Mechanisms and treatment of anemia related to cardiac arrest.

Cardiac arrest is a common and fatal emergency situation. Recently, an increasing number of studies have shown that anemia in patients with cardiac arrest is closely related to high mortality rates and poor neurological outcomes. Anemia is prevalent among patients with post-cardiac arrest syndrome (PCAS), but its specific pathogenesis remains unclear.

Effects of peripheral blood cells on ischemic stroke: Greater immune response or systemic inflammation?

Ischemic stroke is still one of the most serious medical conditions endangering human health worldwide. Current research on the mechanism of ischemic stroke focuses on the primary etiology as well as the subsequent inflammatory response and immune modulation. Recent research has revealed that peripheral blood cells and their components are crucial to the ensuing progression of ischemic stroke.

Minimally invasive puncture combined with a high frequency of urokinase therapy improves outcomes in patients with HICH.

Minimally invasive puncture combined with urokinase is widely used in the treatment of hypertensive intracerebral hemorrhage (HICH). However, the appropriate frequency of urokinase following minimally invasive puncture in patients is still unclear. In total, 55 patients were enrolled in this study.

Cdk1 protects against oxygen-glucose deprivation and reperfusion-induced Golgi fragmentation and apoptosis through mediating GM130 phosphorylation.

Increasing evidence has indicated that the Golgi apparatus (GA) is involved in the development of cerebral ischemia-reperfusion (IR) injury. Finding effective neuroprotective agents targeting GA has become a priority in the treatment of ischemic stroke. GM130, a key structural protein present on the cis-face of the GA, maintains its structure through its phosphorylation and dephosphorylation.

Sodium valproate-induced nocturnal enuresis in epilepsy: Three case reports and a review of the literature.

Background: Enuresis is an uncommon adverse effect of sodium valproate therapy that is unknown to most clinicians. This study provides an overview of the literature on enuresis associated with sodium valproate therapy, discussing the clinical manifestations and possible mechanisms of this side effect.

Methods: We reported three cases of enuresis induced by sodium valproate and reviewed the published enuresis cases associated with sodium valproate therapy retrieved from databases.

Clinical Features of Aortic Dissection in the Emergency Department: A Single-center Experience from South China.

Objectives: Our goal in this study was to determine 1) whether there are any differences in clinical characteristics between Chinese and Western patients with aortic dissection (AD), and 2) the mortality rate of AD patients in the emergency department (ED) and identify the risk predictors for death.

Methods: We retrospectively analyzed patients who were diagnosed with AD and admitted to our ED between September 1, 2017-August 31, 2020. Data on age, gender, clinical manifestation, medical history, routine blood tests, liver and kidney function, coagulation, myocardial enzymology, and mortality were collected.

Extracorporeal membrane oxygenation rescue for severe pneumocystis pneumonia with the Macklin effect: a case report.

Background: Pneumocystis jirovecii pneumonia (PJP) in an immunocompromised host is often associated with the Macklin effect, which can progress to spontaneous pneumomediastinum (SPM), subcutaneous emphysema (SCE), and pneumothorax (PNX). Diagnosing the causative organism of these conditions in non-HIV infected patients and treating hypoxemia while preventing further lung damage can be challenging. This study examines the case of a non-HIV infected male with SPM, SCE, and PNX secondary to severe Pneumocystis jirovecii (PJ) infection.

FDG-PET/CT Assessment of the Cerebral Protective Effects of Hydrogen in Rabbits with Cardiac Arrest.

Background: Anatomical imaging methods and histological examinations have limited clinical value for early monitoring of brain function damage after cardiac arrest (CA) in vivo.

Objective: We aimed to assess the cerebral protective effects of hydrogen in rabbits with CA by using fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT).

Methods: Male rabbits were divided into the hydrogen-treated (n=6), control (n=6), and sham (n=3) groups.

Successful treatment of severe electrolyte imbalance-induced cardiac arrest caused by adrenal tuberculosis with ECMO in the ED.

Background: Tuberculosis (TB) is a chronic infectious disease, common in China. TB bacteria can invade multiple organs throughout the body, but they rarely cause critical illness. We present a complex critically ill case in this report.

Green Tea Polyphenols Protect against Acetaminophen-Induced Liver Injury by Regulating the Drug Metabolizing Enzymes and Transporters.

Green tea polyphenols (GTPs) have been shown to exhibit diverse beneficial effects against a variety of diseases. Acetaminophen (APAP) overdose is one of the most frequent causes of drug-induced liver injury. In the current study, we aimed to investigate the protective effect of GTP on APAP-induced liver injury in mice and the underlying mechanisms involved.

Therapeutical plasma exchange for thrombotic thrombocytopenic purpura in the emergency department: A single center experience.

Introduction: Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening and easily misdiagnosed thrombotic microangiopathy disease. Few studies have reported the use of therapeutic plasma exchange (TPE) for TTP in emergency departments in China. The present study was a retrospective analysis of patients with TTP who were treated with TPE in our emergency intensive care unit (EICU).

PAQR3 protects against oxygen-glucose deprivation/reperfusion-induced injury through the ERK signaling pathway in N2A cells.

Cerebral ischemia-reperfusion injury is pivotal in the development of multiple-subcellular organelle and tissue injury after acute ischemic stroke. Recently, the Golgi apparatus (GA) has been shown to be a key subcellular organelle that plays an important role in neuroprotection against oxygen-glucose deprivation/reperfusion (OGD/R) injury. PAQR3, a scaffold protein exclusively localized in the GA, was originally discovered as a potential tumor suppressor protein.

The circular RNA 001971/miR-29c-3p axis modulates colorectal cancer growth, metastasis, and angiogenesis through VEGFA.

Background: Colorectal cancer (CRC) is one of the most common malignant tumors globally. Angiogenesis is a key event maintaining tumor cell survival and aggressiveness. The expression of vascular endothelial growth factor A (VEGFA), one of the most significant tumor cell-secreted proangiogenic factors, is frequently upregulated in CRC.

Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2.

Background: Hydrogen is received as an inert gas that thought to be non-functional in vivo previously. Recently, emerging evidences showed that in ischemia/reperfusion (IR) condition, hydrogen reduced cellular reactive oxygen species (ROS) production and ameliorated cell apoptosis. However, the underlying mechanism of hydrogen on IR-induced apoptosis remains elusive.

HspB8 mediates neuroprotection against OGD/R in N2A cells through the phosphoinositide 3-kinase/Akt pathway.

In a previous study, we found that Heat shock protein B8 (HspB8) overexpression could prevent the apoptosis and reduced cell viability induced by OGD/R and showed that the neuroprotective effect of HspB8 was mediated by inhibition of the mitochondrial apoptotic pathway. In recent study, HspB8 has been shown to protect the heart against ischemia/reperfusion (I/R) injury via activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. However, whether this protective effect applied to brain I/R injury remained unexplored.

Ischemic postconditioning regulates cardiomyocyte autophagic activity following ischemia/reperfusion injury.

Ischemic postconditioning (IPostC) is a promising protective mechanism for combating reperfusion injury. However, the role of autophagy in the protective effects of IPostC and the associated signaling pathways have remained to be elucidated. Male Sprague Dawley rats were subjected to 30 min ischemia and 1, 2, 3, 6, 12 and 24 h of reperfusion, with or without IPostC treatment.

GOLPH3 Mediated Golgi Stress Response in Modulating N2A Cell Death upon Oxygen-Glucose Deprivation and Reoxygenation Injury.

Increasing evidence implicating that the organelle-dependent initiation of cell death merits further research. The evidence also implicates Golgi as a sensor and common downstream-effector of stress signals in cell death pathways, and it undergoes disassembly and fragmentation during apoptosis in several neurological disorders. It has also been reported that during apoptotic cell death, there is a cross talk between ER, mitochondria, and Golgi.

HspB8 is neuroprotective during oxygen glucose deprivation and reperfusion.

Heat shock protein B8 (HspB8) is a chaperone protein that is highly and constitutively expressed in the brain, cardiac tissue and many other organs. Recently, it has been shown that HspB8 can enhance cardiac function and render cardioprotection. However, the potential benefits of HspB8 action on ischemic stroke and the underlying mechanism(s) are largely unknown.

Mechanism and Regulation of Autophagy and Its Role in Neuronal Diseases.

Autophagy is a constitutive lysosomal catabolic pathway that degrades damaged organelles and protein aggregates. Neuronal survival is highly dependent on autophagy due to its post-mitotic nature, polarized morphology, and active protein trafficking. Autophagic dysfunction has been linked to several neuronal diseases.

Study of GOLPH3: a potential stress-inducible protein from Golgi apparatus.

Although the Golgi apparatus has been studied extensively for over 100 years, the complex structure-function relationships have yet to be elucidated. It is well known that the Golgi complex plays an important role in the transport, processing, sorting, and targeting of numerous proteins and lipids destined for secretion, plasma membrane, and lysosomes. Increasing evidence suggests that the Golgi apparatus is a sensor and common downstream effector of stress signals in cell death pathways.

The role of GRASPs in morphological alterations of Golgi apparatus: mechanisms and effects.

The Golgi apparatus (GA) is a pivotal organelle in cell metabolism, functioning not only in the processing and transportation of cargoes but also in ion homeostasis, cell apoptosis, and stress sensing. We are interested in the intricate role of GA and the recently present novel concept of 'GA stress'. GA shows various morphological alterations in many neurodegenerative diseases and cell apoptosis induced by biochemical reagents, mechanisms in which oxidative stress is strongly involved.

Decreased levels of cell-division cycle 42 (Cdc42) protein in peripheral lymphocytes from ischaemic stroke patients are associated with Golgi apparatus function.

Objectives: To investigate levels of cell-division cycle 42 (Cdc42) protein, and their relationship with Golgi apparatus function in peripheral lymphocytes, in patients following ischaemic stroke.

Methods: Patients with acute cerebral ischaemic stroke (within 24-72 h of the onset of focal neurological symptoms) and healthy control subjects were enrolled in this prospective case-control study. The cellular location of Cdc42 in peripheral lymphocytes was demonstrated using immunofluorescence.