Effect of solvent vapor annealing on TiOPc thin films and the application on hybrid solar cells

This article reports on effect of solvent vapor annealing on TiOPc thin films and the application on hybrid solar cells based on ZnO/TiOPc with DH-alpha6T as an electron blocking layer. The band gap shows a change for the TiOPc thin film solvent vapor annealed with various solvents, which may be due to the phase transition from amorphous to alpha-phase, beta-form or alpha+beta-form. The phase separation could be responsible for the variations of the optical properties. No significant change is observed in the pi-pi* transition at various phase behaviors. Device performance of hybrid solar cells could be improved and open-circuit voltage (VOC), short-circuit current (ISC) and power conversion efficiency (eta) were enhanced by solvent vapor annealing, which originated from amorphous TiOPc films transformed into crystalline alpha-phase, beta-form or alpha+beta-form.nbsp At alpha-TiOPc, the device achieved the highest performance with VOC, ISC and eta of 0.57 V, 1.40 mA/cm2, and 0.22 %, respectively, which originated from alpha-TiOPc with the widest red and near-IR absorption band

Optimization of the moment of inertia and the release conditions of a discus

AbstractThis paper describes the concurrent optimization of the design of a discus and the skill with which it is thrown. The objective function for optimization is the flight distance, where longer is better. Thirteen control variables are considered, twelve of which are concerned with the skill of the thrower. These determine the launch conditions, which are controlled by the thrower when he or she throws the discus. The final variable is concerned with the discus itself. This is the moment of inertia on its transverse axis. The optimization was carried out with the aid of a genetic algorithm, and the entire trend for each generation between the objective function and the control variables could be visualized with the aid of self organizing maps. It was found that the flight distance achieved with concurrent optimization was longer than that optimized for skill alone. In the case of the optimal flight, the angle of attack should always be less than the stalling angle

Octacosanol Attenuates Disrupted Hepatic Reactive Oxygen Species Metabolism Associated with Acute Liver Injury Progression in Rats Intoxicated with Carbon Tetrachloride

We examined whether octacosanol, the main component of policosanol, attenuates disrupted hepatic reactive oxygen species metabolism associated with acute liver injury progression in rats intoxicated with carbon tetrachloride (CCl4). In rats intoxicated with CCl4 (1 ml/kg, i.p.), the activities of serum transaminases increased 6 h after intoxication and further increased at 24 h. In the liver of CCl4-intoxicated rats, increases in lipid peroxide (LPO) concentration and myeloperoxidase activity and decreases in superoxixde dismutase activity and reduced glutathione (GSH) concentration occurred 6 h after intoxication and these changes were enhanced with an increase in xanthine oxidase activity and a decrease in catalase activity at 24 h. Octacosanol (10, 50 or 100 mg/kg) administered orally to CCl4-intoxicated rats at 6 h after intoxication attenuated the increased activities of serum transaminases and the increased hepatic myeloperoxidase and xanthine oxidase activities and LPO concentration and the decreased hepatic superoxide dismutase and catalase activities and GSH concentration found at 24 h after intoxication dose-dependently. Octacosanol (50 or 100 mg/kg) administered to untreated rats decreased the hepatic LPO concentration and increased the hepatic GSH concentration. These results indicate that octacosanol attenuates disrupted hepatic reactive oxygen species metabolism associated with acute liver injury progression in CCl4-intoxicated rats

Mechanism of oxygen release from Li-rich cathode material for lithium ion batteries

For further wide spread of high energy density batteries, one of the most important technological challenges is preventing thermal runaway. For that, a key phenomenon is the oxygen release from cathode active materials, because released oxygen may react with the organic solvent and generate heat. Therefore, it is important to understand the mechanism of oxygen release to ensure safe battery operation. While the reaction of charged cathode material and organic solvent was investigated well [1], the mechanism of oxygen release from cathode material is not understood so far [2]. In this study, oxygen release behavior of Li-rich cathode material Li1.2Mn0.6Ni0.2O2-d was investigated, and the mechanism of oxygen release was discussed based on defect chemistry and thermodynamics. Please click Additional Files below to see the full abstract

TPNに起因する、腸管粘膜防御機能の低下に対する付加的少量低残沙経腸栄養剤の効果

取得学位 : 博士（医学）, 学位授与番号 : 医博甲第1544号, 学位授与年月日 : 平成14年9月30日, 学位授与大学 : 金沢大

Prevention of Cognitive Decline in Alzheimer's Disease by Novel Antioxidative Supplements

Oxidative stress plays a crucial role in Alzheimer's disease (AD) from its prodromal stage of mild cognitive impairment. There is an interplay between oxidative stress and the amyloid beta (A beta) cascade via various mechanisms including mitochondrial dysfunction, lipid peroxidation, protein oxidation, glycoxidation, deoxyribonucleotide acid damage, altered antioxidant defense, impaired amyloid clearance, inflammation and chronic cerebral hypoperfusion. Based on findings that indicate that oxidative stress plays a major role in AD, oxidative stress has been considered as a therapeutic target of AD. In spite of favorable preclinical study outcomes, previous antioxidative components, including a single antioxidative supplement such as vitamin C, vitamin E or their mixtures, did not clearly show any therapeutic effect on cognitive decline in AD. However, novel antioxidative supplements can be beneficial for AD patients. In this review, we summarize the interplay between oxidative stress and the A beta cascade, and introduce novel antioxidative supplements expected to prevent cognitive decline in AD

Clinical and Pathological Improvement in Stroke-Prone Spontaneous Hypertensive Rats Related to the Pleiotropic Effect of Cilostazol

Background and Purpose-Cerebral infarction is a major cause of death or decreasing activities of daily living. This study aimed to investigate the efficacy of commonly used antiplatelet drugs on stroke and motor and cognitive functions in relation to oxidative stress markers and insulin-like growth factor 1 receptor (IGF-1R). Methods-Stroke-prone spontaneously hypertensive rats were treated with vehicle, aspirin, clopidogrel, and cilostazol from 8 to 10 weeks of age. Physiological parameters, regional cerebral blood flow, and serum lipids were examined. Motor and cognitive functions were evaluated weekly by the Rotorod and water maze task. Spontaneous infarct volume, oxidative stress markers for lipid, protein, and DNA at the ischemic boundary zone of spontaneous infarction, and the IGF-1R-positive cell ratio in the hippocampus were immunohistochemically examined in brain sections. IGF-1R beta expression in the hippocampus was assessed by Western blotting. Results-The antiplatelet drugs, cilostazol and clopidogrel, reduced the spontaneous infarct volume more than aspirin. Only cilostazol improved motor and cognitive functions with a significant increase (P<0.05) in the memory-related IGF-1R-positive ratio and IGF-1R beta expression in the hippocampus. Cilostazol reduced the 4 oxidative stress markers in affected neurons in stroke-prone spontaneously hypertensive rats regardless of blood pressure, regional cerebral blood flow, or serum lipid levels. Conclusions-The present results suggest that a possible pleiotropic effect of cilostazol resulted in the reduction of spontaneous infarct volume and preservation of motor and spatial cognitive functions. The increase of IGF-1R-positive cells in the hippocampal CA1 region could partly explain the preservation of spatial cognitive function in stroke-prone spontaneously hypertensive rats

Early detachment of neuromuscular junction proteins in ALS mice with SODG93A mutation

The transgenic animals with mutant copper/zinc superoxide dismutase (SOD1) DNA develop paralytic motor neuron disease resembling human amyotrophic lateral sclerosis (ALS) patients and are commonly used as models for ALS. In the transgenic (Tg) mice with the G93A mutation of the human SOD1 gene SOD1G93A mice), the loss of ventral root axons and the synapses between the muscles and the motor neurons suggested that the motor neuron degeneration might proceed in a dying-back degeneration pattern. To reveal the relationship between axonal degeneration and the progression of the muscle atrophy in the SOD1G93A mice, we investigated the status of the neuromuscular junction along the disease progression. As a presynaptic or postsynaptic marker of neuromuscular junction (NMJ), anti-synaptic vesicle protein 2 (anti-SV2) antibody and α-bungarotoxin (α-BuTX) were chosen in this study and, as a marker of synaptic cleft, anti-agrin antibody was chosen in this study. In the immunohistochemistry of α-BuTX and anti-SV2 antibody, the percentages of double positive NMJs among α-BuTX single positive were decreased in Tg mice through time from ten weeks. The number of postsynaptic acethylcholine receptor (AChR) clusters did not decrease in Tg mice even at the end stage. Immunohistochemistry of α-BuTX and anti-agrin antibody revealed that the increase of immunopositive area of anti-agrin antibody around the muscle fiber in Tg mice from ten weeks of age. In this study, we revealed that the detachment of nerve terminals started at ten weeks in Tg mice. The levels of AChR did not change throughout 5–20 weeks of age in both groups of mice, and AChR remains clustering at NMJs, suggesting that the muscle abnormality is the result of detachment of nerve terminals

In vivo direct reprogramming of glial linage to mature neurons after cerebral ischemia

The therapeutic effect of in vivo direct reprogramming on ischemic stroke has not been evaluated. In the present study, a retroviral solution (1.5-2.0 × 107 /ul) of mock pMX-GFP (n = 13) or pMX-Ascl1/Sox2/NeuroD1 (ASN) (n = 14) was directly injected into the ipsilateral striatum and cortex 3 days after 30 min of transient cerebral ischemia. The reprogrammed cells first expressed neuronal progenitor marker Dcx 7 and 21 days after viral injection, then expressed mature neuronal marker NeuN. This was accompanied by morphological changes, including long processes and synapse-like structures, 49 days after viral injection. Meanwhile, therapeutic improvement was not detected both in clinical scores or infarct volume. The present study provides a future novel self-repair strategy for ischemic stroke with beneficial modifications of the inducer-suppressor balance