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Open Access Research Article Issue
No association of brain CT blend sign with functional outcomes in patients with spontaneous supratentorial intracerebral hemorrhage after craniotomy
Brain Hemorrhages 2025, 6(2): 69-75
Published: 09 August 2024
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Objective

This study retrospectively analyzed the association of blend sign with long-term outcomes in patients who underwent craniotomy following spontaneous supratentorial intracerebral hemorrhage.

Methods

A retrospective analysis was conducted on a cohort comprising 259 patients. Initially, patients were stratified into two groups: the blend sign group and the non-blend sign group. Subsequently, the neurological status of these patients was assessed using the NIHSS, GCS, and mRS following craniotomy. Furthermore, at six months post-craniotomy, patients were categorized into either the “good outcome group” or the “poor outcome group”. A multivariate regression analysis was applied to ascertain the independent correlation between the CT blend sign and prognosis.

Results

No statistically significant disparities were observed in the proportion of patients experiencing favorable outcomes during the follow-up period between the two groups. Nevertheless, it is noteworthy that the incidence of the blend sign was higher among patients in the good outcome group compared to those in the poor outcome group. Multivariate regression analysis disclosed that poor outcomes following craniotomy was not associated with the blend sign.

Conclusions

The presence of the blend sign may not serve as a reliable predictor of functional outcomes in patients undergoing craniotomy for spontaneous supratentorial ICH.

Open Access Research Article Issue
Mitigating the effects of Endothelin-1 following a minimally invasive surgery reduces the blood-brain barrier permeability in a rabbit model of intracerebral hemorrhage
Brain Hemorrhages 2022, 3(4): 177-183
Published: 25 June 2022
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Objective

The aim of the current study is to evaluate if ETB inhibition following ICH can mitigate the deleterious impact of ET-1, e.g., BBB disruption, and improve neurological function.

Methods

A total of 90 male rabbits (2.8–3.4 kg) were randomly assigned to the following groups (n = 10 per group): normal control (NC), pseudo-control (PC), drug control using normal saline (DC), model control (MC + ICH), minimally invasive surgery (MIS + ICH), minimally invasive surgery + ET-1 receptor agonist (MIS + IRL1620 + ICH), IRL1620 + ICH, ET-1 receptor antagonist (BQ788 + ICH), and IS + BQ788 + ICH. ICH was induced in all groups except for NC, DC and PC groups.

Results

The purdy score, ET-1, MDA, MMP-9, BWC, and BBB permeability were decreased in groups treated with BQ788 and increased in groups treated with IRL1620. The combination of MIS + BQ788 markedly decreased these deleterious outcomes (purdy score, ET-1, MDA, MMP-9, BWC, and BBB permeability) compared to the MIS group.

Conclusions

Using a non-selective antagonist of ETB, deleterious outcomes associated with increased levels of ET-1 following ICH were ameliorated.

Open Access Review Issue
Chronic neuroinflammation regulates cAMP response element-binding protein in the formation of drug-resistant epilepsy by activating glial cells
Journal of Neurorestoratology 2022, 10(2): 100006
Published: 11 June 2022
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The cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) is associated with multiple signaling pathways. The signaling pathways leading to epilepsy have been extensively studied and include the Ca2+/CaMKiV/CREB pathway, the MAPK/CREB pathway, and the PI3K/Akt/CREB pathway. The regulation of transcription in cells requires CREB phosphorylation and dephosphorylation. Based on a review of the relevant literature, we found that increasing evidence demonstrates that drug-resistant epilepsy might be closely related to the upregulation and phosphorylation of CREB. Previous studies have shown that the mechanisms of epileptogenesis are associated with the over-excitability and sudden synchronous discharge of neurons. In turn, we have learned that inflammation produces proinflammatory factors that damage the blood–brain barrier and activate microglia (MG) and astrocytes (AS). Activated MG and AS not only play neuroprotective roles, but also cause neuroinflammation, which in turn damages nerve cells through CREB-related signaling pathways, leading to reduced effectiveness of antiepileptic drugs and, ultimately, to drug resistance in patients with epilepsy. Therefore, we hypothesized that the formation of drug-resistant epilepsy is related to the regulation of CREB activation or phosphorylation in glial cells activated by chronic inflammation.

Open Access Research Article Issue
Up-regulation of PPARγ, Nrf2 and HO-1 in microglia activated by thrombin
Brain Hemorrhages 2020, 1(2): 112-117
Published: 22 May 2020
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Objective

To explore the molecular mechanism involved in secondary brain damage caused by intracerebral hemorrhage (ICH), we activated microglia by thrombin, to observe the changes of peroxisome proliferator-activated receptor-gamma (PPARγ), nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) mRNA transcription and protein expression in the microglia cells of primary culturing in vitro.

Methods

Microglial cells were obtained from the brain tissues of the newborn rats and cultured in vitro. The isolated microglia cells were randomly divided into normal control group (NC group) and thrombin stimulation group (TH group). The expression of PPARγ, Nrf2 and HO-1 was tested by immunofluorescence and real-time PCR.

Results

The immunofluorescence showed that the numbers of stained positive cells of PPARγ, Nrf2 and HO-1 in TH group was increased remarkably as compared with NC group. The results of RT-qPCR showed that the mRNA expression of PPARγ, Nrf2 and HO-1 in TH group was increased significantly as compared with NC group (P < 0.01).

Conclusion

The expression of PPARγ, Nrf2 and HO-1 in the microglia cells activated by the thrombin were increased. Therefore, the microglia could be activated by intracerebral hemorrhage and the anti-oxidative stress effects of microglia can be improved.

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