Hysteretic ac loss of superconducting strips simultaneously exposed to ac transport current and phase-different ac magnetic field

A simple analytical expression is presented for hysteretic ac loss $Q$ of a superconducting strip simultaneously exposed to an ac transport current $I_0\cos\omega t$ and a phase-different ac magnetic field $H_0\cos(\omega t+\theta_0)$. On the basis of Bean's critical state model, we calculate $Q$ for small current amplitude $I_0\ll I_c$, for small magnetic field amplitude $H_0\ll I_c/2\pi a$, and for arbitrary phase difference $\theta_0$, where $I_c$ is the critical current and $2a$ is the width of the strip. The resulting expression for $Q=Q(I_0,H_0,\theta_0)$ is a simple biquadratic function of both $I_0$ and $H_0$, and $Q$ becomes maximum (minimum) when $\theta_0=0$ or $\pi$ ($\theta_0=\pi/2$).Comment: 4 pages, 2 figures, submitted to Appl. Phys. Let

Hysteretic ac loss of polygonally arranged superconducting strips carrying ac transport current

The hysteretic ac loss of a current-carrying conductor in which multiple superconducting strips are polygonally arranged around a cylindrical former is theoretically investigated as a model of superconducting cables. Using the critical state model, we analytically derive the ac loss $Q_n$ of a total of $n$ strips. The normalized loss $Q_n/Q_1$ is determined by the number of strips $n$ and the ratio of the strip width $2w$ to the diameter $2R$ of the cylindrical former. When $n>> 1$ and $w/R<< 1$, the behavior of $Q_n$ is similar to that of an infinite array of coplanar strips.Comment: 3 pages, 3 figures, to be published in Applied Physics Letters (2008

Determination of etoposide serum concentrations in small pediatric samples by an improved method of reversed-phase high-performance liquid chromatography.

Several specific assays have been developed for the measurement of etoposide in biological fluids. As large samples are required for high sensitivity, these systems are not appropriate for a pediatric practice. In the present study, however, an improved method for the determination of serum levels of the anticancer drug etoposide was developed, using high-performance liquid chromatography with fixed-wavelength ultraviolet detection. Etoposide was extracted from serum using dichloromethane. The efficiency of extraction from serum was 85.7 +/- 7.7% for etoposide and 81.1 +/- 8.4% for diphenylhydantoin, the internal standard. The serum concentrations of etoposide were measured in 0.2-ml serum samples. The lower limit of detection was 50 ng/ml. Each measurement was completed within 5 min. The linear quantitation range for etoposide was 0.05-50 microg/ml. This assay presents an alternative method for routine measurement of serum levels of etoposide in the pediatric oncology setting.</p

ヘム鉄磁性とタンパク質修飾のヘモグロビンのアロステリック機構に及ぼす影響

金沢大学医学部研究課題/領域番号:57770205, 研究期間(年度):1982出典：研究課題「ヘム鉄磁性とタンパク質修飾のヘモグロビンのアロステリック機構に及ぼす影響」課題番号57770205（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-57770205/）を加工して作

Upregulation of anti-apoptotic factors in upper motor neurons after spinal cord injury in adult zebrafish

Unlike mammals, fish motor function can recover within 6-8 weeks after spinal cord injury (SCI). The motor function of zebrafish is regulated by dual control; the upper motor neurons of the brainstem and motor neurons of the spinal cord. In this study, we aimed to investigate the framework behind the regeneration of upper motor neurons in adult zebrafish after SCI. In particular, we investigated the cell survival of axotomized upper motor neurons and its molecular machinery in zebrafish brain. As representative nuclei of upper motor neurons, we retrogradely labeled neurons in the nucleus of medial longitudinal fasciculus (NMLF) and the intermediate reticular formation (IMRF) using a tracer injected into the lesion site of the spinal cord. Four to eight neurons in each thin sections of the area of NMLF and IMRF were successfully traced at least 1-15 days after SCI. TUNEL staining and BrdU labeling assay revealed that there was no apoptosis or cell proliferation in the axotomized neurons of the brainstem at various time points after SCI. In contrast, axotomized neurons labeled with a neurotracer showed increased expression of anti-apoptotic factors, such as Bcl-2 and phospho-Akt (p-Akt), at 1-6 days after SCI. Such a rapid increase of Bcl-2 and p-Akt protein levels after SCI was quantitatively confirmed by western blot analysis. These data strongly indicate that upper motor neurons in the NMLF and IMRF can survive and regrow their axons into the spinal cord through the rapid activation of anti-apoptotic molecules after SCI. The regrowing axons from upper motor neurons reached the lesion site at 10-15 days and then crossed at 4-6 weeks after SCI. These long-distance descending axons from originally axotomized neurons have a major role in restoration of motor function after SCI. © 2012 Elsevier Ltd. All rights reserved.Thesis of Kazuhiro Ogai / 大貝 和裕 博士論文 金沢大学医薬保健学総合研究科（保健学専攻

Quantitative evaluation for the role of β146 His and β143 His residues in the Bohr effect of human hemoglobin in the presence of 0.1 M chloride ion

Two different methods were used to determine the number of Bohr protons released upon oxygenation of human hemoglobin (Hb A) and Hb A lacking β146 His (des-His Hb A) at the pH ranging from pH 5.0 to 9.0 in the presence of 0.1 M Cl- at 25 °C. One is the direct differential titration method, the other is based on the measurement of oxygen affinity as a function of pH. The results obtained for Hb A or des-His Hb A with two methods were completely mutually consistent. The number of Bohr protons released from des-His Hb A upon oxygenation at pH 7.5 was about 44% less than that from Hb A, while at pH 5.5 the number of Bohr protons taken up by des-His Hb A was 20% greater than that by Hb A. The differences in the number of Bohr protons between Hb A and des-His Hb A could not be simply ascribed to the lack of β146 His from Hb A. The pK(a) values, which were determined by the deuterium exchange method using 1H NMR, were 8.0 for β146 His of deoxy-Hb A and 6.5 for that of CO Hb A, while those of β143 His were 5.2 for deoxy-Hb A and 6.0 for CO Hb A. From these pK(a) values, in addition to those of α1 Val proposed for the modified CO and deoxy-Hb A with carbamylated β chains by Van Beek and de Bruin, it became evident that almost all (about 92%) of the alkaline Bohr protons released upon oxygenation of Hb A in the presence of 0.1 M Cl- could be acountd for by the protons from these 2 residues, although the involvement of other histidine residues could not be denied. About half the acid Bohr protons from Hb A, which corresponds to the higher pH part (above pH 5.0) of the acid Bohr effect, could be explained by the involvement of β143 His residue. The residual acid Bohr effect in the more acidic pH region was presumably contributed by an amino acid residue with pK(a) values of 4.05 and 5.95 for the deoxy- and CO Hb A, respectively, although the amino acid residue was unspecified. In des-His Hb A, however, the acid and alkaline Bohr effects could not be satisfactorily explained if the pK(a) values of β143 His and α1 Val remained unchanged in comparison with those of Hb A and moreover the involvement of other residues in the Bohr effect was not taken into account. These results indicate that removal of β-carboxyl terminal histidine may cause considerably large perturbations to the tertiary structure of the subunit and/or to the deoxy-quaternary structure of des-His Hb A, so that its acid and alkaline Bohr effects may be altered more extensively than would be expected by deletion of only 1 residue

Upregulation of Leukemia Inhibitory Factor (LIF) during the Early Stage of Optic Nerve Regeneration in Zebrafish.

Fish retinal ganglion cells (RGCs) can regenerate their axons after optic nerve injury, whereas mammalian RGCs normally fail to do so. Interleukin 6 (IL-6)-type cytokines are involved in cell differentiation, proliferation, survival, and axon regrowth; thus, they may play a role in the regeneration of zebrafish RGCs after injury. In this study, we assessed the expression of IL-6-type cytokines and found that one of them, leukemia inhibitory factor (LIF), is upregulated in zebrafish RGCs at 3 days post-injury (dpi). We then demonstrated the activation of signal transducer and activator of transcription 3 (STAT3), a downstream target of LIF, at 3–5 dpi. To determine the function of LIF, we performed a LIF knockdown experiment using LIF-specific antisense morpholino oligonucleotides (LIF MOs). LIF MOs, which were introduced into zebrafish RGCs via a severed optic nerve, reduced the expression of LIF and abrogated the activation of STAT3 in RGCs after injury. These results suggest that upregulated LIF drives Janus kinase (Jak)/STAT3 signaling in zebrafish RGCs after nerve injury. In addition, the LIF knockdown impaired axon sprouting in retinal explant culture in vitro; reduced the expression of a regeneration-associated molecule, growth-associated protein 43 (GAP-43); and delayed functional recovery after optic nerve injury in vivo. In this study, we comprehensively demonstrate the beneficial role of LIF in optic nerve regeneration and functional recovery in adult zebrafish

ヒト赤血球によるトリプトファン代謝産物の病態代謝

トリプトファン及びその代謝物質の代謝は生理的に重要である。この代謝系は肝臓や腎臓などほとんどの臓器の細胞に存在するがヒト赤血球でこのような代謝系が存在するかについては報告がなく十分に検討されていなかった。私達はトリプトファンの代謝中間体である3-ヒドロキシキヌレニン(3-HKN)及び3-ヒドロキシアントラニル酸(3-HAT)の代謝をヒト赤血球を用いて調べたところ、他の臓器で知られているような代謝経路とは異った反応経路で反応が進行し、赤褐色の色素に変化することを見い出した。本研究ではこのようなヒト赤血球における3-HKN及び3-HAT、あるいはこれらの物質の構造類似物質であるオルトアミノフェノールの代謝のメカニズムについて詳しく検討した。その結果次のような研究成果がえられた。 1)ヒト赤血球では3-ヒドロキシキヌレニンはキサントマチンという通常生体内では存在しないと考えられている物質に代謝された。この反応速度は比較的速いので今後3-ヒドロキシキヌレニンが血液中に増加している糖尿病患者について検討を行う予定である。2)トリプトファンの代謝中間体である3-ヒドロキシアントラニル酸は2分子縮合してシンナバリン酸へ代謝されることが、ヒト赤血球を用いて示された。ヒト赤血球におけるこの反応は非常に速いのでその生理的,病理的意義を検討中である。3)オルトアミノフェノールは2-アミノフェノキサジン3-オン(オルトアミノフェノールの二分子縮合体である)へとヒト赤血球内で代謝された。4)これらの反応は赤血球内ヘモグロビンの酸化還元反応と共役しておこることが明らかになった。5)以上の代謝産物は褐色色素であり生体でこのような反応がおきていることについては私達の報告が初めてである。Metabolism of tryptophan and its metabolites is physiologically important in human body. The process of metabolism of tryptophan and its metabolites such as 3-hydroxykynurenine and 3-hydroxyanthranilic acid is known to be present in the cells of brain and kidney etc. However, there are few reports on the metabolism of these compounds in human erythrocytes. We investigated whether tryptophan and its metabolites are metabolized in human erythrocytes or not. Interestingly, we found that these compounds were metabolized to brown or yellow pigments such as cinnabarinic acid and xanthommatin in the cells. These processes included dimerization of 3-hydroxykynurenine and 3-hydroxyanthranilic acid by intracellular hemoglobin in human erythrocytes. In this research, the mechanism for metabolism of tryptophan metabolites such as 3-hydroxykynurenine and 3-hydroxyanthranilic acid was investigated extensively.1). 3-Hydroxykynurenine, a metabolite of tryptophan, was metabolized to xanthommatin, which is not usually found in human body, in human erythrocytes. The reaction rates were relatively fast in the cells. We are to investigate the accumulation of this brown pigment in the patients of Diabetes.2). 3-Hydroxyanthranilic acid, a metabolite of 3-hydroxykynurenine in human body, was metabolized to cinnabarinic acid, an orange colored compound, in human erythrocytes. The reaction rates were very fast. The physiological and pathological significance of the accumulation of cinnabarinic acid in human body is now under investigation.3). o-Aminophenol, which has basal structure of 3-hydroxykynurenine and 3-hydroxyanthranilic acid is metabolized to phenoxazine, a brown pigment, in human erythrocytes. Since o-aminophenol causes toxic methemoglobinemia, the accumulation of phenoxazine compound is conceivable in the bloods of the patient.4). It was found that the metabolism of 3-hydroxykynurenine, 3-hydroxyanthranilic acid and o-aminophenol is coupled with oxidation and reduction of intracellular hemoglobin in human erythrocytes.5). The brown or orange colored pigments such as xanthommatin, cinnabarinic acid and phenoxazine are not found in human body before we reported.研究課題/領域番号:60570127, 研究期間(年度):1985–1986出典：「ヒト赤血球によるトリプトファン代謝産物の病態代謝」研究成果報告書　課題番号60570127(KAKEN：科学研究費助成事業データベース（国立情報学研究所）)　　　本文データは著者版報告書より作