Multi-Biomarkers Approach in Different Organs of <Emphasis Type="Italic">Anodonta cygnea</Emphasis> from the Dnister Basin (Ukraine)

The aim of this study was to compare environmental quality in two sites in western Ukraine—rural (R) and urbanized (U)—with the usage of the resident bivalve mollusk Anodonta cygnea. The study was realized during three seasons. The metal uptake and a set of biochemical markers were determined. For each season, Cd and metallothioneins (MTs) contents in the digestive gland and gills of the mollusc were higher at the U site, reflecting its chronic pollution. The oxidative stress in the mollusk was observed at the U site during spring and at the R site during summer and autumn according to the differences in Mn–superoxide dismutase and catalase activities, O₂^•− production, lipid peroxidation, and glutathione levels. The elevated vitellogenin-like protein levels in the hemolymph and the ethoxyresorufin-O-deethylase activity in the digestive gland in summer–autumn suggested pollutions by organic substances at the R site. The acetylcholinesterase activity was similar in both groups. The centroid grouping analysis of biomarkers and morphological and water indexes demonstrated the clear differentiation of general response in each group in spring and, at the R site, in summer and autumn but its similarity at the U site in summer and autumn.     

The mycotoxin Deoxynivalenol inhibits the cell surface expression of activation markers in human macrophages

Deoxynivalenol (DON) is the most prevalent trichothecene mycotoxin in crops in Europe and North America. It exhibits several toxic effects including impaired growth and immune dysregulation. Macrophages play pivotal role in the host defense; upon activation, they express several specific cell surface receptors that are important in adhesion and cell signaling. Several studies have demonstrated that DON can affect macrophages, however, very few data are available concerning the effect of DON on human macrophages, and the effect on macrophage cell surface receptors is unknown. In the present study, human blood monocytes, differentiated in vitro into macrophages, were activated with IFN-γ, in the presence or absence of low concentrations of DON. The expression of CD11c, CD13, CD14, CD18, CD33, CD35, CD54, CD119 and HLA-DP/DQ/DR was analyzed by flow cytometry. As expected, macrophage activation by IFN-γ upregulated the expression of CD54, CD14, CD119 and HLA-DP/DQ/DR. Incubation with DON decrease the cell surface expression of these activation markers in a dose-dependent manner. When cells were treated with 5 μM DON, the mean fluorescence intensity measured for the expression of these receptors was the same as that observed in non-activated macrophages. This inhibitory effect of DON was only observed when the mycotoxin was applied before the activation signal. Taken together, our results suggest that low concentration of DON alter macrophage activation as measured by the expression of cell surface markers. This may have implications for human health when consuming DON contaminated feed.     

Senator, what is your policy on "Other"?

In the midst of the monumentally important 2008 presidential election, information about the candidates' proposals for biomedical research is notably absent. Why is this the case, and more importantly, what can be done about it?     

Photodynamic treatment with mono-phenyl-tri-(N-methyl-4-pyridyl)-porphyrin for pathogen inactivation in cord blood stem cell products

BACKGROUND: Hematopoietic stem cell transplants and culture of hematopoietic progenitor cells require pathogen‐free conditions. The application of a method of pathogen inactivation in red blood cells using photodynamic treatment (PDT) was investigated for the decontamination of cord blood stem cell (CBSC) products. STUDY DESIGN AND METHODS: CBSC products, spiked with Gram‐positive and Gram‐negative bacteria, were treated with PDT using mono‐phenyl‐tri‐(N‐methyl‐4‐pyridyl)‐porphyrin (Tri‐P(4)) and red light. After PDT, in vitro and in vivo evaluation of the CBSC functions were performed. RESULTS: PDT of CBSC products resulted in the inactivation of the bacteria, with Staphylococcus aureus being the most resistant. Complete decontamination was achieved when CBSC products were contaminated with low titers of bacteria. PDT had no effect on white blood cell viability, the ex vivo expansion potential of the progenitor cells, and their capacity to differentiate to various hematopoietic cell lineages. However, PDT reduced the engraftment of human CBSCs in NOD/SCID mice, particularly affecting the B‐cell lineage engraftment. CONCLUSION: Pathogen inactivation of CBSC with Tri‐P(4)‐mediated PDT is feasible at contamination level up to 10 to 20 colony‐forming units per mL and can be considered when ex vivo expansion culture is anticipated. However, this treatment is not recommended for transplantation purposes at this time. Further investigations may elucidate why engraftment is diminished.     

Glomerular and tubulointerstitial diseases

This article provides a general overview of some of the more common or illustrative glomerular and tubulointerstitial disorders encountered in clinical practice. Disorders are grouped into those causing the nephrotic syndrome, the acute nephritic syndrome and rapidly progressive glomerulonephritis (RPGN), and chronic tubulointerstitial disease. This division is useful for narrowing the differential diagnosis and deciding on further testing and management. Elements of the past history, including detailed family, medication, and social histories, and recent symptoms and physical examination findings are as much a part of the diagnostic workup as are urinary and blood tests. An assessment of the tempo and severity of renal deterioration is critical to separate potential medical emergencies, such as RPGN, from those more indolent disorders that can be managed by the primary care physician.     

Arterial stiffness and haemodynamic response to vasoactive medication in subjects with insulin-resistance syndrome

INSR (insulin-resistance syndrome) affects 25% of the Australian population and is associated with increased cardiovascular risk. In the present study, we postulated that early cardiovascular changes in these individuals may be associated with an activated RAS (renin-angiotensin system). We studied 26 subjects: 13 with INSR [waist circumference, 99+/-6 cm; HOMA (homoeostasis model assessment) score, 2.5+/-0.3] and 13 NCs (normals controls; waist circumference, 77+/-2 cm; HOMA score, 1.4+/-0.2). All received intravenous GTN (glyceryl trinitrate; 10, 20 and 40 microg/min), L-NMMA (N(G)-monomethyl-L-arginine; 3 mg/kg of body weight), AngII (angiotensin II; 8 and 16 ng/min), the selective AT(2)R (AngII type 2 receptor) inhibitor PD123319 (10 and 20 microg/min) and AngII (16 ng/min)+PD123319 (20 microg/min). At the end of each infusion, arterial stiffness indices [SI (stiffness index) and RI (reflection index)] and haemodynamic parameters were measured. There was a significantly higher RI response to AngII (P=0.0004 for both 8 and 16 ng/min doses) and to PD123319 (P=0.004 and P=0.03 for 10 and 20 microg/min doses respectively) in subjects with INSR compared with NCs. Co-infusion of AngII and PD123319 did not lead to additive changes in RI. RI responses to L-NMMA and GTN were not significantly different in both groups. No significant differences in SI and haemodynamic responses were detected. In conclusion, AT(1)R (AngII type 1 receptor) and AT(2)R activity produce arterial stiffness changes in subjects with INSR. Evidence of increased AT(1)R- and AT(2)R-mediated responses in small-to-medium-sized arteries in INSR was found, and may play an early role in the pathogenesis of vascular changes in INSR before haemodynamic changes become apparent.