Search Results (6,051)

Ischemic stroke is a multifactorial disease that leads to brain tissue damage and severe neurological deficit. Transient middle cerebral artery occlusion (tMCAO) models are actively used for the molecular, genetic study of stroke. Previously, using high-throughput RNA sequencing (RNA-Seq), we revealed 3774 differentially expressed genes (DEGs) in the penumbra-associated region of the frontal cortex (FC) of rats 24 h after applying the tMCAO model. Here, we studied the gene expression pattern in the striatum that contained an ischemic focus. Striatum samples were obtained from the same rats from which we previously obtained FC samples. Therefore, we compared DEG profiles between two rat brain tissues 24 h after tMCAO. Tissues were selected based on magnetic resonance imaging (MRI) and histological examination (HE) data. As a result, 4409 DEGs were identified 24 h after tMCAO in striatum. Among them, 2609 DEGs were overlapped in the striatum and FC, whereas more than one thousand DEGs were specific for each studied tissue. Furthermore, 54 DEGs exhibited opposite changes at the mRNA level in the two brain tissues after tMCAO. Thus, the spatial regulation of the ischemic process in the ipsilateral hemisphere of rat brain at the transcriptome level was revealed. We believe that the targeted adjustment of the genome responses identified can be the key for the induction of regeneration processes in brain cells after stroke. Full article

Background. The association between malnutrition and poor outcomes in stroke patients has, to date, been evaluated using composite scores derived from laboratory measurements. However, Bioelectrical Impedance Analysis (BIA) and its advanced application, Bioelectrical Impedance Vector Analysis (BIVA), offer a non-invasive, cost-efficient, and rapid alternative. These methods enable precise assessment of body composition, nutritional status, and hydration levels, making them valuable tools in the clinical evaluation of stroke patients. Objective. This study aimed to compare the ordinal distribution of modified Rankin Scale (mRS) scores at 90 days following an acute ischemic stroke, stratifying patients based on their nutritional status at the time of Stroke Unit admission, as determined by the Bioelectrical Impedance Vector Analysis (BIVA) malnutrition parameter. Methods. We conducted a single-centre prospective observational study on all consecutive patients admitted for acute ischemic stroke to our Stroke Unit between 1 April 2024, and 30 September 2024. We applied the IPW (Inverse Probability Weighting) statistical technique and ordinal logistic regression to compare mRS scores in malnourished and non-malnourished patients. Results. Overall, our study included 195 patients with ischemic stroke assessed using BIVA. Of these, 37 patients (19%) were malnourished. After IPW, we found that malnourished patients had significantly lower rates of favorable 90-day functional outcomes (cOR 3.34, 95% CI 1.74–6.41; p = 0.001). Even after accounting for relevant covariates, malnutrition remained an independent predictor of unfavorable outcomes (acOR 2.79, 95% CI 1.37–5.70; p = 0.005), along with NIHSS score at admission (acOR 1.19, 95% CI 1.11–1.28; p < 0.001), intravenous thrombolysis (acOR 0.28, 95% CI 0.15–0.52; p < 0.001), absolute lymphocyte count (cOR 1.01, 95% CI 1.00–1.02; p = 0.027), and albumin concentration (cOR 0.82, 95% CI 0.75–0.89; p < 0.001). Conclusions. Malnutrition, assessed through Bioelectrical Impedance Vector Analysis (BIVA) at the time of admission to the Stroke Unit, is associated with worse clinical outcomes at 90 days following the ischemic cerebrovascular event. Full article

According to the World Health Organization (WHO), peripheral and central neurological disorders affect approximately one billion people worldwide. Ischemic stroke and Alzheimer’s Disease and other dementias are the second and fifth leading causes of death, respectively. In this context, detecting and classifying brain lesions constitute a critical area of research in medical image processing, significantly impacting clinical practice. Traditional lesion detection, segmentation, and feature extraction methods are time-consuming and observer-dependent. In this sense, research in the machine and deep learning methods applied to medical image processing constitute one of the crucial tools for automatically learning hierarchical features to get better accuracy, quick diagnosis, treatment, and prognosis of diseases. This project aims to develop and implement deep learning models for detecting and classifying small brain White Matter hyperintensities (WMH) lesions in magnetic resonance images (MRI), specifically lesions concerning ischemic and demyelination diseases. The methods applied were the UNet and Segmenting Anything model (SAM) for segmentation, while YOLOV8 and Detectron2 (based on MaskRCNN) were also applied to detect and classify the lesions. Experimental results show a Dice coefficient (DSC) of 0.94, 0.50, 0.241, and 0.88 for segmentation of WMH lesions using the UNet, SAM, YOLOv8, and Detectron2, respectively. The Detectron2 model demonstrated an accuracy of 0.94 in detecting and 0.98 in classifying lesions, including small lesions where other models often fail. The methods developed give an outline for the detection, segmentation, and classification of small and irregular morphology brain lesions and could significantly aid clinical diagnostics, providing reliable support for physicians and improving patient outcomes. Full article

Dementia blood biomarkers are becoming increasingly important. Various factors, such as ischemic lesions and inflammation, can influence the pathomechanism of dementia. We aimed to evaluate the effects of past stroke lesions on blood biomarkers (BMs). Following approval from the institutional ethics committee, patients who were admitted to the memory clinic and were consented to written documents were enrolled (n = 111, average [standard deviation] age: 74.5 [9.1] years-old). Brain magnetic resonance imaging, cognitive function, and neuropsychological symptoms were analyzed. The amyloid-β 42 (Aβ42)/Aβ40 ratio, phosphorylated tau181 (p-tau181), glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and Aβ42/p-tau181 ratio were assessed as plasma BMs. The patients were diagnosed with Alzheimer’s disease (n = 45), mild cognitive impairment (n = 56), depression (n = 8), and subjective cognitive impairment (n = 4). Bivariate analysis exhibited that all measured BM indicators were significantly associated with cognitive decline in patients without past stroke lesions. Whereas the patients with stroke lesions presented a significant association only between GFAP and cognitive decline (p = 0.0011). Multiple regression analysis showed that NfL significantly correlated with cognitive decline only in patients without stroke lesions (r = 0.4988, p = 0.0003) and with delusion only in those with stroke lesions (r = 0.5492, p = 0.0121). Past stroke lesions should be addressed in the assessment of the correlation between blood biomarkers and cognitive decline in dementia patients. Full article

Background/Objectives: Kinesiophobia, or the fear of movement, is a significant problem in the rehabilitation of patients after a stroke, especially in individuals with diabetes, who have an increased risk of health complications. The aim of the study was to validate the Tampa Scale for Kinesiophobia (TSK) for assessing kinesiophobia in the context of patients with diabetes complicated by stroke to ensure its adequacy and reliability in this specific group of patients. Methods: After considering exclusion criteria, 166 patients with type 2 diabetes after ischemic stroke, hospitalized in the neurological rehabilitation ward, were included in the analysis. A survey using the TSK was conducted in the study group. A reliability analysis of the questionnaire was conducted, and then exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) were used to disclose the number of factors that characterize the study group. Results: The Cronbach’s alpha value for the entire scale is 0.875. The value for all the questions on the scale was also above 0.86, so they are considered reliable. Removing any question does not increase the value of Cronbach’s alpha or Guttman index. Based on the scree plot, two factors were identified. The first factor includes 12 items and forms a physical factor, while the second factor includes 5 items and forms a psychological factor. The fit of the two-factor model was checked using confirmatory factor analysis. The final two-factor model has an acceptable fit. All the factor loadings are statistically significant. The factor loadings range from 0.262 to 0.729 for the physical factor and from 0.543 to 0.822 for the psychological factor. Conclusions: The TSK is a reliable and valid tool for assessing the level of kinesiophobia in a group of patients with type 2 diabetes complicated by stroke. The results of the study using this tool may contribute to the development of more effective therapeutic strategies that take into account the specific physical and psychological needs of this group of patients. Full article

Background: Omentin (omentin-1, intelectin-1, ITLN-1) is an adipokine considered to be a novel substance. Many chronic, inflammatory, or civilization diseases are linked to obesity, in which omentin plays a significant role. Methods: MEDLINE and SCOPUS databases were searched using the keywords “omentin” or “intelectin-1”. Then the most recent articles providing new perspectives on the matter and the most important studies, which revealed crucial insight, were selected to summarize the current knowledge on the role of omentin in a literature review. Results and Conclusions: The valid role of this adipokine is evident in the course of metabolic syndrome. In most cases, elevated omentin expression is correlated with the better course of diseases, including: type 2 diabetes mellitus, polycystic ovary syndrome, rheumatoid arthritis, metabolic dysfunction-associated steatotic liver disease, Crohn’s disease, ulcerative colitis, atherosclerosis, or ischemic stroke, for some of which it can be a better marker than the currently used ones. However, results of omentin studies are not completely one-sided. It was proven to participate in the development of asthma and atopic dermatitis and to have different concentration dynamics in various types of tumors. All of omentin’s effects and properties make it an attractive subject of research, considering still unexplored inflammation mechanisms, in which it may play an important role. Omentin was proven to prevent osteoarthritis, hepatocirrhosis, and atherosclerosis in mouse models. All of the above places omentin among potential therapeutic products, and not only as a biomarker. However, the main problems with the omentin’s research state are the lack of standardization, which causes many contradictions and disagreements in this field. Full article

Chronic graft-versus-host disease (cGVHD) is a prognostically negative event following hematopoietic stem cell transplant (HSCT). While cGVHD mainly affects the muscles, skin, oral mucosa, eyes, lungs, gastrointestinal tract, and liver, central nervous system (CNS) involvement remains possible and, moreover, is rare when it occurs isolated. CNS-cGVHD can manifest with a wide spectrum of CNS disorders, including cerebrovascular diseases, autoimmune demyelinating diseases, and immune-mediated encephalitis. We present a case of 65-year-old man previously treated with HSCT presenting with progressive cerebrovascular disorder and optic neuropathy without any clear alternative causal processes except for immune-mediated CNS microangiopathy in the context of possible CNS-cGVHD, along with suggestive imaging and instrumental and laboratory findings. Starting one year after HSCT for acute myeloid leukemia, when the first cerebral ischemic event occurred and was then associated with a reduction in visual acuity, an extensive diagnostic work-up had remained inconclusive over many years, leading us to the hypothesis of CNS-cGVHD and, therefore, to the start of immunosuppressive therapy. Our experience highlighted not ignoring the possibility of cGVHD as the underlying mechanism of CNS disorder, even in the absence of other systemic presentations, once more common etiologies of CNS pathological processes have been ruled out. Full article

Background: Stroke and traumatic brain injury (TBI) represent two major health concerns worldwide. There is growing evidence suggesting a potential association between TBI and stroke. In this systematic review and meta-analysis, we aim to explore the association between TBI and stroke risk, with a specific focus on overall stroke risk and subgroup variations based on stroke type, severity, and the post-TBI time period. Methods: PubMed, Web of Science (WOS), Scopus, and Cochrane Library were systematically searched for studies exploring the link between stroke and TBI. The pooled hazard ratios (HRs) with a 95% confidence interval (CI) were calculated. The Comprehensive Meta-Analysis (CMA) software was used for the analysis. Subgroup analyses were conducted based on stroke type, TBI severity, and post-TBI phase. The Newcastle–Ottawa Scale (NOS) was utilized for the quality assessment. Results: We included a total of 13 observational studies, with data from 8 studies used for quantitative analysis. A history of TBI was associated with a significantly higher odds of stroke compared to controls (HR = 2.3, 95% CI (1.79 to 2.958), p < 0.001). The risk was greater for hemorrhagic stroke (HR = 4.8, 95% CI (3.336 to 6.942), p < 0.001) than for ischemic stroke (HR = 1.56, 95% CI (1.28 to 1.9), p < 0.001). Both moderate-to-severe TBI (HR = 3.64, 95% CI (2.158 to 6.142), p < 0.001) and mild TBI (HR = 1.81, 95% CI (1.17 to 2.8), p = 0.007) were associated with a significantly higher risk of stroke. The risk was also higher in the early post-TBI phase (1–30 days) (HR = 4.155, 95% CI (2.25 to 7.67), p < 0.001) compared to later phases (HR = 1.68, 95% CI (1.089 to 2.59), p = 0.019) from 30 days to 1 year and (HR = 1.87, 95% CI (1.375 to 2.544), p < 0.001) after 1 year. Conclusions: This systematic review confirms a significant association between TBI and an increased risk of stroke, regardless of TBI severity, type, or timing of stroke. The findings highlight the need for early monitoring and advocating preventive strategies for stroke in patients with a history of TBI. Full article

Objective: To investigate the predictive value of nutritional status in heart failure (HF) patients with an implantable cardioverter defibrillator (ICD), and to identify factors associated with ICD discharge and mortality. Methods: This retrospective study was conducted by analyzing data from 2017 to 2021. HF patients who underwent ICD implantation for primary prevention were included. Follow-up visits were continued until December 2022. Patients were examined based on ICD shock occurrence (ICD-A: appropriate shock), ICD non-discharge (ICD-X), and mortality. Nutritional status was assessed by the Prognostic Nutritional Index (PNI) and the Controlling Nutritional Status (CONUT) scores. Results: A total of 221 patients were included in the study, 86 of whom were in the ICD-A group (135 in the ICD-X group). Age and sex distribution were similar in these groups. The all-cause mortality rate was 20.36%. A PNI with a cut-off value of <47.25 and a CONUT score with a cut-off value of >2.5 were able to significantly predict all-cause mortality. The PNI had a greater area under the curve compared to the CONUT. Non-ischemic cardiomyopathy and high left-ventricle end-systolic diameter (ESD) were independently associated with appropriate ICD shock. Low systolic blood pressure, high ESD, low sodium, low total cholesterol, low (<47.25) PNI, and ICD shock were independently associated with all-cause mortality. Conclusions: Malnutrition appears to be associated with mortality in patients with primary-prevention ICDs, and the PNI appears to be a more useful indicator than the CONUT for determining the risk of mortality in these patients. Full article

Background and Objectives: The purpose of this study was to determine the factors that cause delay time in patients admitted to the hospital with STEMI. In addition, the effect of this delay on the patient’s prognosis has also been investigated. Materials and Methods: a total of 301 patients diagnosed with STEMI treated with primary percutaneous coronary intervention (pPCI) were included in the study. Reinfarction, revascularization, cerebrovascular event, and cardiac death were determined as major cardiac clinical events. The follow-up period of our study was 475 ± 193 days. Results: Univariate analysis revealed that factors influencing delay time included BMI, hypertension diabetes, smoking habit and variability in pain intensity. In multivariate logistic regression analysis, BMI, diabetes, hypertension, smoking, variation in pain intensity, and infarct-related artery other than the LAD were identified as independent factors associated with increased delay times. We determined the cut-off values predicting the composite endpoint as 122.5 min for patient delay, 95.5 min for system delay, and 371 min for total ischemic time. It was observed that the in-hospital NT pro-BNP values of the patients presenting early were lower (181 vs. 594 pg/mL p < 0.001), had a higher ejection fraction at the first measurement, and even improved at the sixth week of follow-up (p = 0.047). Conclusions: Prolonged ischemia duration was associated with several factors. Early reperfusion in STEMI patients reduces both cardiac death and clinical events. Delays are influenced by patient awareness, emergency care efficiency, and hospital-specific factors. Improving education, response times, and hospital protocols is essential to minimize delays and improve outcomes. Full article

Cutaneous lesions suggestive of vasculitis and/or ischemic dermatopathy (ID) are anecdotally reported in canine leishmaniosis, and the clinicopathological features of these conditions have not been fully characterized. The objective of this case series was to describe six dogs with leishmaniosis and ID. In 5/6 dogs, leishmaniosis was diagnosed at the time of ID diagnosis, whereas in 1/6 dogs, ID developed during the first month of anti-Leishmania conventional treatment. One each of greyhound, Chihuahua, whippet, American bully, hound and mixed breeds were represented, and the median age at presentation was 6 years [2–8]. All patients presented high or very high levels of circulating anti-Leishmania infantum antibodies. The cutaneous lesions were multifocal alopecia with atrophic skin with hyper- or hypopigmentation (6/6), ulcers located on the extremities and trunk (3/6) and onychodystrophy (2/6). Histologically, ID was confirmed by the presence of follicular atrophy (faded follicles) (6/6), perivascular or interstitial lymphoplasmacytic dermatitis or panniculitis (6/6), collagen smudging (3/6), dermal fibrosis (3/6), lymphocytic interface dermatitis (3/6) and ulceration (3/6). Vasculopathy was observed in the superficial and mid-vascular plexuses in 4/6 dogs and characterized by the combination of some of the following lesions: vasocongestion, hemorrhagic foci, mild hyaline mural degeneration, thrombi and fragmented degenerating nuclear debris of neutrophils in the vascular wall. Moreover, myositis was observed in 1/6 cases. Leishmania-specific immunohistochemistry was positive in the skin of 4/6 cases. Leishmaniosis might be considered an underlying cause of ID in dogs. However, the immune mechanisms and pathogenesis need to be elucidated. Full article

Dalbergia odorifera is widely used to treat cardiovascular diseases. Our research group found that Dalbergia odorifera volatile oil has a good anti-myocardial ischemic effect, and its main pharmacodynamic components are trans-nerolol and its oxides. However, the exact mechanisms underlying this effect have not yet been elucidated. This study aimed to explore the potential myocardial protective effects of trans-nerolol and its underlying molecular mechanisms. Molecular docking was used to predict and visualize the possible mechanism of the anti-apoptotic myocardial protection by trans-nerolol. The myocardial protective effect of trans-nerolol was evaluated by observing pathological injury, myocardial enzyme levels, oxidation, antioxidant levels, and the expression of related proteins. Molecular docking results showed that trans-nerolol binds closely to cytochrome C (Cytc) and apoptosis-related proteins, suggesting that it may play a role in interacting with these target proteins. The results showed that pre-treatment with dose-dependent trans-nerolol significantly mitigated the myocardial histological damage; decreased lactate dehydrogenase (LDH), creatinine kinase (CK), alanine transaminase (ALT), and aspartate transaminase (AST) levels; reduced nitric oxide (NO) production, hydrogen peroxide (H₂O₂), and lipid peroxide (LPO); and increased the total antioxidant content (T-AOC), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities compared with the model group. In addition, dose-dependent trans-nerolol significantly increased the Na⁺-K⁺-ATPase and Ca²⁺-Mg²⁺-ATPase levels. Moreover, trans-nerolol markedly reduced the endogenous and external apoptotic pathways; downregulated the protein expression of Cytc, apoptotic protease activating factor-1 (Apaf1), Fibroblast-associated (Fas), Cysteine-aspartate protease 3 (Caspase3), Cysteine-aspartate protease 8 (Caspase8), and Cysteine-aspartate protease 9 (Caspase9); and upregulated the expression of Heat shock protein 70 (Hsp70) and B-cell lymphoma-2 (Bcl-2). These data indicate that trans-nerolol exerts protective effects against myocardial ischemia (MI), and its mechanism is associated with the suppression of the Cytc- and caspase-signaling pathways. Trans-nerolol has a therapeutic effect on MI, and its mechanism of action is related to its anti-apoptotic effect. These results suggest that Dalbergia odorifera has a potential role to be developed as an MI-promoting therapeutic agent. Full article

Early neurological deterioration is associated with poor functional outcomes in stroke patients, but the underlying mechanisms remain unclear. This study aims to understand the progression of stroke-related brain damage using a rhesus monkey model with ischemic occlusion. Multiparameter MRI was used to monitor the progressive evolution of the brain lesion following stroke. Resting-state functional MRI, dynamic susceptibility contrast perfusion MRI, diffusion tensor imaging, and T1- and T2-weighted scans were acquired prior to surgery and at 4–6 h, 48 h, and 96 h following the stroke. The results revealed a sudden increase in infarction volume after the hyper-acute phase but before 48 h on diffusion-weighted imaging (DWI), with a slight extension by 96 h. Lower relative cerebral blood flow (CBF) and time to maximum (Tmax) prior to the stroke, along with a progressive decrease post-stroke, were observed when compared to other stroke monkeys in the same cohort. Functional connectivity (FC) in the ipsilesional secondary somatosensory cortex (S2) and primary motor cortex (M1) exhibited an immediate decline on Day 0 compared to baseline and followed by a slight increase on Day 2 and a further decrease on Day 4. These findings provide valuable insights into infarction progression, emphasizing the critical role of collateral circulation and its impact on early neurological deterioration during acute stroke. Full article

Background/Objectives: The chronic metabolic condition of hyperglycemia in type-2 diabetics is known to cause various neurological disorders and compromise recovery from brain insults. Previously, we reported a delayed and reduced glial cell response and a greater neuronal cell death in different brain regions of diabetic, db/db, mice following cerebral hypoxic- ischemic injury. In this study, we explored the changes in baseline activation of astrocytes and microglia and its impact on vascular permeability in different brain regions. Methods: The numbers of activated astrocytes (GFAP-positive) and microglia/macrophage (Iba-1-positive) in the motor cortex, caudate and hippocampal regions of 12-week old, type-2 diabetic db/db and non-diabetic db/+ mice were quantitated. The leakage of serum IgG and loss of occludin, a tight junctional protein observed in the cortex and caudate of db/db mice, indicated a compromised blood brain barrier. Results: Results indicated significant differences in activation of glial cells in the cortex and caudate along with increased vessel permeability in diabetic mice. Conclusions: The study suggests that a constant activation of glial cells in the diabetic brain may be the cause of impaired inflammatory response and/or degenerating cerebral blood vessels which contribute to neuronal cell death upon CNS injury. Full article

The effect of the gut microbiota extends beyond their habitant place from the gastrointestinal tract to distant organs, including the cardiovascular system. Research interest in the relationship between the heart and the gut microbiota has recently been emerging. The gut microbiota secretes metabolites, including Trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), bile acids (BAs), indole propionic acid (IPA), hydrogen sulfide (H₂S), and phenylacetylglutamine (PAGln). In this review, we explore the accumulating evidence on the role of these secreted microbiota metabolites in the pathophysiology of ischemic and non-ischemic heart failure (HF) by summarizing current knowledge from clinical studies and experimental models. Elevated TMAO contributes to non-ischemic HF through TGF-ß/Smad signaling-mediated myocardial hypertrophy and fibrosis, impairments of mitochondrial energy production, DNA methylation pattern change, and intracellular calcium transport. Also, high-level TMAO can promote ischemic HF via inflammation, histone methylation-mediated vascular fibrosis, platelet hyperactivity, and thrombosis, as well as cholesterol accumulation and the activation of MAPK signaling. Reduced SCFAs upregulate Egr-1 protein, T-cell myocardial infiltration, and HDAC 5 and 6 activities, leading to non-ischemic HF, while reactive oxygen species production and the hyperactivation of caveolin-ACE axis result in ischemic HF. An altered BAs level worsens contractility, opens mitochondrial permeability transition pores inducing apoptosis, and enhances cholesterol accumulation, eventually exacerbating ischemic and non-ischemic HF. IPA, through the inhibition of nicotinamide N-methyl transferase expression and increased nicotinamide, NAD+/NADH, and SIRT3 levels, can ameliorate non-ischemic HF; meanwhile, H₂S by suppressing Nox4 expression and mitochondrial ROS production by stimulating the PI3K/AKT pathway can also protect against non-ischemic HF. Furthermore, PAGln can affect sarcomere shortening ability and myocyte contraction. This emerging field of research opens new avenues for HF therapies by restoring gut microbiota through dietary interventions, prebiotics, probiotics, or fecal microbiota transplantation and as such normalizing circulating levels of TMAO, SCFA, BAs, IPA, H₂S, and PAGln. Full article