Metal-free isotactic-specific radical polymerization of N-isopropylacrylamide with pyridine N-oxide derivatives : the effect of methyl substituents of pyridine N-oxide on the isotactic-specificity and the proposed mechanism for the isotactic-specific radical polymerization

The radical polymerizations of N-isopropylacrylamide (NIPAAm) in chloroform at low temperatures in the presence of pyridine N-oxide (PNO) derivatives were investigated. It was found that the methylation at meta-positions of PNO improved the isotactic-specificity induced by PNO, whereas the methylation at ortho-positions prevented the induction of the isotactic-specificity. NMR analysis revealed that NIPAAm and PNO derivatives formed predominantly 2:1 complex through a hydrogen bonding interaction. Furthermore, the induction of the isotactic-specificity was attributed to the conformationally-limited propagating radicals. Based on these findings, the mechanism of the isotactic-specific radical polymerization was discussed

Hydrogen-bond-assisted isotactic-specific radical polymerization of N-isopropylacrylamide with pyridine N-oxide

Radical polymerization of N-isopropylacrylamide (NIPAAm) in CHCl3 at low temperatures in the presence of pyridine N-oxide (PNO) was investigated. An isotactic poly(NIPAAm) with meso diad content of 61% was successfully prepared at –60°C in the presence of a twofold amount of PNO. Thermodynamic analysis suggested that the isotactic-specificity was entropically induced, probably due to conformational fixation near the propagating chain-end through coordination by PNO

Metal-free isotactic-specific radical polymerization of N-alkylacrylamides with 3,5-dimethylpyridine N-oxide : The effect of the N-substituent and solvent on the isotactic specificity

Radical polymerization of N-methylacrylamide (NMAAm), N-n-propylacrylamide, N-isopropylacrylamide (NIPAAm) and N-benzylacrylamide was investigated in CHCl3, CH2Cl2 and CH3CN, in the presence of 3,5-dimethylpyridine N-oxide (35DMPNO) to examine the effects of the N-substituent and the solvent on the isotactic specificity induced by 35DMPNO. With addition of 35DMPNO to radical polymerization of N-alkylacrylamides in CHCl3, isotactic specificity was significantly induced in NIPAAm polymerization but only slightly induced in NMAAm polymerization. Furthermore, mixed solvents of CH3CN and halomethanes such as CHCl3 and CH2Cl2 enhanced the ability of 35DMPNO to induce isotactic specificity, and poly(NIPAAm) with 74% meso dyad was obtained

The Creation of School Education Bringing up a Student Carrying Tomorrow (3) : The Valuation of "Compulsory Subjects", "Optional Subjects", and "Integrated Subjects"

The purpose of this study is to show the valuation of "Compulsory Subjects", "Optional Subjects", and "Integrated Subjects", to show the relationship between each subjects and "three abilities", "the ability of recognizing othere senses of value", "the ability of self-expression and communication" and "the ability of decision-making" which defined by the project members. The main result of this study is that we should make up the standards which teachers, students and parents recognize as important abilities

Overexpression of TNF-α converting enzyme promotes adipose tissue inflammation and fibrosis induced by high fat diet

Obesity is a state in which chronic low-grade inflammation persists in adipose tissues. Pro-inflammatory cytokines, including TNF-α, produced by adipose tissues have been implicated as active participants in the development of obesity-related diseases. Since TNF-α converting enzyme (TACE) is the major factor that induces soluble TNF-α, TACE has been noted as a pivotal regulator in this field. To reveal the role of TACE in adipose tissue inflammation, TACE-transgenic (TACE-Tg) and wild type (WT) mice were fed with high fat diet (HFD) or control diet for 16 weeks. At 13 weeks after the beginning of the diet, serum TNF-α and macrophage-related cytokine/chemokine levels were elevated in TACE-Tg mice fed with HFD (Tg-HFD mice), and the number of the so-called crown-like adipocyte was significantly increased in adipose tissues of Tg-HFD mice at the end of the experiment. Although macrophage infiltration was not detected in the adipose tissues at this time, fibrosis was observed around the crown-like adipocytes. These findings suggested that TACE overexpression induced macrophage infiltration and subsequent fibrosis in adipose tissues under HFD regimen. The collective evidence suggested that TACE could be a therapeutic target of HFD-induced obesity-related adipose tissue inflammation

Circulating Neutrophil Extracellular Trap Levels in Well-Controlled Type 2 Diabetes and Pathway Involved in Their Formation Induced by High-Dose Glucose

Objectives: Although intensive therapy for type 2 diabetes (T2D) prevents microvascular complications, 10% of well-controlled T2D patients develop microangiopathy. Therefore, the identification of risk markers for microvascular complications in well-controlled T2D patients is important. Recent studies have demonstrated that high-dose glucose induces neutrophil extracellular trap (NET) formation, which can be a risk for microvascular disorders. Thus, we attempted to determine the correlation of circulating NET levels with clinical/laboratory parameters in well-controlled T2D patients and to reveal the mechanism of NET formation induced by high-dose glucose. Methods: Circulating NET levels represented by myeloperoxidase (MPO)-DNA complexes in the serum of 11 well-controlled T2D patients and 13 healthy volunteers were determined by enzyme-linked immunosorbent assay. The pathway involved in the NET formation induced by high-dose glucose was determined using specific inhibitors. Results: Serum MPO-DNA complex levels were significantly higher in some well-controlled T2D patients in correlation with the clinical/laboratory parameters which have been regarded as risk markers for microvascular complications. The aldose reductase inhibitor, ranirestat, could inhibit the NET formation induced by high-dose glucose. Conclusions: Elevated levels of circulating NETs can be a risk marker for microvascular complications in well-controlled T2D patients. The polyol pathway is involved in the NET formation induced by high-dose glucose