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Biomedicines
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Molecular Characteristics of Cerebral Ischemia and Their Therapeutic Applications
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Molecular Characteristics of Cerebral Ischemia and Their Therapeutic Applications

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 4324

Special Issue Editors

Dr. E-Jian Lee

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Guest Editor
Neurophysiology Laboratory, Neurosurgical Service, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70403, Taiwan
Interests: ischemic stroke; cerebral ischemia; neurophysiology; neuroplasticity
Dr. Shengyang Huang

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Guest Editor
Neurophysiology Laboratory, Neurosurgical Service, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70403, Taiwan
Interests: ischemic stroke; neuroplasticity; electrophysiology; bioengineering

Special Issue Information

Dear Colleagues,

This Special Issue entitled "Molecular Characteristics of Cerebral Ischemia and Their Therapeutic Applications" delves into the intricate molecular aspects associated with cerebral ischemia and explores innovative therapeutic approaches including insights into pathophysiology, biomarkers, and novel treatment strategies. Based on your previous publications and expertise in this field of research, we would like to invite you to publish your work in this Special Issue.

Dr. E-Jian Lee
Dr. Shengyang Huang
Guest Editors

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Keywords

  • cerebral ischemia
  • molecular mechanisms
  • pathophysiology
  • biomarkers
  • therapeutic strategies
  • neuroprotection
  • ischemic stroke
  • neuro-inflammation
  • translational research
  • neuroplasticity
  • neurophysiology
  • neuroscience
  • neuroelectrophysiology

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Published Papers (3 papers)

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20 pages, 3903 KiB  
Article
ACTH-like Peptides Compensate Rat Brain Gene Expression Profile Disrupted by Ischemia a Day After Experimental Stroke
by Ivan B. Filippenkov, Yana Yu. Shpetko, Vasily V. Stavchansky, Alina E. Denisova, Leonid V. Gubsky, Lyudmila A. Andreeva, Nikolay F. Myasoedov, Svetlana A. Limborska and Lyudmila V. Dergunova
Biomedicines 2024, 12(12), 2830; https://doi.org/10.3390/biomedicines12122830 - 13 Dec 2024
Cited by 1 | Viewed by 808
Abstract
Background: Ischemic stroke results from a disruption of cerebral blood flow. Adrenocorticotropic hormone (ACTH) serves as the basis for the creation of synthetic peptides as neuroprotective agents for stroke therapy. Previously, using RNA-Seq we first revealed differential expressed genes (DEGs) associated with ACTH(4–7)PGP [...] Read more.
Background: Ischemic stroke results from a disruption of cerebral blood flow. Adrenocorticotropic hormone (ACTH) serves as the basis for the creation of synthetic peptides as neuroprotective agents for stroke therapy. Previously, using RNA-Seq we first revealed differential expressed genes (DEGs) associated with ACTH(4–7)PGP (Semax) and ACTH(6–9)PGP peptides under cerebral ischemia conditions. Analysis was carried out at 4.5 h after transient middle cerebral artery occlusion (tMCAO) model in the ipsilateral frontal cortex of a rat brain. Methods: Here, we analyzed the penumbra-associated frontal cortex of rats and actions under the same peptides at 24 h after tMCAO using RNA-Seq. Results: 3774 DEGs (fold change > 1.5 and Padj < 0.05) were identified under ischemia conditions, whereas 1539 and 2066 DEGs were revealed under Semax and ACTH(6–9)PGP peptides at 24 h after tMCAO. Furthermore, both peptides significantly reduced expression distortions caused by ischemia for 1171 genes associated with immune and neurosignaling pathways. Concomitantly, there were 32 DEGs under ACTH(6–9)PGP versus Semax administration at 24 h after tMCAO. Besides, neurogenesis-, angiogenesis-, protein kinase- and growth factor-related DEGs were revealed under peptides action. Previously, we observed the neuroprotective effect of peptides at the histological level in rat brains at 24 h after tMCAO. Thus, here we demonstrate the transcriptome manifestation of this histological effect. Furthermore, comparison with previous data at the 4.5 h post-tMCAO time point showed that the pattern of peptide action on the transcriptome depends on the time elapsed after tMCAO. Conclusions: We revealed that the effect of ACTH(6–9)PGP was more similar to Semax than different from it a day after tMCAO. At this time point, ACTH-like peptides compensated rat brain gene expression profiles disrupted by ischemia. Thus, our results may be useful for selecting more effective structures for future anti-stroke drugs and appropriate post-stroke time points for their testing. Full article
(This article belongs to the Special Issue Molecular Characteristics of Cerebral Ischemia and Their Therapeutic Applications)
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Graphical abstract
Full article ">Figure 1
<p>Effect of ischemia, ACTH(6–9)PGP and Semax on the transcriptome of FC of rats 24 h after tMCAO. (<b>a</b>,<b>d</b>,<b>g</b>) Results of RNA-Seq analysis for IR24-f vs. SO24-f (<b>a</b>), IS24-f vs. IR24-f (<b>d</b>), IA24-f vs. IR24-f (<b>g</b>). The quantity of DEGs is indicated by the numbers in the diagram sectors. (<b>b</b>,<b>e</b>,<b>h</b>) Volcano plots show a distribution data between the IR24-f and SO24-f (<b>b</b>), IS24-f and IR24-f (<b>e</b>), IA24-f and IR24-f (<b>h</b>) groups. (<b>c</b>,<b>f</b>,<b>i</b>) The top 10 DEGs (Fold change &gt; 1.5; <span class="html-italic">Padj</span> &lt; 0.05) with the highest expression changes in IR24-f vs. SO24-f (<b>c</b>), IS24-f vs. IR24-f (<b>f</b>), IA24-f vs. IR24-f (<b>i</b>). The data are presented as the mean ± standard error of the mean (M ± SEM).</p> Full article ">Figure 2
<p>The gene expression changes for different groups of ischemia, ACTH(6–9)PGP and Semax at 24 h after tMCAO. Venn diagrams represent RNA-Seq results obtained in comparisons between the IR24-f vs. SO24-f (<b>a</b>–<b>c</b>); IS24-f vs. IR24-f (<b>e</b>–<b>g</b>); IA24-f vs. IR24-f (<b>i</b>–<b>k</b>) groups in FC. All (<b>a</b>,<b>e</b>,<b>i</b>), upregulated (<b>b</b>,<b>f</b>,<b>j</b>), and downregulated (<b>c</b>,<b>g</b>,<b>k</b>) DEGs are shown. The top 10 DEGs (Fold change &gt; 1.5; <span class="html-italic">Padj</span> &lt; 0.05) among 1335 (<b>d</b>), 1753 (<b>h</b>) and 1286 (<b>l</b>) in the Venn diagram (<b>d</b>,<b>h</b>,<b>l</b>), respectively, featuring the highest fold changes in the IR24-f vs. SO24-f (<b>d</b>); IS24-f vs. IR24-f (<b>h</b>); IA24-f vs. IR24-f (<b>l</b>) comparison groups. The data are presented as M ± SEM.</p> Full article ">Figure 3
<p>The RNA-Seq results for the IR24-f vs. SO24-f, IS24-f vs. IR24-f, IA24-f vs. IR24-f and IA24-f vs. IS24-f pairwise comparisons. (<b>a</b>) Venn diagrams present comparison of results between the IR24-f vs. SO24-f, IS24-f vs. IR24-f and IA24-f vs. IR24-f groups. The top 10 DEGs that lie within the intersection between the gene sets in the Venn diagram (<b>a</b>) and have the highest fold change in IR24-f vs. SO24-f (<b>b</b>). The top 10 DEGs that lie within the gene sets in the Venn diagram (<b>a</b>) among the overlapping section between IS24-f vs. IR24-f and IA24-f vs. IR24-f but not in the IR24-f vs. SO24-f pairwise comparisons (<b>c</b>). The data are presented as M ± SEM. (<b>d</b>) Hierarchical cluster analysis of all DEGs in IR24-f vs. SO24-f, IS24-f vs. IR24-f, IA24-f vs. IR24-f, where each row represents a DEG; n = 3 per group. Only those genes with cut-off &gt;1.5 and <span class="html-italic">Padj</span> &lt; 0.05 were selected recognized by significant.</p> Full article ">Figure 4
<p>Signaling KEGG pathways associated with DEGs in the FC of rats 24 h after occlusion. DAVID (2021 Update) was used for pathway search in the IR24-f vs. SO24-f, IS24-f vs. IR24-f, IA24-f vs. IR24-f comparisons. (<b>a</b>) 3-set Venn diagram presents a comparison of DEG-related pathways in the IR24-f vs. SO24-f, IS24-f vs. IR24-f, IA24-f vs. IR24-f and IA24-f vs. IS24-f groups. The number on the chart segments indicates the numbers of annotations. (<b>b–d</b>) The most significant pathways in IR24-f vs. SO24-f (<b>b</b>), IS24-f vs. IR24-f (<b>c</b>), IA24-f vs. IR24-f (<b>d</b>) are presented. (<b>e</b>,<b>f</b>) Cluster analysis of overlapped signaling pathways associated with DEGs in IR24-f vs. SO24-f, IS24-f vs. IR24-f, IA24-f vs. IR24-f pairwise comparison. Pathways of inflammatory cluster (IC) (<b>e</b>) and neurotransmitter cluster (NC) (<b>f</b>) are presented. Each column represents a pairwise comparison and each row represents a signaling pathway (KEGG). The green bars represent the pathways with which the majority of upregulated genes are associated, and the red bars represent the pathways with which the majority of downregulated genes are associated. Only DEGs and pathways with <span class="html-italic">Padj</span> &lt; 0.05 were selected as significant, n = 3 of animals per group.</p> Full article ">Figure 5
<p>The search for pathways that reflect gene expression effects of Semax and ACTH(6–9)PGP at 24 h after tMCAO in FC. (<b>a</b>) Venn diagram presents overlapped and unique DEG-related annotations in the IS24-f vs. IR24-f and IA24-f vs. IR24-f pairwise comparisons. Only pathways that have annotations with DEGs in IA24-f vs. IS24-f pairwise comparison are included. The number on the chart segments indicates the numbers of annotations. All pathways were grouped on three pathway clusters (PC1, PC2 and PC3) (<b>b</b>) The gene network of effects of ACTH(6–9)PGP and Semax peptides on transcriptome of FC at 24 h after tMCAO. In the scheme, 13 genes that are DEGs in the IA24-f vs. IS24-f are presented. These genes are grouped by three half rings of rectangles colored according to their differential expression in comparison groups. Each half ring includes the same 32 genes, but the color in the inner half ring indicates DEGs in the IA24-f vs. IS24-f, the color in the central half ring indicates DEGs in the IS24-f vs. IR24-f, and the colour in the outer half ring indicates the DEGs in IA24-f vs. IR24-f. Three pathway clusters (PC1, PC2 and PC3) are grouped in ovals. PC1 represents common pathways that lie within the intersection between the IA24-f vs. IR24-f and IS24-f vs. IR24-f pathway sets in the Venn diagram (<a href="#biomedicines-12-02830-f004" class="html-fig">Figure 4</a>a) and reflects effects of both peptides. PC2 represents unique pathways that lie within the pathway sets among the IS24-f vs. IR24-f but not among the IA24-f vs. IR24-f pairwise comparisons in the Venn diagram (<a href="#biomedicines-12-02830-f004" class="html-fig">Figure 4</a>a). PC3 represents unique pathways that lie within the pathway sets among the IA24-f vs. IR24-f but not among the IS24-f vs. IR24-f pairwise comparisons in the Venn diagram (<a href="#biomedicines-12-02830-f004" class="html-fig">Figure 4</a>a). The lines connecting the genes and pathways indicate association between them. The KEGG databases from DAVID v. 2021 were used to annotate all clustered pathways. Only DEGs and pathways with <span class="html-italic">Padj</span> &lt; 0.05 were selected as significant. The network was constructed using Cytoscape 3.9.2.</p> Full article ">
9 pages, 951 KiB  
Article
Soluble Glycoprotein VI Levels Assessed Locally within the Extra- and Intracerebral Circulation in Hyper-Acute Thromboembolic Stroke: A Pilot Study
by Andreas Starke, Alexander M. Kollikowski, Vivian Vogt, Guido Stoll, Bernhard Nieswandt, Mirko Pham, David Stegner and Michael K. Schuhmann
Biomedicines 2024, 12(10), 2191; https://doi.org/10.3390/biomedicines12102191 - 26 Sep 2024
Viewed by 1038
Abstract
Background: Severe acute ischemic stroke (AIS) is mainly caused by thromboembolism originating from symptomatic carotid artery (ICA) stenosis or in the heart due to atrial fibrillation. Glycoprotein VI (GPVI), a principal platelet receptor, facilitates platelet adherence and thrombus formation at sites of vascular [...] Read more.
Background: Severe acute ischemic stroke (AIS) is mainly caused by thromboembolism originating from symptomatic carotid artery (ICA) stenosis or in the heart due to atrial fibrillation. Glycoprotein VI (GPVI), a principal platelet receptor, facilitates platelet adherence and thrombus formation at sites of vascular injury such as symptomatic ICA stenosis. The shedding of GPVI from the platelet surface releases soluble GPVI (sGPVI) into the circulation. Here, we aimed to determine whether sGPVI can serve as a local biomarker to differentiate between local atherosclerotic and systemic cardiac thromboembolism in AIS. Methods: We conducted a cohort study involving 105 patients undergoing emergency endovascular thrombectomy (EVT) for anterior circulation stroke. First, sGPVI concentrations were measured in systemic arterial plasma samples collected at the ipsilateral ICA level, including groups with significantly (≥50%) stenotic and non-stenotic arteries. A second sample, taken from the intracerebral pial circulation, was used to assess GPVI shedding locally within the ischemic brain. Results: Our analysis revealed no significant increase in systemic sGPVI levels in patients with symptomatic ≥ 50% ICA stenosis (3.2 [95% CI 1.5–5.0] ng/mL; n = 33) compared with stroke patients without significant ICA stenosis (3.2 [95% CI 2.3–4.2] ng/mL; n = 72). Additionally, pial blood samples, reflecting intravascular molecular conditions during collateral flow, showed similar sGPVI levels when compared to the systemic ICA samples in both groups. Conclusions: Our findings indicate that GPVI is not locally cleaved and shed into the bloodstream in significant amounts during hyper-acute ischemic stroke, neither at the level of symptomatic ICA nor intracranially during collateral blood supply. Therefore, sGPVI does not appear to be suitable as a local stroke biomarker despite strong evidence of a major role for GPVI-signaling in stroke pathophysiology. Full article
(This article belongs to the Special Issue Molecular Characteristics of Cerebral Ischemia and Their Therapeutic Applications)
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Figure 1

Figure 1
<p>Concentration of sGPVI (<b>A</b>) and CXCL4 (<b>B</b>) in arterial plasma samples of patients with large-vessel ischemic stroke in the anterior circulation. Blood samples were obtained from the internal carotid artery (systemic) in patients with either ≥ 50% cervical ICA stenosis or ICA dissection (depicted by black points) and patients without significant ICA stenosis and most likely cardiogenic thromboembolism (depicted by grey points), immediately following EVT. The data are presented as a scatter dot plot with the median indicated. A Mann–Whitney-U test was performed to test for significance.</p> Full article ">Figure 2
<p>Local sGPVI and CXCL4 concentrations distal to cerebral artery occlusion in hyper-acute stroke. Local systemic (depicted by black points) and ischemic (depicted by grey points) plasma levels of sGPVI and CXCL4 in patients with either ≥50% cervical ICA stenosis or ICA dissection (<b>A</b>,<b>C</b>) and patients without significant ICA pathology (<b>B</b>,<b>D</b>). The data are presented as a scatter dot plot with the median indicated. A Wilcoxon rank-sum test was performed to test for significance. * <span class="html-italic">p</span>-value &lt; 0.05; ** <span class="html-italic">p</span>-value &lt; 0.01.</p> Full article ">
15 pages, 2751 KiB  
Article
MicroRNA-195-5p Attenuates Intracerebral-Hemorrhage-Induced Brain Damage by Inhibiting MMP-9/MMP-2 Expression
by Yi-Cheng Tsai, Chih-Hui Chang, Yoon Bin Chong, Chieh-Hsin Wu, Hung-Pei Tsai, Tian-Lu Cheng and Chih-Lung Lin
Biomedicines 2024, 12(6), 1373; https://doi.org/10.3390/biomedicines12061373 - 20 Jun 2024
Cited by 3 | Viewed by 1567
Abstract
Intracerebral hemorrhage (ICH) remains a devastating disease with high mortality, and there is a lack of effective strategies to improve functional outcomes. The primary injury of ICH is mechanical damage to brain tissue caused by the hematoma. Secondary injury, resulting from inflammation, red [...] Read more.
Intracerebral hemorrhage (ICH) remains a devastating disease with high mortality, and there is a lack of effective strategies to improve functional outcomes. The primary injury of ICH is mechanical damage to brain tissue caused by the hematoma. Secondary injury, resulting from inflammation, red cell lysis, and thrombin production, presents a potential target for therapeutic intervention. Inflammation, crucial in secondary brain injury, involves both cellular and molecular components. MicroRNAs (miRNAs) are vital regulators of cell growth, differentiation, and apoptosis. Their deregulation may lead to diseases, and modulating miRNA expression has shown therapeutic potential, especially in cancer. Recent studies have implicated miRNAs in the pathogenesis of stroke, affecting endothelial dysfunction, neurovascular integrity, edema, apoptosis, inflammation, and extracellular matrix remodeling. Preclinical and human studies support the use of miRNA-directed gene modulation as a therapeutic strategy for ICH. Our study focused on the effects of miR-195 in ICH models. Neurological tests, including the corner turn and grip tests, indicated that miR-195 treatment led to improvements in motor function impairments caused by ICH. Furthermore, miR-195-5p significantly reduced brain edema in the ipsilateral hemisphere and restored blood–brain barrier (BBB) integrity, as shown by reduced Evans blue dye extravasation. These results suggest miR-195-5p’s potential in attenuating ICH-induced apoptosis, possibly related to its influence on MMP-9 and MMP-2 expression, enzymes associated with secondary brain injury. The anti-apoptotic effects of miR-195-5p, demonstrated through TUNEL assays, further underscore its therapeutic promise in addressing the secondary brain injury and apoptosis associated with ICH. In conclusion, miR-195-5p demonstrates a significant neuroprotective effect against ICH-induced neural damage, brain edema, and BBB disruption, primarily through the downregulation of MMP-9 and MMP-2. Our findings indicate that miR-195-5p holds therapeutic potential in managing cerebral cell death following ICH. Full article
(This article belongs to the Special Issue Molecular Characteristics of Cerebral Ischemia and Their Therapeutic Applications)
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Figure 1

Figure 1
<p>Evaluation of neurobehavioral recovery post-ICH with miR-195-5p treatment. This study showed the percentages of right turn and power of control performed by rats in four groups (Control, ICH, ICH + NC-mimic, and ICH + miR-195-5p treatment) in the (<b>A</b>) corner turn test and (<b>B</b>) grip test, conducted over 28 days following ICH induction by collagenase infusion. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001 compared with the control group. # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt; 0.01, and ### <span class="html-italic">p</span> &lt; 0.001 compared between the ICH + NC-mimic group and the miR-195-5p-treated group.</p> Full article ">Figure 2
<p>Brain edema assessment in the rat model post-ICH treatment. This study showed the percentage of water content in the contralateral and ipsilateral brain hemispheres among four groups: Control, ICH, ICH + NC-mimic, and ICH + miR-195-5p. The analysis was conducted after inducing ICH by collagenase infusion into the caudate nucleus of rats. * <span class="html-italic">p</span> &lt; 0.05 and *** <span class="html-italic">p</span> &lt; 0.001 compared with control group. # <span class="html-italic">p</span> &lt; 0.05 compared with the ICH + NC-mimic group. (<span class="html-italic">n</span> = 6 in each group).</p> Full article ">Figure 3
<p>Assessment of hematoma volume and blood–brain barrier integrity post-ICH. The effects of ICH and the therapeutic intervention with miR-195-5p on brain injury. (<b>A</b>) Hemoglobin content measurements, indicative of hematoma volume, reveal that while the ICH and ICH + NC-mimic groups show an increase in the ipsilateral hemisphere suggestive of larger hematomas, miR-195-5p treatment significantly reduces this volume, indicating its potential to alleviate hemorrhage-associated brain damage. (<b>B</b>) The assessment of BBB integrity through Evans blue dye extravasation demonstrates heightened permeability in the ICH groups, which is notably decreased following treatment with miR-195-5p. (** <span class="html-italic">p</span> &lt; 0.01 and *** <span class="html-italic">p</span> &lt; 0. 001 different from control, ### <span class="html-italic">p</span> &lt; 0. 001 compared with ICH + NC-mimic) (<span class="html-italic">n</span> = 4 in each group).</p> Full article ">Figure 4
<p>TUNEL assay demonstrating apoptotic cell death in response to ICH and treatment with miR-195-5p. The apoptotic response in brain tissue following ICH and the effect of miR-195-5p treatment, as visualized by fluorescence microscopy and quantified through TUNEL staining. (<b>A</b>) In the images, DAPI staining marks all cell nuclei in blue, while TUNEL staining identifies apoptotic cells in green, with merged images providing a comprehensive view of apoptosis within the total cell context. (<b>B</b>) The control group maintains minimal apoptosis, contrasting with the ICH and ICH + NC-mimic groups, which show increased numbers of TUNEL-positive cells. The ICH + miR-195-5p group reveals a marked reduction in apoptotic cells, underscoring the protective role of miR-195-5p in mitigating cell death associated with ICH. (*** <span class="html-italic">p</span> &lt; 0.001 compared with control, ### <span class="html-italic">p</span> &lt; 0.001 compared with ICH + NC-mimic) (<span class="html-italic">n</span> = 4 in each group).</p> Full article ">Figure 5
<p>Matrix metalloproteinase zymography assessing MMP activity post-ICH and miR-195-5p treatment. The impact of ICH on the activity of various MMPs and the modulatory effects of miR-195-5p treatment. (<b>A</b>) The zymogram reveals the activity levels of Pro-MMP-9, MMP-9, and MMP-2, with samples from both unaffected (contralateral) and affected (ipsilateral) brain hemispheres across the control, ICH, and ICH-treated groups with either NC-mimic or miR-195-5p. It highlights a significant upregulation of Pro-MMP-9 and MMP-9 activities in the ipsilateral hemisphere following ICH, which is notably diminished upon treatment with miR-195-5p, indicating its therapeutic potential in mitigating MMP-related pathologies post-ICH. (<b>B</b>) The bar graphs present a quantitative comparison of these enzymes’ activities, showing relative enzyme densities to the control and demonstrating the specific reduction in MMP activity (particularly for Pro-MMP-9 and MMP-9) associated with miR-195-5p treatment. (*** <span class="html-italic">p</span> &lt; 0.001, ** <span class="html-italic">p</span> &lt; 0.01, and * <span class="html-italic">p</span> &lt; 0.05 compared with the control group, ## <span class="html-italic">p</span> &lt; 0.01 compared with the ICH + NC-mimic group) (<span class="html-italic">n</span> = 4 in each group).</p> Full article ">Figure 6
<p>Differential expression of MMP-9 and MMP-2 post-ICH and miR-195-5p intervention as revealed by Western blotting. The effects of ICH and miR-195-5p treatment on MMP-9 and MMP-2 protein expression. (<b>A</b>) Western blots reveal the presence of MMP-9 and MMP-2 proteins, alongside β-actin as a loading control, with samples taken from the control group, the ICH group, and ICH groups treated with either NC-mimic or miR-195-5p in both the unaffected contralateral and the affected ipsilateral brain hemispheres. (<b>B</b>) The quantitative assessment shows a significant increase in MMP-9 expression in the ipsilateral hemisphere following ICH, which is notably decreased after miR-195-5p treatment, suggesting the treatment’s effectiveness in reducing the upregulated levels of MMP-9 associated with ICH. MMP-2 expression also rises post-ICH but is somewhat decreased by miR-195-5p, with levels still above those of the control, reflecting a differential response to the treatment. (*** <span class="html-italic">p</span> &lt; 0.001 and ** <span class="html-italic">p</span> &lt; 0.01 compared with the control group, # <span class="html-italic">p</span> &lt; 0.05 and ## <span class="html-italic">p</span> &lt; 0.01 compared with the ICH + NC-mimic group) (<span class="html-italic">n</span> = 4 in each group).</p> Full article ">
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