Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia.

This study investigated the roles and mechanisms of PINK1 activity in neonatal hypoxia-induced seizures with shRNA intervention targeting translocase outer mitochondrial membrane 7 (TOM7), the positive regulator of PINK1 autophosphorylation, or overlapping with the m-AAA protease 1 homolog (OMA1), the negative regulator of PINK1 autophosphorylation. Studies have suggested that in hypoxia-induced neonatal seizures, the phosphorylation level of PINK1 is significantly increased and the mitophagic pathway is activated, accompanied by neuronal damage and learning-memory deficits. Inhibiting PINK1 phosphorylation by reducing TOM7 expression alleviated mitophagy, mitochondrial oxidative stress, neuronal damage and seizures.

Suppression of PINK1 autophosphorylation attenuates pilocarpine-induced seizures and neuronal injury in rats.

PTEN-induced kinase 1 (PINK1) autophosphorylation triggers the PINK1/Parkin pathway, which is the main mitophagic pathway in the mammalian nervous system. In the present study, we aimed to mechanistically explore the role of PINK1 in pilocarpine-induced status epilepticus (SE) in Sprague-Dawley rats. Evidence from immunohistochemistry, western blotting, biochemical assays, and behavioral testing showed that pilocarpine-induced SE led to increased levels of PINK1 phosphorylation, mitophagy, mitochondrial oxidative stress, neuronal damage and learning and memory deficits.

The Contributions of Thrombospondin-1 to Epilepsy Formation.

Epilepsy is a neural network disorder caused by uncontrolled neuronal hyperexcitability induced by an imbalance between excitatory and inhibitory networks. Abnormal synaptogenesis plays a vital role in the formation of overexcited networks. Recent evidence has confirmed that thrombospondin-1 (TSP-1), mainly secreted by astrocytes, is a critical cytokine that regulates synaptogenesis during epileptogenesis.

Increased thrombospondin-1 levels contribute to epileptic susceptibility in neonatal hyperthermia without seizures via altered synaptogenesis.

Childhood febrile seizures (FS) represent one of the most common types of seizures and may lead to severe neurological damage and an increased risk of epilepsy. However, most children with fevers do not show clinical manifestations of convulsions, and the consequences of hyperthermia without seizures remain elusive. This study focused on hyperthermia not reaching the individual's seizure threshold (sub-FS stimulus).

Inhibition of PTEN-induced kinase 1 autophosphorylation may assist in preventing epileptogenesis induced by pentylenetetrazol.

PTEN-induced kinase 1 (PINK1) autophosphorylation-triggered mitophagy is the main mitophagic pathway in the nervous system. Moreover, multiple studies have confirmed that mitophagy is closely related to the occurrence and development of epilepsy. Therefore, we speculated that the PINK1 autophosphorylation may be involved in epileptogenesis by mediating mitophagic pathway.

Xenon inhalation attenuates neuronal injury and prevents epilepsy in febrile seizure Sprague-Dawley pups.

Background: Febrile seizures (FS) usually occur in childhood and may cause irreversible neuronal damage, cognitive functional defects, and an increase in the risk of epilepsy later in life. Anti-epileptic drugs (AEDs), currently used to treat FS in children, can relieve seizures. However, their effects in preventing the risk of developing epilepsy in later life are unsatisfactory.

The REM microarousal and REM duration as the potential indicator in paradoxical insomnia.

Objective: Although paradoxical insomnia is a prevalent subtype of chronic insomnia, the etiology of it is unclear. Contrary to complaints of little or no sleep, polysomnography (PSG) findings show that paradoxical insomnia patients have near normal sleep macrostructure. The purpose of this study is to determine the changes of microstructure and explore the etiology of paradoxical insomnia.

Attenuated iron stress and oxidative stress may participate in anti-seizure and neuroprotective roles of xenon in pentylenetetrazole-induced epileptogenesis.

The previous studies have demonstrated the excellent neuroprotective effects of xenon. In this study, we verified the anti-seizure and neuroprotective roles of xenon in epileptogenesis and evaluated the involvement of oxidative stress and iron accumulation in the protective roles of xenon. Epileptogenesis was induced by pentylenetetrazole (PTZ) treatment in Sprague-Dawley rats.

IGH/BCL2 Status Better Predicts Clinico-Pathological Behavior in Primary Splenic Follicular Lymphoma than Histological Grade and Other Molecular Markers.

Splenic lymphoma may be primary or secondary. Primary splenic lymphoma's are rare and usually of follicular cell origin representing <1% of Non-Hodgkin's Lymphoma's. Most are secondary with 35% representing Marginal Cell sub-type with the rest being Diffuse Large B-Cell Lymphoma's.

Celastrol inhibits rheumatoid arthritis by inducing autophagy via inhibition of the PI3K/AKT/mTOR signaling pathway.

Objective: Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disorder of the synovial joints. Celastrol (Cel) is a quinone-methylated triterpenoid extracted from Tripterygium wilfordii Hook F (TwHF) that has been proven to be effective in treating RA. However, the underlying molecular mechanism of celastrol in the treatment of RA remains unknown.

Anti-Seizure and Neuronal Protective Effects of Irisin in Kainic Acid-Induced Chronic Epilepsy Model with Spontaneous Seizures.

An increased level of reactive oxygen species is a key factor in neuronal apoptosis and epileptic seizures. Irisin reportedly attenuates the apoptosis and injury induced by oxidative stress. Therefore, we evaluated the effects of exogenous irisin in a kainic acid (KA)-induced chronic spontaneous epilepsy rat model.

Attenuated succinate accumulation relieves neuronal injury induced by hypoxia in neonatal mice.

Hypoxia causes neonatal neuronal damage. However, the underlying mechanism remains unclear. This study aimed to explore the changes in succinate levels and identify the mechanisms underlying their contribution to hypoxia-induced damage in newborn mice.

Mechanism of SMND-309 against lung injury induced by chronic intermittent hypoxia.

Introduction: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common sleep disorder that causes severe physiological disturbance. Evidence showed that OSAHS is an important associated comorbidity that can affect the survival of patients with pulmonary fibrosis. Until now, the potential mechanisms by which OSAHS accelerates the progression of lung fibrosis remain unclear.

The anti-tumor efficacy of 20(S)-protopanaxadiol, an active metabolite of ginseng, according to fasting on hepatocellular carcinoma.

Background: 20(S)-protopanaxadiol (20(S)-PPD), one of the main active metabolites of ginseng, performs a broad spectrum of anti-tumor effects. Our aims are to search out new strategies to enhance anti-tumor effects of natural products, including 20(S)-PPD. In recent years, fasting has been shown to be multi-functional on tumor progression.

The neuroprotective effect and possible therapeutic application of xenon in neurological diseases.

Xenon is an inert gas with stable chemical properties which is used as an anesthetic. Recent in vitro and in vivo findings indicate that xenon also elicits an excellent neuroprotective effect in subanesthetic concentrations. The mechanisms underlying this primarily involve the attenuation of excitotoxicity and the inhibition of N-methyl-d-aspartic acid (NMDA) receptors and NMDA receptor-related effects, such as antioxidative effects, reduced activation of microglia, and Ca -dependent mechanisms, as well as the interaction with certain ion channels and glial cells.

Neuroprotective Effects of Exogenous Irisin in Kainic Acid-Induced Status Epilepticus.

Elevated reactive oxygen species (ROS) level is considered a crucial causative factor for neuronal damage in epilepsy. Irisin has been reported to ameliorate mitochondrial dysfunction and to reduce ROS levels; therefore, in this study, the effect of exogenous irisin on neuronal injury was evaluated in rats with kainic acid (KA)-induced status epilepticus (SE). Our results showed that exogenous irisin treatment significantly increased the expression of brain-derived neurotrophic factor (BDNF) and uncoupling protein 2 (UCP2), and reduced the levels of neuronal injury and mitochondrial oxidative stress.

Succinate accumulation contributes to oxidative stress and iron accumulation in pentylenetetrazol-induced epileptogenesis and kainic acid-induced seizure.

This study explored the role of succinate accumulation in the oxidative stress and iron accumulation in both pentylenetetrazol (PTZ)-induced epileptogenesis and kainic acid (KA)-induced status epilepticus (SE). The levels of succinate, oxidative stress, iron content, iron-related protein expression, and the severity of neuronal injury and seizures were measured in both models. We found that increased concentrations of succinate were associated with increased levels of oxidative stress, iron content, iron regulator protein, and iron importer divalent metal transporter 1, as well as decreased levels of iron exporter ferropotin 1.

Xenon Exerts Neuroprotective Effects on Kainic Acid-Induced Acute Generalized Seizures in Rats Increased Autophagy.

Xenon has been shown to have neuroprotective effects and is clinically used as a favorable safe inhalation anesthetic. We previously confirmed the neuroprotective effects of xenon treatment in epileptic animals. However, the mechanism underlying these protective effects remains unclear.

Attenuation of the mutual elevation of iron accumulation and oxidative stress may contribute to the neuroprotective and anti-seizure effects of xenon in neonatal hypoxia-induced seizures.

Previous studies have suggested that xenon inhalation has neuroprotective and antiepileptic effects; however, the underlying mechanisms involved remain unclear. This study aimed to investigate the possible xenon inhalation mechanisms involved in the neuroprotection and antiepileptic effects. A neonatal hypoxic C57BL/6J mouse model was used for the experiments.

IL-10 provides cardioprotection in diabetic myocardial infarction via upregulation of Heme clearance pathways.

Diabetes is a risk factor for myocardial infarction, and outcomes after myocardial infarction are worse among diabetics compared with nondiabetics. Diabetes is associated with impaired Heme clearance. Here, we determined whether heme toxicity and impaired heme clearance contribute to diabetic myocardial infarction injury and assessed IL-10 as a therapeutic agent for diabetic myocardial infarction.

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats.

Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis.

Somatic Malignant Transformation of a Testicular Teratoma: A Case Report and an Unusual Presentation.

Testicular cancer represents 1% of all malignant tumors in men. About 95% of testicular cancers are germ cell tumors (GCTs). These can be divided into nonseminomatous GCTs (NSGCTs) and seminomas.

Succinate accumulation induces mitochondrial reactive oxygen species generation and promotes status epilepticus in the kainic acid rat model.

Though succinate accumulation is associated with reactive oxygen species (ROS) production and neuronal injury, which play critical roles in epilepsy, it is unclear whether succinate accumulation contributes to the onset of epilepsy or seizures. We sought to investigate changes in succinate, oxidative stress, and mito-SOX levels, as well as mitophagy and neuronal change, in different status epilepticus (SE) rat models. Our results demonstrate that KA-induced SE was accompanied by increased levels of succinate, oxidative stress, and mito-SOX, as well as mitophagy and neuronal degeneration.

Huganpian, a traditional chinese medicine, inhibits liver cancer growth in vitro and in vivo by inducing autophagy and cell cycle arrest.

Huganpian (HGP), a traditional chinese medicine composed of 6 herbs, possesses excellent therapeutic effects in clinical application. In this study, we aimed to elucidate the anti-tumor activity and the underlying mechanisms of HGP in liver cancer. The results of this study indicated that HGP effectively inhibited liver cancer growth in vitro and in vivo in a dose-dependent manner.