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In the roundtable that follows, clinicians discuss a study published in this issue of the Journal in light of its methodology, relevance to practice, and implications for future research. Article discussed: Berrébi A, Assouline C, Bessières M-H, et al. Long-term outcome of children with congenital toxoplasmosis. Am J Obstet Gynecol 2010;203:552.e1-6. [ABSTRACT FROM AUTHOR]

Rapid climate change in the Arctic is altering microbial structure and function, with important consequences for the global ecosystem. Emerging evidence suggests organisms in higher trophic levels may also influence microbial communities, but whether warming alters these effects is unclear. Wolf spiders are dominant Arctic predators whose densities are expected to increase with warming. These predators have temperature-dependent effects on decomposition via their consumption of fungal-feeding detritivores, suggesting they may indirectly affect the microbial structure as well. To address this, we used a fully factorial mesocosm experiment to test the effects of wolf spider density and warming on litter microbial structure in Arctic tundra. We deployed replicate litter bags at the surface and belowground in the organic soil profile and analyzed the litter for bacterial and fungal community structure, mass loss, and nutrient characteristics after 2 and 14 months. We found there were significant interactive effects of wolf spider density and warming on fungal but not bacterial communities. Specifically, higher wolf spider densities caused greater fungal diversity under ambient temperature but lower fungal diversity under warming at the soil surface. We also observed interactive treatment effects on fungal composition belowground. Wolf spider density influenced surface bacterial composition, but the effects did not change with warming. These findings suggest a widespread predator can have indirect, cascading effects on litter microbes and that effects on fungi specifically shift under future expected levels of warming. Overall, our study highlights that trophic interactions may play important, albeit overlooked, roles in driving microbial responses to warming in Arctic terrestrial ecosystems., Importance: The Arctic contains nearly half of the global pool of soil organic carbon and is one of the fastest warming regions on the planet. Accelerated decomposition of soil organic carbon due to warming could cause positive feedbacks to climate change through increased greenhouse gas emissions; thus, changes in ecological dynamics in this region are of global relevance. Microbial structure is an important driver of decomposition and is affected by both abiotic and biotic conditions. Yet how activities of soil-dwelling organisms in higher trophic levels influence microbial structure and function is unclear. In this study, we demonstrate that predicted changes in abundances of a dominant predator and warming interactively affect the structure of litter-dwelling fungal communities in the Arctic. These findings suggest predators may have widespread, indirect cascading effects on microbial communities, which could influence ecosystem responses to future climate change., Competing Interests: The authors declare no conflict of interest.

Atmospheric CO 2 concentration is increasing, largely due to anthropogenic activities. Previous studies of individual free-air CO 2 enrichment (FACE) experimental sites have shown significant impacts of elevated CO 2 (eCO 2 ) on soil microbial communities; however, no common microbial response patterns have yet emerged, challenging our ability to predict ecosystem functioning and sustainability in the future eCO 2 environment. Here we analyzed 66 soil microbial communities from five FACE sites, and showed common microbial response patterns to eCO 2 , especially for key functional genes involved in carbon and nitrogen fixation (e.g., pcc/acc for carbon fixation, nifH for nitrogen fixation), carbon decomposition (e.g., amyA and pulA for labile carbon decomposition, mnp and lcc for recalcitrant carbon decomposition), and greenhouse gas emissions (e.g., mcrA for methane production, norB for nitrous oxide production) across five FACE sites. Also, the relative abundance of those key genes was generally increased and directionally associated with increased biomass, soil carbon decomposition, and soil moisture. In addition, a further literature survey of more disparate FACE experimental sites indicated increased biomass, soil carbon decay, nitrogen fixation, methane and nitrous oxide emissions, plant and soil carbon and nitrogen under eCO 2 . A conceptual framework was developed to link commonly responsive functional genes with ecosystem processes, such as pcc/acc vs. soil carbon storage, amyA/pulA/mnp/lcc vs. soil carbon decomposition, and nifH vs. nitrogen availability, suggesting that such common responses of microbial functional genes may have the potential to predict ecosystem functioning and sustainability in the future eCO 2 environment., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Health care costs are an important consideration in the decision of hysterectomy routes and robotic surgery is often critiqued for its high cost. We sought to compare the cost of robotic-assisted hysterectomies performed after initial acquisition of the robotic surgical system to cases performed after 5 years of experience. The first 20 patients at a community teaching hospital who underwent robotic-assisted hysterectomy for endometrial cancer by a single gynecologic oncology surgeon were designated Group 1 and 20 patients undergoing robotic hysterectomies 5 years later for the same indication were designated Group 2. Direct hospital costs were divided into operative and non-operative costs. Mean operating room cost and cost of anesthesia per minute for Group 1 were adjusted to Group 2 mean costs. Supply costs were adjusted using the 2015 Consumer Price Index. Baseline characteristics of the groups were comparable. After 5 years of experience, there was a 15.5% [95% CI (-$2865, -$407), p = 0.01] reduction in mean total costs (Group 1 = $10,543, Group 2 = $8907) and a 14.3% [95% CI (-$2378, -$390), p ≤ 0.01] reduction in mean operative costs (Group 1 = $9688, Group 2 = $8304). Significant reductions in procedure time, operating room time, operating room cost, and cost of anesthesia were seen from Group 1 to Group 2. There were no differences in mean non-operative costs, estimated blood loss, cost of supplies or surgeon cost. Experience with robotic-assisted hysterectomies is associated with reduction in costs, which is primarily a result of reduced operative times. This is an important factor when considering costs related to robotic surgery.

Climate change over the past ∼50 years has resulted in earlier occurrence of plant life-cycle events for many species. Across temperate, boreal and polar latitudes, earlier seasonal warming is considered the key mechanism leading to earlier leaf expansion and growth. Yet, in seasonally snow-covered ecosystems, the timing of spring plant growth may also be cued by snowmelt, which may occur earlier in a warmer climate. Multiple environmental cues protect plants from growing too early, but to understand how climate change will alter the timing and magnitude of plant growth, experiments need to independently manipulate temperature and snowmelt. Here, we demonstrate that altered seasonality through experimental warming and earlier snowmelt led to earlier plant growth, but the aboveground production response varied among plant functional groups. Earlier snowmelt without warming led to early leaf emergence, but often slowed the rate of leaf expansion and had limited effects on aboveground production. Experimental warming alone had small and inconsistent effects on aboveground phenology, while the effect of the combined treatment resembled that of early snowmelt alone. Experimental warming led to greater aboveground production among the graminoids, limited changes among deciduous shrubs and decreased production in one of the dominant evergreen shrubs. As a result, we predict that early onset of the growing season may favour early growing plant species, even those that do not shift the timing of leaf expansion., (Published by Oxford University Press on behalf of the Annals of Botany Company.)

Although elevated CO2 (eCO2 ) significantly affects the α-diversity, composition, function, interaction and dynamics of soil microbial communities at the local scale, little is known about eCO2 impacts on the geographic distribution of micro-organisms regionally or globally. Here, we examined the β-diversity of 110 soil microbial communities across six free air CO2 enrichment (FACE) experimental sites using a high-throughput functional gene array. The β-diversity of soil microbial communities was significantly (P < 0.05) correlated with geographic distance under both CO2 conditions, but declined significantly (P < 0.05) faster at eCO2 with a slope of -0.0250 than at ambient CO2 (aCO2 ) with a slope of -0.0231 although it varied within each individual site, indicating that the spatial turnover rate of soil microbial communities was accelerated under eCO2 at a larger geographic scale (e.g. regionally). Both distance and soil properties significantly (P < 0.05) contributed to the observed microbial β-diversity. This study provides new hypotheses for further understanding their assembly mechanisms that may be especially important as global CO2 continues to increase., (© 2015 John Wiley & Sons Ltd.)

Microorganisms have a variety of evolutionary adaptations and physiological acclimation mechanisms that allow them to survive and remain active in the face of environmental stress. Physiological responses to stress have costs at the organismal level that can result in altered ecosystem-level C, energy, and nutrient flows. These large-scale impacts result from direct effects on active microbes' physiology and by controlling the composition of the active microbial community. We first consider some general aspects of how microbes experience environmental stresses and how they respond to them. We then discuss the impacts of two important ecosystem-level stressors, drought and freezing, on microbial physiology and community composition. Even when microbial community response to stress is limited, the physiological costs imposed on soil microbes are large enough that they may cause large shifts in the allocation and fate of C and N. For example, for microbes to synthesize the osmolytes they need to survive a single drought episode they may consume up to 5% of total annual net primary production in grassland ecosystems, while acclimating to freezing conditions switches Arctic tundra soils from immobilizing N during the growing season to mineralizing it during the winter. We suggest that more effectively integrating microbial ecology into ecosystem ecology will require a more complete integration of microbial physiological ecology, population biology, and process ecology.

The present study investigates the results of pretreatment with five prostaglandin (PG) synthetase inhibitors on effects of morphine on body temperature, pupillary diameter, body movement and production of exophthalmos in rat. Hyperthermia, induced by a low dose of morphine, was inhibited in animals pretreated with any of the PG synthetase inhibitors. However, PG synthetase inhibitors had no clear effect on hypothermia induced by higher doses of morphine. The duration of morphine-induced catalepsy was attenuated by pretreatment with the PG synthetase inhibitors in a dose-related manner. The exophthalmos induced by all doses of morphine was either shortened in duration or inhibited by sulindac, paracetamol or ibuprofen. Morphine-induced mydriasis was either attenuated or inhibited by paracetamol, ibuprofen or meclofenamic acid. The results suggest that endogenous PGs play a role in morphine-induced hyperthermia, catalepsy, exophthalmos and mydriasis whereas a physiological role for PGs in morphine-induced hypothermia was not indicated.

The effects of intravitreally injected prostaglandins (PG's) E1 and F2alpha were studied on conscious, bromcresol green (BrCG)-pretreated and control rabbits. The electroretinogram (ERG) of both the PG-injected and the contralateral control eyes was recorded with contact lens electrodes; and electrocorticogram and the visually evoked response (VER) were recorded from both hemispheres with previously implanted supradural electrodes. In normal rabbits, intravitreal injection of 0.70 mg of PGE1 resulted in a small reduction in the amplitude of the ERG b-wave and of the slow negative wave (SNW) of the contralateral VER. In BrCG-pretreated rabbits, intravitreal injection of 0.70 mg of PGE1 caused a statistically significant decrease in the amplitude of the ERG b-wave and the SNW. Intravitreal injection of 0.7 mg of PGE1 also caused a significantly prolonged inhibition of the ERG in BrCG-pretreated, but not in normal rabbits, following exposure of the eye to a bright light flash. A smaller dose of PGE1 (0.35 mg/eye) caused more moderate effects on some of these parameters. These effects could not be explained by the PG-induced miosis. PGF2alpha (0.7 mg/eye) caused no significant changes in any of the parameters studied. These results indicate that exogenous PG's can have adverse effects on retinal function and that these effects are enhanced by BrCG, a PG-transport inhibitor. Presumably, this inhibitor blocks the PG-removal mechanisms across the blood-retinal barriers and hence allows the accumulation of PG's in the extracellular fluids of the retina.

Release of prostaglandins (PGs) from brain tissue increases during experimentally-induced and spontaneous seizures. However, whether PGs or other arachidonic acid metabolites have a role in induction of seizures is still unclear. The effectiveness of pretreatment with PG synthetase inhibitors on pentylenetetrazol (PTZ)-induced models of epilepsy was investigated in free-moving rats with chronically-implanted supracortical electrodes. The effects on the electrocortical and motor manifestations of both a subconvulsive (30 mg.kg-1) and a convulsive (60 mg.kg-1) dose of PTZ were examined. Mefenamic acid (15 or 50 mg.kg-1), meclofenamic acid (15 or 50 mg.kg-1), ibuprofen (30 or 90 mg.kg-1) and paracetamol (300 or 450 mg.kg-1) delayed the onset of PTZ-induced convulsions. But mefenamic acid and meclofenamic acid also potentiated the excitatory effects of both subconvulsive and convulsive doses of PTZ. Indomethacin (3, 10 or 30 mg.kg-1) had no significant effect. The results suggest that the differential effects were produced by actions not related to the cyclo-oxygenase inhibition although the more consistent decrease of convulsive behavior may have resulted from inhibition of PG synthesis.

Prostaglandin and thromboxane levels increase in mammalian brain during seizures, but whether a metabolite of arachidonic acid has a role in induction, or is merely a by-product, of seizures is still not clear. It has been shown that nonsteroidal anti-inflammatory drugs block arachidonic acid metabolism through inhibition of the enzyme, cyclooxygenase. In the present study, the antiepileptic action of nonsteroidal antiinflammatory drugs was investigated utilizing penicillin-induced focal (250 IU) and primary generalized (2.5 million IU kg-1) models of epilepsy. The effects of the drugs on the electrocortical and motor manifestations of both models were examined. As a group, the nonsteroidal anti-inflammatory drugs significantly affected the central nervous system excitation produced by penicillin. However, individual drugs affected different parameters of the excitation. Paracetamol, the most effective, delayed and/or blocked spikes and seizures in both models. Ibuprofen was more effective against the primary generalized model. Mefenamic acid decreased the number of seizures and indomethacin decreased the voltage output in both models. The present study, together with earlier papers, suggests that an arachidonic acid metabolite plays a role in induction of several animal models of epilepsy.

The effects of five nonsteriodal prostaglandin (PG) synthetase inhibitors on the electrocorticogram were studied in rats with chronically implanted supracortical electrodes. All of PG synthetase inhibitors produced high voltage activity in the electrocorticogram. However, behavior and spectral analysis of the electrocortical activity suggests that these drugs could be divided into two groups. Meclofenamic acid and mefenamic acid produced dose-related increases in excitation (to seizure) while ibuprofen, paracetamol and indomethacin produced dose-related increases in sedation.

Cats, sedated and paralyzed, showed a significant increase in body temperature after intravenous injection of morphine while animals with additional spinal blockade (C3) from injection of 2% lidocaine solution, did not. The results suggest that motor activity is not necessary for morphine-induced hyperthermia in the cat, as had been suggested in the literature.

Bole of adrenals in morphine-induced hyperthermia was studied in normal, neurotransmitter antagonist-pretreated, chemical-sympathectomized, adrenalectomized or adrenal-demedullated rats. In restrained female rats, 5 mg/kg morphine produced hyperthermia whereas 20 mg/kg and 40 mg/kg produced hypothermia. Pretreatment with either phenoxybenzamine, propranolol, pentolinium or scopolamine inhibited the hyperthermia. After adrenalectomy, neither 5 mg/kg nor chronic administration of 20 mg/kg morphine produced previously demonstrated hyperthermia. After adrenal-demedullation, a dose of 5 mg/kg morphine also did not produce hyperthermia. In contrast to female rats, restrained male rats showed no significant effect on body temperature after 5 mg/kg morphine, requiring 20 mg/kg and 40 mg/kg morphine to produce hyperthermia. In adrenalectomized male rats, 20 mg/kg morphine did not produce the usual hyperthermia. The results suggest that male rats are more resistant to the hyperthermic effects of morphine than female rats and that in the rat, the adrenals, likely the medulla, play an important role in morphine-induced hyperthermia.

To investigate the relationship of prostaglandins (PGs) to seizure induction, the effects of six PG synthetase inhibitors on convulsions induced by flurothyl, picrotoxin, pentetrazol (PTZ), electroshock or bicuculline were evaluated. Ibuprofen, sulindac, mefenamic acid, and low dose meclofenamic acid increased the latency-to-onset in the flurothyl and/or PTZ models; the electroshock, picrotoxin and bicuculline models were not significantly affected by any of the pretreatment agents. These results suggest that PGs are involved in the mechanism(s) underlying fluorthyl- and PTZ-induced convulsions, but not picrotoxin-, electroshock-, or bicuculline-induced convulsions.

Morphine has been reported to both lower blood pressure (BP) and cause excitation in some species. These are seemingly contradictory effects. In this series of experiments, the actions of morphine on BP, heart rate (HR) and pupillary diameter were re-examined in sedated, paralyzed cats under 2 ranges of dosage and 3 types of sedative. Small doses (1--2 mg/kg) lowered BP and HR while larger doses (8--12 mg/kg) increased both BP and HR. The effect of morphine on pupillary diameter, however, was not biphasic in that increasing doses proportionally increased pupillary diameter. In adrenalectomized cats smaller doses of morphine decreased, but larger doses no longer increased, BP and HR as it has in the non-adrenalectomized animals. Morphine also no longer produced mydriasis in the adrenalectomized cats. The results suggest that, in the cat, morphine can have a biphasic effect and that the adrenals may play a role in the excitatory phase.

The role of the adrenal glands, in morphine-induced hyperthermia was studied in normal, chemically-sympathectomized, adrenalectomized, adrenal-demedullated or splanchnicotomized rats. 2. In restrained female rats, 5 mg/kg morphine produced hyperthermia whereas 20 mg/kg and 40 mg/kg produced hyperthermia. 3. After adrenalectomy, 5 mg/kg morphine did not produce hyperthermia. 4. After adrenal-demedullation or adrenal-denervation (splanchnicotomy), 5 mg/kg morphine did not produce hyperthermia. 5. The results suggest that, in the rat, the adrenal medulla plays an important role in morphine-induced hyperthermia, and that morphine acts centrally to stimulate the medulla.

Currently available evidence shows that some cell membranes represent a barrier to passive diffusion of PGs. In contrast, an active transport of PGs was demonstrated across the wall of the rabbit vagina in vitro. Evidence has been obtained indicating that similar carrier-mediated PG transport processes in vivo mediate the uptake of PGs from the circulation into the lung and the removal of these autocoids from the brain and the eye, across the blood--brain and blood--aqueous barriers. It was shown that probenecid, a known inhibitor of PG transport, enhances the effect of PGE1 on the brain, and in general, it appears to alter the distribution and rate of excretion of PGs. The existence of such barriers to the free diffusion of PGs and the saturable, and possibly rate-limiting, transport of these autocoids across some other membranes must be taken into consideration in the design of experiments and in the interpretation of results. Furthermore, the importance of this consideration is emphasized by the observation that many nonsteroidal antiinflammatory agents and PG antagonists are effective inhibitors of PG transport (17,18); hence, they can be expected to affect the distribution and disposition of PGs.