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Trauma and chronic stress are believed to induce and exacerbate psychopathology by disrupting glutamate synaptic strength. However, in vivo in human methods to estimate synaptic strength are limited. In this study, we established a novel putative biomarker of glutamatergic synaptic strength, termed energy-per-cycle (EPC). Then, we used EPC to investigate the role of prefrontal neurotransmission in trauma psychopathology. Healthy control (n=18) and patients with posttraumatic stress (PTSD; n=16) completed 13C-acetate magnetic resonance spectroscopy scans to estimate prefrontal EPC, which is the ratio of neuronal energetic needs per glutamate neurotransmission cycle (VTCA/VCycle). Patients with PTSD were found to have 28% reduction in prefrontal EPC (t=3.0; df=32, p=0.005). There was no effect of sex on EPC, but age was negatively associated with prefrontal EPC across groups (r=–0.46, n=34, p=0.006). Controlling for age did not affect the study results. The feasibility and utility of EPC were established. Patients with PTSD were found to have reduced prefrontal glutamatergic synaptic strength. These findings suggest that reduced glutamatergic synaptic strength may contribute to the pathophysiology of PTSD and could be targeted by new treatments.HighlightsGlutamatergic synaptic strength is critical for brain function in health and disease.In vivo in human methods to estimate glutamatergic synaptic strength are limited.We here propose a new approach to estimate glutamatergic synaptic strength.The new method employs carbon-13 magnetic resonance spectroscopy (13C MRS).The utility of the new approach was demonstrated in posttraumatic stress disorder (PTSD).

Background: DNA hairpins have been used in molecular analysis of PCR products as self-probing amplicons. Either physical separation or fluorescent oligonucleotides with covalent modifications were previously necessary. Methods: We performed asymmetric PCR for 40–45 cycles in the presence of the saturating DNA dye, LCGreen Plus, with 1 primer including a 5′ tail complementary to its extension product, but without any special covalent modifications. Samples were amplified either on a carousel LightCycler for speed or on a 96/384 block cycler for throughput. In addition to full-length amplicon duplexes, single-stranded hairpins were formed by the primer tail “snapping back” and hybridizing to its extension product. High-resolution melting was performed on a HR-1 (for capillaries) or a LightScanner (for plates). Results: PCR products amplified with a snapback primer showed both hairpin melting at lower temperature and full-length amplicon melting at higher temperature. The hairpin melting temperature was linearly related to the stem length (6–28 bp) and inversely related to the log of the loop size (17–135 bases). We easily genotyped heterozygous and homozygous variants within the stem, and 100 blinded clinical samples previously typed for F5 1691G>A (Leiden) were completely concordant by snapback genotyping. We distinguished 7 genotypes in 2 regions of CFTR exon 10 with symmetric PCR using 2 snapback primers followed by product dilution to favor intramolecular hybridization. Conclusions: Snapback primer genotyping with saturating dyes provides the specificity of a probe with only 2 primers that are free of special covalent labels in a closed-tube system.

The Royal Society expedition to Antarctica established a base at Halley Bay, in support of the International Geophysical Year of 1957?1958. Surface ozone was measured during 1958 only, using a prototype Brewer-Mast sonde. The envelope of maximum ozone was an annual cycle from 10 ppbv in January to 22 ppbv in August. These values are 35% less at the start of the year and 15% less at the end than modern values from Neumayer, also a coastal site. This may reflect a general increase in surface ozone since 1958 and differences in summer at the less windy site of Halley, or it may reflect ozone loss on the inlet together with long-term conditioning. There were short periods in September when ozone values decreased rapidly to near-zero, and some in August when ozone values were rapidly halved. Such ozone-loss episodes, catalysed by bromine compounds, became well-known in the Artic in the 1980s, and were observed more recently in the Antarctic. In 1958, very small ozone values were recorded for a week in midwinter during clear weather with light winds. The absence of similar midwinter reductions at Neumayer, or at Halley in the few measurements during 1987, means we must remain suspicious of these small values, but we can find no obvious reason to discount them. The dark reaction of ozone and seawater ice observed in the laboratory may be fast enough to explain them if the salinity and surface area of the ice is sufficiently amplified by frost flowers.

Hyperglycemia is associated with a decrease in serum sodium concentration. Previous methods of estimating the degree of decrease have not considered the fact that glucose will enter certain cells despite relative insulin deficiency; thus, glucose will not contribute directly to the osmotic gradient responsible for water shifts into or out of these tissues. The expected decrease in serum sodium concentration is 1.35 meg/l for every 100mg/dl increase in blood glucose concentration - the metabolic correction factor. Although the numerical difference between this factor and that calculated by others is small, the metabolic implications could be critical. In the hyperglycemic state the water content of tissues not requiring insulin for glucose transport could increase, and where tissue swelling is physically restricted (for example, in the brain) this expansion could seriously affect organ function.