Search

The pollution of marine environments from plastic waste is anticipated to increase with current increases in plastic production. Reciprocally, escalating research efforts provide an improved understanding, monitoring, awareness, and mitigation of plastic contamination. Freshwater streams are recognised as one of the main contributors of microplastic pollution in marine environments. Presented here is the first investigation on the abundance of microplastic contamination (20 μm and5 mm) in freshwater streams in Adelaide, Australia. Composite samples were obtained from the sub-surface waters of eight freshwater streams (Magazine Wetland, Torrens River, Brownhill Creek, Sturt River, Field River, Christie Creek, Onkaparinga River and Pedler Creek), just before their connection to the Gulf St Vincent. Microplastics were found in all samples and microplastic abundance was 6.4 ± 5.5 particles.L

Based on previous systems for generating helper cells and factors from mouse spleen cell cultures, an in vitro system for the production and detection of human helper factors to the synthetic polypeptide antigens (T,G)-A--L and GAT10 was developed. The factors are made by human peripheral blood leucocytes and are antigen-specific, as judged both by functional criteria and specific binding and elution from antigen columns. Out of the first six volunteers studied two were high responders to (T,G)-A--L, but non-responders to GAT, two responders to GAT but not (T,G)-A--L. One subject made factors to both antigens and the sixth reacted to neither. The antigens chosen are known to be under MHC-linked immune response (Ir) gene control in all animal species tested, with some strains being responders while others are not. The selective responsiveness, different between individuals, thus suggests that the response to these antigens in man is under Ir gene control. Because of the small size of the sample initially studied and HLA typed, it was not surprising that there was no clear-cut association of response with any particular histocompatibility type at the HLA-A, B, C or D locus.

Background Early identification of failing free flaps may allow for potential intervention and flap salvage. The predictive ability of flap temperature monitoring has been previously questioned. The present study investigated the ability of an infrared surface temperature monitoring device to detect trends in flap temperature and correlation with anastomotic thrombosis and flap failure. Methods Postoperative measurement of surface temperature was obtained in 47 microvascular free flaps. Differences in temperature between survival and failure groups were evaluated for statistical significance using Student's t test (PResults In total, eight flaps failed. Five of these were re-explored, of which one was salvaged. The three other flaps died a progressive death secondary to presumed thrombosis of the microcirculation despite adequate Doppler signals. Temperatures of the flap failure group during the last 24 h yielded a mean difference of 2°C (3.56°F) compared with surviving flaps (PConclusions A surface temperature measurement device provides reproducible digital readings without physical contact with the flap. Technical difficulties encountered in previous research with implantable or surface contact temperature probes are obviated with this noncontact technique. Flap temperature monitoring revealed a trend in temperature that correlates with anastomotic thrombosis and eventual flap failure.

Crohn's disease has frequently been associated with coagulation abnormalities, causing intravascular deposition of fibrin and local infarction which can subsequently compromise the gut mucosa. Also, arterial and venous thromboembolic complications of larger vessels appear to be associated with Crohn's disease. Coagulation activation in patients with Crohn's disease could be a result of increased serum and tissue levels of cytokines, as reported. We prospectively studied parameters of coagulation and fibrinolysis in 10 patients with active Crohn's disease, who were subsequently treated with a monoclonal anti-tumor necrosis factor-a (TNF) antibody. Ten consecutive patients with active Crohn's disease (CDAI > 150), not responding to a daily dose of at least 20 mg prednisolone, received a single infusion of human/mouse chimeric anti-TNF antibody cA2. All evaluable patients attained complete clinical and endoscopic remission within 4 weeks. Pretreatment plasma concentrations of markers of thrombin generation, thrombin-antithrombin (TAT) complexes and F1 + 2, were increased (22.1 +/- 11.8 mu g/l and 3.46 +/- 1.2 nmol/l, respectively). After treatment with cA2, these levels almost completely normalized within 2 weeks. D dimer plasma levels were increased at baseline (377 +/- 61.3 mu g/l) and decreased to normal levels after cA2 treatment. The levels of plasminogen activator inhibitor (PAI-1) were elevated before treatment and slowly decreased hereafter. The levels of tissue-type plasminogen activator (t-PA) remained unchanged. Von Willebrand factor (vWf) levels were increased at baseline (159 +/- 21%) and showed a downward trend after 2 weeks (121.3 +/- 24%, NS). In conclusion, anti-TNF antibody infusion resulted in a decrease of thrombin generation and endothelium activation markers in patients that were suffering from steroid-refractory Crohn's disease. These findings support the notion that active Crohn's disease is associated with the activation of coagulation and may indicate that this coagulation activation is mediated by TNF.