Multidrug-Resistant Organism Infections of Inpatients in a Hospital in Eastern China from 2015 to 2021.

Background: The prevalence of multidrug-resistant organisms (MDRO) is gradually increasing in the global scope, causing serious burden to patients and society, which is an important public health problem.

Objective: To analyze the distribution and trend of MDROs and provide a reference for hospital infection control.

Methods: Collected data on MDROs infections among inpatients in a Grade III Level A hospital in Suzhou from 2015 to 2021, including drug-resistant bacteria strains and specimen sources, etc.

Eosinophil: A New Circulating Biomarker for Risk of Poor Outcome in Stroke Patients Undergoing Mechanical Thrombectomy.

Objective: Acute ischemic stroke (AIS), caused by occlusion of large vessel, is a serious life-threatening disease. This study aimed to comprehensively investigate the association of 14 common and readily available circulating biomarkers with the 90-day modified Rankin Scale (mRS) score in patients undergoing mechanical thrombectomy (MT).

Methods: This study included patients with anterior circulation large vessel occlusive stroke treated with MT from 05/2017 to 12/2021.

Influences of different referral modes on clinical outcomes after endovascular therapy for acute ischemic stroke.

Background And Purpose: As endovascular thrombectomy (EVT) is time-dependent, it is crucial to refer patients promptly. Current referral modes include Mothership (MS), Drip and Ship (DS) and Drive the Doctor (DD). The purpose of this study was to investigate the influences of different referral modes on the clinical outcomes of patients with acute ischemic stroke after EVT.

Predictors and Dynamic Nomogram to Determine the Individual Risk of Malignant Brain Edema After Endovascular Thrombectomy in Acute Ischemic Stroke.

Background And Purpose: This study aimed to construct an optimal dynamic nomogram for predicting malignant brain edema (MBE) in acute ischemic stroke (AIS) patients after endovascular thrombectomy (ET).

Methods: We enrolled AIS patients after ET from May 2017 to April 2021. MBE was defined as a midline shift of >5 mm at the septum pellucidum or pineal gland based on follow-up computed tomography within 5 days after ET.

Activation of UCP2 by anethole trithione suppresses neuroinflammation after intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a devastating disease, in which neuroinflammation substantially contributes to brain injury. Uncoupling protein 2 (UCP2) is a member of the mitochondrial anion carrier family, which uncouples oxidative phosphorylation from ATP synthesis by facilitating proton leak across the mitochondrial inner membrane. UCP2 has been reported to modulate inflammation.

Cognitive impairment and sleep disturbances after minor ischemic stroke.

Purpose: Post-stroke cognitive impairment (PSCI) is common among stroke survivors, although its risk factors are not well understood. Here, we assessed cognitive function in patients within 14 days after minor stroke and investigated the risk factors of PSCI, including sleep-related factors.

Methods: Patients with minor acute ischemic stroke (n = 86) were continuously recruited from November 2015 to October 2016.

Hydrogen sulfide attenuates ferric chloride-induced arterial thrombosis in rats.

Hydrogen sulfide (H2S) is a novel gaseous transmitter, regulating a multitude of biological processes in the cardiovascular and other systems. However, it remains unclear whether it exerts any effect on arterial thrombosis. In this study, we examined the effect of H2S on ferric chloride (FeCl3)-induced thrombosis in the rat common carotid artery (CCA).

DNA methylation in cystathionine-γ-lyase (CSE) gene promoter induced by ox-LDL in macrophages and in apoE knockout mice.

Recent studies suggest that epigenetic alterations such as DNA methylation control many aspects of monocytes/macrophages and participate in the pathogenesis of atherosclerosis, a lipid-driven inflammatory disorder. Our and other groups demonstrated that dysregulation of cystathionine γ-lyase (CSE) -hydrogen sulfide (H2S) pathway was involved in monocyte/macrophages-mediated inflammation and atherosclerosis. However, it remains unknown whether altered cse methylation in macrophages may play a role in linking CSE-H2S dysregulation and atherosclerosis.

Prognostic Significance of Uric Acid Levels in Ischemic Stroke Patients.

The importance and function of serum uric acid (UA) levels in patients with cardiovascular disease or stroke are unclear. We sought to evaluate the appropriate UA levels for stroke patients and the association between endogenous UA levels and clinical outcomes in acute ischemic stroke (AIS) patients, particularly regarding the possible interaction between gender and UA levels with respect to AIS prognosis. We examined 303 patients who had an onset of ischemic stroke within 48 h.

Homocysteine Triggers Inflammatory Responses in Macrophages through Inhibiting CSE-H2S Signaling via DNA Hypermethylation of CSE Promoter.

Hyperhomocysteinemia (HHcy) is an independent risk factor of atherosclerosis and other cardiovascular diseases. Unfortunately, Hcy-lowering strategies were found to have limited effects in reducing cardiovascular events. The underlying mechanisms remain unclear.

Statins upregulate cystathionine γ-lyase transcription and H2S generation via activating Akt signaling in macrophage.

Hydrogen sulfide (H2S), the third gaseous transmitter, is implicated in various pathophysiologic processes. In the cardiovascular system, H2S exerts effects of cardioprotection, vascular tone regulation, and atherogenesis inhibition. Recent studies demonstrated that atorvastatin, the inhibitor of 3-hydroxyl-3-methyl coenzyme A reductase, affected H2S formation in kidney and other organs.

Dysregulation of cystathionine γ-lyase (CSE)/hydrogen sulfide pathway contributes to ox-LDL-induced inflammation in macrophage.

Hydrogen sulfide (H2S), mainly produced by cystathionine γ-lyase (CSE) in vascular system, emerges as a novel gasotransmitter exerting anti-inflammatory and anti-atherosclerotic effects. Alterations of CSE/H2S pathway may thus be involved in atherosclerosis pathogenesis. However, the underlying mechanisms are poorly understood.

[Autophagy of human vascular endothelial cells by oxidized low-density lipoprotein: involvement of oxidative stress but no oxidized low density lipoprotein-1].

Objective: Our previous studies found that 100 µg/ml oxidized low-density lipoprotein (ox-LDL) could up-regulate the autophagic level in human umbilical vein endothelial cells (HUVEC). The present study was conducted to observe the roles of oxidative stress and lectin-like oxidized low density lipoprotein-1 (LOX-1) in the ox-LDL-induced up-regulation of autophagy.

Methods: Prior to the ox-LDL exposure, LOX-1mAb, vitamin C and vitamin E were used to study the roles of LOX-1 and oxidative stress in the activation of autophagy.

Protective role of autophagy in AGE-induced early injury of human vascular endothelial cells.

Advanced glycation end-products (AGEs) contribute to the pathogenesis of diabetes mellitus and atherosclerosis by promoting vascular endothelial cell proliferation, migration, damage and death. In this study, we examined the role of autophagy in HUVECs exposed to AGE-modified bovine serum albumin (AGE-BSA). HUVECs incubated with AGE-BSA for 6 h showed an increase in the formation of acidic vesicular organelles and autophagosomes.

[Protective effects of autophagy against oxidized LDL-induced injury in endothelial cells].

Objective: To investigate the role of autophagy in oxidized low density lipoprotein (ox-LDL) induced injury of human umbilical vein endothelial cells (HUVEC).

Methods: The cultured HUVECs were randomly divided into four groups of control, ox-LDL, ox-LDL + rapamycin and ox + 3-methyladenine (3-MA). The cells were used to detect the ratio of LC3-II/LC3-I by Western blot while the proliferation and apoptosis of cells measured by MTT and flow cytometry.