Repetitive negative thinking as a unique transdiagnostic risk factor for suicidal ideation.

Repetitive negative thinking (RNT) is a transdiagnostic symptom observed across mood and anxiety disorders and is characterized by frequent, distressing thoughts that are perceived as uncontrollable. Specific forms of RNT have been linked to increased suicide risk. However, most work examining links between RNT and suicide has been conducted within specific disorders and subtypes of RNT (e.g., rumination in individuals with depression). The present study aimed to investigate associations between transdiagnostic RNT and suicidal ideation. We hypothesized RNT would be associated with suicide risk beyond disorder-specific clinical symptoms. Fifty-four participants with mood, anxiety, and/or traumatic stress disorders completed an interview assessing suicidal risk (Columbia-Suicide Severity Rating Scale (C-SSRS)) and self-report questionnaires assessing transdiagnostic RNT, depression, and anxiety. Based on C-SSRS, we divided participants into high or low suicide risk groups. We analyzed the relationship between suicidal risk group and RNT and found that RNT was uniquely associated with suicidal risk group, controlling for depression and anxiety severity. Our results suggest including assessments of RNT may have clinical utility for understanding the degree of suicide risk in individuals and point to the potential utility of including clinical interventions to target this symptom for those at high risk of suicide.

Observations of ionospheric ELF and VLF wave generation by excitation of the thermal cubic nonlinearity.

Extremely-low-frequency (ELF, 3-3000 Hz) and very-low-frequency (VLF, 3-30 kHz) waves generated by the excitation of the thermal cubic nonlinearity are observed for the first time at the High-Frequency Active Auroral Research Program high-frequency transmitter in Gakona, Alaska. The observed ELF and VLF field amplitudes are the strongest generated by any high frequency (HF, 3-30 MHz) heating facility using this mechanism to date. This manner of ELF and VLF generation is independent of naturally forming currents, such as the auroral electrojet current system. Time-of-arrival analysis applied to experimental observations shows that the thermal cubic ELF and VLF source region is located within the collisional D-region ionosphere. Observations are compared with the predictions of a theoretical HF heating model using perturbation theory. For the experiments performed, two X-mode HF waves were transmitted at frequencies ω1 and ω2, with |ω2-2ω1| being in the ELF and VLF frequency range. In contrast with previous work, we determine that the ELF and VLF source is dominantly produced by the interaction between collision frequency oscillations at frequency ω2-ω1 and the polarization current density associated with the lower frequency HF wave at frequency ω1. This specific interaction has been neglected in past cubic thermal nonlinearity work, and it plays a major role in the generation of ELF and VLF waves.

Mice with gene targetted prion protein alterations show that Prnp, Sinc and Prni are congruent.

Classical genetic analysis has identified Sinc/Prni as the major gene controlling mouse scrapie incubation time. Sinc/Prni is linked to Prnp, the gene encoding the prion protein (PrP). Prnp alleles express distinct PrP protein variants, PrP A and PrP B, which arise from codon 108L/F and 189 T/V dimorphisms. Prnp genotype segregates with incubation time length which suggests, but does not prove, that incubation time is controlled by PrP dimorphisms, and that the Sinc/Prni and Prnp loci are congruent. We have used gene targetting to construct mice in which the endogenous Prnp allele has been modified to express PrP B instead of PrP A. Challenge with a mouse-adapted BSE strain results in dramatically shortened incubation times and demonstrates that PrP dimorphisms at codon 108 and/or 189 control incubation time, and that Sinc/Prni and Prnp are congruent.

Microplastics in beluga whale (Delphinapterus leucas) prey: An exploratory assessment of trophic transfer in the Beaufort Sea.

Microplastics (MPs, <5 mm in length) have been identified as emerging contaminants in marine environments, with ingestion by a variety of biota being of increasing concern. Few studies exist on MP ingestion in Arctic fish, and there are currently no such data from the Beaufort Sea. We investigated MP abundance in five ecologically valuable species from three sampling sites in the Eastern Beaufort Sea to evaluate possible trophic-level pathways of MPs from prey to beluga whales. Polymer analysis confirmed that 21% of fish gastrointestinal tracts (n = 116) contained microplastic particles. Fish that contained MPs had a mean abundance of 1.42 ±â€¯0.44 particles per individual and an overall mean abundance of 0.37 ±â€¯0.16 particles. No plastic particles >5 mm were found, and 78% of the particles observed were fibers. Based on energetic needs, we estimate that individual beluga may ingest between 3800 and 145,000 microplastics annually through trophic transfer, with uncertain health implications.

Microplastics in beluga whales (Delphinapterus leucas) from the Eastern Beaufort Sea.

Microplastics (MPs, particles <5 mm) represent an emerging global environmental concern, having been detected in multiple aquatic species. However, very little is known about the presence of MPs in higher trophic level species, including cetaceans. We worked with community based monitors and Inuvialuit hunters from Tuktoyaktuk (Northwest Territories, Canada) to sample seven beluga whales (Delphinapterus leucas) in 2017 and 2018. Microplastics were detected in the gastrointestinal tracts in every whale. We estimate that each whale contained 18 to 147 MPs in their GI tract (average of 97 ±â€¯42 per individual). FTIR-spectroscopy revealed over eight plastic polymer types, with nearly half being polyester. Fibres made up 49% of MPs. The diversity of MP shapes and polymeric identities in beluga points to a complex source scenario, and ultimately raises questions regarding the significance and long-term exposure of this pollutant in this ecologically and culturally valuable species.

Defining regions and rearrangements of the Silene latifolia Y chromosome.

We combine data from published marker genotyping of three sets of S. latifolia Y chromosome deletion mutants with changed sex phenotypes and add genotypes for several new genic markers to refine the deletion map of the Y chromosome and compare it with the X chromosome genetic map. We conclude that the Y chromosome of this species has been derived through multiple rearrangements of the ancestral gene arrangement and that none of the rearrangements so far detected was involved in stopping X-Y recombination. Different Y genotypes may also differ in their gene content and possibly arrangements, suggesting that mapping the Y-linked sex-determining genes will be difficult, even if many further genic markers are obtained. Even in determining the map of Y chromosome markers to discover all the rearrangements, physical mapping by FISH or other experiments will be essential. Future deletion mapping work should ensure that markers are studied in the parents of deletion mutants and should probably include additional deletions that were not ascertained by causing mutant sex phenotypes.

A common mechanism of chromosomal translocation in T- and B-cell neoplasia.

The chromosomal breakpoint involved in the t(8;14)(q24;q11) chromosome translocation in the SKW-3 cell line, which directly involves the 3' flanking region of the c-myc gene, was cloned and sequenced. The breakpoint on chromosome 8 mapped to a position 3 kb 3' of c-myc while the chromosome 14 breakpoint occurred 36 kb 5' of the gene for the constant region of the alpha chain of the T-cell receptor (TCR). The translocation resulted in a precise rearrangement of sequences on chromosome 8 and what appears to be a functional J alpha segment on chromosome 14. Signal sequences for V-J joining occurred at the breakpoint positions on both chromosomes 14 and 8, suggesting that the translocation occurs during TCR gene rearrangement and that it is catalyzed by the enzymatic systems involved in V-J joining reactions. The involvement of c-myc in the translocation and the association of joining signals at the breakpoints provides a parallel to the situation observed in the translocations involving c-myc and the immunoglobulin loci in B-cell neoplasms and suggests that common mechanisms of translocation and oncogene deregulation are involved in B- and T-cell malignancies.

Towards efficient and broadband four-wave-mixing using short-length dispersion tailored lead silicate holey fibers.

We demonstrate four-wave-mixing based wavelength conversion at 1.55 mum in a 2.2 m-long dispersion-shifted lead-silicate holey fiber. For a pump peak power of ~6 W, a conversion efficiency of -6 dB is achieved over a 3-dB bandwidth of ~30 nm. Numerical simulations are used to predict the performance of the fiber for different experimental conditions and to address the potential of dispersion-tailored lead silicate holey fibers in wavelength conversion applications utilizing four-wave-mixing. It is shown that highly efficient and broadband wavelength conversion, covering the entire C-band, can be achieved for such fibers at reasonable optical pump powers and for fiber lengths as short as ~2 m.

Screening for neurocognitive impairment in HIV-positive adults aged 50 years and older: Montreal Cognitive Assessment relates to self-reported and clinician-rated everyday functioning.

As the HIV+ population ages, the risk for and need to screen for HIV-associated neurocognitive disorders (HAND) increases. The aim of this study is to determine the utility and ecological validity of the Montreal Cognitive Assessment (MoCA) among older HIV+ adults. A total of 100 HIV+ older adults aged 50 years or over completed a comprehensive neuromedical and neurocognitive battery, including the MoCA and several everyday functioning measures. The receiver operating characteristic curve indicates ≤26 as the optimal cut-off balancing sensitivity (84.2%) and specificity (55.8%) compared to "gold standard" impairment as measured on a comprehensive neuropsychological battery. Higher MoCA total scores are significantly (p < .01) associated with better performance in all individual cognitive domains except motor abilities, with the strongest association with executive functions (r = -0.49, p < .01). Higher MoCA total scores are also significantly (p <.01) associated with fewer instrumental activities of daily living declines (r = -0.28), fewer everyday cognitive symptoms (r = -0.25), and better clinician-rated functional status (i.e., Karnofsky scores; r = 0.28); these associations remain when controlling for depressive symptoms. HIV+ individuals who are neurocognitively normal demonstrate medium-to-large effect size differences in their MoCA performance compared to those with asymptomatic neurocognitive impairment (d = 0.85) or syndromic HAND (mild neurocognitive disorder or HIV-associated dementia; d = 0.78), while the latter two categories do not differ. Although limited by less than optimal specificity, the MoCA demonstrates good sensitivity and ecological validity, which lends support to its psychometric integrity as a brief cognitive screening tool among older HIV+ adults.

Ataxia in prion protein (PrP)-deficient mice is associated with upregulation of the novel PrP-like protein doppel.

The novel locus Prnd is 16 kb downstream of the mouse prion protein (PrP) gene Prnp and encodes a 179 residue PrP-like protein designated doppel (Dpl). Prnd generates major transcripts of 1.7 and 2.7 kb as well as some unusual chimeric transcripts generated by intergenic splicing with Prnp. Like PrP, Dpl mRNA is expressed during embryogenesis but, in contrast to PrP, it is expressed minimally in the CNS. Unexpectedly, Dpl is upregulated in the CNS of two PrP-deficient (Prnp(0/0)) lines of mice, both of which develop late-onset ataxia, suggesting that Dpl may provoke neurodegeneration. Dpl is the first PrP-like protein to be described in mammals, and since Dpl seems to cause neurodegeneration similar to PrP, the linked expression of the Prnp and Prnd genes may play a previously unrecognized role in the pathogenesis of prion diseases or other illnesses.

Accumulation and perchlorate exposure potential of lettuce produced in the Lower Colorado River region.

The Colorado River is contaminated with perchlorate concentrations of 1.5-8 microg/L, an anion linked to thyroid dysfunction. Over 90% of the lettuce (Lactuca sativa L.) consumed during the winter months in the United States is produced in the Lower Colorado River region. Studies were conducted in this region to survey the potential for lettuce perchlorate accumulation and estimate potential human exposure to perchlorate from lettuce. Total uptake of perchlorate in the above-ground plant of iceberg lettuce was approximately 5 g/ha. Exposure estimates ranged from 0.45 to 1.8 microg/day depending on lettuce types and trimming. For all lettuce types, hypothetical exposures were less than 4% of the reference dose recommended by the National Academy of Sciences. Results show the relative iodide uptake inhibition potential because of lettuce nitrate was 2 orders of magnitude greater than that associated with the corresponding trace levels of perchlorate. These data support the conclusion that potential perchlorate exposures from lettuce irrigated with Colorado River water are negligible relative to acute or long-term harmful amounts.

Cloning and sequencing of the cDNA encoding the murine mammary gland long-form prolactin receptor.

The nucleotide sequence of a 1992-bp cDNA encoding the long form of the murine mammary prolactin receptor (PRL-R) has been determined. The deduced 68-kDa protein has high sequence identity with long forms of prolactin receptors from rat ovary and rabbit mammary gland.

Primary structure of the speC gene encoding biosynthetic ornithine decarboxylase in Escherichia coli.

A 2.91-kb fragment of the Escherichia coli chromosome containing the speC gene, encoding biosynthetic ornithine decarboxylase (ODC) was sequenced. The speC gene is encoded by a 2133-bp ORF; the deduced amino-acid sequence contains 711 residues whose predicted molecular mass is 79,505 Da.

The synergistic effect of aphidicolin on the yield of X-ray-induced chromosome aberrations throughout the cell cycle in JU56 cells.

The effect of a 2-h post-treatment with aphidicolin at a dose sufficient to inhibit DNA synthesis on the yield of X-ray-induced chromosomal aberrations throughout the cell cycle was measured. Exposure to aphidicolin during and after irradiation brought about an increase in exchanges in cells irradiated in G2, in sister unions only in cells irradiated in S, and in all chromosome aberration types (fragments, sister unions, and dicentrics) in cells irradiated in G1. It is suggested that, during G1 and G2 but not during S inhibiting the repair enzyme alpha-polymerase brings about the conversion of some X-ray-induced DNA lesions to double-strand which can then take part in aberrations.

Time sequence of events leading to chromosomal aberration formation.

Investigations have been carried out which have measured the influence of the repair polymerases on the yield of different types of chromosomal aberrations. The studies were mainly concerned with the effect of inhibiting the polymerases on the yield of aberrations. The polymerases fill in single strand regions, and the fact that their inhibition affects the yield of aberrations suggests that single strand lesions are influential in aberration formation. The results indicate that-- 1. There are two actions of polymerases in clastogenesis. One is in their involvement in a G2 repair system, in which the pair of chromatids is concerned, and which does not yield aberrations unless the inhibition is still operating when the cells enter mitosis. The second also operates in G1 and S, and is such that when repair is inhibited, further damage accrues. 2. The second action is affected by inhibiting polymerase but operates even when the repair enzymes are active. 3. The production of chromosomal exchanges involves a series of reactions, some of which are reversible. 4. The time span over which the reactions occur is much longer than has been envisaged previously (e.g., most of a cell cycle).

Chromosomal aberration types in cells at the second division after irradiation in G1 or G2.

Cultures of JU-56 cells were irradiated in either G1 or G2 and examined either in their first post-irradiation metaphase (in diploids) or in their second post-irradiation metaphase (in colcemid-induced tetraploids). The timing of fixation, together with tritiated thymidine pulse labelling, allowed selection for scoring only metaphases of cells that were in the G1 or G2 phase of the cell cycle during irradiation. With G1 irradiation it was found that many of the aberrations observed at the first division were not present (as derivatives) at the second division, and also that new aberrations were found at the second division, which were not derived from aberrations at the first division. Clonogenic survival was also measured in populations of cells irradiated in G1. It was found that cells containing chromosomal aberrations at the first division were not numerous enough to explain lack of survival. When frequencies of aberrations following G2 irradiation scored at the second division were compared with those scored at the first, there was a significant increase in dicentrics as compared with their progenitor asymmetrical chromatid interchanges, and of mirror-image dicentrics as compared with their progenitor sister unions. A substantial number of sister unions were also observed at the second division. We conclude that some aberrations are lost during the interphase between the first and the second post-irradiation metaphase and that new chromosomal aberrations arise during the second post-irradiation interphase.

Effects of 1-beta-D-arabinofuranosylcytosine on chromosomes, depending upon the cell cycle stage at the time of exposure.

1-beta-D-Arabinofuranosyl cytosine (ara-C) is a clinically important cytotoxic drug which is a potent inhibitor of DNA but which has a minimal effect on other cellular processes. The cytotoxic action of ara-C on mammalian cells has been suggested to be due to the chromosome aberrations induced by this compound. Using a marsupial cell line (JU56), the cells of which contain only 9 readily identified chromosomes, the different types of chromosome aberrations induced by a pulse of ara-C have been quantified, and the cell cycle dependence of the damage has been assessed. It was found that, for cells exposed in G2, both chromatid-type and chromosome-type lesions were produced. The frequency of these lesions was reduced by a chase of deoxycytidine, and there was some evidence that the initial lesions are gaps which may later be converted to true breaks. In early G2 and late S cells, lesions were produced chiefly at one chromosome locations; this location was not specifically late-replicating. At all stages of S, lesions were chiefly chromatid-type, and some exchanges occurred. The level of damage in S cells was not influenced by a deoxycytidine chase. There was negligible damage in cells exposed in G1. It is suggested that the reason previous investigators have obtained very different cell cycle dependence of chromosome damage is that the delaying effects of ara-C on cell cycle progression was not taken into account.

Studies of X-ray-induced chromosome aberrations in cells of the black-tailed wallaby. I. Non-random exchange in peripheral blood cells irradiated in Go.

The distribution of exchanges between individual chromosome arms in mitotic peripheral blood cells following X-irradiation in Go has been measured. It was found that, although all arms exchanged with each other, there were small but significant departures from the frequencies expected on the basis of random breakage and exchange. It is suggested that non-randomness may reflect the non-uniform state of condensation of chromatin in Go lymphocytes.

Synergism of 1-beta-D-arabinofuranosylcytosine with itself and aphidicolin.

JU56 cells have been exposed to 1-beta-D-arabinofuranosylcytosine (ara-C) in S phase, and again to aphidicolin (APC) or ara-C during G2, and examined for chromosomal aberrations at c-metaphase. It was found that the two exposures acted synergistically in the production of chromosomal lesions of both the chromatid and isochromatid type. The results were interpreted as indicating that inhibition of the G2 repair system prevented the repair of DNA single-strand regions produced by the incorporation of ara-C during semi-conservative DNA synthesis.