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• Identification of a novel role for type IV collagen in bone biology. • Col4a1 mutant mouse models of Gould syndrome exhibit skeletal abnormalities. • Elevated TGFβ signaling contributes to skeletal pathogenesis in Col4a1 mutant mice. • Phenotypic and mechanistic overlap between Gould syndrome and other collagen-related ECM disorders. Skeletal defects are hallmark features of many extracellular matrix (ECM) and collagen-related disorders. However, a biological function in bone has never been defined for the highly evolutionarily conserved type IV collagen. Collagen type IV alpha 1 (COL4A1) and alpha 2 (COL4A2) form α1α1α2 (IV) heterotrimers that represent a fundamental basement membrane constituent present in every organ of the body, including the skeleton. COL4A1 and COL4A2 mutations cause Gould syndrome, a variable and clinically heterogenous multisystem disorder generally characterized by the presence of cerebrovascular disease with ocular, renal, and muscular manifestations. We have previously identified elevated TGFβ signaling as a pathological insult resulting from Col4a1 mutations and demonstrated that reducing TGFβ signaling ameliorate ocular and cerebrovascular phenotypes in Col4a1 mutant mouse models of Gould syndrome. In this study, we describe the first characterization of skeletal defects in Col4a1 mutant mice that include a developmental delay in osteogenesis and structural, biomechanical and vascular alterations of mature bones. Using distinct mouse models, we show that allelic heterogeneity influences the presentation of skeletal pathology resulting from Col4a1 mutations. Importantly, we found that TGFβ target gene expression is elevated in developing bones from Col4a1 mutant mice and show that genetically reducing TGFβ signaling partially ameliorates skeletal manifestations. Collectively, these findings identify a novel and unsuspected role for type IV collagen in bone biology, expand the spectrum of manifestations associated with Gould syndrome to include skeletal abnormalities, and implicate elevated TGFβ signaling in skeletal pathogenesis in Col4a1 mutant mice. [ABSTRACT FROM AUTHOR]

Retinal vein occlusion (RVO) and cerebrovascular disease share common risk factors and may be independently associated; however, the strength and nature of this association remain unclear. We conducted a systematic review and meta-analysis, informed by studies from PubMed, Scopus, EMBASE, Web of Science, and Google Scholar until January 6, 2024, aimed to clarify this relationship. Eligible studies included cohorts observing stroke incidence in RVO patients for over a year. Pooled effect estimates were calculated using random-effects models, with subgroup analyses evaluating associations between RVO types (central and branch) and stroke subtypes (ischemic and hemorrhagic). Ten cohort studies with a total of 428,650 participants (86,299 RVO patients) were included. Compared to controls, RVO patients exhibited a significantly increased risk of stroke (pooled risk ratio [RR]=1.38, 95 % confidence interval (95 %CI)=1.34–1.41). Subgroup analyses indicated elevated risk for both ischemic (RR=1.37, 95 %CI=1.32–1.42) and hemorrhagic (RR=1.55, 95 %CI=1.08–2.22) strokes in RVO patients. Additionally, both central (RR=1.50, 95 %CI=1.27–1.78) and branch (RR=1.41, 95 %CI=1.32–1.50) RVO were associated with stroke risk. Sensitivity analyses confirmed consistent results across various criteria, and funnel plots indicated no publication bias. RVO significantly increases the risk of both ischemic and hemorrhagic stroke, regardless of RVO type, suggesting a strong independent association between these conditions. [ABSTRACT FROM AUTHOR]

Randomized controlled trials (RCTs) provide information on appropriate management protocols in patients with cerebrovascular diseases. Despite growing evidence of race and ethnicity being independent predictors of outcomes, recent literature has drawn attention to inadequate reporting of these demographic profiles across RCTs. To our knowledge, the adherence to reporting race and/or ethnicity in cerebrovascular RCTs remains undescribed. Our study describes trends in the reporting of race and/or ethnicity across cerebrovascular RCTs. Web of Science was searched to identify the top 100-cited cerebrovascular RCTs. Additional articles were retrieved from guidelines issued by the American Heart Association for the management of ischemic stroke, intracerebral hemorrhage, and aneurysmal subarachnoid hemorrhage. Univariate and multivariate analyses were performed to assess for factors influencing reporting of race/ethnicity. Sixty-five percent of cerebrovascular RCTs lacked reporting of participant race and/or ethnicity. Multivariate regression revealed that studies from North America had a 14.74- fold higher odds (95% CI: 4.574–47.519) of reporting race/ethnicity. Impact factor of the journal was associated with 1.007-fold odds of reporting race/ethnicity (95% CI: 1.000–1.013). Reporting of race and/or ethnicity did not increase with time, or vary according to the number of participating centers, median number of study participants, source of funding, or category of RCT. Among RCTs that reported race, Blacks and Asians were underrepresented compared to Whites. Sixty-five percent of prominent cerebrovascular RCTs lack adequate reporting of participant race/ethnicity. Reasons for inadequate reporting of these variables remain unclear and warrant additional investigation. [ABSTRACT FROM AUTHOR]

White matter hyperintensities (WMH) are associated with cortical thinning. Although they are primarily detected in older participants, these lesions can appear in younger and midlife individuals. Here, we tested whether WMH are associated with cortical thinning in relatively younger (26–50 years) and relatively older (58–84) participants who were free of dementia, and how these associations are moderated by WMH localization. WMH were automatically quantified and categorized according to the localization of three classes of white matter tracts: association, commissural and projection fibers. Mediation analyses were used to infer whether differences in cortical thickness between younger and older participants were explained by WMH. Our results revealed that total WMH explained between 20.6 % and 65.5 % of the effect of age on cortical thickness in AD-signature regions including the lateral temporal lobes and supramarginal gyrus, among others. This mediation was slightly stronger for projection WMH, although it was still significant for association and commissural WMH. These results suggest that there is an interplay between vascular and AD causes of cognitive impairment that starts at younger ages. • White matter hyperintensities (WMH) are apparent in middle-age. • WMH correlate with cortical thickness, especially in younger adults. • WMH explain up to 65.6 % of age-related cortical thickness differences. • The effect of WMH on atrophy starts during the mid-life. [ABSTRACT FROM AUTHOR]

Observational studies have suggested that mental disorders and cerebrovascular diseases (CVDs) may be risk factors for each other, but genetic evidence of a causal relationship is still lacking. We used Mendelian randomization (MR) studies to explore the causal relationship between mental disorders and CVDs from the genetic perspective. To investigate the causal association between major depressive disorder (MDD), anxiety, attention deficit/hyperactivity disorder (ADHD), bipolar disorder and schizophrenia five kinds of mental disorders and CVDs using two-sample two-way MR analysis based on publicly available genome-wide association study (GWAS) data. We used as instrumental variables (IVs) single-nucleotide polymorphisms (SNPs) that were strongly associated with mental disorders and CVDs. IVW method was used as the main analysis method, and MR-IVW, MR-Egger methods, MR-PRESSO test, leave-one-out analysis and funnel plot were used for sensitivity analysis. We further conducted a meta-analysis to summarize the currently available MR analyses. The results of forward MR study showed that there was a significant causal relationship between ADHD and AS (any stroke) (p (AS) = 0.001, OR (95%CI) =1.118 (1.047–1.195)), any ischemic stroke (AIS) (p (AIS) = 0.004, OR (95%CI) =1.118(1.035–1.206)) and large artery stroke (LAS) (p (LAS) = 0.026, OR (95%CI): 1.206(1.023–1.422)). No heterogeneity, pleiotropy and outliers were found in sensitivity analysis. The reverse MR study showed that IA (intracranial aneurysm) (p (IA) = 0.033, OR (95%CI) = 1.123(1.009–1.249)) and UIA (unruptured intracranial aneurysm) (p (UIA) = 0.015, OR (95%CI) =1.040(1.008–1.074)) were risk factors for schizophrenia. Sensitivity analysis showed no pleiotropy, but there was heterogeneity. After excluding outliers, MR analysis showed that IA and UIA were still risk factors for schizophrenia. Our meta-analyses found statistical significance in causal relationships between ADHD and LAS (OR (95%CI) =1.18 (1.06–1.32), p = 0.003), IA and schizophrenia (OR (95%CI) =1.05 (1.02–1.08), p = 0.002) and UIA and schizophrenia (OR (95%CI) =1.03 (1.01–1.06), p = 0.010). The MR study and meta-analysis suggest that genetically predicted ADHD is a risk factor for LAS, and IA and UIA increase the risk of schizophrenia. The result has implications for the development of feasible prevention strategies in the future. • To investigate the causal association between mental disorders and CVDs using two-sample two-way MR analysis. • ADHD is a risk factor for large artery stroke, and intracranial aneurysm increases the risk of schizophrenia. • The study obtain a more comprehensive understanding of the interaction between mental disorders and CVDs. [ABSTRACT FROM AUTHOR]

High cardiorespiratory fitness (CRF) has been associated with a lower risk of depression, anxiety, and cerebrovascular disease. The aim was to explore CRF changes over-time associated with these outcomes. This large-scale prospective cohort study, using data from Swedish population-wide registries and databases (during 1972–2020), included men (n =131,431), with measures of estimated CRF (estCRF) in late adolescence (maximal cycle test) and adulthood (submaximal cycle test) (mean years between 24.6, SD 8.8). The study explored how change in estCRF was associated with incident depression, anxiety, and cerebrovascular disease using Cox proportional hazards models. Analyses were performed in 2023. Higher estCRF in late adolescence and adulthood were associated with a lower risk of incident depression, anxiety, and cerebrovascular disease later in life. For all three outcomes, an increase in estCRF (mL/min/kg and z-score) between the two-time points was associated with a lower risk. Further, decreasing from moderate or high estCRF in adolescence to low estCRF in adulthood, compared to staying at a moderate or high level, was associated with a higher risk of depression and anxiety (HR: 1.24 95% CI 1.07–1.45 and 1.25 95% CI 1.06–1.49, respectively). Conversely, increasing from moderate to high estCRF was associated with a lower risk of incident anxiety (HR: 0.84 95% CI 0.71–0.99). The findings indicate that there is a longitudinal association between negative change in estCRF and increased risk of depression, anxiety, and cerebrovascular disease later in life. Decreasing levels of estCRF could be a helpful indicator when identifying these disorders at a population level. [ABSTRACT FROM AUTHOR]

Platelet activation of protease-activated receptor 4 (PAR4) and thrombin are at the top of a chain of events leading to fibrin deposition, microinfarcts, blood-brain barrier disruption, and inflammation. We evaluated mRNA expression of the PAR4 gene F2RL3 in human brain and global cognitive performance in participants with and without cognitive impairment or dementia. Data were acquired from the Religious Orders Study (ROS) and the Rush Memory and Aging Project (MAP). F2RL3 mRNA was elevated in AD cases and was associated with worse retrospective longitudinal cognitive performance. Moreover, F2RL3 expression interacted with clinical AD diagnosis on longitudinal cognition whereas this relationship was attenuated in individuals without cognitive impairment. Additionally, when adjusting for the effects of AD neuropathology, F2RL3 expression remained a significant predictor of cognitive decline. F2RL3 expression correlated positively with transcript levels of proinflammatory markers including TNFα, IL-1β, NFκB, and fibrinogen α/β/γ. Together, these results reveal that F2RL3 mRNA expression is associated with multiple AD-relevant outcomes and its encoded product, PAR4, may play a role in disease pathogenesis. • F2RL3 mRNA was elevated in AD and associated with worse cognitive performance. • F2RL3 mRNA interacted with clinical AD diagnosis on longitudinal cognition. • F2RL3 mRNA correlated with β-amyloid, tau, and severity of CAA. • F2RL3 mRNA correlated with transcript levels of proinflammatory markers. [ABSTRACT FROM AUTHOR]

Despite the increasing prevalence of cervical odontoid fractures in older adults, the treatment strategy is controversial. The objectives of the current study are to investigate the prognosis and complications of cervical odontoid fractures in elderly patients and to identify factors associated with worsening of ambulation after 6 months. This multicenter, retrospective study included 167 patients aged 65 years or older with odontoid fractures. Patient demographic and treatment data were investigated and compared according to the treatment strategy. To determine associations with worsening ambulation after 6 months, we focused on the treatment strategies (nonsurgical treatment [collar immobilization or halo vest], conversion to surgery, or initial surgery) and patients' background. Patients who received nonsurgical treatment were significantly older, and patients who underwent surgery had more Anderson-D'Alonzo type 2 fractures. Of the patients initially treated nonsurgically, 26% later underwent surgery. Numbers of complications, including death, and degrees of ambulation after 6 months did not differ significantly among treatment strategies. Patients who had worsened ambulation after 6 months were significantly more likely to be older than 80 years, to have needed assistance with walking before injury, and to have cerebrovascular disease. Multivariable analysis showed that a score of ≥2 on the 5-item modified frailty index (mFI-5) was significantly associated with worsening ambulation. Preinjury mFI-5 scores of ≥2 were significantly associated with worsening ambulation 6 months after treatment of cervical odontoid fractures in older adults. [ABSTRACT FROM AUTHOR]

We investigated the feasibility of using compressed sensitivity encoding (CS-SENSE) to accelerate high-resolution black-blood T1-weighted imaging with variable flip angles (T1WI-VFA) for efficient visualization and characterization of lenticulostriate arteries (LSAs) on a 3.0 T MR scanner. Twenty-five healthy volunteers and 18 patients with the cerebrovascular disease were prospectively enrolled. Healthy volunteers underwent T1WI-VFA sequences with different acceleration factors (AFs), including conventional sensitivity encoding (SENSE) AF = 3 and CS-SENSE AF = 3, 4, 5, and 6 (SENSE3, CS3, CS4, CS5, CS6, respectively) at 3 Tesla MRI scanner. Objective evaluation (contrast ratio and number, length, and branches of LSAs) and subjective evaluation (overall image quality and LSA visualization scores) were used to assess image quality and LSA visualization. Comparisons were performed among the 5 sequences to select the best AF. All patients underwent both T1WI-VFA with the optimal AF and digital subtraction angiography (DSA) examination, and the number of LSAs observed by T1WI-VFA was compared with that by DSA. Pair-wise comparisons among CS3, CS4, and SENSE3 revealed no significant differences in both objective measurements and subjective evaluation (all P > 0.05). In patients, there was no significant difference in LSA counts on the same side between T1WI-VFA with CS4 and DSA (3, 3–4 and 3, 3–3, P = 0.243). CS3 provided better LSA visualization but a longer scan duration compared to CS4. And, CS4 strikes a good balance between LSA visualization and acquisition time, which is recommended for routine clinical use. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) is increasingly recognized as a common condition in the general population and causes significant OSA-associated morbidities including cardiovascular and cerebrovascular events such as cerebral small vessel disease (CSVD) and stroke. In this study, using sensitive ELISA immunoassays, we measured subset of endothelial/vascular and inflammatory biomarkers as well as neurofilament light chain (NfL), a sensitive marker for neuroaxonal injury, using plasma from OSA patients post-stroke (Acute Cerebral Infarction (ACI), N = 26) to determine their usefulness as potential prognostic markers in disease progression. Our results showed significantly increased plasma TNFα and NfL concentrations and decreased concentrations of platelet derived growth factor (PDGF-AA) in post-stroke OSA patients with more severe white matter hyperintensities (WMHs). And after separating the patients based on sex, compared to females, male post-stroke OSA patients with severe WMHs have increased circulating levels of inflammatory chemokine CXCL10 and cytokine Interleukin-10 (IL-10) and significantly decreased levels of Angiopoietin-1 (Ang-1) an important protein responsible for endothelial/vascular integrity functions. Importantly, in a subset of newly diagnosed OSA patients (without prior history of stroke), significantly increased plasma CXCL10 levels and decreased plasma Ang-1 levels were also readily observed when compared to healthy controls, indicating possible altered endothelial integrity and ongoing vascular inflammation in these newly diagnosed OSA patients. In summary, our study has identified a novel set of plasma biomarkers including PDGF-AA, CXCL10 and Ang-1 for their potential prognostic value for disease outcomes pre- and post-stroke in OSA patients and use as surrogate markers to measure efficacy of treatment modalities. • Increased plasma Neurofilament light (NfL) were seen in post-stroke OSA patients. • Decreased plasma levels of PDGF-AA were seen in post-stroke OSA patients. • In post-stroke OSA males, decreased levels of Angiopoietin-1 (Ang-1) were seen. • In newly diagnosed OSA patients, increased plasma CXCL10 levels were detected. • In newly diagnosed OSA patients, decreased plasma Ang-1 levels were observed. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most prevalent sleep and respiratory disorder. This syndrome can induce severe cardiovascular and cerebrovascular complications, and intermittent hypoxia is a pivotal contributor to this damage. Vascular pathology is closely associated with the impairment of target organs, marking a focal point in current research. Vascular lesions are the fundamental pathophysiological basis of multiorgan ailments and indicate a shared pathogenic mechanism among common cardiovascular and cerebrovascular conditions, suggesting their importance as a public health concern. Increasing evidence shows a strong correlation between OSAHS and vascular lesions. Previous studies predominantly focused on the pathophysiological alterations in OSAHS itself, such as intermittent hypoxia and fragmented sleep, leading to vascular disruptions. This review aims to delve deeper into the vascular lesions affected by OSAHS by examining the microscopic pathophysiological mechanisms involved. Emphasis has been placed on examining how OSAHS induces vascular lesions through disruptions in the endothelial barrier, metabolic dysregulation, cellular phenotype alterations, neuroendocrine irregularities, programmed cell death, vascular inflammation, oxidative stress and epigenetic modifications. This review examines the epidemiology and associated risk factors for OSAHS and vascular diseases and subsequently describes the existing evidence on vascular lesions induced by OSAHS in the cardiovascular, cerebrovascular, retinal, renal and reproductive systems. A detailed account of the current research on the pathophysiological mechanisms mediating vascular lesions caused by OSAHS is provided, culminating in a discussion of research advancements in therapeutic modalities to mitigate OSAHS-related vascular lesions and the implications of these treatment strategies. • OSAHS can lead to vascular lesions in various systems throughout the body. • OSAHS mediates vascular lesions through multiple molecular and cellular mechanisms. • The treatment of vascular lesions concurrent with OSHAS has been explored but still faces numerous challenges. [ABSTRACT FROM AUTHOR]

• A systematic review of the pathophysiologic processes of SAH was conducted. • The role of natural compounds in the pathophysiologic process of SAH. • Signaling pathway mechanisms by which natural compounds act in SAH. • Natural compounds are categorized in detail. • Evaluate the prognostic potential of natural compounds to improve SAH. Subarachnoid hemorrhage (SAH) is a common and fatal cerebrovascular disease with high morbidity, mortality and very poor prognosis worldwide. SAH can induce a complex series of pathophysiological processes, and the main factors affecting its prognosis are early brain injury (EBI) and delayed cerebral ischemia (DCI). The pathophysiological features of EBI mainly include intense neuroinflammation, oxidative stress, neuronal cell death, mitochondrial dysfunction and brain edema, while DCI is characterized by delayed onset ischemic neurological deficits and cerebral vasospasm (CVS). Despite much exploration in people to improve the prognostic outcome of SAH, effective treatment strategies are still lacking. In recent years, numerous studies have shown that natural compounds of plant origin have unique neuro- and vascular protective effects in EBI and DCI after SAH and long-term neurological deficits, which mainly include inhibition of inflammatory response, reduction of oxidative stress, anti-apoptosis, and improvement of blood–brain barrier and cerebral vasospasm. The aim of this paper is to systematically explore the processes of neuroinflammation, oxidative stress, and apoptosis in SAH, and to summarize natural compounds as potential targets for improving the prognosis of SAH and their related mechanisms of action for future therapies. [ABSTRACT FROM AUTHOR]

Stroke is a leading cause of morbidity and mortality in the United States among older adults. However, the impact of demographic and geographic risk factors remains ambiguous. A clear understanding of these associations and updated trends in stroke mortality can influence health policies and interventions. This study characterizes stroke mortality among older adults (age ≥55) in the US from January 1999 to December 2020, sourcing data from the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research. Segmented regression was used to analyze trends in crude mortality rate and age-adjusted mortality rate (AAMR) per 100,000 individuals stratified by stroke subcategory, sex, ethnicity, urbanization, and state. A total of 3,691,305 stroke deaths occurred in older adults in the US between 1999 and 2020 (AAMR = 233.3), with an overall decrease in AAMR during these years. The highest mortality rates were seen in nonspecified stroke (AAMR = 173.5), those 85 or older (crude mortality rate1276.7), men (AAMR = 239.2), non-Hispanic African American adults (AAMR = 319.0), and noncore populations (AAMR = 276.1). Stroke mortality decreased in all states from 1999 to 2019 with the greatest and least decreases seen in California (−61.9%) and Mississippi (−35.0%), respectively. The coronavirus pandemic pandemic saw increased stroke deaths in most groups. While there's a decline in stroke-related deaths among US older adults, outcome disparities remain across demographic and geographic sectors. The surge in stroke deaths during coronavirus pandemic reaffirms the need for policies that address these disparities. [ABSTRACT FROM AUTHOR]

Vascular neurosurgery has developed significantly in Nigeria, but its burden and challenges remain unclear. This study systematically reviewed vascular neurosurgical literature from Nigeria. Four research databases and gray literature sources were searched from 1962–2021. ROBINS-I tool was used to assess risk of bias. Descriptive, narrative, and statistical analyses were conducted on all variables. Where appropriate, paired t-tests and Chi-squared independence tests were used (α = 0.05). 56 articles were included and 3203 patients pooled for analysis. Risk of bias was moderate-high. Most articles were published over the last 20 years with retrospective cohort studies and case reports being the most common study designs. The cohort had a relatively even gender split and an average age of 49 years (±22). Cerebrovascular accidents accounted for over 85% of diagnoses, with most etiologies being traumatic. Headache and motor deficit were the most prevalent clinical features. X-ray and carotid angiography were the most commonly reported imaging modalities, closely followed by computed tomography (CT) and CT angiography. The top two radiological diagnoses were ischemic cerebrovascular disease and intracerebral hematoma. Aneurysmal clipping and hematoma evacuation were the most commonly reported treatment modalities. Outcome at last follow-up was favorable in 48%. The mortality rate was 6%. Post-treatment complications included chest infection and rebleeding. This study illustrates the epidemiological burden of neurovascular pathology (based on the available data in published literature) in Nigeria, and raises awareness amongst service providers and researchers of the attendant challenges and epochal trends seen within vascular neurosurgery in Nigeria. [ABSTRACT FROM AUTHOR]

Chikungunya virus outbreaks have been associated with excess deaths at the ecological level. Previous studies have assessed the risk factors for severe versus mild chikungunya virus disease. However, the risk of death following chikungunya virus disease compared with the risk of death in individuals without the disease remains unexplored. We aimed to investigate the risk of death in the 2 years following chikungunya virus disease. We used a population-based cohort study and a self-controlled case series to estimate mortality risks associated with chikungunya virus disease between Jan 1, 2015, and Dec 31, 2018, in Brazil. The dataset was created by linking national databases for social programmes, notifiable diseases, and mortality. For the matched cohort design, individuals with chikungunya virus disease recorded between Jan 1, 2015, and Dec 31, 2018, were considered as exposed and those who were arbovirus disease-free and alive during the study period were considered as unexposed. For the self-controlled case series, we included all deaths from individuals with a chikungunya virus disease record, and each individual acted as their own control according to different study periods relative to the date of disease. The primary outcome was all-cause natural mortality up to 728 days after onset of chikungunya virus disease symptoms, and secondary outcomes were cause-specific deaths, including ischaemic heart diseases, diabetes, and cerebrovascular diseases. In the matched cohort study, we included 143 787 individuals with chikungunya virus disease who were matched, at the day of symptom onset, to unexposed individuals using sociodemographic factors. The incidence rate ratio (IRR) of death within 7 days of chikungunya symptom onset was 8·40 (95% CI 4·83–20·09) as compared with the unexposed group and decreased to 2·26 (1·50–3·77) at 57–84 days and 1·05 (0·82–1·35) at 85–168 days, with IRR close to 1 and wide CI in the subsequent periods. For the secondary outcomes, the IRR of deaths within 28 days after disease onset were: 1·80 (0·58–7·00) for cerebrovascular diseases, 3·75 (1·33–17·00) for diabetes, and 3·67 (1·25–14·00) for ischaemic heart disease, and there was no evidence of increased risk in the subsequent periods. For the self-controlled case series study, 1933 individuals died after having had chikungunya virus disease and were included in the analysis. The IRR of all-cause natural death within 7 days of symptom onset of chikungunya virus disease was 8·75 (7·18–10·66) and decreased to 1·59 (1·26–2·00) at 57–84 days and 1·09 (0·92–1·29) at 85–168 days. For the secondary outcomes, the IRRs of deaths within 28 days after disease onset were: 2·73 (1·50–4·96) for cerebrovascular diseases, 8·43 (5·00–14·21) for diabetes, and 2·38 (1·33–4·26) for ischaemic heart disease, and there was no evidence of increased risk at 85–168 days. Chikungunya virus disease is associated with an increased risk of death for up to 84 days after symptom onset, including deaths from cerebrovascular diseases, ischaemic heart diseases, and diabetes. This study highlights the need for equitable access to approved vaccines and effective anti-chikungunya virus therapeutics and reinforces the importance of robust vector-control efforts to reduce viral transmission. Brazilian National Research Council (CNPq), Fundação de Amparo à Pesquisa do Estado da Bahia, Wellcome Trust, and UK Medical Research Council. For the Portuguese translation of the abstract see Supplementary Materials section. [ABSTRACT FROM AUTHOR]

• In a population of non-institutionalized 75 years-old subjects, lncRNA H19 predicts all-cause mortality over a follow-up of 14 years. • lncRNA H19 is differentially expressed in males and females, and it is a possible feature of sex differences in lifespan. • low-levels of lncRNA NKILA are associated with an increased risk of lacunar stroke, detected by magnetic resonance, over a follow-up of 7.5 years. Differential expression of long non-coding RNAs (lncRNAs) is a hallmark of cardiovascular aging, cerebrovascular diseases, and neurodegenerative disorders. This research article investigates the association between a panel of lncRNAs and the risk of death and ischemic stroke in a cohort of non-institutionalized elderly subjects. A total of 361 healthy individuals aged 75 years old, prospectively recruited in the Vienna Transdanube Aging (VITA) cohort, were included. Expression of lncRNAs at baseline was assessed using quantitative polymerase chain reaction PCR with pre-amplification reaction, using 18S for normalization. The primary endpoint was all-cause mortality; the secondary endpoint was the incidence of new ischemic brain lesions. Death was assessed over a 14-year follow-up, and ischemic brain lesions were evaluated by magnetic resonance imaging (MRI) over a 90-month follow-up. Ischemic brain lesions were divided into large brain infarcts (Ø ≥ 1.5 cm) or lacunes (Ø < 1.5 cm) The primary endpoint occurred in 53.5 % of the study population. The incidence of the secondary endpoint was 16 %, with a 3.3 % being large brain infarcts, and a 12.7 % lacunes. After adjustment for potential confounders, the lncRNA H19 predicted the incidence of the primary endpoint (HR 1.194, 95 % C.I. 1.012–1.409, p = 0.036), whereas the lncRNA NKILA was associated with lacunar stroke (HR 0.571, 95 % C.I. 0.375–0.868, p = 0.006). In a prospective cohort of non-institutionalized elderly subjects, high levels of lncRNA H19 are associated with a higher risk of death, while low levels of lncRNA NKILA predict an increased risk of lacunar stroke. [Display omitted] [ABSTRACT FROM AUTHOR]

Cet article traite de la prise en charge de la maladie thromboembolique veineuse chez les patients atteints de tumeurs cérébrales malignes, primitives ou secondaires (métastatiques). Les données disponibles concernant les risques de récidive veineuse thromboembolique et de risque hémorragique chez les patients atteints de tumeurs cérébrales sont limitées, ces patients ayant été exclus de la plupart des essais cliniques randomisés, interventionnels, comparant les héparines de bas poids moléculaire aux anti-vitamine K ou aux inhibiteurs directs du facteur Xa administrés par voie orale. Des études observationnelles rétrospectives, généralement menées sur de faibles effectifs et comportant un risque élevé de facteurs confondants, fournissent davantage d'informations. Leurs conclusions suggèrent que l'utilisation d'inhibiteurs directs du facteur Xa est associée à des taux plus faibles d'hémorragies intracrâniennes que les héparines de bas poids moléculaire. Dans l'ensemble, le profil de sécurité des inhibiteurs directs du facteur Xa, lorsqu'ils sont utilisés pour prévenir la récidive de la maladie thromboembolique veineuse chez les patients atteints de tumeurs cérébrales primitives ou secondaires, semble favorable. Les données disponibles sont en faveur de l'utilisation d'un anticoagulant à une dose thérapeutique chez les patients atteints de tumeurs cérébrales primitives et secondaires ayant présenté événement thromboembolique veineux, mais ne sont toutefois pas encore suffisamment solides pour permettre de recommander un inhibiteur direct du facteur Xa plutôt qu'une héparine de bas poids moléculaire. This article addresses the management of venous thromboembolism in patients with malignant brain tumours, including both primary and secondary (metastatic) tumours. The available data on patients on venous thromboembolism recurrence and bleeding risks in patients with brain tumours is limited, since these patients have been excluded from most randomised, interventional, head-to-head, clinical trials comparing low molecular weight heparins to vitamin K antagonists or to direct oral factor Xa inhibitors. More information is available from retrospective observational studies, which however were generally small, and carried a high risk of confounding. Their findings suggest that direct factor Xa inhibitor use is associated with lower rates of intracranial haemorrhage compared with low molecular weight heparins. Overall, the safety profile of direct oral factor Xa inhibitors when used to prevent venous thromboembolism recurrence in patients with either primary or secondary brain tumours appears to be favourable. The available data are in favour of using an anticoagulant at a full therapeutic dose in patients with primary and secondary brain tumours experiencing a venous thromboembolism, although they are not yet sufficiently robust to permit recommending a direct factor Xa inhibitor over low-molecular weight heparin. [ABSTRACT FROM AUTHOR]

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Guidelines no longer recommend low-fat diets and currently recommend more plant-based diets to reduce atherosclerotic cardiovascular disease (ASCVD) risk. Furthermore, these guidelines have consistently recommended salt-reduced diets. This article describes current self-reported use and time-trends in the self-reported use of low-fat, low-salt and vegetarian diets in ASCVD patients and examines patient characteristics associated with each diet. 9005 patients with ASCVD included between 1996 and 2019 in the UCC-SMART cohort were studied. The prevalence of self-reported diets was assessed and multi-variable logistic regression was used to identify the determinants of each diet. Between 1996-1997 and 2018–2019, low-fat diets declined from 22.4 % to 3.8 %, and low-salt diets from 14.7 % to 4.6 %. The prevalence of vegetarian diets increased from 1.1 % in 1996–1997 to 2.3 % in 2018–2019. Patients with cerebrovascular disease (CeVD) and peripheral artery disease or an abdominal aortic aneurysm (PAD/AAA) were less likely to report a low-salt diet than coronary artery disease (CAD) patients (OR 0.62 [95%CI 0.49–0.77] and 0.55 [95%CI 0.41–0.72]). In the period 1996 to 2019 amongst patients with ASCVD, the prevalence of self-reported low-fat diets was low and decreased in line with changes in recommendations in major guidelines. The prevalence of self-reported vegetarian diets was low but increased in line with societal and guideline changes. The prevalence of self-reported low-salt diets was low, especially in CeVD and PAD/AAA patients compared to CAD patients, and decreased over time. Renewed action is needed to promote low-salt diets in ASCVD patients. • A small and decreasing proportion of patients with ASCVD reports a low-salt diet. • Renewed efforts are needed to promote low-salt diets in this population. • While still low, an increasing number of CVD patients reports a vegetarian diet. • Further research is needed on the vegetarian diet's health impact in CVD patients. [ABSTRACT FROM AUTHOR]

Numerous studies suggest that the gut microbiota closely linked to cerebrovascular diseases, such as Intracranial aneurysm (IA) and aneurysmal subarachnoid hemorrhage (aSAH). Nevertheless, the confirmation of a definitive causal connection between gut microbiota, IA, and aSAH is still pending. The aim of our research is to explore the potential bidirectional causality among them. This bidirectional Mendelian Randomization (MR) study used single nucleotide polymorphisms linked to gut microbiota, IA, and aSAH from Genome-Wide Association Studies. The Inverse Variance Weighted (IVW) method was used to explore causality. To assess the robustness of the result, sensitivity analyses were further performed, including weighted-median method, MR-Egger regression, Maximum-likelihood method, MR pleiotropy residual sum and outlier test and leave-one-out analysis. In the IVW method, the family Porphyromonadaceae (odds ratio [OR] 0.63; 95% CI 0.47–0.85; P : 0.002) and genus Bilophila (OR 0.66; 95% CI 0.50–0.86; P : 0.002) showed a significant negative association with the risk of IA. Similarly, the genus Bilophila (OR: 0.68; 95% CI: 0.50–0.93; P : 0.017) and genus Ruminococcus1 (OR: 0.48; 95% CI: 0.30–0.78; P : 0.003) were linked to reduced risk of aSAH. The sensitivity analysis yielded similar outcomes in the IVW approach. Through the adoption of reverse MR analysis, a potential correlation between IA and decreased abundance of genus Ruminococcus1 was identified (OR 0.94; 95% CI 0.90–0.99; P 0.024). This MR analysis investigated the causal associations between gut microbiota, IA, and aSAH risks. The findings expanded current knowledge of the microbiota-gut-brain axis and offered novel perspectives on preventing and managing these conditions. [ABSTRACT FROM AUTHOR]

Apart from their diagnostic, monitoring, or prognostic utility in clinical settings, molecular biomarkers may be instrumental in understanding the pathophysiology of psychiatric disorders, including schizophrenia. Using untargeted metabolomics, we recently identified eight cerebrospinal fluid (CSF) metabolites unique to first-episode psychosis (FEP) subjects compared to healthy controls (HC). In this study, we sought to investigate the CSF proteomic signatures associated with FEP. We employed 16-plex tandem mass tag (TMT) mass spectrometry (MS) to examine the relative protein abundance in CSF samples of 15 individuals diagnosed with FEP and 15 age-and-sex-matched healthy controls (HC). Multiple linear regression model (MLRM) identified 16 differentially abundant CSF proteins between FEP and HC at p < 0.01. Among them, the two most significant CSF proteins were collagen alpha-2 (IV) chain (COL4A2: standard mean difference [SMD] = −1.12, p = 1.64 × 10−4) and neuron-derived neurotrophic factor (NDNF: SMD = −1.03, p = 4.52 × 10−4) both of which were down-regulated in FEP subjects compared to HC. We also identified several potential CSF proteins associated with the pathophysiology and the symptom profile and severity in FEP subjects, including COL4A2, NDNF, hornerin (HRNR), contactin-6 (CNTN6), voltage-dependent calcium channel subunit alpha-2/delta-3 (CACNA2D3), tropomyosin alpha-3 chain (TPM3 and TPM4). Moreover, several protein signatures were associated with cognitive performance. Although the results need replication, our exploratory study suggests that CSF protein signatures can be used to increase the understanding of the pathophysiology of psychosis. [Display omitted] • Quantification of 1888 proteins from first-episode psychosis (FEP) and healthy control (HC) subjects. • Identification of 72 differentially abundant CSF proteins between FEP and HC subjects. • Analyses of potential CSF biomarkers of FEP that imply synaptic, cerebrovascular, and metabolic dysfunctions. [ABSTRACT FROM AUTHOR]

• Non-invasive imaging enhances atherosclerosis evaluation beyond anatomy. • CTA identifies high-risk plaque features in coronary heart disease. • FAI and PCAT offer cardiac event prediction. • MRI enables precise phenotyping of vulnerable plaque components. • Insightful molecular imaging reveals plaque development and rupture. Atherosclerosis is a chronic inflammatory disease characterized by the buildup of plaques in arterial walls, leading to cardiovascular diseases and high morbidity and mortality rates worldwide. Non-invasive imaging techniques play a crucial role in evaluating patients with suspected or established atherosclerosis. However, there is a growing body of evidence suggesting the need to visualize the underlying processes of plaque progression and rupture to enhance risk stratification. This review explores recent advancements in non-invasive assessment of atherosclerosis, focusing on computed tomography, magnetic resonance imaging, and nuclear imaging. These advancements provide valuable insights into the assessment and management of atherosclerosis, potentially leading to better risk stratification and improved patient outcomes. [ABSTRACT FROM AUTHOR]

The occurrence of dural arteriovenous fistulas (DAVFs) at the craniocervical junction (CCJ) is an uncommon vascular malformation. The diagnosis and treatment of CCJ DAVFs present a formidable challenge. This study aims to investigate the effect of endovascular embolization and microsurgery on improving patient prognosis. This retrospective study included patients diagnosed with CCJ DAVFs who received treatment at the First Affiliated Hospital of Fujian Medical University between January 2000 and January 2023. The clinical records, imaging data, and treatment methods were obtained from the hospital's medical record system. The patients were classified into microsurgery and embolization groups based on the surgical technique employed for treatment. The primary outcome measures were surgical-associated neurological dysfunction (SAND) and long-term neurological outcomes. The Cox proportional hazard regression was utilized to determine hazard ratios and 95% confidence intervals (CI) to assess the relationship between treatment methods and prognosis. Kaplan-Meier survival analysis was employed to evaluate the incidence of SAND in both cohorts. This study recruited 46 patients with an average age of 53.72 ± 13.83 years. In the microsurgery group, there were 12 cases (26.1%) observed. While in the embolization group, there were 34 cases (73.9%). Of these patients, 16 (34.8%) experienced SAND after treatment. In the microsurgery group, there were 8 cases (75.0%), while in the embolization group, only 8 cases (23.5%) were reported. Specifically, the embolization group exhibited a significantly lower risk of SAND [adjusted hazard ratio = 0.259, 95% CI = 0.096–0.700; P = 0.008)] compared to the microsurgery group. Additionally, the combined Borden grade 2–3 was found to be significantly associated with SAND (adjusted hazard ratio = 3.150, 95% CI = 1.132–8.766; P = 0.028). The results of the Kaplan-Meier survival analysis indicated a statistically significant difference in the occurrence of favorable functional outcomes between the 2 groups (log-rank P = 0.0081). CCJ DAVFs are uncommon disorders characterized by a diverse range of clinical manifestations. The functional prognosis of endovascular treatment may be superior to microsurgery. [ABSTRACT FROM AUTHOR]

Moyamoya disease (MMD) is a rare and complex cerebrovascular disorder that is diagnosed through imaging studies, such as computed tomography or magnetic resonance imagin, which show progressive narrowing of the terminal portion of the internal carotid arteries and the development of compensatory capillary collaterals. The objective of our study was to identify and clarify the predictive factors for seizures in patients with MMD. From January 2019 to March 2023, a total of 102 patients with MMD were enrolled in this study. Ten patients with seizures after surgery as the main presentation were included. Patients with epilepsy were compared to those without epilepsy in terms of their clinical characteristics. Multivariable analysis was applied to determine factors linked with postoperative seizures. Ten patients developed seizures after revascularization for MMD. Logistic regression analysis revealed that early seizure (odds ratio [OR], 0.068; 95% CI, 0.014–0.342; P = 0.001), cortical involvement (OR, 9.593; 95% CI, 2.256–40.783; P = 0.002), and postoperative hyperperfusion (OR, 7.417; 95% CI, 1.077–51.093; P = 0.042) were significantly associated with seizures. In a multivariate analysis, it was found that early seizures were significantly associated with a higher likelihood of experiencing seizures (OR, 5.88; 95% CI, 1.01–33.96; P = 0.048), while patients who had seizures were more likely to have cortical involvement (OR, 8.90; 95% CI, 1.55–50.96; P = 0.014) or postoperative hyperperfusion (OR, 12.44; 95% CI, 1.21–127.74; P = 0.034). Epilepsy in patients with MMD link with several clinical factors. In patients with MMD who undergo bypass surgery, early seizures, cortical involvement, and postoperative hyperperfusion are significant independent predictive factors for the development of epilepsy. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage (SAH) is a cerebrovascular disorder with significant mortality and morbidity. Neural injury in SAH is mediated through a variety of pathophysiological processes. Currently available treatments are either nonspecific in targeting the basic pathophysiological mechanisms that result in neural damage in SAH, or merely focus on vasospasm. Ferroptosis is a type of programmed iron dependent cell death, which has received attention due to its possible role in neural injury in SAH. Herein, we review how intracellular iron overload mediates the production of reactive free radicals and lipid peroxidation through a variety of biochemical pathways in SAH. This in turn results in induction of ferroptosis, as well as exacerbation of vasospasm. We also discuss several therapeutic agents that have been shown to inhibit ferroptosis through targeting different steps of the process. Such agents have proven effective in ameliorating vasospasm, neural damage, and neurobehavioral outcomes in animal models of SAH. Human studies to test the safety and efficacy of intrathecal or parenteral administration of the inhibitors of ferroptosis in improving outcomes of SAH patients are warranted. There are currently a few ongoing clinical trials pursuing this therapeutic concept, the results of which will be critical to determine the value of ferroptosis as a novel therapeutic target in SAH. [ABSTRACT FROM AUTHOR]

• We leveraged genetic variants associated specifically with hypertension (122,620 cases and 332,683 controls), systolic (469,767 individuals), diastolic (490,469 individuals) blood pressure, pulse pressure (810,865 individuals) and mean arterial pressure (over 1 million individuals) to evaluate their effects on brain cortex surficial area (51,665 individuals) and cortex thickness (51,665 individuals). • Our findings revealed a significant correlation between elevated systolic blood pressure and abnormal reduction in brain cortex surficial area (β=−1330.69, 95% confident interval [CI]: −2655.35 to −6.02, p = 0.0489). However, no significant relationship was found between systolic blood pressure and brain cortex thickness (β=−0.0078, p = 0.1287). • No significant associations were observed between hypertension (β=−200.05, p = 0.6884; β=−0.0051, p = 0.1179, respectively), diastolic blood pressure (β=−460.63, p = 0.5160; β=0.0047, p = 0.2448, respectively), pulse pressure (β=1041.84, p = 0.3725; β=−0.0112, p = 0.2212, respectively), mean arterial pressure (β=−18.84, p = 0.8841; β=0.0002, p = 0.7654, respectively) and both brain cortex surficial area and brain cortex thickness. Hypertension has been recognized as a significant risk factor for cerebrovascular diseases and cognitive decline. However, the specific impact of hypertension, systolic/diastolic blood pressure, pulse pressure (PP) and mean arterial pressure (MAP) on brain cortical structure remains unclear. Mendelian randomization (MR) provides a robust approach to investigate the causal relationship between blood pressure components and brain cortical changes. In this MR study, data from large-scale genome-wide association studies for blood pressure components and neuroimaging were utilized to conduct our analyses. We leveraged genetic variants associated specifically with hypertension (122,620 cases and 332,683 controls), systolic (469,767 individuals), diastolic (490,469 individuals) blood pressure, PP (810,865 individuals) and MAP (over 1 million individuals) to evaluate their effects on brain cortex surficial area (51,665 individuals) and cortex thickness (51,665 individuals). Our findings revealed a significant correlation between systolic blood pressure and abnormal reduction in brain cortex surficial area (β=-1330.69, 95% confident interval [CI]: -2655.35 to -6.02, p = 0.0489); however, no significant relationship was found between systolic blood pressure and brain cortex thickness (β=-0.0078, 95% CI: -0.0178 to 0.0022, p = 0.1287). Additionally, no significant associations were observed between hypertension (β=-200.05, p = 0.6884; β=-0.0051, p = 0.1179, respectively), diastolic blood pressure (β=-460.63, p = 0.5160; β=0.0047, p = 0.2448, respectively), PP (β=1041.84, p = 0.3725; β=-0.0112, p = 0.2212, respectively), MAP (β=-18.84, p = 0.8841; β=0.0002, p = 0.7654, respectively) and both brain cortex surficial area and brain cortex thickness. Our MR study provides evidence supporting the hypothesis that systolic blood pressure, rather than diastolic blood pressure, PP or MAP, is associated with abnormal changes in brain cortical structure. [ABSTRACT FROM AUTHOR]

It has not been fully elucidated that nutritional parameters affect the change of activities of daily living (ADL) during pneumonia treatment. This study assessed the impact of nutritional status, including erector spinae muscle (ESM) size on ADL changes from admission to discharge among older patients with community-acquired pneumonia (CAP). We retrospectively included patients (age: ≥65 years) who were admitted to the hospital for CAP and underwent chest computed tomography (CT) on admission. ADL was evaluated using the Barthel index, and patients were divided into the maintained or improved ADL group and the declined ADL group from admission through discharge. The ESM cross-sectional area was measured on a single-slice CT image. Logistic regression models were applied for assessing factors associated with changes in ADL. A total of 523 patients hospitalized for CAP (median age 86 years) were evaluated. The declined group had significantly higher ADL levels on admission, a greater frequency of smoking history and malignancy, and a lower frequency of cerebrovascular disease and dementia. No significant difference in ESM size was observed between the groups. Multivariate analysis revealed that higher ADL levels on admission (odds ratio 1.034, interquartile range 1.026–1.043) and malignancy (3.002, 1.150–7.836) were associated with a decline in ADL, whereas cerebrovascular disease (0.579, 0.373–0.900) was related to improvement or maintenance of ADL. Although nutritional status might not affect the change of ADL among older patients hospitalized with pneumonia, a cerebrovascular disease history may be a good predictor for ADL improvement. [ABSTRACT FROM AUTHOR]

People with schizophrenia are at a greater risk of poor physical health than the general population. This study investigated the annual incidence of physical illnesses after a new schizophrenia diagnosis, which has rarely been investigated in the literature. The authors collected data from Taiwan's National Health Insurance Research Database from January 1, 1996, to December 31, 2013, and enrolled 1910 patients with newly diagnosed schizophrenia cases aged 10–40 years and 7640 age- and sex-matched controls from the general population. They estimated the 1-year prevalence and annual incidence rate ratio (IRR) of specified physical diseases across 3 years in the schizophrenia group compared with the controls. Several physical illnesses were prevalent within 1 year of schizophrenia diagnosis. Regarding incident physical illnesses, patients had a moderate to strong risk of numerous physical illnesses (IRR > 3.0: ischemic heart disease, cerebrovascular disease, diabetes mellitus, and cancer; IRR 1.8–3.0: other forms of heart disease, vein and lymphatic diseases, pneumonia, chronic hepatic disease, and ulcer disease) within the first year after schizophrenia diagnosis. The IRRs of most physical illnesses declined over 3 years, except for that of cerebrovascular disease, which significantly increased (IRR > 3.0) over the 3 years after schizophrenia diagnosis. Cerebrovascular disease had a significant incidence risk (IRR > 3) persistently across the 3 years. Various comorbid physical illnesses can occur in the early stages of schizophrenia. Clinicians should consider these vulnerabilities to physical illnesses during the evaluation of patients with newly diagnosed schizophrenia by attempting to prevent, screen for, and manage them. [ABSTRACT FROM AUTHOR]

Cerebral microbleeds (CMB) are often associated with vascular risk factors and/or cerebral amyloid angiopathy and are frequently identified in people with dementia. The present study therefore aimed to estimate the pooled prevalence and associations of CMB in Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), using meta-analytic methods. Sixty-five MRI studies were included after a systematic search on major electronic databases. We found that the prevalence of CMB was comparable across the three dementia subtypes (31–36%) and was highly influenced by the MRI techniques used. CMB in AD were associated with a history of hypertension and amyloid-β burden. In contrast, CMB in DLB, despite being predominantly lobar, were associated with hypertension, but not amyloid-β burden. These findings suggest that the underlying pathophysiology of CMB in DLB might differ from that of AD. There was substantially larger number of AD studies identified and more studies evaluating CMB in Lewy body dementias are warranted. • Microbleeds were present in approximately one-third of common dementia diagnoses. • The prevalence of microbleeds is highly influenced by MRI techniques. • The pathophysiology of microbleeds might differ between dementia subtypes. • More studies investigating microbleeds in Lewy body dementias are needed. [ABSTRACT FROM AUTHOR]

Limited published data exists that collates serious adverse outcomes involving ketamine as a psychiatric intervention. This systematic review assesses the reported incidence of medical serious adverse events (MSAEs), including but not limited to cardiovascular events, in patients receiving sub-anesthetic doses of ketamine for psychiatric disorders to guide practitioners during treatment planning, risk-benefit analyses, and the informed consent process. Pubmed database was searched for clinical trials of sub-anesthetic ketamine for psychiatric disorders in non-pregnant adult patients. Of the 2275 articles identified, 93 met inclusion criteria, over half of which were published in 2017 or later. Only studies that reported adverse events were included, and the incidence of MSAEs was calculated. Of the 3756 participants who received at least one sub-anesthetic dose of ketamine, four participants experienced a MSAE, resulting in an incidence of approximately 0.1 % of individuals. The four MSAEs resolved without reported sequelae. Eighty-three percent of studies reported screening for medical illness and exclusion of high-risk patients. There were no serious cardiac adverse events or deaths observed in any participants; however, most trials' study designs excluded those with high cardiovascular complication risk. Most studies were small, underpowered for detecting rare MSAEs, at potential high-risk of bias of non-report of MSAEs, and limited mostly to intranasal and intravenous routes. Findings suggest that with basic medical screening there is a very low incidence of MSAEs including adverse cardiac or cerebrovascular events in individuals receiving sub-anesthetic ketamine for psychiatric disorders. • 0.1% of individuals who received ketamine for psychiatric disorders experienced a medical serious adverse event • There were no serious cardiac adverse events in any of the 3,756 participants • Transient elevations of heart rate and blood pressure with use of sub-anesthetic ketamine are usually not dangerous [ABSTRACT FROM AUTHOR]

Moyamoya disease (MMD) cannot be found commonly as a rare type compared with other vascular disease, such as aneurysm. However, it cannot be ignored for its high fatality and disability rates. In addition, exact pathogenesis study of this disease is still on the way. The ivy sign is always observed in MMD, but the clinical importance of this sign in MMD isn't clearly known. The main purpose of this research was to specifically investigate the clinical significance. In this retrospective cohort study to gather the baseline clinical and imaging study, the patients with MMD were hospitalized from January 2016 to 2020. In the analysis, univariate and multivariate logistic regression was used to testify whether ivy sign was independently associated with MMD characteristics including cerebrovascular morphology, cerebral hemodynamics, cerebrovascular events, and postoperative collateral formation (PCF). We included 156 patients with 312 hemispheres. As for the result of multivariate logistic regression analysis, we could discover a fact that ivy sign was tightly connected to the Suzuki stage ≥IV (odds ratio [OR], 1.386; 95% confidence interval [CI], 1.055–1.822; P = 0.019), cerebral blood flow (CBF) decreased type (OR, 2.330; 95% CI, 1.733–3.133; P = 0.000), age acted as a protective factor for CBF (OR, 0.966; 95% CI, 0.946–0.986; P = 0.001), the elder was more likely associated with decreased CBF. Ivy sign also played a significant role in ischemic cerebrovascular events (OR, 5.653; 95% CI, 3.092–10.336; P = 0.003), their remarkable connection could be seen on the study. We could also find that ivy sign was closely connected to the good PCF (OR, 2.830; 95% CI, 1.329–6.027; P = 0.007), and we couldn't ignore the fact that age was associated with good PCF as well (OR, 0.933; 95% CI, 0.882–0.987; P = 0.015). We could be more aware of the connection between ivy sign and Moyamoya disease from this study in order to implement diagnosis, treatment, and prognosis more efficiently. [ABSTRACT FROM AUTHOR]

Mild-to-moderate obstructive sleep apnea (mmOSA) is highly prevalent in the general population. However, studies on its association with incident cardiovascular and/or cerebrovascular disease (CBVD) are limited. We examined the association between mild-to-moderate OSA and incident cardiovascular and/or cerebrovascular (CBVD) in a general population sample, and whether age modifies this association. A total of 1173 adults from the Penn State Adult Cohort (20-88 years) without CBVD or severe OSA at baseline were followed-up after 9.2 (±4.1) years. Incident CBVD was defined based on a self-report of a physician diagnosis or treatment for heart disease and/or stroke. Logistic regression examined the association of mild-to-moderate OSA (AHI 5-29.9) with incident CBVD and the combined effect of mmOSA and MetS on incident CBVD after adjusting for multiple confounders. Age significantly modified the association between mmOSA with incident CBVD (p-interaction = 0.04). Mild-to-moderate OSA was significantly associated with incident CBVD in adults aged <60 years (OR = 1.74, 95%CI = 1.06-2.88, p = 0.029), but not in adults aged ≥60 years (OR = 0.71, 95%CI = 0.39-1.27, p = 0.247). Even mild OSA (AHI 5-14.9) carried a significant risk for incident CBDV in adults aged <60 years (OR = 1.86, 95%CI = 1.05-3.28, p = 0.032). An additive effect was found between mmOSA and MetS with incident CBVD in those aged <65 years (OR = 3.84, 95%CI = 1.95-7.56, p<0.001). The risk of incident CBVD is increased in young and middle-aged but not older adults with mmOSA, which may affect the way we currently diagnose and treat this highly prevalent sleep-related breathing disorder. • Mild-to-moderate sleep apnea (mmOSA) is associated with heart problems and stroke. • This risk is stronger in young and middle-aged than in older adults. • These data may affect the way we diagnose/treat mmOSA in young vs. older adults. [ABSTRACT FROM AUTHOR]

Bioactive compounds derived from herbal medicinal plants modulate various therapeutic targets and signaling pathways associated with cardiovascular diseases (CVDs), the world's primary cause of death. Ginkgo biloba , a well-known traditional Chinese medicine with notable cardiovascular actions, has been used as a cardio- and cerebrovascular therapeutic drug and nutraceutical in Asian countries for centuries. Preclinical studies have shown that ginkgolide B, a bioactive component in Ginkgo biloba , can ameliorate atherosclerosis in cultured vascular cells and disease models. Of clinical relevance, several clinical trials are ongoing or being completed to examine the efficacy and safety of ginkgolide B-related drug preparations in the prevention of cerebrovascular diseases, such as ischemia stroke. Here, we present a comprehensive review of the pharmacological activities, pharmacokinetic characteristics, and mechanisms of action of ginkgolide B in atherosclerosis prevention and therapy. We highlight new molecular targets of ginkgolide B, including nicotinamide adenine dinucleotide phosphate oxidases (NADPH oxidase), lectin-like oxidized LDL receptor-1 (LOX-1), sirtuin 1 (SIRT1), platelet-activating factor (PAF), proprotein convertase subtilisin/kexin type 9 (PCSK9) and others. Finally, we provide an overview and discussion of the therapeutic potential of ginkgolide B and highlight the future perspective of developing ginkgolide B as an effective therapeutic agent for treating atherosclerosis. Ginkgolide B possesses the antiatherosclerotic advantage of "multitarget and multipathway", which is closely linked to its regulating endothelial dysfunction, thrombosis, leukocyte action, and risk factors. [Display omitted] [ABSTRACT FROM AUTHOR]

[Display omitted] • Norad-Pum2 axis participates in the process of neuronal apoptosis after SAH. • Pum2 upregulation improves brain injury and neurobehavior in SAH mice. • Norad knockdown enhances the inhibitory effect of Pum2 on target RNA. Subarachnoid Hemorrhage (SAH) is a cerebrovascular disorder that has been found to have severe consequences, including a high mortality and disability rate. Research has indicated that neuronal death, particularly apoptosis, plays a major role in the neurological impairment that follows SAH. RNA-binding protein Pum2 can interfere with translation or other biological functions by connecting to the UGUAHAUA sequence on RNA. Noncoding RNA activated by DNA damage (Norad) contains some Pum2 recognition sequences, which may bind to Pum2 protein and affect its capacity to attach to target mRNA. The time course expression of Norad and Pum2 after SAH is analyzed by establishing a mouse SAH model. Subsequently, the purpose of this study is to investigate the potential role and mechanism of the Norad-Pum2 axis after SAH using lentivirus overexpression of Pum2 and knockdown of Norad. Analysis of Pum2 and Norad levels reveal that the former is significantly reduce and the latter is significantly increased in the SAH group compared to the sham group. Subsequent overexpression of Pum2 and Norad knockdown is found to reduce SAH-induced oxidative stress, neuronal apoptosis, and ultimately improve behavioral and cognitive changes in SAH mice. Our study indicates that Norad-Pum2 acts as a neuromodulator in SAH, and that by increasing Pum2 and decreasing Norad levels, SAH-induced neuronal apoptosis can be reduced and neurological deficits alleviated. Consequently, Norad-Pum2 may be a promising therapeutic target for SAH. [ABSTRACT FROM AUTHOR]

As a common hemorrhagic cerebrovascular disease, subarachnoid hemorrhage (SAH) has high mortality and disability. Delayed cerebral ischemia (DCI) is among the major complications after SAH, severely affecting the patient prognosis. Through bibliometric analysis, this study investigated the global research status, trends, and hotspots of DCI after SAH from 2013 to 2022, providing a scientific reference for researchers in this field. We searched the Web of Science Core Collection for articles and associated records from 2013 to 2022. The data were analyzed and presented using VOSviewer software. This study covered 3436 articles, and the number of publications issued by DCI after SAH study increased annually. The United States published the most papers and had the highest number of citations. Harvard University and World Neurosurgery were the institutions and journals with the most published papers. Keyword analysis indicated that the recent research on DCI after SAH has focused on its pathophysiological mechanisms. DCI after SAH has drawn increasing interest in academic circles during the past decade. This study presented an objective, systematic, and comprehensive analysis of the literature on DCI after SAH. Currently, the hotspots in this field focus on pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Despite an increase in the number of genes associated with pediatric stroke, imaging phenotypes in children have not been well reported. Guidelines are needed to facilitate the identification and treatment of patients with monogenic causes of cerebrovascular disorders. We performed a retrospective review of imaging and medical records of patients aged zero to 21 years with monogenic causes of vascular malformations, small or large vessel disease, transient ischemic attacks, and/or ischemic or hemorrhagic stroke. We classified patients according to their imaging phenotype and reviewed neurological and systemic features and management strategies. We reviewed the literature to identify genes associated with cerebrovascular disorders presenting in childhood. We identified 18 patients with monogenic causes of cerebrovascular disorders and classified each patient as belonging to one or more of three cerebrovascular phenotypes according to predominant imaging characteristics: small vessel disease, large vessel disease, and/or vascular malformations. Preventative treatments included aspirin, N -acetylcysteine, tocilizumab, therapeutic low-molecular-weight heparin, and resection of vascular malformations. Classifying pediatric patients with cerebrovascular disorders by imaging phenotype can aid in determining the next steps in genetic testing and treatment. [ABSTRACT FROM AUTHOR]

Dementia is a multifactorial disorder that is likely influenced by both Alzheimer's disease (AD) and vascular pathologies. We evaluated domain-specific cognitive and neuropsychiatric dysfunction using a two-neuroimaging biomarker construct (beta-amyloid [Aβ] and cerebrovascular disease [CeVD]). We analyzed data from 216 memory clinic participants (mean age = 75.9 ± 6.9; 56.5% female) with neuropsychological and neuropsychiatric assessments, 3T-MRI, and Aβ-PET imaging. Structural equation modeling showed that the largest Aβ (A+) effect was on memory (B = −1.50) and apathy (B = 0.26), whereas CeVD effects were largest on language (B = −1.62) and hyperactivity (B = 0.32). Group comparisons showed that the A+C+ group had greater memory impairment (B = −1.55), hyperactivity (B = 0.79), and apathy (B = 0.74) compared to A−C+; and greater language impairment (B = −1.26) compared to A+C−. These potentially additive effects of Aβ and CeVD burden underline the importance of early detection and treatment of Aβ alongside optimal control of vascular risk factors as a potential strategy in preventing cognitive and neurobehavioral impairment. [ABSTRACT FROM AUTHOR]

• What is the primary question addressed by this study? We investigated associations of the cortical thickness signature of Alzheimer's disease (AD) and white matter hyperintensity volumes with a composite index of health and financial literacy given that the ability to access, understand, and utilize health and financial information influences older adults' health outcomes. • What is the main finding of this study? For 303 participants without dementia from the Rush Memory and Aging Project, reduced AD signature cortical thickness was associated with baseline levels of and faster declines in literacy. White matter hyperintensities were associated with the level of but not change in literacy. • What is the meaning of the finding? Results support the assertion that biological vulnerability associated with AD may predict a broader spectrum of behavior than originally recognized, even in non-demented older adults. The cortical thickness "signature" of Alzheimer's disease (AD-CT) and white matter hyperintensity (WMH) burden have each been associated with cognitive aging and incident AD and related dementias. Less is known about how these structural neuroimaging markers associate with other critical behaviors. We investigated associations of AD-CT and WMH volumes with a composite index of health and financial literacy given that the ability to access, understand, and utilize health and financial information significantly influences older adults' health outcomes. Participants were 303 adults without dementia (age∼80 years; 74% women) from the Rush Memory and Aging Project. Baseline 3T MRI T1-weighted structural and T2-weighted FLAIR data were used to assess AD-CT and WMH volumes, respectively. Literacy was measured using questions designed to assess comprehension of health and financial information and concepts, yielding a total literacy score. Multivariable linear mixed effects regression models determined the relationship of each neuroimaging marker, first separately and then combined, with the level of and change in literacy. Reduced AD-CT and higher WMH at baseline were each associated with lower levels of literacy; only AD-CT was associated with the rate of decline in literacy over time. The association of AD-CT with change in literacy persisted when both neuroimaging markers were included in the same model. The cortical thickness signature of AD predicts changes in health and financial literacy in nondemented older adults suggesting that the multidimensional construct of health and financial literacy relies on specific brain networks implicated in AD. [ABSTRACT FROM AUTHOR]

Local recurrence (LR) rates in nasopharyngeal carcinoma (NPC) following definitive radiation (RT) ± chemotherapy (CT) range from 7–15%. A prospective trial comparing endoscopic surgery and reirradiation in recurrent cases found that surgery improved survival in a carefully chosen group of patients with low-volume mucosal recurrence. However, the fact that the recurrent disease is mostly multifocal and infiltrative in nature makes a limited group of patients suitable for surgery. In this study, we aimed to report our stereotactic ablative radiotherapy (SABR) outcomes in cases diagnosed with recurrent NPC. The data of 83 patients who underwent SABR in our department between 2007 and 2022 with the diagnosis of local-regional recurrent NPC, which was unresectable or had surgical margin positivity after resection were evaluated retrospectively. The Kaplan-Meier method was used for survival analyses (IBM SPSS v.23). Patient, tumor, and treatment characteristics are presented in Table 1. The median age was 53 (range, 19-78). The median follow-up was 24 months (range, 3–151 months). The median interval between patients' first and second RT's was 39 months (range, 4–238 months). The initial response evaluation following reirradiation found a complete response in 38%, a partial response in 40%, stable disease in 8%, and progression in 1%. In follow-up, LR developed in 20 patients (24%) and distant metastasis (DM) developed in 14 patients (17%). The most common sites of DM were the lung, bone, and liver. SABR provided 76% local control (LC). The 1- and 2-year overall survival (OS), local recurrence-free survival (LRFS), and distant metastasis-free survival (DMFS) rates were 67% and 53%, 65% and 46%, and 62% and 49%, respectively. In univariate analysis, LRFS (60% vs. 34%, p=0.002) and DMFS (63% vs. 31%, p=0.007) rates were higher in patients with recurrent tumor volume ≤36 cc compared to patients with tumor volume >36 cc. Age (≤53 vs. >53 years), gender (male vs. female), interval between RTs (≤2 vs. >2 years), surgery before SBRT (yes vs. no), SBRT dose (≤30 vs. >30 Gy) and device (robotic- vs. linear accelerator-based), and site of recurrence (primary vs. neck recurrence) could not be identified for prognostic significance for OS, LRFS, and DMFS parameters. A notable proportion of patients experienced late toxicity, with 20% exhibiting grade 3 or 4 toxicity and 12% experiencing grade 5 toxicity. Fourteen patients (17%) experienced massive hemorrhage as a result of carotid blow-out syndrome (CBOS); two patients (2%) suffered from cerebrovascular disease as a result of carotid artery stenosis; five patients (6%) experienced brain parenchymal necrosis; three patients (3.5%) had permanent gastrostomies; and three patients (3.5%) had hearing loss. There was no observed disparity in toxicity levels between doses administered consecutively or every other day. [Display omitted] Using SABR as a reirradiation method for people with recurrent NPC has shown to be very effective at achieving LC while keeping treatment-related side effects at a level that can be tolerated. There is a positive correlation between a smaller recurring tumor volume and higher levels of local recurrence-free survival (LRFS) and distant metastasis-free survival (DMFS). [ABSTRACT FROM AUTHOR]

• RNF213 protein expression is upregulated in the ischemic penumbra. • Rnf213 knockout decreases infarct volume and alleviates neurological deficits. • Rnf213 knockout ameliorates neuronal apoptosis in the ischemic penumbra. • Rnf213 knockout activates the Akt/GSK-3β/β-catenin/Bcl-2 signalling pathway. Previous studies by us and others have shown that RING finger protein 213 (RNF213) is associated with cerebrovascular disease and systemic vasculopathy. Indeed, Rnf213 mRNA expression is increased in cerebral ischemia reperfusion injury (CIRI). The purpose of the present study was to investigate the role of Rnf213 in CIRI. Using the middle cerebral artery occlusion (MCAO) model, we confirmed that the expression of RNF213 protein was significantly upregulated in neurons in the ischemic penumbra. Rnf213 knockout mice were successfully generated using CRISPR/Cas9 technology. According to TTC staining and Bederson neurological scale, removal of Rnf213 decreased brain infarct volume and improved neurological deficit score, although the restoration of cerebral blood flow after MCAO was similar in WT and Rnf213−/− mice. In addition, the levels of p-Akt, p-GSK-3β, β-catenin and Bcl-2 were significantly increased 24 h after MCAO in the ischemic penumbra of the Rnf213−/− mice compared to WT mice, indicating that Rnf213 removal may ameliorate neuronal apoptosis by regulating the Akt/GSK-3β/β-catenin/Bcl-2 signaling pathway. Taken together, our study reveals that Rnf213 regulates neuronal apoptosis in CIRI, therefore impacting on brain infarct volume in brain ischemia. [ABSTRACT FROM AUTHOR]

With the increasing incidence of malignancies, the importance of cancer-associated stroke is emphasized. Although moyamoya disease is a leading cause of stroke, no reports have documented cancer-associated stroke in patients with this condition. We aimed to investigate cerebrovascular events during malignancy treatments in patients with moyamoya disease. A total of 405 patients with moyamoya disease who visited our hospital between January 2000 and March 2022 were retrospectively examined. We evaluated the management of moyamoya disease, presence of the ring finger protein 213 p.Arg4810Lys variant, treatments for malignant tumors, presence of cerebrovascular events during treatment, and follow-up periods and outcomes. Among the 405 patients, 17 patients with moyamoya disease (4.2%) were diagnosed with malignancies. Among patients aged 60 years and over, 7 out of 67 (10.4%) had malignancies. Of the 17 patients, 11 (64.7%) were symptomatic, and 7 (41.2%) had revascularization surgery. 9 patients were treated with oral antiplatelet drugs. There was no significant difference between the groups with and without malignancy regarding the presence of the ring finger protein 213 p.Arg4810Lys variant (80.0% vs. 62.7%, P = 0.33). All patients underwent surgical treatment, and 7 (41.2%) received chemotherapy. One death due to tumor progression was reported. No cerebrovascular event was observed during malignancy treatments and follow-up periods, which had a mean duration of 6 years. In our cohort, malignancy treatments in patients with moyamoya disease were safely conducted without cerebrovascular events. However, it is advisable to avoid hypotension, dehydration, hyperventilation, and long-term discontinuation of antiplatelet drugs during the treatment of malignant tumors. [ABSTRACT FROM AUTHOR]

Background: Although the prognosis of incomplete cervical spinal cord injury (SCI) diagnosed as American Spinal Injury Association Impairment Scale grade C (AIS C) is generally favorable, some patients remain non-ambulatory. The present study explored the clinical factors associated with the non-ambulatory state of AIS C patients.Methods: This study was a single-center retrospective observational study. Seventy-three participants with AIS C on admission were enrolled and divided into two groups according to ambulatory ability after one year. Prognostic factors of SCI were compared in ambulatory (A-group) and non-ambulatory participants (NA-group). Univariable and multivariable logistic regression analyses were performed on demographic information, medical history, mechanism of injury, presence of fracture, ASIA motor scores (MS) of the extremities, neurological findings, including an anorectal examination on admission, and imaging findings.Results: Forty-one patients were included in the A-group and 32 in the NA-group. Univariable analysis revealed that the following factors were related to poor outcomes (p < 0.05): older age, history of cerebrovascular disorder, impairment/absence of S4-5 sensory score, deep anal pressure (DAP) (-), voluntary anal contraction (VAC) (-), anorectal tone (-), anal wink reflex (-), and low MS of the upper and lower extremities. In the multivariable analysis using age, presence or absence of sacral abnormality, and history of cerebrovascular disorders (adjusted for these three factors), older age and presence of sacral abnormality on admission were independent risk factors for a non-ambulatory state at the 1-year follow-up.Conclusions: Incomplete AIS C SCI individuals with older age and/or impairment of anorectal examination could remain non-ambulatory at 1-year follow-up. [ABSTRACT FROM AUTHOR]

• Present a novel multiscale model to capture the dynamic blood flow and autoregulation in the brain vasculature. • Dynamic behaviour due to the fluid-wall interactions affects blood flow. • Important to achieve accurate, scale-invariant and computationally feasible coupling at the vessel-capillary interface. • The myogenic response might be insufficient by itself to restore blood flow following a drop in blood pressure. • Parameter space analysis gives insight into the range and influence of the model parameters prior to data extraction. Models of the micro-circulatory blood flow in the brain can play a key role in understanding the variety of cerebrovascular diseases that occur in the microvasculature. These conditions are often linked to structural modifications in the vessel network, alterations in the blood flow patterns, as well as impairment in the autoregulatory response, all of which are pathological changes that the model should be able to address if it were to have any clinical value. Furthermore, if the model results were to be validated against clinical MRI data, the model simulations need to be computationally feasible when used on networks on the scale of an MRI voxel. This requires some form of an upscaling approach that bypasses the need for an explicit architectural representation of the whole network while maintaining the relevant anatomical connections. To this end, we developed a hybrid multiscale model of blood flow and autoregulation that traces the dynamic changes in blood flow, volume, and pressure in the cortical microvasculature, where the discrete topology of the penetrating vessels is preserved, and these are then appropriately coupled to the homogenised capillary bed by a spatially distributing support function in the terminal endings. In contrast to the other multiscale models, the model developed here accounts for the dynamic physiological phenomena of the blood flow and the autoregulation processes in the microvessels. We show how the adaptive meshing scheme for the capillary bed developed in this study can be employed to ensure a scale-invariant coupling formulation and numerically accurate simulations, all without compromising the computational feasibility of the model. A statistically accurate cortical network on the scale of an MRI voxel is generated, and the model parameter values are calibrated using a Monte Carlo Filtering analysis to ensure that the model results are physiologically informed. The model is found to be able to capture the steep pressure gradients that have been reported to occur at coupling interfaces. Furthermore, in response to an upstream pressure drop, the network is found to be able to recover cerebral blood flow while exhibiting the characteristic autoregulatory behaviour in terms of changes in vessel calibre and the biphasic flow response. Overall, the model developed here offers a high-quality characterisation of dynamic flow and autoregulation in the microvasculature at improved computational efficiency and lays the ground for whole-brain dynamic simulations. [ABSTRACT FROM AUTHOR]

Brain areas exhibiting negative blood oxygenation-level dependent cerebrovascular reactivity (BOLD-CVR) responses to carbon dioxide (CO 2) are thought to suffer from a completely exhausted autoregulatory cerebrovascular reserve capacity and exhibit vascular steal phenomenon. If this assumption is correct, the presence of vascular steal phenomenon should subsequently result in an equal negative fMRI signal response during a motor-task based BOLD-fMRI study (increase in metabolism without an increase in cerebral blood flow due to exhausted reserve capacity) in otherwise functional brain tissue. To investigate this premise, the aim of this study was to further investigate motor-task based BOLD-fMRI signal responses in brain areas exhibiting negative BOLD-CVR. Seventy-one datasets of patients with cerebrovascular steno-occlusive disease without motor defects, who underwent a CO 2 -calibrated motor task-based BOLD-fMRI study with a fingertapping paradigm and a subsequent BOLD-CVR study with a precisely controlled CO 2 -challenge during the same MRI examination, were included. We compared BOLD-fMRI signal responses in the bilateral pre- and postcentral gyri – i.e. Region of Interest (ROI) with the corresponding BOLD-CVR in this ROI. The ROI was determined using a second level group analysis of the BOLD-fMRI task study of 42 healthy individuals undergoing the same study protocol. An overall decrease in BOLD-CVR was associated with a decrease in BOLD-fMRI signal response within the ROI. For patients exhibiting negative BOLD-CVR, we found both positive and negative motor-task based BOLD-fMRI signal responses. We show that the presence of negative BOLD-CVR responses to CO 2 is associated with heterogeneous motor task-based BOLD-fMRI signal responses, where some patients show -more presumed- negative BOLD-fMRI signal responses, while other patient showed positive BOLD-fMRI signal responses. This finding may indicate that the autoregulatory vasodilatory reserve capacity does not always need to be completely exhausted for vascular steal phenomenon to occur. • The common vascular steal phenomenon theorem assumes a negative BOLD-CVR response to carbon dioxide. • We have shown the presence of both negative and positive motor BOLD-fMRI signal responses in voxels with steal phenomenon. • This indicates that the vasodilatory reserve capacity does not always need to be exhausted for vascular steal to occur. [ABSTRACT FROM AUTHOR]

Cerebrovascular diseases are associated with high incidence of health care–associated infections (HAIs) and poor prognosis in elderly patients. This study aimed to investigate the incidence and clinical characteristics of HAIs in elderly patients with cerebrovascular disease in the intensive care unit (ICU). Patients admitted with cerebrovascular disease, aged ≥65 years, were included. The clinical data of the patients were retrospectively analyzed to determine the risk factors, infection type, distribution, and pathogenic characteristics of HAIs in the context of cerebrovascular diseases. Out of 381 ICU inpatients monitored, 79 (20.73%) developed HAIs. Risk analysis revealed number of ventilator days as significant risk factors for HAIs in elderly patients with cerebrovascular diseases in the comprehensive ICU. In the HAI group, 56 patients (70.89%) had respiratory tract infection (RTI). Sixty-five patients (82.28%) were infected with Gram-negative bacteria (GNB), and 42 (53.16%) with multi-drug–resistant organism (MDRO). The length of hospitalization days, ventilator days, and overall hospitalization costs were higher in the HAI group than in the non-HAI group (P < 0.05), but there was no significant difference between groups in the treatment outcome of patients. Patients with MDRO infection had longer duration and higher cost of hospitalization than those infected with non-MDRO (P < 0.05), but there was no significant difference between the groups in the treatment outcome of patients. HAIs occurred mostly due to RTI and GNB infection. The hospitalization cost and duration, as well as the length of ventilator days, were higher for cerebrovascular patients with HAIs than for non-HAIs patients. [ABSTRACT FROM AUTHOR]

Here, we tested that standard eyes-closed resting-state electroencephalographic (rsEEG) rhythms may characterize patients with mild cognitive impairment due to chronic kidney disease at stages 3–4 (CKDMCI-3&4) in relation to CKDMCI patients under hemodialysis (CKDMCI-H) and mild cognitive impairment (MCI) patients with cerebrovascular disease (CVMCI). Clinical and rsEEG data in 22 CKDMCI-3&4, 15 CKDMCI-H, 18 CVMCI, and 30 matched healthy control (HC) participants were available in a national archive. Spectral rsEEG power density was calculated from delta to gamma frequency bands at scalp electrodes. Results showed that (1) all MCI groups over the HC group showed decreased occipital rsEEG alpha power density; (2) compared to the HC and CVMCI groups, the 2 CKDMCI groups had higher rsEEG delta–theta power density; and (3) the CKDMCI-3&4 group showed the lowest parietal rsEEG alpha power density. The present rsEEG measures may be useful to monitor the impact of circulating uremic toxins on brain regulation of cortical arousal for quiet vigilance in CKDMCI patients. [ABSTRACT FROM AUTHOR]

Catalpol, an iridoid glucoside isolated from Rehmannia glutinosa , has gained attention due to its potential use in treating cardio-cerebrovascular diseases (CVDs). This extensive review delves into recent studies on catalpol's protective properties in relation to various CVDs, such as atherosclerosis, myocardial ischemia, infarction, cardiac hypertrophy, and heart failure. The review also explores the compound's anti-oxidant, anti-inflammatory, and anti-apoptotic characteristics, emphasizing the role of vital signaling pathways, including PGC-1α/TERT, PI3K/Akt, AMPK, Nrf2/HO-1, estrogen receptor (ER), Nox4/NF-κB, and GRP78/PERK. The article discusses emerging findings on catalpol's ability to alleviate diabetic cardiovascular complications, thrombosis, and other cardiovascular-related conditions. Although clinical studies specifically addressing catalpol's impact on CVDs are scarce, the compound's established safety and well-tolerated nature suggest that it could be a valuable treatment alternative for CVD patients. Further investigation into catalpol and related iridoid derivatives may unveil new opportunities for devising natural and efficacious CVD therapies. [Display omitted] • Catalpol demonstrates promising therapeutic potential for a variety of CVDs. • Catalpol has anti-oxidant, anti-inflammatory, and anti-apoptotic effects. • Catalpol protects cardio-cerebrovascular system through multiple signaling pathways. [ABSTRACT FROM AUTHOR]

Despite declines in morbidity and mortality in recent years, ischemic stroke (IS) remains one of the leading causes of death and disability from cerebrovascular diseases. Addressing the controllable risk factors underpins the successful clinical management of IS. Hypertension is one of the most common treatable risk factors for IS and is associated with poor outcomes. Ambulatory blood pressure monitoring has revealed that patients with hypertension have a higher incidence of blood pressure variability (BPV) than those without hypertension. Meanwhile, increased BPV has been identified as a risk factor for IS. The risk of IS is higher and the prognosis after infarction is worse with higher BPV, no matter in the acute or subacute phase. BPV is multifactorial, with alterations reflecting individual physiological and pathological changes. This article reviews the current research advances in the relationship between BPV and IS, with an attempt to raise awareness of BPV among clinicians and IS patients, explore the increased BPV as a controllable risk factor for IS, and encourage hypertensive patients to control not only average blood pressure but also BPV and implement personalized blood pressure management. [ABSTRACT FROM AUTHOR]

Explore the consequences of the coronavirus pandemic (COVID-19) on patients suffering from cerebrovascular disorders necessitating interventions. Using the National Surgical Quality Improvement Program database, patients with cerebrovascular disease who underwent procedures before (2018–2019) and during (2020–2021) COVID-19 were identified. ICD-10 and Current Procedure Terminology codes were employed to classify diseases and elective cases, respectively. Our study analyzed variations in diagnoses, procedures, demographics, mortality and morbidity likelihood scores, and outcomes. Analysis was conducted using R 4.2.1 with tidyverse, haven, and Ime4 packages. Statistical significance was defined as P < 0.05. There was a significant rise in cerebrovascular accidents (CVAs) (9.96% vs. 12.28%) and a decrease in elective carotid endarterectomies (92.30% vs. 87.22%). Carotid stenting increased significantly (7.63% vs. 12.62%), and mortality probability scores rose for CVAs and carotid interventions. Ethnic (Hispanic) and racial minorities (Asians and Black/African American) were disproportionately affected (P < 0.001). Conditions from delayed care increased, and total operative times rose (117.46 vs. 124.33 minutes). Various patient outcomes worsened (P < 0.05), and multivariate analyses showed Hispanic patients had higher mortality and morbidity probability scores (P < 0.05). The pandemic led to more severe disease progression and reduced diagnoses due to screening delays, indicating deferred care. Prolonged operative times, extended hospital stays, and worsening outcomes, including infections and thrombotic events, hint at the repercussions of persistent staff shortages in health care facilities. Ethnic and racial minorities faced disproportionate impacts. To minimize harm to patients with cerebrovascular disease in future public health crises, it is crucial to develop policies that address these findings. [ABSTRACT FROM AUTHOR]