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Brown trout, Salmo trutta, and rainbow trout, Oncorhynchus mykiss, have been introduced to freshwaters in Hokkaido, Japan. Today, it is recognized that these introduced salmonids have negative impacts on native salmonids such as white-spotted charr, Salvelinus leucomaenis, and masu salmon, O. masou. In particular, interspecific competition may be an important mechanism that could contribute to the exclusion for native salmonids. In this study, experimental pairwise contests were conducted to compare interference competitive ability between native and introduced salmonids. We demonstrated that brown trout were competitively superior to white-spotted charr and masu salmon whereas rainbow trout were superior to white-spotted charr. We suggest that introduced brown trout negatively impact both white-spotted charr and masu salmon, and introduced rainbow trout negatively impact white-spotted charr.

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Using an artificial stream, habitat use by two sympatric native salmonids in the presence and absence of introduced salmonid species was investigated experimentally. When only native white-spotted charr Salvelinus leucomaenis and masu salmon Oncorhynchus masou were sympatric, they occupied different microhabitats. In the presence of introduced brown trout Salmo trutta or rainbow trout Oncorhynchus mykiss, however, white-spotted charr and masu salmon were observed to use a similar habitat and interspecific competition between white-spotted charr and masu salmon was initiated. The study suggested that the coexistence of native salmonids was negatively affected through interspecific competition between native and introduced salmonids.

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During severe hypoxia, pretreatment with FBP completely preserves adenosine triphosphate and almost completely preserves cell morphology but does not alter hypoxia-induced decreases in intracellular pH. Pretreatment also substantially augments the flux of glucose into the pentose-phosphate pathway.

Summary:  A patient with Williams syndrome, craniosynostosis, and infantile spasms is described. At age 6 months, the infant demonstrated infantile spasms and craniosynostosis and was operated on for craniosynostosis and treated with adrenocorticotropic hormone (ACTH) for the infantile spasms. ACTH completely controlled the seizures, but was halted because of the progression of ventricular hypertrophy. The seizure returned, and he was found to have elfin face, failure‐to‐thrive, developmental delay, and dental malformation in addition to congenital heart defects. High‐resolution chromosome analysis revealed interstitial deletion of 7q11.22‐q11.23. Therefore his clinical and cytogenetic diagnosis was Williams syndrome. Thyrotropin‐releasing hormone (TRH) therapy reduced his seizures and improved the findings of EEG without cardiac side effects. In addition, his psychomotor development was slightly improved.

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