BackgroundProtein kinase RNA (PKR-regulated) is a double-stranded RNA activated protein kinase whose expression is induced by interferon. The role of PKR in cell growth regulation is controversial, with some studies supporting a tumour suppressor function and others suggesting a growth-promoting role. However, it is possible that the function of PKR varies with the type of cancer in question.MethodsWe report here a detailed study to evaluate the function of PKR in hepatitis C virus genotype 4 (HCV-4) infected patients. PKR gene was quantitated in HCV related malignant and non-malignant liver tissue by RT-PCR technique and the association of HCV core and PKR was assessed.ResultsIf PKR functions as a tumour suppressor in this system, its expression would be higher in chronic hepatitis tissues. On the contrary our study demonstrated the specific association of HCV-4 with PKR expressed in hepatocellular carcinoma (HCC) tissues, leading to an increased gene expression of the kinase in comparison to chronic hepatitis tissues. This calls into question its role as a tumour suppressor and suggests a positive regulatory role of PKR in growth control of liver cancer cells. One limitation of most of other studies is that they measure the levels rather than the quantitation of PKR gene.ConclusionThe findings suggest that PKR exerts a positive role in cell growth control of HCV-4 related HCC, obtaining a cut-off value for PKR expression in liver tissue provides the first evidence for existence of a viral activator of PKR.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1267826959682402.

Petroleum oil pollution is a worldwide problem that results from the continuous exploration, production, and consumption of oil and its products. Petroleum hydrocarbons are produced as a result of natural or anthropogenic practices, and their common source is anthropogenic activities, which impose adverse effects on the ecosystem’s nonliving and living components including humans. Phytoremediation of petroleum hydrocarbon-polluted soils is an evolving, low-cost, and effective alternative technology to most traditional remediation methods. The objective of this study is to evaluate the phytoremediation potentiality of Vinca rosea for crude oil-contaminated soil by understanding its properties and involvement in the enhanced degradation of crude oil. The remediation potentiality was determined by evaluating the total petroleum hydrocarbon degradation percentage (TPH%) and changes in the molecular type composition of saturated and aromatic hydrocarbon fractions. TPH% was estimated gravimetrically, and changes in the molecular type composition of saturated and aromatic fractions were measured using gas chromatography and high-performance liquid chromatography, respectively. Sulfur concentration was measured using X-ray fluorescence. Cadmium and lead quantification was measured using Inductively Coupled Plasma-Atomic Emission Spectrometry (ICP-AES). The results revealed that V. rosea enhanced total petroleum hydrocarbon (TPH) degradation and altered the molecular composition of the crude oil. The saturated hydrocarbons increased and the aromatic hydrocarbons decreased. The saturated hydrocarbon fraction in the crude oil showed a wider spectrum of n-paraffin peaks than the oil extracted from unplanted and V. rosea-planted soils. Polyaromatic hydrocarbon degradation was enhanced in the presence of V. rosea, which was reflected in the increase of monoaromatic and diaromatic constituents. This was parallel to the increased sulfur levels in planted soil. The determination of sulfur and heavy metal content in plant organs indicated that V. rosea can extract and accumulate high amounts from polluted soils. The ability of V. rosea to degrade TPH and alter the composition of crude petroleum oil by decreasing the toxicity of polyaromatic hydrocarbons in soil, as well as its capability to absorb and accumulate sulfur and heavy metals, supports the use of plant species for the phytoremediation of crude oil-polluted sites.

Abstracts: The current study demonstrates amygdalin’s (vitamin B17) postulated mechanism of action on cancer cells where it kills cells by selective toxicity, promotes apoptosis via cell cycle arrest, induces apoptosis via intrinsic cell death pathway (the mitochondria-initiated pathway), and enhances immunity. Thus, amygdalin can be considered a valuable natural cancer therapeutic agent. The toxicity of Amygdalin was reviewed. Moreover, solutions to avoid the cyanide poisoning have been proposed.

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