Analysis of the common complications and recurrence-related factors of superior parasagittal sinus meningioma.

Objectives: Parasagittal meningioma resection is prone to postoperative complications and tumor recurrence because the tumor invades the superior sagittal sinus. This study aimed to clarify the incidence of perioperative complications and the recurrence of superior sagittal paranasal meningiomas and explored potential predictors in this context.

Methods: The study retrospectively reviewed the clinical, imaging, and follow-up data of parasagittal meningiomas among patients who underwent microsurgical resection in the authors' institution from January 2008 to December 2017.

Cortical network switching: possible role of the lateral septum and cholinergic arousal.

Background: Cortical networks undergo large-scale switching between states of increased or decreased activity in normal sleep and cognition as well as in pathological conditions such as epilepsy. We previously found that focal hippocampal seizures in rats induce increased neuronal firing and cerebral blood flow in subcortical structures including the lateral septal area, along with frontal cortical slow oscillations resembling slow wave sleep. In addition, stimulation of the lateral septum in the absence of a seizure resulted in cortical deactivation with slow oscillations.

Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro.

Background: Translocation of high-mobility group box 1 (HMGB1) from nucleus could trigger inflammation. Extracellular HMGB1 up-regulates inflammatory response in sepsis as a late mediator. However, little was known about its role in subarachnoid hemorrhage-inducible inflammation, especially in the early stage.

Biphasic activation of nuclear factor kappa B and expression of p65 and c-Rel after traumatic brain injury in rats.

Background And Object: Nuclear factor kappa B (NF-κB) functions as a key regulator in the central nervous system and regulates the inflammatory pathway. There are two peaks of cerebral NF-κB activation after neonatal hypoxia-ischemia and subarachnoid hemorrhage. Our previous studies found that NF-κB activity was up-regulated at an early stage and remained elevated at day 7 after traumatic brain injury (TBI).

Glycyrrhizic acid confers neuroprotection after subarachnoid hemorrhage via inhibition of high mobility group box-1 protein: a hypothesis for novel therapy of subarachnoid hemorrhage.

Subarachnoid hemorrhage usually results in poor clinical outcome and devastating neurological deficits. The early brain injury and delayed vasospasm after subarachnoid hemorrhage (SAH) are involved in the poor prognosis to the patients, while the mechanisms have not been well elucidated. Previous studies found an up-regulation of Toll-like receptor 4 (TLR4), inflammatory factors and high-mobility group box 1 (HMGB1) in the cortex after SAH.

Expression of the NLRP3 inflammasome in cerebral cortex after traumatic brain injury in a rat model.

Inflammatory response plays an important role in the pathogenesis of secondary damage after traumatic brain injury (TBI). The inflammasome is a multiprotein complex involved in innate immunity and a number of studies have suggested that the inflammasome plays a critical role in a host inflammatory signaling. Nucleotide-binding domain, leucine-rich repeat, pyrin domain containing 3 (NLRP3) is a key component of the NLRP3-inflammasome, which also includes apoptotic speck-containing protein (ASC) with a cysteine protease (caspase)-activating recruitment domain and pro-caspase1.

Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: a pilot study.

Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH.

Expression of intestinal CD40 after experimental traumatic brain injury in rats.

Background: Nuclear factor kappa B (NF-κB) has been shown to be activated in the intestine after traumatic brain injury (TBI), and results in gastrointestinal mucosal injury. In addition, CD40 has a major role in the activation of NF-κB and is up-regulated in inflammatory bowel disease. However, we found no study in the literature investigating the intestinal expression of CD40 after TBI.

[Role of Bid protein in the mitochondria and Endoplasmic Reticulum associated apoptotic pathway].

Objective: To explore the role of Bid protein in the mitochondria and endoplasmic reticulum (ER) associated apoptotic pathway.

Methods: Apoptosis of MUTZ-1 cells induced by homoharringtonine (HHT) was measured by FACS. Mitochondria and ER associated apoptotic pathway was detected by RT-PCR and Western blotting.

[Experimental study on the effects of hydrogen peroxide on caveolin in human lens epithelial cells].

Objective: To observe the expression and distribution of caveolin and phosphorylated caveolin-1 in human lens epithelial cells (HLECs) under H(2)O(2) treatment.

Methods: HLECs (SRA01/04) were exposed to different concentrations of H(2)O(2) for different periods of time. The distribution of caveolin and phosphorylated caveolin-1 in H(2)O(2) treated cells was observed by laser scanning confocal microscopy and fluorescence microscopy.

[Effects of tumor necrosis factor alpha on expression of phospholamban and intracellular calcium in cardiomyocytes].

Objective: To explore the effects of tumor necrosis factor alpha (TNFalpha) on the expression of phospholamban (PLB) and sarco (endo) plasmic reticulum Ca(2+)-ATPase (SERCA2a) and concentration of intracellular free calcium in myocardiocytes.

Methods: The neonatal rat myocardiocytes were randomly divided into 6 groups: treatment with different concentrations of TNFalpha (1,10,30,50,and 70 microg/L, respectively) and without TNFalpha (control). The mRNA and protein expression of PLB and SERCA2a were detected with one-step reverse transcription-polymerase chain reaction and Western blotting.

[Therapeutic neovascularization with autologous bone marrow CD34+ cells transplantation in hindlimb ischemia].

Objective: To explore whether transplantation of autologous bone marrow stem cells might augment angiogenesis and collateral vessel formation in a canine model of hindlimb ischemia.

Methods: CD34(+) stem cells were centrifugation through Ficoll and an immune magnetic cell sorting system from bone marrow (20 ml) of canine (n = 5) and induced into endothelial cells with VEGF in vitro, and expression of von Willebrand factor. Bilateral hindlimb ischemia was surgically induced in canines and Dil fluorescence labeled autologous stem cells were transplanted into the ischemic tissues.