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A wearable surgical navigation system is developed for intraoperative imaging of surgical margin in cancer resection surgery. The system consists of an excitation light source, a monochromatic CCD camera, a host computer, and a wearable headset unit in either of the following two modes: head-mounted display (HMD) and Google glass. In the HMD mode, a CMOS camera is installed on a personal cinema system to capture the surgical scene in real-time and transmit the image to the host computer through a USB port. In the Google glass mode, a wireless connection is established between the glass and the host computer for image acquisition and data transport tasks. A software program is written in Python to call OpenCV functions for image calibration, co-registration, fusion, and display with augmented reality. The imaging performance of the surgical navigation system is characterized in a tumor simulating phantom. Image-guided surgical resection is demonstrated in an ex vivo tissue model. Surgical margins identified by the wearable navigation system are co-incident with those acquired by a standard small animal imaging system, indicating the technical feasibility for intraoperative surgical margin detection. The proposed surgical navigation system combines the sensitivity and specificity of a fluorescence imaging system and the mobility of a wearable goggle. It can be potentially used by a surgeon to identify the residual tumor foci and reduce the risk of recurrent diseases without interfering with the regular resection procedure.

The aim of this study is to investigate the expression of tumor-associated macrophages (TAMs) M1, M2 phenotypic in human glioma tissues, and to explore the clinical significance and prognostic value of TAMs in glioma patients. A total of 50 glioma samples were obtained from patients diagnosed in our hospital from 2007 to 2010. Clinical follow-up was conducted via return visits and telephone interviews after discharge. Progression free survival (PFS) was calculated based on tumor progression by MRI and CT examination from the primary operation. Overall survival (OS) time was calculated from the initial surgical operation date to end date of follow-up or death. Kaplan-Meier methodology was used to evaluate the survival of patients and log-rank test for comparing differences between groups. The expression levels of CD16 and CD206 were investigated in the 4 μm serial paraffin sections by immunohistochemistry. M1-type macrophages filtrated in all the grades of glioma samples, and the lower expression level was associated with high grade glioma. A negative correlation was found between WHO pathological grades and the expression of M1-type macrophages by Spearman correlation analysis. M2-type macrophages filtrated in all the grades of glioma samples with the higher expression level associated with high grade glioma. A positive correlation was found between WHO pathological grades and the expression of M2-type macrophages by Spearman correlation analysis. The PFS and OS among patients with high levels of M1-type macrophages (CD16+++) were significantly higher than those with less expression. The PFS and OS among patients with high levels of M2-type macrophages (CD206+++) were significantly lower than those with low expression. M1-type macrophages may inhibit the tumor growth and improve the therapeutic outcome of glioma patients. M2 ratios are associated with tumor proliferation and poor prognosis. TAMs phenotypes of glioma samples are the potential biomarkers in assessing the degree of malignancy, tumor invasion, and patient prognosis in clinic.

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The chemokine fractalkine (CX3CL1) and its receptor CX3CR1 play a fundamental role in the pathophysiology of stroke. Previous studies have focused on a paracrine interaction between neurons that produce fractalkine and microglia that express CX3CR1 receptors in the central nervous system. Recent findings have demonstrated the functional expression of CX3CR1 receptors by hippocampal neurons, suggesting their involvement in neuroprotective and neurodegenerative actions. To elucidate the roles of neuronal CX3CR1 in neurodegeneration induced by ischemic stroke, a mouse model of permanent middle cerebral artery occlusion (pMCAO) was employed. In the pMCAO mice, increased CX3CR1 levels, apoptosis-associated morphological changes, and Caspase 3-positive neuronal cells were observed in the striatum and in the hippocampus 24 hours after occlusion. Upregulation of CX3CR1 in ischemic neurons is associated with neuronal apoptotic cell death. In contrast, ischemia-induced apoptotic neuronal cell death was decreased in CX3CR1 deficient mice. Cultured primary hippocampal neurons obtained from CX3CR1 deficient mice were more resistant to glutamate-induced excitotoxicity by blocking calcium influx than those from wild-type mice. For the first time, we reported that neuronal CXCR1 mediates neuronal apoptotic cell death in ischemia. Our results suggest that modulating CXCR1 activity offers a novel therapeutic strategy for stroke.

Striatal transplantation of dopaminergic (DA) neurons or neural stem cells (NSCs) has been reported to improve the symptoms of Parkinson’s disease (PD), but the low rate of cell survival, differentiation, and integration in the host brain limits the therapeutic efficacy. We investigated the therapeutic effects of intracranial co-transplantation of mesencephalic NSCs stably overexpressing human glial-derived neurotrophic factor (GDNF-mNSCs) together with fetal DA neurons in the 6-OHDA rat model of PD. Striatal injection of mNSCs labeled by the contrast enhancer superparamagnetic iron oxide (SPIO) resulted in a hypointense signal in the striatum on T2-weighted magnetic resonance images that lasted for at least 8 weeks post-injection, confirming the long-term survival of injected stem cells in vivo. Co-transplantation of GDNF-mNSCs with fetal DA neurons significantly reduced apomorphine-induced rotation, a behavioral endophenotype of PD, compared to sham-treated controls, rats injected with mNSCs expressing empty vector (control mNSCs) plus fetal DA neurons, or rats injected separately with either control mNSCs, GDNF-mNSCs, or fetal DA neurons. In addition, survival and differentiation of mNSCs into DA neurons was significantly greater following co-transplantation of GDNF-mNSCs plus fetal DA neurons compared to the other treatment groups as indicated by the greater number of cell expressing both the mNSCs lineage tracer enhanced green fluorescent protein (eGFP) and the DA neuron marker tyrosine hydroxylase. The success of cell-based therapies for PD may be greatly improved by co-transplantation of fetal DA neurons with mNSCs genetically modified to overexpress trophic factors such as GDNF that support differentiation into DA cells and their survival in vivo.

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