This study conducted a bibliometric and visualization analysis of research on stroke-related sleep disorders from 2015 to 2026. It aims to elucidate the current research landscape, identify key hotspots, and discern potential future trends within this field.

We retrieved relevant publications on stroke-related sleep disorders from the Web of Science Core Collection database for the period from January 1, 2016, to December 31, 2025. Using Citespace (Version 6.2.R4), we generated and visualized knowledge maps encompassing analyses of authors, countries, institutions, keywords, co-cited references, co-cited authors, and co-cited journals.

A total of 607 publications were ultimately included. The annual publication count demonstrated a general upward trend over the past decade. Publication output peaked in 2025 with a transient decline in 2019. The United States emerged as the most productive country, followed closely by China. Network analyses revealed strong collaborative relationships among countries, institutions, and authors, shaping influential research clusters represented by scholars such as Devin L. Brown and Ronald D. Chervin. Among institutions, Harvard University contributed the most publications and exhibited a notably high centrality (0.06). Keyword co-occurrence analysis identified eight major thematic clusters and 20 keywords with the strongest citation bursts, with "ischemic stroke" and "apnea" emerging as the predominant core keywords.

Sleep apnea, particularly obstructive sleep apnea (OSA) and insomnia, remains the most extensively investigated sleep disorder in stroke populations. Hypertension emerged as one of the most frequent keywords among the identified influencing factors. Acute ischemic stroke represented the most common stroke type linked to sleep disturbances. Future investigations are likely to emphasize the identification of underlying pathophysiological mechanisms, systematic exploration of influencing factors, and the development of robust risk prediction models, ultimately aiming to inform clinical decision-making and improve long-term patient outcomes.

This experimental study investigated theaflavin (TF) as a potential treatment for atherosclerosis (AS), focusing on its regulation of macrophage pyroptosis and autophagy via GSK-3β.

Human aortic tissues from controls and subjects with AS, twelve male ApoE^-/- mice, and ox-LDL-induced Ana-1 mouse macrophages, including Gsdmd/Caspase-1-overexpressing and Gsdmd-deficient cells, were studied.

After 6 weeks of high-fat feeding, mice received TF (10 mg/kg/day, intraperitoneally) or PBS for 6 weeks; macrophages were stimulated with ox-LDL (20 μg/mL) and treated with TF for 48 h.

Oil Red O staining, immunofluorescence, Western blotting, ELISA, CRISPR/Cas9, molecular docking, cellular thermal shift assay, and co-immunoprecipitation were performed. Data were expressed as mean ± SD and analyzed using unpaired two-tailed t-tests or ANOVA with Dunnett's test.

TF attenuated aortic plaque formation and reduced GSDMD-N, C-CASP1, NLRP3, and IL-1β. In vitro, TF suppressed lipid uptake in Gsdmd- or Caspase-1-overexpressing macrophages but showed no effect in Gsdmd-deficient cells. TF interacted with GSK-3β, reduced p-GSK-3β(Tyr216), promoted autophagy, and enhanced GSK-3β-cathepsin B interaction.

TF attenuates AS progression by suppressing pyroptosis-mediated foam cell formation and promoting autophagy through modulation of GSK-3β activity.

Sepsis-induced cardiomyopathy is a serious complication of sepsis characterized by acute myocardial dysfunction and substantial mortality. This study evaluated the therapeutic effects of BGP-15 and the potential involvement of SIRT3/SOD2-associated signaling in a mouse model of cecal ligation and puncture (CLP)-induced sepsis.

BGP-15 (20 or 40 mg/kg) was administered intravenously once at 6 h after CLP surgery. Survival, cardiac function, myocardial injury, oxidative stress, and inflammatory responses were evaluated. Myocardial SIRT3 expression, SOD2 Lys68 acetylation, and total SOD2 protein were assessed. The SIRT3 inhibitor 3-TYP was co-administered to investigate the potential involvement of SIRT3-related signaling in the effects of BGP-15.

Sepsis was associated with cardiac dysfunction, increased mortality and myocardial injury, reduced myocardial SIRT3 expression, increased SOD2 Lys68 acetylation, and decreased total SOD2 protein. BGP-15 treatment improved survival and cardiac function, reduced serum CK-MB and LDH levels, and attenuated myocardial oxidative and inflammatory injury. High-dose BGP-15 increased SIRT3 expression, both BGP-15 doses reduced the Acetyl-SOD2/SOD2 ratio, and total SOD2 protein was increased. Co-administration of 3-TYP attenuated several cardiac, oxidative, and inflammatory effects associated with BGP-15 treatment, whereas its apparent attenuation of the 14-day survival benefit did not reach statistical significance (log-rank P = 0.1103).

These findings support the involvement of SIRT3-related signaling in the cardioprotective effects associated with BGP-15 in experimental sepsis and support further preclinical investigation of BGP-15 for septic cardiomyopathy. SIRT3 and SOD2 enzymatic activities were not measured directly.

Hypoxic-ischemic brain injury (HIBI) is characterized by complex pathological processes that contribute to acute neuronal damage. Photobiomodulation (PBM) and hydrogen inhalation have each demonstrated neuroprotective effects in ischemic and hypoxic models; however, the effects of their combined application in acute HIBI have not been directly evaluated. In this study, HIBI was induced in mice, followed by treatment with PBM alone, hydrogen inhalation alone, or their combination. Behavioral performance, physiological parameters, and molecular markers of neuronal survival, glial activation, neuroinflammation, apoptosis, and hypoxia signaling were evaluated at 24 h after injury. While PBM or hydrogen alone partially attenuated HIBI-induced alterations, combined treatment more effectively preserved locomotor activity, stabilized physiological parameters, and reduced neuronal loss. These effects were accompanied by decreased glial activation and inflammatory signaling, suppression of apoptotic pathways, and improved regulation of hypoxia-related signaling. Collectively, these findings demonstrate that combined PBM and hydrogen inhalation confers enhanced neuroprotection compared with monotherapies by modulating multiple pathological mechanisms in acute HIBI.

The reduced blood flow and energy substrates to the affected area during ischemia and sudden exposure to these molecules after ischemia is called reperfusion. Reperfusion can be as damaging to cells and tissues as ischemia. This study aims to examine the effects of brain Ischemia-Reperfusion (I/R) and 1-week 3',4'-Dihydroxyflavonol (DiOHF) treatment on Matrix Metalloproteinasease (MMP), occludin, claudin-5, and β-actin levels in frontal cortex and hippocampus tissue in male rats. In this study, twenty-eight male Wistar-Albino rats were allocated into four experimental groups: Control, Sham, Ischemia-Reperfusion (I/R), and Ischemia-Reperfusion + DiOHF. Under general anesthesia, bilateral carotid artery ligation was performed to induce ischemia for 30 min, followed by reperfusion. DiOHF supplementation (10 mg/kg) was administered for one week. At the end of the treatment period, the animals were sacrificed under general anesthesia, and the frontal cortex and hippocampus tissues were harvested. Gene expression levels of MMP-3, MMP-9, occludin, claudin-5, and β-actin in the collected tissues were analyzed using real-time PCR. While I/R suppressed the levels of claudin-5 and occludin in the frontal cortex and hippocampus, it increased the levels of β-actin, matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-9 (MMP-9). 3',4'-Dihydroxyflavonol supplementation for 1 week corrected the deteriorations caused by I/R. The study results show that 1 week of 3',4'-Dihydroxyflavonol treatment after I/R corrects the changes in structural damage indicators caused by transient bilateral carotid occlusion-induced ischemia-reperfusion in the frontal cortex and hippocampus to a certain extent.

To synthesize the experiences and perceptions of lay bystanders before, during, and after responding to out-of-hospital cardiac arrests.

Seven English and Chinese databases were searched from their inception to July 31, 2026, supplemented with citation tracking. Two reviewers independently selected studies, appraised methodological quality using the Joanna Briggs Institute (JBI) critical appraisal checklist for qualitative research, and extracted the findings and supporting illustrations. Unequivocal and credible findings were synthesized using JBI meta-aggregation, and confidence was assessed using confidence in the evidence from reviews of qualitative research.

Eight studies involving 209 participants were included. Thirty-three findings were grouped into 12 categories and 4 were synthesized findings concerning the motivators and inhibitors of response, recognition and appraisal of out-of-hospital cardiac arrest, conditions facilitating or impeding cardiopulmonary resuscitation and automated external defibrillator use, and post-event psychological responses and adjustment. Confidence in the evidence from reviews of qualitative research was moderate for the 1st 3 synthesized findings, and low for the 4th.

Bystander response is a continuum that extends from event recognition and action to post-event adjustment. Out-of-hospital cardiac arrest systems should provide realistic preparations, clear on-scene support, proportionate information, and psychological support after an event.

Hypertensive emergency complicated by acute ischemic stroke (AIS) represents a life-threatening clinical condition. Abrupt elevations in blood pressure not only increase the risk of stroke-related complications but also predispose patients to cerebral perfusion imbalance and target-organ injury. However, there is no consensus regarding the optimal antihypertensive strategy or individualized management protocol in this setting.

Three individuals with preexisting chronic hypertension developed acute ischemic stroke in the context of a hypertensive emergency, posing challenges in evaluating disease evolution, optimizing individualized treatment strategies, and assessing long-term prognosis.

Based on clinical manifestations and imaging examinations, all 3 cases were diagnosed as hypertensive emergencies with concomitant AIS.

In the emergency department, all patients were managed with urapidil administered through a continuous microinfusion pump to achieve blood pressure control. Following stabilization, intravenous thrombolysis was performed in case 1, whereas mechanical thrombectomy was undertaken in cases 2 and 3.

After therapeutic intervention, all patients achieved blood pressure stabilization within the target range and demonstrated significant neurological recovery in the acute phase. Cases 1 and 2 demonstrated favorable clinical recovery without major complications during follow-up. Case 3 underwent successful emergency thrombectomy but was transferred to another institution shortly thereafter and was subsequently lost to follow-up.

Treating hypertensive emergency in the setting of AIS demands careful appraisal of the patient's condition, hemodynamic profile, and cerebral perfusion needs to guide individualized therapy. Effective yet safe blood pressure reduction is critical to avoid cerebral hypoperfusion. Long-term prognosis can be further optimized through a multidisciplinary team (MDT), close follow-up, strict medication compliance, and targeted lifestyle interventions.

Platelet-derived growth factor subunit B (PDGFB) is a key regulator of vascular remodeling, angiogenesis, and blood-brain barrier integrity. Although elevated PDGFB levels have been reported after ischemic injury, whether stroke liability itself causally influences circulating PDGFB levels remains unclear. We performed a two-sample Mendelian randomization (MR) analysis to assess the causal effects of genetically predicted all stroke, ischemic stroke, and cardioembolic stroke on plasma PDGFB concentrations. Genetic instruments were obtained from large-scale GIGASTROKE genome-wide association studies, and outcome data were derived from a proteomics GWAS. Instruments were then filtered by removing variants associated with established cardiovascular risk factors in a phenome-wide screen and outliers identified by RadialMR. The inverse variance-weighted (IVW) method was used as the primary analysis, complemented by weighted median, weighted mode, and MR-Egger approaches. Sensitivity analyses included Cochran's Q statistics, MR-Egger intercept tests, single-SNP analyses, leave-one-out analyses, and MR-PRESSO. IVW analysis demonstrated a significant positive causal association between genetic liability to all stroke and plasma PDGFB levels (β = 0.209, SE = 0.062, 95% CI 0.088 to 0.331, p = 7.3 × 10^-4). A similar association was observed for ischemic stroke (β = 0.155, SE = 0.059, 95% CI 0.039 to 0.270, p = 0.009), with directionally consistent results across sensitivity analyses. MR-Egger regression for ischemic stroke initially suggested pleiotropy.After removal of a radial-MR outlier (rs2289252), the intercept was attenuated and no longer statistically significant (- 0.0190, p = 0.282). In contrast, no evidence of a causal association was found between cardioembolic stroke liability and plasma PDGFB levels across all MR methods (β = - 0.078, SE = 0.087, 95% CI - 0.248 to 0.092, p = 0.368). These findings provide genetic evidence that liability to stroke, particularly ischemic stroke, is causally associated with increased circulating PDGFB levels, whereas cardioembolic stroke does not show such an effect. This suggests that elevated PDGFB reflects vascular responses specific to ischemic stroke rather than a general consequence of all stroke subtypes.

We employed Mendelian randomization (MR) to explore causal relationships between gut microbiota (GM), coronary atherosclerotic heart disease (CAHD), and potential metabolic mediators. We utilized summary statistics from genome-wide association studies (GWAS), encompassing data on 473 GM traits from comprehensive microbiome GWAS, 61 lipoprotein-mediated cholesterol transport and distribution data from large-scale metabolic biomarker studies, and coronary atherosclerosis (CA) data from the GWAS catalog (study accession GCST90043957) involving 456,348 European participants. Bidirectional MR analyses were conducted to investigate the causal relationships between GM and CA. Two-sample Mendelian randomization analyses were performed to identify potential mediating metabolites and quantify the mediation proportion. Ultimately, the GM GCA-900066755, identified through MR as having a potential causal relationship, was selected to investigate its potential effects on CA by influencing cholesterol transport and distribution. Our results indicated that GCA-900066755 was positively associated with an increased risk of CA (odds ratio = 1.156). CA did not significantly affect the levels of GCA-900066755 (odds ratio = 1.009). GCA-900066755 was negatively correlated with total cholesterol levels in medium high-density lipoprotein, which reduced CA risk, and was positively correlated with total cholesterol levels in low-density lipoprotein (LDL), large LDL, medium LDL, and small LDL, which were positively associated with CA. Mediation analysis showed 7 data points mediating the association between GCA-900066755 and CA. Our MR study supports a causal relationship between specific GM groups and the risk of CAHD, highlighting that cholesterol traits are not merely outcomes associated with the relationship between GM and CAHD, but are important mediating factors. Understanding the biological mechanisms of these traits can provide a concrete foundation for future targeted interventions.

Economic immigrants are selected into Canada using a point system, which accounts for immigrants' language proficiency, education, and experience. We examined the impact of three policy changes associated with increasingly strict language requirements on mental health care utilization of immigrants in Canada. Using administrative health care data from Ontario, Canada, covering 1997 to 2015, we employed a difference-in-differences approach to study the effects of language requirement-related policies on economic immigrants' (i.e., skilled workers) mental health care use, relative to several comparison groups not impacted by the policy, including immigrants from the Anglosphere (i.e., immigrants from countries that have English as an official language or national language) and non-points-based immigrants (i.e., immigrants in the family class). Following policy changes that coincided with periods of increased English proficiency as an entry requirement, we found that mental health care utilization (i.e., visits to general practitioners for mental health reasons and psychiatrists) decreased for economic immigrants from non-Anglosphere countries, compared to those from Anglosphere countries, but increased compared to non-points-based immigrants. Additionally, non-mental health care utilization increased for economic immigrants from non-Anglosphere countries, compared to those from Anglosphere countries and non-points-based immigrants, following the later policy changes. This study sheds light on the impact of immigration policies, namely language requirements, on health care utilization and provides a starting point to understanding potential barriers that immigrants may face in accessing mental health care in a host country.