Comprehensive immune modulation mechanisms of Angong Niuhuang Wan in ischemic stroke: Insights from mass cytometry analysis.

Background: Angong Niuhuang Wan (AGNHW, ), is a classical medicinal formula in Traditional Chinese Medicine (TCM) that has been appreciated for its neuroprotective properties in ischemic cerebral injuries, yet its intricate mechanisms remain only partially elucidated.

Aims: This study leverages advanced Mass cytometry (CyTOF) to analyze AGNHW's multifaceted immunomodulation effects in-depth, emphasizing previously underexplored areas.

Results: AGNHW mitigated monocyte-derived macrophages (MoDM) infiltration in the brain, distinguishing its effects on those from microglia.

Metabolic changes with the occurrence of atherosclerotic plaques and the effects of statins.

Atherosclerosis is a common cardiovascular disease caused by the abnormal expression of multiple factors and genes influenced by both environmental and genetic factors. The primary manifestation of atherosclerosis is plaque formation, which occurs when inflammatory cells consume excess lipids, affecting their retention and modification within the arterial intima. This triggers endothelial cell (EC) activation, immune cell infiltration, vascular smooth muscle cell (VSMC) proliferation and migration, foam cell formation, lipid streaks, and fibrous plaque development.

Effects of remote ischemic postconditioning on the pro-inflammatory neutrophils of peripheral blood in acute cerebral infarction.

Background: Neutrophils play crucial roles in the inflammatory response after acute cerebral infarction (ACI). Previous studies revealed neutrophils are non-homogeneous and can be divided into at least two subtypes, pro-inflammatory and anti-inflammatory, correlated with patients' prognosis.

Objective: We aimed to explore the correlation between disease severity and peripheral blood neutrophils in patients with ACI and determine whether remote ischemic postconditioning (RIPostC) exerts neuroprotective effects by regulating neutrophils.

A review of stress-induced hyperglycaemia in the context of acute ischaemic stroke: Definition, underlying mechanisms, and the status of insulin therapy.

The transient elevation of blood glucose produced following acute ischaemic stroke (AIS) has been described as stress-induced hyperglycaemia (SIH). SIH is common even in patients with AIS who have no previous diagnosis of diabetes mellitus. Elevated blood glucose levels during admission and hospitalization are strongly associated with enlarged infarct size and adverse prognosis in AIS patients.

Neutrophil Heterogeneity and its Roles in the Inflammatory Network after Ischemic Stroke.

As the first peripheral immune cells to enter the brain after ischemic stroke, neutrophils are important participants in stroke-related neuroinflammation. Neutrophils are quickly mobilized from the periphery in response to a stroke episode and cross the blood-brain barrier to reach the ischemic brain parenchyma. This process involves the mobilization and activation of neutrophils from peripheral immune organs (including the bone marrow and spleen), their chemotaxis in the peripheral blood, and their infiltration into the brain parenchyma (including disruption of the blood-brain barrier, inflammatory effects on brain tissue, and interactions with other immune cell types).

Systematic Study of Immune Cell Diversity in ischemic postconditioning Using High-Dimensional Single-Cell Analysis with Mass Cytometry.

Ischemic postconditioning (IPostC) is a concept of ischemic stroke treatment, in which several cycles of brief reocclusion after reperfusion are repeated. It is essential to have an accurate understanding of the immune response in IPostC. By using high parametric single-cell mass cytometry, immune cell subsets and characterize their unique functions from ischemic brain and peripheral blood were identified after IPostC.

Review Cerebral Ischemic Tolerance and Preconditioning: Methods, Mechanisms, Clinical Applications, and Challenges.

Stroke is one of the leading causes of morbidity and mortality worldwide, and it is increasing in prevalence. The limited therapeutic window and potential severe side effects prevent the widespread clinical application of the venous injection of thrombolytic tissue plasminogen activator and thrombectomy, which are regarded as the only approved treatments for acute ischemic stroke. Triggered by various types of mild stressors or stimuli, ischemic preconditioning (IPreC) induces adaptive endogenous tolerance to ischemia/reperfusion (I/R) injury by activating a multitude cascade of biomolecules, for example, proteins, enzymes, receptors, transcription factors, and others, which eventually lead to transcriptional regulation and epigenetic and genomic reprogramming.

Systematic Study of the Immune Components after Ischemic Stroke Using CyTOF Techniques.

Stroke induces a robust inflammatory response. However, it still lacks a systematic view of the various immune cell types due to the limited numbers of fluorophore used in the traditional FACS technique. In our current study, we utilized the novel technique mass cytometry (CyTOF) to analyze multiple immune cell types.

Mechanisms underlying astrocytic connexin-43 autophagy degradation during cerebral ischemia injury and the effect on neuroinflammation and cell apoptosis.

Connexin-43 (Cx43) is the most abundant gap junction protein in the nervous system. It enables cell communication and has important physiological roles including ion transport and substrate exchange, all of which have been implicated in cerebral ischemia injury. Our previous in vitro and in vivo studies have demonstrated that Cx43 is internalized and degraded during ischemia stress.

Vinpocetine Protects Against Cerebral Ischemia-Reperfusion Injury by Targeting Astrocytic Connexin43 via the PI3K/AKT Signaling Pathway.

Vinpocetine (Vinp) is known for its neuroprotective properties. However, the protective mechanism of Vinp against cerebral ischemia/reperfusion (I/R) injury should be further explored. This study was designed to investigate the neuroprotective effects of Vinp against oxygen-glucose deprivation/reoxygenation (OGD/R) injury and cerebral I/R injury and explore whether this mechanism would involve enhancement of astrocytic connexin 43 (Cx43) expression via the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway.

Potential Mechanism of Venous System for Leukoaraiosis: From post-mortem to in vivo Research.

Background: Leukoaraiosis (LA), widely accepted as a feature of cerebral small vessel disease, significantly increases the incidence of stroke, dementia, and death. Cerebral small artery disease has been considered as one of the main causes of LA. However, since the term "venous collagenosis" (VC) was proposed in an atrophy research in 1995, there have been pathological and neuroimaging studies proving the association between the venous system and LA in aging, Alz-heimer's disease (AD), and Parkinson's disease.

Potential Applications of Remote Limb Ischemic Conditioning for Chronic Cerebral Circulation Insufficiency.

Chronic cerebral circulation insufficiency (CCCI) refers to a chronic decrease in cerebral blood perfusion, which may lead to cognitive impairment, psychiatric disorders such as depression, and acute ischemic stroke. Remote limb ischemic conditioning (RLIC), in which the limbs are subjected to a series of transient ischemic attacks, can activate multiple endogenous protective mechanisms to attenuate fatal ischemic injury to distant organs due to acute ischemia, such as ischemic stroke. Recent studies have also reported that RLIC can alleviate dysfunction in distant organs caused by chronic, non-fatal reductions in blood supply (e.

Silencing the lncRNA in pro-inflammatory macrophages attenuates acute experimental ischemic stroke via LCP1 in mice.

Long noncoding RNAs (lncRNA) expression profiles change in the ischemic brain after stroke, but their roles in specific cell types after stroke have not been studied. We tested the hypothesis that lncRNA modulates brain injury by altering macrophage functions. Using RNA deep sequencing, we identified 73 lncRNAs that were differentially expressed in monocyte-derived macrophages (MoDMs) and microglia-derived macrophages (MiDMs) isolated in the ischemic brain three days after stroke.

Gerstmann-Sträussler-Scheinker disease: A case report.

Background: Gerstmann-Sträussler-Scheinker (GSS) disease is an inherited prion disease that is clinically characterized by the early onset of progressive cerebellar ataxia. The incidence of GSS is extremely low and it is particularly rare in China. Therefore, clinicians may easily confuse this disease with other diseases that also cause ataxia, resulting in its under-diagnosis or misdiagnosis.

Increased expression of claudin-12 promotes the metastatic phenotype of human bronchial epithelial cells and is associated with poor prognosis in lung squamous cell carcinoma.

A prior study by our group using cDNA array analysis identified the tight junction component claudin-12 (CLDN12) to be an upregulated gene in lung squamous cell carcinoma (SqCC) cells compared with normal human bronchial epithelial cells. The present study aimed to explore the effect and underlying molecular mechanism of CLDN12 with regard to the malignant phenotype of SqCC. Firstly, the expression patterns of CLDN12 in SqCC tissues, lung adenocarcinoma tissues and histologically non-neoplastic lung epithelial tissues were investigated by immunohistochemistry and western blotting.

Increased expression of claudin-17 promotes a malignant phenotype in hepatocyte via Tyk2/Stat3 signaling and is associated with poor prognosis in patients with hepatocellular carcinoma.

Background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer death in Asia; however, the molecular mechanism in its tumorigenesis remains unclear. Abnormal expression of claudins (CLDNs), a family of tight junction (TJ) proteins, plays an important role in the metastatic phenotype of epithelial-derived tumors by affecting tight junction structure, function and related cellular signaling pathways. In a previous study, we used a tissue chip assay to identify CLDN17 as an upregulated gene in HCC.

Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate.

Following cerebral ischemia/reperfusion (I/R) injury, a series of pathophysiological processes are stimulated in both the central nervous system (CNS) and the periphery, including, but not limited to, the peripheral immune and endocrine systems and underregulation of the neuroendocrine-immune network. Glutamate (Glu) is an important excitatory neurotransmitter in the CNS; its excitotoxicity following cerebral ischemia has been a focus of study for several decades. In addition, as a novel immunoregulator, Glu also regulates immune activity in both the CNS and periphery and may connect the CNS and periphery through regulation of the neuroendocrine-immune network.

Management of multiple neurological complications in mixed connective tissue disease: A case report.

Rationale: Mixed connective tissue disease (MCTD) refers to an overlapping condition of different autoimmune disorders such as systemic lupus erythematosus, cutaneous systemic sclerosis, rheumatoid arthritis, polymyositis, and dermatomyositis. However, MCTD manifesting as transverse myelitis is extremely rare. Herein, we report a case of MCTD with both central and peripheral nervous system involvement.

Astrocytic gap junction inhibition by carbenoxolone enhances the protective effects of ischemic preconditioning following cerebral ischemia.

Background: Stroke is the second leading cause of death worldwide and the most common cause of adult-acquired disability in many nations. Thus, attenuating the damage after ischemic injury and improving patient prognosis are of great importance. We have indicated that ischemic preconditioning (IP) can effectively reduce the damage of ischemia reperfusion and that inhibition of gap junctions may further reduce this damage.

The prevalence of depression in rheumatoid arthritis in China: A systematic review.

This systematic review is to explore the prevalence of depression in patients with rheumatoid arthritis (RA) in China. Articles of prevalence rates for depression in adult RA patients published before October 2015 were identified from PubMed, Embase, The Cochrane Library, CNKI, CBM, VIP, and Wanfang database and other internet databases. Relevant journals and the recommendations of expert panels were also searched manually.

Characteristics of cardio-Cerebrovascular modulation in patients with generalized anxiety disorder: an observational study.

Background: Generalized anxiety disorder (GAD) has been shown in previous studies to display abnormal cerebral blood flow velocity (CBFV); however, the characteristics of cardio-cerebrovascular modulation are unknown. We aimed to analyze cardio-cerebrovascular modulation using parameters from a supine-to-standing test.

Methods: There are 2 parts to this study; in Part 1, 125 participants with Hamilton Anxiety scale scores ≥14 were enrolled, and 33 age- and sex-matched medically and psychiatrically healthy volunteers were recruited as control participants.

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning.

Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in membrane channel function, and activation of protein kinases.

Noninvasive and quantitative intracranial pressure estimation using ultrasonographic measurement of optic nerve sheath diameter.

We aimed to quantitatively assess intracranial pressure (ICP) using optic nerve sheath diameter (ONSD) measurements. We recruited 316 neurology patients in whom ultrasonographic ONSD was measured before lumbar puncture. They were randomly divided into a modeling and a test group at a ratio of 7:3.

Cortical spreading depression-induced preconditioning in the brain.

Cortical spreading depression is a technique used to depolarize neurons. During focal or global ischemia, cortical spreading depression-induced preconditioning can enhance tolerance of further injury. However, the underlying mechanism for this phenomenon remains relatively unclear.