Radical-induced ionic polymerization in the presence of maleic anhydride. I. Mechanism of polymerization of maleic anhydride by radical initiators

Three kinds of trapped radicals are observed in poly(maleic anhydride) (Poly-MAH) which were prepared by the use of radical initiators such as AIBN or BPO. It was found that these radicals were transformed to the active species so as to initiate the cationic polymerization. The structure of these radicals was studied by the ESR and the kinetic analysis of MAH polymerization in the presence of various additives.     

PVC、EPR和CSM材料辐照后热氧化降解的反应动力学分析

采用气相色谱定量测量了聚氯乙烯(PVC)、乙丙橡胶(EPR)和氯磺化聚乙烯(CSM)等线缆绝缘材料经辐照后在不同温度下热老化过程中的O2消耗量.对实验数据进行了反应动力学分析,发现线缆绝缘材料的热氧化降解反应为一级反应.同时获得了不同温度下的反应常数,并与根据Arrhenius 方程计算的理论结果进行了比较.     

Downregulation of miR-122-5p Activates Glycolysis via PKM2 in Kupffer Cells of Rat and Mouse Models of Non-Alcoholic Steatohepatitis

Non-alcoholic steatohepatitis (NASH) has pathological characteristics similar to those of alcoholic hepatitis, despite the absence of a drinking history. The greatest threat associated with NASH is its progression to cirrhosis and hepatocellular carcinoma. The pathophysiology of NASH is not fully understood to date. In this study, we investigated the pathophysiology of NASH from the perspective of glycolysis and the Warburg effect, with a particular focus on microRNA regulation in liver-specific macrophages, also known as Kupffer cells. We established NASH rat and mouse models and evaluated various parameters including the liver-to-body weight ratio, blood indexes, and histopathology. A quantitative phosphoproteomic analysis of the NASH rat model livers revealed the activation of glycolysis. Western blotting and immunohistochemistry results indicated that the expression of pyruvate kinase muscle 2 (PKM2), a rate-limiting enzyme of glycolysis, was upregulated in the liver tissues of both NASH models. Moreover, increases in PKM2 and p-PKM2 were observed in the early phase of NASH. These observations were partially induced by the downregulation of microRNA122-5p (miR-122-5p) and occurred particularly in the Kupffer cells. Our results suggest that the activation of glycolysis in Kupffer cells during NASH was partially induced by the upregulation of PKM2 via miR-122-5p suppression.     

Mutated KIT Tyrosine Kinase as a Novel Molecular Target in Acute Myeloid Leukemia

KIT is a type-III receptor tyrosine kinase that contributes to cell signaling in various cells. Since KIT is activated by overexpression or mutation and plays an important role in the development of some cancers, such as gastrointestinal stromal tumors and mast cell disease, molecular therapies targeting KIT mutations are being developed. In acute myeloid leukemia (AML), genome profiling via next-generation sequencing has shown that several genes that are mutated in patients with AML impact patients’ prognosis. Moreover, it was suggested that precision-medicine-based treatment using genomic data will improve treatment outcomes for AML patients. This paper presents (1) previous studies regarding the role of KIT mutations in AML, (2) the data in AML with KIT mutations from the HM-SCREEN-Japan-01 study, a genome profiling study for patients newly diagnosed with AML who are unsuitable for the standard first-line treatment (unfit) or have relapsed/refractory AML, and (3) new therapies targeting KIT mutations, such as tyrosine kinase inhibitors and heat shock protein 90 inhibitors. In this era when genome profiling via next-generation sequencing is becoming more common, KIT mutations are attractive novel molecular targets in AML.     

The quantum relative entropy as a rate function and information criteria

We prove that the quantum relative entropy is a rate function in large deviation principle. Next, we define information criteria for quantum states and estimate the accuracy of the use of them. Most of the results in this paper are essentially based on Hiai-Ohya-Tsukada theorem.

     

An integrated photodetector-amplifier using a-Si p-i-n photodiodesand poly-Si thin-film transistors

The authors propose a photodetector-amplifier circuit consisting of a bridge photodetector circuit and a CMOS differential amplifier, both monolithically integrated on a transparent substrate. A test circuit was fabricated using a-Si p-i-n photodiodes and poly-Si thin-film transistors on a quartz substrate. A clear effect of the differential amplifier was demonstrated in the test circuit. It is shown that the circuit performance can be controlled by changing the bias current of the differential amplifier. With a relatively low bias current on the order of 10^-11 A, the circuit works digitally with output voltages either close to 0 V or V_DD. The power consumption of the circuit is approximately 60 μW, which is low enough for use in two-dimensional arrays