Tianjin Neurosurgical Institute

Tianjin, China

Tianjin Neurosurgical Institute

Tianjin, China
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Cao Y.,Tianjin Medical University | Cao Y.,Tianjin Huanhu Hospital | Pu K.,Tianjin Huanhu Hospital | Pu K.,Tianjin Neurosurgical Institute | And 8 more authors.
World Neurosurgery | Year: 2017

Objective To investigate the efficacy of antibiotic prophylaxis (AP) and the risk factors for postoperative infections in clean neurosurgery. Methods Data were retrospectively collected on all patients who had undergone clean neurosurgical operation at our institution between January 2009 and December 2014. From January 2009 until October 2011, AP was administered to every clean neurosurgical patient. From November 2011 to December 2014, no AP (n-AP) was prescribed for all clean neurosurgical operations. The efficacy of AP and independent risk factors for infection were studied. Results A total of 808 clean neurosurgical cases were included. The AP group comprised 360 surgical cases, including 29 meningitis cases and 2 cases of incision infections, whereas the n-AP group consisted of 448 surgical cases, including 35 meningitis cases and 4 cases of incision infections (P = 0.848). Microorganisms were identified in 7 of 29 cases in the AP group compared with their identification in 22 of 35 cases in the n-AP group (P = 0.002). The percentage of patients with multidrug-resistant bacterial meningitis in the AP group was 57.1% compared with 13.6% in the n-AP group (P = 0.038). The risk factors for postoperative infection were cerebrospinal fluid leakage (odds ratio, 27.8; 95% confidence interval, 9.38–28.55) and surgery time (odds ratio, 1.12; 95% confidence interval, 1.02–1.22). Conclusions Our results show that in our data set, AP had no preventive effect on postoperative infections in clean neurosurgery. In addition, AP appeared to decrease the positive bacterial culture rate and to promote the emergence of multidrug-resistant bacteria. Cerebrospinal fluid leakage and surgery time were the risk factors for postoperative infection. © 2017 Elsevier Inc.


Wang B.,Tianjin HuanHu Hospital | Wang B.,Tianjin Key Laboratory of Cerebrovascular Disease and Neurodegenerative Disease | Wang B.,Tianjin Neurosurgical Institute | Wang D.,Tianjin Medical University | And 19 more authors.
Neurological Sciences | Year: 2016

During pathological conditions, extracellular-5′-nucleotidase/CD73 can protect neurons by reducing the permeability of the blood brain barrier. In recent years, it has been demonstrated that CD73 can negatively contribute to the growth of gliomas; however, the function of CD73 in glioma blood vessels is not clear. We analysed the expression of CD73 in 72 glioma patients using immunohistochemistry and correspondingly compared the results with the Edema index (EI). We established an in vitro model of the blood-tumour barrier and analysed the expression of CD73 in vascular endothelial cells. Lastly, CD73 expression was inhibited in endothelial cells, and the effects of this inhibition on tight junction structure and transendothelial resistance were observed. Compared to normal brains, the expression of CD73 in blood vessels of glioma patients was significantly decreased, and the amount was lower in the centre of the tumour than the periphery. The proportion of CD73-positive blood vessels had a positive correlation with the EI. The expression of CD73 in the in vitro endothelial cell blood-tumour barrier model was decreased. Lastly, inhibiting CD73 was found to decrease the expression of tight junction related proteins in endothelial cells and to decrease the value of transendothelial electric resistance. The expression of CD73 in glioma blood vessels was significantly decreased, which may play a multi-functional role in decreasing the expression of tight junction related proteins of brain microvascular endothelial cells and may also increase blood-tumour barrier permeability and accelerate the formation of PTBE. © 2016, Springer-Verlag Italia.


Wu Q.,Tianjin Neurosurgical Institute | Liu G.,Chongqing Medical University | Xu L.,Tianjin Neurosurgical Institute | Wen X.,Tianjin University | And 5 more authors.
Neurochemical Research | Year: 2016

Tacrolimus (FK506), an immunophilin ligand, has been widely shown to be neuroprotective in a posttraumatic period. The nuclear factor of activated T cells (NFATc1) pathway plays an important role in regenerating neurological function following traumatic brain injury (TBI), but the precise mechanism underlying FK506-induced repair of neurological functions remains unclear. In the present study, a total of 210 SD rats were enrolled and randomly divided into sham group, TBI group and FK506 group. The rats in the TBI and FK506 groups were inflicted with moderate TBI left lateral fluid percussion impact. A modified neurological severity score (mNSS) system was used to evaluate the severity of effects on nerve function. mNSS levels were significantly lower in the FK506 group than in the TBI group. The zaccumulation of cerebral water content was lower, cerebral Aquaporin 4 (AQP4) mRNA level was lower, the number of growth-associated protein-43 (GAP-43)-positive cells was higher, and the distribution of vesicles containing excitatory neurotransmitters was altered in the injured cortex in the FK506 group. Moreover, the cortical mRNA and serum protein expression levels of interleukin-2 (IL-2) and interferon-γ (IFN-γ) were decreased in FK506 group, especially at 6 h and at 1 day after TBI. At days 1–28 after TBI, the expression of cleaved-caspase 3, which indicates apoptosis, was lower in the FK506 group than in the TBI group. Mechanistically, FK506 significantly down-regulated the mRNA and protein levels of calcium-regulated phosphatase (calcineurin, CaN) and inhibited the activation of NFATc1. These results demonstrate that FK506 relieved inflammatory responses by regulating the NFATc1 signaling pathway and promoting the synaptic reconstruction of neurons and glial cells by regulating cell apoptosis, thereby facilitated improvements in neurological function. © 2016 Springer Science+Business Media New York


PubMed | Tianjin Neurosurgical Institute, Tianjin Medical University and Tianjin HuanHu Hospital
Type: Journal Article | Journal: Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology | Year: 2016

During pathological conditions, extracellular-5-nucleotidase/CD73 can protect neurons by reducing the permeability of the blood brain barrier. In recent years, it has been demonstrated that CD73 can negatively contribute to the growth of gliomas; however, the function of CD73 in glioma blood vessels is not clear. We analysed the expression of CD73 in 72 glioma patients using immunohistochemistry and correspondingly compared the results with the Edema index (EI). We established an in vitro model of the blood-tumour barrier and analysed the expression of CD73 in vascular endothelial cells. Lastly, CD73 expression was inhibited in endothelial cells, and the effects of this inhibition on tight junction structure and transendothelial resistance were observed. Compared to normal brains, the expression of CD73 in blood vessels of glioma patients was significantly decreased, and the amount was lower in the centre of the tumour than the periphery. The proportion of CD73-positive blood vessels had a positive correlation with the EI. The expression of CD73 in the in vitro endothelial cell blood-tumour barrier model was decreased. Lastly, inhibiting CD73 was found to decrease the expression of tight junction related proteins in endothelial cells and to decrease the value of transendothelial electric resistance. The expression of CD73 in glioma blood vessels was significantly decreased, which may play a multi-functional role in decreasing the expression of tight junction related proteins of brain microvascular endothelial cells and may also increase blood-tumour barrier permeability and accelerate the formation of PTBE.

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