Landspreading with co-digested cattle slurry, with or without pasteurisation, as a mitigation strategy against pathogen, nutrient and metal contamination associated with untreated slurry.

North Atlantic European grassland systems have a low nutrient use efficiency and high rainfall. This grassland is typically amended with unprocessed slurry, which counteracts soil organic matter depletion and provides essential plant micronutrients but can be mobilised during rainfall events thereby contributing to pathogen, nutrient and metal incidental losses. Co-digesting slurry with waste from food processing mitigates agriculture-associated environmental impacts but may alter microbial, nutrient and metal profiles and their transmission to watercourses, and/or soil persistence, grass yield and uptake. The impact of EU and alternative pasteurisation regimes on transmission potential of these various pollutants is not clearly understood, particularly in pasture-based agricultural systems. This study utilized simulated rainfall (Amsterdam drip-type) at a high intensity indicative of a worst-case scenario of ~11 mm hr-1 applied to plots 1, 2, 15 and 30 days after grassland application of slurry, unpasteurised digestate, pasteurised digestate (two conditions) and untreated controls. Runoff and soil samples were collected and analysed for a suite of potential pollutants including bacteria, nutrients and metals following rainfall simulation. Grass samples were collected for three months following application to assess yield as well as nutrient and metal uptake. For each environmental parameter tested: microbial, nutrient and metal runoff losses; accumulation in soil and uptake in grass, digestate from anaerobic co-digestion of slurry with food processing waste resulted in lower pollution potential than traditional landspreading of slurry without treatment. Reduced microbial runoff from digestate was the most prominent advantage of digestate application. Pasteurisation of the digestate further augmented those environmental benefits, without impacting grass output. Anaerobic co-digestion of slurry is therefore a multi-beneficial circular approach to reducing impacts of livestock production on the environment.

Adipose tissue is influenced by hypoxia of obstructive sleep apnea syndrome independent of obesity.

AIMS: Obstructive sleep apnea syndrome (OSAS) is associated with increased cardiovascular risk and diabetes independent of obesity. We investigated whether adipose tissue dysfunction is exacerbated due to increased tissue hypoxia. METHODS: Adipose tissue (AT) oxygenation was measured with a Clarke-type electrode (pATO2) in 16 men with OSAS before and after 4 months of continuous positive airway pressure therapy (CPAP) and in BMI-matched controls. Oxygenation was simultaneously monitored in arterial blood by pulse oximetry (SaO2); mixed blood in AT microcirculation by reflectance spectroscopy (SATO2) along with blood flow. Markers of hypoxia, adipo- and angiogenesis, inflammation and fibrosis were analysed in AT and serum. RESULTS: OSAS subjects were more insulin resistant. Despite lower arterial SaO2 (95.4±1.3% vs. 97.1±1.6%, P=0.013) in subjects with OSAS, there was no difference in the oxygen content of AT microcirculation (61.6±18.4 vs. 72.2±7.0%, P=0.07) or pATO2 (49.2±7.5 vs. 50.4±14.7mmHg, P=0.83) between groups. Resting AT blood flow was higher in OSAS compared to controls (108.5±22.7 vs. 78.9±24.9au, P<0.005) and strongly associated with inflammation markers IL-6 and MCP-1. AT of OSAS subjects showed increased inflammation (TNFA P=0.049) and fibrosis (COL3A1 P=0.02), a trend of higher HIF1A expression (P=0.06) and reduced adipogenesis (PPARG P=0.006). After CPAP, only expression of the lipid deposition marker LPL increased (30%, P=0.047). CONCLUSIONS: Adipose tissue of awake OSAS subjects appears no more hypoxic than adipose tissue of BMI-matched controls despite daytime hypoxaemia. Increased adipose tissue blood flow may be explained by an increased inflammatory response. We observe features of adipose dysfunction in subjects with OSAS, which attribute to increased cardiometabolic risk associated with this condition.

Microstructure and mechanics of human resistance arteries.

Vascular diseases such as diabetes and hypertension cause changes to the vasculature that can lead to vessel stiffening and the loss of vasoactivity. The microstructural bases of these changes are not presently fully understood. We present a new methodology for stain-free visualization, at a microscopic scale, of the morphology of the main passive components of the walls of unfixed resistance arteries and their response to changes in transmural pressure. Human resistance arteries were dissected from subcutaneous fat biopsies, mounted on a perfusion myograph, and imaged at varying transmural pressures using a multimodal nonlinear microscope. High-resolution three-dimensional images of elastic fibers, collagen, and cell nuclei were constructed. The honeycomb structure of the elastic fibers comprising the internal elastic layer became visible at a transmural pressure of 30 mmHg. The adventitia, comprising wavy collagen fibers punctuated by straight elastic fibers, thinned under pressure as the collagen network straightened and pulled taut. Quantitative measurements of fiber orientation were made as a function of pressure. A multilayer analytical model was used to calculate the stiffness and stress in each layer. The adventitia was calculated to be up to 10 times as stiff as the media and experienced up to 8 times the stress, depending on lumen diameter. This work reveals that pressure-induced reorganization of fibrous proteins gives rise to very high local strain fields and highlights the unique mechanical roles of both fibrous networks. It thereby provides a basis for understanding the micromechanical significance of structural changes that occur with age and disease.

Grazing intensity is a poor indicator of waterborne Escherichia coli O157 activity.

Contamination of watercourses with fecal matter represents a significant risk to public health due to the associated risk from human pathogens (e.g. Escherichia coli O157, norovirus). In addition, water contamination may also perpetuate the re-infection cycle of human pathogens within domesticated and wild animal populations. While diffuse pollution from agricultural fields has been identified as a major source of these pathogens, the relationship between livestock grazing intensity and subsequent pathogen persistence in water is not well established. Our aim was to critically evaluate the importance of land use management on the activity of E. coli O157 in freshwaters collected from a livestock dominated catchment in the UK. We inoculated replicate batches of both filter-sterilised and non-sterile freshwaters with a chromosomally lux-marked E. coli O157 and monitored pathogen survival and activity over a 5 d period. Our results indicate that the greatest risk for pathogens entering freshwater is probably associated with high intensity livestock areas, although their subsequent survival is greatest in waters from low intensity livestock areas. We ascribe this enhanced persistence in the latter to reduced competition and predation within these aquatic environments. These results have serious implications for the reliability of pathogen risk exposure maps which are based on grazing intensity alone.

Measurements of H-->D-->(gamma-->,pi) and implications for the convergence of the Gerasimov-Drell-Hern integral.

We report new measurements of inclusive pi production from frozen-spin HD for polarized photon beams covering the Delta(1232) resonance. These provide data simultaneously on both H and D with nearly complete angular distributions of the spin-difference cross sections entering the Gerasimov-Drell-Hearn (GDH) sum rule. Recent results from Mainz and Bonn exceed the GDH prediction for the proton by 22 microb, suggesting as yet unmeasured high-energy components. Our pi0 data reveal a different angular dependence than assumed in Mainz analyses and integrate to a value that is 18 microb lower, suggesting a more rapid convergence. Our results for deuterium are somewhat lower than published data, considerably more precise, and generally lower than available calculations.

Experimentally induced pneumonia in scid/beige mice, using a bovine isolate of Pasteurella haemolytica.

BACKGROUND AND PURPOSE: Intranasal challenge of immunocompetent mice with Pasteurella haemolytica results in little or no pulmonary inflammation. The study reported here was designed to investigate the inflammatory response in the lungs of immunodeficient scid/beige mice after similar challenge. METHODS: Fifty-five scid/beige mice were challenged intranasally with saline or one of three doses (2.8 x 10(6), 3.4 x 10(9), or 3.3 x 10(11) colony-forming units [CFU]/ml) of P. haemolytica. The lungs were examined for changes in weight, bacterial count, and presence of gross and microscopic lesions at 24, 48, or 96 hours after challenge. RESULTS: Intranasal challenge with concentrations > or = 3.4 x 10(9) CFU/ml of P. haemolytica induced significantly heavier lung weight, with severe pulmonary lesions, and development of suppurative and fibrinous bronchopneumonia in dose- and time-dependent manner 48 hours after challenge. Pasteurella haemolytica was consistently isolated from the lungs at 24 hours after challenge. CONCLUSIONS: Bronchopneumonia was induced by P. haemolytica in mice without manipulation of the mouse or the bacteria. The lesions were similar to those that develop in the lungs of cattle infected with P. haemolytica and indicate potential use of the model for the study of this host/bacterial interaction.

Large granular lymphocytic leukemia in a mixed breed dog.

A mixed breed dog was diagnosed with large granular lymphocytic leukemia. Immunophenotypic analysis indicated the lymphocytes were CD3+, CD8+ T cells expressing the alpha beta T cell receptor and a leukointegrin, alpha d. Chemotherapy and splenectomy resulted in an initial reduction in the lymphocyte count.

Immunocytologic detection of Chlamydia psittaci from cervical and vaginal samples of chronically infected ewes.

An immunocytologic method was developed for the detection of chronic Chlamydia psittaci infection from the reproductive tract of ewes. Vaginal and cervical samples from 8 infected and 2 non-infected ewes were stained with a C. psittaci-specific monoclonal antibody. Cells containing C. psittaci were only detected from the 8 infected ewes and the level of detection varied with respect to the estrus cycle. An increased number of infected cells were observed during the periovulation period, thus indicating an optimal window for detection.

Effect of prostaglandins on the ontogenic response of rat gastric mucosa to luminal H+.

We have characterized the ontogeny of gastric mucosal permeability responses to luminal H+ and investigated the effect of prostaglandins (PGs) on these responses in the neonate. Mucosal responses to instillation of HCl (100-600 mN) were measured in rats between 10 and 60 days after birth. Permeability changes were expressed as H+ loss and Na+, K+, and protein appearance in the luminal instillate. Responses to 100 and 200 mN HCl were low at all ages. Instillation of 300 or 400 mN HCl produced larger transmucosal fluxes of ions and protein in animals older than 20 days of age compared with younger animals. High concentrations of acid (500-600 mN HCl) produced large fluxes of ions and protein at every age examined. The responses in suckling animals were less than those seen in rats 25 days of age or older. In each age group mucosal HCO-3 secretion was inhibited by HCl concentrations greater than 100 mN. In each age group the mucosal response to 350 mN HCl was reduced by either 16,16-dimethyl-PGE2 (2 micrograms/kg ig) or a PGI2 analogue (Iloprost; 100 micrograms/kg ig). The effect of either prostanoid was greater in animals younger than 25 days of age compared with older rats. PGE2 and 6-keto-PGF1 alpha were detected in the gastric mucosa at all ages examined. Suckling animals had higher levels of either prostanoid. PGE2 levels decreased after 30 days, while levels of 6-keto-PGF1 alpha remained constant. These data suggest that 1) the susceptibility of H+-induced alterations in mucosal permeability to ions and protein increases as the animal ages, 2) the gastric mucosa of weanling rats is sensitive to PGs, and 3) PGE2 and 6-keto-PGF1 alpha are present in neonatal rat mucosa.

Neonatal and maternal prostaglandin in the ontogenic response of rat gastric mucosa to H+.

We have previously demonstrated that neonatal rat stomach is less susceptible to luminal H+ when compared with the adult. In the present study we investigate the role of endogenous prostaglandins (PG) in the ontogeny of gastric permeability responses to H+. Responses to luminal instillation of 250 mN HCl were measured in rats at 10, 15, 20, and 25 days after birth. Mucosal responses were measured in terms of loss of H+ and appearance of Na+, K+, and protein in the luminal instillate. Indomethacin (IM; 8 mg/kg sc) administration to rat pups reduced mucosal levels of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha). In response to intraluminal HCl, the reduction of mucosal PG did not significantly affect transmucosal fluxes of ions and protein when compared with control pups. IM was also given to lactating dams on days just prior to the pups being 10, 15, 20, and 25 days old. IM treatment significantly reduced the content of PGE2 and 6-keto-PGF1 alpha in maternal milk. Permeability responses in pups from IM-treated dams were increased over pups from control dams. This effect was not observed in 25-day-old rats. Treatment of pups from IM-injected dams with PGE2 but not PGI2 partially restored the permeability responses to luminal H+ to levels observed in pups from control dams.(ABSTRACT TRUNCATED AT 250 WORDS)