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Cu nonmagnetic metallic nanoclusters were embedded in the ZnO thin film by using nanocluster beam deposition. No presence of secondary phase was detected in X-ray diffraction (XRD) analysis, but secondary phases CuO and Cu2O nanoclusters were detected in films by transmission electron microscopy (TEM). Cu nanoclusters embedded in ZnO films have the average particle size around 8-10 nm. Cu atoms were surrounded by ZnO matrix, and the interface effect caused overlapping of p-orbital from O contributed by ZnO and d-orbital contributed by Cu as suggested by XPS and UV-Vis absorbance results. Alternating gradient field magnetometer (AGM) results show that the embedment of nonmagnetic Cu nanoclusters in ferromagnetic ZnO thin films can enhance the room temperature ferromagnetism of ZnO thin film up to maximum Ms = 2.64 emu/cc with small coercivities lower than 70 Oe. The saturation magnetization (Ms) value increases with Cu volume fraction in ZnO and decreases with Cu volume fraction after certain volume fractions of Cu were achieved. Based on the clues given by XPS results, +1 valence state of Cu is in the ferromagnetism favorable state, indicating possible spin polarization occurred and ferromagnetism induced in the system.

1. In the rabbit jejunum nerveside causes alternating contractions of the longitudinal and circular muscles, which are similar to the peristaltic reflex produced by distension of the gut. These effects are abolished by dibucaine (Nupercaine) and tetrodotoxin. The site of action is located in Auerbach's plexus. 2. Circular muscle contractions due to nerveside are blocked by hexamethonium, nicotine, morphine, atropine and hyoscine. There is no circular response to nerveside after removal of Auerbach's plexus. It is suggested that nerveside acts by stimulating presynaptic nerve terminals which are cholinergic and that the circular muscle is innervated by cholinergic nerve fibres. 3. Longitudinal muscle contractions due to nerveside are not affected by hexamethonium but can be blocked by paralysis of myenteric ganglia with nicotine. They are not abolished by morphine or by cholinolytic drugs. It is suggested that nerveside acts by stimulating either receptors insensitive to acetylcholine in ganglion cells or non-cholinergic presynaptic nerve terminals. It is further suggested that the longitudinal muscle of the rabbit gut is supplied by non-cholinergic as well as cholinergic nerve fibres.

The incidence of aortic incompetence complicating ventricular septal defect has been estimated as varying from 2-5% (Glasser et alii, 1972) to 5% (Nadas et alii, 1964). Although numerous publications have appeared describing the clinical, pathological and surgical aspects of this syndrome in different parts of the world, documentation of its occurrence in Asian patients has been rare except for reports from Japan (Tatsuno et alii, 1973; Mizuno and Saegusa, 1967). This paper describes our experience of 12 cases collected over 10 years.

"Nerveside", a phosphopeptide extracted from ox and dog brains by Toh, was injected into one lateral ventricle of four rats previously prepared for the injection as well as for recordings of the EEG of the dorsal hippocampus (field CA1) and sensorimotor cortex. "Nerveside" in doses of 150 and 300 micrograms/animal induced a transient stereotyped behaviour and longer lasting alterations of the EEG activity and vigilance pattern. Wakefulness was increased, slow wave sleep and REM-sleep were diminished. The vigilance pattern was characterized by rapid shifts between all three vigilance states. The effects of "nerveside" were visible for about three hours.

1. An enzyme which can be extracted from brain inactivates nerveside in the optimum pH range 5·8–7·0. 2. The polybasic acids trypan blue and its analogue trypan red, bromphenol blue and its analogue bromthymol blue at concentrations of 0·22 m M and ethylenediaminetetra-acetic acid (EDTA) at a concentration of 1 m M are strong inhibitors of the enzyme. 3. Penicillin which is a monobasic carboxylic acid also inhibits the enzyme but only if concentrations as high as 3·6 m M are used. The antibiotic streptomycin which is a basic substance does not inhibit the enzyme. 4. Caffeine at a concentration of 7·2 m M only weakly inhibits the enzyme. 5. Chymotrypsin and wheat germ acid phosphatase also inactivate nerveside at pH 5·9 and are inhibited by the acidic dyes and penicillin. EDTA inhibits wheat germ phosphatase but activates chymotrypsin. 6. Inactivation of nerveside by the brain enzyme and by wheat germ phosphatase is different from the action of chymotrypsin. Nerveside solutions incubated with chymotrypsin completely lose all biological activity whereas if incubation is carried out with either the brain enzyme or wheat germ acid phosphatase a residual biological activity remains even when the concentration of these two enzymes is increased. This residual biological activity is due to a peptide as it is destroyed by chymotrypsin. 7. The manner in which nerveside is inactivated by the brain enzyme is uncertain as the preparation of the latter contained phosphodiesterase and protease activities which were similarly inhibited by the acid dyes, penicillin and EDTA. 8. Pentylenetetrazole, picrotoxin, strychnine and tetanus toxin do not inhibit the brain enzyme. 9. The nerveside-inactivating enzyme is not identical with the Substance P-inactivating enzyme in brain as the former is inhibited by EDTA while the latter is not.

Besides histamine another smooth muscle stimulating substance has been found in the nasal mucosa of dog and sheep. It is an acid which is readily oxidized by neutral aqueous potassium permanganate and osmium tetroxide, and is thermostable at pH 10.8 but not at pH 2.8. The purification of this acid has been followed by using the atropinized tortoise intestine as a test object, which is insensitive to acetylcholine, 5-hydroxytryptamine and small amounts of histamine. Both the tortoise intestine and rat colon are contracted by this acidic substance. The amount of histamine found in sheep nasal mucosa ranged from 12 to 23 μg./g. tissue and in dog nasal mucosa from 6 to 13 μg./g. tissue.