Interfacial Energy Alignment at the ITO/Ultra-Thin Electron Selective Dielectric Layer Interface and Its Effect on the Efficiency of Bulk-Heterojunction Organic Solar Cells.

We have investigated the photovoltaic properties of an inverted bulk heterojunction (BHJ) cell in a device with an indium-tin-oxide (ITO)/electron selective layer (ESL)/P3HT:PCBM active layer/MoOx/Ag multilayered structure. The insertion of only single layer of poly(diallyl-dimethyl-ammonium chloride) (PDDA) cationic polymer film (or poly(ethyleneimine) (PEI) polymeric interfacial dipole layer) and titanium oxide nanosheet (TN) films as an ESL effectively improved cell performance. Abnormal S-shaped curves were observed in the inverted BHJ cells owing to the contact resistance across the ITO/active layer interface and the ITO/PDDA/TN/active layer interface. The series resistance across the ITO/ESL interface in the inverted BHJ cell was successfully reduced using an interfacial layer with a positively charged surface potential with respect to ITO base electrode. The positive dipole in PEI and the electronic charge phenomena at the electrophoretic deposited TN (ED-TN) films on ITO contributed to the reduction of the contact resistance at the electrode interface. The surface potential measurement revealed that the energy alignment by the transfer of electronic charges from the ED-TN to the base electrodes. The insertion of the ESL with a large positive surface potential reduced the potential barrier for the electron injection at ITO/TN interface and it improved the photovoltaic properties of the inverted cell with an ITO/TN/active layer/MoOx/Ag structure.

[Trial of the integrated cross-field pharmaceutical education in the first year of faculty of pharmacy].

The six-year pharmacist education course has begun, and now first-year students receive clinical training. Interdisciplinary problem-solving capabilities covering chemistry, biology, molecular biology, pharmacology, pathology, and pharmacokinetics are necessary for new pharmacists. However, the conventional pharmaceutical science education was so separate from other fields that education for interdisciplinary cooperative capability was insufficient. This was especially true of elemental science courses, because they are not directly connected with clinical knowledge, and there is a problem of low student interest in those courses. As a result, students acquired only recall-level knowledge in clinical courses and their problem-solving capabilities in clinical treatment and drug development deteriorated. Therefore we offered a trial lecture aimed to help students recognize the important relationship between elemental science courses and clinical courses and increase their motivation to enroll in these courses. Specifically, the trial lecture covered cancer therapy, in reference to mechanisms of carcinogenesis, epidemiology, physiology of cancer, anticancer drugs with explanations of the mechanism of action of carcinogens, anticancer drugs, and molecular-targeted drugs from the viewpoints of organic chemistry and biochemistry by a specialized teacher. This paper reports on this experimental lecture with evaluations from students.

Effects of the α1-adrenoceptor agonist phenylephrine on SART stress-induced orthostatic hypotension in rats.

BACKGROUND: Specific alternation of rhythm in temperature (SART)-stressed rats, an animal model of autonomic imbalance, exhibit low blood pressure and tachycardia during consciousness and under anesthesia. In addition, these rats easily develop orthostatic hypotension (OH) as a response to postural manipulation. Hence, we studied the influence of the adrenalin α1-receptor agonist phenylephrine on stress-induced OH in SART-stressed rats and unstressed rats. METHODS: Male Wistar rats weighing 250-300 g were used. Rats were fixed in the supine position under urethane anesthesia. Blood pressure was directly measured from the left common carotid artery and ECG was recorded simultaneously. RESULTS: The maximum decrease in blood pressure and the area under the blood pressure-time curve were both large, while the %reflex was small in the SART-stressed rats compared with unstressed rats. In the SART-stressed rats, prolonged intravenous administration of phenylephrine reduced OH at a dose that barely affected unstressed rats. CONCLUSION: The results suggested that sympathetic dysfunction is a factor underlying SART stress-induced OH.

Specific alternation of rhythm in temperature (SART) stress-induced irritable bowel syndrome-like changes in mice and effects of drugs.

Stress is closely associated with the manifestation and progress of irritable bowel syndrome (IBS). For the purpose of establishing experimentally the relationship between IBS and stress, the transportation capacity of the small intestine in specific alternation of rhythm in temperature (SART)-stressed animals was studied using charcoal transportation method. The charcoal suspension was administered orally into the stomach of fasting mice. Mice were sacrificed after a certain time and %charcoal transit (%CT) of the small intestine was measured. The %CTs in SART-stressed mice were greater than those in unstressed or continuously cold-stressed mice. This increase in %CT remained for 1 week after discontinuation of SART stress loading. Cholinergic blockers decreased %CTs in SART-stressed mice. Increases in %CT by a cholinesterase inhibitor were less in SART-stressed mice than in unstressed mice. Increases of %CT in SART-stressed mice were suppressed by Neurotropine. These results suggested that the parasympathetic hypertonicity, not just cold, played a role in the increases in the transportation capacity in SART-stressed mice and that these animals can be a useful tool for elucidation of the mechanism of IBS.

Suppressed neutrophil respiratory burst in patients with haemorrhagic stroke.

The pathophysiology underlying the high incidence of post-stroke infectious complications has not been fully understood. We measured the respiratory burst of neutrophils as an index of their bactericidal function in patients with haemorrhagic stroke, and we also measured the plasma concentrations of noradrenalin, cortisol and neutrophil function-related amino acids. Blood samples were obtained from patients who underwent emergency craniotomies for haemorrhagic stroke (n=11) or CT-guided stereotaxic aspiration of intracerebral haematomas (n=6). Neutrophils were isolated, and their chemiluminescence response to N-formyl-methionyl-leucyl-phenylalanine was measured. Healthy volunteers served as controls (n=15). In patients with stroke, the chemiluminescence response of the isolated neutrophils was significantly lower than in the controls, and it was significantly inversely correlated with the plasma noradrenalin concentration. By Day 30, this value approached control levels. Other parameters measured were not significantly correlated with the chemiluminescence response. Stroke-induced suppression of the neutrophil respiratory burst may be responsible for frequent post-stroke infectious complications.

Effects of some beta-adrenoceptor antagonists on orthostatic hypotension in repeatedly cold- (SART-) stressed rats.

Rats stressed by specific alternation of rhythm in temperature (SART) show various symptoms of disautonomia, increased pulse rates, continuous hypotension, and severe orthostatic hypotension (OH) when they are subjected to postural change. The OH symptoms are improved by muscarinic M2-receptor blockers. In the present study, effects of beta-adrenoceptor blocking agents on OH in SART-stressed rats were investigated. Anesthetized rats were restrained on a board in the supine position, and direct blood pressure and ECG were measured automatically using Fluclet Jr.2. Postural change was performed by raising the rat's head up to a 60 degrees angle for 4 min. Unstressed rats treated with hexamethonium showed large decrease in blood pressure, small reflex from the bottom of pressure and decreased tachycardia reflex, whereas isoproterenol showed little changes. In SART-stressed rats, isoproterenol alleviated the decrease in blood pressure in postural change, brought large reflex from the bottom of pressure and increased tachycardia reflex, whereas hexamethonium had little changes. Propranolol and atenolol induced the similar changes as those seen by hexamethonium. ICI-118,551, a selective beta2-adrenoceptor antagonist showed large reflex from the bottom of pressure and increased tachycardia reflex in stressed rats, whereas little changes in unstressed rats. In conclusion, it was suggested that the hypotension in OH manifestation time of rats reflects the state of peripheral blood vessels, and beta1-adrenoceptors played a role in compensatory tachycardia reflex and beta2-adrenoceptors in blood pressure reflex. The circulatory regulation in SART-stressed rats seems to be poorly functioning in nervous reflex in postural changes.

Effects of AF-DX116 and other muscarinic receptor antagonists on orthostatic hypotension in autonomic imbalanced (SART-stressed) rats.

SART (specific alternation of rhythm in temperature)-stressed rats are an animal model of autonomic imbalance created by exposing animals to repeated cold stress. The SART-stressed rats have been shown to easily develop orthostatic hypotension (OH). In this study, effects of AF-DX116, a selective M(2) antagonist, and other muscarinic receptor antagonists on OH were investigated in SART-stressed and unstressed rats. Each anesthetized rat was canulated into the left common carotid artery, and blood pressure (BP) and heart rate were measured. Stimulation for postural change was initiated by head-up tilting. As the indices of OH, the maximum fall of BP, % reflex (recovery from maximum fall), and the area enclosed between the baseline and the recovery curve for BP (AUC) were used. Large AUC and small % reflex in SART-stressed rats were changed, becoming similar to those of the unstressed rats by AF-DX116 and methoctoramine. Atropine and methylatropine had similar effects to AF-DX116. However, the effects of methoctoramine, atropine, and methylatropine were less than that of AF-DX116. Pirenzepine was not effective. In conclusion, it was suggested in SART-stressed rats that OH was related to hyperactivity in the parasympathetic nerve and the M(2) receptor played the major role in OH.

A role for corticotropin-releasing factor in repeated cold stress-induced anxiety-like behavior during forced swimming and elevated plus-maze tests in mice.

SART (specific alternation of rhythm in temperature) stress is known to cause anxiety-like behavior in mice/rats in several anxiety-related behavioral tests. In the present study, we investigated possible roles for corticotropin-releasing factor (CRF) and glucocorticoids in SART stress-induced anxiety-like behavior in two different anxiety-related behavioral tests. In the forced swimming test, CRF, administered intracerebroventricular (i.c.v.) at 0.5-2 pmol/mouse, dose-dependently reduced immobility time in unstressed and SART-stressed mice. alpha-Helical CRF, a specific CRF receptor antagonist, administered i.c.v. at 0.1-1 nmol/mouse, dose-dependently increased immobility time in SART-stressed mice, but not in unstressed mice. In the elevated plus-maze test, CRF at 10-20 pmol/mouse significantly decreased the time spent in open arms in unstressed mice. CRF at a high dose tended to decrease this time in SART-stressed mice, but this decrease was not statistically significant. alpha-Helical CRF failed to modify the time in unstressed mice. In contrast, alpha-helical CRF at 0.38 and 0.75 nmol/mouse increased the time in SART-stressed mice. Both immobility time in the forced swimming test and time spent in open arms in the elevated plus-maze test in unstressed and SART-stressed mice were unaffected by adrenalectomy. These results suggest that CRF plays an important role in anxiety-like behavior caused by SART stress.