of interneurons that stained positively for c-Fos (black arrows) were those that colocalized VIP ( D ) and ChAT ( E ), but not SOM or PV (open arrows in F or G ). H , Quantitative analysis of specifically labeled c-Fos-positive COX-2 pyramidal cells and subgroups of GABA interneurons in layers II–IV of the contralateral barrel cortex. * p
    Figure Legend Snippet: Distribution of double-immunostained c-Fos nuclei in cells identified with markers of pyramidal cells and interneurons in the stimulated contralateral barrel cortex. A , Distribution of c-Fos-positive COX-2 pyramidal cells in superficial layers of the contralateral somatosensory cortex. B , Higher magnification of c-Fos-positive COX-2 pyramidal cells (black arrows) in layers II/III of the activated barrel cortex. Several COX-2 pyramidal cells are not double stained for c-Fos (open arrow). C , COX-1 immunoreactivity was limited to microglial cells that did not exhibit c-Fos-stained nuclei (open arrows). Among the subsets of interneurons that stained positively for c-Fos (black arrows) were those that colocalized VIP ( D ) and ChAT ( E ), but not SOM or PV (open arrows in F or G ). H , Quantitative analysis of specifically labeled c-Fos-positive COX-2 pyramidal cells and subgroups of GABA interneurons in layers II–IV of the contralateral barrel cortex. * p

    Techniques Used: Staining, Labeling

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    Staining:

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    Article Title: Reactivating the extracellular matrix synthesis of sulfated glycosaminoglycans and proteoglycans to improve the human skin aspect and its mechanical properties
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    Immunohistochemistry:

    Article Title: Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type
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    Incubation:

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    Article Title: Exposure to an open-field arena increases c-Fos expression in a subpopulation of neurons in the dorsal raphe nucleus, including neurons projecting to the basolateral amygdaloid complex
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    Article Snippet: .. On the third day, sections were washed four times for 5 min in 0.1 M PB, incubated with a biotinylated secondary antibody (biotinylated donkey anti-goat; 1:500; Jackson ImmunoResearch, 705-065-147; or biotinylated donkey anti-rabbit; 1:500; Jackson ImmunoResearch, 711-065-152) for 1 hour at RT, followed by incubation in avidin-biotin-peroxidase solution (VECTASTAIN Elite ABC HRP Kit, Vector Laboratories, PK-6100) for 1 hour at RT and initiation of color reaction with a peroxidase substrate kit (SG Peroxidase Substrate Kit, Vector Laboratories, SK-4700). .. All stained sections were mounted, dehydrated, and coverslipped with mounting medium (EUKITT medium, Sigma-Aldrich, catalog no. 03989).

    Plasmid Preparation:

    Article Title: Early Neuronal and Glial Fate Restriction of Embryonic Neural Stem Cells
    Article Snippet: .. We further used the ABC Vectastain kit for DAB detection as well as the Substrate Kit Vector SG (Vector Laboratories, West Grove, CA). .. Immunolabeling of cultures or tissue sections and detection of β-galactosidase enzymatic activity were as described previously ( )., , and were obtained using a confocal laser microscope (Leica, Nussloch, Germany), and the software used was Leica lite, NIH ImageJ, and Photoshop (Adobe Systems, San Jose, CA).

    Article Title: Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type
    Article Snippet: .. Double-labelling IHC was performed on selected 70 µm sections using the α-syn antibody described above together with the Vector Labs, Burlingame, CA, USA, SG (SK-4700; Vector) blue chromogen and the SMI-311 mab (1:1000; Covance, Princeton, NJ, USA), the rabbit polyclonal antibody (pab) for oligodendrocyte-specific protein (1:400; Abcam, Cambridge, UK) and the anti-oligo2 antibody (1:400; Millipore, Billerica, MA, USA). .. For double-labelling immunofluorescence (IF), 15 µm frozen sections were microwaved in 10 mM citrate buffer, pH 6.0, for 15 min; blocked in 2% FBS with 0.1 M Tris and incubated with the mouse mab syn-506 (specific for α-synuclein, amino acids 1–89; 1:10 000; CNDR [ ]) and rabbit pab Olig2 (specific for oligodendrocytes; 1:250; Millipore), rat mab TA51 (specific for phosphorylated heavy and medium molecular weight neurofilament; 1:10; CNDR [ ]), rabbit pab NFL1/2 (specific for low molecular weight neurofilament; 1:1000; CNDR [ ]) or rabbit pab 17028 (a microtubule associated protein 2 specific antibody; 1:500; CNDR, unpubl. data), followed by a goat anti-mouse Alexa Fluor® 546-labelled IgG (H+L) antibody, a goat anti-rabbit Alexa Fluor® 588-labelled IgG (H+L) antibody and a goat anti-rat Alexa Fluor® 588-labeld IgG (H+L) antibody (1:500; Invitrogen, Carlsbad, CA, USA) in 2%FBS in 0.1 M Tris.

    Article Title: Exposure to an open-field arena increases c-Fos expression in a subpopulation of neurons in the dorsal raphe nucleus, including neurons projecting to the basolateral amygdaloid complex
    Article Snippet: .. After 15 h, tissue was washed twice in 0.3% PBST followed by incubation with a biotinylated swine anti-rabbit polyclonal antibody (Cat. No. E0353, 1:200; DakoCytomation Ltd, Cambridgeshire, UK) in 0.1% PBST for 90 min. Tissue was washed twice in 0.3% PBST followed by incubation with an avidin-biotin-peroxidase complex (Elite ABC reagent, Cat. No. PK-6100, 1:200; Vector Laboratories, Peterborough, UK) in 0.1% PBST for 90 min. Last, tissue was washed in 0.3% PBST, then in PBS, and incubated in peroxidase chromogen substrate (Vector SG; Vector Laboratories; Cat. No. SK4700; diluted as recommended by the vendor) in PBS for 23 min. After the chromogen reaction, tissue was immediately washed in PBS, 1% hydrogen peroxide in PBS, PBS, and 0.3% PBST respectively. .. Then, slices were incubated with sheep anti-TrpOH antibody in 0.1% PBST for 18 h. All subsequent steps were identical to those described above used for the immuno-peroxidase localization of c-Fos-immunoreactivity, except for the secondary antibody and chromogen reaction steps; these used a rabbit anti-sheep secondary antibody (Cat. No. PK-6106, 1:200, Vector Laboratories Ltd.), and a peroxidase chromogen substrate solution consisting of 0.01% 3,3′-diaminobenzidine tetrahydrochloride (DAB) and 0.0015% hydrogen peroxide in PBS (20 min).

    Article Title: HDAC2 dysregulation in the nucleus basalis of Meynert during the progression of Alzheimer’s disease
    Article Snippet: .. All tissue was developed with the Vector SG Substrate Kit (blue-gray reaction product, Vector Laboratories). .. Immunohistochemical controls were performed to rule out any cross-reactivity or non-specific staining, including omission of the primary and secondary antibodies.

    Avidin-Biotin Assay:

    Article Title: Exposure to an open-field arena increases c-Fos expression in a subpopulation of neurons in the dorsal raphe nucleus, including neurons projecting to the basolateral amygdaloid complex
    Article Snippet: .. After 15 h, tissue was washed twice in 0.3% PBST followed by incubation with a biotinylated swine anti-rabbit polyclonal antibody (Cat. No. E0353, 1:200; DakoCytomation Ltd, Cambridgeshire, UK) in 0.1% PBST for 90 min. Tissue was washed twice in 0.3% PBST followed by incubation with an avidin-biotin-peroxidase complex (Elite ABC reagent, Cat. No. PK-6100, 1:200; Vector Laboratories, Peterborough, UK) in 0.1% PBST for 90 min. Last, tissue was washed in 0.3% PBST, then in PBS, and incubated in peroxidase chromogen substrate (Vector SG; Vector Laboratories; Cat. No. SK4700; diluted as recommended by the vendor) in PBS for 23 min. After the chromogen reaction, tissue was immediately washed in PBS, 1% hydrogen peroxide in PBS, PBS, and 0.3% PBST respectively. .. Then, slices were incubated with sheep anti-TrpOH antibody in 0.1% PBST for 18 h. All subsequent steps were identical to those described above used for the immuno-peroxidase localization of c-Fos-immunoreactivity, except for the secondary antibody and chromogen reaction steps; these used a rabbit anti-sheep secondary antibody (Cat. No. PK-6106, 1:200, Vector Laboratories Ltd.), and a peroxidase chromogen substrate solution consisting of 0.01% 3,3′-diaminobenzidine tetrahydrochloride (DAB) and 0.0015% hydrogen peroxide in PBS (20 min).

    Article Title: Determinants of seeding and spreading of α-synuclein pathology in the brain
    Article Snippet: .. On the third day, sections were washed four times for 5 min in 0.1 M PB, incubated with a biotinylated secondary antibody (biotinylated donkey anti-goat; 1:500; Jackson ImmunoResearch, 705-065-147; or biotinylated donkey anti-rabbit; 1:500; Jackson ImmunoResearch, 711-065-152) for 1 hour at RT, followed by incubation in avidin-biotin-peroxidase solution (VECTASTAIN Elite ABC HRP Kit, Vector Laboratories, PK-6100) for 1 hour at RT and initiation of color reaction with a peroxidase substrate kit (SG Peroxidase Substrate Kit, Vector Laboratories, SK-4700). .. All stained sections were mounted, dehydrated, and coverslipped with mounting medium (EUKITT medium, Sigma-Aldrich, catalog no. 03989).

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    Vector Laboratories antibody anti cd34
    ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to <t>CD34</t> marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values
    Antibody Anti Cd34, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 97/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    antibody anti cd34 - by Bioz Stars, 2021-02
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    ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to CD34 marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values

    Journal: Clinical, Cosmetic and Investigational Dermatology

    Article Title: Reactivating the extracellular matrix synthesis of sulfated glycosaminoglycans and proteoglycans to improve the human skin aspect and its mechanical properties

    doi: 10.2147/CCID.S116548

    Figure Lengend Snippet: ( A ) Immunostaining of cells only positive to PDGFR alpha merker (red signal is indicated by black arrows). ( B ) Immunostaining of cells only positive to CD34 marker (blue signal is indicated by black arrow). ( C ) Immunostaining of cells positive to both markers PDGFR alpha and CD34 (superposition of red and blue signals is indicated by black arrow). Notes: ( D ) A chart representative of the percentage of positive cells to both CD34 and PDGFR alpha found in skin explants treated with or without the composition As shown in D , a statistically significant increase by 26% of the percentage of cells double marked with CD34 and PDGFR was observed in skin explants treated with the composition in comparison to untreated skin explants. The statistical significance was determined by Student’s t -test and represented by * for p -values

    Article Snippet: Successively, the slides were incubated overnight at room temperature with the antibody anti-CD34 and revealed by SG (blue staining, Ref. SK-4700; Vector Laboratories).

    Techniques: Immunostaining, Marker

    Morphology and timeline of glial and neuronal α-syn aggregation in multiple system atrophy of the cerebellar type (MSA-C). Here and in the subsequent two figures we show images of 70-µm-thick sections because they were used to enable to see the histology and pathology in a more three-dimensional manner than conventional 6-µm-thick sections wherein objects have a more two-dimensional appearance. Hence, this figure shows a richer morphology of α-syn aggregation in the inferior olive (IO) ( A – G ) and the pontine nuclei ( H – L ) as depicted by Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry. ( A ) The most frequent pathology in MSA-C consisted of α-syn-positive glial cytoplasmic inclusions (GCIs; arrowheads), whereas α-syn-positive Nis (arrow) were rare. GCIs frequently were seen in oligodendroglial cells with a swollen nucleus and expanded cytoplasm. ( B ) Nis were often seen in association with neurons that showed cytoplasmic and nuclear swelling as well as a loosening of cytoplasmic lipofuscin pigment and the arrow identifies swollen cell of the IO, arrowhead shows enlarged nucleus. ( C ) This may represent changes that are followed by the development of α-syn inclusions (arrow), and, consecutively, by the occurrence of increasingly bulky cytoplasmic neuronal inclusion (NI) ( D ) and the arrow depicts a neuron with both nuclear and cytoplasmic NIs, arrowhead shows GCI). ( E, F ) Cytoplasmic NIs (as shown by arrow in E ) increased to fill most of the neuronal perikarya. In parallel, neurons became surrounded by an increasing numbers of neuritic α-syn inclusions (NRIs), presumablly in dendrites. ( G ) Finally, neuronal loss became apparent by free lipofuscin pigment remnants in the extracellular space. ( H ) Arrowhead depicts neuronal abnormalities as evidenced by cytoplasmic and nuclear swelling of a pontine neuron and the arrow shows an incipient nuclear NI. ( I ) Arrow depicts pontine neuron with nuclear NI. ( J ) Arrow shows pontine neuron including both nuclear and cytoplasmic NI, arrowhead shows GCI. ( K ) Affected neuron (arrow) is increasingly surrounded by GCI. ( L ) After neuronal degeneration, large cytoplasmic NI is observed free in the extracellular space. All scale bars in this figure represent 20 µm.

    Journal: Neuropathology and applied neurobiology

    Article Title: Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type

    doi: 10.1111/nan.12362

    Figure Lengend Snippet: Morphology and timeline of glial and neuronal α-syn aggregation in multiple system atrophy of the cerebellar type (MSA-C). Here and in the subsequent two figures we show images of 70-µm-thick sections because they were used to enable to see the histology and pathology in a more three-dimensional manner than conventional 6-µm-thick sections wherein objects have a more two-dimensional appearance. Hence, this figure shows a richer morphology of α-syn aggregation in the inferior olive (IO) ( A – G ) and the pontine nuclei ( H – L ) as depicted by Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry. ( A ) The most frequent pathology in MSA-C consisted of α-syn-positive glial cytoplasmic inclusions (GCIs; arrowheads), whereas α-syn-positive Nis (arrow) were rare. GCIs frequently were seen in oligodendroglial cells with a swollen nucleus and expanded cytoplasm. ( B ) Nis were often seen in association with neurons that showed cytoplasmic and nuclear swelling as well as a loosening of cytoplasmic lipofuscin pigment and the arrow identifies swollen cell of the IO, arrowhead shows enlarged nucleus. ( C ) This may represent changes that are followed by the development of α-syn inclusions (arrow), and, consecutively, by the occurrence of increasingly bulky cytoplasmic neuronal inclusion (NI) ( D ) and the arrow depicts a neuron with both nuclear and cytoplasmic NIs, arrowhead shows GCI). ( E, F ) Cytoplasmic NIs (as shown by arrow in E ) increased to fill most of the neuronal perikarya. In parallel, neurons became surrounded by an increasing numbers of neuritic α-syn inclusions (NRIs), presumablly in dendrites. ( G ) Finally, neuronal loss became apparent by free lipofuscin pigment remnants in the extracellular space. ( H ) Arrowhead depicts neuronal abnormalities as evidenced by cytoplasmic and nuclear swelling of a pontine neuron and the arrow shows an incipient nuclear NI. ( I ) Arrow depicts pontine neuron with nuclear NI. ( J ) Arrow shows pontine neuron including both nuclear and cytoplasmic NI, arrowhead shows GCI. ( K ) Affected neuron (arrow) is increasingly surrounded by GCI. ( L ) After neuronal degeneration, large cytoplasmic NI is observed free in the extracellular space. All scale bars in this figure represent 20 µm.

    Article Snippet: Double-labelling IHC was performed on selected 70 µm sections using the α-syn antibody described above together with the Vector Labs, Burlingame, CA, USA, SG (SK-4700; Vector) blue chromogen and the SMI-311 mab (1:1000; Covance, Princeton, NJ, USA), the rabbit polyclonal antibody (pab) for oligodendrocyte-specific protein (1:400; Abcam, Cambridge, UK) and the anti-oligo2 antibody (1:400; Millipore, Billerica, MA, USA).

    Techniques: Staining, Immunohistochemistry

    α-syn pathology in the cerebellum of multiple system atrophy of the cerebellar type. ( A ) Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry (IHC) [pigment-Nissl (PN) + α-syn] depicts the selective pattern of cerebellar involvement by α-syn pathology and neuronal loss: glial cytoplasmic inclusions (GCIs) most severely affect subcortical white matter (SWM), whereas the deep white matter (DWM) surrounding the dentate nucleus (indicated by arrowheads) is much less affected. Mild GCI pathology can be detected in the granular layer (GL), whereas the molecular layer (MOL) remains free of α-syn inclusions. ( B, C ) PN + α-syn IHC shows more detailed view of GCI (examples shown by arrowheads) in SWM and GL, whereas the ML is unaffected. ( D ) Myelin stain shows severe demyelination of SWM, whereas DWM surrounding dentate nucleus (arrowheads) is well preserved. ( E ) Combined Campbell-Switzer silver staining (CS) and α-syn IHC shows GCI that are argyrophilic (arrow) and not argyrophilic (arrowhead) in SWM of cerebellum. ( F, G ) Combined CS and myelin staining show spatial relation of GCI (arrowhead) to myelinated axons (arrow), and the asterisk in G indicates a Purkinje cell (PC). ( H ) Combined CS and myelin staining shows a GCI (arrowhead) and myelinated axon (arrow) that is ensheathed by argyrophilic processes, most likely oligodendroglial processes. ( I ) Combined CS + PN staining shows loss of PCs in of cerebellar cortex (area indicated by arrowhead). ( J ) Provides more detailed view of i) showing PCs (example depicted by arrow), area with PC loss (arrowhead) and swelling of PC axon (‘torpedo’, indicated by asterisk). ( K ) Combined CS + myelin staining shows multiple torpedoes (asterisks) of proximal PC (arrow) axons; asterisk indicates GCI in subcortical white matter. ( L ) Combined CS + myelin staining shows PC (arrow) with distortion of dendrites (arrowheads) and axonal swelling (asterisk). Scale Bar is equivalent to 1 mm in A and D , 200 µm in B, F, G , and K , 500 µm in I , 100 µm in C, E , and M , and 50 µm in H .

    Journal: Neuropathology and applied neurobiology

    Article Title: Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type

    doi: 10.1111/nan.12362

    Figure Lengend Snippet: α-syn pathology in the cerebellum of multiple system atrophy of the cerebellar type. ( A ) Darrow red aldehyde fuchsin staining combined with α-syn immunohistochemistry (IHC) [pigment-Nissl (PN) + α-syn] depicts the selective pattern of cerebellar involvement by α-syn pathology and neuronal loss: glial cytoplasmic inclusions (GCIs) most severely affect subcortical white matter (SWM), whereas the deep white matter (DWM) surrounding the dentate nucleus (indicated by arrowheads) is much less affected. Mild GCI pathology can be detected in the granular layer (GL), whereas the molecular layer (MOL) remains free of α-syn inclusions. ( B, C ) PN + α-syn IHC shows more detailed view of GCI (examples shown by arrowheads) in SWM and GL, whereas the ML is unaffected. ( D ) Myelin stain shows severe demyelination of SWM, whereas DWM surrounding dentate nucleus (arrowheads) is well preserved. ( E ) Combined Campbell-Switzer silver staining (CS) and α-syn IHC shows GCI that are argyrophilic (arrow) and not argyrophilic (arrowhead) in SWM of cerebellum. ( F, G ) Combined CS and myelin staining show spatial relation of GCI (arrowhead) to myelinated axons (arrow), and the asterisk in G indicates a Purkinje cell (PC). ( H ) Combined CS and myelin staining shows a GCI (arrowhead) and myelinated axon (arrow) that is ensheathed by argyrophilic processes, most likely oligodendroglial processes. ( I ) Combined CS + PN staining shows loss of PCs in of cerebellar cortex (area indicated by arrowhead). ( J ) Provides more detailed view of i) showing PCs (example depicted by arrow), area with PC loss (arrowhead) and swelling of PC axon (‘torpedo’, indicated by asterisk). ( K ) Combined CS + myelin staining shows multiple torpedoes (asterisks) of proximal PC (arrow) axons; asterisk indicates GCI in subcortical white matter. ( L ) Combined CS + myelin staining shows PC (arrow) with distortion of dendrites (arrowheads) and axonal swelling (asterisk). Scale Bar is equivalent to 1 mm in A and D , 200 µm in B, F, G , and K , 500 µm in I , 100 µm in C, E , and M , and 50 µm in H .

    Article Snippet: Double-labelling IHC was performed on selected 70 µm sections using the α-syn antibody described above together with the Vector Labs, Burlingame, CA, USA, SG (SK-4700; Vector) blue chromogen and the SMI-311 mab (1:1000; Covance, Princeton, NJ, USA), the rabbit polyclonal antibody (pab) for oligodendrocyte-specific protein (1:400; Abcam, Cambridge, UK) and the anti-oligo2 antibody (1:400; Millipore, Billerica, MA, USA).

    Techniques: Staining, Immunohistochemistry, Silver Staining