Management of surgical instruments with radio frequency identification tags.

PURPOSE: To prevent malpractices, medical staff has adopted inventory time-outs and/or checklists. Accurate inventory and maintenance of surgical instruments decreases the risk of operating room miscounting and malfunction. In our previous study, an individual management of surgical instruments was accomplished using Radio Frequency Identification (RFID) tags. The purpose of this paper is to evaluate a new management method of RFID-tagged instruments. DESIGN/METHODOLOGY/APPROACH: The management system of RFID-tagged surgical instruments was used for 27 months in clinical areas. In total, 13 study participants assembled surgical trays in the central sterile supply department. FINDINGS: While using the management system, trays were assembled 94 times. During this period, no assembly errors occurred. An instrument malfunction had occurred after the 19th, 56th, and 73 th uses, no malfunction caused by the RFID tags, and usage history had been recorded. Additionally, the time it took to assemble surgical trays was recorded, and the long-term usability of the management system was evaluated. ORIGINALITY/VALUE: The system could record the number of uses and the defective history of each surgical instrument. In addition, the history of the frequency of instruments being transferred from one tray to another was recorded. The results suggest that our system can be used to manage instruments safely. Additionally, the management system was acquired of the learning effect and the usability on daily maintenance. This finding suggests that the management system examined here ensures surgical instrument and tray assembly quality.

Enhanced tumor growth elicited by L-type amino acid transporter 1 in human malignant glioma cells.

OBJECTIVE: To study the expression and function of L-type amino acid transporter 1 (LAT1), a major catalytic subunit of system L that is responsible for the transport of large neutral amino acids, including most essential amino acids, in concert with the covalently bound 4F2 heavy chain, and is implicated in tumorigenesis. METHODS: Human glioma cell lines and tumor specimens were analyzed for LAT1 expression using Western blotting and reverse transcription polymerase chain reaction analysis. The rate of neutral amino acid uptake was measured using L-[C]leucine. The proliferation and apoptosis rates were analyzed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide and terminal deoxynucleotidyl transferase-mediated nick end-labeling assays, respectively, on inhibition of system L by 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid. The effects on proliferation and tumor growth caused by exogenously overexpressed LAT1 were similarly analyzed. RESULTS: LAT1 was expressed in most human high-grade gliomas and glioma cell lines at various levels, with more ubiquitous expression of 4F2 heavy chain. Glioma cells with high LAT1 expression exhibited a marked increase in the uptake rate of L-[C]leucine. 2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid treatment not only suppressed deoxyribonucleic acid synthesis in association with the up-regulation of the cyclin-dependent kinase inhibitor p21 but also enhanced apoptosis with caspase activation, thereby exerting both cytostatic and cytocidal effects in glioma cells with high LAT1 expression levels. Furthermore, overexpression of LAT1 in glioma cells with low endogenous LAT1 expression significantly enhanced the rates of tumor cell growth in athymic mice. CONCLUSION: LAT1, the major transporter of system L, is frequently expressed at higher levels in high-grade gliomas than in low-grade gliomas and brain tissues, and it may play an important role in enhancing the rates of tumor cell proliferation and growth in vivo.

Prognostic significance of O6-methylguanine-DNA methyltransferase protein expression in patients with recurrent glioblastoma treated with temozolomide.

BACKGROUND: Temozolomide (TMZ) is active against newly diagnosed glioblastoma (GBM), and O(6)-methylguanine-DNA methyltransferase (MGMT) is implicated in resistance to TMZ and nitrosoureas. We evaluated the efficacy and safety of the standard 5-day TMZ regimen in patients with recurrent GBM after initial therapy including nitrosourea-based chemotherapy, in conjunction with an analysis of the prognostic value of MGMT protein expression regarding response to TMZ and survival. METHODS: From September 2003 to January 2007, 30 patients having recurrent GBM received 150-200 mg/m(2)/day of TMZ for five consecutive days every 28 days. Tumor tissue from 19 patients was analysed for MGMT protein expression using western blotting, and 17 of them were assessable for a response. RESULTS: The overall response rate was 23.5% (one complete response and three partial responses). Six patients had stable disease (35.3%). Median progression-free survival (PFS) time was 2.2 months, and median overall survival (OS) time was 9.9 months from the initiation of TMZ therapy. Patients with low MGMT protein expression had a significantly improved PFS (P = 0.016) and OS (P = 0.019) compared to those with high expression. Both low MGMT expression (P = 0.040) and re-resection at relapse (P = 0.014) persisted as significant independent favorable prognostic factors for OS. The most common grade 3 and 4 hematological toxicity was lymphopenia (22.2%). CONCLUSIONS: The standard 5-day TMZ regimen resulted in moderate antitumor activity with an acceptable safety profile in patients with nitrosourea-pretreated recurrent GBM, and protein expression of MGMT is an important prognostic factor for patients treated with TMZ even after recurrence.

Oligodendrocyte lineage transcription factor 2 inhibits the motility of a human glial tumor cell line by activating RhoA.

The basic helix-loop-helix transcription factor, oligodendrocyte lineage transcription factor 2 (OLIG2), is specifically expressed in the developing and mature central nervous system and plays an important role in oligodendrogenesis from neural progenitors. It is also expressed in various types of glial tumors, but rarely in glioblastoma. Although we previously showed that OLIG2 expression inhibits glioma cell growth, its role in tumorigenesis remains incompletely understood. Here, we investigated the effect of OLIG2 expression on the migration of the human glioblastoma cell line U12-1. In these cells, OLIG2 expression is controlled by the Tet-off system. Induction of OLIG2 expression inhibited both the migration and invasiveness of U12-1 cells. OLIG2 expression also increased the activity of the GTPase RhoA as well as inducing the cells to form stress fibers and focal adhesions. Experiments using short interfering RNA against p27(Kip1) revealed that up-regulation of the p27(Kip1) protein was not essential for RhoA activation, rather it contributed independently to the decreased motility of OLIG2-expressing U12-1 cells. Alternatively, semiquantitative reverse transcription-PCR analysis revealed that mRNA expression of RhoGAP8, which regulates cell migration, was decreased by OLIG2 expression. Furthermore, expression of C3 transferase, which inhibits Rho via ADP ribosylation, attenuated the OLIG2-induced inhibition of cell motility. Imaging by fluorescence resonance energy transfer revealed that in U12-1 cells lacking OLIG2, the active form of RhoA was localized to protrusions of the cell membrane. In contrast, in OLIG2-expressing cells, it lined almost the entire plasma membrane. Thus, OLIG2 suppresses the motile phenotype of glioblastoma cells by activating RhoA.

Predominant expression of OLIG2 over ID2 in oligodendroglial tumors.

OLIG2 is a basic helix-loop-helix transcription factor regulating the generation of oligodendrocytes from neural progenitor cells, and the function of OLIG2 is inhibited posttranslationally through the interaction with ID2. This study aims to examine if the analysis of OLIG2 and ID2 expression in glioma tissues helps the differential diagnosis of chemosensitive oligodendroglial tumors from astrocytic tumors. Expression levels of OLIG2 and ID2 in 11 oligodendroglial and 27 astrocytic tumors were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR, and immunohistochemistry. The mean expression level of OLIG2 was higher in oligodendroglial tumors than astrocytic tumors, but some astrocytic tumors showed high OLIG2 expression, indicating that OLIG2 cannot be an independent marker of oligodendroglial tumors. No significant difference was observed between ID2 expression in oligodendroglial tumors and astrocytic tumors. It was notable that OLIG2 expression was predominant over ID2 expression in oligodendroglial tumors, while ID2 expression was predominant over OLIG2 expression in astrocytic tumors. Comparative genomic hybridization revealed that gliomas with loss on chromosome 1p, which is closely associated with chemosensitivity, also showed the predominant expression of OLIG2 over ID2. These results indicate that the immunohistochemical study on the relative expression level of OLIG2 to ID2 can be a useful screening for oligodendroglial tumors.

A novel function of OLIG2 to suppress human glial tumor cell growth via p27Kip1 transactivation.

The basic helix-loop-helix transcription factor OLIG2 is specifically expressed in cells of the oligodendrocyte lineage. It is also expressed in various tumors originating from glial cells; however, the expression of OLIG2 is rare or weak in glioblastomas, the most malignant gliomas. The role of OLIG2 in glioma remains unclear. To investigate the function of OLIG2 in glial tumor cells, we have established a glioblastoma cell line, U12-1, in which the expression of OLIG2 is induced by the Tet-off system. Induction of OLIG2 resulted in suppression of both the proliferation and anchorage-independent growth of U12-1. It also resulted in an increase in the expression of p27(Kip1). A luciferase assay revealed that the CTF site of the p27(Kip1) gene promoter was essential for OLIG2-dependent activation of p27(Kip1) gene transcription. Electrophoretic mobility shift assays confirmed that a nuclear extract of OLIG2-expressing U12-1 cells contained a protein complex that binds to the CTF site of the p27(Kip1) gene promoter. Furthermore, siRNA against p27(Kip1) rescued the OLIG2-mediated growth and DNA synthesis inhibition of U12-1 cells. These results indicate that OLIG2 suppresses the proliferation of U12-1 and that this effect is mediated by transactivation of the p27(Kip1) gene, and low expression of OLIG2 may be related to the malignant behavior of human glioblastoma.

Congenital gemistocytic astrocytoma in a fetus.

INTRODUCTION: Congenital brain tumors, especially tumors diagnosed before birth, are very rare. This report presents a case of a congenital gemistocytic astrocytoma diagnosed by antenatal intrauterine ultrasound. CASE REPORT: An intrauterine MRI revealed hydrocephalus and a mass lesion including massive hemorrhage in the right occipital lobe of a fetus. The patient was delivered by cesarean section and a total excision of the hemorrhagic tumor was carried out on the third day of his life. The histological study revealed gemistocytic astrocytoma (WHO grade II). Neither adjuvant chemotherapy nor radiation was given after the first surgery. Ten months after his birth, a recurrent tumor was depicted on follow-up MRI. The second total excision of the recurrent tumor and chemotherapy using cisplatin and vincristine were performed. OUTCOME: The patient is free of disease at the age of 2 years and 6 months.

Clinico-pathological features of pilomyxoid astrocytoma of the optic pathway.

Five cases of pilomyxoid astrocytoma (PmA) characterized by a monophasic pattern with a myxoid background were selected for a clinicopathological study from 23 cases previously diagnosed as pilocytic astrocytoma (PA). All PmA patients were either infants or young children (mean age 2.1 years), and all tumors were located in the optic chiasm/hypothalamus region. All cases received chemotherapy, which reduced tumor size, and the location of the tumor became confined to the optic chiasm. In two cases, tumor recurrence occurred 3 and 7 years after chemotherapy. Histology of the recurrent tumors showed the biphasic pattern of classical PA. Hence, we conclude that PmA might be an infantile form of PA and speculate that a subset of PmA in the optic pathway/hypothalamus originates from the optic chiasm, possibly derived from radial glia existing in the embryonic optic chiasm.

Clear cell ependymoma of the fourth ventricle.

Two cases of clear cell ependymoma (CCE) of the fourth ventricle are reported in a 49-year-old woman with dysphagia and a 59-year-old woman with dizziness and gait disturbance. CCE is a relatively new variant of ependymoma added to the WHO classification of tumors in 1993. Tumor cells display an oligodendroglioma-like appearance with a clear perinuclear halo. Most infratentorial CCE tumors are located in the cerebellum. There are only three cases, including the present two cases, that have been reported to affect the fourth ventricle.

High uptake on 11C-methionine positron emission tomographic scan of basal ganglia germinoma with cerebral hemiatrophy.

We herein describe a 12-year-old male patient with a germinoma of the basal ganglia who presented with progressive hemiparesis. MR imaging showed ipsilateral cerebral hemiatrophy predominantly in the left basal ganglia, whereas no mass or enhancement was depicted. Single photon emission CT revealed no significant uptake of thallium, whereas (11)C-methionine positron emission tomography showed clearly discernible uptake in the left putamen. Stereotactic biopsy, referencing the results of (11)C-methionine positron emission tomography, was performed, allowing histologic verification of germinoma to be established. (11)C-methionine positron emission tomography was the only technique that indicated the precise localization of the tumor in our patient and enabled biopsy-based final diagnosis of the basal ganglia germinoma without any overt mass formation.

Expression of the oligodendroglial lineage-associated markers Olig1 and Olig2 in different types of human gliomas.

Because a specific group of oligodendrogliomas is susceptible to adjuvant therapy, it is important to elucidate the biological characteristics of these tumors. In situ hybridization analyses have revealed that Olig genes are expressed in oligodendroglial lineage cells and are highly expressed in oligodendrogliomas. To clarify whether OLIG is a tumor-specific marker for oligodendrogliomas, we have investigated the expression of Olig transcripts by semiquantitative RT-PCR assay and OLIG2 protein with a new antibody in a variety of glial tumors. The semiquantitative RT-PCR revealed that high levels of expression of Olig1 and Olig2 mRNAs were present in anaplastic oligodendrogliomas and anaplastic astrocytomas, while expression of these mRNAs in grade IV glioblastomas was lower than in grade II and grade III gliomas (p < 0.01). Immunohistochemical analyses demonstrated that the mean immunopositive proportion of OLIG2 was 82% in anaplastic oligodendrogliomas but only 34% in anaplastic astrocytomas. Therefore, although OLIG2 expression was detected in a range of gliomas not specific for oligodendrogliomas, the expression level in anaplastic oligodendrogliomas was more uniform and intense than that in other glial tumors. In conclusion, combining Olig mRNA expression and immunohistochemistry of OLIG2 enables oligodendrogliomas to be distinguished from glioblastomas and other astrocytic glial tumors.