Hemorrhage is one of the most prominent manifestations produced by the parenteral administration of various snake venoms especially of Habu (Mitsuhashi et al., 1959; Ohsaka et al., 1961) and other species of Crotalidae (Fidler et al., 1940; Taube et al., 1937). In order to study the principle(s) responsible for hemorrhage caused by snake venom, a quantitative method for the determination of hemorrhagic activity is required. Up to date, however, few attempts have been made to establish the quantitative estima tion of hemorrhagic activity of snake venom. Minton (1956) and Mitsuhashi et al. (1959) tried to estimate the hemorrhagic activity but the results they obtained were not repro ducible in our hands. The present authors proposed a new method, which consists of the following procedures; (1) intracutaneous injection of venom into the depilated back skin of rabbits; (2) accurate measurement of the size of hemorrhagic spot carried out from the inside of the removed skin; (3) application of the parallel line assay method for the estimation. By this method it was possible to study the relationships of hemorrhagic activity to proteolytic and other pathological activities of Habu venom (Ohsaka et al., 1960, 1961). In this paper, details of the new method will be presented. MATERIALS AND METHODS Snake venom: The work to be reported here dealt with the venom from a species of Trimeresurus flavoviridis (Habu).* Each pool of the crude venom was dried, powdered and then stored at room temperature until used. These preparations, dissolved in M/30 phosphate buffered saline (pH

A sufficient supply of NADPH is a critical factor in L-lysine production by Corynebacterium glutamicum. Endogenous NAD-dependent glyceraldehyde 3-phosphate dehydrogenase (GAPDH) of C. glutamicum was replaced with nonphosphorylating NADP-dependent glyceraldehyde 3-phosphate dehydrogenase (GapN) of Streptococcus mutans, which catalyzes the reaction of glyceraldehyde 3-phosphate to 3-phosphoglycerate with the reduction of NADP ؉ to NADPH, resulting in the reconstruction of the functional glycolytic pathway. Although the growth of the engineered strain on glucose was significantly retarded, a suppressor mutant with an increased ability to utilize sugars was spontaneously isolated from the engineered strain. The suppressor mutant was characterized by the properties of GapN as well as the nucleotide sequence of the gene, confirming that no change occurred in either the activity or the basic properties of GapN. The suppressor mutant was engineered into an L-lysine-producing strain by plasmid-mediated expression of the desensitized lysC gene, and the performance of the mutant as an L-lysine producer was evaluated. The amounts of L-lysine produced by the suppressor mutant were larger than those produced by the reference strain (which was created by replacement of the preexisting gapN gene in the suppressor mutant with the original gapA gene) by ϳ70% on glucose, ϳ120% on fructose, and ϳ100% on sucrose, indicating that the increased L-lysine production was attributed to GapN. These results demonstrate effective L-lysine production by C. glutamicum with an additional source of NADPH during glycolysis.

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We report on a 3-year-old girl with respiratory syncytial virus (RSV) encephalitis manifested by disturbance of consciousness, conjugate eye deviation, anuria, truncal ataxia and intention tremor. T2-weighted magnetic resonance imaging (MRI) showed hyperintense areas in the cerebellar cortex. No lesion was detected in the cerebral cortex, pons or spinal cord. The hyperintense areas in the cerebellar cortex diminished with recovery from the clinical manifestations and had resolved 2 months after onset. The MRI lesions in the cerebellum were considered to be due to oedema. SPECT and positron emission tomography (PET), performed 3 months after onset, disclosed areas of hypoperfusion and hypometabolism at the same sites. One year after onset, MRI showed mild atrophy of the cerebellum. Hypoperfusion on SPECT and hypometabolism on PET remained. Neuroimaging showed that ataxia and tremor in this case were the result of cerebellitis. The patient has no neurological deficit except for mild truncal ataxia. This patient is a rare example of RSV encephalitis.