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The programmed cell death 4 (PDCD4) tumor-suppressor gene regulates cell apoptosis, protein translation, signal transduction, and induction of mediators of inflammation. However, the mechanism by which PDCD4 is down-regulated and regulates tumor growth remains elusive. In this study, we showed that PDCD4 is down-regulated in glioma cells and acts as a tumor suppressor. Based on the TCGA data, we confirmed that AKT2, but not AKT1 or AKT3, interacts with PDCD4, thus leading to the suppression of PDCD4 in glioma cells. Moreover, the analysis suggested that PDCD4 regulates the expression of IL-5, CCL-5, VEGF, and CXCL10 via the NF-kB pathway. Additionally, depletion of levels of PDCD4 promoted angiogenic activity of glioma cells via the VEGF-STAT3 pathway. When tumor cells over-expressing PDCD4 were injected into nude mice, the increased expression of PDCD4 blocked tumorigenesis and prolonged overall survival. Our study indicates the need to develop drugs that can modulate the expression of PDCD4 and test their efficacy in clinical trials.

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Objective To investigate the protective effect of mild hypothermia on cerebral ischemia-reperfusion injury in rats and the effect of mild hypothermia on the expression of inhibitor of differentiation 2 (Id2) protein.Methods A total of 72 adult male rats were randomly divided into a sham operation group,a normothermia group,and a mild hypothermia group.A model of middle cerebral artery occlusion was induced by a suture method.The mild hypothermia group was treated with low temperature (anal temperature 33±1 ℃,tympanic membrane temperature 31±1 ℃).Modified Neurological Severity Score (mNSS) was used to evaluate neurological deficits,triphenyltetrazolium chloride staining was used to detect infarct volume,and Western blot was used to detect the Id2 expression in the ischemic cortex at ischemia-reperfusion 6,12,24,and 72 h,respectively.ResultsThe mNSS scores in the mild hypothermia group were significantly lower than those in the normothermia group,the infarct volumes were significantly smaller than those in the normothermia group at ischemia-reperfusion 6,12,24,and 72 h (all P<0.001).Western blot analysis showed that the Id2 expressions in the ischemic cortex in the mild hypothermia group were significantly lower than those in the normothermia group at ischemia-reperfusion 6,12,24,and 72 h (all P<0.05).Conclusion s Mild hypothermia can decrease neurological deficits and reduce infarct volume after cerebral ischemia-reperfusion,its mechanism may be associated with the down-regulation of the Id2 expression.

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We report a case with both traumatic subdural effusion (TSE) and associated hydrocephalus. A collapse of the sinuses is known to be present in some infants with external hydrocephalus, but collapsed sinuses have not been previously described in patients with TSE and associated hydrocephalus. Therefore, a preoperative magnetic resonance imaging venography was performed, with thrombosis in the left transverse and sigmoid sinuses identified. The infant was treated with subdural peritoneostomy. We hypothesized that an occlusive cerebral venous sinus thrombosis may well be the culprit, or an exacerbating factor for TSE associated with hydrocephalus.

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Objective To investigate the diagnosis and treatment of cerebral venous sinus thrombosis ( CVST) in early pregnancy.Methods The clinical data of 4 patients with CVST in early pregnancy were analyzed retrospectively.Results The age of the 4 patients with CVST during early pregnancy was 22 -28 years old.The clinical symptom was headache, and 1 case with seizure.The clinical sign was papilledema.The MRI and MRV examination showed that the superior sagittal sinus thrombosis in 1 case, the superior sagittal sinus and left transverse sinus thrombosis in 1 case, and the left transverse sinus and sigmoid sinus thrombosis in 2 cases.The patients were received anticoagulant therapy with low molecular weight heparin, 1 case was added endovascular thrombolytic therapy.After therapy, 2 cases were cured, and 2 cases improved.Conclusions CVST in early pregnancy is easy to be misdiagnosed.MRI and MRV are helpful to diagnose it.The mainly therapies are endovascular thrombolysis and anticoagulation therapy with low molecular weight heparin.

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Objective To investigate the effect of inhibition of endoplasmic reticulum stress (ERS) in ischemic preconditioning-induced cerebral ischemia tolerance.Methods A total of 120 adult male SpragueDawley rats were randomly allocated into three groups:sham operation,global cerebral ischemic and ischemic preconditioning groups (ischemic preconditioning for 3 minutes,and global cerebral ischemia for 15 minutes after 2 days).Three time points (day 1,day 3 and day 7) were set.Sugawara method was used to observe the changes of neurological behavior in rats.TUNEL staining was used to observe the conditions of cortical neuronal apoptosis.Immunofluorescence staining and Western blot analysis were used to detect the expression levels of ERS-related protein CHOP,GRP78,and caspase-12.Results The neurological behavior score showed that the sham operation group did not have neurological deficits.Both the global cerebral ischemic group and the ischemic preconditioning group had obvious neurological deficits,and they improved gradually with the passage of time,but after modeling,the neurological scores at each time point in the global cerebral ischemic were significantly lower than those in the ischemic preconditioning group:at day 1∶11.00 ±0.63 vs.14.33 ±0.33 (t =21.74,P＝0.001); at day 3∶ 12.17±0.31vs.15.17±0.48 (t=27.93,P =0.000); at day 7:14.67±0.49 vs.16.33 ±0.33 (t =7.81,P=0.020).TUNEL staining showed that at day 7 after ischemia,the positive cell count per mm2 in the sham operation,global cerebral ischemic and ischemic preconditioning groups were 4.83 ±1.85vs.395.67± 43.43 and 146.17± 27.38 respectively (F=23.62,P=0.001).The ischemic preconditioning group was significantly lower than that in the global cerebral ischemic group (P =0.001).Immunofluorescence staining showed that at day 7 after ischemia,the numbers of positive cells of CHOP (26.50±3.89vs.82.33±4.25; P=0.000),GRP78 (15.00±2.02vs.35.67±2.99; t=0.000),and caspase-12 (22.33 ± 2.76 vs.66.50± 7.25; P=0.000) in the ischemic preconditioning group were significantly less than those in the global cerebral ischemic group.Western blotting showed that at day 7 after ischemia,the expression levels of CHOP (1.22 ± 0.38 vs.3.22 ± 0.51; t =24.50,P =0.001),GRP78 (1.78 ± 0.45 vs.3.16 ± 0.76; t =14.29,P =0.005),and caspase-12 (2.89 ± 0.53 vs.5.96 ± 0.67; t =77.73; P =0.000) in the ischemic preconditioning group were significantly lower than those in the global cerebral ischemic group.Conclusions Ischemic preconditioning demonstrated a neuroprotective effect for the second lethal ischemia,its mechanism may be associated with the relief of ERS and downregulation of ERS-related protein.

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Glioblastoma multiforme (GBM) is the most common primary brain tumor and the most malignant astrocytoma in adults, with rare extra-cranial metastases, especially for subcutaneous metastases. It could be easily misdiagnosed as primary subcutaneous tumor. In this report, we describe a patient with pontine GBM who developed a subcutaneous swelling at the ipsilateral posterior cervical region 8 months after operation, and the pathological and immunocytochemical examination carry the same characteristics as the primary intracranial GBM cells, which defined it as subcutaneous metastasis. GBM with subcutaneous metastasis is extremely rare, and knowledge of a prior intracranial GBM, pathological examinations and immunocytochemical tests with markers typically expressed by GBM are of vital importance for the diagnosis of GBM metastasis. Surgical resection of subcutaneous swelling, followed by chemotherapy and radiotherapy, could be the best strategy of treatment for the patients with GBM subcutaneous metastasis.

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Sophocarpine, one of the major alkaloid compounds isolated from Sophora pachycarpa, is highly valued and important in traditional Chinese medicine. In the present study, we aimed to explore the possible mechanisms underlying sophocarpine-mediated neuroprotection against transient focal cerebral ischemia. Sophocarpine (5, 10, or 20mg/kg) was given 30min before focal ischemia was induced in rats by occlusion of the middle cerebral artery. After sophocarpine treatment, the total infarct volume was significantly decreased in comparison to the ischemia-reperfusion values. The results of a neurological evaluation were significantly improved in the sophocarpine treated group when compared to controls. The number of TUNEL-positive cells was significantly reduced compared to the untreated ischemic group. Results of Western blotting and immunohistochemical staining indicated that pretreatment with sophocarpine down-regulated the expression of acid-sensing ion channel 1 (ASIC1) in the ischemic cortex. These results suggest that sophocarpine ameliorated the ischemic injury induced by transient focal cerebral ischemia in rats and that this neuroprotective effect might be related to the anti-ASIC1 channel and anti-apoptotic action of sophocarpine.

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Objective To investigate the neuroprotective effect of sophocarpine against transient focal cerebral ischemia via down-regulation of the acid-sensing ion channel 1(ASICl) in rats.Methods Twenty-five SD rats were randomly allocated into sham operation,cerebral ischemia/reperfusion,and 5,10,and 20 mg/kg sophocarpine pretreatment groups (n=5 in each group).A rat focal ischemia model was induced by the intraluminal suture method.Five,10 and 20 mg/kg sophocarpine were injected intraperitoneally for pretreatrnent.2,3,5-triphenyltetrazolium chloride staining was used to detect cerebral infarct volume.TUNEL staining was used to detect apoptosis.Immunohistochemistry and Western blot were used to detect the expression of ASIC1 and ASIC2.Results The infarct volume after ischemia-reperfusion was(181.21±9.21)mm3,while the 5,10,and 20 mg/kg sophocarpine pretreatment groups were(150.12±6.19),(52.31±4.20),and(32.18±3.82)mm3,respectively;the neurological function scores in the cerebral ischemia/reperfusion group was(3.62±0.36),while the 5,10,and 20 mg/kg sophocarpine pretreatment grows were(3.15±0.36),(1.92±0.18),and(1.85±0.21),respectively;The surviving neurons only accounted for(31.2±2.8)% of the total cell number in the cerebral ischemia-reperfusion group,while they accounted for(51.2±3.7)%,(76.5±2.1)%,and(77.1±4.1)% in the 5,10,and 20 mg/kg sophocarpine pretreatnmat groups.Compared with the cerebral ischemia/reperfusion group,the cerebral infarct volume was decreased significantly in the sophocarpine pretreatrnent groups(all P<0.01),the neurological function scores were decreased significantly(all P<0.01),and the number of apoptotic cells was decreased significantly (all P<0.01).Immunohistochemistry showed that the number of ASIC-1 positive cells in the sham operation,cerebral ischemia-reperfusion,and 5,10,and 20 mg/kg sophocarpine pretreatment groups were(162.5±8.3),(165.1±5.3),(138.3±7.2),(82.1±6.3),and(69.2±5.5)/mm respectively;Western blot showed that the ASIC1 protein expression was decreased sigaificantly in the 10 and 20 mg/ky sophocarpine pretreatment groups (P<0.01),while there WaS no significant difference in the ASIC2 protein expression.Condusions Sophocarpine may play a neuroprotective role for cerebral ischemia-reperfusion injury in rats via down-regulating the expression of ASIC1 protein.

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The experimental study of cerebral ischemia plays an important role for understanding the pathogenesis of ischemic brain injury, but its correlation with the clinical therapeutic strategies has certain limitations. One of its main reasons is that the experimental models and methods can not or only partially repeat the pathophysiological processes of natural cerebral ischemia. In order to promote the understanding and interpretation of the experimental data, we review the commonly used experimental animal models and modeling methods and mainly elaborate the methods of current different in vivo and in vitro clinical evaluation. Based on these studies, we believe that the standardized clinical evaluations are hugely important for assessing the experimental results and clinical transformation.

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Objective To investigate the clinical characteristics, operation time and methods for patients with central brain herniation caused by bifrontal contusions. Methods A retrospective study was performed on the medical records of patients with central brain herniation caused by bifrontal contusions admitted from January 2000 to December 2006. There were 45 males and 18 females, at age range of 20-72 years (average 43 years). The majority of the patients were victims of falls and traffic accidents. There were 29 patients treated with immediate operation and 34 with emergency operation. All the operations involved simultaneous bilateral craniectomy for decompression, including 17 patients treated with bilateral decompressive craniectomy and 46 with unilateral decompressive craniectomy. Results The prognosis was favorable in 19 patients with GOS score of 5 or 4 points, severely disabled in seven with GOS score of 3 points, vegetative in four with GOS score of 4 points and the worst in seven with GOS score of 1 point. Of all, 19 patients suffered severe mental disorders especially personality change and disturbance of intelligence. Seven patients were complicated by epilepsy and three by hydrocephalus. Conclusions Based on early clinical manifestations of central brain herniation combined with imaging manifestations, bilateral balance decompression craniectomy can reduce the mortality and morbidity and improve the cure rate of patients with central herniation caused by bifrontal brain contusions.

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BACKGROUND: There are different reports about operative methods for the treatment of hypertensive intracerebral hematomas. Our experience of transsylvian-transinsular microsurgical approach to hypertensive putaminal hematomas was analyzed. METHODS: A retrospective analysis was performed on 28 consecutive patients with hypertensive intracerebral hematomas who underwent surgical treatment at the Department of Neurosurgery, Renji Hospital, from January 2004 to December 2007. RESULTS: The transsylvian-transinsular approach to evacuate the hypertensive putaminal hematoma gains a good result. We believe it allows decompression of important deep-seated neurostructures with a more suitable angle and shorter distance from the cortex to the hematoma; allows easier access to vessels responsible for the bleeding, reducing the rate of rebleeding postoperatively; and avoids damage to the temporal or frontal cortex. CONCLUSIONS: Transsylvian-transinsular approach for hypertensive putaminal hematoma is advocated.

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OBJECTIVE@#To investigate the anatomical relationship among optic nerve, posterior ethmoid sinus and ophthalmic artery to further provide surgical instruction for endoscopic transsphenoidal optic nerve decompression.@*METHOD@#Messerklinger technique was adopted in eight cases of adult cadaveric head to expose the posterior ethmoid sinus and sphenoid sinus. The optic-carotid recess and optic canal were identified. The adjacent structure of optic canal was observed. After removal of the bony wall of optic canal, the relationship between the optic nerve and the ophthalmic artery was disrupted.@*RESULT@#the optic-carotid recess was observed in all specimens. The occurrence of optic nerve prominence was 62%. Three patterns of the syntropy of optic nerve were observed. Optic nerve was border by posterior ethmoid sinus anteriorly and sphenoid sinus posteriorly in 8 cases (50%), by sphenoid sinus in 5 (31%), and by posterior ethmoid sinus in 3 (19%). At the cranial end, The ophthalmic artery was observed, 9 (56%) inferior-medially, 4 (25%) inferiorly and 3 (19%) inferior-laterally relative to optic nerve. At the ophthalmic end, the artery was observed 3 (19%) inferiorly and 13 (81%) inferior-laterally relative to optic nerve.@*CONCLUSION@#The optic-carotid recess can be regarded as the first landmark. The ophthalmic artery injury should be avoided with regard to its relationship with optic nerve during endoscopic decompression surgery.

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Objective To investigate the mRNA and protein expressions of Nav 1.1 and Nav 1.2 in hippocampus following traumatic brain injury ( TBI) in rats.Methods After the lateral fluid percussion model was established in adult male Sprague Dawley rats,the rats were sacrificed at 2,12,24 and 72 hours after percussion and collected ipsilateral hippocampus for detecting mRNA and protein expressions of Nav 1.1 and Nav 1.2 by means of fluorescent quantitation RT-PCR,Western blot and immunofluo rescence staining.Results The mRNA expressions of Nav 1.1 and Nav 1.2 were significantly down-regulated (P<0.01) in hippocampus and reached the lowest level at 2 hours following TBI.The protein expression of Nav 1.1 was significantly down-regulated (P<0.01) but recovered near to level of control group at 72 hours after TBI.While there was no statistical difference on protein expression of Nav 1.2 in hippocampus after TBI compared with control group (P>0.05).Conclusion TBI induces significant down-regulated mRNA and protein expressions of Nav 1.1 in the hippocampus,which may be one of molecular mechanisms for functional alternation of sodium channels and excitotoxic action following TBI.

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<p><b>OBJECTIVE</b>To study the effect of endoscopic-assisted keyhole operation (EAKO) on treating hypertensive intracranial hematomas and the value of our patent dissector applied during the operation.</p><p><b>METHODS</b>A total of 25 patients with hypertensive intracranial hematomas underwent endoscopic-assisted keyhole evacuation, during which, the viewing dissector, which had recently achieved national patent, was connected to the tip of endoscope and used to help dissect hematomas. The outcome of this procedure were compared with those of 22 comparable cases undergone conventional surgical treatment (large or smaller craniotomy). The items for comparison included the volume of remaining hematoma, the duration of operation, postsurgical Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS).</p><p><b>RESULTS</b>Remaining hematoma was ascertained 48 h after operation with the use of computerized tomography (CT) scans. In the case of EAKO, nearly complete evacuation (> 84%) was achieved in 21 cases; GCS was evaluated at 7 d postsurgery resulting in GCS > 12 in 9 patients, GCS 9 - 12 in 12 patients and GCS < 9 in 4 patients. The follow-up period ranged from 6 to 21 mon. GOS was estimated at half a year and good recovery rate as defined by GOS was assigned to 76% of the EAKO patients. There are significant differences in the volumes of remaining hematomas and the duration of operation between the EAKO and craniotomy group (P < 0.05). In addition, better clinical outcomes were obtained in EAKO.</p><p><b>CONCLUSION</b>EAKO has the advantage of being minimally invasive, improving surgical results and the prognosis of hypertensive intracranial hematoma patients. We conclude that keyhole operation is a safe, effective alternative for removal of hypertensive intracranial hematoma, particularly during acute stages.</p>

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Objective To investigate the change on monoamine neurotransmitter in cerebral cortex motor area of traumatic asphyxia canines and provide scientific basis for its therapy.Methods The model of canine traumatic asphyxia was established,the change on monoamine neurotransmitter in cerebral cortex (motor area) and the products of metabolism during different time were tested with HPLC DC method.Results At 2 h after damage in cerebral cortex 5 hydroxyindolecetic acid (5 HIAA) elevated remarkably; At 8 h after da mage 5 hydroxytryptamine (5 HT), homovanillic acid (HVA) elevated; but there was no obvious change on norepinephrine(NE) and 3,4 dihydroxyphenyl acetic acid (DOPAC).Conclusion The monoamine neurotransmitters might play an important role in the pathological course of secondary brain injury after traumatic asphyxia.The utilization of 5 HT antagonists or compound inhibitor at early stage was a reliable method for treating brain injury after traumatic asphyxia.