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The terrestrialization of floodplains has become a concern to river managers and ecologists because it has degraded habitats for floodplain-dependent organisms. We examined the temporal distributions of the endangered deepbody bitterling (Acheilognathus longipinnis) throughout its life history, which is an autumn-spawning annual fish spending its egg and larval stages in unionid mussels and emerging in spring, to understand its population decline in the terrestrialized floodplains of the Kiso River, central Japan. We first validated our A. longipinnis environmental DNA (eDNA) sampling method and observed an 89.3% probability of consistency between the eDNA and the direct capture surveys of 56 floodplain waterbodies (FWBs). Subsequently, the temporal distributions with autumn dispersal (9 of 14 FWBs) were found using time-series eDNA samples collected from 14 FWBs on a floodplain with a length and width of 1.4 and 0.2 km, respectively. In the following spring, juveniles were only detected in the two FWBs connected to the river channel. Moreover, the direct capture data revealed that juveniles occurred in 52.9% (9/17) of the connected FWBs, but only in 5.1% (2/39) of the FWBs isolated from the river channel. Autumn dispersal of A. longipinnis would be disadvantageous for reproduction in terrestrialized floodplains with numerous isolated FWBs.

Overproduction of proinflammatory cytokines is characteristic of hemophagocytic syndrome (HPS), a highly lethal inflammatory disease. Peripheral blood monocytes include two distinct subpopulations according to surface antigen expression: a major type, CD14+/CD16− (classical monocytes), and a minor type, CD14+/CD16bright (proinflammatory monocytes). Among peripheral blood monocytes from HPS patients, CD14+/CD16bright cells were increased, together with lipopolysaccharide-induced production of tumor necrosis factor (TNF)-α and interleukin (IL)-6. By three-color immunofluorescence, CD14+/CD16bright monocytes exhibited more intense human leukocytic antigen DR than CD14+/CD16− monocytes, consistent with greater maturity. Serum IL-6, TNF-α, and IL-8 were increased in HPS patients. A sensitive inflammatory marker, neutrophil CD64 expression, also was significantly elevated in HPS patients. In conclusion, expansion of proinflammatory monocytes and increased expression of neutrophil CD64 appeared to be important in the pathophysiology of HPS. Expansion of CD14+/CD16bright monocytes and neutrophil CD64 expression could serve as indicators of the inflammatory state in HPS. [ABSTRACT FROM AUTHOR]

This study investigated the effect of hyperbaric oxygen (HBO)on the gene expression of the extracellular matrix proteins of the ruptured anterior cruciate ligament (ACL). In each of 80 Sprague-Dawley rats, ACL was lacerated at the tibial insertion. Forty rats were exposed to 100% oxygen at 2.5 ATA for 2 hours for 5 days a week, beginning the day of surgery(Group H), whereas the remaining 40 control rats were housed in normal room air(Group C). The animals were sacrificed at 3. 7, 14, and 28 days postoperatively, and ACLs were harvested after macroscopic examination. RNA was extracted from the harvested ACL and the gene expression of type I and type HI procollagen, three kinds of matrix metalloproteinases(MMP) (collagenase 3, gelatinase A and B), and tissue inhibitor of matrix metalloproteinase (TIMP) l and 2 was examined semi-quantitatively by the RT-PCR method. None of the lacerated ACL healed macroscopically. The gene expression of type I and type III procollagen and TIMP 1 and 2 in Group H was higher than that in Group C, whereas there was no significant difference in the gene expression of each MMP between the groups. It is suggested that the administration of HBO enhances collagen synthesis and inhibits tissue degradation by decreasing the ratio of MMP to TIMP in ruptured ACL. Although it is unlikely that the administration of HBO heals the ruptured ACL by itself, it may be useful as an adjunct after primary repair of ACL. [ABSTRACT FROM AUTHOR]

Treatment of L929 cells with tumour necrosis factor-α (TNF-α) plus actinomycin D induced DNA damage (indicated by the appearance of a sub-G1 peak due to extracellular leakage of low molecular weight DNA following DNA fragmentation) before significant cell lysis occurred. The DNA damage occurred in parallel with a decrease of the intracellular total glutathione content and an increase of intracellular reactive oxygen intermediates (ROI), as indicated by increased dihydrorhodamine 123 oxidation. Because the inhibition of mitochondrial respiration suppressed the increase of dihydrorhodamine 123 oxidation and DNA damage as well as the decrease in the total glutathione content, it was suggested that increased mitochondrial formation of ROI was responsible for DNA damage after TNF treatment. Deferoxamine (a ferric iron chelator) and dithiothreitol (a sulfhydryl reagent) both prevented DNA damage and cell killing, indicate that hydroxyl radicals generated from O2- and H2O2 produced by the mitochondria in a process catalysed by iron contributed to DNA damage and that this pathway may be involved in TNF-αinduced cytotoxicity. An inhibitor of poly(ADP)-ribose polymerase (3-aminobenzamide), worsened DNA damage, but was protective against cell lysis, suggesting that DNA repair subsequent to injury was more important than DNA damage per se in development of TNF-α cytotoxicity. [ABSTRACT FROM AUTHOR]