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In Japan, stocked chum salmon (Oncorhynchus keta) fry may have become the perfect prey for non-native brown trout (Salmo trutta), which are popular targets of anglers. If this is the case, fry stocking which is intended to boost commercial fishing may be helping to sustain the populations of an invasive predator. We used dietary and biochemical analyses to examine whether brown trout quickly restore their nutritional status following wintertime declines by preying upon chum salmon fry that are stocked in spring. We targeted six rivers in Hokkaido, Japan, three with fry stocking and three without. Changes in brown trout condition factor, triglyceride contents in muscle and serum, serum insulin-like growth factor-1 (IGF-1; an indicator of short-term growth), and docosahexaenoic acid (DHA; an essential fatty acid abundant in fish) content in muscle were examined between before stocking and during the stocking period in the six rivers. Dietary analysis showed that brown trout preyed on fry during the stocking period in all stocked rivers. Their nutritional status tended to be higher during the stocking period than before stocking in stocked rivers, but not in unstocked rivers. These results suggest that the massive stocking of chum salmon fry provides brown trout with the perfect prey to quickly restore their nutritional status and fuel increased growth; this may therefore be a controversial issue among stakeholders.

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Nematodes that parasitize salmonids are found in both seawater and freshwater. Unlike seawater species such as those in family Anisakidae, freshwater species have not been well studied. In particular, the influences of these nematodes on the body condition of salmonids remain unclear. We studied the effects of Salmonema cf. ephemeridarum on the body condition of masu salmon Oncorhynchus masou. We found a positive relationship between the number of parasites and fish fork length. In contrast, we found a negative relationship between the body condition (condition factor) of fish and the number of parasites. These results suggest that nematode infection could affect host energy reserves for future growth.

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Increases in prey population size can affect the physiology and ecology of upper-trophic level organisms. This phenomenon is known as a bottom-up effect. For example, the increased abundance of prey resources can trigger physiological (internal) changes in predators, such as improvements in nutritional status. However, these physiological aspects of bottom-up effects have not been considered. In this study, we tested the hypothesis that white-spotted charr Salvelinus leucomaenis, a salmonid fish, increases body stores of omega-3 fatty acids, especially docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), by preying upon stocked hatchery-reared masu salmon Oncorhynchus masou fry in streams. The dynamics of fatty acid contents in charr inhabiting salmon-stocked and unstocked streams clearly support this hypothesis: fatty acid contents (DHA, EPA, and total fatty acid) increased after stocking in stocked streams, but not in unstocked streams. In addition, DHA increased with increasing body size of white-spotted charr and vice versa for EPA. The impacts of human activities, such as fish stocking, on freshwater ecosystems are a matter of serious concern for conservation. Future attempts to gain a comprehensive understanding of the impacts of fish stocking should consider not only community ecology but also physiology.

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Domestication and captive breeding can compromise the obstacle- and predator-avoidance capabilities of animals in the wild. Whereas previous studies only examined these effects in combination, here we examine them individually by comparing the abilities of wild, F1 (offspring of wild parents) and captive-bred (approx. F15) masu salmon Oncorhynchus masou to avoid a falling object under experimental conditions. Rates of avoidance failure were low (wild, 12.5%; F1, 10.7%; captive-bred, 8%) under light conditions, but increased under dark conditions (wild, 11.1%; F1, 32.1%; captive-bred, 60.0%). We attribute the elevated avoidance failure rate among F1 fish to the lack of learning opportunities in hatchery environments (i.e. domestication), and the further elevation of avoidance failure rate among captive-bred fish to the degradation of sensory organ function (i.e. captive breeding). These results imply reduced survival rates for F1 and captive-bred fish in the wild and are consistent with the low stocking efficiencies reported for captive-bred masu salmon.

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Because captive-bred animals gradually adapt to artificial rearing environments due to evolving life history traits, such individuals sometimes show lessened performance in natural environments. The lateral line system, one of the principal sensory organs of fishes, varies according to habitat environments, sometimes differing even within the same species. A reduction in lateral line elements may also occur in successive generations of captive-bred fish. Such a reduction, involving neuromasts over the entire body, was examined for the first time in captive-bred masu salmon Oncorhynchus masou masou. The total number of neuromasts in captive-bred fish was ca. 10% lower than in wild-caught and F1 fishes, suggesting that the system in captive-bred fish had reduced in number due to domestication. Furthermore, differences in total neuromast numbers between captive-bred and wild fish were greater than between anadromous and fluvial populations of the species. The lower number of neuromasts could be one of the reasons behind the lower survival of captive-bred fish in natural environments.

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Pulsed supplies of prey generally increase predator food intake. However, it is unclear whether this holds true when predators and pulsed prey are in the same guild (i.e. intraguild (IG) predators and prey). IG prey may increase IG-predator food intake through predation, but they may decrease food intake through competition. To test these hypotheses, we compared the food intake of white-spotted charr (Salvelinus leucomaenis) (IG predator) in streams that were stocked or unstocked with masu salmon (Oncorhynchus masou) fry (IG prey) in streams in Hokkaido, Japan. One day after stocking, mean stomach content weight of charr was six times higher than in unstocked streams due to fry consumption. In particular, large charr showed intense piscivory. However, predation on fry was rare after about three weeks. Some factors that could explain this time-limited IG predation include the growth and decreasing abundance of fry over time and the acquisition of predator-avoidance behaviour. In days other than the first-day post-stocking, food intake by charr did not differ between stocked and unstocked streams. No effects of interspecific competition on charr food intake were observed.

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UNLABELLED: Newborn screening studies indicate the expected high incidence of later-onset Fabry disease with silent Fabry nephropathy while, with recent improved clinical care of premature infants, children with congenital oligonephropathy caused by premature embryonal development of the kidney are thought to be increasing. However, the coexistence of Fabry nephropathy and oligonephropathy has not been reported previously. We present the case of a 13-year-old boy who was diagnosed with Fabry nephropathy accompanied with histological features of oligonephropathy. He was born as a preterm baby, and a renal biopsy was performed because of mild renal dysfunction and mild proteinuria. He had neither characteristic early symptoms nor a family history of Fabry disease. Histologic findings demonstrated diffuse global enlargement and foamy change of podocytes with markedly decreased number and enlargement of the glomeruli. Both his plasma and leukocyte α-galactosidase A (GLA) activities were markedly decreased, and the plasma globotriaosylsphingosine and urine globotriaosylceramide levels were increased. Gene analysis revealed a missense mutation, R112H, in the GLA gene, which had been reported in the later-onset phenotype of Fabry patients. He is now under treatment with enzyme replacement therapy and an angiotensin-converting enzyme inhibitor. CONCLUSION: This case indicated the possible co-occurrence of Fabry nephropathy and oligonephropathy. For early diagnosis and timely management, careful examinations for proteinuria and renal function, in addition to establishing an effective screening system for Fabry disease, will be necessary.

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N-Methyl-D-aspartate-mediated neurotoxicity is known to involve nitric oxide production and to be augmented in an environment of reactive oxygen species. We used TUNEL staining and homogenous cytosolic immunoreactivity of cytochrome c in an acute brain slice preparation to investigate the influence of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, on N-methyl-D-aspartate-induced apoptosis. Cerebrocortical slices were obtained from parietal lobes of 7-day-old Sprague-Dawley rats, superfused with well-oxygenated artificial cerebrospinal fluid, and metabolically recovered. Subsequent 30-min exposures to 10 microM N-methyl-D-aspartate in treated and untreated slices were followed by 4 h of recovery superfusion with oxygenated artificial cerebrospinal fluid. Outcomes were compared for three groups of slices: "the N-methyl-D-aspartate-only group"; "the edaravone treatment group", which had 20 microM edaravone present throughout and subsequent to N-methyl-D-aspartate exposure; the "control group", in which slices were superfused only with oxygenated artificial cerebrospinal fluid. At the conclusion of recovery (t = 4 h), the percentage of TUNEL-positive cells in the edaravone treatment group (7.0+/-3.3%) was significantly reduced from the percentage for the N-methyl-D-aspartate-only group (21.9+/-4.1%), and insignificantly greater than the percentage for the control group (3.4+/-2.1%). Percentages of cytochrome c positive cells at t = 1 h were significantly increased (p < 0.01) in the N-methyl-d-aspartate-only group (30.6+/-1.9%) compared to percentages for both the control group (11.4+/-2.6%) and the edaravone treatment group (15.2+/-2.1%). Edaravone's reduction in TUNEL staining and cytochrome c release provides evidence of reactive oxygen species mechanisms and antioxidant benefits in cytochrome c-mediated apoptosis during N-methyl-D-aspartate excitotoxicity.

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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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We performed a tissue culture study using embryonic rat brain to investigate the effect of excessive stimulation of NMDA receptors on neuronal migration in the cerebral cortex. After progenitor cells in the ventricular zone of E16 cerebral cortex explants were labeled with [(3)H]thymidine, the explants were cultured for 48 h, and distributions of labelled cells were evaluated autoradiographically. Stimulation of NMDA receptors by NMDA and ibotenate, NMDA receptor agonists added to the culture medium in separate studies, caused percentages of labeled cells to decrease significantly in the intermediate zone and increase in the ventricular zone. The results suggest that in rat cerebral cortex, agonist stimulation of NMDA receptors inhibits neuronal migration.

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