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Given the high costs associated with fruit fly (Tephritidae) invasions, there is a need to better understand and predict the risks of future invasions. We assembled a global database of historical Tephritidae invasions with the objective to identify the biological and socioeconomic drivers that explain these invasions. We investigate the tendencies of certain species to invade and the characteristics of regions that make them more prone to invasions. We used various published sources and online databases to assemble a database documenting the occurrence (presence/absence) and status (native/non-native) of individual species for each country in the world. Values of several socio-economic and environmental variables were also assembled and considered as explanatory variables. A generalized linear mixed-effects model framework was used to evaluate the utility of these variables for predicting the country-level occurrence of each species outside of its native range. A total 44 species were identified as having been accidentally introduced in the world. Most species of invading Tephritidae have established in only five or fewer countries. The number of invasions has rapidly increased since the 1950s. Climatic similarity between native and invaded countries, gross domestic product of the invaded country and distance from the native range are significant predictors of tephritid invasions. Our analysis revealed that both economic and biological factors explain patterns of historical Tephritid invasions. Despite the rising efforts to prevent new invasions, additional species may continue to invade, and many currently established species will likely continue to expand their ranges into new areas.

This work shows that S-atom substitution in phosphate, controls the directionality of hole transfer processes between base and sugar-phosphate backbone in DNA systems. The investigation combines synthesis, electron spin resonance (ESR) studies in supercooled homogeneous solution, pulse radiolysis in aqueous solution at ambient temperature and density functional theory (DFT) calculations of in-house synthesized model compound dimethylphosphorothioate (DMTP(O(−))=S) and nucleotide (5’-O-methoxyphosphorothioyl-2’-deoxyguanosine (G-P(O(−))=S)). ESR investigations show that DMTP(O(−))=S reacts with Cl(2)(•−) to form the σ(2)σ*(1) adduct radical -P-S∸Cl which subsequently reacts with DMTP(O(−))=S to produce [-P-S∸S-P-](−). -P-S∸Cl in G-P(O(−))=S undergoes hole transfer to Gua forming the cation radical (G(•+)) via thermally activated hopping. However, pulse radiolysis measurements show that DMTP(O(−))=S forms the thiyl radical (-P-S•) by one-electron oxidation which did not produce [-P-S∸S-P-](−). Gua in G-P(O(−))=S is oxidized unimolecularly by -P-S• intermediate in sub-picosecond range. DFT thermochemical calculations explain the differences in ESR and pulse radiolysis results obtained at different temperatures.

We report on the physicochemical processes and the products of DNA damage involved in Ne-22 ion-beam radiation of hydrated (12 ± 3 H2O/nucleotide) salmon testes DNA at 77 K. Free radicals trapped at 77 K were identified using electron spin resonance (ESR) spectroscopy. The measurement of DNA damage using two different techniques of mass spectrometry revealed the formation of numerous DNA products. Results obtained by ESR spectroscopy showed that as the linear energy transfer (LET) of the ion-beam radiation increases along the beam track, the production of DNA radicals correspondingly increases until just before the Bragg peak is reached. Yields of DNA products along the ion-beam track were in excellent agreement with the radical production. This work is the first to use the combination of ESR spectroscopy and mass spectrometric techniques enabling a better understanding of mechanisms of radiation damage to DNA by heavy ion beams detailing the formation of DNA free radicals and their subsequent products.

A novel high-performance computing algorithm, developed in response to the next generation of computational challenges associated with burning plasma regimes in ITER-scale tokamak devices, has been tested and is described herein. The Lorentz-orbit code for use in stellarators and tokamaks (LOCUST) is designed for computationally scalable modelling of fast-ion dynamics, in the presence of detailed first wall geometries and fine 3D magnetic field structures. It achieves this through multiple levels of single instruction, multiple thread parallelism and by leveraging general-purpose graphics processing units. This enables LOCUST to rapidly track the full-orbit trajectories of kinetic Monte Carlo markers to deliver high-resolution fast-ion distribution functions and plasma-facing component power loads. LOCUST has been tested against the prominent NUBEAM and ASCOT fast-ion codes. All codes were compared for collisional plasmas in both high and low-aspect ratio toroidal geometries, with full-orbit and guiding-centre tracking. LOCUST produces statistically consistent results in line with acceptable theoretical and Monte Carlo uncertainties. Synthetic fast-ion D-α diagnostics produced by LOCUST are also compared to experiment using FIDASIM and show good agreement.

Invited for the cover of this issue are the groups of Roman Dembinski, Mehran Mostafavi, and Amitava Adhikary at the Polish Academy of Sciences, Université Paris-Saclay, and Oakland University. The image depicts a doughnut as a way of illustrating the hole transfer process. Read the full text of the article at 10.1002/chem.202000247.

The directionality of the hole-transfer processes between DNA backbone and base was investigated by using phosphorodithioate [P(S- )=S] components. ESR spectroscopy in homogeneous frozen aqueous solutions and pulse radiolysis in aqueous solution at ambient temperature confirmed initial formation of G.+ -P(S- )=S. The ionization potential of G-P(S- )=S was calculated to be slightly lower than that of guanine in 5'-dGMP. Subsequent thermally activated hole transfer from G.+ to P(S- )=S led to dithiyl radical (P-2S. ) formation on the μs timescale. In parallel, ESR spectroscopy, pulse radiolysis, and density functional theory (DFT) calculations confirmed P-2S. formation in an abasic phosphorodithioate model compound. ESR investigations at low temperatures and higher G-P(S- )=S concentrations showed a bimolecular conversion of P-2S. to the σ2 -σ*1 -bonded dimer anion radical [-P-2S - . 2S-P-]- [ΔG (150 K, DFT)=-7.2 kcal mol-1 ]. However, [-P-2S - . 2S-P-]- formation was not observed by pulse radiolysis [ΔG° (298 K, DFT)=-1.4 kcal mol-1 ]. Neither P-2S. nor [-P-2S - . 2S-P-]- oxidized guanine base; only base-to-backbone hole transfer occurs in phosphorodithioate.

FER-1 is required for fusion of specialized vesicles, called membranous organelles, with the sperm plasma membrane during Caenorhabditis elegans spermiogenesis. To investigate its role in membranous organelle fusion, we examined ten fer-1 mutations and found that they all cause the same defect in membrane fusion. FER-1 and the ferlin protein family are membrane proteins with four to seven C2 domains. These domains commonly mediate Ca2+-dependent lipid-processing events. Most of the fer-1 mutations fall within these C2 domains, showing that they have distinct, non-redundant functions. We found that membranous organelle fusion requires intracellular Ca2+ and that C2 domain mutations alter Ca2+ sensitivity. This suggests that the C2 domains are involved in Ca2+ sensing and further supports their independent function. Using two immunological approaches we found three FER-1 isoforms, two of which might arise from FER-1 by proteolysis. By both light and electron microscopy, these FER-1 proteins were found to be localized to membranous organelle membranes. Dysferlin, a human homologue of FER-1 involved in muscular dystrophy, is required for vesicle fusion during Ca2+-induced muscle membrane repair. Our results suggest that the ferlin family members share a conserved mechanism to regulate cell-type-specific membrane fusion.

Dissection of the phenotypic and molecular details of development and differentiation is a centuries-old topic in evolutionary biology. However, an adequate understanding is missing for the molecular evolution of genes that are expressed differentially throughout development-across time, tissues, and the sexes. In this study, we investigate the dynamics of gene evolution across Caenorhabditis elegans ontogeny and among genes expressed differentially between each sex and gamete type. Using gene classes identified by genome-wide gene expression developmental time series and comparative sequence analysis with the congener C. briggsae, we demonstrate that genes expressed predominantly after reproductive maturity evolve more rapidly than genes expressed earlier in development and that genes expressed transiently during embryogenesis evolve faster than other embryonic transcripts. These results are indicative of relaxed selection on genes expressed after maturity, in accord with the mutation-accumulation model of aging. Furthermore, genes involved in spermatogenesis reveal more rapid evolution than other phenotypic classes of genes. Average rates of evolution among male soma-related genes indicates that selection acts to maintain males in these androdioecious species, despite their rarity, and the rapid evolution of sperm genes suggests that sexual selection acts on sperm development and function.

Cholesterol is a structural component of animal membranes that influences fluidity, permeability and formation of lipid microdomains. It is also a precursor to signalling molecules, including mammalian steroid hormones and insect ecdysones. The nematode Caenorhabditis elegans requires too little cholesterol for it to have a major role in membrane structure. Instead, its most probable signalling functions are to control molting and induce a specialized non-feeding larval stage, although no cholesterol-derived signalling molecule has yet been identified for these or any other functions.

The soil nematode Caenorhabditis elegans is an example of a species in which self-fertilizing hermaphrodites predominate, but functional males continue to persist – allowing outcrossing to persevere at low levels. Hermaphrodites can produce male progeny as a consequence of sex chromosome non-disjunction or via outcrossing with males. Consequently, the genetics of sex determination coupled with the efficiency by which males find, inseminate and obtain fertilizations with hermaphrodites will influence the frequency at which males and outcrossing occurs in such populations. Behavioural and physiological traits with a heritable basis, as well as ecological characters, may influence male reproductive success and therefore sex ratio. Because sex ratio is tied to male reproductive success, sex ratio greatly affects outcrossing rates, patterns of genetic variation, and the ability of natural selection to act within populations. In this paper we explore the determinants of male frequency in C. elegans with a mathematical model and experimental data. We address the role of the genetic machinery of sex determination via sex chromosome non-disjunction on sex ratio and the influence of physiological components of C. elegans' life history that contribute to variation in sex ratio by way of male reproductive success. Finally, we discuss the short-term and long-term factors that are likely to affect sex ratio and breeding system evolution in species like C. elegans.

During spermiogenesis, Caenorhabditis elegans spermatids activate and mature into crawling spermatozoa without synthesizing new proteins. Mutations in the spe-12 gene block spermatid activation, rendering normally self-fertile hermaphrodites sterile. Mutant males, however, are fertile. Surprisingly, when mutant hermaphrodites mate with a male, their self-spermatids activate and form functional spermatozoa, presumably due to contact with male seminal fluid. Here we show that, in addition to its essential role in normal activation of hermaphrodite-derived spermatids, SPE-12 also plays a supplementary but nonessential role in mating-induced activation. We have identified the spe-12 gene, which encodes a novel protein containing a single transmembrane domain. spe-12 mRNA is expressed in the sperm-producing germ line and the protein localizes to the spermatid cell surface. We propose that SPE-12 functions downstream of both hermaphrodite- and male-derived activation signals in a spermatid signaling pathway that initiates spermiogenesis.

During maturation of spermatids to motile spermatozoa in Caenorhabditis elegans, large vesicles called membranous organelles (MOs) fuse with the spermatid plasma membrane. Mutations in the gene fer-1 cause abnormal spermatozoa in which the MOs do not fuse, although they abut the plasma membrane normally. Here we describe the fer-1 gene, which we found to be approximately 8.6 kb in length and to encode a 6.2 kb transcript whose expression is limited to the primary spermatocytes, the cells in which the MOs form. fer-1 is predicted to encode a 235 kDa protein which is highly charged except for a putative transmembrane domain near the C terminus. We identified the mutations associated with five fer-1 alleles, all of which are missense mutations causing single amino acid changes. FER-1 is not similar to any characterized proteins in sequence databases, nor does it contain known functional motifs other than the predicted transmembrane domain. The C-terminal transmembrane domain makes FER-1 resemble some viral fusion proteins, suggesting it may play a direct role in MO-plasma membrane fusion. FER-1 does show significant sequence similarity to several predicted human proteins of unknown function. Two of the identified fer-1 mutations are located in regions of similarity between FER-1 and two of these predicted proteins. This strengthens the biological significance of these similarities and suggests these regions of similarity represent functionally important domains of FER-1 and the human proteins.

We describe a protocol for artificial insemination of Caenorhabditis elegans which we used to evaluate the viability of sperm from different strains and of sperm activated in vitro. Worms can be artificially inseminated with almost 100% success. Both male and hermaphrodite sperm can be used for insemination. Sperm from a sterile hermaphrodite [fem-3(q23ts)] were found to be viable. As with normal mating, male sperm inseminated into hermaphrodites artificially outcompete the hermaphrodite's own sperm, even though they have not been ejaculated with seminal fluid. Spermatozoa that were activated in vitro from spermatids by the weak base triethanolamine were viable. In contrast, spermatozoa activated in vitro by protease treatment were not.

Caenorhabditis elegans spermatozoa move by crawling. Their motility requires thin cytoskeletal filaments assembled from a unique cytoskeletal protein, the major sperm protein (MSP). During normal sperm development the MSP is segregated to developing sperm by assembly into filaments that form a paracrystalline array in a transient organelle, the fibrous body-membranous organelle. Mutations in the spe-6 gene cause sterility because they lead to defective primary spermatocytes that do not form spermatids. In these mutant spermatocytes the MSP fails to assemble into fibrous body filaments. Instead, the unassembled MSP distributes throughout the cytoplasm and nucleus. Thus, the spe-6 gene product is necessary for normal MSP localization and assembly during sperm development. In addition to their MSP assembly defect, spe-6 mutant spermatocytes arrest meiosis at diakinesis although their spindle pole bodies still replicate and separate. This results in spermatocytes with four half-spindles surrounding condensed, but unsegregated, chromosomes. All four spe-6 alleles, as well as a chromosome III deficiency that deletes the spe-6 gene, fail to complement two small overlapping chromosome IV deficiencies, eDf18 and eDf19. This non-allele-specific second site non-complementation suggests a concentration-dependent interaction between the spe-6 gene product and products of the gene(s) under eDf18 and eDf19, which include a cluster of sperm-specific genes. Since MSP filament assembly is highly concentration-dependent in vitro, the non-complementation might be expected if the sperm-specific gene products under eDf18 and eDf19 were needed together with the spe-6 gene product to promote MSP assembly.

Rapidly emerging mobile communications platforms, such as mobile phones, in countries across Africa, Iraq, and Afghanistan offer new opportunities for direct public engagement in health systems, placing tools and timely information into the hands of those who need it most. Early results from pioneering work suggest real benefits of mobile devices in addressing access to care, monitoring and treating diseases, and providing continuous medical education and training. The Military Health System, a $43-billion global healthcare system within the U.S. Department of Defense, in partnership with other U.S. government agencies and nongovernmental organizations and the international health sector, can make valuable contributions to creating a sustainable global m-health infrastructure.

Influenza epidemics cause numerous deaths and millions of hospitalizations each year. Because of the alarming emergence of resistance to anti-influenza drugs, there is a need to identify new naturally occurring antiviral molecules. We tested the hypothesis that pomegranate polyphenol extract (PPE) has anti-influenza properties. Using real time PCR, plaque assay, and TCID 50% hemagglutination assay, we have shown that PPE suppresses replication of influenza A virus in MDCK cells. PPE inhibits agglutination of chicken red blood cells (cRBC) by influenza virus and is virucidal. The single-cycle growth conditions indicated that independent of the virucidal effect PPE also inhibits viral RNA replication. PPE did not alter virus ribonucleoprotein (RNP) entry into nucleus or translocation of virus RNP from nucleus to cytoplasm in MDCK cells. We evaluated four major Polyphenols in PPE (ellagic acid, caffeic acid, luteolin, and punicalagin) and demonstrated that punicalagin is the effective, anti-influenza component of PPE. Punicalagin blocked replication of the virus RNA, inhibited agglutination of chicken RBC's by the virus and had virucidal effects. Furthermore, the combination of PPE and oseltamivir synergistically increased the anti-influenza effect of oseltamivir. In conclusion, PPE inhibited the replication of human influenza A/Hong Kong (H3N2) in vitro. Pomegranate extracts should be further studied for therapeutic and prophylactic potential especially for influenza epidemics and pandemics.

The isolation and properties of a gene encoding a histone H1 protein of Caenorhabditis elegans, his-24, are described. The predicted protein sequence is similar to histone H1 proteins of other eukaryotes. However, the gene structure of his-24 is atypical for a histone H1 gene; it contains an intron and encodes a polyadenylated mRNA. A family of approximately five histone H1 genes is defined by cross-hybridization to his-24. All appear to encode polyadenylated mRNAs. One gene is expressed specifically in male germ cells. These histone H1 genes are dispersed individually in the genome, apart from the previously described clusters of core histone genes (H2A, H2B, H3 and H4), which probably all encode non-polyadenylated mRNAs. This histone gene organization, with clustered core histone genes, encoding non-polyadenylated transcripts, and dispersed, histone H1 genes from which it appears only polyadenylated messages arise, suggests that C. elegans is at a stage of evolution of the histone gene family intermediate between lower eukaryotes (e.g. yeast) and the most advanced forms.

C-reactive protein (CRP) activates endothelial cells to express adhesion molecules, VCAM and ICAM, and Monocyte Chemotactic Protein, and CRP decreases the availability of nitric oxide. Thus, it is a proinflammatory substance and its serum level is also a predictor of future vascular events. White blood cell counts are independent predictors of cardiovascular events. Lipoprotein-associated phospholipase A2 (Lp-PLA2) may have both proinflammatory and antiinflammatory effects. High Lp-PLA2 levels predict future cardiovascular events. Myeloperoxidase is proinflammatory and its serum level is a predictor of prognosis of cardiovascular events in patients. In troponin-negative acute coronary syndrome (ACS) patients, elevated pregnancy-associated plasma protein-A is an independent predictor of adverse outcome during 6 months of follow-up. Elevated serum amyloid A at hospital admission in patients with unstable angina predicts a poorer prognosis. CD40 and CD40 ligand levels predict prognosis in patients with ACS. The primary proinflammatory cytokines are interleukin-1 and -6 and tumor necrosis factor-α. Increased serum levels of the proinflammatory cytokines are associated with a poorer prognosis, development of congestive heart failure (CHF), and of progressive atherosclerosis. Increased serum levels of interleukin-10 are associated with a better prognosis in patients with coronary artery disease (CAD).

Atherosclerotic plaque ulceration and fissuring lead to thrombosis and vasoconstriction. Local coagulation factors and blood components, in addition to plaque fissuring and ulceration, contribute to determining the development of thrombosis. Several different imaging procedures, including intravascular ultrasound, elastography, thermography, optical coherence tomography (OCT), magnetic resonance imaging (MRI), and computed tomography (CT) are being developed to detect vulnerable atherosclerotic plaques. Although it is variable among patient groups, perhaps 20% to 40% of patients with acute coronary artery syndromes have more than one vulnerable plaque, suggesting a relatively widespread inflammatory state within the coronary arteries.