The flux of emerging aquatic insects from streams can provide a significant energy subsidy to riparian web‐building spiders. However, despite the high temporality of aquatic insect emergence, the effects of such aquatic insect dynamics on spider distribution are poorly understood. To examine the relationship, the aquatic insect flux from a headwater stream in a northern Japanese deciduous forest was experimentally manipulated by using a greenhouse‐type covering, during May to July. Under natural conditions, the aquatic and terrestrial insect abundances dramatically decreased and increased from May through July, respectively. The experimental reduction of aquatic insect flux depressed the density of horizontal orb weavers (Tetragnathidae) in both May and June, but not in July when aquatic insects were scarce, indicating a temporal limitation on spider distribution by aquatic insect flux. In contrast, the densities of both vertical orb weavers (Araneidae) and sheet weavers (Linyphiidae) were unaffected by the manipulation throughout the study period. These various responses, differing among months or spider guilds, may be attributed to the degree of specialization for aquatic prey in the spiders and their mobility in response to aquatic insect flux. The experimental results provided direct evidence that the temporal dynamics of aquatic insect flux, as well as spider characteristics, were primary factors determining the distributional patterns of riparian web‐building spiders.

These data suggest that patients with acute type B dissection who have a large aortic diameter (> or = 40 mm) and a patent primary entry site in the thorax should be treated surgically during the acute phase on the condition that the surgical risk in this phase is limited.

1. We examined effects of water temperature on the community structure of a three trophic level food chain (predatory fish, herbivorous caddisfly larvae and periphyton) in boreal streams. We used laboratory experiments to examine (i) the effects of water temperature on feeding activities of fish and caddisfly larvae and on periphyton productivity, to evaluate the thermal effects on each trophic level (species-level experiment), and (ii) the effects of water temperature on predation pressure of fish on abundance of the lower trophic levels, to evaluate how temperature affects top-down control by fish (communitylevel experiment). 2. In the species-level experiment, feeding activity of fish was high at 12°C, which coincides with the mean summer temperature in forested streams of Hokkaido, Japan, but was depressed at 3°C, which coincides with the mean winter temperature, and also above 18°C, which coincides with the near maximum summer temperatures. Periphyton productivity increased over the range of water temperatures. 3. In the community-level experiments, a top-down effect of fish on the abundance of caddisfly larvae and periphyton was clear at 12°C. This effect was not observed at 3 and 21°C because of low predation pressure of fish at these temperatures. 4. These experiments revealed that trophic cascading effects may vary with temperature even in the presence of abundant predators. Physiological depression of predators because of thermal stress can alter top-down control and lead to changes in community structure. 5. We suggest that thermal habitat alteration can change food web structure via combinations of direct and indirect trophic interactions.

T cell receptor α chain–deficient (TCR-α−/−) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4+TCR-ββ (CD4+ββ) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4+ββ T cells, we treated TCR-α−/− mice with anti–IL-4 monoclonal antibody (mAb). Approximately 60% of TCR-α−/− mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti–IL-4 mAb–treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab–treated mice. Although TCR-α−/− mice treated with either specific or mock Ab developed CD4+ββ T cells, only those treated with anti–IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon γ–specific expression. These findings suggest that IL-4–producing Th2-type CD4+ββ T cells play a major immunopathological role in the induction of IBD in TCR-α−/− mice, a role that anti–IL-4 mAb inhibits by causing Th2-type CD4+ββ T cells to shift to the Th1 type.