Biological Control of Fenusa pusilla (Hymenoptera: Tenthredinidae) in the Northeastern United States: A Thirty-four Year Perspective on Efficacy

Parasitoid releases against the birch leafminer Fenusa pusilla (Lepeletier) (Hymenoptera: Tenthredinidae) in eastern North America began in 1974, with releases in eastern Canada, followed by others in the Middle Atlantic States and New England. Of 4 parasitoids released, only 1, the ichneumonid Lathrolestes nigricollis (Thompson), established and spread widely. Studies of its preliminary impacts were made in several locations in the 1980s and 1990s, but full impact of the parasitoid on host density was not yet achieved in that period. Here we report results of surveys in 7 states (MA, CT, RI, NY, PA, NJ, DE) in 2007 documenting the current birch leaf miner levels (as % of leaves mined in spring) and parasitism. Survey results show that the pest has declined dramatically to barely detectable levels in 5 states (MA, CT, RI, NY, PA) but that in southern NJ, the pest remains abundant (ca 50% leaves mined) despite significant parasitism levels. Survey results, in context with previous evaluations made when populations were still declining, show that the project has been completely successful in much of the northeastern USA, but that there is a southern limit to efficacy in mid-New Jersey. Possible reasons for lack of control in this area, in contrast to high levels of control elsewhere, are discussed

Effects of di(n-butyl) phthalate exposure on foetal rat germ-cell number and differentiation: identification of age-specific windows of vulnerability: DBP effects on foetal germ cells

Environmental factors are implicated in increased incidence of human testicular germ‐cell cancer (TGCC). TGCC has foetal origins and may be one component of a testicular dysgenesis syndrome (TDS). Certain phthalates induce TDS in rats, including effects on foetal germ cells (GC). As humans are widely exposed to phthalates, study of the effects of phthalates on foetal rat GC could provide an insight into the vulnerability of foetal GC to disruption by environmental factors, and thus to origins of TGCC. This study has therefore characterized foetal GC development in rats after in utero exposure to di(n‐butyl) phthalate (DBP) with emphasis on GC numbers/proliferation, differentiation and time course for inducing effects. Pregnant rats were treated orally from embryonic day 13.5 (e13.5) with 500 mg/kg/day DBP for varying periods. GC number, proliferation, apoptosis, differentiation (loss of OCT4, DMRT1 expression, DMRT1 re‐expression, GC migration) and aggregation were evaluated at various foetal and postnatal ages. DBP exposure reduced foetal GC number by ∼60% by e15.5 and prolonged GC proliferation, OCT4 and DMRT1 immunoexpression; these effects were induced in the period immediately after testis differentiation (e13.5–e15.5). In contrast, DBP‐induced GC aggregation stemmed from late gestation effects (beyond e19.5). Foetal DBP exposure delayed postnatal resumption of GC proliferation, leading to bigger deficits in numbers, and delayed re‐expression of DMRT1 and radial GC migration. Therefore, DBP differentially affects foetal GC in rats according to stage of gestation, effects that may be relevant to the human because of their nature (OCT4, DMRT1 effects) or because similar effects are demonstrable in vitro on human foetal testes (GC number). Identification of the mechanisms underlying these effects could give a new insight into environment‐sensitive mechanisms in early foetal GC development that could potentially be relevant to TGCC origins

Dynamic changes in DNA modification states during late gestation male germ line development in the rat

BACKGROUND: Epigenetic reprogramming of fetal germ cells involves the genome-wide erasure and subsequent re-establishment of DNA methylation. Mouse studies indicate that DNA demethylation may be initiated at embryonic day (e) 8 and completed between e11.5 and e12.5. In the male germline, DNA remethylation begins around e15 and continues for the remainder of gestation whilst this process occurs postnatally in female germ cells. Although 5-methylcytosine (5mC) dynamics have been extensively characterised, a role for the more recently described DNA modifications (5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC)) remains unclear. Moreover, the extent to which the developmental dynamics of 5mC reprogramming is conserved across species remains largely undetermined. Here, we sought to describe this process during late gestation in the male rat. RESULTS: Using immunofluorescence, we demonstrate that 5mC is re-established between e18.5 and e21.5 in the rat, subsequent to loss of 5hmC, 5fC and 5caC, which are present in germ cells between e14.5 and e16.5. All of the evaluated DNA methyl forms were expressed in testicular somatic cells throughout late gestation. 5fC and 5caC can potentially be excised through Thymine DNA Glycosylase (TDG) and repaired by the base excision repair (BER) pathway, implicating 5mC oxidation in active DNA demethylation. In support of this potential mechanism, we show that TDG expression is coincident with the presence of 5hmC, 5fC and 5caC in male germ cell development. CONCLUSION: The developmental dependent changes in germ cell DNA methylation patterns suggest that they are linked with key stages of male rat germline progression

Nitrogen forms affect root structure and water uptake in the hybrid poplar

The study analyses the effects of two different forms of nitrogen fertilisation (nitrate and ammonium) on root structure and water uptake of two hybrid poplar (Populus maximowiczii x P. balsamifera) clones in a field experiment. Water uptake was studied using sap flow gauges on individual proximal roots and coarse root structure was examined by excavating 18 whole-root systems. Finer roots were scanned and analyzed for architecture. Nitrogen forms did not affect coarse-root system development, but had a significant effect on fine-root development. Nitrate-treated trees presented higher fine:coarse root ratios and higher specific root lengths than control or ammonium treated trees. These allocation differences affected the water uptake capacity of the plants as reflected by the higher sapflow rate in the nitrate treatment. The diameter of proximal roots at the tree base predicted well the total root biomass and length. The diameter of smaller lateral roots also predicted the lateral root mass, length, surface area and the number of tips. The effect of nitrogen fertilisation on the fine root structure translated into an effect on the functioning of the fine roots forming a link between form (architecture) and function (water uptake)

In utero exposure to cigarette smoke dysregulates human fetal ovarian developmental signalling

STUDY QUESTION How does maternal cigarette smoking disturb development of the human fetal ovary?<p></p> SUMMARY ANSWER Maternal smoking increases fetal estrogen titres and dysregulates several developmental processes in the fetal ovary.<p></p> WHAT IS KNOWN ALREADY Exposure to maternal cigarette smoking during gestation reduces human fetal ovarian cell numbers, germ cell proliferation and subsequent adult fecundity.<p></p> STUDY DESIGN, SIZE, DURATION The effects of maternal cigarette smoking on the second trimester human fetal ovary, fetal endocrine signalling and fetal chemical burden were studied. A total of 105 fetuses were studied, 56 from mothers who smoked during pregnancy and 49 from those who did not.<p></p> PARTICIPANTS/MATERIALS, SETTING METHODS Ovary, liver and plasma samples were collected from electively terminated, normally progressing, second trimester human fetuses. Circulating fetal hormones, levels of 73 fetal ovarian transcripts, protein localization, density of oocytes/primordial follicles and levels of 16 polycyclic aromatic hydrocarbons (PAHs) in the fetal liver were determined.<p></p> MAIN RESULTS AND THE ROLE OF CHANCE Circulating fetal estrogen levels were very high and were increased by maternal smoking (ANOVA, P = 0.055–0.004 versus control). Smoke exposure also dysregulated (two-way ANOVA, smoking versus gestation weeks interaction, P = 0.046–0.023) four fetal ovarian genes (cytochrome P450 scc [CYP11A1], NOBOX oogenesis homeobox [NOBOX], activator of apoptosis harakiri [HRK], nuclear receptor subfamily 2, group E, member 1 [NR2E1]), shifted the ovarian Inhibin βA/inhibin α ratio (NHBA/INHA) transcript ratio in favour of activin (ANOVA, P = 0.049 versus control) and reduced the proportion of dominant-negative estrogen receptor 2 (ERβ: ESR2) isoforms in half the exposed fetuses. PAHs, ligands for the aryl hydrocarbon receptor (AHR), were increased nearly 6-fold by maternal smoking (ANOVA, P = 0.011 versus control). A fifth transcript, COUP transcription factor 1 (nuclear receptor subfamily 2, group F, member 1: NR2F1, which contains multiple AHR-binding sites), was both significantly increased (ANOVA, P = 0.026 versus control) and dysregulated by (two-way ANOVA, smoking versus gestation weeks interaction, P = 0.021) maternal smoking. NR2F1 is associated with repression of FSHR expression and smoke-exposed ovaries failed to show the normal increase in FSHR expression during the second trimester. There was a significantly higher number of DEAD (Asp-Glu-Ala-Asp) box polypeptide 4 (DDX4) VASA-positive (ANOVA, P = 0.016 versus control), but not POU domain, class 1, transcription factor 1 (POU5F1) OCT3/4-positive, oocytes in smoke-exposed fetuses and this matched with a significantly higher number of primordial follicles (ANOVA, P = 0.024 versus control).<p></p> LIMITATIONS, REASONS FOR CAUTION The effects of maternal smoking on establishment of the maximum fetal primordial follicle pool cannot be reliably studied in our population since the process is not completed until 28 weeks of gestation and normal fetuses older than 21 weeks of gestation are not available for study. Our data suggest that some fetal ovaries are affected by smoke exposure while others are not, indicating that additional studies, with larger numbers, may show more significant effects.<p></p> WIDER IMPLICATIONS OF THE FINDINGS Fetal exposure to chemicals in cigarette smoke is known to lead to reduced fecundity in women. Our study suggests, for the first time, that this occurs via mechanisms involving activation of AHR, disruption of inhibin/activin and estrogen signalling, increased exposure to estrogen and dysregulation of multiple molecular pathways in the exposed human fetal ovary. Our data also suggest that alterations in the ESR2 positive and dominant negative isoforms may be associated with reduced sensitivity of some fetuses to increased estrogens and maternal smoking

Distribution of \u3cem\u3eCotesia rubecula\u3c/em\u3e (Hymenoptera: Braconidae) and Its Displacement of \u3cem\u3eCotesia glomerata\u3c/em\u3e in Eastern North America

A survey was conducted from May to Oct of 2011 of the parasitoid community of the imported cabbageworm, Pieris rapae (Lepidoptera: Pieridae), in cole crops in part of the eastern United States and southeastern Canada. The findings of our survey indicate that Cotesia rubecula (Hymenoptera: Braconidae) now occurs as far west as North Dakota and has become the dominant parasitoid of P. rapae in the northeastern and north central United States and adjacent parts of southeastern Canada, where it has displaced the previously common parasitoid Cotesia glomerata (Hymenoptera: Braconidae). Cotesia glomerata remains the dominant parasitoid in the mid-Atlantic states, from Virginia to North Carolina and westward to southern Illinois, below latitude N 38° 48′. This pattern suggests that the released populations of C. rubecula presently have a lower latitudinal limit south of which they are not adapted

Additive multiple predator effects can reduce mosquito populations

1. Multiple predator interactions may profoundly alter ecological community dynamics and can complicate predictions of simpler pairwise predator–prey interaction strengths. In particular, multiple predator effects may lessen or enhance prey risk, with implications for community‐level stability. Such emergent effects may modulate natural enemy efficacy towards target organisms. 2. In the present study, a functional response approach was used to quantify emergent multiple predator effects among natural enemies towards the disease vector mosquito complex, Culex pipiens. Conspecific multiple predator–predator interactions of the cyclopoid copepod Macrocyclops albidus (intermediate predator) were quantified by comparing multiple predator consumption simulations, based on individual consumption rates, with multiple predator consumption rates that were experimentally observed. Further, the study examined the influence of the presence of a predator at a higher trophic level, Chaoborus flavicans, on copepod group predation. 3. Both predators displayed type II functional responses, with C. flavicans consuming significantly more prey than M. albidus individually. Overall consumption levels of mosquitoes increased with greater predator density and richness. Antagonistic or synergistic emergent multiple predator effects between conspecifics of M. albidus were not detected, and the higher‐level predator did not reduce effects of the intermediate predator. Accordingly, evidence for additive multiple predator interactions was found. 4. The lack of predator–predator interference between cyclopoid copepods and larval chaoborid midges provides strong support for their combined application in mosquito biocontrol. It is proposed that there should be increased examination of multiple predator effects in assessments of natural enemy efficacies to better understand overall predatory effects within communities and utilities in vector control

Comparative Effects of Di(n-Butyl) Phthalate Exposure on Fetal Germ Cell Development in the Rat and in Human Fetal Testis Xenografts

Background: Phthalate exposure induces germ cell effects in the fetal rat testis. Although experimental models have shown that the human fetal testis is insensitive to the steroidogenic effects of phthalates, the effects on germ cells have been less explored.Objectives: We sought to identify the effects of phthalate exposur on human fetal germ cellsin a dynamic model and to establish whether the rat is an appropriate model for investigatingsuch effects.Methods: We used immunohistochemistry, immunofluorescence, and quantitative real-time polymerase chain reaction to examine Sertoli and germ cell markers on rat testes and human fetal testis xenografts after exposure to vehicle or di(n‑butyl) phthalate (DBP). Our study included analysis of germ cell differentiation markers, proliferation markers, and cell adhesion proteins.Results: In both rat and human fetal testes, DBP exposure induced similar germ cell effects, namely, germ cell loss (predominantly undifferentiated), induction of multinucleated gonocytes(MNGs), and aggregation of differentiated germ cells, although the latter occurred rarely in the human testes. The mechanism for germ cell aggregation and MNG induction appears to be loss of Sertoli cell–germ cell membrane adhesion, probably due to Sertoli cell microfilament redistribution.Conclusions: Our findings provide the first comparison of DBP effects on germ cell number, differentiation, and aggregation in human testis xenografts and in vivo in rats. We observed comparable effects on germ cells in both species, but the effects in the human were muted compared with those in the rat. Nevertheless, phthalate effects on germ cells have potential implications for the next generation, which merits further study. Our results indicate that the rat is a human-relevant model in which to explore the mechanisms for germ cell effects

Of mongooses and mitigation: ecological analogues to geoengineering

Anthropogenic global warming is a growing environmental problem resulting from unintentional human intervention in the global climate system. If employed as a response strategy, geoengineering would represent an additional intentional human intervention in the climate system, with the intent of decreasing net climate impacts. There is a rich and fascinating history of human intervention in environmental systems, with many specific examples from ecology of deliberate human intervention aimed at correcting or decreasing the impact of previous unintentionally created problems. Additional interventions do not always bring the intended results, and in many cases there is evidence that net impacts have increased with the degree of human intervention. In this letter, we report some of the examples in the scientific literature that have documented such human interventions in environmental systems, which may serve as analogues to geoengineering. We argue that a high degree of system understanding is required for increased intervention to lead to decreased impacts. Given our current level of understanding of the climate system, it is likely that the result of at least some geoengineering efforts would follow previous ecological examples where increased human intervention has led to an overall increase in negative environmental consequences