Hepatic injury induced by radio frequency waves emitted from conventional Wi-Fi devices in Wistar rats.

In this study, the impact of standard 2.45 GHz radio frequency source (averaged whole-body specific absorption rate 0.01 W kg-1 24 h-1 daily for 40 consecutive days) on the liver of Wistar female rats was investigated. The rats were randomly divided into control and Wi-Fi-exposed groups. At the end of the exposure, liver samples were dissected from rats. Rats' livers were inspected through the evaluation of some oxidative stress parameters and the evaluation of glutamic oxaloacetic transaminase and glutamic-pyruvic transaminase levels as well as through the molecular investigation using Fourier transform infrared spectroscopy. Histopathological examination in addition to ultrastructure examination was also performed. The present data revealed that Wi-Fi exposure leads to severe oxidative stress in the rat liver. Furthermore, Wi-Fi exposure resulted in deleterious effects in the liver function and alters its molecular structure. Moreover, severe histological and ultrastructural alterations are reported in the hepatic tissues points to hepatotoxic effects induced by Wi-Fi exposure. In conclusion, care must be taken when using Wi-Fi emitting devices due to their severe impact on the liver. Public awareness of the need to decrease exposure time and increase the distance from Wi-Fi exposure sources must be raised wherever possible.

Interaction of genetic and environmental factors in Saccharomyces cerevisiae meiosis: the devil is in the details.

One of the most important principles of scientific endeavour is that the results be reproducible from lab to lab. Although research groups rarely redo the published experiments of their colleagues, research plans almost always rely on the work of someone else. The assumption is that if the same experiment were repeated in another lab, results would be so similar that the same interpretation would be favoured. This notion allows one researcher to compare his/her own results to earlier work from other labs. An essential prerequisite for this is that the experiments are done in identical conditions and therefore the methodology must be clearly stated. While this may be scientific common sense, adherence is difficult because "standard" methods vary from one laboratory to another in subtle ways that are often not reported. More importantly, for many years the field ofyeast meiotic recombination considered typical differences to be innocuous. This chapter will highlight the documented environmental and genetic variables that are known to influence meiotic recombination in Saccharomyces cerevisiae. Other potential methodological sources of variation in meiotic experiments are also discussed. A careful assessment of the effects of these variables, has led to insights into our understanding of the control of recombination and meiosis.

Matrix metalloproteinases and their tissue inhibitors direct cell fate during cancer development.

Matrix metalloproteinases (MMPs) were initially recognised for their extracellular matrix (ECM)-degrading capability during tissue remodelling. Their importance was further highlighted by their role in metastasis. Clinical trials have since evaluated the potential of MMP inhibitors as anticancer therapeutics, but without success. These initial studies point to the complex, multifunctional capacity of MMPs in cancer as shown by their function, not only as strident mediators of advanced malignancies, but also as effectors of early stage tumorigenesis. Research now shows that MMPs, and their tissue inhibitors, affect tumour initiation and growth through loss of cell adhesion, evasion of apoptosis, and deregulation of cell division. The extracellular nature of the metalloproteinase axis situates it as a master regulator of cell fate.

Metalloproteinases, inflammation, and rheumatoid arthritis.

Ideally, the inflammatory response occurs rapidly to terminate infection. It also must halt in a timely manner to stop this reaction from inflicting self damage. Such a highly regulated process results from altering balances in pro- and anti-inflammatory signals orchestrated by multiple cell types and factors within the tissue microenvironment. The discovery of new substrates of metalloproteinases within this microenvironment has disclosed a new function in inflammation. The role of these proteases now extends beyond extracellular matrix remodelling enzymes to that of mediators of inflammatory signals involving various chemokines and cytokines. As natural inhibitors of these metalloproteinases, TIMPs have the potential of regulating the inflammatory response and affecting diseases such as rheumatoid arthritis. TIMP-3, in particular, stands out as an important regulator of inflammation with its ability to specifically inhibit proinflammatory cytokines and tissue destruction in the joint.