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In order to gain an obvious insight into the role of water in the mechanism of the excimer laser ablation of the cornea, we have macroscopically investigated the ablation behavior of collagen gel in the swelled state by direct photoetching using an ArF excimer laser with time-resolved photography, and furthermore, the thermal effects on the microscopic structures of the collagen molecules by FTIR–ATR spectroscopy. The hydrated collagen film (HF) has a smaller threshold fluence than the dried collagen film (DF). From the time-resolved photographs, the ejected materials were detected only for HF. It was predicted that the effect of bubble formation for HF contributes to the etching. The FTIR–ATR spectroscopic results revealed that the existence of the water suppressed the denaturation of the collagen to gelatin on the surface in the irradiated region. Overall, it was inferred that during the ablation process for HF, the laser energy would be mostly consumed as the latent heat of evaporation of water, that is, the water in the gel matrix would contribute to the suppression of the increment in the temperature in the irradiated region.

We investigated the interaction of KSG-504 with CCK-8- or pentagastrin-induced gallbladder and gastrointestinal responses in vitro and in vivo. KSG-504 (10(-7)-10(-4) M) inhibited CCK-8-induced contractions of both isolated guinea pig gallbladder and rabbit terminal cavity of the bile duct in a concentration-dependent manner. Furthermore, intravenous administration of KSG-504 also dose-dependently inhibited CCK-8-induced gallbladder contraction in anesthetized guinea pigs with an IC50 value of 0.23 mg/kg. In conscious mice, KSG-504 inhibited both CCK-8- and egg yolk-stimulated gallbladder emptying in a dose-dependent manner (IC50: 13.3 and 9.6 mg/kg, respectively). The CCK-8-induced delay of gastric emptying in conscious rats was also antagonized by KSG-504 with an IC50 value of 3.78 mg/kg, i.v., whereas pentagastrin-stimulated gastric acid secretion in anesthetized rats was not affected by KSG-504 at all. KSG-504 (1 mg/kg, i.v.) also inhibited CCK-8-induced duodenal and jejunal contractions in anesthetized rabbits. These results indicate that KSG-504 exerts an antagonistic effect on CCK-A receptors in the gastrointestinal tract, but not on gastrin receptors in the stomach.

We investigated the protective and/or therapeutic effects of a new cholecystokinin receptor antagonist, KSG-504, on different types of experimental pancreatitis in the rat and mouse. The intravenous injection of KSG-504 (10, 25, 50 and 100 mg/kg) before caerulein administration to the rat inhibited the increases in plasma amylase, lipase and of pancreatic wet weight in a dose-dependent manner. The histological changes due to caerulein-induced acute pancreatitis were also decreased by KSG-504 when KSG-504 (25, 50 and 100 mg/kg) was administered after the induction of acute pancreatitis; the increases in plasma amylase, lipase and pancreatic wet weight were reduced, but the histological changes of the pancreas were not decreased significantly. In the second experiment, acute pancreatitis was induced in rats by injecting 0.3 ml of 6% sodium taurocholate into the pancreatic interstitial tissue. KSG-504 administered immediately and 1.5 hr after sodium-taurocholate injection at 100 mg/kg reduced the increases of pancreatic enzymes in the plasma, pancreatic wet weight and ascites. Moreover, KSG-504 (50 and 100 mg/kg, i.v., x 2) mitigated the histological changes of taurocholate-induced acute pancreatitis. Another type of acute pancreatitis was induced in mice by dl-ethionine (0.5 g/kg, p.o., x 4) and a choline-deficient diet. KSG-504 (10, 30 and 100 mg/kg) was subcutaneously administered five times every 12 hr during the experiment. KSG-504 elongated the survival of mice in a dose-dependent manner. These findings suggest that KSG-504 has potent protective and/or therapeutic effects against acute pancreatitis and that cholecystokinin may be involved in the development of pancreatitis.

The formation of nap-type structures induced by UV-laser irradiation of renatured gelatin films with various triple helix contents was observed by an atomic force microscope. Surface topography was found to be dependent on degree of helix content (DHC), fluence, and number of applied pulses (PN). The surface roughness (Ra) increased with PN following a hyperbolic curve for the renatured gelatin films with DHC of more than ca. 7%. The increment of Ra tended to be depressed with increasing DHC.

The formation of nap-type or wall-type structures on laser irradiated collagen related biopolymers films is reported. An atomic force microscope (AFM) allows a highly sensitive surface characterization of the same area of the irradiated sample between subsequent laser pulses. A change in surface topography was found to be dependent on the fluence and number of applied pulses. A successive measurement technique of AFM gave significant information on the mechanism of surface structure formation.

The parametric decay instability which is excited by the CO 2 laser light (10 12 W/cm 2 ) in a high-pressure hydrogen plasma characterized by n e ≈10 19 cm -3 , T e ≈2–5 keV, T i ≈5–10 keV is detected for the first time by the forward scattering (4.3°±0.3°) of the ruby laser light. The wavenumber k is about 9×10 3 cm -1 and the frequencies of the low frequency wave ω L and the high frequency wave ω H are 3×10 13 rad/sec and 1.6×10 14 rad/sec respectively. Considering ω H +ω L ≈ω co 2 =1.8×10 14 rad/sec, the parametric decay instability is excited by the electric field of the CO 2 laser. It is not clear whether phonon-plasmon decay instability is excited or not.

The non-destructive production of compressed mega-gauss magnetic field in a plasma focus is experimentally investigated. Interferometric, magneto-optical and electrodynamical measurements show that the maximum field strength is about 1 MG in the converging plasma layer which has a pure magnetohydrodynamic shock structure.