[A decade of pecision neurosurgery: the informative and systematic upgrading of brain glioma surgery].

Precision neurosurgery concept as well as the establishment of it's technical platform, have played essential roles in promoting the modern surgical management of brain gliomas in China.In the past decade,the multidisciplinary integration of medical sciences and technology innovations has significantly promoted the clinical implementation of new imaging and novel navigation technology.With active clinical translational research and practice,precision neurosurgery has developed from "startup prologue" (simple anatomical navigation) to "precision neurosurgery 1.0" (intraoperative MRI with multimodal neuronavigation),followed by "precision neurosurgery 2.0" (informative and systematic upgrading).In the past decade,Chinese researchers have made significant and remarkable achievements in precision neurosurgery through continuous efforts and innovation.In the future,state-of-art technologies such as artificial intelligence on deep learning and machine learning,multimodal real-time navigation,intraoperative optical imaging,and targeted molecular imaging technology will promote the development of precision neurosurgery in a coordinated manner, leading to the advent of "precision neurosurgery 3.0".

[Implement of multimodal navigation-based virtual reality in the needle biopsy of intracranial eloquent lesions].

Objective: To investigate the clinical value of multimodal navigation-based virtual reality (MNVR) in the needle biopsy of intracranial eloquent lesions. Methods: From January 2016 to January 2017, 20 patients with intracranial deep-seated lesions involving eloquent brain areas underwent MNVR-aided needle biopsy at Department of Neurosurgery, People's Liberation Army General Hospital. Preoperatively, MNVR was used to propose and revise the biopsy planning. Intraoperatively, navigation helped trajectory avoid the eloquent structures. Intraoperative MRI (iMRI) was performed to prove the biopsy accuracy and detect the intraoperative complications. Perioperative neurological status, iMRI findings, intraoprative complications, surgical outcome and pathological diagnosis were recorded. Wilcoxon rank-sum test was conducted to compare the preoperative and postoperative neurological scores. Results: MNVR helped revised 45%(9/20) initial biopsy trajectories, which would probably injury the nearby eloquent structures. Navigation helped biopsy trajectories spare the eloquent structures during the operation. No statistical difference was found between postoperative and preoperative neurological status, despite all the lesions were adjacent to eloquent areas. Additionally, 20 patients totally received 21 iMRI scanning. iMRI helped revise incorrect biopsy site in one case and detected intraoperative hemorrhage in another case, both of cases were treated immediately and effectively. No MNVR related adverse events and complications occurred. Conclusions: MNVR-aided needle biopsy of intracranial eloquent lesions is a safe, novel and efficient biopsy modality. This technique is helpful to reduce the incidence of surgery related neurological deficits.

[Implementation of multimodal navigation combined with intraoperative magnetic resonance imaging in the frameless stereotactic biopsy of intracranial lesions].

Objective: To investigate the impact and value of multimodal navigation and intraoperative magnetic resonance imaging (iMRI) on the biopsy of intracranial lesions. Methods: From February, 2009 to December, 2016, this study enrolled 156 patients, who underwent multimodal navigation and iMRI-guided brain biopsy in the Neurosurgery Department of PLA General Hospital. Metabolic information was used for biopsy target selection. Intraoperative guidance helped biopsy trajectory avoid the eloquent structures. iMRI was performed to prove the biopsy accuracy and to revise the incorrect biopsy. Diagnostic rate, perioperative neurological status, surgical parameter, and surgical outcome were recorded. Results: The first iMRI helped to revise 7 (4.5%) incorrect biopsy sites, and final iMRI confirmed biopsy accuracy in all cases. Postoperative diagnostic rate was 96.8% (151/156). No statistical difference was found between postoperative and preoperative neurological statuses, despite 86 (55.1%) lesions were adjacent to eloquent areas. Additionally, iMRI detected 6 (3.8%) intraoperative hematomas that were treated immediately. Conclusions: Brian biopsy with iMRI and multimodal navigation is a safe, accurate and efficient biopsy modality. This technique may help increase the biopsy accuracy with low morbidity and mortality.

Effect of human umbilical cord mesenchymal stem cells on endometriotic cell proliferation and apoptosis.

The objective of this study was to observe the effects of human umbilical cord mesenchymal stem cells (UCMSCs) on the proliferation and apoptosis of endometriotic cells. Endometriotic cells and UCMSCs were primarily cultured in vitro. In the experimental group, a UCMSC and endometriotic cell non-contact co-culture system was established. The control group consisted of 1 x 10(5) endometriotic cells cultured alone. The proliferation and apoptosis of endometriotic cells were respectively detected using the MTT method and flow cytometry. The mRNA expression level of the tensin homologue gene (PTEN) in endometriotic cells was detected by reverse transcription-polymerase chain reaction amplification. Compared with the control group, the proliferation of endometriotic cells in the experimental group was clearly inhibited (P < 0.05) and time-dependent (P < 0.05). In addition, the number of apoptotic cells were significantly increased (P < 0.05), and the amount of cells, which entered S phase from G1 phase, decreased significantly. Furthermore, the mRNA expression level of the PTEN gene in the experimental group was significantly higher than in the control group (P < 0.05). These results suggest that UCMSCs might inhibit the proliferation of human endometriotic cells in vitro and promote their apoptosis by upregulating the expression of PTEN.

Tumor-associated fibroblast-conditioned medium promotes tumor cell proliferation and angiogenesis.

This study aimed to explore how tumor-associated fibroblasts (TAFs) promote the proliferation and angiogenesis of tumor cells via the paracrine mechanism in vitro. Conditioned media (CM) of ovarian TAFs and normal fibroblasts (NFs) were collected. Ovarian cancer cells (OCCs) were treated with 2 mL TAFs-CM and NFs-CM in experimental and control groups, respectively; 20 mM SB431512, a specific small molecule inhibitor of transforming growth factor-ß (TGF-ß), was added in the experimental group as the intervention group. The cell cycle was determined in each group. mRNA expressions of proliferating cell nuclear antigen (PCNA), α-smooth muscle actin (α-SMA), and vascular endothelial growth factor (VEGF), and protein expressions of α-SMA and VEGF were detected in each group. Proliferation of OCCs was significantly promoted in the experimental group compared with that of the control group. The proliferative effect was obviously inhibited in the intervention group. The mRNA expressions of PCNA, α-SMA, and VEGF, and protein expressions of α-SMA and VEGF were all dramatically up-regulated in each group, and were strongly inhibited by SB-431512. TAFs promote the proliferation of OCCs via paracrine and up-regulated expression of angiogenic genes and proteins, which can be effectively inhibited by inhibiting the TGF-ß signaling pathway.

Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig.

Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta). To further explore the potential link between brain trauma and neurodegeneration, we conducted neuropathological studies using a pig model of diffuse brain injury. Brain injury was induced in anesthetized animals via nonimpact head rotational acceleration of 110 degrees over 20 ms in the coronal plane (n = 15 injured, n = 3 noninjured). At 1, 3, 7, and 10 days post-trauma, control and injured animals were euthanized and immunohistochemical analysis was performed on brain sections using antibodies specific for A beta, beta-amyloid precursor protein (betaPP), tau, and neurofilament (NF) proteins. In addition to diffuse axonal pathology, we detected accumulation of A beta and tau that colocalized with immunoreactive betaPP and NF in damaged axons throughout the white matter in all injured animals at 3-10 days post-trauma. In a subset of brain injured animals, diffuse A beta-containing plaque-like profiles were found in both the gray and white matter, and accumulations of tau and NF rich inclusions were observed in neuronal perikarya. These results show that this pig model of diffuse brain injury is characterized by accumulations of proteins that also form pathological aggregates in AD and related neurodegenerative diseases.

Evolution of neurofilament subtype accumulation in axons following diffuse brain injury in the pig.

Although accumulation of neurofilament (NF) proteins in axons has been recognized as a prominent feature of brain trauma, the temporal course of the accumulation of specific NF subtypes has not been well established. In the present study, 17 miniature swine were subjected to nonimpact inertial brain injury. At 3 hours (h), 6 h, 24 h, 3 days, 7 days, and 10 days post-trauma, immunohistochemical analysis was performed to determine axonal accumulation of NF-light (NF-L), the rod and sidearm domains and sidearm phosphorylation states of NF-medium (NF-M), and heavy (NF-H). We found that NF-L accumulation was easily identified in damaged axons by 6 h post-trauma, but NF-M and H accumulation was not clearly visualized until 3 days following injury. In addition, the axonal accumulation of NF-M and H appeared to be primarily comprised of the sidearm domains. While the accumulating NF was found to be predominantly dephosphorylated, we also detected accumulation of phosphorylated NF. Finally, we found that developing axonal pathology may proceed either towards axotomy with discrete terminal bulb formation or towards the development of varicose swellings encompassing long portions of axons. These findings suggest that there is a differential temporal course in NF subtype disassembly, dephosphorylation, and accumulation in axons following initial brain trauma and that these processes occur in morphologically distinct phenotypes of maturing axonal pathology.

Diffuse axonal pathology detected with magnetization transfer imaging following brain injury in the pig.

This study was designed to evaluate with magnetization transfer imaging (MTI) and conventional magnetic resonance (MR) imaging the manifestation of diffuse axonal injury (DAI) in an animal model of injury via nonimpact coronal plane rotational acceleration. A second objective was to investigate the diagnostic use of quantitative MTR imaging based on statistical parameters in a single subject, as opposed to grouped analysis. Seven mini-swine were subjected to brain trauma known to produce isolated DAI and to MR imaging at two time points. Following sacrifice, the brains were harvested for histopathologic examination. Magnetization transfer ratio (MTR) maps were generated for double-blinded comparison of regions with abnormal MTR values and regions with documented DAI. Positive and negative predictive values for MTR detection of DAI were 67 and 56%, respectively, and in acute studies alone, 89 and 61%. Gains in sensitivity over conventional imaging for detection of DAI were demonstrated.

Characterization of diffuse axonal pathology and selective hippocampal damage following inertial brain trauma in the pig.

Dynamic deformation applied to white matter tracts is a common feature of human brain trauma, and may result in diffuse axonal injury (DAI). To produce DAI in an experimental model, we have utilized nonimpact inertial loading to induce brain trauma in miniature swine. This species was chosen due to its large gyrencephalic brain with substantial white matter domains. Twenty anesthetized (2% isoflurane) miniature swine were subjected to pure impulsive centroidal rotation 110 degrees in the coronal plane in 4 to 6 ms; peak accelerations ranged from 0.6 to 1.7 x 10(5) rad/s2. Seven days following injury, the brains were fixed (4% paraformaldehyde). Histopathologic examination was performed on 40 microns sections stained with cresyl violet (Nissl), antibodies targeting neurofilament (axonal damage), GFAP (astrocytes), and pig IgG (protein extravasation). Widespread multifocal axonal injury was observed in combination with gliosis throughout the brain, most commonly in the root of gyri and at the interface of the gray and white matter. Very little vascular disruption was noted in regions of axonal injury. Neuronal damage was primarily found in the CA1 and CA3 subfields of the hippocampus. These results suggest that this model is clinically relevant and useful for evaluating mechanisms of inertial brain trauma.

Pathophysiology of brain swelling after acute experimental brain compression and decompression.

Global ischemia was created by controlled expansion of an epidural balloon for 25 minutes in Group A (six cats) and for 5 minutes in Group B (six cats). The alterations of intracranial pressure, arteriovenous oxygen content difference, cerebral metabolic rate of oxygen, cerebral blood flow, and electroencephalogram were observed until brain death or 24 hours' survival with normal intracranial pressure. The animals were then killed for brain histological examination. In four other cats, a 2% solution of Evans blue dye (4 mg/kg) was injected intravenously--immediately after deflation--resulting in 25 minutes of global ischemia. Two other cats received 5 minutes of global ischemia. The cats were killed 1 hour later. Abrupt swelling occurred in Group A, and no swelling was found in Group B. A transient absolute hyperemia was found immediately after deflation in both groups. The cerebral blood flow and cerebral metabolic rate of oxygen decreased markedly with low arteriovenous oxygen content difference and flat electroencephalogram in Group A, compared with gradual recovery of cerebral blood flow and cerebral metabolic rate of oxygen with high arteriovenous oxygen content difference and reappearance of electroencephalogram activity in Group B. The extravasation of Evans blue was observed on the compressed cerebral hemisphere, thalamus, hypothalamus, and brain stem in swelling animals and only on the compressed hemisphere in nonswelling animals. Histologically, the damage and congestive dilation of capillary, degeneration, and necrosis of neuronal and glial cell were found prominently on the hypothalamus and brain stem in the swelling group.(ABSTRACT TRUNCATED AT 250 WORDS)

Location of myocardial infarction and its surface cardioelectric representation. An experimental study.

In order to explore the relationship between the different location of myocardial infarction (MI) and reflections of pathognomonic Q potentials on the body surface, an experimental study was carried out in 28 dogs. The results were (1) in 27 of a total 28 dogs after MI formation, abnormal Q maps appeared; (2) right ventricular MI, posterior wall MI and some lateral and apical MI are prone to miss abnormal Q potentials in the conventional 12-lead ECG; and (3) the MI location and relative size diagnosed through electrocardiographic peak mapping (EPM) correlated to acute MI in dog ventricles fairly well. The unexpected Q map reflections of right ventricular MI provide new clues for improving our automatic diagnosis system after further correlative studies. The results strongly support the feasibility of the application of EPM in clinical diagnosis.

[Intracranial pressure monitoring in clinical practice. Report of 180 cases].

180 severe neurosurgical cases were monitored by intraventricular, epidural and subdural measurements. Intracranial infection rate was 1.1% and the intracranial hypertension rate was 83.3%. Increased intracranial pressure was most often seen in group of head injury. The outcome was poor in cases of uncontrol intracranial hypertension. It was found that intracranial pressure monitoring is useful for diagnosis, treatment and estimation of prognosis and has practical clinical value. This method and indications should be used appropriately according to the different situations. The patients with acute intracranial hypertension should be monitored intensively.