Yanming Qu

Publications (3)8.28 Total impact

• Article: Localization of transverse-sigmoid sinus junction using preoperative 3D computed tomography: application in retrosigmoid craniotomy.

  Lei Xia, Mingshan Zhang, Yanming Qu, Ming Ren, Haoran Wang, Hongwei Zhang, Chunjiang Yu, Mingwang Zhu, Jianhua Li
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  ABSTRACT: In retrosigmoid craniotomy, neurosurgeons usually depend on surface landmarks and their experience to evaluate the position of transverse-sigmoid sinus junction (TSSJ) and place an appropriate initial burr-hole, which is not accurate each time because of variability in different craniums. The authors introduce a simple procedure based on 3D computed tomography (CT) to localize the TSSJ in retrosigmoid craniotomy. Eighteen patients who underwent retrosigmoid craniotomy were analyzed. On the internal view of skull in 3D CT image, a simulative burr-hole was placed on the margin of transverse-sigmoid sinus groove junction. Then, on the external view of skull in 3D CT image, the center of the simulative burr-hole was marked and a coordinate system was established based on a line connected the digastric point and the asterion. Then the coordinate of the burr-hole's center was measured in this coordinate system. In operation, the burr-hole was placed according to the coordinate measured previously and craniotomy was performed. The margin of TSSJ was exposed in each case. No damage of venous sinus was encountered. Post-operative skull base CT demonstrated a good match between the actual and predicted burr-hole and bone defects only existed along the cut line. This simple method could help in localizing the TSSJ and avoiding the risk of sinus injury and reducing the bone defect. It is sufficiently precise for practical application at surgical planning.
  Neurosurgical Review 05/2012; 35(4):593-9. · 2.04 Impact Factor
• Source

  Available from: ccmu.edu.cn

  Article: VCAM-1 siRNA reduces neointimal formation after surgical mechanical injury of the rat carotid artery.

  Yanming Qu, Xiangen Shi, Hongwei Zhang, Wei Sun, Song Han, Chunjiang Yu, Junfa Li
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  ABSTRACT: Restenosis is one of several complications following carotid endarterectomy (CEA). The pathogenesis of restenosis may be related to postsurgery inflammation and leukocyte recruitment mediated by cellular adhesion molecules. In this study, we examine the role of vascular cell adhesion molecule-1 (VCAM-1) in carotid neointimal hyperplasia following carotid surgical mechanical de-endothelialization (CSMDE) in a rat model of CEA. The inhibition of siRNA on VCAM-1 protein expression was determined by using the methods of immunostaining and Western blot. Ultrasound imaging and morphometric analysis were applied to measure the degree of CSMDE-induced carotid artery neointimal hyperplasia of rats. We found that a lentivirus-based construct expressing a small interfering RNA (siRNA) against VCAM-1 could effectively (P < .05, n = 10 per group) reduce VCAM-1 protein expression in the carotid arteries of rats undergoing CSMDE (CSMDE+RNAi: 135.0 +/- 27.6%) when compared that of CSMDE with scrambled siRNA (CSMDE+CON: 182.7 +/- 36.4%). Doppler ultrasonography revealed that CSMDE+RNAi was accompanied by a significant reduction in the extent of stenosis demonstrated by increased blood velocity (665.85 +/- 48.37 mm/s) and linear diameter (0.59 +/- 0.77 mm) compared to CSMDE+CON (46.72 +/- 28.67 mm/s with undetectable linear diameter, P < .05, n = 10 per group). In addition, morphometric analysis of hematoxylin and eosin (HE)-stained sections indicated that the intima (innermost layer of media at lesion site)/media area ratio (I/M) was significantly increased (P < .05, n = 10 per group) both in the CSMDE (3.99 +/- 0.65) and CSMDE+CON (4.33 +/- 0.59) groups compared with the SHAM group (0.35 +/- 0.13). However, CSMDE+RNAi resulted in a significant (P < .05, n = 10 per group) decrease in the I/M ratio (1.79 +/- 0.43) compared to CSMDE+CON, whereas there were no significant differences in the total arterial area and medial areas among the groups. These results suggest that perivascular events mediated by VCAM-1 are likely to play an important role in the pathogenesis of carotid artery neointimal hyperplasia in rats after CSMDE.
  Journal of vascular surgery: official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter 12/2009; 50(6):1452-8. · 3.52 Impact Factor
• Source

  Available from: ccmu.edu.cn

  Article: Increased isoform-specific membrane translocation of conventional and novel protein kinase C in human neuroblastoma SH-SY5Y cells following prolonged hypoxia.

  Junfa Li, Yanming Qu, Pengyu Zu, Song Han, Ge Gao, Qunyuan Xu, Li Fang
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  ABSTRACT: Several studies have suggested that protein kinase C (PKC) plays a key role in the mechanism of cerebral ischemic/hypoxic preconditioning (I/HPC). However, detailed information regarding PKC isoforms in response to brain ischemia/hypoxia and their potential role in neuroprotection is unclear. Previous studies in our laboratory have demonstrated that the levels in membrane translocation of conventional PKC (cPKC) betaII, gamma, and novel PKCepsilon (nPKC), but not cPKCalpha, betaI, nPKCdelta, eta, mu, theta, and atypical PKC (aPKC) zeta and iota/lambda, were increased significantly in the hippocampus and cortex of intact mice with hypoxic preconditioning. To further detect cPKC and nPKC isoforms activation following prolonged hypoxia in vitro, we tested the membrane translocation (an indicator of PKC activation) of cPKCalpha, betaI, betaII, and gamma, and nPKCdelta, epsilon, eta, mu, and theta in a human neuroblastoma SH-SY5Y cell line following sustained hypoxic exposure (1% O(2)/5% CO(2)/94% N(2)). Using Western blot and immunocytochemistry methods, we found that the levels of cPKCalpha, betaI, betaII, and nPKCepsilon, but not nPKCdelta, eta, mu, and theta, membrane translocation were increased significantly (P < 0.05, n = 8) in a time-dependent manner (from 0.5 to 24 h) following sustained hypoxic exposure. Similarly, the immunostaining experiment also showed a noticeable translocation of cPKCalpha, betaI, betaII, and nPKCepsilon from the cytosol to the perinuclear or membrane-related areas after 6 h posthypoxic exposure. In addition, no cPKCgamma was detected in this cell line under either a normoxic or hypoxic condition. These results suggested that prolonged hypoxia may induce the activation of cPKCalpha, betaI, betaII, and nPKCepsilon by triggering their membrane translocation in SH-SY5Y cells.
  Brain Research 07/2006; 1093(1):25-32. · 2.73 Impact Factor