• Cooking method
• Gut microbiota
• Ischemic stroke
• Rhubarb
• SCFAs

• CI2021A04205, CI2021B015 Scientific and technological innovation project of China Academy of Chinese Medical Sciences
• CI2021A04205, CI2021B015 Scientific and technological innovation project of China Academy of Chinese Medical Sciences
• ZXKT23007, ZXKT21030 Fundamental Research Funds for the Central public welfare research institutes
• ZXKT23007, ZXKT21030 Fundamental Research Funds for the Central public welfare research institutes
• ZZ15-YQ-034 Special program for outstanding young scientific and technological talents (innovation) of China Academy of Chinese Medical Sciences of China Academy of Chinese Medical Sciences

• P0.1
• PMI
• inspiratory effort
• mechanical ventilation
• pressure support ventilation
• ΔPocc

• brain network topology
• microbiota-gut-brain axis
• poststroke aphasia
• resting-state fMRI

• National Natural Science Foundation of China

• Animals
• Female
• Rats
• Cognitive Dysfunction/etiology
• Cognitive Dysfunction/drug therapy
• Disease Models, Animal
• Gastrointestinal Microbiome/drug effects
• Insulin-Like Growth Factor I/metabolism
• Insulin-Like Growth Factor I/administration & dosage
• Neuroprotective Agents/pharmacology
• Neuroprotective Agents/therapeutic use
• Rats, Sprague-Dawley
• Stroke/complications

• RF1 NS119872 NINDS NIH HHS

• Gastrointestinal bleeding
• Pneumonia
• Stroke
• Temporal sequence

• Humans
• Male
• Female
• Ischemic Stroke/epidemiology
• Ischemic Stroke/complications
• Ischemic Stroke/etiology
• Gastrointestinal Hemorrhage/etiology
• Gastrointestinal Hemorrhage/epidemiology
• Aged
• Pneumonia/complications
• Pneumonia/epidemiology
• Middle Aged
• Time Factors
• Risk Factors
• Hospitalization/statistics & numerical data
• Length of Stay/statistics & numerical data
• Aged, 80 and over
• Logistic Models

• 2020-1-2041 Beijing Municipal Commission of Health and Family Planning
• 81471208 National Natural Science Foundation of China
• L223028 Beijing Natural Science Foundation

• proton pump inhibitor
• upper gastrointestinal bleeding
• severe stroke
• nomogram model

• Humans
• Retrospective Studies
• Critical Illness
• Gastrointestinal Hemorrhage/epidemiology
• Gastrointestinal Hemorrhage/etiology
• Risk Factors
• Prognosis
• Stroke/complications

• ChAT
• Gastrointestinal dysfunction
• Stroke
• Vagus nerve
• α7nAChR

• Nomogram
• Post-endoscopic model
• Pre-endoscopic model
• Prognosis prediction
• Retrospective study
• Upper gastrointestinal bleeding

• Aspiration
• Gastric contents
• Gastrointestinal endoscopy
• Nomogram
• Outpatient

• Humans
• Male
• Outpatients
• Nomograms
• Retrospective Studies
• Gastroscopy
• Hypnotics and Sedatives/adverse effects

• anticoagulants
• cerebrovascular accident
• gastrointestinal bleeding
• gastrointestinal hemorrhage
• ischemic stroke

• Acute ischaemic stroke
• Gut microbiome
• Metabolome
• Multi-omics
• Tibetan miniature pig

• Animals
• Swine
• Swine, Miniature/genetics
• RNA, Ribosomal, 16S/genetics
• RNA, Ribosomal, 16S/analysis
• Tibet
• Brain Ischemia/genetics
• Genes, rRNA
• Feces/microbiology
• Stroke/genetics
• Metabolomics/methods
• Metabolome
• Biomarkers/analysis
• Ischemic Stroke/genetics
• ATP-Binding Cassette Transporters/genetics

• Bile acids
• Ischemic stroke
• Lipopolysaccharides
• Phenylacetylglutamine
• Short-chain fatty acids
• Trimethylamine N-oxide

• Humans
• Gastrointestinal Microbiome/physiology
• Ischemic Stroke
• Dysbiosis/metabolism
• Stroke/microbiology
• Bacteria/metabolism

• Humans
• Ischemic Stroke
• Dysbiosis
• Stroke/complications
• Central Nervous System
• Gastrointestinal Diseases/etiology

• bibliometric analysis
• gut microbiota
• hotspots
• research trends
• stroke

• Ileum
• Intestinal motility
• Jejunum
• Myenteric Plexus
• Systemic inflammation

• GCS
• age
• gastrointestinal bleeding
• predictors
• prognosis
• stress ulcer prophylaxis
• stroke

• neuroscience
• stroke

• Male
• Animals
• Swine
• Ischemic Stroke
• Tumor Necrosis Factor-alpha
• Stroke/therapy
• Neural Stem Cells/pathology
• Inflammation/pathology
• Fatty Acids, Volatile
• Nanoparticles

• R01 CA247769 NCI NIH HHS
• R01 CA257851 NCI NIH HHS
• R01 NS093314 NINDS NIH HHS
• R01NS093314 NINDS NIH HHS
• National Institute of Neurological Disorders and Stroke
• Georgia Experimental Agricultural Station

• Mendelian randomization
• causality
• gastrointestinal disorders
• risk
• stroke

• Gut-brain axis
• Inflammasome
• Photothrombotic stroke
• Pyroptosis

• Animals
• Mice
• Pyroptosis
• Inflammasomes/metabolism
• Endothelial Cells/metabolism
• Brain-Gut Axis
• Caspases/metabolism
• Stroke
• Thrombotic Stroke

• Biological sciences
• Immunology
• Metabolomics
• Transcriptomics

• R01 AI154630 NIAID NIH HHS
• R01 DK109560 NIDDK NIH HHS

Stroke is a disease with high incidence, mortality and disability rates. It is also the main cause of adult disability in developed countries. Stroke is often caused by small emboli on the inner wall of the blood vessels supplying the brain, which can lead to arterial embolism, and can also be caused by cerebrovascular or thrombotic bleeding. With the exception of recombinant tissue plasminogen activator (rt-PA), which is a thrombolytic drug used to recanalize the occluded artery, most treatments have been demonstrated to be ineffective. Stroke can also induce peripheral organ damage. Most stroke patients have different degrees of injury to one or more organs, including the lung, heart, kidney, spleen, gastrointestinal tract and so on. In the acute phase of stroke, severe inflammation occurs in the brain, but there is strong immunosuppression in the peripheral organs, which greatly increases the risk of peripheral organ infection and aggravates organ damage. Nonneurological complications of stroke can affect treatment and prognosis, may cause serious short-term and long-term consequences and are associated with prolonged hospitalization and increased mortality. Many of these complications are preventable, and their adverse effects can be effectively mitigated by early detection and appropriate treatment with various medical measures. This article reviews the pathophysiological mechanism, clinical manifestations and treatment of peripheral organ injury after stroke.

• gastrointestinal tract
• heart
• kidney
• lung
• peripheral organ injury
• spleen
• stroke

• Neurocritical care
• Stress ulcer prophylaxis
• Upper gastrointestinal bleeding

• Aged
• Analgesics, Opioid/adverse effects
• Brain
• Humans
• Hypnotics and Sedatives/adverse effects
• Middle Aged
• Prospective Studies

Background: While there have been major advances in unveiling the mechanisms comprising the ischemic cascade of CNS, stroke continues to be a significant burden. There is a need to extend the focus toward peripheral changes, and the brain–gut axis has recently gained much attention. Our study aimed to evaluate gut inflammation and its association with blood variables in stroke using fecal calprotectin (FC). Methods: Fecal samples were obtained from 27 stroke patients and 27 control subjects. FC was quantitatively measured using a commercial ELISA. Laboratory data on the fecal sample collection were also collected, including CBC, ESR, glucose, creatinine, total protein, albumin, transaminases, and CRP. Results: There was a significant increase in FC levels in stroke patients compared to the controls. Furthermore, FC in stroke patients was negatively correlated with the Glasgow Coma Scale. Moreover, FC in stroke patients was positively correlated with CRP and negatively correlated with lymphocyte count and albumin. Conclusions: Our findings show that increased FC is associated with consciousness and systemic response in stroke and warrants further studies to elucidate the usefulness of FC in the management of stroke.

• blood flow
• fermented soybeans
• gut microbiota
• inflammation
• post-stroke hyperglycemia

• blood glucose
• blood pressure
• body temperature
• gut microbiota
• hydration
• immune response
• oxygen
• schemic stroke

Stroke is the second leading cause of death worldwide. Patients who have a stroke are susceptible to many gastrointestinal (GI) complications, such as dysphagia, GI bleeding, and fecal incontinence. However, there are few studies focusing on the GI tract after stroke. The current study is to investigate the changes of intestinal structure and function in mice after ischemic stroke. Ischemic stroke was made as a disease model in mice, in which brain and ileal tissues were collected for experiments on the 1^st and 7^th day after stroke. Intestinal motility of mice was inhibited, and intestinal permeability was increased after stroke. Hematoxylin-eosin (HE) staining showed the accumulation of leucocytes in the intestinal mucosa. Myeloperoxidase (MPO) activity and inflammatory proteins (nuclear factor kappa-B (NF-κB), inducible nitric oxide synthase (iNOS)) in the small intestine were significantly increased in mice after stroke. The expression of tight junction (TJ) proteins (zonula occludens-1 (ZO-1), occludin, and claudin-1) was downregulated, and transmission electron microscopy (TEM) showed broken TJ of the intestinal mucosa after stroke. Glial fibrillary acidic protein (GFAP) and the apoptosis-associated proteins (tumor necrosis factor (TNF-α), caspase-3, and cleaved caspase-3) were notably upregulated as well. Ischemic stroke led to negative changes on intestinal structure and function. Inflammatory mediators and TNF-α-induced death receptor signaling pathways may be involved and disrupt the small intestinal barrier function. These results suggest that stroke patients should pay attention to GI protection.

The intestinal microbiome, the largest reservoir of microorganisms in the human body, plays an important role in neurological development and aging as well as in brain disorders such as an ischemic stroke. Increasing knowledge about mediators and triggered pathways has contributed to a better understanding of the interaction between the gut-brain axis and the brain-gut axis. Intestinal bacteria produce neuroactive compounds and can modulate neuronal function, which affects behavior after an ischemic stroke. In addition, intestinal microorganisms affect host metabolism and immune status, which in turn affects the neuronal network in the ischemic brain. Here we discuss the latest results of animal and human research on two-way communication along the gut-brain axis in an ischemic stroke. Moreover, several reports have revealed the impact of an ischemic stroke on gut dysfunction and intestinal dysbiosis, highlighting the delicate play between the brain, intestines and microbiome after this acute brain injury. Despite our growing knowledge of intestinal microflora in shaping brain health, host metabolism, the immune system and disease progression, its therapeutic options in an ischemic stroke have not yet been fully utilized. This review shows the role of the gut microflora-brain axis in an ischemic stroke and assesses the potential role of intestinal microflora in the onset, progression and recovery post-stroke.

• amyloid
• brain ischemia
• gut microbiota
• stroke
• tau protein
• trimethylamine-n-oxide

• 16S ribosomal RNA sequencing
• gut microbiota
• post-stroke affective disorder
• post-stroke cognitive impairment
• stroke

After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understanding of cerebral plasticity is pivotal to design effective therapeutic strategies. Experimental models and clinical studies have fueled the current understanding of the cellular and molecular processes responsible for plastic remodeling. In this review, we describe the known mechanisms, in patients and animal models, underlying cerebral reorganization and contributing to functional recovery after ischemic stroke. We also discuss the manipulations and therapies that can stimulate neural plasticity. We finally explore a new topic in the field of ischemic stroke pathophysiology, namely the brain-gut axis.

• Brain-gut axis
• ischemia
• microbiota
• neuro-inflammation
• recovery

• Animals
• Gastrointestinal Microbiome/physiology
• Humans
• Models, Animal
• Neuronal Plasticity/physiology
• Recovery of Function/physiology
• Stroke/physiopathology

• Diarrhea
• Enteric nutrition
• Intensive care unit
• Predictive model
• Stroke

• acute ischemic stroke
• nomogram
• prediction
• stroke-associated pneumonia

• bloodstream infection
• gastrointestinal bleeding
• inverse probability of treatment weighting (IPTW)
• propensity score
• sepsis

Postoperative cerebral complications (PCC) are common and serious postoperative complications for patients with Stanford type A aortic dissection (AAD). The aim of this study was to evaluate the risk factors for PCC in these patients and to provide a scientific basis for effective prevention of PCC.

In this retrospective case-control study, 125 patients with AAD who underwent thoracotomy in our department from October 2017 to October 2018 in the department of cardiovascular surgery, Fujian Medical University Union Hospital were divided into two groups: patients with PCC (n = 12), and patients without PCC (n = 113). The general clinical data, the types of corrective surgeries, the intraoperative situations, the postoperative complications, and the midterm outcomes of the patients were analyzed.

The patients with PCC were significantly older than the patients without PCC (P = 0.016), and the incidence of the preoperative cerebral disease history in the patients with PCC was significantly higher than those of the PCC (−) group (P = 0.024). The Euro SCORE II of patients with PCC was dramatically higher than the patients without PCC (P = 0.005). There were significant differences between the two groups in terms of the duration of cardiopulmonary bypass (CPB) (P = 0.010) and the length of moderate hypothermic circulatory arrest (MHCA) combined with selective cerebral perfusion (SCP) (P = 0.000). The monitoring of rcSO₂ indicated that there was significant difference between the two groups in terms of the bilateral baseline (P = 0.000). Patients with PCC were observed to have experienced significantly longer intubation times (P = 0.000), ICU stays (P = 0.001), and postoperative hospital stays (P = 0.009), and they also had dramatically higher rates of pulmonary infection (P = 0.000), multiple organ dysfunction syndrome (P = 0.041) and tracheotomy (P = 0.022) after surgeries. The duration of MHCA+SCP (OR:9.009, P = 0.034) and the average baseline value of rcSO₂ (OR:0.080, P = 0.009) were ultimately identified as significant risk factors.

PCC has a serious influence on the prognoses of patients following surgical treatment with AAD. The duration of MHCA+SCP and the average baseline value of rcSO₂ were the independent risk factors for PCC.

• Aneurysm, dissecting
• Circulatory arrest, deep hypothermia induced
• Oximetry
• Postoperative complications

• Disorder
• Dysphagia
• EAT-10
• Eat
• Eating
• Swallowing
• Tool

• Adult
• Aged
• Aged, 80 and over
• Belgium
• Cohort Studies
• Deglutition/physiology
• Deglutition Disorders/diagnosis
• Eating/physiology
• Female
• Humans
• Language
• Male
• Middle Aged
• ROC Curve
• Reproducibility of Results
• Surveys and Questionnaires

• Gastrointestinal hemorrhage
• acute ischemic stroke
• anticoagulation
• brain herniation
• mortality
• risk factors.

We systematically reviewed literature regarding “Lewy body constipation”, i.e., constipation due to Lewy body diseases (LBD), with minimal neurologic symptoms. Epidemiology and pathology studies showed that LBD can start with constipation alone, mostly due to neuronal loss and appearance of Lewy bodies in the myenteric plexus. Because LBD significantly increases with age, “Lewy body constipation” may also increase with age. Neuroimaging methods such as metaiodobenzylguanidine (MIBG) scintigraphy and dopamine transporter (DAT) scan provide a way to detect “Lewy body constipation.” Key for “Lewy body constipation” includes minimal non-motor features such as REM sleep behavior disorder (night talking). Add-on therapy may be required to ameliorate constipation in patients. Diagnosis is not always easy; therefore, collaboration of gastroenterologists and neurologists is highly recommended to maximize patients' quality of life. In conclusion, “Lewy body constipation” might become a distinct category among geriatric constipation, regarding patients' follow-up and their management.

• Lewy body constipation
• Parkinson's disease
• constipation
• dementia with Lewy bodies
• neuroimaging

Background and Purpose: The gut communicates with the brain bidirectionally via neural, humoral and immune pathways. All these pathways are affected by acute brain lesions, such as stroke. Brain-gut communication may therefore impact on the overall outcome after CNS-injury. Until now, contradictory reports on intestinal function and translocation of gut bacteria after experimental stroke have been published. Accordingly, we aimed to specifically investigate the effects of transient focal cerebral ischemia on intestinal permeability, gut associated lymphoid tissue and bacterial translocation in an exploratory study using a well-characterized murine stroke model.

Methods: After 60 min of middle cerebral artery occlusion (MCAO) we assessed intestinal morphology (time points after surgery day 0, 3, 5, 14, 21) and tight junction protein expression (occludin and claudin-1 at day 1 and 3) in 12-week-old male C57Bl/6J mice. Lactulose/mannitol/sucralose test was performed to assess intestinal permeability 24–72 h after surgery. To investigate the influence of cerebral ischemia on the local immune system of the gut, main immune cell populations in Peyer's patches (PP) were quantified by flow cytometry. Finally, we evaluated bacterial translocation to extraintestinal organs 24 and 72 h after MCAO by microbiological culture and fluorescence in situ hybridization targeting bacterial 16S rRNA.

Results: Transient MCAO decreased claudin-1 expression in the ileum but not in the colon. Intestinal morphology (assessed by light microscopy) and permeability did not change measurably after MCAO. After MCAO, animals had significantly fewer B cells in PP compared to naïve mice.

Conclusions: In a murine model of stroke, which leads to large brain infarctions in the middle cerebral artery territory, we did not find evidence for overt alterations neither in gut morphology, barrier proteins and permeability nor presence of intestinal bacterial translocation.

• bacterial translocation
• gut associated lymphatic tissue
• gut permeability
• gut-brain axis
• immune system
• stroke
• tight junctions

• autonomic function
• constipation
• heart rate variability
• ischemic stroke
• transcutaneous electrical acustimulation

• Bacterial infection
• Immunosuppression
• Stroke
• Therapeutics

• enteric nervous system
• focal cerebral ischaemia
• global cerebral ischaemia
• nitric oxide synthase
• vasoactive intestinal peptide

• Aneurysmal subarachnoid hemorrhage
• Delayed cerebral ischemia
• Outcome
• Risk factors

• Population-based study
• Taiwan
• gastroesophageal reflux disease
• stroke

• Chronic Traumatic Encephalopathy
• Concussion
• Gut
• Gut-brain axis
• Intestinal dysfunction
• Microbiota
• Microglia
• Neurodegenerative disease
• Neuroinflammation
• Traumatic Brain Injury

• Animals
• Brain/immunology
• Brain/physiopathology
• Brain Diseases/immunology
• Brain Diseases/microbiology
• Brain Diseases/physiopathology
• Brain Injuries, Traumatic/immunology
• Brain Injuries, Traumatic/microbiology
• Brain Injuries, Traumatic/physiopathology
• Encephalitis/immunology
• Encephalitis/microbiology
• Encephalitis/physiopathology
• Gastrointestinal Microbiome
• Humans

Spontaneous subarachnoid hemorrhage (SAH) is a devastating disease, and gastrointestinal hemorrhage is one of several potential complications of acute strokes. We aim to analyze its prevalence, risk factors, and association with in-hospital prognosis following SAH. A total of 1047 adult patients with a primary diagnosis of spontaneous SAH were retrospectively enrolled. We retrieved medical information from the administrative database utilizing diagnostic and procedure codes of the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). Patients with SAH included 418 men and 629 women, and their mean age was 57.2 (standard deviation 14.6) years (range, 18–93 years). Gastrointestinal hemorrhage occurred in 30 of the 1047 patients, accounting for 2.9%. In a multivariate logistic regression model, the independent risk factors for gastrointestinal hemorrhage were liver disease and hydrocephalus. The in-hospital mortality rates were 43.3% and 29.3% in patients with and without gastrointestinal hemorrhage, respectively, but the difference was not statistically significant. In conclusion, the prevalence of gastrointestinal hemorrhage was 2.9% in patients hospitalized for spontaneous SAH. Underlying liver disease and the presence of hydrocephalus were both independent risk factors for this complication, which is a reminder to clinicians to pay increased attention in such cases.