ArticleBrain research2008
Neuronal and astrocytic apoptosis after subarachnoid hemorrhage: a possible cause for poor prognosis.
Article in Brain research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 82 citations in OpenAlex.
- Effects of autolysis and prolonged formalin fixation on histomorphology and immunohistochemistry of normal canine brain tissue: an experimental study.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2024Article
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
- Neuroprotective Effects of Piceatannol on Olfactory Bulb Injury after Subarachnoid Hemorrhage.Molecular neurobiology · 2023Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- PTEN and AKT/GSK-3β/CRMP-2 signaling pathway are involved in neuronal apoptosis and axonal injury in early brain injury after SAH in rats.Genes & diseases · 2022Article
- The role of the astrocyte in subarachnoid hemorrhage and its therapeutic implications.Frontiers in immunology · 2022Review
- Irreversible Neuronal Damage Begins Just After Aneurysm Rupture in Poor-Grade Subarachnoid Hemorrhage Patients.Translational stroke research · 2021Article
- Microglia as target for anti-inflammatory approaches to prevent secondary brain injury after subarachnoid hemorrhage (SAH).Journal of neuroinflammation · 2021Article
- Attenuation in Proinflammatory Factors and Reduction in Neuronal Cell Apoptosis and Cerebral Vasospasm by Minocycline during Early Phase after Subarachnoid Hemorrhage in the Rat.BioMed research international · 2021Article
- Effect of astaxanthin on neuron damage, inflammatory factors expressions and oxidative stress in mice with subarachnoid hemorrhage.American journal of translational research · 2021Article
- Neuroprotective Effect of Ultrasound Triggered Astaxanthin Release Nanoparticles on Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in chemistry · 2021Article
- β-Caryophyllene Liposomes Attenuate Neurovascular Unit Damage After Subarachnoid Hemorrhage in Rats.Neurochemical research · 2020Article
- Neuroprotective roles of total flavones of Camellia on early brain injury andcognitive dysfunction following subarachnoid hemorrhage in rats.Metabolic brain disease · 2020Article
- Endoplasmic reticulum stress mediates cortical neuron apoptosis after experimental subarachnoid hemorrhage in rats.International journal of clinical and experimental pathology · 2020Article
- Innate immunity activation in the early brain injury period following subarachnoid hemorrhage.Journal of neuroinflammation · 2019Article
- Morphological Characteristics of Neuronal Death After Experimental Subarachnoid Hemorrhage in Mice Using Double Immunoenzymatic Technique.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Article
- Neuroinflammation and Microvascular Dysfunction After Experimental Subarachnoid Hemorrhage: Emerging Components of Early Brain Injury Related to Outcome.Neurocritical care · 2019Review
- Elucidating the novel biomarker and therapeutic potentials of High-mobility group box 1 in Subarachnoid hemorrhage: A review.AIMS neuroscience · 2019Review
- Receptor-Mediated Delivery of Astaxanthin-Loaded Nanoparticles to Neurons: An Enhanced Potential for Subarachnoid Hemorrhage Treatment.Frontiers in neuroscience · 2019Article
- Melatonin attenuates early brain injury after subarachnoid hemorrhage by the JAK-STAT signaling pathway.International journal of clinical and experimental pathology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Clinical evidence suggests that factors other than cerebral vasospasm, such as delayed neuronal and astrocytic cell death, may play a role in the poor prognosis of patients with subarachnoid hemorrhage (SAH). Here we examined this using immunohistochemistry and confocal microscopy in 3 different brain areas in a dog model of SAH. Using antibodies against neuronal marker neuronal nuclear protein (NeuN) and astrocyte marker glial fibrillary acidic protein (GFAP) in conjunction with apoptosis marker (cleaved caspase-3), we quantified neurons and astrocytes to monitor the degree of apoptosis in both groups. Experimental SAH group showed 44 +/- 1% caspase-3 positive neurons in comparison to the 2.0 +/- 0.1% in the control group (P < 0.001, 6 animals each group). For astrocytes, a total 25 +/- 1% were caspase-3 positive in day 7 SAH group, as compared to 0.40 +/- 0.01% for controls (P < 0.001). Regional analysis revealed that neuronal caspase-3 immunoreactivity in all 3 regions were significantly higher (P < 0.001) in SAH animals than that in the control animals. However, the analysis of total area, size and signal co-localization of GFAP with caspase-3 indicated that astrocytic reactivity and proliferation are seen primarily in the hippocampal area, with the least changes detectable in the brainstem. We conclude that in the dog model, there was a significant increase of neuronal and astrocytic cleaved caspase-3, possibly reflecting apoptosis, following SAH induction. These changes coupled with neurological deterioration seen in patients may present a possible reason for the poor outcome in SAH patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.