A flowing-afterglow apparatus coupled with a low pressure chamber has been used to measure product ion distributions and rate constants in the charge-transfer reactions of Ar+ with CH4, C2Hn(n=2,4,6), and C3Hn(n=6,8) at thermal energy. Only parent cation is formed for C2H2 due to energy restriction. Major product channels are dissociative charge transfer followed by cleavage of C–H bond(s) for CH4, C2H4, C2H6, and C3H6, while by cleavage of a C–C bond for C3H8. A comparison of the product ion distributions with the photoelectron–photoion coincidence data for CH4, C2H4, and C2H6 leads us to conclude that the mean energies of precursor (pre)dissociative states are 15.3–15.5 eV, which are 0.3–0.5 eV below the resonance states. Thus the fractions of available energy deposited into internal modes of precursor parent ions at the instant of charge transfer are estimated to be 85%–95%, indicating that most of the CT reactions occurs without significant momentum transfer. The total rate constants for CH4, C2Hn(n=4,6), and C3Hn(n=6,8) are (0.78–1.1)×10−9 cm3 s−1, corresponding to 60%–92% of the calculated values from the Langevin theory. The rate constant for C2H2, 4.2×10−10 cm3 s−1, amounts to 38% of the kcalcd value. The small kobsd/kcalcd ratio is attributed to the lack of ionic states with favorable Franck–Condon factors for ionization.
The relationships between plasma concentrations of diphenylhydantoin (DPH), phenobarbital (PB), carbamazepine (CBZ), and 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810), a new anticonvulsant agent, and their anticonvulsant and neurotoxic effects were studied in various species of animals. Anticonvulsant activities of test drugs were examined by the maximal electroshock seizure (MES) test. Neurotoxicities were determined by the rotorod performance test in mice and rats and by behavioral observations in rabbits, dogs, and monkeys. It was demonstrated that both the anticonvulsant effects and the neurotoxic effects of the drugs tested were more closely correlated with their plasma concentrations than with the dosages administered. There was a critical plasma concentration for each drug to show an anticonvulsant effect or to cause a neurotoxic effect in an individual animal. The critical plasma concentrations for anticonvulsant and neurotoxic effects of each drug were relatively constant among different species, with the exception of DPH in rabbits, which had twice the value in other species. The therapeutic ranges of plasma concentrations of DPH, PB, and CBZ determined in various species of animals coincided well with those recommended clinically. AD-810 was found to be effective against MES without signs of neurological toxicity in the ranges of plasma concentrations of 9.8 to 74.0, 10.8 to 95.0, 9.6 to 117.0, and 12.6 to 96.2 microgram/ml in mice, rats, rabbits, and dogs, respectively. These results seem to suggest that AD-810 may be effective clinically at plasma concentrations above 10 microgram/ml, with a therapeutic range up to 70 microgram/ml, which is much wider than the therapeutic ranges of DPH (10--20 microgram/ml), PB (10--30 microgram/ml), and CBZ (4--10 microgram/ml).
The objective of the present study is to investigate the suitable impeller geometry for a mini turbo-pump, which is defined as the size having impeller diameter between around 5 mm and 50 mm. This is treated because those pumps having the above size are regarded as low efficiency machines if efficiency is less than 40 percent or 50 percent. Considering that not only low Reynolds number and tip clearance but the design method are the major causes for low performance, we carried out the performance test experimentally using two semi-open centrifugal impellers: one is named as Impeller B of 36 mm diameter and the other is Impeller C of 34 mm diameter. And the former is designed by a conventional method and the latter is based on the proposed method. In the performance tests, rotational speed was varied between 3000 rpm and 10,000 rpm and the axial clearance at the blade tip of impeller exit was between 0.2 mm and 0.8 mm. It is clearly seen from the results that Impeller C gives the better hydraulic performance. It is also clarified that the effect of tip clearance on Impeller C performance is much smaller than that of the Impeller B. Further, we conducted numerical calculation of impeller performance, where the commercial CFD code named TASCflow was used with k-ω turbulence model. From the results, the turbulent flow analysis is reasonably usable to study the flow in the above mini impellers.
Abstract--Prolonged ischemia by bilateral carotid artery ligation in rats resulted in cerebral edema with a reduced energy state. Mitochondria isolated from the ischemic brain showed an impairment of oxidative phosphorylation.The ischemic brain was also characterized by a remarkable accumulation of free fatty acids known to have properties as an uncoupling factor. The major components of increased free fatty acids were palmitic, stearic, oleic and arachidonic acids. The analysis of saponified myelin and mitochondrial lipids from the ischemic brain showed a decrease in fatty acid contents.The main components of decreased fatty acids in these subcellular fractions corresponded to those of free fatty acids accumulating in the ischemic brain. These results indicate that cerebral energy failure in the ischemic brain is related to the accumulation of free fatty acids, which are derived from endogenous brain lipids.Although considerable efforts have been devoted to the study on experimental brain edema, the biochemical alterations associated with the pathogenesis still remain to be eluci dated. Current evidence suggests that cerebral swelling is accompanied by a reduction of the cerebral energy state (1-3) and an impairment of mitochondrial function (4-6). A deficiency of available energy is assumed to cause a disturbance of active ionic transport across the cell membrane, which could lead to cerebral swelling or cell damage. In a previous report (7), we showed that unilateral brain edema produced in rats by the combination of ischemia and hypoxic exposure was characterized by a considerable increase of free fatty acids in the brain. Our experiments also demonstrated that oleic and arachidonic acids, which increased markedly in the edematous brain, inhibited oxidative phosphorylation of in vitro mitochondrial preparations (7). These observations provided information for further study on the biochemical mechanism of cerebral energy failure in brain edema.In the present study, we investigated cerebral energy metabolism in another form of brain edema produced in rats by a permanent ligation of bilateral carotid arteries. This paper deals with biochemical events associated with cerebral energy failure and the free fatty acid change in the subcellular lipids of the edematous brain.
MATERIALS AND METHODS
Brain ischennaMale Wistar rats weighing 80-100 g were anesthetized with sodium hexobarbital (150 mg/
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