Stability of peatland carbon to rising temperatures.

Peatlands contain one-third of soil carbon (C), mostly buried in deep, saturated anoxic zones (catotelm). The response of catotelm C to climate forcing is uncertain, because prior experiments have focused on surface warming. We show that deep peat heating of a 2 m-thick peat column results in an exponential increase in CH4 emissions. However, this response is due solely to surface processes and not degradation of catotelm peat. Incubations show that only the top 20-30 cm of peat from experimental plots have higher CH4 production rates at elevated temperatures. Radiocarbon analyses demonstrate that CH4 and CO2 are produced primarily from decomposition of surface-derived modern photosynthate, not catotelm C. There are no differences in microbial abundances, dissolved organic matter concentrations or degradative enzyme activities among treatments. These results suggest that although surface peat will respond to increasing temperature, the large reservoir of catotelm C is stable under current anoxic conditions.

Gaseous mercury fluxes from forest soils in response to forest harvesting intensity: a field manipulation experiment.

Forest harvesting leads to changes in soil moisture, temperature and incident solar radiation, all strong environmental drivers of soil-air mercury (Hg) fluxes. Whether different forest harvesting practices significantly alter Hg fluxes from forest soils is unknown. We conducted a field-scale experiment in a northern Minnesota deciduous forest wherein gaseous Hg emissions from the forest floor were monitored after two forest harvesting prescriptions, a traditional clear-cut and a clearcut followed by biomass harvest, and compared to an un-harvested reference plot. Gaseous Hg emissions were measured in quadruplicate at four different times between March and November 2012 using Teflon dynamic flux chambers. We also applied enriched Hg isotope tracers and separately monitored their emission in triplicate at the same times as ambient measurements. Clearcut followed by biomass harvesting increased ambient Hg emissions the most. While significant intra-site spatial variability was observed, Hg emissions from the biomass harvested plot (180 ± 170 ng m(-2)d(-1)) were significantly greater than both the traditional clearcut plot (-40 ± 60 ng m(-2)d(-1)) and the un-harvested reference plot (-180 ± 115 ng m(-2)d(-1)) during July. This difference was likely a result of enhanced Hg(2+) photoreduction due to canopy removal and less shading from downed woody debris in the biomass harvested plot. Gaseous Hg emissions from more recently deposited Hg, as presumably representative of isotope tracer measurements, were not significantly influenced by harvesting. Most of the Hg tracer applied to the forest floor became sequestered within the ground vegetation and debris, leaf litter, and soil. We observed a dramatic lessening of tracer Hg emissions to near detection levels within 6 months. As post-clearcutting residues are increasingly used as a fuel or fiber resource, our observations suggest that gaseous Hg emissions from forest soils will increase, although it is not yet clear for how long such an effect will persist.

Water quality, sediment, and soil characteristics near Fargo-Moorhead urban areas as affected by major flooding of the Red River of the North.

Spring flooding of the Red River of the North (RR) is common, but little information exits on how these flood events affect water and overbank sediment quality within an urban area. With the threat of the spring 2009 flood in the RR predicted to be the largest in recorded history and the concerns about the flooding of farmsteads, outbuildings, garages, and basements, the objectives of this study, which focused on Fargo, ND, and Moorhead, MN, were to assess floodwater quality and to determine the quantity and quality of overbank sediment deposited after floodwaters recede and the quality of soil underlying sediment deposits. 17ß-Estradiol was detected in 9 of 24 water samples, with an average concentration of 0.61 ng L. Diesel-range organics were detected in 8 of 24 samples, with an average concentration of 80.0 µg L. The deposition of sediment across locations and transects ranged from 2 to 10 kg m, and the greatest mass deposition of chemicals was closest to the river channel. No gasoline-range organics were detected, but diesel-range organics were detected in 26 of the 27 overbank sediment samples (maximum concentration, 49.2 mg kg). All trace elements detected in the overbank sediments were within ranges for noncontaminated sites. Although flooding has economic, social, and environmental impacts, based on the results of this study, it does not appear that flooding in the RR in F-M led to decreased quality of water, sediment, or soil compared with normal river flows or resident soil.

Smoking and a complement gene polymorphism interact in promoting cardiovascular disease morbidity and mortality.

We have demonstrated previously that carriers of a genotype called C4B*Q0 (silent allele of the C4B gene) have a substantially increased risk to suffer from myocardial infarction or stroke, and are selected out from the healthy elderly population. Because smoking carries a major risk for cardiovascular disease (CVD), it seemed worthwhile to study if these two factors interact. Study 1 involved 74 patients with angina pectoris (AP), 85 patients with recent acute myocardial infarction (AMI) and 112 survivors of a previous AMI and 382 controls from Iceland. Study 2 involved 233 patients with severe CVD and 274 controls from Hungary. Smoking habits were registered for each subject. The number of C4A and C4B genes was determined by phenotyping or genotyping. Compared to controls, C4B*Q0 carrier frequency was significantly higher at diagnosis in Icelandic smokers with AP (P = 0.005) and AMI (P = 0.0003) and Hungarian smokers with severe coronary artery disease (P = 0.023), while no such difference was observed in non-smoking subjects. Age-associated decrease in C4B*Q0 observed previously in two remote Caucasian populations was found, in the present study, to be associated strongly with smoking, and to already occur in smokers after age 50 years both in Iceland and Hungary. Our findings indicate that the C4B*Q0 genotype can be considered as a major covariate of smoking in precipitating the risk for AMI and associated deaths.

Defective prevention of immune precipitation in autoimmune diseases is independent of C4A*Q0.

Increased prevalence of C4 null alleles is a common feature of autoimmune diseases. We have shown previously that complement-dependent prevention of immune precipitation (PIP) is defective in patients with systemic lupus erythematosus (SLE), and correlated this defect with C4A*Q0 and low levels of the C4A isotype. To further clarify the role of C4A in the aetiology of SLE, we now extend our studies to other diseases which have been associated with C4A*Q0. The frequency of C4A*Q0 was increased in Icelandic patients with coeliac disease (0.50; P < 0.001), Grave's disease (0.30; P = 0.002) and insulin-dependent diabetes mellitus (0.23; P = 0.04) and in British patients with dermatitis herpetiformis (0.42; P = 0.002) and this was reflected in low levels of C4A. In spite of this, PIP was normal in these patients, and in marked contrast to our previous observations on connective tissue diseases, PIP measurements in these patient groups correlated more strongly with levels of C4B (r = 0.51, P = 0.0000004) than C4A. Patients with increased levels of anti-C1q antibodies had significantly lower PIP than patients without such antibodies (P < 0.01) and a negative association of PIP with anti-C1q antibodies was also reflected in an increased prevalence (P = 0.006) and levels (P = 0.006) of anti-C1q antibodies in patients with subnormal PIP, as well as a negative correlation between PIP and anti-C1q antibodies (r = - 0.25, P = 0.02). These results show that the PIP defect cannot be explained by low levels of C4A alone and suggest that measurements of anti-C1q antibodies may be useful in future studies on the molecular cause of the PIP defect in autoimmune connective tissue disease.

Increased frequency of C4B*Q0 alleles in patients with Henoch-Schönlein purpura.

Henoch-Schonlein purpura (HSP) is a vasculitis of unknown aetiology, possibly involving immune complexes. The complement system is essential for the clearance of immune complexes. Our aim was to explore the hypothesis that patients with HSP have abnormal complements, contributing to the development of the disease. The study included 56 patients diagnosed with HSP at the Children's Hospital, Iceland between 1984 and 2000, and 98 blood donors as controls. Serum levels of immunoglobulin A, C4A, C4B and mannan-binding lectin were measured and compared between the two groups. C4 null alleles were significantly more common in HSP patients than in controls (P = 0.018) and were carried by 66.1% of the patients compared with 41.2% of the controls. This difference was due to an increased frequency of C4B*Q0 allele in the HSP group (0.25 versus 0.11 in the control group; P = 0.002). The fact that the majority of our patients carried a C4 null allele indicates that children with C4 deficiencies may have an increased risk of developing HSP. This may reflect inadequate complement activity and possibly present an opportunity to identify patients at risk of developing serious morbidity associated with HSP.

Patients with systemic lupus erythematosus are deficient in complement-dependent prevention of immune precipitation.

OBJECTIVE: A functional deficiency of complement has been implicated but not conclusively demonstrated in the pathogenesis of systemic lupus erythematosus (SLE). To test this, we studied several aspects of complement in 44 patients with SLE, 46 patients with rheumatoid arthritis and 102 blood donors. METHODS: Prevention of immune precipitation (PIP) was measured by an enzyme immunoassay, levels of C1q, C4 and C3 by rocket immunoelectrophoresis, C4A, C4B and C3d by enzyme-linked immunosorbent assay (ELISA), complement haemolysis (CH50) by standard methods and C4 allotypes by high-voltage agarose electrophoresis and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). RESULTS: PIP was significantly reduced in SLE (P<0.001); the defect was revealed by a sensitive assay measuring this function of complement but not by the other tests employed. The patients were clinically well at the time of study, and levels of C3d, which have been shown to correlate with disease activity, were normal. The defect was more common in patients with early disease (P = 0.009), supporting a role in aetiology or early pathophysiology. PIP was positively correlated with levels of C4 (P = 3 x 10(-5)) and in particular the C4A isotype (P = 9 x 10(-10)) whereas C4B was redundant. CONCLUSIONS: Our results reveal a defect in prevention of immune precipitation in SLE that is apparent at an early stage in the disease and correlates with low levels of C4A. These results indicate that subtle deficiencies of complement may predispose to SLE.

Deficiency of complement-dependent prevention of immune precipitation in systemic sclerosis.

BACKGROUND: Previous studies have indicated that complement may be activated or inherently abnormal in systemic sclerosis (SSc), and it has been suggested that immune complex deposition plays a part in the microvascular damage of this disease. OBJECTIVE: To study several aspects of the complement system in 24 patients with SSc. METHODS: Complement dependent prevention of immune precipitation (PIP) was measured by a sensitive enzyme immunoassay, levels of C1q, C4, and C3 by rocket immunoelectrophoresis, C4 allotypes by high voltage agarose electrophoresis, and C4A, C4B, and C3d by an enzyme linked immunosorbent assay (ELISA). RESULTS: PIP was markedly decreased in the patients with SSc (p<0.001). Abnormal complement activation was detected in nine patients as raised levels of the complement split product C3d. However, a relation between low PIP and complement activation was not seen. PIP was significantly lower in patients who carried the C4A*Q0 allotype (p=0.03), and a strong correlation was found between PIP and C4A concentration (p<0.00001). The PIP defect may, at least in some patients, be associated with the initial phase of the disease. CONCLUSIONS: The results show a previously unrecognised functional defect of complement in SSc; the defect correlates with low levels of classical pathway components and, in particular, C4A.

Ultrastructural alterations of bacteria during the postantibiotic effect.

Ultrastructural alterations of Staphylococcus aureus and Pseudomonas aeruginosa were examined during the postantibiotic effect (PAE) with transmission electron microscopy. After exposure to dicloxacillin the staphylococci were characterized by an increase in the number of crosswalls, rifampin produced thickening of the cell wall, but only minimal changes were induced by gentamicin. Intracellular electrondense aggregates were observed in P. aeruginosa after exposure to imipenem, tobramycin and ciprofloxacin, and imipenem caused globoid cell formations. These alterations were not uniform in every organism, but they correlated well with the duration of the PAE determined by viable counts.

Metabolic and ultrastructural effects induced by ciprofloxacin in Staphylococcus aureus during the postantibiotic effect (PAE) phase.

The new quinolone antibacterial agents have been found to produce a postantibiotic effect (PAE) of 1-4 h in bacteria but the underlying mechanism is still unknown. After exposure to ciprofloxacin in concentrations of 1-16 x MIC for 1 hr the DNA synthesis in S. aureus ATCC 25923 was investigated during the PAE. Ultrastructure was also investigated by electron microscopy after exposure to a concentration of 2 x MIC. The rate of DNA synthesis per organism (measured as CPM/cfu/ml) increased progressively up to a maximum value at 1 1/2 h after drug removal. The maximal 3H-thymidine incorporation per organism at this moment correlated directly with the duration of the PAE. Bacterial swelling with scarcity and vacuole-formation of the cytoplasm characterized the majority of the staphylococci during the PAE. The physiological importance of the increased DNA synthesis is unknown, but the increased metabolic activity, coincident with increased duration of the PAE, suggests a possible common mechanism.