Biological Characteristics and Fishery Assessment of Alaska Plaice, Pleuronectes quadrituberculatus, in the Eastern Bering Sea

Alaska plaice, Pleuronectes quadrituberculatus, is one of the major flatfishes in the eastern Bering Sea ecosystem and is most highly concentrated in the shallow continental shelf of the eastern Bering Sea. Annual commercial catches have ranged from less than 1,000 metric tons (t) in 1963 to 62,000 t in 1988. Alaska plaice is a relatively large flatfish averaging about 32 cm in length and 390 g in weight in commercial catches. They are distributed from nearshore waters to a depth of about 100 m in the eastern Bering Sea during summer, but move to deeper continental shelf waters in winter to escape sea ice and cold water temperatures. Being a long-lived species (>30 years), they have a relatively low natural mortality rate estimated at 0.20. Maturing at about age 7, Alaska plaice spawn from April through June on hard sandy substrates of the shelf region, primarily around the 100 m isobath. Prey items primarily include polychaetes and other marine worms. In comparison with other flatfish, Alaska plaice and rock sole, Pleuronectes bilineatus, have similar diets but different habitat preferences with separate areas of peak population density which may minimize interspecific competition. Yellowfin sole, Pleuronectes asper, while sharing similar habitat, differs from these two species because of the variety of prey items in its diet. Competition for food resources among the three species appears to be low. The resource has experienced light exploitation since 1963 and is currently in good condition. Based on the results of demersal trawl surveys and age-structured analyses, the exploitable biomass increased from 1971 through the mid-1980’s before decreasing to the 1997 level of 500,000 t. The recommended 1998 harvest level, Allowable Biological Catch, was calculated from the Baranov catch equation based on the FMSY harvest level and the projected 1997 biomass, resulting in a commercial harvest of 69,000 t, or about 16% of the estimated exploitable biomass

Thermal Properties of Graphene, Carbon Nanotubes and Nanostructured Carbon Materials

Recent years witnessed a rapid growth of interest of scientific and engineering communities to thermal properties of materials. Carbon allotropes and derivatives occupy a unique place in terms of their ability to conduct heat. The room-temperature thermal conductivity of carbon materials span an extraordinary large range - of over five orders of magnitude - from the lowest in amorphous carbons to the highest in graphene and carbon nanotubes. I review thermal and thermoelectric properties of carbon materials focusing on recent results for graphene, carbon nanotubes and nanostructured carbon materials with different degrees of disorder. A special attention is given to the unusual size dependence of heat conduction in two-dimensional crystals and, specifically, in graphene. I also describe prospects of applications of graphene and carbon materials for thermal management of electronics.Comment: Review Paper; 37 manuscript pages; 4 figures and 2 boxe

A transcriptomic snapshot of early molecular communication between Pasteuria penetrans and Meloidogyne incognita

© The Author(s). 2018Background: Southern root-knot nematode Meloidogyne incognita (Kofoid and White, 1919), Chitwood, 1949 is a key pest of agricultural crops. Pasteuria penetrans is a hyperparasitic bacterium capable of suppressing the nematode reproduction, and represents a typical coevolved pathogen-hyperparasite system. Attachment of Pasteuria endospores to the cuticle of second-stage nematode juveniles is the first and pivotal step in the bacterial infection. RNA-Seq was used to understand the early transcriptional response of the root-knot nematode at 8 h post Pasteuria endospore attachment. Results: A total of 52,485 transcripts were assembled from the high quality (HQ) reads, out of which 582 transcripts were found differentially expressed in the Pasteuria endospore encumbered J2 s, of which 229 were up-regulated and 353 were down-regulated. Pasteuria infection caused a suppression of the protein synthesis machinery of the nematode. Several of the differentially expressed transcripts were putatively involved in nematode innate immunity, signaling, stress responses, endospore attachment process and post-attachment behavioral modification of the juveniles. The expression profiles of fifteen selected transcripts were validated to be true by the qRT PCR. RNAi based silencing of transcripts coding for fructose bisphosphate aldolase and glucosyl transferase caused a reduction in endospore attachment as compared to the controls, whereas, silencing of aspartic protease and ubiquitin coding transcripts resulted in higher incidence of endospore attachment on the nematode cuticle. Conclusions: Here we provide evidence of an early transcriptional response by the nematode upon infection by Pasteuria prior to root invasion. We found that adhesion of Pasteuria endospores to the cuticle induced a down-regulated protein response in the nematode. In addition, we show that fructose bisphosphate aldolase, glucosyl transferase, aspartic protease and ubiquitin coding transcripts are involved in modulating the endospore attachment on the nematode cuticle. Our results add new and significant information to the existing knowledge on early molecular interaction between M. incognita and P. penetrans.Peer reviewedFinal Published versio

Pairing symmetry and properties of iron-based high temperature superconductors

Pairing symmetry is important to indentify the pairing mechanism. The analysis becomes particularly timely and important for the newly discovered iron-based multi-orbital superconductors. From group theory point of view we classified all pairing matrices (in the orbital space) that carry irreducible representations of the system. The quasiparticle gap falls into three categories: full, nodal and gapless. The nodal-gap states show conventional Volovik effect even for on-site pairing. The gapless states are odd in orbital space, have a negative superfluid density and are therefore unstable. In connection to experiments we proposed possible pairing states and implications for the pairing mechanism.Comment: 4 pages, 1 table, 2 figures, polished versio

An Analysis of Human MicroRNA and Disease Associations

It has been reported that increasingly microRNAs are associated with diseases. However, the patterns among the microRNA-disease associations remain largely unclear. In this study, in order to dissect the patterns of microRNA-disease associations, we performed a comprehensive analysis to the human microRNA-disease association data, which is manually collected from publications. We built a human microRNA associated disease network. Interestingly, microRNAs tend to show similar or different dysfunctional evidences for the similar or different disease clusters, respectively. A negative correlation between the tissue-specificity of a microRNA and the number of diseases it associated was uncovered. Furthermore, we observed an association between microRNA conservation and disease. Finally, we uncovered that microRNAs associated with the same disease tend to emerge as predefined microRNA groups. These findings can not only provide help in understanding the associations between microRNAs and human diseases but also suggest a new way to identify novel disease-associated microRNAs

Dengue Virus Targets the Adaptor Protein MITA to Subvert Host Innate Immunity

Dengue is one of the most important arboviral diseases caused by infection of four serotypes of dengue virus (DEN). We found that activation of interferon regulatory factor 3 (IRF3) triggered by viral infection and by foreign DNA and RNA stimulation was blocked by DEN-encoded NS2B3 through a protease-dependent mechanism. The key adaptor protein in type I interferon pathway, human mediator of IRF3 activation (MITA) but not the murine homologue MPYS, was cleaved in cells infected with DEN-1 or DEN-2 and with expression of the enzymatically active protease NS2B3. The cleavage site of MITA was mapped to LRR↓96G and the function of MITA was suppressed by dengue protease. DEN replication was reduced with overexpression of MPYS but not with MITA, while DEN replication was enhanced by MPYS knockdown, indicating an antiviral role of MITA/MPYS against DEN infection. The involvement of MITA in DEN-triggered innate immune response was evidenced by reduction of IRF3 activation and IFN induction in cells with MITA knockdown upon DEN-2 infection. NS2B3 physically interacted with MITA, and the interaction and cleavage of MITA could be further enhanced by poly(dA:dT) stimulation. Thus, we identified MITA as a novel host target of DEN protease and provide the molecular mechanism of how DEN subverts the host innate immunity

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition