脑胶质瘤( Glioma )是最常见的颅内肿瘤〔1〕,约占颅内原发肿瘤的一半,其恶性率是全身肿瘤的2％ ～3％ 〔2〕.Glioma 可分为低级别胶质瘤和高级别胶质瘤.高级别胶质瘤具有迅速性侵袭生长、血管不正常增生、容易破坏脑组织等生物学特性,这使得恶性胶质瘤治疗难度大,且预后较差.胶质母细胞瘤( GBM)是常见的脑恶性肿瘤,经过系统治疗后其中位生存时间仍少于15个月〔3,4〕.目前,GBM经过手术、放化疗等治疗后效果仍达不到患者及家属的心理预期.本文对Glioma治疗现状及临床进展进行综述.

Background Radiation therapy is the primary method of treatment for glioblastoma (GBM). Therefore, the suppression of radioresistance in GBM cells is of enormous significance. Ribophorin II (RPN2), a protein component of an N-oligosaccharyl transferase complex, has been associated with chemotherapy drug resistance in multiple cancers, including GBM. However, it remains unclear whether this also plays a role in radiation therapy resistance in GBM. Methods We conducted a bioinformatic analysis of RPN2 expression using the UCSC Cancer Genomics Browser and GEPIA database and performed an immunohistochemical assessment of RPN2 expression in biopsy specimens from 34 GBM patients who had received radiation-based therapy. We also studied the expression and function of RPN2 in radiation-resistant GBM cells. Results We found that RPN2 expression was upregulated in GBM tumors and correlated with poor survival. The expression of RPN2 was also higher in GBM patients with tumor recurrence, who were classified to be resistant to radiation therapy. In the radiation-resistant GBM cells, the expression of RPN2 was also higher than in the parental cells. Depletion of RPN2 in resistant cells can sensitize these cells to radiation-induced apoptosis, and overexpression of RPN2 had the reverse effect. Myeloid cell leukemia 1 (MCL1) was found to be the downstream target of RPN2, and contributed to radiation resistance in GBM cells. Furthermore, STAT3 was found to be the regulator of MCL1, which can be activated by RPN2 dysregulation. Conclusion Our study has revealed a novel function of RPN2 in radiation-resistant GBM, and has shown that MCL1 depletion or suppression could be a promising method of therapy to overcome the resistance promoted by RPN2 dysregulation.

Objective To investigate the effects of interleukin-2 ( IL-2 ) activated NK cells on gliomas in animal models. Methods The nude mice were divided into seven groups. A:sterile nude mice control group;B:in vivo transplan-tation GBM group;C:in vivo injection of IL-2 group;D:injection of NK cells group;E:simultaneous transplantation of BGM tissue and NK cells group;F:simultaneous transplantation of IL-2 and NK cells group;G:simultaneoustransplantation of BGM,NK cells and IL-2 group. To observe the growth of nude mice,the growth of tumor in nude mice,the emergence time of the tumor,the growth of the tumor ( size and weight) data etc,and carry out statistical analysis. Results NK cells have hadinhibition and killing effect on GBM,and IL-2 can promote the inhibition and killing effect of NK cells on GBM,and can coulddelay the growth of glioma. Conclusion NK cells have the effect of inhibiting the human brain glioma and lay the foundation for the clinical immunotherapy of glioma.

颅脑外伤（Traumatic Brain Injury,TBI）)是神经外科中常见的多发病,其治疗过程中出现低钠血症是较为常见的电解质紊乱 [1] 。轻度的低钠患者会出现疲倦乏力和性格改变,严重的低钠血症会导致意识改变或癫痫发作,有时候会诱发心律失常甚至导致患者死亡 [2] 。因此,对TBI患者密切关注其离子变化情况,病因诊断及制定科学的诊疗计划有重

Objective To study the water channel protein 4 (Aquaporins-4,AQP4) in the genetic rule of hydrocephalus rats,to explore the role of AQP4 inherited in hydrocephalus.WTHZMethods By randomly selecting not seen hydrocephalus AQP4 knockout mice AQP4 knockout female mating,with its F1,F2,F3 generations to establish genetic map,genetic study on its rule.Extracting total RNA of brain tissue,making its role in the genetic gene chip research.Results In the phenotype of AQP4 knockout is heritable and has nothing to do with sex,at the same time is not a single gene heredity,and for euchromosome inheritance;Entirely on gene chip showed that AQP4 knock out mice under the background of the occurrence of hydrocephalus phenotype with the participation of other genes.Conclusion By making genetic map and gene chip in mice,prove that AQP4 has important role in the pathogenesis of congenital hydrocephalus.

生长激素（ GH）型垂体腺瘤是缓慢进展的疾病，临床主要表现为巨人症和肢端肥大症，且具有侵袭性生长的倾向，特别是对视交叉，视丘下部及海绵窦的侵犯，单独手术很难治愈，其手术治疗肿瘤复发率达20％～50％〔1〕。放射治疗是垂体瘤治疗的重要手段之一，包括常规放射和立体定向放射。对于控制肿瘤生长、减少肿瘤复发、改善内分泌功能有积极作用。

This case report deals with multiple intracranial metastatic tumors and studies of expression and regulation characteristics of aquaporins (AQPs) of cerebellar metastatic tumor and brain tissue surrounding tumor. In this work, we try to understand the role of abnormal expression of AQPs in formation and elimination of brain edema and provide new ideas for the treatment of brain edema induced by tumor. The work involves resection of intracranial occupying lesions to get cerebellar metastatic tumor organization. Total RNA was extracted, RT-PCR was done, and immunohistochemical staining was done to study the expression and regulation characteristics of AQPs. We found that AQP4 had a high expression in the peritumoral brain tissue and no expression in the center of brain metastasis tumor organization. Around the tumor tissue, the AQP4 staining was junior in the more distant region from tumor and it added significantly in close to the tumor tissue region. It demonstrated that the AQP4 expression was upregulated, obviously with the distance drawing near gradually to tumor tissue. In addition, stained AQP1 was not observed on cerebellar metastatic tumor and peritumoral brain microvascular endothelial cells. The phenomenon that AQP4 had an increased expression in the surrounding region of cerebellar metastatic tumor and, moreover, increased significantly in the region next to the cerebellar metastatic tumor tightly is probably related to the formation of peritumoral brain edema and plays an important role in cytotoxic brain edema mechanism. AQP1 was not expressed on cerebellar metastatic tumor and peritumoral brain tissue microvascular endothelial cells, and this may be an important factor that the peritumoral interstitial brain edema is removed ineffectively to cause ‘small tumor, big edema.’

脑心综合征是指脑出血、蛛网膜下腔出血、急性颅脑外伤等原因致使下丘脑、脑干自主神经中枢受到影响,临床症状和心电图表现出类似急性心肌梗死、心内膜下出血、心肌缺血、心律失常或心力衰竭的症状.当脑部疾病得到控制或好转后心脏病症状及心电图异常情况随之改善甚至消失[1].其主要表现包括心电图改变、心律失常、心肌酶活性升高、心功能障碍及心率改变等[2].这种心脏损害对脑出血预后影响较大,甚至可导致患者猝死.近年来,临床医师越来越关注急性脑出血后心电图及心肌酶的变化,并将其作为衡量脑出血严重程度的指标和判断脑出血预后的因素.

OBJECTIVE To explore the risk factors for pulmonary infection in postoperative coma patients complicated by cerebral hemorrhage after tracheotomy and the measures of prevention and control.METHODS From Jan.2010 to Jan.2011,medical records of 187 patients with intracerebral hemorrhage after tracheotomy were retrospectively reviewed and prospectively monitored.RESULTS Among 187 cases,69 cases suffered from hospital infections,62 of 69 suffered from lung infection with the infection rate of 33.15%.The pulmonary infection rate of the patients aged ≥45(42.45%) was significantly higher than that of the patients aged 45(6.25%)(P0.05).Patients with tracheotomy time≥5 d(36.31%) were higher than those 5 d(5.26%)(P0.05);the patients with suction(37.03%) were higher than patients without(8.00%)(P0.05),the pulmonary infection rate of the patients with smoking history combined with COPD was 58.59%,statistically different(P0.05)compared with the patients without smoking history.CONCLUSION Invasive operations such as inhalation,endotracheal intubation,tracheotomy and use of ventilator are the predominant risks for pulmonary infection after tracheotomy.Risk factors should be monitored and controlled to effectively reduce the incidence of pulmonary tract infection and the mortality of cerebral hemorrhage postoperative coma patients.

老年糖尿病是指年龄≥60岁的糖尿病患者,按发病时间可分为老年期起病的糖尿病和青壮年起病而延续至老年期者.目前我国成人糖尿病患病率为3%,其中60岁以上的人群中占5%,随着我国人口老龄化,老年糖尿病已成为危害老年人健康的常见病之一.