Epigallocatechin Gallate Preferentially Inhibits O-Methylguanine DNA-Methyltransferase Expression in Glioblastoma Cells Rather than in Nontumor Glial Cells.

Objective: O-methylguanine (O6-meG) DNA-methyltransferase (MGMT) is a main regulator of temozolomide (TMZ) resistance in glioblastomas. Some MGMT inhibitors have been studied in clinical trials but with very little success, because their inhibiting effects were not tumor-selective, and often cause severe toxicity in normal tissues in the presence of TMZ. The goal of this study is to explore whether Epigallocatechin gallate (EGCG), a natural small molecule, could preferentially modulate MGMT in glioblastoma cells.

FM19G11 inhibits O -methylguanine DNA-methyltransferase expression under both hypoxic and normoxic conditions.

FM19G11 is a small molecular agent that inhibits hypoxia-inducible factor-1-alpha (HIF-1α) and other signaling pathways. In this study, we characterized the modulating effects of FM19G11 on O -methylguanine DNA-methyltransferase (MGMT), the main regulator of temozolomide (TMZ) resistance in glioblastomas. This study included 2 MGMT-positive cell lines (GBM-XD and T98G).

Postoperative pneumocephalus increases the recurrence rate of chronic subdural hematoma.

Objectives: Pneumocephalus is a common operative complication of chronic subdural hematoma. This study is to analyze the relationship between postoperative pneumocephalus and the recurrence and surgical outcomes.

Patients And Methods: This is a retrospective case-cohort study, including a pneumocephalus group (n = 46) and a control group (n = 181).

Microvascular Decompression for Trigeminal Neuralgia: Zone Exploration and Decompression Techniques.

Objective: The aim of this study is to introduce zone exploration of the trigeminal nerve and decompression techniques for different types of vasculars.

Methods: The trigeminal nerve was sectioned into 5 zones. Zone 1, 2, 3, 4 was located at the rostral, caudal, ventral, and dorsal part of the nerve root entry zone (REZ) respectively, and zone 5 was located at the distal of the nerve root.

Management of vessels passing through the facial nerve in the treatment of hemifacial spasm.

Background: In hemifacial spasm, it is extremely rare to find a vessel passing through the facial nerve. In this study, we present our experience of the surgical treatment of four such patients.

Methods: From January 2010 to Match 2015, we treated 2,576 hemifacial spasm patients with microvascular decompression in our department.

Nimodipine-mediated re-myelination after facial nerve crush injury in rats.

This study aimed to investigate the mechanism of nimodipine-mediated neural repair after facial nerve crush injury in rats. Adult Sprague-Dawley rats were divided into three groups: healthy controls, surgery alone, and surgery plus nimodipine. A facial nerve crush injury model was constructed.

The mechanism of hemifacial spasm: a new understanding of the offending artery.

Although neurovascular confliction was believed to be the cause of hemifacial spasm (HFS), the mechanism of the disorder remains unclear to date. Current theories, merely focusing on the facial nerve, have failed to explain the clinical phenomenon of immediate relief following a successful microvascular decompression surgery (MVD). With the experience of thousands of microvascular decompression surgeries and preliminary investigations, we have learned that the offending artery may play a more important role than the effect of merely mechanical compression in the pathogenesis of the disease.

The strategy of microvascular decompression for hemifacial spasm: how to decide the endpoint of an MVD surgery.

Objective: Microvascular decompression (MVD) has become the standard treatment for hemifacial spasm. As not all patients get complete relief, this strategy is still controversial. The study aimed to figure out how to tell the proper endpoint to the surgery.

The role of autonomic nervous system in the pathophysiology of hemifacial spasm.

Objectives: Despite the vascular compression of the seventh cranial nerve has been verified by the microvascular decompression surgery as the cause of hemifacial spasm (HFS), the mechanism of the disease is still unknown. We believe that the autonomic nervous system in adventitia of the offending artery may contribute to the HFS. To prove our hypothesis, we performed an experiment in SD rats.

[The immunogenicity of mouse neural stem cells].

Aim: To explore the immunogenicity of mouse neural stem cells (NSCs), thus help to solve the problem of immunologic rejection in NSCs transplantation.

Methods: (1) Thirty C57BL/6 mice were assigned randomly into two groups, then the two groups were immuned by intraperitoneal injection respectively with BALB/c mice's NSCs or hepatic cells (as control). Afterwards one-way mixed lymphocyte culture was performed with BALB/c mice's NSCs or hepatic cells and immuned C57BL/6 mice's T lymphocytes.

Surgery for posttraumatic syringomyelia: a retrospective study of seven patients.

Objective: To analyze retrospectively the clinical symptoms, signs, radiological findings and results of treatment of posttraumatic syringomyelia.

Methods: The data of 7 patients with posttraumatic syringomyelia confirmed by computerized tomography (CT) and magnetic resonance imaging (MRI) in our hospital between 1999 and 2004 were reviewed retrospectively. The patients underwent decompressive laminectomy or syringo-subarachnoid (S-S) shunting with microsurgery.

A novel method for culturing neural stem cells.

The standard culture method for neural stem cells cannot prevent the attachment of neurospheres, which eventually result in differentiation. This study developed a new method for long-term neural stem cell cultivation. In the antiattachment group, neural stem cells were cultured in flasks coated with 1.

Transplantation of neural stem cells into the traumatized brain induces lymphocyte infiltration.

Objective: This study examined the lymphocyte infiltration induced by neural stem cell grafts in the traumatized brain.

Methods: Sixty Sprague-Dawley rats were assigned randomly to transplantation (n = 30) or control (n = 30) groups, and each rat was subjected to brain contusion. The neural stem cells derived from Wistar rats were transplanted into the lesion of the transplantation group, and saline was injected instead into the controls.

Bcl-2 gene therapy for apoptosis following traumatic brain injury.

Objective: To investigate the therapeutic effect of Bcl-2 fusion protein on apoptosis in brain following traumatic brain injury.

Methods: Bcl-2 gene was cloned by RT-PCR. Bcl-2 and EGFP genes were linked together and inserted into pAdeno-X vector.