自然言語符号化における言語横断的な転移学習、圧縮、白色化の効果の分析

Tohoku University博士（情報科学）thesi

自然言語符号化における言語横断的な転移学習、圧縮、白色化の効果の分析

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Study on relation between spatial distribution and release rate of hydrophobic compounds incorporated in polymer micelles with anomalous small angle X-ray scattering

Amphiphilic block copolymers in aqueous solution undergo self-assembly into polymer micelles composed of hydrophobic core and hydrophilic shell. The polymer micelles can solubilize hydrophobic compounds in aqueous solution by incorporating them in the hydrophobic core. Therefore, they have been expected to be a drug career in drug delivery system (DDS). In DDS, controlling of the drug release behavior and retention stability are critical issues. However, tuning release rate and stability of retention of drug molecules is significantly difficult. Since the hydrophobic molecules must pass through the hydrophobic cores and hydrated corona layers to go out the polymer micelles, their release properties should strongly depend on spatial distribution of drug molecules in polymer micelles. Therefore, to elucidate the relation between spatial distribution of drug molecules and release properties of drug molecules is of significant importance to design a novel DDS. Thus, the aim of this study is to clarify the relation between spatial distribution of hydrophobic compounds in polymer micelles and their release and retention property. Poly(methyl methacrylate)-block-poly(N,N-(dimethylamino)ethyl methacrylate) (Poly-1) as amphiphilic block copolymer was synthesized by reversible addition-fragmentation radical polymerization. The weight- and number-average molecular weights of the resulting Poly-1 were 1.6104 g mol-1 and 1.9104 g mol-1, respectively. Three kinds of compounds (9-bromofluorene (BrF), 4-bromobenzyl alcohol (BrBzOH), 4-bromophenol (BrPh)) were employed as bromine-labeled hydrophobic compounds. Poly-1 and a hydrophobic compound were mixed at 10 wt% of a hydrophobic compound against Poly-1. Please click Additional Files below to see the full abstract

肝臓・腎臓の恒常性維持に関与する核内受容体HNF4ファミリーの同定と機能解明

学位記番号：理工博甲34

Inhibition of tibialis anterior spinal reflex circuits using frequency-specific neuromuscular electrical stimulation

Arai S., Sasaki A., Tsugaya S., et al. Inhibition of tibialis anterior spinal reflex circuits using frequency-specific neuromuscular electrical stimulation. Artificial Organs , (2024); https://doi.org/10.1111/aor.14737.Background: Neuromuscular electrical stimulation (NMES) can generate muscle contractions and elicit excitability of neural circuits. However, the optimal stimulation frequency for effective neuromodulation remains unclear. Methods: Eleven able-bodied individuals participated in our study to examine the effects of: (1) low-frequency NMES at 25 Hz, (2) high-frequency NMES at 100 Hz; and (3) mixed-frequency NMES at 25 and 100 Hz switched every second. NMES was delivered to the right tibialis anterior (TA) muscle for 1 min in each condition. The order of interventions was pseudorandomized between participants with a washout of at least 15 min between conditions. Spinal reflexes were elicited using single-pulse transcutaneous spinal cord stimulation applied over the lumbar enlargement to evoke responses in multiple lower-limb muscles bilaterally and maximum motor responses (Mmax) were elicited in the TA muscle by stimulating the common peroneal nerve to assess fatigue at the baseline and immediately, 5, 10, and 15 min after each intervention. Results: Our results showed that spinal reflexes were significantly inhibited immediately after the mixed-frequency NMES, and for at least 15 min in follow-up. Low-frequency NMES inhibited spinal reflexes 5 min after the intervention, and also persisted for at least 10 min. These effects were present only in the stimulated TA muscle, while other contralateral and ipsilateral muscles were unaffected. Mmax responses were not affected by any intervention. Conclusions: Our results indicate that even a short-duration (1 min) NMES intervention using low- and mixed-frequency NMES could inhibit spinal reflex excitability of the TA muscle without inducing fatigue

Effect of the angiotensin-converting enzyme inhibitor imidapril on reactive hyperemia in patients with essential hypertension: relationship between treatment periods and resistance artery endothelial function

AbstractOBJECTIVESThe purpose of this study was to evaluate the effects of the angiotensin-converting enzyme (ACE) inhibitor imidapril and the calcium antagonist amlodipine on endothelial function before and after 2, 4, 8, 12, 24 and 48 weeks of treatment.BACKGROUNDThere are limited data on whether and how long endothelial function is improved after initiation of ACE inhibitor treatment and how the grade of endothelial function further progresses after improvement of endothelial dysfunction in patients with essential hypertension.METHODSThe forearm blood flow (FBF) was measured in 25 patients with essential hypertension and in 25 normotensive subjects by using strain-gauge plethysmography during reactive hyperemia (RH) (280 mm Hg for 5 min) and after sublingual administration of nitroglycerin (NTG, 0.3 mg).RESULTSThe FBF of patients with essential hypertension during RH was significantly less than that of normotensive subjects. The increase in FBF after sublingual NTG was similar in both groups. Both imidapril (n = 13) and amlodipine (n = 12) significantly reduced systolic blood pressure and diastolic after eight weeks of treatment from the pretreatment values. Forearm vascular resistance was significantly decreased after two weeks of treatment. Imidapril significantly augmented RH after 12 weeks of treatment from the pretreatment values (31.6 ± 5.7 to 38.2 ± 6.0 ml/min per 100 ml tissue, p < 0.05), whereas amlodipine did not alter RH for each treatment period. The ability of imidapril to improve RH was maintained throughout the 48-week treatment period. There was no significant difference in RH at 12, 24 and 48 weeks. The increase in FBF after sublingual administration of NTG was similar in all treatment periods for the two groups. The infusion of NG-monomethyl-L-arginine, a nitric oxide (NO) synthase inhibitor, abolished the enhancement of RH in hypertensive patients treated with imidapril.CONCLUSIONSThese findings suggest that the ACE inhibitor imidapril augments RH after 12 weeks of treatment in patients with essential hypertension and that this ACE inhibitor-induced augmentation of RH may be due to an increase in NO

Continuous release of O2−/ONOO− in plasma-exposed HEPES-buffered saline promotes TRP channel-mediated uptake of a large cation

Although the externally controllable extracellular supply of the short-lived reactive oxygen and nitrogen species, such as O2•−, •NO, and ONOO−, could potentially manipulate cellular functions, their simple administration to cells is likely to be ineffective due to their rapid deactivation. In this study, we found a method of a continuous supply of O2•−/ONOO− over a few minutes, which is triggered by irradiation of a nonequilibrium atmospheric pressure plasma to commonly used organic buffers (e.g., 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid, HEPES). In addition, a continuous low-dose O2•−/ONOO− supply was shown to induce a physiologically relevant Ca2+ response and subsequently the uptake of a large cation mediated by transient receptor potential channel family member(s). Our results provide a novel approach to the continuous O2•−/ONOO− supply, requiring controllable and mass-volume treatments

Repetitive Passive Finger Movement Modulates Primary Somatosensory Cortex Excitability

Somatosensory inputs induced by repetitive passive movement (RPM) modulate primary motor cortex (M1) excitability; however, it is unclear whether RPM affects primary somatosensory cortex (S1) excitability. In this study, we investigated whether RPM affects somatosensory evoked potentials (SEPs) and resting state brain oscillation, including alpha and beta bands, depend on RPM frequency. Nineteen healthy subjects participated in this study, and SEPs elicited by peripheral nerve electrical stimulation were recorded from the C3’ area in order to assess S1 excitability (Exp. 1: n = 15). We focused on prominent SEP components such as N20, P25 and P45-reflecting S1 activities. In addition, resting electroencephalograms (EEGs) were recorded from C3’ area to assess the internal state of the brain network at rest (Exp. 2: n = 15). Passive abduction/adduction of the right index finger was applied for 10 min at frequencies of 0.5, 1.0, 3.0, and 5.0 Hz in Exp. 1, and 1.0, 3.0, and 5.0 Hz in Exp. 2. No changes in N20 or P25 components were observed following RPM. The 3.0 Hz-RPM decreased the P45 component for 20 min (p &lt; 0.05), but otherwise did not affect the P45 component. There was no difference in the alpha and beta bands before and after any RPM; however, a negative correlation was observed between the rate of change of beta power and P45 component at 3.0 Hz-RPM. Our findings indicated that the P45 component changes depending on the RPM frequency, suggesting that somatosensory inputs induced by RPM influences S1 excitability. Additionally, beta power enhancement appears to contribute to the P45 component depression in 3.0 Hz-RPM

Low body mass index is a risk factor forimpaired endothelium-dependent vasodilation in humans: role of nitric oxide and oxidative stress

AbstractObjectivesThe purpose of this study was to evaluate the relationship between body mass index (BMI), including low BMIs, and endothelial function.BackgroundEpidemiologic study has demonstrated that not only obesity but also a low BMI may be a risk factor for cardiovascular disease.MethodsThe forearm blood flow (FBF) response to acetylcholine (ACh) and isosorbide dinitrate (ISDN) was measured in 87 healthy young men (15 low BMI, 51 normal, 14 obese, and 7 extremely obese).ResultsPlasma concentrations of 8-hydroxy-2′-deoxyguanosine and serum concentrations of malondialdehyde-modified low-density lipoprotein were higher in low BMI, obese, and extremely obese subjects than in normal subjects and were similar among the low BMI, obese, and extremely obese groups. The FBF response to ACh was greater in the normal group than in the other groups (p < 0.001), and was lower in the extremely obese group as compared with the other groups (p < 0.001). The ACh-stimulated vasodilation was similar between the low BMI group and the obese group. The ISDN-stimulated vasodilation was similar in all four groups. There were no significant differences in ACh-stimulated vasodilation between the four groups after the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine infusion. Co-infusion of vitamin C augmented the FBF response to ACh in low BMI, obese, and extremely obese groups—but not in normal BMI group.ConclusionsThese findings suggest that not only obesity but also a low BMI may be a risk factor for impaired endothelium-dependent vasodilation through the increased oxidative stress, leading to the reduced bioavailability of NO