Source 1primary paper2012Asian Pacific Journal of Cancer Prevention
Toolkit/immunohistochemistry
immunohistochemistry
Also known as: IHC
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Immunohistochemistry is an antibody-based tissue staining assay used in the cited stroke study alongside transcriptomics and real-time polymerase chain reaction to examine post-stroke tissue in aged rats and post-stroke patients. In that context, it supported assessment of angiogenesis-related histological features such as vascular density after stroke.
Usefulness & Problems
Why this is useful
This assay is useful for visualizing tissue-associated biological features in situ using antibody staining. In the supplied evidence, it contributed histological assessment of post-stroke angiogenesis-related tissue changes when combined with molecular profiling approaches.
Problem solved
Immunohistochemistry helps address the problem of assessing tissue-level angiogenesis after stroke within intact specimens rather than relying only on transcript measurements. In the cited study context, it supported comparison of vascular density and related post-stroke tissue features between young and old rats and in post-stroke patient material.
Problem links
provides protein-level or histological evidence for the proposed Smad4-linked mechanism
LiteratureIt helps assess whether the protective pathway is associated with suppression of Smad4 expression.
Source:
It helps assess whether the protective pathway is associated with suppression of Smad4 expression.
provides tissue-based evidence that supports non-homogeneous astrocyte properties
LiteratureIt helps assess whether astrocyte properties vary across locations or conditions in situ.
Source:
It helps assess whether astrocyte properties vary across locations or conditions in situ.
supports anatomical and marker-based assessment of stress-associated cell subtype changes
LiteratureIt helps identify where and in which cell subtypes stress-associated molecular or phenotypic changes occur.
Source:
It helps identify where and in which cell subtypes stress-associated molecular or phenotypic changes occur.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete measurement method used to characterize an engineered system.
Mechanisms
antibody-based tissue stainingTarget processes
No target processes tagged yet.
Input: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: sensor
The available evidence indicates use of immunohistochemistry in combination with real-time polymerase chain reaction and stroke transcriptomics in aged rats and post-stroke patients. No further practical details are provided on fixation, antigen retrieval, detection chemistry, construct design, or required reagents beyond antibody-based tissue staining.
The supplied evidence does not specify the antibodies, antigens, staining protocol, quantification method, or imaging modality used for immunohistochemistry. It also does not provide performance metrics such as sensitivity, specificity, reproducibility, or independent benchmarking for this assay in the described application.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2review2023Frontiers in Neuroscience
Source 3primary paper2023
Source 4review2019Annual Review of Neuroscience
Source 5primary paper2026MED
Source 6primary paper2014Frontiers in Aging Neuroscience
Ranked Claims
CD44 and miR-146a reduce apoptosis in tendinopathic tenocytes and tendons by modulating the AKT/miR-146a/Smad4 signalling pathway.
By modulating the AKT/miR-146a/Smad4 signalling pathway, CD44 and miR-146a effectively reduce apoptosis in tendinopathic tenocytes and tendons.
Overexpression of CD44 and miR-146a reduces apoptosis in rat primary tendinopathic tenocytes compared with controls.
Overexpression of CD44 and miR-146a in tendinopathic tenocytes resulted in significantly reduced apoptosis compared to controls.
apoptosis significantly reduced compared to controls
The reviewed literature uses chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry approaches to investigate the role of specific cell subtypes in the stress response.
many studies have used state-of-the-art tools such as chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry to investigate the role of specific cell subtypes in the stress response
Recent availability of RNA sequencing, immunohistochemistry, electron microscopy, morphological reconstruction, and imaging data has challenged the view that astrocytes are a homogeneous population across the CNS.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
Approval Evidence
6 sources5 linked approval claimsfirst-pass slug immunohistochemistry
In situ hybridization (ISH) and immunohistochemistry (IHC) were performed to examine the pathway's effect on Smad4 expression in tendinopathic tenocytes and tendons.
Source:
many studies have used state-of-the-art tools such as ... immunohistochemistry to investigate the role of specific cell subtypes in the stress response
Source:
Using a combination of immunohistochemistry
Source:
this view has been challenged in the last few years with the availability of RNA sequencing, immunohistochemistry, electron microscopy, morphological reconstruction, and imaging data
Source:
by combining stroke transcriptomics with immunohistochemistry in aged rats and post-stroke patients
Source:
Using real time polymerase chain reaction and immunohistochemistry techniques
Source:
tool usage summarysupports
The reviewed literature uses chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry approaches to investigate the role of specific cell subtypes in the stress response.
many studies have used state-of-the-art tools such as chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry to investigate the role of specific cell subtypes in the stress response
Source:
field summarysupports
Recent availability of RNA sequencing, immunohistochemistry, electron microscopy, morphological reconstruction, and imaging data has challenged the view that astrocytes are a homogeneous population across the CNS.
Source:
comparative biological observationsupports
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Source:
comparative biological observationsupports
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
Source:
human observationsupports
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
Source:
Comparisons
Source-stated alternatives
ISH was used alongside IHC for Smad4-related pathway examination, while TUNEL was used for apoptosis assessment.; The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.; Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Source:
ISH was used alongside IHC for Smad4-related pathway examination, while TUNEL was used for apoptosis assessment.
Source:
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Source-backed strengths
The evidence shows that immunohistochemistry was integrated with real-time polymerase chain reaction and stroke transcriptomics, indicating utility as a complementary tissue-level assay in multimodal studies. In the cited work, it supported biological observations about vigorous angiogenesis after stroke and age-associated differences in vascular density by day 14.
Source:
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Source:
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Source:
However, the young rats had a higher vascular density by day 14 post-stroke.
Compared with chemogenetic circuit manipulation
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Compared with electron microscopy
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Compared with electrophysiology
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Compared with imaging
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Compared with imaging surveillance
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Compared with microscopy
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Compared with morphological reconstruction
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Compared with optogenetic
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
The abstract lists chemogenetic, optogenetic, genetic manipulation, electrophysiology, and pharmacology as other tools used in the same literature.
Compared with RNA sequencing
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Shared frame: source-stated alternative in extracted literature
Strengths here: used as a mechanistic readout in the study; presented as a state-of-the-art tool in the reviewed literature; named as one of the evidence streams supporting astrocyte diversity.
Relative tradeoffs: abstract does not specify antibody validation, quantification, or resolution of cell-type specificity; the abstract does not specify markers, throughput, or subtype resolution.
Source:
Other evidence streams named in the abstract include RNA sequencing, electron microscopy, morphological reconstruction, and imaging.
Ranked Citations
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