Heavy metal accumulation in small terrestrial rodents infected by cestodes or nematodes

The aim of the present study was to assess whether there is a difference in accumulation of heavy metal ions (Cd, Cr, Cu, Mn, Ni, Pb and Zn) in hosts (small mammals) infected by cestode parasites when compared to those without cestode infection. The abundance of gastrointestinal parasites and bioaccumulation of heavy metals in host livers and kidneys were measured. Contents of heavy metals in hosts were determined by ICP OES method. The hosts with cestode infection (Paranoplocephala sp.) had lower contents of heavy metals in their livers and kidneys compared to hosts with nematode infection (Mastophorus muris). The content of Pb, Cd, Cr, Cu and Ni was higher in kidneys than in livers, in both (cestode and nematode infected) rodents while the content of Mn was higher in livers. Content of Zn was similar. The content of heavy metals in host was decreasing with the increasing abundance of cestodes (Paranoplocephala sp.). Species-response models to particular heavy metals are presented

Heavy metal accumulation in small terrestrial rodents infected by cestodes or nematodes

The aim of the present study was to assess whether there is a difference in accumulation of heavy metal ions (Cd, Cr, Cu, Mn, Ni, Pb and Zn) in hosts (small mammals) infected by cestode parasites when compared to those without cestode infection. The abundance of gastrointestinal parasites and bioaccumulation of heavy metals in host livers and kidneys were measured. Contents of heavy metals in hosts were determined by ICP OES method. The hosts with cestode infection (Paranoplocephala sp.) had lower contents of heavy metals in their livers and kidneys compared to hosts with nematode infection (Mastophorus muris). The content of Pb, Cd, Cr, Cu and Ni was higher in kidneys than in livers, in both (cestode and nematode infected) rodents while the content of Mn was higher in livers. Content of Zn was similar. The content of heavy metals in host was decreasing with the increasing abundance of cestodes (Paranoplocephala sp.). Species-response models to particular heavy metals are presented

Heavy metal accumulation in small terrestrial rodents infected by cestodes or nematodes

The aim of the present study was to assess whether there is a difference in accumulation of heavy metal ions (Cd, Cr, Cu, Mn, Ni, Pb and Zn) in hosts (small mammals) infected by cestode parasites when compared to those without cestode infection. The abundance of gastrointestinal parasites and bioaccumulation of heavy metals in host livers and kidneys were measured. Contents of heavy metals in hosts were determined by ICP OES method. The hosts with cestode infection (Paranoplocephala sp.) had lower contents of heavy metals in their livers and kidneys compared to hosts with nematode infection (Mastophorus muris). The content of Pb, Cd, Cr, Cu and Ni was higher in kidneys than in livers, in both (cestode and nematode infected) rodents while the content of Mn was higher in livers. Content of Zn was similar. The content of heavy metals in host was decreasing with the increasing abundance of cestodes (Paranoplocephala sp.). Species-response models to particular heavy metals are presented

A case for strain-induced fluid flow as regulators of BMU-coupling and osteonal alignment

Throughout life, human bone is renewed continuously in a tightly controlled sequence of resorption and formation. This process of bone remodeling is remarkable because it involves cells from different lineages, collaborating in so-called basic multicellular units (BMUs) within small spatial and temporal boundaries. Moreover, the newly formed (secondary) osteons are aligned to the dominant load direction and have a density related to its magnitude, thus creating a globally optimized mechanical structure. Although the existence of BMUs is amply described, the cellular mechanisms driving bone remodeling—particularly the alignment process—are poorly understood. In this study we present a theory that explains bone remodelling as a self-organizing process of mechanical adaptation. Osteocytes thereby act as sensors of strain-induced fluid flow. Physiological loading produces stasis of extracellular fluid in front of the cutting cone of a tunneling osteon, which will lead to osteocytic disuse and (continued) attraction of osteoclasts. However, around the resting zone and the closing cone, enhanced extracellular fluid flow occurs, which will activate osteocytes to recruit osteoblasts. Thus, cellular activity at a bone remodeling site is well related to local fluid flow patterns, which may explain the coordinated progression of a BMU

Mechanotransduction by bone cells in vitro: mechanobiology of bone tissue

Mechanical force plays an important role in the regulation of bone remodelling in intact bone and bone repair. In vitro, bone cells demonstrate a high responsiveness to mechanical stimuli. Much debate exists regarding the critical components in the load profile and whether different components, such as fluid shear, tension or compression, can influence cells in differing ways. During dynamic loading of intact bone, fluid is pressed through the osteocyte canaliculi, and it has been demonstrated that fluid shear stress stimulates osteocytes to produce signalling molecules. It is less clear how mechanical loads act on mature osteoblasts present on the surface of cancellous or trabecular bone. Although tissue strain and fluid shear stress both cause cell deformation, these stimuli could excite different signalling pathways. This is confirmed by our experimental findings, in human bone cells, that strain applied through the substrate and fluid flow stimulate the release of signalling molecules to varying extents. Nitric oxide and prostaglandin E2 values increased by between two- and nine-fold after treatment with pulsating fluid flow (0.6±0.3 Pa). Cyclic strain (1000 μstrain) stimulated the release of nitric oxide two-fold, but had no effect on prostaglandin E2. Furthermore, substrate strains enhanced the bone matrix protein collagen I two-fold, whereas fluid shear caused a 50% reduction in collagen I. The relevance of these variations is discussed in relation to bone growth and remodelling. In applications such as tissue engineering, both stimuli offer possibilities for enhancing bone cell growth in vitro