Exploration of sedimentary deposits in the Atacama Desert, Chile, using integrated geophysical techniques

The Atacama Desert is a unique landscape to understand the evolution of the Earth in extremely arid environments. Clay pans are crucial to comprehend the surface and subsurface processes in areas limited by water availability. We present an integrated geoscientific study to investigate the sedimentary deposits of the Paranal clay pan located in the hyperarid core of the Atacama Desert. We used the loop source transient electromagnetic (TEM) method complemented by magnetics and active seismics to resolve different subsurface properties at different spatial scales. A total of 116 soundings were processed, analyzed, and inverted to investigate the resistivity distribution of the clay pan. The TEM-1D inversion results reveal a three-layered resistivity structure with reliable information down to a depth of 250 m. Colluvial and lacustrine sediments reach a maximum thickness of about 160 +/- 10 m. The shape of the lacustrine sediments suggests the presence of an old paleochannel that might be part of the former main Paranal drainage network. In addition, the basement below the clay pan can be partly interpreted as a damaged zone of an inferred strike-slip fault system. Subsequent 2D magnetic modeling confirms the basement depth derived from the TEM results. The seismic transects reveal accurate structural information of the upper 60 m and are consistent with TEM-1D models. High P wave velocities correlate with high electrical conductivity layers and are interpreted as lacustrine sediments. Our work provides key information with respect to the sedimentary thickness above the basement contributing to paleoclimate research in northern Chile

Exercise-induced changes in gene expression do not mediate post exertional malaise in Gulf War illness

Background: Post-exertional malaise (PEM) is considered a characteristic feature of chronic multi-symptom illnesses (CMI) like Gulf War illness (GWI); however, its pathophysiology remains understudied. Previous investigations in other CMI populations (i.e., Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) have reported associations between PEM and expression of genes coding for adrenergic, metabolic, and immune function. Objectives: To investigate whether PEM is meditated by gene expression in Veterans with GWI. Methods: Veterans with GWI (n = 37) and healthy control Gulf War Veterans (n = 25) provided blood samples before and after 30-min of cycling at 70% of age-predicted heart rate reserve. Relative quantification of gene expression, symptom measurements, and select cardiopulmonary parameters were compared between groups at pre-, 30 minpost-, and 24 hpost-exercise using a doubly multivariate repeated measures analysis of variance (RM-MANOVA). Mediation analyses were used to test indirect effects of changes in gene expression on symptom responses (i.e., PEM) to the standardized exercise challenge. Results: Veterans with GWI experienced large symptom exacerbations following exercise compared to controls (Cohen's d: 1.65; p < 0.05). Expression of β-actin (ACTB), catechol-O-methyltransferase (COMT), and toll-like receptor 4 (TLR4) decreased in Veterans with GWI at 30 min (p < 0.05) and 24 h post-exercise (p < 0.05). Changes in gene expression did not mediate post-exercise symptom exacerbation in GWI (Indirect Effect Slope Coefficient: 0.06 – 0.02; 95% CI: 0.19, 0.12). Conclusion: An acute bout of moderate intensity cycling reduced the expression of select structural, adrenergic, and immune genes in Veterans with GWI, but the pathophysiological relevance to PEM is unclear

Structural basis for binding of hypoxia-inducible factor to the oxygen-sensing prolyl hydroxylases.

The oxygen-dependent hydroxylation of proline residues in the alpha subunit of hypoxia-inducible transcription factor (HIFalpha) is central to the hypoxic response in animals. Prolyl hydroxylation of HIFalpha increases its binding to the von Hippel-Lindau protein (pVHL), so signaling for degradation via the ubiquitin-proteasome system. The HIF prolyl hydroxylases (PHDs, prolyl hydroxylase domain enzymes) are related to the collagen prolyl hydroxylases, but form unusually stable complexes with their Fe(II) cofactor and 2-oxoglutarate cosubstrate. We report crystal structures of the catalytic domain of PHD2, the most important of the human PHDs, in complex with the C-terminal oxygen-dependent degradation domain of HIF-1alpha. Together with biochemical analyses, the results reveal that PHD catalysis involves a mobile region that isolates the hydroxylation site and stabilizes the PHD2.Fe(II).2OG complex. The results will be of use in the design of PHD inhibitors aimed at treating anemia and ischemic disease