[Analysis of misdiagnosis causes of suprasellar arachnoid cysts].

Objective: To investigate the causes of misdiagnosis of suprasellar arachnoid cysts, analyze its characteristics and put forward the diagnostic basis and differential points. Methods: The clinical data fo 97 cases of suprasellar arachnoid cysts diagnosed and treated in the neurosurgery department of Beijing Tiantan Hospital and Hebei General Hospital from March 2015 to March 2019 were analyzed retrospectively. All patients underwent CT and MRI scans with obstructive hydrocephalus. 13 cases were misdiagnosed, including 7 males and 6 females. First visit age 1-31 years old, with an average age of 6.3 years. There were 10 patients younger than 6 years old. The remaining 15-year-old patients, 31-year-old patients and 26-year-old patients each have one case. 11 cases were misdiagnosed as obstructive hydrocephalus, 2 cases as cystic craniopharyngioma. Results: 13 cases were misdiagnosed and mistreated, 11 cases were treated with intraventricular and abdominal shunt, 9 cases were treated with neuroendoscopy and recovered well. One cases of intracranial hematomas underwent craniotomy again, the hematomas were removed again and the bone slise were decompressed. One case had fissured stable after shunt. There were no operative deaths and no complications in this group. After endoscopic reoperation, CT and/or MRI scans showed that the ventricle narrowed in varying degrees, some of them returned to normal size and the flow of cerebrospinal fluid (cerebrospinal fluid) was unobstruct at the end of magnetic resonance cerebrospinal fluid angiography (MRI) fistula after endoscopic reoperation. Conclusions: The incidence of suprasellar arachnoid cysts is low, it is rare in clinic and it is easy to misdiagnose and mistreate. At present, it is recognized that the best treatment methods are partial resection of endoscope cyst wall, cyst ventricle fistula and third ventricle floor fisthla.

Immunization with dendritic cells pulsed with tumor extract increases survival of mice bearing intracranial gliomas.

The purpose of this study is to investigate the efficacy of dendritic cell-mediated immunotherapy against intracranial gliomas. Cloned DC2.4 dendritic cells originating from C57BL/6 mice were pulsed with glioma GL261 cell extracts and administered i.p. to C57BL/6 mice with intracranial GL261 gliomas. The survival of mice with and without pulsed dendritic cells was monitored after intracranial implantation of the GL261 glioma cells. Fluorescence activated cell sorting (FACS) analysis showed that DC2.4 cells express high levels of MHC class I and class II molecules, costimulatory molecules B7-1 and B7-2, and the cell adhesion molecule ICAM-1. Antigen-presenting capabilities in these dendritic cells were initially characterized in vitro by a mixed lymphocyte reaction, showing that Balb/c CD4+ and CD8+ T cells were able to generate allogeneic responses to DC2.4 cells. Tumor extract-pulsed DC2.4 dendritic cells were then used for the treatment of C57BL/6 mice with syngeneic GL261 gliomas. Animals with intracranial GL261 gliomas and vaccinated i.p. with pulsed DC2.4 dendritic cells exhibited significantly enhanced survival, relative to animals treated with saline or non-pulsed DC2.4 cells alone. In addition, cured animals showed an increased delayed-type hypersensitivity response to GL261 cells and survived when rechallenged with intracranial GL261 gliomas. In summary these results indicate that dendritic cells pulsed with tumor extract can enhance immune responses to tumor antigen and therefore represent a potential immunotherapeutic approach for treating patients with intracranial gliomas.

In vitro efficacy of recombinant diphtheria toxin-murine interleukin-4 immunoconjugate on mouse glioblastoma and neuroblastoma cell lines and the additive effect of radiation.

OBJECT: The prognosis for patients with primary malignant brain tumors is poor despite aggressive treatment, and tumor recurrence is common regardless of the chosen therapy. Although multimodal treatment does not provide a cure, it is necessary to determine which treatment modalities have the greatest cytotoxic effect and can potentially prolong survival. Immunotoxin therapy is a novel approach for the treatment of tumors, and it has been successfully used in the central nervous system. Because the interleukin (IL)-4 receptor is commonly expressed on brain tumor cells, the purpose of this study was to evaluate the cytotoxic effect of using a modified diphtheria toxin-murine IL-4 (DT390- mIL4) immunoconjugate for the treatment of murine brain tumor cell lines and to determine whether the addition of radiation therapy could potentiate the effect of this agent. METHODS: Spontaneous murine glioblastoma (SMA-560) and two neuroblastoma (Neuro-2a and NB41A3) cell lines were treated using DT390-mIL4 at different concentrations, and the anti-mouse IL-4 monoclonal antibody (11B11) was used for blocking its cytotoxicity. Other SMA-560 and Neuro-2a cell lines were treated using 500 cGy of radiation 3 hours before DT390-mIL4 treatment. Cytotoxity was evaluated using a trypan blue viability assay. The immunoconjugate exhibited a dose-dependent cytotoxic effect with 50% inhibitory concentration values of 0.56 x 10(-9) M in SMA-560, 1.28 x 10(-9) M in Neuro-2a, and 0.95 x (-10) M in NB41A3 cell lines. The cytotoxicity of DT390-mIL4 was specifically blocked by an excess of 11B11. Cytotoxicity was additive when the DT390-mIL4 at 10(-9) M immunoconjugate administration was followed by radiation therapy. CONCLUSIONS: These results indicate that the IL-4 receptor can be a target for diphtheria toxin fusion proteins and that radiation can potentiate the effects of DT390-mIL4. The development of multimodal approaches to treat malignant brain tumors with agents that have different mechanisms of action may be beneficial.

Phosphatidylinositol 3 kinase activity is not essential for B7-1-mediated costimulation of proliferation or development of cytotoxicity in murine T cells.

It has been suggested that induction of phosphatidylinositol (PI) 3 kinase activity upon CD28 costimulation may contribute to CD28-mediated signaling. In this report, T cell stimulation by microspheres bearing coimmobilized anti-TCR mAb and purified B7-1 ligand was examined. This approach allows study of cosignaling mediated by CD28 interaction with its native ligand in the absence of potentially confounding contributions from other receptor-ligand interactions. For murine CD4+ and CD8+ T cells, costimulation with B7-1 up-regulated PI3 kinase activity assayed in vitro, and this was blocked by treatment of the cells with wortmannin, a specific inhibitor of PI3 kinase, before stimulation. However, wortmannin failed to inhibit B7-1-dependent T cell proliferation or development of cytotoxicity in CD8+ cells. These results indicate that the enzymatic activity of PI3 kinase is not essential in the CD28-mediated signaling involved in the costimulation of proliferation or induction of CTL activity in precursor CTL.