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Emerald ash borer, Agrilus planipennis Fairmaire (Coleoptera: Buprestidae), is one of the most serious forest pests in the United States. Ongoing research indicates that establishment of larval parasitoids depends upon the season-long availability of host stages susceptible to parasitism. We monitored emerald ash borer overwintering stages at 90 sites across 22 states to: 1) produce a model of the percentage of emerald ash borer overwintering as non-J larvae; 2) link that model to establishment of Tetrastichus planipennisi; and 3) explore changes to our model under climate change scenarios. Accumulated growing degree days (GDD) is an important predictor of the proportion of emerald ash borer overwintering as non-J larvae (1-4 instar larvae under the bark; available to parasitoids emerging in spring) versus J-larvae (fourth-instar larvae in pupal chambers in the outer wood; unavailable to parasitoids). From north to south, the availability of non-J emerald ash borer larvae in the spring decreases as accumulated GDD increases. In areas where the model predicted >46-75%, >30-46%, >13-30%, or ≤13% of emerald ash borer overwintering as non-J larvae, the probability of establishment of T. planipennisi was 92%, 67%, 57%, and 21%, respectively. We determined that 13% of emerald ash borer overwintering as non-J larvae was the lowest threshold for expected T. planipennisi establishment. Additional modeling predicts that under climate change, establishment of T. planipennisi will be most affected in the Central United States, with areas that are currently suitable becoming unsuitable. Our results provide a useful tool for the emerald ash borer biological control program on how to economically and successfully deploy emerald ash borer biological control agents., (Published by Oxford University Press on behalf of Entomological Society of America 2020.)

We describe approaches to addressing the perennial challenge of collecting a sufficient diversity of nontarget insects for host-specificity testing of candidate biocontrol agents of invasive wood-borers such as the Asian longhorned beetle, Anoplophora glabripennis (Motschulsky) (Coleoptera: Cerambycidae). Multifunnel and intercept traps, retrofitted to maintain live insects and baited with cerambycid-specific pheromone lures, were deployed in diverse forests in southeastern Massachusetts. We collected 1,288 adult beetles comprising 56 species, mostly from the subfamilies targeted by the lures (Cerambycinae and Lamiinae). The type of trap and tree species in which the trap was hung did not seem to affect the species caught. Methods used to induce egg laying and techniques to rear cerambycid larvae are described. Dastarcus helophoroides (Fairmaire) (Coleoptera: Bothrideridae) is the most common Asian longhorned beetle parasitoid in China; therefore, we conducted tests to determine whether cerambycids native to North America would be at risk should this species be released. D. helophoroides attacked all six species tested: Monochamus scutellatus (Say) (Coleoptera: Cerambycidae: Lamiinae), Monochamus notatus (Drury) (Coleoptera: Cerambycidae: Lamiinae), Apriona rugicollis Chevrolat (Coleoptera: Cerambycidae: Lamiinae), Enaphalodes rufulus (Haldeman) (Coleoptera: Cerambycidae: Cerambycinae), Graphisurus fasciatus (DeGeer) (Coleoptera: Cerambycidae: Lamiinae), and Neoclytus acuminatus (F.) (Coleoptera: Cerambycidae: Cerambycinae). Parasitism of native cerambycids was not statistically different from parasitism of Asian longhorned beetle, except for N. acuminatus, which is a considerably smaller species than Asian longhorned beetle, and for M. notatus and M. scutellatus, which attack pine trees rather than hardwood trees like Asian longhorned beetle and the other native species tested. Our testing indicates that many native cerambycids would be vulnerable to D. helophoroides and we conclude that D. helophoroides should not be considered for release as a biocontrol agent in North America.

The forkhead domain (FHD)-containing developmental transcription factor FOXC1 is mutated in patients presenting with Axenfeld-Rieger malformations. In this paper, we report the introduction of positive, negative or neutral charged amino acids into critical positions within the forkhead domain of FOXC1 in an effort to better understand the essential structural and functional determinants within the FHD. We found that FOXC1 is intolerant of mutations at I87. Additionally, alterations of amino acids within alpha-helix 1 of the FOXC1 FHD affected both nuclear localization and transactivation. Amino acids within alpha-helix 3 were also found to be necessary for transactivation and can have roles in correct localization. Interestingly, changing amino acids within alpha-helix 3, particularly R127, resulted in altered DNA-binding specificity and granted FOXC1 the ability to bind to a novel DNA sequence. Given the limited topological variation of FHDs, due to the high conservation of residues, we anticipate that models of forkhead domain function derived from these data will be relevant to other members of the FOX family of transcription factors.

Bone remodeling reflects an equilibrium between bone resorption and formation. The local expression of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) in bone determines the entry of monoblastic precursors into the osteoclast lineage and subsequent bone resorption. Nitric oxide (NO) inhibits osteoclastic bone resorption in vitro and regulates bone remodeling in vivo. An interaction of NO with RANKL and OPG has not been studied. Here, we show that treatment of ST-2 murine stromal cells with the NO donor sodium nitroprusside (100 microm) for 24 h inhibited 1,25 dihydroxyvitamin D(3)-induced RANKL mRNA to less than 33 +/- 7% of control level, whereas OPG mRNA increased to 204 +/- 19% of control. NOR-4 replicated these NO effects. The effects of NO were dose dependent and associated with changes in protein levels: RANKL protein decreased and OPG protein increased after treatment with NO. PTH-induced RANKL expression in primary stromal cells was inhibited by sodium nitroprusside, indicating that the NO effect did not require vitamin D. NO donor did not change the stability of RANKL or OPG mRNAs, suggesting that NO affected transcription. Finally, cGMP, which can function as a second messenger for NO, did not reproduce the NO effect, nor did inhibition of endogenous guanylate cyclase prevent the NO effect on these osteoactive genes. The effect of NO to decrease the RANKL/OPG equilibrium should lead to decreased recruitment of osteoclasts and positive bone formation. Thus, drugs and conditions that cause local increase in NO formation in bone may have positive effects on bone remodeling.

IGF-I, a ubiquitous polypeptide, plays a key role in longitudinal bone growth and acquisition. The most predominant effect of skeletal IGF-I is acceleration of the differentiation program for osteoblasts. However, in vivo studies using recombinant human (rh) IGF-I and/or rhGH have demonstrated stimulation of both bone formation and resorption, thereby potentially limiting the usefulness of these peptides in the treatment of osteoporosis. In this study, we hypothesized that IGF-I modulates bone resorption by regulating expression of osteoprotegerin (OPG) and receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL) in bone cells. Using Northern analysis in ST2 cells, we found that human IGF-I suppressed OPG mRNA in a time- and dose-dependent manner: 100 micro g/LIGF-I (13 nM) decreased OPG expression by 37.0 +/- 1.8% (P < 0.002). The half maximal inhibitory dose of IGF-I was reached at 50 micro g/liter ( approximately 6.5 nM) with no effect of IGF-I on OPG message stability. Conditioned media from ST2 cells confirmed that IGF-I decreased secreted OPG, reducing levels by 42%, from 12.1-7 ng/ml at 48 h (P < 0.05). Similarly, IGF-I at 100 micro g/liter (13 nM) increased RANKL mRNA expression to 353 +/- 74% above untreated cells as assessed by real-time PCR. In vivo, low doses of rhGH when administered to elderly postmenopausal women only modestly raised serum IGF-I (to concentrations of 18-26 nM) and did not affect circulating OPG concentrations; however, administration of rhIGF-I (30 micro g/kg.d) for 1 yr to older women resulted in a significant increase in serum IGF-I (to concentrations of 39-45 nM) and a 20% reduction in serum OPG (P < 0.05). In summary, we conclude that IGF-I in a dose- and time-dependent manner regulates OPG and RANKL in vitro and in vivo. These data suggest IGF-I may act as a coupling factor in bone remodeling by activating both bone formation and bone resorption; the latter effect appears to be mediated through the OPG/RANKL system in bone.

Adrenomedullin (AM) exerts profound natriuretic and vasodilatory effects in conscious animals. This newly discovered hormone also acts in the central nervous system to inhibit water drinking and in the pituitary gland to reduce basal and stimulated ACTH release. We investigated whether the natriuretic action of AM in kidney was matched by a central nervous system action to decrease salt intake. Isotonic hypovolemia induced in male rats by pretreatment with polyethylene glycol potently stimulates both water and salt water (0.3 mol/liter NaCl) drinking. Saline drinking was significantly inhibited when AM was administered into the lateral cerebroventricle before the drinking interval. The effect was dose related (dose range, 44-88 pmol), long lasting (> 5 h), and reversible (resolved at 24 h). When hypovolemic rats were administered antiserum to AM (intracerebroventricular administration) before the drinking interval, a significant 2-fold augmentation of saline drinking was observed. These data suggest that in addition to peripheral actions on cardiovascular and renal function and pituitary actions to inhibit ACTH release, AM may act within the central nervous system to determine fluid and electrolyte balance and, ultimately, blood pressure.

Peptide fragments of the larger 167 amino acid obesity gene related peptide (OBGRP), leptin, were tested for their ability to inhibit feeding in the rat. The C-terminal fragment, OBGRP 116-167 exerted only minimal inhibition of feeding when administered into the lateral cerebroventricle. No alteration in feeding was observed following administration of OBGRP 57-92. We hypothesized that the satiety effects of leptin reside in the N-terminal region of the peptide sequence. Significant, dose-related, and reversible inhibition of food intake was observed following central administration of the 35 amino acid fragment OBGRP 22-56. These results suggest that a small, readily synthesized fragment of the 167 amino acid peptide leptin may exert physiologically relevant satiety effects in brain revealing an endocrine feedback mechanism by which the adipocyte may modulate hypothalamic function.

The novel hormone, adrenomedullin (AdM), which exerts potent hypotensive effects in the periphery and natriuretic actions in the kidney, was found to be antidipsogenic. Cerebroventricular injection of AdM (22, 44, and 88 pmol) resulted in a dose-related diminution of water drinking in response to subsequent central administration of 100 pmol angiotensin II. Additionally, 88 pmol AdM significantly inhibited the drinking response to overnight water deprivation and hyperosmotic challenge. No significant effects of AdM in the doses tested were observed on blood pressure, heart rate, or motor activity. These results suggest that this novel hormone can act within the nervous system to complement its peripheral actions on fluid and electrolyte homeostasis, independent of a central action on cardiovascular function or locomotion.