Publications by authors named "K Tokiyoshi"

Article Synopsis
  • The study introduces MS-DIAL 5, a software designed for analyzing complex mass spectrometry data to better understand lipid structures and localization, integrating a species-specific lipidome database for enhanced accuracy.* -
  • With optimized settings, MS-DIAL 5 accurately identified lipid structures for 96.4% of tested standards and effectively assigned specific positions in lipids, particularly for complex molecules found in the eye.* -
  • The research also identified an enzyme (glycerol 3-phosphate acyltransferase) linked to the incorporation of important fatty acids into lipids, using both mass spectrometry techniques and experimental validation.*
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Article Synopsis
  • - This study focuses on enhancing untargeted lipidomics using fast liquid chromatography (LC) and tandem mass spectrometry (MS) by combining data-dependent acquisition (DDA) and SWATH-DIA techniques for better lipid annotation rates.
  • - A new workflow is presented that utilizes an 8.6-minute LC gradient and employs quality control samples with various SWATH-DIA methods to address MS signal drift, leading to improved data quality.
  • - The approach significantly increases lipid annotation coverage by 1.7 times compared to conventional methods, identifying 95.3% of lipids, which benefits both large-scale and small-scale research, impacting clinical applications and basic biology.
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Common regions of deletion(s) on chromosome 22q and the correlations between loss of heterozygosity and patient survival were analysed in 18 deoxyribonucleic acid samples from astrocytic tumors (3 astrocytomas, 5 anaplastic astrocytomas, and 11 glioblastomas) and matched normal brain tissues. The polymerase chain reaction products using five microsatellite markers were electrophoresed on polyacrylamide gels and the ethidium bromide stained bands were photographed. Loss of heterozygosity was observed in 14 (74%) of 19 samples, with similar incidences in astrocytomas, anaplastic astrocytomas, and glioblastomas (67%, 80%, and 82%, respectively).

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To prognosticate the implications of various allelic losses on chromosome 17 in the morphology and biology of astrocytic tumors, we have examined loss of heterozygosity (LOH) at 14 microsatellite loci on chromosome 17 in a series of 19 astrocytic tumors (3 astrocytomas, 5 anaplastic astrocytomas, and 11 glioblastomas). The DNA samples extracted from tumor and matched normal brain tissue were amplified by polymerase chain reaction (PCR) followed by polyacrylamide gel electrophoresis and photography under UV transillumination. The molecular genetic data were compared with immunohistochemistry performed with antibodies to glial fibrillary acidic protein (GFAP), MIB-1 and p53 protein.

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We analyzed 19 samples of various astrocytic tumors (3 astrocytomas, 5 anaplastic astrocytomas, and 11 glioblastomas) for loss of heterozygosity (LOH) on chromosome 9p at 6 microsatellite loci (D9S54, IFNA, D9S171, D9S104, D9S165, and D9S166). Polymerase chain reaction was performed and the products were electrophoresed on polyacrylamide gel. As many as 16 of the 19 samples (84%) exhibited LOH.

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