Ultrastructure of the spermatozoon of the digenean Plagiorchis elegans (Rudolphi, 1802) (Plagiorchioidea,Plagiorchiidae)

The ultrastructure of the mature spermatozoon of the type genus of the Plagiorchiidae Plagiorchis elegans (Rudolphi, 1802), a parasite of the Golden hamster, Mesocricetus auratus is described. This study is the first ultrastructural study of the spermatozoon of a Plagiorchis, the second of a plagiorchiid species and only the third in the Plagiorchioidea. Previously data on spermatozoon ultrastructure existed only for the plagiorchiid Enodiotrema reductum and the omphalometrid Rubenstrema exasperatum. The mature spermatozoon of P. elegans exhibited the general pattern described in most digenean species, namely two axonemes of the 9 + “1” Trepaxonemata pattern, nucleus, mitochondria, external ornamentation of the plasma membrane, spine‐like bodies, and glycogen granules. However, the rather typical expansion of the plasma membrane is not found in P. elegans. Another peculiarity of the spermatozoon of P. elegans is the presence of a structure called thin cytoplasm termination. Spermatozoon ultrastructure of P. elegans is compared with that of E. reductum and R. exasperatum. Spermatozoon of P. elegans conforms to the general pattern described in E. reductum. Thus, this study further expands our knowledge on the spermatozoon ultrastructure among the members of the Plagiorchioidea, one of the most phylogenetically derived groups of the digenea. J. Morphol. 274:965–972, 2013. © 2013 Wiley Periodicals, Inc.     

Choice in multi-alternative environments: A trial-by-trial implementation of the Sequential Choice Model

The sequential choice model (SCM) proposes that latencies to accept options presented alone can be used to predict preferences between these options when they are presented simultaneously. SCM has been proposed and tested in experiments where only two alternatives were present. To further challenge the model, we trained and tested European starlings (Sturnus vulgaris) in an environment with a background of four alternatives differing in delay to reinforcement. Unexpected binary choices between the six possible pairs of alternatives were used to assess preference. The model's predictions of the strength of preference roughly corresponded to the bird's choices for each of the six choice situations. More importantly, a trial-by-trial test of the model correctly predicted 84% of all individual choice trials.     

How does mutation affect the distribution of phenotypes?

The potential for mutational processes to influence patterns of neutral or adaptive phenotypic evolution is not well understood. If mutations are directionally biased, shifting trait means in a particular direction, or if mutation generates more variance in some directions of multivariate trait space than others, mutation itself might be a source of bias in phenotypic evolution. Here, we use mutagenesis to investigate the affect of mutation on trait mean and (co)variances in zebrafish, Danio rerio. Mutation altered the relationship between age and both prolonged swimming speed and body shape. These observations suggest that mutational effects on ontogeny or aging have the potential to generate variance across the phenome. Mutations had a far greater effect in males than females, although whether this is a reflection of sex‐specific ontogeny or aging remains to be determined. In males, mutations generated positive covariance between swimming speed, size, and body shape suggesting the potential for mutation to affect the evolutionary covariation of these traits. Overall, our observations suggest that mutation does not generate equal variance in all directions of phenotypic space or in each sex, and that pervasive variation in ontogeny or aging within a cohort could affect the variation available to evolution.     

Postanoxic oxidative injury in rat hepatocytes: lactate-dependent protection against tert-butylhydroperoxide.

Previous studies in this laboratory showed that hypoxia and anoxia enhance the susceptibility of hepatocytes to tert-butylhydroperoxide (TBH)-induced oxidative injury. To determine whether preceding exposure to anoxia affects postanoxic sensitivity to oxidative injury, viability was studied in hepatocytes incubated under anoxic conditions followed by reoxygenation without or with tert-butylhydroperoxide addition. Results showed that a preceding exposure to 60 min of anoxia substantially increased the vulnerability of cells to injury by the oxidant. Because substantial tissue lactate can accumulate during anoxia, the effect of increased lactate on postanoxic injury due to TBH was determined. Results showed that added lactate protected in a concentration-dependent manner. The TBH elimination rate was stimulated by lactate, and the pyruvate production rate approached the rate of TBH elimination. Thus, lactate protects against postanoxic oxidative injury by supplying reducing equivalents for peroxide reduction. This suggests that lactate accumulation during ischemia may be beneficial and that supplementation with lactate could be considered as a means to protect against postischemic injury.