COMPARISON OF CHLOROPHYLL A AND THE ALGAL GROWTH POTENTIAL IN THE WEST LAKE

The present work studied environmental factors, such as temperature, nitrogen, phosphorus, chlorophyll a and transparency of the West Lake. Algal growth potential test (AGP) was performed to determine the influence of the environment elements on the potential of algal growth, and to explain what conditions were necessary for algal reproduction.Article信州大学理学部附属諏訪臨湖実験所報告 11: 35-39(1999)departmental bulletin pape

自然発症慢性膵炎WBN/KobラットにおけるTumor Protein p53-Induced Nuclear Protein1(TP53INP1)の発現 : 動態と抗膵炎薬の効果

取得学位 : 博士（医学）, 学位授与番号 : 医博甲第1741号 , 学位授与年月日 : 平成18年3月22日, 学位授与大学 : 金沢大

How tyramine β-hydroxylase controls the production of octopamine, modulating the mobility of beetles

Biogenic amines perform many kinds of important physiological functions in the central nervous system (CNS) of insects, acting as neuromodulators, neurotransmitters, and neurohormones. The five most abundant types of biogenic amines in invertebrates are dopamine, histamine, serotonin, tyramine, and octopamine (OA). However, in beetles, an important group of model and pest insects, the role of tyramine beta-hydroxylase (T beta H) in the OA biosynthesis pathway and the regulation of behavior remains unknown so far. We therefore investigated the molecular characterization and spatiotemporal expression profiles of T beta H in red flour beetles (Triboliun castaneum). Most importantly, we detected the production of OA and measured the crawling speed of beetles after dsTcT beta H injection. We concluded that TcT beta H controls the biosynthesis amount of OA in the CNS, and this in turn modulates the mobility of the beetles. Our new results provided basic information about the key genes in the OA biosynthesis pathway of the beetles, and expanded our knowledge on the physiological functions of OA in insects

Micro-patterned TiO2 films for photocatalysis

Titanium dioxide film as a stable material plays an important role in photocatalytic degradation of pollutants. One of the ways to improve photocatalytic efficiency is to increase the active sites on the semiconductor surface. Photolithography is a manufacturing technique for controlling precisely micrographics on surface. Here grating-structured, square-structured and hexagon-structured TiO2 films were prepared by photolithography and the effects of various surface structures on photocatalysis were studied. It was demonstrated that the photocatalytic activity of TiO2 film was not always improved as the surface area increased. The micro-patterned surface would also impede the mass transfer in the process of photocatalysis. (C) 2019 Elsevier B.V. All rights reserved

Effect of gemcitabine on the expression of apoptosis-related genes in human pancreatic cancer cells

金沢大学がん研究所分子標的がん医療研究開発センターAim: To investigate the expression of genes involved in the gemcitabine-induced cytotoxicity in human pancreatic cancer cells. Methods: A human pancreatic cancer cell line, PANC-1, was cultured. 1 × 104 PANC-1 cells were plated in 96-well microtiter plates. After being incubated for 24 h, gemcitabine was added to the medium at concentrations ranging 2.5 -1 000 mg/L. The AlamarBlue dye method was used for cell growth analysis. DNA fragmentation was quantitatively assayed using a DNA fragmentation enzyme-linked immunosorbent assay (ELISA) kit. PAP and TP53INP1 mRNA expression was determined using the reverse transcription-polymerase chain reaction with semi-quantitative analysis. The expression of GSK-3β and phospho-GSK-3β proteins was examined with Western blot analysis. Results: The IC50 for the drug after a 48-h exposure to gemcitabine was 16 mg/L. The growth of PANC-1 cells was inhibited by gemcitabine in a concentration-dependent manner (P< 0.0001) and the cell growth was also inhibited throughout the time course (P<0.0001). The DNA fragmentation rate in the gemcitabine-treated group at 48 h was 44.7 %, whereas it was 25.3 % in the untreated group. The PAP mRNA expression was decreased after being treated with gemcitabine, whereas the TP53INP1 mRNA was increased by the gemcitabine treatment. Western blot analysis showed that phospho-GSK-3βser9 was induced by the gemcitabine treatment. Conclusion: Gemcitabine suppresses PANC-1 cell proliferation and induces apoptosis. Apoptosis is considered to be associated with the inhibition of PAP and GSK-3β, and the activation of TP53INP1 and pospho-GSK-3βser9. © 2006 The WJG Press. All rights reserved

Effect of gemcitabine on the expression of apoptosis-related genes in human pancreatic cancer cells.

金沢大学がん研究所Aim: To investigate the expression of genes involved in the gemcitabine-induced cytotoxicity in human pancreatic cancer cells. Methods: A human pancreatic cancer cell line, PANC-1, was cultured. 1 × 104 PANC-1 cells were plated in 96-well microtiter plates. After being incubated for 24 h, gemcitabine was added to the medium at concentrations ranging 2.5 -1 000 mg/L. The AlamarBlue dye method was used for cell growth analysis. DNA fragmentation was quantitatively assayed using a DNA fragmentation enzyme-linked immunosorbent assay (ELISA) kit. PAP and TP53INP1 mRNA expression was determined using the reverse transcription-polymerase chain reaction with semi-quantitative analysis. The expression of GSK-3β and phospho-GSK-3β proteins was examined with Western blot analysis. Results: The IC50 for the drug after a 48-h exposure to gemcitabine was 16 mg/L. The growth of PANC-1 cells was inhibited by gemcitabine in a concentration-dependent manner (P< 0.0001) and the cell growth was also inhibited throughout the time course (P<0.0001). The DNA fragmentation rate in the gemcitabine-treated group at 48 h was 44.7 %, whereas it was 25.3 % in the untreated group. The PAP mRNA expression was decreased after being treated with gemcitabine, whereas the TP53INP1 mRNA was increased by the gemcitabine treatment. Western blot analysis showed that phospho-GSK-3βser9 was induced by the gemcitabine treatment. Conclusion: Gemcitabine suppresses PANC-1 cell proliferation and induces apoptosis. Apoptosis is considered to be associated with the inhibition of PAP and GSK-3β, and the activation of TP53INP1 and pospho-GSK-3βser9. © 2006 The WJG Press. All rights reserved