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Su J.,Shanghai JiaoTong University | Zhou H.,Fudan University | Tao Y.,Ouyang Hospital | Guo J.,State Key Laboratory of Medical Neurobiology | And 7 more authors.
PLoS ONE | Year: 2015

Granulocyte-colony stimulating factor (G-CSF) has been shown to play a neuroprotective role in ischemic stroke by mobilizing bone marrow (BM)-derived endothelial progenitor cells (EPCs), promoting angiogenesis, and inhibiting apoptosis. Impairments in mobilization and function of the BM-derived EPCs have previously been reported in animal and human studies of diabetes where there is both reduction in the levels of the BM-derived EPCs and its ability to promote angiogenesis. This is hypothesized to account for the pathogenesis of diabetic vascular complications such as stroke. Here, we sought to investigate the effects of GCSF on diabetes-associated cerebral vascular defect. We observed that pretreatment of the cultured human brain vascular endothelial cells (HBVECs) with G-CSF largely prevented cell death induced by the combination stimulus with high glucose, free fatty acids (FFA) and hypoxia by increasing cell viability, decreasing apoptosis and caspase-3 activity. Cell ultrastructure measured by transmission electron microscope (TEM) revealed that GCSF treatment nicely reduced combination stimulus-induced cell apoptosis. The results from fluorescent probe Fluo-3/AM showed that G-CSF greatly suppressed the levels of intracellular calcium ions under combination stimulus. We also found that G-CSF enhanced the expression of cell cycle proteins such as human cell division cycle protein 14A (hCdc14A), cyclinB and cyclinE, inhibited p53 activity, and facilitated cell cycle progression following combination stimulus. In addition, activation of extracellular signal-regulated kinase1/ 2 (ERK1/2) and Akt, and deactivation of c-Jun N terminal kinase (JNK) and p38 were proved to be required for the pro-survival effects of G-CSF on HBVECs exposed to combination stimulus. Overall, G-CSF is capable of alleviating HBVECs injury triggered by the combination administration with high glucose, FFA and hypoxia involving the mitogenactivated protein kinases (MAPK) and Akt signaling cascades. G-CSF may represent a promising therapeutic agent for diabetic stroke. Copyright: © 2015 Su et al. Source

Jiang S.,Fudan University | Xu W.,Fudan University | Xu W.,State Key Laboratory of Medical Neurobiology | Shen Y.,Fudan University | And 2 more authors.
Annals of Plastic Surgery | Year: 2012

Purpose: The optimal treatment for cubital tunnel syndrome is widely debated. The purpose of this study is to describe the technique of an endoscopic-assisted ulnar nerve decompression using carbon dioxide insufflation in association with subcutaneous anterior transposition and to assess the success or failure of the method of treatment. Methods: In all, 8 male and 4 female patients with an average age of 42 years (range, 25-56) who presented signs, symptoms, and abnormal neurophysiological studies of cubital tunnel syndrome were recruited in the retrospective study. Between August 2008 and June 2009, they were operated on using a 0-degree lens endoscope. Preoperatively, they were classified according to the Dellon scale, and the Bishop rating system was used to evaluate the postoperative outcomes. Results: Preoperatively, 5 patients were rated as mild, another 5 as moderate, and the remaining 2 as severe. The average length of the incision was 15 ± 3 mm, the mean length of the ulnar nerve decompression was 18 ± 2 cm, and the whole duration of surgery (skin to skin) lasted 30 ± 5 minutes. The endoscopic-assisted cubital tunnel release under carbon dioxide insufflation and subcutaneous anterior transposition surgeries in all patients were performed with no difficulty. All the patients had improvement in symptoms of cubital tunnel syndrome and 10 of 12 patients scored excellent according to the modified Bishop Rating System at a minimum of 1 year after surgery. Conclusions: Endoscopy-assisted cubital tunnel release under carbon dioxide insufflation demonstrated similar results compared with conventional open surgeries, besides, it may avoid problems such as long incision, painful scarring, and have additional advantages of providing an extended endoscopic view, which is safe and mini-invasive with favorable results in a 12-month follow-up. © 2012 by Lippincott Williams & Wilkins. Source

Jiang S.,Fudan University | Li Z.-Y.,Shanghai JiaoTong University | Hua X.-Y.,Fudan University | Xu W.-D.,Fudan University | And 3 more authors.
Microsurgery | Year: 2010

The purpose of our study was to establish the profile of cortical reorganization in whole BPAI on rats and evaluate changes of cortical reorganization after repair of the median nerve with the contralateral C7 root transfer. Forty adult SD rats underwent whole roots avulsion of left brachial plexus, among them 20 received contralateral C7 root transfer to the injured median nerve. Intracortical microstimulation was performed in primary motor cortex (M1) at intervals of 3, 5, 7, and 10 months, postoperatively. The maps of motor cortical responses were constructed. Five normal rats were used as the control. Results showed that stimulating right M1 elicited motion of left vibrissae, submaxilla, neck, back, and left hindlimb after left BPAI, among them neck representation area replaced the forelimb area throughout the reorganization process. The left forelimb representation area was found in the left motor cortex 5 months after the contralateral C7 root transfer and existed in both motor cortexes at 7th postoperative month. The left forelimb representation area was detected only in rightmotor cortex at 10thmonth, postoperatively. In conclusions, after the contralateral C7 root transfer for repair of the median nerve in BPAI, the cortical reorganization occurred in a time-dependent reorganization. The findings from this study demonstrate that brain involves in the functional recovery after BPAI and repair with nerve transfer and suggest that efforts to improve the results fromnerve repair should address the peripheral nerve as well as the brain. © 2010 Wiley-Liss, Inc. Source

Jiang S.,Fudan University | Xu W.-D.,Fudan University | Xu W.-D.,State Key Laboratory of Medical Neurobiology | Shen Y.-D.,Fudan University | And 2 more authors.
Anatomical Science International | Year: 2011

For surgeries aimed at the dissection of full-length phrenic nerve, a full appreciation of its trajectory, blood supply and correlation with adjacent anatomical structures is necessary, especially for endoscopic manipulations. A fresh cadaver study was conducted with the purpose of avoiding surgical complications and ensuring further efficacy and efficiency of endoscopic manipulations. Ten fresh adult cadavers were dissected. Special attention was paid to the topography of the origin, the trajectory of the phrenic nerve, and its anatomic communication with the surrounding vessels and organs. In the second side of the cadavers, thoracic endoscopic manipulations and observations were also performed. The full length of the phrenic nerve was 24.6 ± 1.7 and 30.6 ± 1.8 cm on the right and left side, respectively; the blood supply of the phrenic nerve in the thoracic cavity came exclusively from the pericardiacophrenic artery; the distance between the origin of the pericardiacophrenic artery and that of the internal thoracic artery ranged from 0.5 to 5.2 cm on the right side, and from 1.4 to 5.6 cm on the left; most of the pericardiacophrenic veins intermingled with small vessels of pericardium and pleura, forming a venous network and joining the innominate vein. Endoscopic dissection of the thoracic phrenic nerve together with the accompanying pericardiacophrenic artery can be performed. Extreme attention should be paid during surgery to a section of about 6 cm in length of the artery originating from the internal thoracic artery, while the accompanying veins do not require to be spared. © 2011 Japanese Association of Anatomists. Source

Zhang J.,Xian Jiaotong University | Shi Q.,Xian Jiaotong University | Chen X.,Xian Jiaotong University | Yang P.,Xian Jiaotong University | And 8 more authors.
International Journal of Molecular Medicine | Year: 2012

We have previously reported that 5 copies of the hypoxia response element (HRE) can conditionally regulate brain-derived neurotrophic factor gene expression under hypoxic/ischemic conditions in mice. In the present study, we investigated the controlled expression of neurotrophin-3 (NT-3) by HRE under hypoxic conditions and determined the protective effects of conditionally expressed NT-3 on hypoxia-induced apoptosis in PC12 cells. Five copies of the HRE (5HRE) and the simian virus 40 minimal promoter (SV40mp) were employed to construct a cassette, and transfer of therapeutic gene, NT-3, into PC12 cells was achieved using a retroviral vector. Our results showed that the retroviral vector, pLNC-5HRE-NT3, was successfully constructed and transfected into PC12 cells. Compared with normal conditions, in which NT-3 was expressed at low levels, the expression of NT-3 significantly increased under hypoxic conditions in 5HRE-NT3 transgenic PC12 cells (P<0.05). By contrast, in NT-3 transgenic PC12 cells without HRE, we found no significant difference in NT-3 expression between the normoxic and hypoxic groups. The conditional adjustment of NT-3 expression by 5HRE significantly reduced apoptosis induced by hypoxia in 5HRE-NT3 transgenic PC12 cells (P<0.05) but not in 5HRE-enhanced green fluorescent protein (EGFP) transgenic PC12 cells and PC12 cells without gene transfer. In addition, the hypoxia-induced upregulation of both p38 and caspase-3 activities was suppressed in 5HRE-NT3 transgenic PC12 cells under hypoxic conditions (P<0.05). Taken together, these results demonstrate that 5HRE-SV40mp regulates NT-3 gene expression in response to hypoxia in PC12 cells. The data presented in this study may prove useful in future gene therapy studies for the treatment of ischemic diseases. Source

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