Microwave radiometry and its potential applications in biology and medicine: experimental studies.

This paper presents experimental data on : (1) the natural emission of microwave radiation by biological systems, and (2) the effect of drugs as well as microwave radiation on specimen microwave emission. Experiments were conducted on guinea pigs, mice, rabbits, and human subjects. The results were obtained with two different radiometers, one of the correlation type and one of the Dicke type, operating in the X-band at about 9 GHz with a sensitivity of approximately 0.1 degrees K. The results demonstrate the feasibility of this technique and suggestions are made for its use in bilogy, medicine, and in the field of biocommunications.     

Scale dependency of metapopulation models used to predict climate change impacts on small mammals

To investigate potential range shifts in a changing climate it is becoming increasingly common to develop models that account for demographic processes. Metapopulation models incorporate the spatial configuration of occupied habitat (i.e. arrangement, size and quality), population demographics, and inter‐patch dispersal making them suitable for investigating potential threats to small mammal range and abundance. However, the spatial scale (resolution) used to represent species–environment dynamics may affect estimates of range shift and population resilience by failing to realistically represent the spatial configuration of suitable habitat, including stepping stones and refugia. We aimed to determine whether relatively fine‐scale environmental information influenced predictions of metapopulation persistence and range shift. Species distribution models were constructed for four small terrestrial mammals from southern Australia using environmental predictors measured at 0.1 × 0.1 km (0.01 km²) or 1.0 × 1.0 km (1 km²) resolution, and combined with demographic information to parameterise coupled niche‐population models. These models were used to simulate population dynamics projected over 40‐yr under a stable and changing climate. Initial estimates of the area of available habitat were similar at both spatial scales. However, at the fine‐scale, habitat configuration comprised a greater number of patches (ca 12 times), that were more irregular in shape (ca 8 times the perimeter:area), and separated by a tenth of the distance than at the coarse‐scale. While small patches were not more prone to extinction, populations generally declined at a higher rate and were associated with a lower expected minimum abundance. Despite increased species vulnerability at the fine‐scale, greater range shifts were measured at the coarse‐scale (for species illustrating a shift at both scales). These results highlight the potential for range shifts and species vulnerability information to be misrepresented if advanced modelling techniques incorporating species demographics and dispersal inadequately represent the scale at which these processes occur.     

EGFR Inhibitor Erlotinib Delays Disease Progression but Does Not Extend Survival in the SOD1 Mouse Model of ALS

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that causes progressive paralysis due to motor neuron death. Several lines of published evidence suggested that inhibition of epidermal growth factor receptor (EGFR) signaling might protect neurons from degeneration. To test this hypothesis in vivo, we treated the SOD1 transgenic mouse model of ALS with erlotinib, an EGFR inhibitor clinically approved for oncology indications. Although erlotinib failed to extend ALS mouse survival it did provide a modest but significant delay in the onset of multiple behavioral measures of disease progression. However, given the lack of protection of motor neuron synapses and the lack of survival extension, the small benefits observed after erlotinib treatment appear purely symptomatic, with no modification of disease course.     

Genetic Associations of Angiotensin-Converting Enzyme with Primary Intracerebral Hemorrhage: A Meta-analysis

Background

A number of studies have reported an association of angiotensin-converting enzyme (ACE) gene polymorphism with primary intracerebral hemorrhage (PICH), however the reports have demonstrated inconclusive results. To clarify this conflict, we updated the previously performed meta-analysis by Peck et al., which revealed negative results, by investigating the ACE polymorphism and its correlation to PICH.

Methods

PubMed and Embase databases (through Dec 2012) were searched for English articles on the relationship of the I/D polymorphism in ACE with PICH in humans. Summary odds ratios (ORs) were estimated and potential sources of heterogeneity and bias were explored.

Results

A total of 805 PICH cases and 1641 control cases obtained from 8 case-control studies were included. The results suggest that in dominant genetic models, the ACE I/D polymorphic variant was associated with a 58% increase in susceptibility risk of PICH (OR = 1.58; 95% CI = 1.07–2.35 for DD vs. DI+II). However, in the subgroup analysis based on race, a significant increased risk was found in Asian DD homozygote carriers (OR = 1.76 and 95% CI = 1.16–2.66 for DD vs. DI+II), but not in Caucasian DD homozygote carriers (OR = 1.18, 95% CI = 0.36–3.88, P = 0.784 for DD vs. DI+II). The heterogeneity between studies was remarkable, and its major sources of heterogeneity were due to the year in which the study was published. No potential publication bias was observed in dominant genetic models.

Conclusions

These data demonstrated evidence of a positive association between ACE I/D polymorphism with PICH, and suggested that the ACE gene is a PICH susceptible gene in Asian populations.     

Dietary Supplementation of Polyunsaturated Fatty Acids in Caenorhabditis elegans

Fatty acids are essential for numerous cellular functions. They serve as efficient energy storage molecules, make up the hydrophobic core of membranes, and participate in various signaling pathways. Caenorhabditis elegans synthesizes all of the enzymes necessary to produce a range of omega-6 and omega-3 fatty acids. This, combined with the simple anatomy and range of available genetic tools, make it an attractive model to study fatty acid function. In order to investigate the genetic pathways that mediate the physiological effects of dietary fatty acids, we have developed a method to supplement the C. elegans diet with unsaturated fatty acids. Supplementation is an effective means to alter the fatty acid composition of worms and can also be used to rescue defects in fatty acid-deficient mutants. Our method uses nematode growth medium agar (NGM) supplemented with fatty acidsodium salts. The fatty acids in the supplemented plates become incorporated into the membranes of the bacterial food source, which is then taken up by the C. elegans that feed on the supplemented bacteria. We also describe a gas chromatography protocol to monitor the changes in fatty acid composition that occur in supplemented worms. This is an efficient way to supplement the diets of both large and small populations of C. elegans, allowing for a range of applications for this method.