Key factors influencing Hg levels and trends in unperturbed oligotrophic temperate and boreal lakes.

Mercury (Hg) is a toxic metal that presents a major risk to ecosystems, biota, human health, and remains a priority concern. In temperate and boreal lakes Hg and methylmercury (MMHg) are expected to vary as a function of atmospheric Hg deposition, lake water chemistry, catchment characteristics and climate variables. The aim of this study was to quantify Hg and MMHg in unperturbed oligotrophic lakes and to identify the factors controlling their distribution. We first hypothesized that lake Hg (and MMHg to lesser extent) spatial variations are linked to atmospheric deposition, catchment characteristics, and terrestrial exportation of dissolved organic carbon (DOC). We secondly examined if lake Hg concentrations have followed the decrease in atmospheric Hg emission observed between the mid-1990s to the end-2010s. We found that overall, atmospheric Hg has little impact on lake Hg and MMHg concentrations, which are both primarily influenced by DOC input originating from the forest catchment. The relationship between DOC and Hg differed between the spring and the fall, with a Hg-to-DOC ratio twice as high in spring. This seems related to snowmelt input of Hg (with a relatively reduced input of DOC) or the internal lake build-up of Hg during the ice-covered period. Of the 10 lakes intensively visited over a 20-year period, only 3 showed significant lake Hg decreases despite significant negative trends in atmospheric Hg concentrations, suggesting a lag between atmospheric and surface water temporal trends. Overall, terrestrial catchments retain around 80% of atmospheric Hg implying that large Hg pools have been built up in soils in the last decades. As such, the reduction of atmospheric Hg alone will not necessarily result in Hg decreases in lakes, since the Hg concentrations may be modulated by DOC export trends and catchment characteristics. This stresses the need to improve our understanding of the processes governing Hg transfers from catchments into lakes.

Comparison of social cognitive functioning in schizophrenia and high functioning autism: more convergence than divergence.

BACKGROUND: Individuals with schizophrenia and individuals with high-functioning autism (HFA) seem to share some social, behavioral and biological features. Although marked impairments in social cognition have been documented in both groups, little empirical work has compared the social cognitive functioning of these two clinical groups. METHOD: Forty-four individuals with schizophrenia, 36 with HFA and 41 non-clinical controls completed a battery of social cognitive measures that have been linked previously to specific brain regions. RESULTS: The results indicate that the individuals with schizophrenia and HFA were both impaired on a variety of social cognitive tasks relative to the non-clinical controls, but did not differ from one another. When individuals with schizophrenia were divided into negative symptom and paranoid subgroups, exploratory analyses revealed that individuals with HFA may be more similar, in terms of the pattern of social cognition impairments, to the negative symptom group than to the paranoia group. CONCLUSIONS: Our findings provide further support for similarities in social cognition deficits between HFA and schizophrenia, which have a variety of implications for future work on gene-brain-behavior relationships.

Some of the effects of the selective sigma ligand (+)pentazocine are mediated via a naloxone-sensitive receptor.

Recently, in an attempt to isolate the nonopioid sigma receptor, Su and colleagues purified a protein from rat liver and brain which appeared to resemble the original sigma opioid receptor as proposed by Martin in 1976, and for which the nonopiate sigma-1 ligand (+)pentazocine presents a high affinity. Previous in vivo electrophysiological studies from our laboratory have demonstrated that several selective sigma-1 ligands potentiate the neuronal response to NMDA. The goal of the present series of experiments was to assess the effects of some selective sigma-1 ligands on the potentiation of the NMDA response and to determine if this potentiation was mediated by the naloxone-sensitive sigma receptor. Extracellular unitary recordings from pyramidal neurons of the CA3 region of the rat dorsal hippocampus were obtained. The sigma-1 ligands BD 737, L 687-384, and JO-1784 (igmesine), administered intravenously at low doses, potentiated the NMDA response but the opiate antagonist naloxone failed to reverse this potentiation. However, the potentiation of the NMDA response induced by the sigma-1 ligand (+)pentazocine was suppressed by naloxone but not by the mu antagonist cyprodime hydrobomide, the kappa antagonist DIPPA nor by the delta antagonist naltrindole. (+/-) Cyclazocine, which presents a high affinity for the above-mentioned sigma-opiate receptor acted as an antagonist by suppressing the potentiation of the NMDA response induced by both JO-1784 and (+)pentazocine. These results suggest that the effects induced by some sigma-1 ligands may, in fact, be sensitive to naloxone while others may not. The original classification of sigma receptors as opiates might have been partly accurate.

Modeling of frequency doubling and tripling with measured crystal spatial refractive-index nonuniformities.

Efficient frequency doubling and tripling are critical to the successful operation of inertial confinement fusion laser systems such as the National Ignition Facility currently being constructed at the Lawrence Livermore National Laboratory and the Omega laser at the Laboratory for Laser Energetics. High-frequency conversion efficiency is strongly dependent on attainment of the phase-matching condition. In an ideal converter crystal, one can obtain the phase-matching condition throughout by angle tuning or temperature tuning of the crystal as a whole. In real crystals, imperfections in the crystal structure prohibit the attainment of phase matching at all locations in the crystal. We have modeled frequency doubling and tripling with a quantitative measure of this departure from phase matching in real crystals. This measure is obtained from interferometry of KDP and KD*P crystals at two orthogonal light polarizations.

Modulation of the neuronal response to N-methyl-D-aspartate by selective sigma2 ligands.

It has now been accepted for several years that sigma (sigma) receptors exist in, at least, two distinct entities denoted sigma1 and sigma2. Previous electrophysiological studies from our laboratory have demonstrated that several selective sigma1 ligands potentiate the neuronal response to NMDA. The nonselective sigma1/sigma2 ligand DTG also potentiates the NMDA response. However, when DTG is administered at doses between 3 and 40 microg/kg, the increase of NMDA-induced activation turns to an epileptoid activity. Until recently, the physiological role of sigma2 receptors had been less studied due to the lack of selective sigma2 ligands. The goal of the present electrophysiological studies was to assess the effect of the intravenous administration of new selective sigma2 ligands on the neuronal response to NMDA in the CA3 region of the rat dorsal hippocampus. Lu 28-179 and BD 1008 potentiated dose-dependently the NMDA response and generated bell-shaped dose-response curves. These ligands failed to generate any epileptoid activity on their own but the subsequent administration of a low dose of a sigma1 agonist (JO-1784) induced an epileptoid activity. Interestingly, the potentiations of the NMDA response induced by Lu 28-179 or BD 1008 were not reversed by haloperidol, by the neurosteroid progesterone, nor by the selective sigma1 antagonist NE-100. Ibogaine, a high affinity sigma2 ligand, slightly increases the NMDA response, which was reversed by progesterone. These data suggest that, similarly to sigma1 ligands, sigma2 agonists potentiate the NMDA response and that the coactivation of sigma1 and sigma2 receptors could be necessary to induce an epileptoid activity. They also suggest that haloperidol may not act as a sigma2 antagonist and that several subtypes of sigma2 receptors could exist.

Recombination walking: genetic selection of clones from pooled libraries of yeast artificial chromosomes by homologous recombination.

Recombination walking is based on the genetic selection of specific human clones from a yeast artificial chromosome (YAC) library by homologous recombination. The desired clone is selected from a pooled (unordered) YAC library, eliminating labor-intensive steps typically used in organizing and maintaining ordered YAC libraries. Recombination walking represents an efficient approach to library screening and is well suited for chromosome-walking approaches to the isolation of genes associated with common diseases.

A multisubunit ribozyme that is a catalyst of and template for complementary strand RNA synthesis.

Derivatives of the sunY self-splicing intron efficiently catalyzed the synthesis of complementary strand RNA by template-directed assembly of oligonucleotides. These ribozymes were separated into three short RNA fragments that formed active catalytic complexes. One of the multisubunit sunY derivatives catalyzed the synthesis of a strand of RNA complementary to one of its own subunits. These results suggest that prebiotically synthesized oligonucleotides might have been able to assemble into a complex capable of self-replication.

Phylogenetic and genetic evidence for base-triples in the catalytic domain of group I introns.

Understanding the mechanisms by which ribozymes catalyse chemical reactions requires a detailed knowledge of their structure. The secondary structure of the group I introns has been confirmed by comparison of over 70 published sequences, by chemical protection studies, and by genetic experiments involving compensatory mutations. Phylogenetic data can also be used to identify tertiary interactions in RNA molecules. This was first done by Levitt, who predicted tertiary interactions in transfer RNA, which were subsequently confirmed by X-ray crystallography. More recently, sequence comparison data have been used to predict tertiary interactions in ribosomal RNA. We have searched a complete alignment of the core regions of group I introns for evolutionary covariations that could not be ascribed to classical Watson-Crick or wobble base pairings. Here we describe two examples of phylogenetic covariation that are most simply explained by postulating hydrogen-bonded base-triples similar to those found in tRNA. Genetic experiments with the Tetrahymena and sunY introns confirm the importance of these interactions for the structure of the ribozyme.

Mutational analysis of conserved nucleotides in a self-splicing group I intron.

We have constructed all single base substitutions in almost all of the highly conserved residues of the Tetrahymena self-splicing intron. Mutation of highly conserved residues almost invariably leads to loss of enzymatic activity. In many cases, activity could be regained by making additional mutations that restored predicted base-pairings; these second site suppressors in general confirm the secondary structure derived from phylogenetic data. At several positions, our suppression data can be most readily explained by assuming non-Watson-Crick base-pairings. In addition to the requirements imposed by the secondary structure, the sequence of the intron is constrained by "negative interactions", the exclusion of particular nucleotide sequences that would form undesirable secondary structures. A comparison of genetic and phylogenetic data suggests sites that may be involved in tertiary structural interactions.

Preservation of short-term energy balance in clinically stable patients with AIDS.

Malnutrition in patients with acquired immune deficiency syndrome (AIDS) is common and multifactorial. The possible causes of malnutrition were evaluated by performing studies of energy balance in five clinically stable outpatients with AIDS, six seronegative homosexual control subjects, and five seronegative heterosexual control subjects. The AIDS group was significantly depleted of body cell mass compared with the control subjects but the values did not change significantly over 6 wk. Food intake was normal in the AIDS group whereas intestinal absorptions of the pentose sugar xylose and of the triglyceride triolein were both significantly diminished. The AIDS patients were hypometabolic as compared with the control subjects and with predictions of metabolic rate based on the Harris-Benedict equation. We conclude that short-term energy balance can be maintained in clinically stable patients with AIDS. Hypometabolism is an appropriate metabolic response to the combination of body-cell-mass depletion and nutrient malabsorption.