Interactive Effects of Anthropogenic, Environmental, and Biotic Stressors on Multiple Endpoints in Hyla chrysoscelis

Multiple stressors have been proposed as causative agents for declining populations and increased incidence of malformations in amphibians although few studies have examined possible interactions among these stressors. We measured interactive effects of UV radiation, three chemicals, and interspecific competition (with Rana 1phenocephala) on multiple endpoints in Hyla chrysoscelis using a center point- and chemical-free control-enhanced 24 factorial design. UV radiation was transmitted or filtered using OP-4 or OP-3 acrylite filters installed above 72, 500-liter mesocosms on 16 May 1997. Methyl mercury, chlorpyrifos, and atrazine were applied at levels of 0, 10, 50, and 100 % of 400 ppb, 30 ppb, and 192 ppb, respectively, on 8 June. Hatching success and larval mortality were assessed 1, 2, 4, 8, 16, and 32 days after chemical application. After sampling on day 32, chemicals were reapplied to 24 mesocosms, initial water levels were restored in 24 additional mesocosms, and the remaining mesocosms were unmanipulated. On day 33, we placed 25 Hyla eggs in each mesocosm to perform a complete larval assessment of interacting stressors on growth, development, metamorphosis, and incidence of malformations. Interactions among stressors affected hatching success, developmental time, number of metamorphs, and incidence of malformation. Single effects of stressors were uncommon in that only larval mortality was unaffected by potential stressor interactions. If interactive effects of stressors are not evaluated in experiments examining population declines and malformations, results may be misinterpreted leading to ineffective conservation efforts

Probing Life Qualification through Expanded Voir Dire

The conventional wisdom is that most trials are won or lost in jury selection. If this is true, then in many capital cases, jury selection is literally a matter of life or death. Given these high stakes and Supreme Court case law setting out standards for voir dire in capital cases, one might expect a sophisticated and thoughtful process in which each side carefully considers which jurors would be best in the particular case. Instead, it turns out that voir dire in capital cases is woefully ineffective at the most elementary task--weeding out unqualified jurors. Empirical evidence reveals that many capital jurors are in fact unqualified to serve. Moreover, the ineffectiveness of the process is far from even-handed. A juror is not death-qualified if she would always vote against a death sentence, regardless of the circumstances, and a handful of the jurors who actually serve in capital cases are in fact unqualified for this reason. On the other hand, a juror is not life qualified” if she would always vote for a death sentence upon the proof of capital murder; if she is a burden shifter, a person who requires the defendant to demonstrate why she deserves to live; or because she is mitigation impaired, a person who is unwilling to consider one or more mitigating factors that the Supreme Court has said jurors must be willing to consider. In contrast to the small number of death unqualified jurors who actually serve in capital cases, far larger numbers of jurors who are not life qualified serve in capital cases. Part II of this article will summarize the law relevant to determining who is qualified to sit as a juror in a capital case, and then demonstrate the magnitude of the problem of unqualified jurors as revealed by the current empirical findings of capital juror studies. Part III then examines how and why voir dire malfunctions in capital cases, thereby allowing unqualified jurors to sentence defendants to death. Part IV will suggest several ways in which courts may help rectify the problem of the unconstitutional empanelment of jurors who are uncommonly willing to condemn a man to die

Probing Life Qualification through Expanded Voir Dire

The conventional wisdom is that most trials are won or lost in jury selection. If this is true, then in many capital cases, jury selection is literally a matter of life or death. Given these high stakes and Supreme Court case law setting out standards for voir dire in capital cases, one might expect a sophisticated and thoughtful process in which each side carefully considers which jurors would be best in the particular case. Instead, it turns out that voir dire in capital cases is woefully ineffective at the most elementary task--weeding out unqualified jurors. Empirical evidence reveals that many capital jurors are in fact unqualified to serve. Moreover, the ineffectiveness of the process is far from even-handed. A juror is not death-qualified if she would always vote against a death sentence, regardless of the circumstances, and a handful of the jurors who actually serve in capital cases are in fact unqualified for this reason. On the other hand, a juror is not life qualified” if she would always vote for a death sentence upon the proof of capital murder; if she is a burden shifter, a person who requires the defendant to demonstrate why she deserves to live; or because she is mitigation impaired, a person who is unwilling to consider one or more mitigating factors that the Supreme Court has said jurors must be willing to consider. In contrast to the small number of death unqualified jurors who actually serve in capital cases, far larger numbers of jurors who are not life qualified serve in capital cases. Part II of this article will summarize the law relevant to determining who is qualified to sit as a juror in a capital case, and then demonstrate the magnitude of the problem of unqualified jurors as revealed by the current empirical findings of capital juror studies. Part III then examines how and why voir dire malfunctions in capital cases, thereby allowing unqualified jurors to sentence defendants to death. Part IV will suggest several ways in which courts may help rectify the problem of the unconstitutional empanelment of jurors who are uncommonly willing to condemn a man to die

Developmental learning impairments in a rodent model of nodular heterotopia

Developmental malformations of neocortex—including microgyria, ectopias, and periventricular nodular heterotopia (PNH)—have been associated with language learning impairments in humans. Studies also show that developmental language impairments are frequently associated with deficits in processing rapid acoustic stimuli, and rodent models have linked cortical developmental disruption (microgyria, ectopia) with rapid auditory processing deficits. We sought to extend this neurodevelopmental model to evaluate the effects of embryonic (E) day 15 exposure to the anti-mitotic teratogen methylazoxymethanol acetate (MAM) on auditory processing and maze learning in rats. Extensive cortical anomalies were confirmed in MAM-treated rats post mortem. These included evidence of laminar disruption, PNH, and hippocampal dysplasia. Juvenile auditory testing (P21–42) revealed comparable silent gap detection performance for MAM-treated and control subjects, indicating normal hearing and basic auditory temporal processing in MAM subjects. Juvenile testing on a more complex two-tone oddball task, however, revealed a significant impairment in MAM-treated as compared to control subjects. Post hoc analysis also revealed a significant effect of PNH severity for MAM subjects, with more severe disruption associated with greater processing impairments. In adulthood (P60–100), only MAM subjects with the most severe PNH condition showed deficits in oddball two-tone processing as compared to controls. However, when presented with a more complex and novel FM sweep detection task, all MAM subjects showed significant processing deficits as compared to controls. Moreover, post hoc analysis revealed a significant effect of PNH severity on FM sweep processing. Water Maze testing results also showed a significant impairment for spatial but not non-spatial learning in MAM rats as compared to controls. Results lend further support to the notions that: (1) generalized cortical developmental disruption (stemming from injury, genetic or teratogenic insults) leads to auditory processing deficits, which in turn have been suggested to play a causal role in language impairment; (2) severity of cortical disruption is related to the severity of processing impairments; (3) juvenile auditory processing deficits appear to ameliorate with maturation, but can still be elicited in adulthood using increasingly complex acoustic stimuli; and (4) malformations induced with MAM are also associated with generalized spatial learning deficits. These cumulative findings contribute to our understanding of the behavioral consequences of cortical developmental pathology, which may in turn elucidate mechanisms contributing to developmental language learning impairment in humans

Ischemia–reperfusion impairs blood–brain barrier function and alters tight junction protein expression in the ovine fetus

The blood–brain barrier is a restrictive interface between the brain parenchyma and the intravascular compartment. Tight junctions contribute to the integrity of the blood–brain barrier. Hypoxic–ischemic damage to the blood–brain barrier could be an important component of fetal brain injury. We hypothesized that increases in blood–brain barrier permeability after ischemia depend upon the duration of reperfusion and that decreases in tight junction proteins are associated with the ischemia-related impairment in blood–brain barrier function in the fetus. Blood–brain barrier function was quantified with the blood-to-brain transfer constant (Ki) and tight junction proteins by Western immunoblot in fetal sheep at 127 days of gestation without ischemia, and 4, 24, or 48 h after ischemia. The largest increase in Ki (P \u3c 0.05) was 4 h after ischemia. Occludin and claudin-5 expressions decreased at 4 h, but returned toward control levels 24 and 48 h after ischemia. Zonula occludens-1 and -2 decreased after ischemia. Inverse correlations between Ki and tight junction proteins suggest that the decreases in tight junction proteins contribute to impaired blood–brain barrier function after ischemia. We conclude that impaired blood–brain barrier function is an important component of hypoxic–ischemic brain injury in the fetus, and that increases in quantitatively measured barrier permeability (Ki) change as a function of the duration of reperfusion after ischemia. The largest increase in permeability occurs 4 h after ischemia and blood–brain barrier function improves early after injury because the blood–brain barrier is less permeable 24 and 48 than 4 h after ischemia. Changes in the tight junction molecular composition are associated with increases in blood–brain barrier permeability after ischemia

Cladoceran birth and death rates estimates

I. Birth and death rates of natural cladoceran populations cannot be measured directly. Estimates of these population parameters must be calculated using methods that make assumptions about the form of population growth. These methods generally assume that the population has a stable age distribution. 2. To assess the effect of variable age distributions, we tested six egg ratio methods for estimating birth and death rates with data from thirty-seven laboratory populations of Daphnia pulicaria. The populations were grown under constant conditions, but the initial age distributions and egg ratios of the populations varied. Actual death rates were virtually zero, so the difference between the estimated and actual death rates measured the error in both birth and death rate estimates. 3. The results demonstrate that unstable population structures may produce large errors in the birth and death rates estimated by any of these methods. Among the methods tested, Taylor and Slatkin's formula and Paloheimo's formula were most reliable for the experimental data. 4. Further analyses of three of the methods were made using computer simulations of growth of age-structured populations with initially unstable age distributions. These analyses show that the time interval between sampling strongly influences the reliability of birth and death rate estimates. At a sampling interval of 2.5 days (equal to the duration of the egg stage), Paloheimo's formula was most accurate. At longer intervals (7.5–10 days), Taylor and Slatkin's formula which includes information on population structure was most accurate

Multi-level evidence of an allelic hierarchy of USH2A variants in hearing, auditory processing and speech/language outcomes.

Language development builds upon a complex network of interacting subservient systems. It therefore follows that variations in, and subclinical disruptions of, these systems may have secondary effects on emergent language. In this paper, we consider the relationship between genetic variants, hearing, auditory processing and language development. We employ whole genome sequencing in a discovery family to target association and gene x environment interaction analyses in two large population cohorts; the Avon Longitudinal Study of Parents and Children (ALSPAC) and UK10K. These investigations indicate that USH2A variants are associated with altered low-frequency sound perception which, in turn, increases the risk of developmental language disorder. We further show that Ush2a heterozygote mice have low-level hearing impairments, persistent higher-order acoustic processing deficits and altered vocalizations. These findings provide new insights into the complexity of genetic mechanisms serving language development and disorders and the relationships between developmental auditory and neural systems

Effects of epibiosis on consumer-prey interactions

In many benthic communities predators play a crucial role in the population dynamics of their prey. Surface characteristics of the prey are important for recognition and handling by the predator. Because the establishment of an epibiotic assemblage on the surface of a basibiont species creates a new interface between the epibiotized organism and its environment, we hypothesised that epibiosis should have an impact on consumer-prey interactions. In separate investigations, we assessed how epibionts on macroalgae affected the susceptibility of the latter to herbivory by the urchin Arbacia punctulata and how epibionts on the blue mussel Mytilus edulis affected its susceptibility to predation by the shore crab Carcinus maenas. Some epibionts strongly affected consumer feeding behavior. When epibionts were more attractive than their host, consumer pressure increased. When epibionts were less attractive than their host or when they were repellent, consumer pressure decreased. In systems that are controlled from the top-down, epibiosis can strongly influence community dynamics. For the Carcinus/Mytilus system that we studied, the insitu distribution of epibionts on mussels reflected the epibiosis-determined preferences of the predator. Both direct and indirect effects are involved in determining these epibiont-prey-consumer interactions