Hatchery selection promotes boldness in newly hatched brown trout (Salmo trutta): implications for dominance

By using newly hatched (approximately 2 weeks old) brown trout(Salmo trutta) from six families of wild and six families ofsea-ranched origin (seventh generation), we tested the hypothesesthat (1) the hatchery environment selects for increased boldness,and (2) boldness predicts dominance status. Sea-ranched troutspend their first 2 years in the hatchery before being releasedinto the wild at the onset of seaward migration. Trout werepresented with a novel object (tack) and with food (brine shrimp),and their responses were measured and scored in terms of boldness.Siblings with increasing difference in boldness were then pairedin dyadic contests. Fish of sea-ranged origin were on averagebolder than were fish of wild origin, and bolder individualswere more likely to become dominant regardless of origin. Boldnesswas not related to RNA levels, indicating that bold behaviorwas not a consequence of higher metabolism or growth rate. Neitherwas size a predictor of bold behavior or the outcome of dyadiccontests. These results are consistent with studies on olderlife stages showing increased boldness toward predators in hatchery-selectedfish, which suggests that behavioral consequences of hatcheryselection are manifested very early in life. The concordancebetween boldness and dominance may suggest that these behaviorsare linked in a risk prone-aggressive phenotype, which may bepromoted by hatchery selection. However, we also found significantvariation in behavioral and growth-related traits among families,suggesting that heritable variation has not been exhausted bysea-ranching procedures.     

The mechanism of inhibition of S-adenosyl-L-homocysteine hydrolase by fluorine-containing adenosine analogs

(Z)-4',5'-Didehydro-5'-deoxy-5'-fluoroadenosine (I), 5'-deoxy-5'-difluoroadenosine (II), and 4',5'-didehydro-5'-deoxy-5'-fluoroarabinosyl-adenosine (III) are inhibitors of rat liver S-adenosyl-L-homocysteine hydrolase. Compounds I and II are time-dependent and irreversible inhibitors of the enzyme. Both I and II are oxidized by E.NAD to produce E.NADH, and fluoride anion is formed in the inactivation reaction (0.7 to 1.0 mole fluoride/mole of enzyme subunit, and 1.7 moles fluoride/mole of enzyme subunit from I and II, respectively). The enzyme is stoichiometrically labeled with [8-3H]-I, but the label is lost upon denaturation of the protein either with or without treatment of the labeled complex with sodium borohydride. The compound III, the arabino derivative of I, is a competitive inhibitor of the enzyme. The mechanism of the inhibition of S-adenosyl-L-homocysteine hydrolase by these inhibitors is discussed.     

Antiretroviral activity of mechanism-based irreversible inhibitors of S-adenosylhomocysteine hydrolase.

S-Adenosylhomocysteine hydrolase (AdoHcy-nase) is a key enzyme in transmethylation reactions. The objective of the present study was to examine the potential antiretroviral activities of novel mechanism-based irreversible AdoHcy-nase inhibitors. (Z)-4',5'-didehydro-5'-deoxy-5'-fluoroadenosine (ZDDFA), (E)-4',5'-didehydro-5'-deoxy-5'-fluoroadenosine (EDDFA), (Z)-4',5'-didehydro-5'-deoxy-5'-chloroadenosine (ZDDCA) and 5'-deoxy-5'-acetylenic adenosine (DAA) inhibited AdoHcy-nase activity with Ki values of 0.55, 1.04, greater than 10.0 and 3.30 microM, respectively. These four compounds were tested for antiviral activity in vitro against Moloney leukemia virus (MoLV) in the XC-plaque assay. MoLV replication in murine fibroblasts (SC-1) was inhibited by ZDDFA, EDDFA and DAA with IC50 values of 0.05, 0.25 and 3.30 micrograms/ml, respectively. ZDDCA did not inhibit MoLV infection at the concentrations tested. Antiviral activity correlated with the ability of the individual compounds to maintain sustained elevations in intracellular S-adenosylhomocysteine (AdoHcy) concentrations in the SC-1 cells. ZDDFA, the most potent inhibitor of AdoHcy-nase and MoLV was also the most active in maintaining sustained elevations in intracellular AdoHcy levels. The antiviral activity of ZDDFA was also examined in murine C3H1OT1/2 fibroblasts which constitutively produce MoLV. Pretreatment with ZDDFA (1.0 microgram/ml) for 24 hr inhibited virus production by 88%. Similar to the SC-1 cells, and concomitant with enzyme inhibition, there was a 300-fold increase in AdoHcy levels in ZDDFA (1.0 microgram/ml) treated C3H1OT1/2 cells. Incorporation of a [3H]methyl group from tritiated S-adenosylmethionine into total RNA in C3H1OT1/2 cells was inhibited by ZDDFA without affecting cell viability. These results suggest that mechanism-based inhibitors of AdoHcy-nase, such as ZDDFA, may have potential as antiretroviral agents.     

华西银腊梅挥发油化学成分的研究

用水蒸气蒸馏法提取华西银腊梅挥发油,并用气相色谱-质谱(GC-MS)联用技术对其挥发油的化学成分进行分析,结果共鉴定了其中的39种成分,所鉴定成分含量约占总检出量的87.83%。其化学成分主要为(Z,Z)-9,12-十八碳二烯酸甲酯(9.00%),壬醛(5.83%),二十一烷(5.69%),二十烷(5.08%),辛炔酸(4.50%),2,6,10,15-四甲基十七烷(3.93%),(Z)-6-十八烯酸甲酯(3.65%),3,8-二甲基十一烷(3.52%),1-十六碳炔(3.31%),肉豆蔻酸(2.86%),月桂醛(2.81%),壬酸(2.23%),5,6,7,7α-四氢-4,4,7α三甲基-2(4H)-苯并呋喃酮(2.18%)等。     

European checkerspots (Melitaeini: Lepidoptera,Nymphalidae) are not aposematic – the point of view of great tits (Parus major)

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Multiplex panels of polymorphic microsatellite loci for two cryptic bat species of the genus Pipistrellus,developed by cross‐species amplification within the family Vespertilionidae

The paper presents multiplex panels of polymorphic microsatellites for two closely related cryptic species Pipistrellus pipistrellus and Pipistrellus pygmaeus. We tested the cross‐species amplification of 34 microsatellite loci, originally developed for five vespertilionid bat species. Ten and nine polymorphic loci in P. pipistrellus (mean number of alleles per locus = 10.5) and P. pygmaeus (8.1), respectively, in three multiplex polymerase chain reactions per species were amplified. All loci can be analysed in a single fragment analysis and can be used as markers to the study of evolution and the ecology of structured populations of socially living bats.     

Total sleep deprivation does not significantly degrade semantic encoding

ABSTRACT

Sleep deprivation impairs performance on cognitive tasks, but it is unclear which cognitive processes it degrades. We administered a semantic matching task with variable stimulus onset asynchrony (SOA) and both speeded and self-paced trial blocks. The task was administered at the baseline and 24 hours later after 30.8 hours of total sleep deprivation (TSD) or matching well-rested control. After sleep deprivation, the 20% slowest response times (RTs) were significantly increased. However, the semantic encoding time component of the RTs remained at baseline level. Thus, the performance impairment induced by sleep deprivation on this task occurred in cognitive processes downstream of semantic encoding.