Sestrin2 protects against lethal sepsis by suppressing the pyroptosis of dendritic cells.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sestrin2 (SESN2), a highly evolutionarily conserved protein, is critically involved in the cellular response to various stresses and has been confirmed to maintain the homeostasis of the internal environment. However, the potential effects of SESN2 in regulating dendritic cells (DCs) pyroptosis in the context of sepsis and the related mechanisms are poorly characterized.

Sestrin2 protects dendritic cells against endoplasmic reticulum stress-related apoptosis induced by high mobility group box-1 protein.

Sestrin2 (SESN2) is a highly evolutionary conserved protein and involved in different cellular responses to various stresses. However, the potential function of SESN2 in immune system remains unclear. The present study was designed to test whether dendritic cells (DCs) could express SESN2, and investigate the underlying molecular mechanism as well as its potential significance.

Endoplasmic reticulum stress regulates oxygen-glucose deprivation-induced parthanatos in human SH-SY5Y cells via improvement of intracellular ROS.

Aims: Endoplasmic reticulum (ER) stress has been demonstrated to regulate neuronal death caused by ischemic insults via activation of apoptosis, but it still remains unclear whether ER stress participates in regulation of parthanatos, a new type of programmed cell death characterized by PARP-1 overactivation and intracellular accumulation of PAR polymer.

Methods: we used oxygen-glucose deprivation (OGD) and human SH-SY5Y cells to simulate neuronal damage caused by ischemia.

Results: Oxygen-glucose deprivation induced time-dependent death in SH-SY5Y cells, which was accompanied with upregulation of PARP-1, accumulation of PAR polymer, decline of mitochondrial membrane potentials and nuclear translocation of AIF.

Protection of ischemic postconditioning against neuronal apoptosis induced by transient focal ischemia is associated with attenuation of NF-κB/p65 activation.

Background And Purpose: Accumulating evidences have demonstrated that nuclear factor κB/p65 plays a protective role in the protection of ischemic preconditioning and detrimental role in lethal ischemia-induced programmed cell death including apoptosis and autophagic death. However, its role in the protection of ischemic postconditioning is still unclear.

Methods: Rat MCAO model was used to produce transient focal ischemia.

Sellar Chordoma Presenting as Pseudo-macroprolactinoma with Unilateral Third Cranial Nerve Palsy.

We described a 61-year-old female with a sellarchordoma, which presented as pseudo-macroprolactinoma with unilateral third cranial nerve palsy. Physical examination revealed that her right upper lid could not be raised by itself, right eyeball movement limited to the abduction direction, right pupil dilated to 4.5 mm with negative reaction to light, and hemianopsia in bitemporal sides.

Proteasome inhibitor MG-132 induces C6 glioma cell apoptosis via oxidative stress.

Aim: Proteasome inhibitors have been found to suppress glioma cell proliferation and induce apoptosis, but the mechanisms are not fully elucidated. In this study we investigated the mechanisms underlying the apoptosis induced by the proteasome inhibitor MG-132 in glioma cells.

Methods: C6 glioma cells were used.

Large cystic hypoglossal schwannoma with fluid-fluid level: a case report.

Hypoglossal schwannomas are rare skull base tumors. Furthermore, cystic hypoglossal schwannomas are extremely uncommon. We report the first case of a large cystic hypoglossal schwannoma with a fluid-fluid level.

Two subtypes of meningiomas with different imaging co-existed at sphenoid ridge.

Intracranial multiple meningiomas are not uncommon, but multiple meningiomas consisting of different subtypes are rare. Here, we describe an adult male patient with two meningiomas located at sphenoid ridge, with different features on MRI and CTA. Histological examination revealed that one was fibrous meningioma and the other was psammomatous meningioma.

Inhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells.

Aim: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the effect of autophagy on the destiny of glioma cells remains unclear.

[Expression of Aurora-B in human glioma tissue and its significance].

Objective: To study the expression of Aurora-B in human glioma tissue and its significance.

Methods: The total RNA was extracted from 41 human glioma tissues and 11 normal brain tissues by Trizol reagent. After reverse transcription of the total RNA into cDNAs, Aurora-B mRNA expressions in these samples were detected by quantitative real-time PCR.

[Study on the activities' alteration of the proteasome in neurons of cortex and its relation with delayed neuron death after reperfusion following ischemia].

Objective: To investigate the activities' alteration of the proteasome in neurons of cortex and its relation with delayed neuron death after reperfusion following ischemia.

Methods: 20 minutes transient global ischemia rat model was used. Following different reperfusion period, all the 50 rats were divided into 5 groups, sham-operation group, 0.