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延伸されたボリエチレンテレフタラートが熱処理されると収縮を起こす。その原因を微細構造の熱処理による変化から知ることを目的とした。その結果,低倍率延伸試料および高倍率延伸試料の130℃以下の熱処理では,引きのばされた分子鎖の配向低下により収縮が超こると考えられる。高延伸された試料を熱処理したときに,長周期,密度,収縮率の間に相間関係が見いだされ,このことから,熱収縮にfold(折りたたみ)構造が関与していると結論した。

Background Peroxisome proliferator-activated receptor γ (PPAR-γ) has been shown to play an important role in the control of inflammatory responses acting on macrophages, mast cells, T cells, and eosinophils. The present study was aimed at investigating the effects of PPAR-γ agonist on nasal symptoms and eosinophil accumulations in nasal mucosa by using a murine allergic rhinitis model. Furthermore, we examined the expression of PPAR-γ in the nasal mucosa in mice. Methods BALB/c mice were sensitized and challenged intranasally with ovalbumin. Ciglitazone, a PPAR-γ agonist, was administered orally 6 hours before each nasal challenge. Results Administration of PPAR-γ agonist significantly decreased the number of nasal rubs, nasal histamine responsiveness, serum IgE, IL-5 production from the spleen, and eosinophilic infiltration in the nasal mucosa. Furthermore, PPAR-γ was expressed in eosinophils and epithelial cells in the nasal mucosa by immunohistochemistry. Conclusions PPAR-γ was expressed in eosinophils and epithelial cells in the nasal mucosa. Also, the oral administration of ciglitazone is effective in upper airway allergic inflammation in mice.

We investigated the origin of the non-specialized cells proliferated in primary expiant culture of human parotid gland. The predominant cells in surface layer were morphologically epithelial origin with desmosomes and intercellular digitations. The cultured cells did not show any specific affinity to parotin isolated from bovine parotid gland, which seemed to be one of the marker for duct cell. However, it was demonstrated autoradiographycally that DNA synthesis in the cells was rapidly induced by isoproterenol, a potent stimulator of acinar cell. From these results, the non-specialized epithelial cells in expiant culture seemed to be derived from acinar cell in human parotid gland.

We have studied insulin resistance in a 12-year-old Japanese boy who presented with congenital generalized lipodystrophy. Oral glucose tolerance test exhibited a diabetic pattern with normal fasting plasma glucose. Results from euglycemic glucose clamp study showed decreases in both insulin sensitivity and responsiveness. Both the patient's erythrocytes and Epstein-Barr virus transformed lymphocytes showed low-normal insulin binding with a slight reduction in binding affinity in the latter. Insulin binding to the cultured fibroblasts was decreased due to a lowered affinity. In addition, they displayed a rightward shift of the insulin dose-response curve for D-14C-glucose uptake with no decrease in the maximum uptake. Insulin-stimulated autophosphorylation and kinase activity of the wheat germ agglutinin purified receptors from the Epstein-Barr virus-transformed lymphocytes appeared normal. The reason for some discrepancies in insulin binding among the cells remains unknown, and we cannot formulate a conclusion as to whether or not a primary binding defect of insulin receptors exists and contributes to insulin resistance in the patient. The decrease in insulin responsiveness demonstrated in the glucose clamp study may result from a defect at the rate-limiting step in the postbinding process of insulin action, presumably a defect in the glucose transport system in muscle tissues. The defect may be secondary to changes in in vivo circumstances.

The purpose of this study is to clarify the role of peptide leukotrienes(LTs) on the onset of characteristic hyperreactive nasal symptoms of nasal allergy by observing the time course of the correlation among degrees of nasal symtoms, and by observing the amount of chemical mediators and the number of inflammatory cells in the nasal lavage fluid after nasal antigen challenge in subjects with Japanese cedar pollinosis during off season. Sneezing was terminated within 10 minutes and nasal discharge within 2 hours. However, time course change of the percent increase of nasal airway resistance showed dual response consisting of immediate and late phase responses. The peak of the former was seen at 30 minutes and the latter was at 7 hours after provocation. The significant increase of eosinophils in the nasal lavage fluid was observed during both the immediate and the late phase responses, but during the late phase response, the increase was more prominent. Basophilic cells definitely increased during the late phase response. The amount of LTs in the nasal lavage fluid increased significantly during both the immediate and the late phase responses. In contrast, the level of histamine increased significantly only during the immediate phase response.Considering that LTs, especially LTD, , has potent and persistent effect on causing swelling of nasal mucosa, LTs may play important role in causing nasal obstruction during both the immediate and the late phase responses after antigen challenge. On the other hand, the role of histamine may be confined to cause the hyperreactive nasal symptoms during the immediate phase response. Our results also indicate that the source of LTs in the nasal lavage fluid during the immediate phase response is mast cells in nasal mucosa, and during the late phase response, eosinophils and basophils are important as the source of LTs in addition to mast cells.