Land use modification causes slow, but predictable, change in soil microbial community composition and functional potential.

BACKGROUND: Bacterial communities are critical to ecosystem functioning and sensitive to their surrounding physiochemical environment. However, the impact of land use change on microbial communities remains understudied. We used 16S rRNA gene amplicon sequencing and shotgun metagenomics to assess soil microbial communities' taxonomic and functional responses to land use change. We compared data from long-term grassland, exotic forest and horticulture reference sites to data from sites that transitioned from (i) Grassland to exotic forest or horticulture and from (ii) Exotic forest to grassland. RESULTS: Community taxonomic and functional profiles of the transitional sites significantly differed from those within reference sites representing both their historic and current land uses (P < 0.001). The bacterial communities in sites that transitioned more recently were compositionally more similar to those representing their historic land uses. In contrast, the composition of communities from sites exposed to older conversion events had shifted towards the compositions at reference sites representing their current land use. CONCLUSIONS: Our study indicates that microbial communities respond in a somewhat predictable way after a land use conversion event by shifting from communities reflecting their former land use towards those reflecting their current land use. Our findings help us to better understand the legacy effects of land use change on soil microbial communities and implications for their role in soil health and ecosystem functioning. Understanding the responsiveness of microbial communities to environmental disturbances will aid us in incorporating biotic variables into soil health monitoring techniques in the future.

Plastics and the microbiome: impacts and solutions.

Global plastic production has increased exponentially since manufacturing commenced in the 1950's, including polymer types infused with diverse additives and fillers. While the negative impacts of plastics are widely reported, particularly on marine vertebrates, impacts on microbial life remain poorly understood. Plastics impact microbiomes directly, exerting toxic effects, providing supplemental carbon sources and acting as rafts for microbial colonisation and dispersal. Indirect consequences include increased environmental shading, altered compositions of host communities and disruption of host organism or community health, hormone balances and immune responses. The isolation and application of plastic-degrading microbes are of substantial interest yet little evidence supports the microbial biodegradation of most high molecular weight synthetic polymers. Over 400 microbial species have been presumptively identified as capable of plastic degradation, but evidence for the degradation of highly prevalent polymers including polypropylene, nylon, polystyrene and polyvinyl chloride must be treated with caution; most studies fail to differentiate losses caused by the leaching or degradation of polymer monomers, additives or fillers. Even where polymer degradation is demonstrated, such as for polyethylene terephthalate, the ability of microorganisms to degrade more highly crystalline forms of the polymer used in commercial plastics appears limited. Microbiomes frequently work in conjunction with abiotic factors such as heat and light to impact the structural integrity of polymers and accessibility to enzymatic attack. Consequently, there remains much scope for extremophile microbiomes to be explored as a source of plastic-degrading enzymes and microorganisms. We propose a best-practice workflow for isolating and reporting plastic-degrading taxa from diverse environmental microbiomes, which should include multiple lines of evidence supporting changes in polymer structure, mass loss, and detection of presumed degradation products, along with confirmation of microbial strains and enzymes (and their associated genes) responsible for high molecular weight plastic polymer degradation. Such approaches are necessary for enzymatic degraders of high molecular weight plastic polymers to be differentiated from organisms only capable of degrading the more labile carbon within predominantly amorphous plastics, plastic monomers, additives or fillers.

Toward the improvement of total nitrogen deposition budgets in the United States.

Frameworks for limiting ecosystem exposure to excess nutrients and acidity require accurate and complete deposition budgets of reactive nitrogen (Nr). While much progress has been made in developing total Nr deposition budgets for the U.S., current budgets remain limited by key data and knowledge gaps. Analysis of National Atmospheric Deposition Program Total Deposition (NADP/TDep) data illustrates several aspects of current Nr deposition that motivate additional research. Averaged across the continental U.S., dry deposition contributes slightly more (55%) to total deposition than wet deposition and is the dominant process (>90%) over broad areas of the Southwest and other arid regions of the West. Lack of dry deposition measurements imposes a reliance on models, resulting in a much higher degree of uncertainty relative to wet deposition which is routinely measured. As nitrogen oxide (NOx) emissions continue to decline, reduced forms of inorganic nitrogen (NHx = NH3 + NH4+) now contribute >50% of total Nr deposition over large areas of the U.S. Expanded monitoring and additional process-level research are needed to better understand NHx deposition, its contribution to total Nr deposition budgets, and the processes by which reduced N deposits to ecosystems. Urban and suburban areas are hotspots where routine monitoring of oxidized and reduced Nr deposition is needed. Finally, deposition budgets have incomplete information about the speciation of atmospheric nitrogen; monitoring networks do not capture important forms of Nr such as organic nitrogen. Building on these themes, we detail the state of the science of Nr deposition budgets in the U.S. and highlight research priorities to improve deposition budgets in terms of monitoring and flux measurements, leaf- to regional-scale modeling, source apportionment, and characterization of deposition trends and patterns.

Impact of electrokinetic remediation on microbial communities within PCP contaminated soil.

Electrokinetic techniques have been used to stimulate the removal of organic pollutants within soil, by directing contaminant migration to where remediation may be more easily achieved. The effect of this and other physical remediation techniques on the health of soil microbial communities has been poorly studied and indeed, largely ignored. This study reports the impact on soil microbial communities during the application of an electric field within ex situ laboratory soil microcosms contaminated with pentachlorophenol (PCP; 100mg kg(-1) oven dry soil). Electrokinetics reduced counts of culturable bacteria and fungi, soil microbial respiration and carbon substrate utilisation, especially close to the acidic anode where PCP accumulated (36d), perhaps exacerbated by the greater toxicity of PCP at lower soil pH. There is little doubt that a better awareness of the interactions between soil electrokinetic processes and microbial communities is key to improving the efficacy and sustainability of this remediation strategy.

Molecular analysis of arsenate-reducing bacteria within Cambodian sediments following amendment with acetate.

The health of millions is threatened by the use of groundwater contaminated with sediment-derived arsenic for drinking water and irrigation purposes in Southeast Asia. The microbial reduction of sorbed As(V) to the potentially more mobile As(III) has been implicated in release of arsenic into groundwater, but to date there have been few studies of the microorganisms that can mediate this transformation in aquifers. With the use of stable isotope probing of nucleic acids, we present evidence that the introduction of a proxy for organic matter ((13)C-labeled acetate) stimulated As(V) reduction in sediments collected from a Cambodian aquifer that hosts arsenic-rich groundwater. This was accompanied by an increase in the proportion of prokaryotes closely related to the dissimilatory As(V)-reducing bacteria Sulfurospirillum strain NP-4 and Desulfotomaculum auripigmentum. As(V) respiratory reductase genes (arrA) closely associated with those found in Sulfurospirillum barnesii and Geobacter uraniumreducens were also detected in active bacterial communities utilizing (13)C-labeled acetate in microcosms. This study suggests a direct link between inputs of organic matter and the increased prevalence and activity of organisms which transform As(V) to the potentially more mobile and thus hazardous As(III) via dissimilatory As(V) reduction.

Severe coronary artery disease in the absence of supravalvular stenosis in a patient with Williams syndrome.

Williams syndrome is a complex syndrome comprising developmental abnormalities, craniofacial dysmorphic features, and cardiac anomalies. The most common cardiac anomaly is supravalvular aortic stenosis. We report a case of a 6-year-old girl with Williams syndrome who presented with decompensated heart failure due to ischemic cardiomyopathy. Her only significant cardiac anomaly was severe stenosis of the left main coronary artery. She subsequently died despite surgical revascularization. Isolated coronary anomalies are rare in Williams syndrome but should be considered especially in the presence of heart failure or ischemia.

Does intrathecal fentanyl produce acute cross-tolerance to i.v. morphine?

We have examined the hypothesis that intrathecal fentanyl at operation can increase postoperative i.v. morphine requirements. We studied 60 patients undergoing Caesarean section. All received intrathecal 0.5% plain bupivacaine 2 ml combined with either fentanyl 0.5 ml (25 micrograms) (group F) (n = 30) or normal saline 0.5 ml (group S) (n = 30). In addition, 10 ml of an extradural solution (fentanyl 1 ml (50 micrograms) combined with 0.5% bupivacaine 9 ml) was administered after delivery. Extradural solution was only given before delivery if the intrathecal injection failed to produce a block above T6 or the patient required further analgesia. Postoperative analgesia was provided with i.v. morphine patient-controlled analgesia. At operation, intrathecal fentanyl reduced the need to administer extradural solution before delivery, increased the anaesthetist's satisfaction with analgesia and reduced nausea, but increased pruritus. Up to 6 h after delivery there was no difference in postoperative morphine requirements or pain scores. Between 6 h and 23 h there was a 63% increase in morphine requirements in group F. We consider the most likely explanation for this finding to be that intrathecal fentanyl induced acute spinal opioid tolerance.

Neurogenic pulmonary oedema.

Neurogenic pulmonary oedema followed a subarachnoid haemorrhage secondary to an arteriovenous malformation in an eight-year-old boy. Despite a complicated course, he made a full recovery. Neurogenic pulmonary oedema is rare in childhood. It is sudden in onset, and potentially fatal, but is amenable to prompt and vigorous treatment.

Comparison of pulse oximeters in healthy sleeping infants.

Four commercially available pulse oximeters were compared on normal infants to determine incidence and correct identification of movement artefact, and to assess their other features, in order to guide the potential user in the most appropriate choice of a machine to suit their purposes. Measurements of arterial oxygen saturation by pulse oximetry are distorted by movement artefact. During five one hour recording periods, over 100 artefacts occurred with each machine. The incidence of movement artefact differed between oximeters. Twice as many occurred when the Criticare 500 was used. The four oximeters differed in their ability to identify artefacts. The Novametrix 500 was best able to do this. A visual display aided observer recognition of artefacts. Other features of the different machines are described. An expansion of the use of pulse oximetry beyond the intensive care unit is suggested.

Extracellular volume of the human placenta in vitro.

The extracellular volume of fresh and perfused human placenta has been measured in two sets of experiments. In the first set fragments of placenta which had been dually perfused for either 45 or 110 min as well as fragments from unperfused areas of the same placenta were incubated for 4 h in Earle's bicarbonate buffer containing 51Cr-EDTA as an extracellular marker. The 51Cr-EDTA space, as a proportion of wet weight, was 76.5 +/- (SE) 1.4 (n = 11) and 79.4 +/- 1.8% (n = 6) for the short and long perfusions, respectively; these did not significantly differ from each other or from the values for the equivalent unperfused placenta: 75.2 +/- 1.0 (n = 11) and 77.7 +/- 0.9% (n = 6). In the second set of experiments 51Cr-EDTA and 14C-inulin were perfused through the maternal and fetal circulations of the placental lobules for 1, 2, or 4 h, and simultaneously unperfused fragments from the same placenta were incubated with the markers for 1, 2, or 4 h. The 51Cr-EDTA space was found to be significantly higher than the 14C-inulin space in both perfusion and incubation determinations. Irrespective of the marker, the incubation spaces were unaltered with time and were significantly higher than the perfusion spaces at all three time points. However, the difference decreased with the length of perfusion, so that by 4 h it was less than 10%. (At 4 h incubation the 51Cr-EDTA space was 76.2 +/- 0.9% and the perfusion space 67.4 +/- 1.1%, n = 6; the 14C-inulin incubation space was 60.9 +/- 2.2% and the perfusion space 52.5 +/- 2.6%, n = 5). As there was no evidence of increasing placental permeability with time, as judged by clearance of creatinine, it was concluded that the placental extracellular volume is large irrespective of the method of measurement.

Pupillometer for use during anaesthesia.

This paper presents the design for a pupillometer based on a fixed focal length microscope; it is suitable for use during anaesthesia. The pupillometer has been tested and found to give reliable results. A certain amount of practice is necessary to make measurements quickly. The pupillometer was designed to allow the study of pupil diameter in relation to 'depth of anaesthesia'.

Disposition and metabolism of fenbufen in several laboratory animals.

Absorption, distribution, metabolism and excretion studies with gamma-oxo-(1,1'-biphenyl)-4-butanoic acid (fenbufen) have been conducted in several laboratory animal species. Single oral doses of 14C-fenbufen were administered to rats, guinea pigs, rabbits and dogs (10, 40 and 100 mg/kg) and to mice and monkeys (40 and 100 mg/kg); rats, rabbits and dogs received an i.v. dose of 10 mg/kg. Multiple oral doses of 40 mg/kg of non-radiolabelled fenbufen were studied in the rat and dog. Plasma concentrations of fenbufen and its metabolites were dose dependent with areas under the curve showing general linearity both within and among species over the range studied (10--100 mg/kg). Radioactivity was present in all tissues examined following a dose of 10 mg/kg 14C-fenbufen orally to rats and guinea pigs. Except for gastrointestinal tract, liver and kidney these tissue levels were usually lower than the corresponding plasma level through 24 h post dose. The major drug-related material in plasma of the rat, guinea pig and dog was (1,1'-biphenyl)-4-acetic acid; in the monkey it was gamma-hydroxy(1,1'-biphenyl)-4-butanoic acid. These two compounds together with unchanged fenbufen were present in the plasma of all the animals studied. In addition 4'-hydroxy(1,1'-biphenyl)-4-acetic acid was found in rat plasma and beta, gamma-dihydroxyl(1,1'-biphenyl)-4-butanoic acid in dog plasma. The plasma profiles of fenbufen and metabolites did not change during multiple, daily oral doses of 40 mg/kg in either the rat (up to 10 days) or the dog through 18 months. In varying proportions, a total of 11 metabolites (including those listed above) together with fenbufen itself were isolated and characterized from the urine of mice, rats, guinea pigs, dogs and/or monkeys dosed with fenbufen. Within each of the species studied, excretion patterns of drug-related materials in the urine and feces following an i.v. dose were similar to those following the oral doses. In general urine was the major excretory pathway.

Metabolic and pharmacokinetic studies with fenbufen in man.

Single oral doses of 600 mg of 14C-labelled gamma-oxo(1,1'-biphenyl)-4-butanoic acid (fenbufen) were administered to three male volunteers. Additional male and female subjects received single (500-700 mg) or multiple (300-400 mg b.i.d.) doses of non-isotopically labelled drug. Fenbufen was rapidly absorbed from the gastroiintestinal tract to the extent of at least 78%. Food reduced the rate but not the extent of absorption. Peak serum concentrations of total drug related compounds were reached by 2 h, at which time fenbufen accounted for only 11% of these substances. The remaining drug related material consisted of two metabolites: gamma-hydroxy(1,1'-biphenyl)-4-butanoic acid and (1,1'-biphenyl)-4-acetic acid. Steady state serum concentrations were reached within a week with multiple dosing regimens. The ratio of fenbufen to its circulating metabolites did not change over a month of daily dosing. Only traces of fenbufen and metabolites were present in the cellular components of blood or in human milk, but significant amounts (concentrations one-third those in serum) were measured in the synovial fluid of arthritic patients. Fenbufen and its circulating metabolites were highly bound (> 98%) to human serum in vitro, but at therapeutic levels showed very small or no effects on the serum binding of various other commonly used drugs. Concomitant administration of fenbufen and acetylsalicylic acid (ASA) resulted in decreased serum concentration of fenbufen and its metabolites compared to those obtained from fenbufen administration alone. In addition to the serum metabolites, three more transformation products were identified in urine: 4'-hydroxy(1,1'-biphenyl)-4-acetic acid, gamma,4'-dihydroxy(1,1'-biphenyl)-4-butanoic acid and beta, gamma-dyhydroxy(1,1'-biphenyl)-4-butanoic acid.