A Calculation Method of Deposition Profiles in CVD Reactors Using Genetic Algorithms

AbstractIn this study, we introduced a novel and generalized calculation method to reproduce the deposition profiles in various types of chemical vapor deposition reactors. Robust and accurate calculations along with reduced computing cost were achieved by this method. Both boundary value problems and initial value problems for estimating the mass balance equations of the deposition species by iterations of numerical integrations were changed into problems of finding the linear combinations consisting of a few “basis functions,” which are inherent in the reactors and deposition species. The coefficients of the linear combinations were optimized using genetic algorithms. We could demonstrate the validity of the proposed method using various examples of the reaction mechanisms and conditions

OCTAD-S: Digital Fast Fourier Transform Spectrometers by FPGA

We have developed a digital fast Fourier transform (FFT) spectrometer made of an analog-to-digital converter (ADC) and a field-programmable gate array (FPGA). The base instrument has independent ADC and FPGA modules, which allow us to implement different spectrometers in a relatively easy manner. Two types of spectrometers have been instrumented, one with 4.096 GS/s sampling speed and 2048 frequency channels and the other with 2.048 GS/s sampling speed and 32768 frequency channels. The signal processing in these spectrometers has no dead time and the accumulated spectra are recorded in external media every 8 ms. A direct sampling spectroscopy up to 8 GHz is achieved by a microwave track-and-hold circuit, which can reduce the analog receiver in front of the spectrometer. Highly stable spectroscopy with a wide dynamic range was demonstrated in a series of laboratory experiments and test observations of solar radio bursts.Comment: 20 pages, 7 figures, accepted for publication in Earth, Planets and Spac

Infrequent RAS mutation is not associated with specific histological phenotype in gliomas

BACKGROUND: Mutations in driver genes such as IDH and BRAF have been identified in gliomas. Meanwhile, dysregulations in the p53, RB1, and MAPK and/or PI3K pathways are involved in the molecular pathogenesis of glioblastoma. RAS family genes activate MAPK through activation of RAF and PI3K to promote cell proliferation. RAS mutations are a well-known driver of mutation in many types of cancers, but knowledge of their significance for glioma is insufficient. The purpose of this study was to reveal the frequency and the clinical phenotype of RAS mutant in gliomas. METHODS: This study analysed RAS mutations and their clinical significance in 242 gliomas that were stored as unfixed or cryopreserved specimens removed at Kyoto University and Osaka National Hospital between May 2006 and October 2017. The hot spots mutation of IDH1/2, H3F3A, HIST1H3B, and TERT promoter and exon 2 and exon 3 of KRAS, HRAS, and NRAS were analysed with Sanger sequencing method, and 1p/19q codeletion was analysed with multiplex ligation-dependent probe amplification. DNA methylation array was performed in some RAS mutant tumours to improve accuracy of diagnosis. RESULTS: RAS mutations were identified in four gliomas with three KRAS mutations and one NRAS mutation in one anaplastic oligodendroglioma, two anaplastic astrocytomas (IDH wild-type in each), and one ganglioglioma. RAS-mutant gliomas were identified with various types of glioma histology. CONCLUSION: RAS mutation appears infrequent, and it is not associated with any specific histological phenotype of glioma

Activated leukocyte cell adhesion molecule expression correlates with the WNT subgroup in medulloblastoma and is involved in regulating tumor cell proliferation and invasion.

Cluster of differentiation (CD) 166 or activated leukocyte cell adhesion molecule (ALCAM) is a transmembrane molecule known to be an intercellular adhesion factor. The expression and function of ALCAM in medulloblastoma (MB), a pediatric brain tumor with highly advanced molecular genetics, remains unclear. Therefore, this study aimed to clarify the significance and functional role of ALCAM expression in MB. ALCAM expression in 45 patients with MB was evaluated by immunohistochemical analysis of formalin-fixed paraffin-embedded clinical specimens and the relationship between ALCAM expression and pathological type/molecular subgroup, such as WNT, SHH, Group 3, and Group 4, was examined. Eight ALCAM positive (18%), seven partially positive (16%), and 30 negative (67%) cases were detected. All seven cases of the WNT molecular subgroup were ALCAM positive and ALCAM expression strongly correlated with this subgroup (P < 0.0001). In addition, functional studies using MB cell lines revealed ALCAM expression affected proliferation and migration as a positive regulator in vitro. However, ALCAM silencing did not affect survival or the formation of leptomeningeal dissemination in an orthotopic mouse model, but did induce a malignant phenotype with increased tumor cell invasion at the dissemination sites (P = 0.0029). In conclusion, our results revealed that ALCAM exhibited highly specific expression in the WNT subgroup of MB. Furthermore, we demonstrated that the cell kinetics of MB cell lines can be altered by the expression of ALCAM