Can the Q Link Ally,a form of Sympathetic Resonance Technology (SRT), attenuate acute mobile phone-related changes to neural function?

OBJECTIVES: Exposure to active mobile phones (MP) has been shown to affect human neural function as shown by the electroencephalogram (EEG). Although it has not been determined whether such effects are harmful, a number of devices have been developed that attempt to minimize these MP-related effects. One such device, the Q Link Ally (QL; Clarus Products, International, L.L.C., San Rafael, CA), is argued to affect the human organism in such a way as to attenuate the effect of MPs. The present pilot study was designed to determine whether there is any indication that QL does alter MP-related effects on the human EEG. DESIGN: Twenty-four (24) subjects participated in a single-blind, fully counterbalanced crossover design in which subjects' resting EEG and phase-locked neural responses to auditory stimuli were assessed under conditions of either active MP or active MP plus QL. RESULTS: The addition of QL to the MP condition increased resting EEG in the gamma range and did so as a function of exposure duration, and it attenuated MP-related effects in the delta and alpha range (at trend-level). The addition of the QL also affected phase-locked neural responses, with a laterality reversal in the alpha range and an alteration to changes over time in the delta range, a reduction of the MP-related beta decrease over time at fronto-posterior sites, and a global reduction in the gamma range that increased as a function of exposure duration. No unambiguous relations were found between these changes and either performance or psychologic state. CONCLUSIONS: This pilot study suggests that the addition of the QL to active MP-exposure does affect neural function in humans, altering both resting EEG patterns and the evoked neural response to auditory stimuli, and that there is a tendency for some MP-related changes to the EEG to be attenuated by the QL.     

Role of molecular diagnostics in forensic science

Since the first use of DNA to identify the perpetrator of a murder in 1985, forensic science has witnessed dramatic changes in the field of human identification. The technology has altered by adopting novel methods developed originally for use in the field of medical genetics. Currently, millions of samples from blood, semen, hair and tissues are analyzed to determine the origin of the samples. The processes used at present rely on the separation of polymorphic DNA fragments by electrophoresis. Although rapid, this process represents a bottleneck in the automation of the process. Recent advances in chip-based techniques offer a rapid and highly automated solution, provided that the necessary DNA polymorphisms can be examined in this way. This review examines the immediate future of human identification and considers possible routes for future developments.     

Genetic complexity and serum reactivity of HVR1 quasispecies of hepatitis C virus in patients with cirrhosis

OBJECTIVE: The RNA genome of hepatitis C virus varies considerably, especially within the hypervariable region 1 (HVR1), a domain located on the 5' end of the E2/NS1 envelope region. Our previous study has suggested there were greater numbers of quasispecies in the liver than in matched serum, independent of the viral load. However, the significance of this finding has not been examined extensively at genetic and serological levels. METHODS: By large scale cloning and sequencing, we studied the genetic complexity of HVR1 quasispecies in two selected patients with cirrhosis. The serum reactivity of peptides representing different HVR1 quasispecies isolated from these cases was also estimated by standard ELISA format. RESULTS: We found the same major (dominant and/or subdominant) viral quasispecies variants in serum and in the cirrhotic liver. Genetic analysis suggested that the evolutionary pressure on HVR1 was higher than on its flanking region in quasispecies derived from the liver, whereas this trend is attenuated in quasispecies from serum. The immunoreactivity to peptides representing different HVR1 quasispecies variants showed considerable cross-reactivity with heterologous sera, whereas the reactivity was strongest against the dominant HVR1 peptide over time in homologous sera. CONCLUSIONS: These findings indicate that the formation and selection of HVR1 quasispecies may not be driven solely by humoral immune pressure, at least in these two cases.     

Etoposide-mediated deregulation of the G2M checkpoint in myeloid leukaemic cell lines results in loss of cell survival

The K562 leukaemic cell line expresses an inherent survival signal due to the antiapoptotic properties of Bcr-abl, which is, in part, mediated by prolonging the G2M checkpoint and allowing DNA repair mechanisms to operate post genotoxic insult. Arrest of the cell cycle is mediated by retaining an inactivating state of phosphorylation of cyclin-dependent kinase 1 (Cdk1) on tyrosine 15. Our data confirmed that cell survival in K562 was promoted by cell cycle arrest at G2M in response to the genotoxin etoposide. There was no predicted cell cycle arrest in Bcr-abl-positive derivative cell lines of K562 that did not survive the same genotoxic insult but, paradoxically, Cdk1 tyrosine phosphorylation was enhanced to a higher extent compared with the parental cell line where arrest of the cell cycle was observed. To ascertain that this was not an anomaly of the derivative lines, HL60 cells were treated with concentrations of etoposide that induced arrest of the cell cycle or apoptosis. Only HL60 cells that subsequently underwent apoptosis elicited the same effect of increased Cdk1 tyrosine phosphorylation. It is proposed that the augmented tyrosine phosphorylation status of Cdk1 is associated with the abolition of cell survival, in addition to the previously reported induction of cell cycle arrest in myeloid cell lines.     

Targeted disruption of the protein kinase C epsilon gene abolishes the infarct size reduction that follows ischaemic preconditioning of isolated buffer-perfused mouse hearts

OBJECTIVE: Activation of protein kinase C (PKC) isoforms is associated with the cardioprotective effect of early ischaemic preconditioning (IP). PKC consists of at least 10 different isoforms, encoded by separate genes, which mediate distinct physiological functions. Although the PKC-epsilon isoform has been implicated in preconditioning, uncertainty remains. We investigated whether preconditioning still occurs in a mouse line lacking cardiac PKC-epsilon protein due to a targeted disruption within the pkc-epsilon allele. METHODS: The isolated buffer-perfused hearts from knockout mice lacking PKC-epsilon (-/-) and sibling heterozygous mice (+/-), with a normal PKC-epsilon complement, were preconditioned by 4 x 4 min ischaemia/6 min reperfusion. Hearts then underwent 45 min of global ischaemia followed by 1.5 h of reperfusion. RESULTS: In PKC-epsilon (+/-) hearts ischaemic preconditioning reduced infarction volume as a percentage of myocardial volume (24.3+/-4.5 vs. 41.3+/-4.7%, P<0.001). In contrast, in PKC-epsilon (-/-) hearts preconditioning failed to diminish infarction (36.4+/-2.9 vs. 38.8+/-4.5%). Surprisingly however, although preconditioning did not reduce infarct size, it did enhance contractile recovery in PKC-epsilon (-/-) mice (43.1+/-3.9 vs. 24.9+/-5.1%, P<0.05), similar to the level seen in PKC-epsilon (+/-) hearts (35.2+/-3.9 vs. 20.9+/-5.0%, P<0.05). CONCLUSIONS: These data suggest that PKC-epsilon is essential for the reduction in infarction that follows early ischaemic preconditioning, but is not associated with the improvement in functional recovery.