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The body fluid status in acute stroke is a crucial determinant in early stroke recovery but a real-time method to monitor body fluid status is not available. This study aims to evaluate the relationship between salivary conductivity and body fluid status during the period of intravenous fluid hydration. Between June 2020 to August 2022, patients presenting with clinical signs of stroke at the emergency department were enrolled. Salivary conductivities were measured before and 3 h after intravenous hydration. Patients were considered responsive if their salivary conductivities at 3 h decreased by more than 20% compared to their baseline values. Stroke severity was assessed using the National Institutes of Health Stroke Scale, and early neurological improvement was defined as a decrease of ≥ 2 points within 72 h of admission. Among 108 recruited patients, there were 35 of stroke mimics, 6 of transient ischemic attack and 67 of acute ischemic stroke. Salivary conductivity was significantly decreased after hydration in all patients (9008 versus 8118 µs/cm, p  = 0.030). Among patients with acute ischemic stroke, the responsive group, showed a higher rate of early neurological improvement within 3 days compared to the non-responsive group (37% versus 10%, p  = 0.009). In a multivariate logistic regression model, a decrease in salivary conductivity of 20% or more was found to be an independent factor associated with early neurological improvement (odds ratio 5.42, 95% confidence interval 1.31–22.5, p  = 0.020). Real-time salivary conductivity might be a potential indicator of hydration status of the patient with acute ischemic stroke.

Background Necrotizing soft tissue infections (NSTI) are rapidly progressing and life-threatening conditions that require prompt diagnosis. However, differentiating NSTI from other non-necrotizing skin and soft tissue infections (SSTIs) remains challenging. We aimed to evaluate the diagnostic value of the biochemical analysis of soft tissue infectious fluid in distinguishing NSTIs from non-necrotizing SSTIs. Methods This cohort study prospectively enrolled adult patients between May 2023 and April 2024, and retrospectively included patients from April 2019 to April 2023. Patients with a clinical suspicion of NSTI in the limbs who underwent successful ultrasound-guided aspiration to obtain soft tissue infectious fluid for biochemical analysis were evaluated and classified into the NSTI and non-necrotizing SSTI groups based on their final discharge diagnosis. Common extravascular body fluid (EBF) criteria were applied. Results Of the 72 patients who met the inclusion criteria, 10 patients with abscesses identified via ultrasound-guided aspiration were excluded. Based on discharge diagnoses, 39 and 23 patients were classified into the NSTI and non-necrotizing SSTI groups, respectively. Biochemical analysis revealed significantly higher albumin, lactate, lactate dehydrogenase (LDH), and total protein levels in the NSTI group than in the non-necrotizing SSTI group, and the NSTI group had significantly lower glucose levels and pH in soft tissue fluids. In the biochemical analysis, LDH demonstrated outstanding discrimination (area under the curve (AUC) = 0.955; p  < 0.001) among the biochemical markers. Albumin (AUC = 0.884; p  < 0.001), lactate (AUC = 0.891; p  < 0.001), and total protein (AUC = 0.883; p  < 0.001) levels also showed excellent discrimination. Glucose level (AUC = 0.774; p  < 0.001) and pH (AUC = 0.780; p  < 0.001) showed acceptable discrimination. When the EBF criteria were evaluated, the total scores of Light’s criteria (AUC = 0.925; p  < 0.001), fluid-to-serum LDH ratio (AUC = 0.929; p  < 0.001), and fluid-to-serum total protein ratio (AUC = 0.927; p  < 0.001) demonstrated outstanding discrimination. Conclusion Biochemical analysis and EBF criteria demonstrated diagnostic performances ranging from acceptable to outstanding for NSTI when analyzing soft tissue infectious fluid. These findings provide valuable diagnostic insights into the recognition of NSTI. Further research is required to validate these findings.

Background: Branch atheromatous disease (BAD) is a subtype of ischemic stroke associated with early neurological deterioration (END) and poor outcomes. Although BAD shares features with large artery atherosclerosis, optimal treatment strategies remain undefined. Objectives: To assess the efficacy and safety of early dual antiplatelet therapy (DAPT) and high-intensity statins in reducing END and improving outcomes in BAD. Design: A prospective, single-arm study with a historical control group. Methods: This study reports the results of the Statin and Dual Antiplatelet Therapy in Preventing Early Neurological Deterioration in Branch Atheromatous Disease trial. Patients with BAD-related ischemic stroke were treated with aspirin, clopidogrel, and high-intensity statins within 24 h of symptom onset. Outcomes were compared with a historical control cohort treated with single antiplatelet therapy and moderate- or low-intensity statins. The primary outcome was the composite of END (defined as an National Institutes of Health Stroke Scale score increase ⩾2 points within 7 days) or recurrent stroke within 30 days. Secondary outcomes included severe END, functional outcomes at 90 days, and safety events. Results: A total of 91 patients received intensive therapy and 285 received standard treatment. The primary endpoint occurred less frequently in the intensive group (34.1% vs 48.1%; adjusted risk ratio (aRR), 0.71; 95% confidence interval (CI), 0.52–0.98; p = 0.034). Intensive therapy significantly reduced END at 7 days (34.1% vs 47.0%; aRR, 0.73; 95% CI, 0.54–1.00; p = 0.049) but not recurrent stroke at 30 days (2.2% vs 1.8%; aRR, 1.16; 95% CI, 0.25–5.43). Good outcomes at 90 days (modified Rankin Scale ⩽2) were more common with intensive therapy (73.6% vs 57.2%; aRR, 1.27; 95% CI, 1.09–1.48; p = 0.002). Major bleeding and mortality did not differ between groups. Conclusion: Early intensive therapy with DAPT and high-intensity statins significantly reduced END and improved recovery in BAD without compromising safety. Further studies are warranted to validate these findings. Trial registration: ClinicalTrials.gov; Identifier: NCT04824911 (https://clinicaltrials.gov/study/NCT04824911). Plain language summary Early treatment with statin and dual antiplatelet therapy may help prevent worsening stroke symptoms in a specific type of acute ischemic stroke Some people who experience a certain type of acute ischemic stroke called branch atheromatous disease (BAD) may get worse within the first few days, even after receiving medical care. This early worsening can lead to more severe disability. In this study, we tested whether starting a combination of dual antiplatelet therapy—aspirin and clopidogrel—along with a high-dose statin (a cholesterol-lowering medication) within 24 hours of stroke onset could help prevent this early decline. We treated 91 patients with this intensive therapy and compared their outcomes to 285 patients from previous years who had received standard treatment. We found that those who received the early intensive therapy were less likely to experience worsening stroke symptoms during the first week and more likely to have better recovery after three months. The treatment did not increase the risk of serious side effects, although mild bleeding occurred slightly more often. These findings suggest that early use of dual antiplatelet therapy and a strong statin may help improve outcomes in people with this specific kind of stroke. More research is needed to confirm these results and guide future treatment recommendations.

Background To survive and thrive, many animals, including humans, have evolved goal-directed behaviors that can respond to specific physiological needs. An example is thirst, where the physiological need to maintain water balance drives the behavioral basic instinct to drink. Determining the neural basis of such behaviors, including thirst response, can provide insights into the way brain-wide systems transform sensory inputs into behavioral outputs. However, the neural basis underlying this spontaneous behavior remains unclear. Here, we provide a model of the neural basis of human thirst behavior. Results We used fMRI, coupled with functional connectivity analysis and serial-multiple mediation analysis, we found that the physiological need for water is first detected by the median preoptic nucleus (MnPO), which then regulates the intention of drinking via serial large-scale spontaneous thought-related intrinsic network interactions that include the default mode network, salience network, and frontal-parietal control network. Conclusions Our study demonstrates that the transformation in humans of sensory inputs for a single physiological need, such as to maintain water balance, requires large-scale intrinsic brain networks to transform this input into a spontaneous human behavioral response.

Background: Branch atheromatous disease (BAD) is a primary cause of early neurological deterioration (END) in penetrating artery occlusion, leading to poor functional outcomes. While it has been proposed to classify BAD under large artery atherosclerosis, uncertainty exists regarding the optimal treatment strategy, including cholesterol-lowering targets. Objectives: We aimed to assess the clinical implications and temporal changes of atherosclerotic plaques before and after high-intensity statin treatment. Design: This is a high-resolution vessel-wall imaging sub-analysis of the trial of Statin and Dual Antiplatelet Therapy in Preventing Early Neurological Deterioration in Branch Atheromatous Disease (SATBRAD). Methods: In this prospective, single-group cohort study, participants in the treatment arm of the SATBRAD trial received early dual antiplatelet therapy and high-intensity statin treatment. The majority of these participants subsequently underwent high-resolution vessel-wall magnetic resonance imaging (MRI). Those with atheromatous plaques in the parent artery continued high-intensity statin treatment for 6 months, followed by a repeat MRI to monitor plaque changes. Results: There were 57 patients who underwent vessel-wall imaging and 24 exhibited contrast-enhanced plaques. Patients with contrast-enhanced plaques showed higher rates of END (29.2% vs 6.1%, p = 0.027), perfusion defects (62.5% vs 24.2%, p = 0.004), and lower rates of good outcomes at 3 months (50.0% vs 81.8%, p = 0.011). After adjusting for confounding factors, contrast-enhanced plaque had a negative impact on achieving a good outcome at 3 months (adjusted odds ratio = 0.04; 95% confidence interval = <0.01–0.60). Following high-intensity statin treatment in 36 patients, there was a notable reduction in stenosis (33.7% vs 29.3%, p = 0.005) and contrast-enhanced plaque volume (16.3 vs 11.6 mm3, p = 0.015). Conclusion: The study highlighted the association between contrast-enhanced atherosclerotic plaques, END, and poor functional outcomes, with high-intensity treatment leading to plaque volume reduction. These results underscore the shared pathology between BAD and intracranial atherosclerosis, emphasizing the necessity for further research and tailored treatment strategies for BAD. Trial registration: ClinicalTrials.gov; Identifier: NCT04824911 (https://clinicaltrials.gov/study/NCT04824911). Plain language summary Changes in atherosclerosis and its impact on health after statin treatment: what we learned from detailed vessel imaging in the SATBRAD trial Branch atheromatous disease (BAD) is a major cause of early worsening of stroke symptoms, leading to poor recovery. While some experts believe BAD should be treated like large artery disease, the best treatment approach, including cholesterol-lowering targets, remains unclear. This study aimed to assess how high-intensity statin treatment affects atherosclerotic plaques over time and its impact on patient health. Analyzing detailed vessel images from the SATBRAD trial, where patients received high-intensity statins and magnetic resonance imaging, revealed that 24 out of 57 patients had plaques that showed up clearly with contrast enhancement. These patients were more likely to experience early worsening of stroke symptoms and perfusion compromise and had poorer outcomes. After six months of high-intensity statin treatment, there was a significant reduction in plaque size and vessel narrowing. The study concluded that contrast-enhanced plaques are linked to worse early stroke symptoms and poor recovery, but high-intensity statin treatment can reduce plaque size, suggesting that BAD may share similarities with larger artery disease and highlighting the need for further research and tailored treatments for BAD.

IntroductionBranch atheromatous disease (BAD) contributes to small-vessel occlusion in cases of occlusion or stenosis of large calibre penetrating arteries, and it is associated with a higher possibility of early neurological deterioration (END) and recurrent stroke in acute ischaemic stroke. As the pathology of BAD is due to atherosclerosis, we postulate that early intensive medical treatment with dual antiplatelet therapy (DAPT) and high-intensity statins may prevent END and recurrent stroke in acute small subcortical infarction caused by BAD.Methods and analysisIn this prospective, single-centre, open-label, non-randomised, single-arm study using a historical control, we will compare early DAPT and high-intensity statin treatment with a historical control group of patients with BAD who were treated with single antiplatelet therapy without high-intensity statin treatment. Patients will be eligible for enrolment if they are admitted for acute ischaemic stroke within 24 hours, have a National Institutes of Health Stroke Scale (NIHSS) score of 1–8 and are diagnosed with BAD by MRI. Patients will take aspirin, clopidogrel and high-intensity statins (atorvastatin or rosuvastatin) within 24 hours of stroke onset, followed by aspirin or clopidogrel alone from day 22. The primary endpoint is the percentage of patients who develop END within 7 days of stroke onset (defined as an increase in the NIHSS score ≥2 points) and recurrent stroke within 30 days. The total sample sizes will be 138 for the intervention group and 277 for the control group. A historical control group will be drawn from previous prospective observation studies.Ethics and disseminationThe protocol of this study has been approved by the Institutional Review Board of Chang Gung Memorial Hospital (202001386A3). All participants will have to sign and date an informed consent form. The findings arising from this study will be disseminated in peer-reviewed journals and academic conferences.Trial registration numberNCT04824911.

Background Accurately predicting mortality in patients with skin and soft-tissue infections (SSTIs) remains challenging. Machine learning models offer rapid processing, algorithmic impartiality, and strong predictive accuracy, which may improve early risk stratification in the emergency department (ED). Methods We retrospectively analyzed clinical data from 1,294 ED patients diagnosed with SSTIs between March 2015 and December 2020. Five machine learning algorithms—logistic regression (LR), k-nearest neighbours (KNN), support vector machine (SVM), random forest (RF), and Extreme Gradient Boosting (XGBoost)—were developed using 20 candidate variables, with model performance evaluated in independent runs. A simplified XGBoost model using only the six most influential predictors was also derived for bedside application. Results Among the five models, XGBoost achieved the highest performance (AUC = 0.892, sensitivity = 86.9%, specificity = 93.4%). The streamlined six-variable XGBoost model further improved predictive metrics (AUC = 0.922, sensitivity = 88.5%, specificity = 95.4%), matching or slightly surpassing the full model while reducing data requirements. Conclusions XGBoost outperformed LR, KNN, SVM, and RF in predicting SSTI mortality, offering both higher accuracy and operational efficiency. Its sequential tree-building, regularization, and robust handling of missing data enable superior discrimination in tabular clinical datasets. The simplified model, requiring only standard admission variables, provides a fast, cost-effective, and highly accurate tool for early identification of high-risk patients in the ED.

Background/Objectives: Small-vessel occlusion, previously referred to as lacunar infarcts, accounts for approximately one-third of all ischemic strokes, using an axial diameter of less than 20 mm on diffusion-weighted imaging. However, this threshold may not adequately differentiate small-vessel occlusion from other pathologies, such as branch atheromatous disease (BAD) and embolism. This study aimed to assess the clinical significance and pathological implications of acute small subcortical infarctions (SSIs) based on infarct diameter. Methods: We conducted a retrospective case–control study using data from stroke patients recorded between 2016 and 2021 of the Stroke Registry in Chang Gung Healthcare System. Patients with acute SSIs in penetrating artery territories were included. Key variables such as patient demographics, stroke severity, and medical history were collected. Infarcts were categorized based on size, and the presence of early neurological deterioration (END) and favorable functional outcomes were assessed. Results: Among the 855 patients with acute SSIs, the median age was 70 years and the median National Institutes of Health Stroke Scale (NIHSS) score at arrival was four. END occurred in 97 patients (11.3%). Those who experienced END were significantly less likely to achieve a favorable functional outcome compared to those who did not (18.6% vs. 59.9%, p < 0.001). The incidence of END increased progressively with infarct sizes of 15 mm or larger, with the optimal threshold for predicting END identified as 15.5 mm and for BAD, it was 12.1 mm. A multiple logistic regression analysis revealed that motor tract involvement [adjusted odds ratio (aOR) 2.3; 95% confidence interval (CI) 1.1–4.7], an initial heart rate greater than 90 beats per minute (aOR 2.3; 95% CI 1.2–4.3), and a larger infarct size (15 mm to less than 20 mm vs. 10 mm to less than 15 mm; aOR 3.0; 95% CI 1.4–6.3) were significantly associated with END. Conclusions: Our findings suggest that setting the upper limit for small-vessel occlusion at 15 mm would be more effective in distinguishing it from BAD. However, these findings should be interpreted in the context of the retrospective design and study population. Further multi-center research utilizing high-resolution vessel wall imaging is necessary to refine this threshold and enhance diagnostic accuracy.

IntroductionDual antiplatelet therapy and high-intensity statins are the mainstay treatment in patients with acute stage, symptomatic intracranial atherosclerotic stenosis (ICAS). Alirocumab is a monoclonal antibody that can inhibit proprotein convertase subtilisin–kexin type 9 and effectively lower low-density lipoprotein cholesterol levels with less side effects than statins. We hypothesise that alirocumab treatment in addition to statin therapy could stabilise intracranial plaque and reduce arterial stenosis.Methods and analysisIn this prospective, randomised, open-label, blinded end-point study, we will use high-resolution vessel-wall MRI to evaluate the efficacy and safety of alirocumab in patients who had an acute ischaemic stroke from ICAS. We will recruit 66 patients who had an acute ischaemic stroke within 7 days of symptom onset, who had symptomatic intracranial artery stenosis (>30%) at the middle cerebral artery, basilar artery or intracranial internal carotid artery. Among them, 22 patients will be randomised to the intervention group to receive treatment with 75 mg alirocumab subcutaneously every 2 weeks for a total of 26 weeks, while those in the control group will not. All patients in both groups will receive antiplatelet agents and high-intensity statins, including 20 mg rosuvastatin or 40–80 mg atorvastatin or at the maximum tolerated dose. All of them will undergo MRI at recruitment and after 26 weeks. The primary outcomes are changes in intracranial atherosclerotic plaques in the MRI before and after 6 months treatment. This trial is being conducted at Chang Gung Memorial Hospital at Chiayi, Taiwan.Ethics and disseminationThis trial has been approved by the Institutional Review Board of Chang Gung Memorial Hospital (approval no. 202 002 482A3). Written informed consent will be obtained from all research participants. Study results will be published as peer-reviewed articles.Trial registration numberClinicalTrials.gov, Identifier: NCT05001984; Pre-results.

This study investigated whether alcoholic intoxication (AI) increases the risk of inflammatory bowel disease (IBD) by using a population-based database in Taiwan. This retrospective matched-cohort study included 57 611 inpatients with new-onset AI (AI cohort) and 230 444 randomly selected controls (non-AI cohort). Each patient was monitored for 10 years to individually identify those who were subsequently diagnosed with Crohn disease (CD) and ulcerative colitis (UC) during the follow-up period. Cox proportional hazard regression analysis was conducted to determine the risk of IBD in patients with AI compared with controls without AI. The incidence rate of IBD during the 10-year follow-up period was 2.69 per 1 000 person-years and 0.49 per 1 000 person-years in the AI and non-AI cohorts, respectively. After adjustment for age, sex, and comorbidity, the AI cohort exhibited a 3.17-fold increased risk of IBD compared with the non-AI cohort (hazard ratio [HR] = 3.17, 95% confidence interval [CI] = 2.19-4.58). Compared with the non-AI cohort, the HRs of CD and UC were 4.40 and 2.33 for the AI cohort, respectively. After stratification for the severity of AI according to the duration of hospital stay, the adjusted HRs exhibited a significant correlation with the severity; the HRs of IBD were 1.76, 6.83, and 19.9 for patients with mild, moderate, and severe AI, respectively (p for the trend < .0001). The risk of IBD was higher in patients with AI and increased with the length of hospital stay.