A novel synthesis of sequential polypeptides.
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Biomedical subjects
Publications and source records attributed to K Uno.
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A 73-year-old man with mild inactive interstitial pneumonitis and non-small cell bronchogenic carcinoma developed a cell-mediated hypersensitivity pneumonitis within 15 days following a second exposure to paclitaxel. Histological features of transbronchial lung biopsy were consistent with interstitial pneumonitis. Bronchoalveolar lavage showed increased lymphocytes and eosinophils, and decreased helper/suppressor T lymphocyte ratio. Leukocyte migration inhibitory test was positive for paclitaxel. These results support the possibility that paclitaxel-induced pneumonitis is due to delayed type hypersensitivity; they also support the hypothesis of a central role of T lymphocytes in drug-induced pneumonitis.
It has been shown that lipoprotein(a) (Lp[a]) may interfere with the fibrinolytic system and that the Lp(a) level in an individual remains constant. To evaluate the effects of Lp(a) on the fibrinolytic system in patients with unstable angina, we measured plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, and the thrombin-antithrombin III complex. The latter is a marker of thrombin generation, and the alpha 2-plasmin inhibitor-plasmin complex is an indicator of plasminogen activation. Venous plasma samples were taken from 18 patients with unstable angina and 18 patients with stable exertional angina who had been matched for clinical variables. On admission, plasma levels of Lp(a) were significantly higher in patients with unstable angina than in those with stable exertional angina (319 +/- 193 mg/l versus 191 +/- 141 mg/l, respectively; p less than 0.05). On admission, plasma levels of the alpha 2-plasmin inhibitor-plasmin complex and of the thrombin-antithrombin III complex were also significantly higher in patients with unstable angina than in those with stable exertional angina (0.78 +/- 0.42 micrograms/ml and 3.6 +/- 1.3 ng/ml versus 0.41 +/- 0.13 micrograms/ml and 1.9 +/- 0.5 ng/ml, respectively; p less than 0.01). In nine of the 18 patients with unstable angina, serial changes of plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, the thrombin-antithrombin III complex, and the acute-phase proteins C-reactive protein and alpha 1-antitrypsin were examined for 3 weeks after admission.(ABSTRACT TRUNCATED AT 250 WORDS)
A new method was proposed to prepare monocored water-loaded microcapsules with diameters of 50 microns or larger by making use of the process of interfacial polymer deposition. A solution of ethylcellulose or polystyrene in dichloromethane was added dropwise to an O/W emulsion in which n-hexane was dispersed as fine droplets in aqueous gelatin solution. Successive evaporation of dichloromethane at 40 degrees C and n-hexane at 80 degrees C gave monocored water-loaded ethylcellulose or polystyrene microcapsules. Monocored water-loaded ethylcellulose/polystyrene composite microcapsules were similarly prepared using mixed solutions of the two polymers in dichloromethane instead of ethylcellulose or polystyrene solution. When those mixed solutions which exhibit phase separation were used, the composite microcapsules obtained had a patchwork-like structure in which polystyrene-rich islands are dispersed in the ethylcellulose-rich sea.
Inward permeation from the surrounding medium of phenobarbital through the wall of water-loaded ethylcellulose microcapsules was investigated as a function of capsule size under the conditions of constant total capsule volume and constant total capsule surface area. The experimental data obtained were analysed in terms of capsule wall density and drug partition coefficient. The drug permeability coefficients calculated according to an equation derived from Fick's first law of diffusion were found to increase with decreasing capsule size in both constant total capsule volume and constant total capsule surface area experiments. The wall density and the drug partition coefficient also exhibited the same trend. Based on these findings, it was concluded that the drug permeation through ethylcellulose microcapsule membrane occurs predominantly by a solution-diffusion mechanism.
To estimate change of cerebral glucose metabolism by anticancer drugs, positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) was performed in 11 patients with malignancies who did not show neurological symptoms. In a patient treated with intravenous high-dose methotrexate (HD-MTX) and intrathecal MTX, apparent decrease of glucose metabolism was observed. HD-MTX and intrathecal MTX may cause cerebral glucose metabolism disorder primarily. Cerebral glucose metabolism was also mildly reduced by chemotherapy with drugs other than MTX and by radiotherapy outside the brain, with a corresponding change of blood data. It may reflect a psychosomatic change in whole body.