Central role of detachment faults in accretion of slow-spreading oceanic lithosphere

Author Posting. © Macmillan Publishers, 2008. This is the author's version of the work. It is posted here by permission of Macmillan Publishers for personal use, not for redistribution. The definitive version was published in Nature 455 (2008): 790-794, doi:10.1038/nature07333.The formation of oceanic detachment faults is well established from inactive, corrugated fault planes exposed on seafloor formed along ridges spreading at less than 80 km/My1-4. These faults can accommodate extension for up to 1-3 Myrs5, and are associated with one of two contrasting modes of accretion operating along the northern Mid-Atlantic Ridge (MAR). The first is symmetrical accretion, dominated by magmatic processes with subsidiary high-angle faulting and formation of abyssal hills on both flanks. The second is asymmetrical accretion involving an active detachment fault6 along one ridge flank. An examination of ~2500 km of the MAR between 12.5 and 35°N reveals asymmetrical accretion along almost half of the ridge. Hydrothermal activity identified to date in the study region is closely associated with asymmetrical accretion, which also exhibits high-levels of near continuous hydroacoustically and teleseismically recorded seismicity. Enhanced seismicity is probably generated along detachment faults accommodating a sizeable proportion of the total plate separation. In contrast, symmetrical segments have lower levels of seismicity, which concentrates primarily at their ends. Basalts erupted along asymmetrical segments have compositions that are consistent with crystallization at higher pressures than basalts from symmetrical segments, and with lower extents of partial melting of the mantle. Both seismic and geochemical evidence indicate that the axial lithosphere is thicker and colder at asymmetrical sections of the ridge, either because associated hydrothermal circulation efficiently penetrates to greater depths, or because the rising mantle is cooler. We suggest that much of the variability in seafloor morphology, seismicity and basalt chemistry found along slow-spreading ridges can be thus attributed to the frequent involvement of detachments in oceanic lithospheric accretion.Supported by CNRS (JE), NSF (DKS, HS, JC, CL and SE), WHOI (JE, DKS, HS and JC), Harvard University (JE, CL and SE), Univ. of Leeds (JC), and MIT (JE)

Complete mitochondrial DNA sequences provide new insights into the Polynesian motif and the peopling of Madagascar

More than a decade of mitochondrial DNA (mtDNA) studies have given the 'Polynesian motif' renowned status as a marker for tracing the late-Holocene expansion of Austronesian speaking populations. Despite considerable research on the Polynesian motif in Oceania, there has been little equivalent work on the western edge of its expansion - leaving major issues unresolved regarding the motif's evolutionary history. This has also led to considerable uncertainty regarding the settlement of Madagascar. In this study, we assess mtDNA variation in 266 individuals from three Malagasy ethnic groups: the Mikea, Vezo, and Merina. Complete mtDNA genome sequencing reveals a new variant of the Polynesian motif in Madagascar; two coding region mutations define a Malagasy-specific sub-branch. This newly defined 'Malagasy motif' occurs at high frequency in all three ethnic groups (13-50%), and its phylogenetic position, geographic distribution, and estimated age all support a recent origin, but without conclusively identifying a specific source region. Nevertheless, the haplotype's limited diversity, similar to those of other mtDNA haplogroups found in our Malagasy groups, best supports a small number of initial settlers arriving to Madagascar through the same migratory process. Finally, the discovery of this lineage provides a set of new polymorphic positions to help localize the Austronesian ancestors of the Malagasy, as well as uncover the origin and evolution of the Polynesian motif itself

The development of an intervention programme to reduce whole-body vibration exposure at work induced by a change in behaviour: a study protocol

<p>Abstract</p> <p>Background</p> <p>Whole body vibration (WBV) exposure at work is common and studies found evidence that this exposure might cause low back pain (LBP). A recent review concluded there is a lack of evidence of effective strategies to reduce WBV exposure. Most research in this field is focussed on the technical implications, although changing behaviour towards WBV exposure might be promising as well. Therefore, we developed an intervention programme to reduce WBV exposure in a population of drivers with the emphasis on a change in behaviour of driver and employer. The hypothesis is that an effective reduction in WBV exposure, in time, will lead to a reduction in LBP as WBV exposure is a proxy for an increased risk of LBP.</p> <p>Methods/Design</p> <p>The intervention programme was developed specifically for the drivers of vibrating vehicles and their employers. The intervention programme will be based on the most important determinants of WBV exposure as track conditions, driving speed, quality of the seat, etc. By increasing knowledge and skills towards changing these determinants, the attitude, social influence and self-efficacy (ASE) of both drivers and employers will be affected having an effect on the level of exposure. We used the well-known ASE model to develop an intervention programme aiming at a change or the intention to change behaviour towards WBV exposure. The developed programme consists of: individual health surveillance, an information brochure, an informative presentation and a report of the performed field measurements.</p> <p>Discussion</p> <p>The study protocol described is advantageous as the intervention program actively tries to change behaviour towards WBV exposure. The near future will show if this intervention program is effective by showing a decrease in WBV exposure.</p

A dearth of small particles in the transiting material around the white dwarfWD 1145+017

White dwarf WD 1145+017 is orbited by several clouds of dust, possibly emanating from actively disintegrating bodies. These dust clouds reveal themselves through deep, broad, and evolving transits in the star's light curve. Here, we report two epochs of multi-wavelength photometric observations of WD 1145+017, including several filters in the optical, K$_\mathrm{s}$ and 4.5 $\mu$m bands in 2016 and 2017. The observed transit depths are different at these wavelengths. However, after correcting for excess dust emission at K$_\mathrm{s}$ and 4.5 $\mu$m, we find the transit depths for the white dwarf itself are the same at all wavelengths, at least to within the observational uncertainties of $\sim$5%-10%. From this surprising result, and under the assumption of low optical depth dust clouds, we conclude that there is a deficit of small particles (with radii $s \lesssim$ 1.5 $\mu$m) in the transiting material. We propose a model wherein only large particles can survive the high equilibrium temperature environment corresponding to 4.5 hr orbital periods around WD 1145+017, while small particles sublimate rapidly. In addition, we evaluate dust models that are permitted by our measurements of infrared emission

Dilated Thin-Walled Blood and Lymphatic Vessels in Human Endometrium: A Potential Role for VEGF-D in Progestin-Induced Break-Through Bleeding

Progestins provide safe, effective and cheap options for contraception as well as the treatment of a variety of gynaecological disorders. Episodes of irregular endometrial bleeding or breakthrough bleeding (BTB) are a major unwanted side effect of progestin treatment, such that BTB is the leading cause for discontinued use of an otherwise effective and popular medication. The cellular mechanisms leading to BTB are poorly understood. In this study, we make the novel finding that the large, dilated, thin walled vessels characteristic of human progestin-treated endometrium include both blood and lymphatic vessels. Increased blood and lymphatic vessel diameter are features of VEGF-D action in other tissues and we show by immunolocalisation and Western blotting that stromal cell decidualisation results in a significant increase in VEGF-D protein production, particularly of the proteolytically processed 21 kD form. Using a NOD/scid mouse model with xenografted human endometrium we were able to show that progestin treatment causes decidualisation, VEGF-D production and endometrial vessel dilation. Our results lead to a novel hypothesis to explain BTB, with stromal cell decidualisation rather than progestin treatment per se being the proposed causative event, and VEGF-D being the proposed effector agent

Mapping post-glacial expansions: The peopling of Southwest Asia

Archaeological, palaeontological and geological evidence shows that post-glacial warming released human populations from their various climate-bound refugia. Yet specific connections between these refugia and the timing and routes of post-glacial migrations that ultimately established modern patterns of genetic variation remain elusive. Here, we use Y-chromosome markers combined with autosomal data to reconstruct population expansions from regional refugia in Southwest Asia. Populations from three regions in particular possess distinctive autosomal genetic signatures indicative of likely refugia: one, in the north, centered around the eastern coast of the Black Sea, the second, with a more Levantine focus, and the third in the southern Arabian Peninsula. Modern populations from these three regions carry the widest diversity and may indeed represent the most likely descendants of the populations responsible for the Neolithic cultures of Southwest Asia. We reveal the distinct and datable expansion routes of populations from these three refugia throughout Southwest Asia and into Europe and North Africa and discuss the possible correlations of these migrations to various cultural and climatic events evident in the archaeological record of the past 15,000 years

Low Densities of Serotonin and Peptide YY Cells in the Colon of Patients with Irritable Bowel Syndrome

Background The gut hormones are important in regulating gastrointestinal motility. Disturbances in gastrointestinal motility have been reported in patients with irritable bowel syndrome (IBS). Reduced endocrine cell density, as revealed by chromogranin A, has been reported in the colon of IBS patients. Aims To investigate a possible abnormality in the colonic endocrine cells of IBS patients. Methods A total of 41 patients with IBS according to Rome Criteria III and 20 controls were included in the study. Biopsies from the right and left colon were obtained from both patients and controls during colonoscopy. The biopsies were immunostained for serotonin, peptide YY (PYY), pancreatic polypeptide (PP), entroglucagon, and somatostatin cells. Cell densities were quantified by computerized image analysis. Results Serotonin and PYY cell densities were reduced in the colon of IBS patients. PP, entroglucagon, and somatostatin- immunoreactive cells were too few to enable reliable quantification

Human PTCHD3 nulls: rare copy number and sequence variants suggest a non-essential gene

<p>Abstract</p> <p>Background</p> <p>Copy number variations (CNVs) can contribute to variable degrees of fitness and/or disease predisposition. Recent studies show that at least 1% of any given genome is copy number variable when compared to the human reference sequence assembly. Homozygous deletions (or CNV nulls) that are found in the normal population are of particular interest because they may serve to define non-essential genes in human biology.</p> <p>Results</p> <p>In a genomic screen investigating CNV in Autism Spectrum Disorders (ASDs) we detected a heterozygous deletion on chromosome 10p12.1, spanning the Patched-domain containing 3 (<it>PTCHD3</it>) gene, at a frequency of ~1.4% (6/427). This finding seemed interesting, given recent discoveries on the role of another Patched-domain containing gene (<it>PTCHD1</it>) in ASD. Screening of another 177 ASD probands yielded two additional heterozygous deletions bringing the frequency to 1.3% (8/604). The deletion was found at a frequency of ~0.73% (27/3,695) in combined control population from North America and Northern Europe predominately of European ancestry. Screening of the human genome diversity panel (HGDP-CEPH) covering worldwide populations yielded deletions in 7/1,043 unrelated individuals and those detected were confined to individuals of European/Mediterranean/Middle Eastern ancestry. Breakpoint mapping yielded an identical 102,624 bp deletion in all cases and controls tested, suggesting a common ancestral event. Interestingly, this CNV occurs at a break of synteny between humans and mouse. Considering all data, however, no significant association of these rare <it>PTCHD3 </it>deletions with ASD was observed. Notwithstanding, our RNA expression studies detected <it>PTCHD3 </it>in several tissues, and a novel shorter isoform for <it>PTCHD3 </it>was characterized. Expression in transfected COS-7 cells showed <it>PTCHD3 </it>isoforms colocalize with calnexin in the endoplasmic reticulum. The presence of a patched (Ptc) domain suggested a role for <it>PTCHD3 </it>in various biological processes mediated through the Hedgehog (Hh) signaling pathway. However, further investigation yielded one individual harboring a homozygous deletion (<it>PTCHD3 </it>null) without ASD or any other overt abnormal phenotype. Exon sequencing of <it>PTCHD3 </it>in other individuals with deletions revealed compound point mutations also resulting in a null state.</p> <p>Conclusion</p> <p>Our data suggests that <it>PTCHD3 </it>may be a non-essential gene in some humans and characterization of this novel CNV at 10p12.1 will facilitate population and disease studies.</p

Parallel Adaptive Divergence among Geographically Diverse Human Populations

Few genetic differences between human populations conform to the classic model of positive selection, in which a newly arisen mutation rapidly approaches fixation in one lineage, suggesting that adaptation more commonly occurs via moderate changes in standing variation at many loci. Detecting and characterizing this type of complex selection requires integrating individually ambiguous signatures across genomically and geographically extensive data. Here, we develop a novel approach to test the hypothesis that selection has favored modest divergence at particular loci multiple times in independent human populations. We find an excess of SNPs showing non-neutral parallel divergence, enriched for genic and nonsynonymous polymorphisms in genes encompassing diverse and often disease related functions. Repeated parallel evolution in the same direction suggests common selective pressures in disparate habitats. We test our method with extensive coalescent simulations and show that it is robust to a wide range of demographic events. Our results demonstrate phylogenetically orthogonal patterns of local adaptation caused by subtle shifts at many widespread polymorphisms that likely underlie substantial phenotypic diversity

Inducible viral receptor, A possible concept to induce viral protection in primitive immune animals

A pseudolysogen (PL) is derived from the lysogenic Vibrio harveyi (VH) which is infected with the VHS1 (Vibrio harveyi Siphoviridae-like 1) bacteriophage. The lysogenic Vibrio harveyi undergoes an unequivalent division of the extra-chromosomal VHS1 phage genome and its VH host chromosome and produces a true lysogen (TL) and pseudolysogen (PL). The PL is tolerant to super-infection of VHS1, as is of the true lysogen (TL), but the PL does not contain the VHS1 phage genome while the TL does. However, the PL can become susceptible to VHS1 phage infection if the physiological state of the PL is changed. It is postulated that this is due to a phage receptor molecule which can be inducible to an on-and-off regulation influence by an alternating condition of the bacterial host cell. This characteristic of the PL leads to speculate that this phenomenon can also occur in high organisms with low immunity such as shrimp. This article proposes a hypothesis that the viral receptor molecule on the target cell can play a crucial role in which the invertebrate aquaculture animals can become tolerant to viral infection. A possible mechanism may be that the target cell disrupts the viral receptor molecule to prevent super infection. This concept can explain a mechanism for the prevention of viral infection in invertebrate animals which do not have acquired immunity in response to pathogens. It can guide us to develop a mechanism of immunity to viral infection in low-evolved-immune animals. Also, it can be an additional mechanism that exists in high immune organism, as in human for the prevention of viral infectio