Showing papers by "Hua Feng published in 2013"

Deferoxamine attenuates iron-induced long-term neurotoxicity in rats with traumatic brain injury.

Abstract: This study investigated whether deferoxamine (DFO), an iron chelator attenuates iron-induced toxicity in rats with traumatic brain injury. In this study, three groups of Sprague-Dawley rats (sham, injury and DFO groups) were examined. Rats were killed on day 28 after Morris water maze testing and brains perfused for either non-heme brain binding or hemosiderin staining. Western blotting was used to measure protein levels of ferritin, transferrin and transient receptor potential canonical channel 6 (TRPC6). In TBI rats, there was a significant increase in brain iron on day 28, ferritin L, ferritin H, transferrin and TRPC6 levels were all significantly elevated post-TB1. There were also deficits in spatial learning and memory; however, DFO administration attenuated these effects in TBI rats supporting the notion that DFO may reduce brain injury accentuated by iron overload.

Immediate splenectomy down-regulates the MAPK-NF-κB signaling pathway in rat brain after severe traumatic brain injury.

Abstract: BACKGROUNDThe treatment of severe traumatic brain injury (TBI) remains a difficult process. One key to improving treatment efficacy is to reduce secondary brain injury. Local and systemic inflammatory responses play an important role in secondary injury after TBI, which if unchecked can lead to fata

Superoxide mediates direct current electric field-induced directional migration of glioma cells through the activation of AKT and ERK.

Abstract: Direct current electric fields (DCEFs) can induce directional migration for many cell types through activation of intracellular signaling pathways. However, the mechanisms that bridge extracellular electrical stimulation with intracellular signaling remain largely unknown. In the current study, we found that a DCEF can induce the directional migration of U87, C6 and U251 glioma cells to the cathode and stimulate the production of hydrogen peroxide and superoxide. Subsequent studies demonstrated that the electrotaxis of glioma cells were abolished by the superoxide inhibitor N-acetyl-l-cysteine (NAC) or overexpression of mitochondrial superoxide dismutase (MnSOD), but was not affected by inhibition of hydrogen peroxide through the overexpression of catalase. Furthermore, we found that the presence of NAC, as well as the overexpression of MnSOD, could almost completely abolish the activation of Akt, extracellular-signal-regulated kinase (Erk)1/2, c-Jun N-terminal kinase (JNK), and p38, although only JNK and p38 were affected by overexpression of catalase. The presenting of specific inhibitors can decrease the activation of Erk1/2 or Akt as well as the directional migration of glioma cells. Collectively, our data demonstrate that superoxide may play a critical role in DCEF-induced directional migration of glioma cells through the regulation of Akt and Erk1/2 activation. This study provides novel evidence that the superoxide is at least one of the “bridges” coupling the extracellular electric stimulation to the intracellular signals during DCEF-mediated cell directional migration.

Specific frequency band of amplitude low-frequency fluctuation predicts Parkinson's disease

Abstract: a b s t r a c t Resting-state functional magnetic resonance imaging (RS-fMRI) has been considered for development as a biomarker and analytical tool for evaluation of Parkinson's disease (PD). Here we utilized analysis of the amplitude low-frequency fluctuations (ALFF) to determine changes in intrinsic neural oscillations in 72 patients with PD. Two different frequency bands (slow-5: 0.01-0.027 Hz; slow-4: 0.027-0.073 Hz) were analyzed. In the slow-5 band, PD patients compared with controls had increased ALFF values mainly in the caudate and several temporal regions, as well as decreased ALFF values in the cerebellum and the parieto-temporo-occipital cortex. Additionally, in the slow-4 band, PD patients relative to controls exhibited reduced ALFF value in the thalamus, cerebellum, and several occipital regions. Together, our data demonstrate that PD patients have widespread abnormal intrinsic neural oscillations in the corti- costriatal network in line with the pathophysiology of PD, and further suggest that the abnormalities are dependent on specific frequency bands. Thus, frequency domain analyses of resting state BOLD sig- nals may provide a useful means to study the pathophysiology of PD and the physiology of the brain's dopaminergic pathways. © 2013 Elsevier B.V. All rights reserved.

Implantation of GL261 neurospheres into C57/BL6 mice: A more reliable syngeneic graft model for research on glioma-initiating cells

Abstract: Recent studies have demonstrated that inflammatory cells and inflammatory mediators are indispensable components of the tumor-initiating cell (TIC) niche and regulate the malignant behavior of TICs However, conventional animal models for glioma-initiating cell (GIC) studies are based on the implantation of GICs from human glioblastoma (GBM) into immunodeficient mice without the regulation of immune system Whether animal models can mimic the cellular microenvironment of malignancy and evaluate the biological features of GICs accurately is unclear Here, we detected the biological features of neurosphere-like tumor cells derived from the murine GBM cell line GL261 (GL261-NS) and from primary human GBM (PGBM-NS) in vitro, injected GL261-NS into syngeneic C57/BL6 mouse brain and injected PGBM-NS into NOD/SCID mouse brain, respectively The tumorigenic characteristics of the two different orthotopic transplantation models were analyzed and the histological discrepancy between grafts and human primary GBM was compared We found that GICs enriched in GL261-NS, GL261-NS and PGBM-NS exhibited increased GIC potential and enhanced chemoresistance in vitro GL261-NS was significantly more aggressive compared to GL261 adhesive cells (GL261-AC) in vivo and the enhanced aggression was more significant in syngeneic mice compared to immunodeficient mice The discrepancy of tumorigenicity between GL261-NS and GL261-AC in C57/BL6 mice was also larger compared to that between PGBM-NS and PGBM-AC in immunodeficient mice Syngrafts derived from GL261-NS in C57/BL6 mice corresponded to the human GBM histologically better, compared with xenografts derived from PGBM-NS in NOD/SCID mice, which lack inflammatory cells and inflammatory mediators We conclude that the inflammatory niche is involved in the tumorigenicity of GICs and implantation of GL261-NS into C57/BL6 mice is a more reliable syngeneic graft model for in vivo study on GICs relative to the immunodeficiency model

Experimental high-altitude intracerebral hemorrhage in minipigs: histology, behavior, and intracranial pressure in a double-injection model.

Abstract: Background Specific pathophysiological mechanism in intracerebral hemorrhage (ICH) at high altitude is unclear, and at present, there is no relevant and suitable animal model.

Angiographic findings in 2 children with cerebral paragonimiasis with hemorrhage

Abstract: Hemorrhagic events associated with cerebral paragonimiasis are not rare, especially in children and adolescents; however, angiographic evidence of cerebrovascular involvement has not been reported. The authors describe angiographic abnormalities of the cerebral arteries seen in 2 children in whom cerebral paragonimiasis was associated with hemorrhagic stroke. The patients presented with acute intracerebral and subarachnoid hemorrhage. Angiography revealed a beaded appearance and long segmental narrowing of arteries, consistent with arteritis. In both patients, involved vessels were seen in the area of the hemorrhage. The vascular changes and the hemorrhage, together with new lesions that developed close to the hemorrhage and improved after praziquantel treatment, were attributed to paragonimiasis. Further study of the frequency and mechanism of hemorrhagic cerebrovascular complications associated with cerebral paragonimiasis is needed.