Objective:To examine the impact of hyperbaric oxygen intervention on oxidative stress and nerve growth factor in patients with craniocerebral injury.Methods:Using the random number table method, 40 patients with craniocerebral injury who were treated at the First People's Hospital of Nantong were randomly assigned to either the control group or the hyperbaric oxygen group, with 20 patients in each group. The control group received routine intervention for clinical traumatic brain injury, while the hyperbaric oxygen group received additional hyperbaric oxygen intervention during the 7 to 30 days of routine intervention. Indicators of oxidative stress and nerve growth factor levels were compared between the two groups at the time of admission and 30 days after therapy.Results:The serum levels of superoxide dismutase, endothelium-derived relaxing factor-nitric oxide, and nerve growth factor in the hyperbaric oxygen group increased more significantly than in the control group. The serum malondialdehyde concentration was also significantly reduced in the hyperbaric oxygen group.Conclusion:Hyperbaric oxygen intervention can successfully lower systemic oxidative stress response and increase the expression level of nerve growth factor in patients with craniocerebral injury.

Marine red beds (MRBs) as a special geological phenomenon have been considered relevant to specific palaeogeographic or paleoclimatic conditions. The Wuchiapingian Yundoutan Formation in Xikou, Shaanxi, Central China is characterized by a huge thick succession of red limestones, which is a unique deposition among marine strata of China during the Wuchiapingian. The lithology, mineralogy, and geochemistry features of the Yundoutan Formation MRBs were analyzed by using techniques of field measurement, polarized optical microscope, field emission scanning electron microscope (FESEM), diffuse absorbance spectroscopy (DAS), X-ray diffraction (XRD), and geochemical analysis, which were used to discuss their origin and palaeogeographic and paleoclimatic responses. The results show that the stain mineral for the MRBs is mainly weakly-crystalline hematite which can not be observed in the FESEM but was detected from the DAS first derivative spectra with featured peaks around 570 nm. The similar trend of Fe with refractory elements and the strong positive correlation between Fe and Al suggest Fe is mainly a terrestrial source. Limestones of the Yundoutan Formation contain different colors including red, light gray, and dark gray. Red limestones have comparable contents of Fe with dark gray limestones, which are larger than that of light gray limestones, but they are depleted in redox-sensitive elements (Cr, Ni, Cu, Zn, Mo, U) and riched in Fe(III) compared with dark gray limestones. Those indicate that the formation of red limestones needs both enough terrestrial Fe and strong oxic conditions. A mechanism proposed for the formation of red limestones was that Fe was transported from the highlands, which were then deposited under a strong oxic environment and transformed into hematite. We suggest the Wuchiapingian MRBs formed in Central China represent a unique paleogeography and palaeoclimate association. During that time, the study area attached to the northern margin of the United North China-Qinling Block received terrestrial materials from its northward highlands, which provided Fe under a warm climate. Meanwhile, the study area located between the South and North China blocks was on the narrow seaway connecting the Palaeotethys and Panthalassa, which produced relatively fast exchanging rates of seawater and thus a high content of oxygen that can easily transform terrestrial-sourced Fe into hematite. The gradual transition among color-different limestones may be driven by the changes in rainfall that influenced river transportation on terrestrial materials or sea-level changes that influenced the redox state of the water-sediment interface.

Background An inhibitor of apoptosis (IAP) family member, baculoviral IAP repeat containing five (BIRC5) plays an important role in the occurrence and development of tumors. However, the underlying mechanism in human cancers remains unclear. Methods In this study, we investigated BIRC5 expression and explored the prognostic value of BIRC5 in different human cancers via bioinformatics analysis, including the databases of Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, GEPIA, DriverDBv3, GeneMANIA, WEB-based Gene Set Analysis Tool (WebGestalt) and TIMER. Results In most human cancers, BIRC5 usually had higher expression compared to normal human tissues. High expression of BIRC5 could increase the mortality of patients with adrenocortical carcinoma (ACC), kidney renal clear cell carcinoma (KIRC), low-grade glioma (LGG), liver hepatocellular carcinoma (LIHC), and lung adenocarcinoma (LUAD) (P<0.05). Cox analysis demonstrated that high BIRC5 expression was an independent factor for poor overall survival (OS) [hazard ratio, (HR) >1, P<0.05]. There were differences in BIRC5 expression in the case of TP53 mutation, different tumor grades, and stages. Interactive genes for BIRC5 mainly participated in apoptosis, cell division, cell cycle, and cancer pathways, strongly suggesting its oncogenic role in promoting cancer cell proliferation and cancer development. In addition, BIRC5 expression exhibited a close correlation with immune infiltration, which was related to the cumulative survival rate, especially in LGG. The elevated expression of BIRC5 could be regulated through TP53 mutation, tumor stage, and tumor grade (P<0.05). Conclusions As a result of our findings, BIRC5 appears to be an independent unfavourable prognostic biomarker in human cancers. BIRC5 may become a potential clinical target in the future for the treatment of cancers.

Introduction: Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis, a serious neurological autoimmune disorder caused by autoantibodies with diverse clinical manifestations, may simultaneously onset with antimyelin oligodendrocyte glycoprotein (MOG) demyelination after recurrent central nervous system (CNS) demyelination. Case Report: We present a case of anti-NMDAR encephalitis combining with anti-MOG CNS demyelination following recurrent CNS demyelination. A 38-year-old man admitted to hospital developed epileptic seizures following recurrent episodes of cross-sensory disturbance and dizziness. Magnetic resonance imaging (MRI) showed a demyelinating lesion in the right brainstem initially. Despite a good response to methylprednisolone pulse therapy at the beginning, the patient still had relapses and progression after corticosteroid reduction or withdrawal. Then brain MRI discovered new serpentine lesions involving extensive cerebral cortex on his second relapse. Repeat autoantibodies test indicated cerebrospinal fluid (CSF) NMDAR antibodies coexisted with MOG-Abs simultaneously, suggesting the diagnosis of anti-NMDAR encephalitis with anti-MOG CNS demyelination. Results: After a definite diagnosis, the patient was treated with mycophenolate mofetil (MMF) and corticosteroid. He was discharged after his symptoms ameliorated. No neurological sequels remained, and there were no effects on his activities of daily living after 6 months of immunoregulatory therapy of MMF and corticosteroid. Conclusion: For individuals with recurrent CNS demyelination, especially combining with cortical encephalitis, repeated detection of autoantibodies against AE, and demyelination in CSF/serum can be helpful to enable a definite early diagnosis. For patients who suffer from anti-NMDAR encephalitis combining with anti-MOG CNS demyelination, second-line immunotherapy is recommended when first-line treatment such as steroids, intravenous immunoglobulin G (IVIG) and plasma exchange has been proven ineffective to prevent the relapse of disease.

单核细胞增生李斯特菌脑膜脑炎是由单核细胞增生李斯特菌侵入脑膜及脑实质而引起的中枢神经系统感染性疾病,病死率高达17％～24％[1].脑积水主要是由于脑脊液分泌过多或循环障碍而引起的脑室系统扩大.单核细胞增生李斯特菌脑膜脑炎并发脑积水,病情危重,常预后不佳.现报道一例单核细胞增生李斯特菌脑膜脑炎并发脑积水的患者,旨在提高临床医师的认识,以便在临床工作中做出正确诊断和及时治疗,进而改善患者预后.

帕金森病(PD)是中老年人常见的神经系统变性疾病,存在运动症状和非运动症状.冲动控制障碍是PD非运动症状之一,但常被临床忽视.本文从PD冲动控制障碍危险因素、发病机制、临床表现、辅助检查、治疗等方面展开综述.

经颅直流电刺激(tDCS)是一种非侵入性的调节大脑皮质神经元活动的物理治疗方法,在临床疾病康复治疗中应用十分广泛.脑卒中作为一种常见的具有高发病率和高致残率的脑血管疾病,其康复治疗得到广泛的关注.tDCS作为一种新型的神经康复治疗手段,已在脑卒中康复治疗中逐渐得到推广和应用,并获得很好的疗效.本文就tDCS作用机理及其在脑卒中康复治疗中的应用展开综述.

目的 探讨精神障碍合并癫痫发作的神经梅毒的诊治.方法 分析以“精神障碍合并癫痫发作”为主症的2例不典型神经梅毒患者的临床资料,并复习相关文献.结果 2例均有精神异常伴癫痫发作,1例有吸毒及冶游史,2例血清、脑脊液RPR及TPPA均阳性,1例脑脊液蛋白升高.经驱梅治疗后,临床症状均明显好转.结论 以不明原因的精神障碍合并癫痫发作为首发症状的患者建议常规行梅毒筛查;确诊神经梅毒的患者应及时规范应用青霉素驱梅治疗.

Objective To investigate the role of AHR／SOCS2 pathway on astrocyte inflammatory response after oxygen deprivation.Methods Astrocytes ( AS) were isolated and cultured in vitro to establish astrocyte oxygen glucose deprivation (OGD／R) model.AS were divided into the following groups as ctrl group (normal culture ), OGD／R group, OGD／R+negative control group, OGD／R+AHR overexpression group , OGD／R+AHR overexpression +SOCS2 knockdown group.Western blot and RT-PCR were used to detect the expression of AHR , SOCS2 and inflammatory factors in each group.It was used to confirm whether SOCS2 could block the expression of AS inflammatory factors TNF-α, IL-6 and iNOS after OGD／R which was regulated by AHR.Results The expression levels of TNF-α, IL-6 and iNOS were increased after overexpression of AHR and SOCS2.Knocking down SOCS2 could block the up-regulation of TNF-α, IL-6 and iNOS which was caused by AHR.Conclusion The AHR／SOCS2 pathway is involved in the regulation of AS inflammation after OGD／R.

PBL(Problem Based Learning)联合CBL(Case Based Learning)是当下较为高效的教学方法,突破了传统的以老师为中心的教学模式,主张以问题为导向,在临床案例的基础上,充分发挥学生的主观能动性.而神经病学是一门专业性较强的学科,内容深奥难懂,传统的教学模式难以获得良好的教学效果,我们将PBL联合CBL教学方法运用在神经病学见习教学中,旨在提高见习教学质量,培养优秀人才.

甲基丙二酸血症( Methylmalonic acidemia,MMA)是常见的先天性有机酸代谢缺陷性疾病.根据发病年龄将≤1岁定义为早发型;>1岁为晚发型.早发型较常见,病情呈进行性加重,病死率高,即便存活也可能留下重度神经系统损害[1].晚发型较为少见,由于缺乏典型的临床表现,常常造成临床医师的误诊、漏诊,这导致相当一部分晚发型甲基丙二酸血症未得到及时合理的治疗.正因为如此,患者病情进一步发展、恶化,并最终导致不可逆的神经损害.晚发型甲基丙二酸血症导致的神经损害严重降低了患者的生活质量,给家庭及社会带来了沉重的负担.了解晚发型甲基丙二酸血症神经损害的各项表现,有利于临床医生发现诊断线索并及早做出正确诊断,这对改善患者预后、降低医疗费用、减轻社会医疗负担有着重要的意义.

Cerebral ischemia,brain tumor,and spinal cord injury (SCI) are the central nerve disease which usually cause irreversible,severe neurologic deficits or death.Inflammation plays a key role in the associated secondary damage after central nervous system (CNS) injury.Epidermal growth factor receptor (EGFR) excessive activation has been closely implicated in the initiation and progression of inflammation.Previous studies have shown that through depressing CNS inflammation,EGFR inhibitors may play a role in the therapeutic treatment of CNS disorders.We mainly reviewed the mechanisms of EGFR signaling pathway activation mediating inflammatory damage in CNS.

Objective To investigate the characteristics of cognitive impairment in chronic subjective tinnitus pa-tients. Methods 103 patients with chronic subjective tinnitus and 52 healthy volunteers were tested by the audiometer to detect the hearing threshold,the tinnitus Handicap Inventory (THI) to assess the severity of tinnitus,the Cognitive Abilities Screening Instrument (CASI) and auditory evoked potential P300 to evaluate cognitive ability. Results There was no sig-nificant difference in CASI sum score between the two groups (P=0. 168). However,the scores of short-term memory (P<0. 001),attention ability (P<0. 001) and orientation ability (P<0. 05) of CASI in tinnitus group were lower than those in control group. Furthermore,tinnitus patients exhibited a longer P300 latency(P<0. 001). The analysis revealed that tinnitus severity (THI score) was negatively correlated with CASI score(r= -0. 873,P<0. 001)and positively correlated with the latency of P300 (r=0. 345,P<0. 001). Conclusion "Short-term memory","Attention" and "Orientation" are the main clinical features of cognitive impairment in chronic subjective tinnitus patients.

Objective: To characterize the microenvironment following blood-spinal cord barrier (BSCB) damage and to evaluate the role of BSCB disruption in secondary damage of spinal cord injury (SCI). Methods: A model of BSCB damage was established by co-culture of primary microvascular endothelial cells and glial cells obtained from rat spinal cord tissue followed by oxygen glucose deprivation/re-oxygenation (OGD/R). Permeability was evaluated by measuring the transendothelial electrical resistance (TEER) and the leakage test of Fluorescein isothiocyanate-dextran (FITC-dextran). The expression of tight junction (TJ) proteins (occludin and zonula occludens-1 (ZO-1) were evaluated by Western blot and immunofluorescence microscopy. Proinflammatory factors (TNF-alpha, iNOS, COX-2 and IL-1 beta), leukocyte chemotactic factors (MIP-l alpha, MIP-1 beta) and leukocyte adhesion factors (ICAM-1, VCAM-1) were detected in the culture medium under different conditions by enzyme-linked immuno sorbent assay (ELISA). Results: The model of BSCB damage induced by OGD/R was successfully constructed. The maximum BSCB permeability occurred 6-12 hours but not within the first 3 h after OGD/R-induced damage. Likewise, the most significant period of TJ protein loss was also detected 6-12 hours after induction. During the hyper-acute period (3 h) following OGD/R-induced damage of BSCB, leukocyte chemotactic factors and leukocyte adhesion factors were significantly increased in the BSCB model. Pro-inflammation factors (TNF-alpha, IL-1 beta, iNOS, COX-2), leukocyte chemotactic factors (MIP-1 alpha, MIP-1 beta) and leukocyte adhesion factors (ICAM-1, VCAM-1) were also sharply produced during the acute period (3-6 hours) and maintained plateau levels 6-12 hours following OGD/R-induced damage, which overlapped with the period of BSCB permeability maximum. A negative linear correlation was observed between the abundance of proinflammatory factors and the expression of TJ proteins (ZO-1 and occludin) and transepithelial electrical resistance (TEER), and a positive linear correlation was found with transendothelial FITC-dextran. Conclusions: Secondary damage continues after primary BSCB damage induced by OGD/R, exhibiting close ties with inflammation injury.