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Chiu T.-L.,Tzu Chi University | Chiu T.-L.,Neuro Medical Scientific Center | Peng C.-W.,Tzu Chi University | Wang M.-J.,Buddhist Tzu Chi General Hospital
Oncology Reports | Year: 2011

Microglia have been found to infiltrate into malignant brain tumors. However, their function is usually reversed by cancerous cells thus contributing to cancer growth and metastasis. We propose that microglial immuno-activity can be modulated with interleukin-12, by which the anti-cancer ability might be restored. To this end, a strategy was designed using AAV2 carrying interleukin-12 to activate microglia to eliminate cancerous cells. Under this strategy, recombinant AAV2 encoding interleukin-12 was constructed and evaluated for its transduction efficacy on cancerous and CNS cells. The bioactivity of microglia modulated by interleukin-12 was examined and death receptors 4 and 5 were detected on cancerous cells. The effects of interleukin-12 on microglial cytotoxicity were evaluated by MTT assay. The human cell line DBTRG, surgical specimens of GBM and rat astrocytes expressed AAV2-mediated GFP quite strongly. Interleukin-12 secretion was detected in DBTRG, RG2 and astrocytes after the transduction of AAV2 encoding interleukin-12. TRAIL releasing and phagocytotic activity of microglia were significantly increased after interleukin-12 stimulation. MTT assay of microglial cytotoxicity elicited significant increase after the stimulation with interleukin-12 protein. In conclusion, AAV2 is an effective vector in transferring therapeutic genes such as interleukin-12 to enhance microglial anti-cancer activity and to eliminate cancerous cells.

Chang T.-P.,Neuro Medical Scientific Center | Wu Y.-C.,Antien Ear
Laryngoscope | Year: 2010

We report a case of a tiny infarct on the left dorsolateral pons in a 50-year-old man who presented with prolonged and isolated vertigo. The clinical features mimic vestibular neuritis and can easily lead to misdiagnosis. Selective involvement of the left superior vestibular nucleus might explain the resemblance to acute peripheral vestibulopathy. © 2010 The American Laryngological, Rhinological and Otological Society, Inc.

Chiu S.C.,Taichung Tzu Chi Hospital | Huang S.Y.,Mackay Memorial Hospital | Chen S.P.,Tzu Chi Stem Cells Center | Su C.C.,Changhua Christian Hospital | And 3 more authors.
Prostate Cancer and Prostatic Diseases | Year: 2013

BACKGROUND:Tanshinone IIA (Tan-IIA) is one of the major lipophilic components isolated from the root of Salviae Miltiorrhizae Radix. We explored the mechanisms of cell death induced by Tan-IIA treatment in prostate cancer cells in vitro and in vivo.METHODS:Cells were treated with Tan-IIA and growth inhibition was assessed. Cell cycle profiles after Tan-IIA treatment were determined by flow cytometry. Expression levels of cell cycle regulatory proteins and apoptosis-related proteins were determined after Tan-IIA treatment. Expression levels of endoplasmic reticulum (ER) stress-regulated genes were determined to investigate their role in Tan-IIA-induced cell death. GADD153 expression was knocked down by small interfering RNA (siRNA) transfection. Rate of cell death and proliferation was obtained by 3-(4,5-dimethyl thizol-2-yl)-2,5-diphenyl tetrazolium bromide assay. Antitumor activity of Tan-IIA was performed in LNCaP xenograft model.RESULTS:Our results showed that Tan-IIA caused prostate cancer cell death in a dose-dependent manner, and cell cycle arrest at G0/G1 phase was noted, in LNCaP cells. The G0/G1 phase arrest correlated with increase levels of CDK inhibitors (p16, p21 and p27) and decrease of the checkpoint proteins. Tan-IIA also induced ER stress in prostate cancer cells: activation and nuclear translocation of GADD153/CCAAT/enhancer- binding protein-homologous protein (CHOP) were identified, and increased expression of the downstream molecules GRP78/BiP, inositol-requiring protein-1 and GADD153/CHOP were evidenced. Blockage of GADD153/CHOP expression by siRNA reduced Tan-IIA-induced cell death in LNCaP cells. Tan-IIA also suppressed LNCaP xenograft tumor growth, causing 86.4% reduction in tumor volume after 13 days of treatment.CONCLUSIONS:Our findings suggest that Tan-IIA causes G0/G1 cell cycle arrest in LNCaP cells and its cytotoxicity is mediated at least partly by ER stress induction. These data provide evidence supporting Tan-IIA as a potential anticancer agent by inducing ER stress in prostate cancer. © 2013 Macmillan Publishers Limited All rights reserved.

Chang T.-P.,Neuro Medical Scientific Center | Wu Y.-C.,Antien ENT Clinic | Hsu Y.-C.,Foundation Medicine
Acta Neurologica Taiwanica | Year: 2013

Purpose: Vestibular paroxysmia is defined as paroxysmal, brief, and carbamazepine-responsive vertigo. Although neurovascular cross-compression (NVCC) of the vestibulocochlear nerve is believed to be the cause of vestibular paroxysmia, the mechanism remains controversial. Herein, we describe the case of a man with NVCC who presented with paroxysmal vertigo associated with paroxysmal pulsatile tinnitus. Case Report: A 68-year-old man presented with paroxysmal vertigo for one month. Paroxysmal pulsatile tinnitus in the right ear occurred simultaneously with the vertigo. Magnetic resonance imaging demonstrated that the right anterior inferior cerebellar artery was compressing the right vestibulocochlear nerve. The vertigo and tinnitus completely disappeared within one week after treatment with carbamazepine. Conclusion: The pulsatile nature of the patient's tinnitus implied that the auditory nerve was being compressed by a pulsating artery and was found to consolidate the causal relationship between NVCC and vestibular paroxysmia.

Chiu T.-L.,Neuro Medical Scientific Center | Tsai S.-T.,Neuro Medical Scientific Center | Chiu C.-H.,Buddhist Tzu Chi General Hospital
Journal of Clinical Neuroscience | Year: 2012

Augmentation of the cerebral blood supply to correct cerebral hemodynamic insufficiency by extracranial-intracranial bypass may be an appropriate method to reduce the risk of ischemic stroke. Eighty-five patients with ischemic symptoms, decreased regional cerebral blood flow, and decreased regional cerebrovascular reactivity were recruited for surgery. The post-bypass mean regional blood flow increased by 35.8% compared to the pre-bypass value (p < 0.001). Only minor re-establishment of vasculature after anastomosis was detected in three of four patients with middle cerebral artery stenosis, which suggests that there are fewer benefits of bypass surgery in this situation. Cerebral infarction occurred immediately post-operation in one patient who was predisposed to stroke due to a bilateral carotid occlusion. Hyperperfusion injury was infrequent in this series; only one patient developed intracerebral hemorrhage three weeks after the bypass. One ischemic and one hemorrhagic stroke occurred during the 90 months following surgery. © 2012 Elsevier Ltd. All rights reserved.

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