Divergent northern and southern populations and demographic history of the pearl oyster in the western Pacific revealed with genomic SNPs

In the open ocean without terrain boundaries, marine invertebrates with pelagic larvae can migrate long distances using ocean currents, suggesting reduced genetic diversification. Contrary to this assumption, however, genetic differentiation is often observed in marine invertebrates. In the present study, we sought to explain how population structure is established in the western Pacific Ocean, where the strong Kuroshio Current maintains high levels of gene flow from south to north, presumably promoting genetic homogeneity. We determined the population structure of the pearl oyster, Pinctada fucata, in the Indo-Pacific Ocean using genome-wide genotyping data from multiple sampling localities. Cluster analysis showed that the western Pacific population is distinct from that of the Indian Ocean, and that it is divided into northern (Japanese mainland) and southern (Nansei Islands, China, and Cambodia) populations. Genetic differentiation of P. fucata can be explained by geographic barriers in the Indian Ocean and a local lagoon, and by environmental gradients of sea surface temperature (SST) and oxygen concentration in the western Pacific. A genome scan showed evidence of adaptive evolution in genomic loci, possibly associated with changes in environmental factors, including SST and oxygen concentration. Furthermore, Bayesian simulation demonstrated that the past population expansion and division are congruent with ocean warming after the last glacial period. It is highly likely that the environmental gradient forms a genetic barrier that diversifies P. fucata populations in the western Pacific. This hypothesis helps to explain genetic differentiation and possible speciation of marine invertebrates

Detection of a novel locus involved in non-seed-shattering behaviour of Japonica rice cultivar, Oryzasativa ‘Nipponbare’

Asian cultivated rice, Oryzasativa, was domesticated from its wild ancestor, O.rufipogon. Loss of seed shattering is one of the most recognisable traits selected during rice domestication. Three quantitative trait loci (QTLs), qSH1, qSH3, and sh4, were previously reported to be involved in the loss of seed shattering of Japonica cultivated rice, O.sativa ‘Nipponbare’. However, the introgression line (IL) carrying ‘Nipponbare’ alleles at these three loci in the genetic background of wild rice, O.rufipogon W630, showed a lower value for detaching a grain from the pedicel than ‘Nipponbare’. Here, we investigated abscission layer formation in the IL and found a partially formed abscission layer in the central region between the epidermis and vascular bundles. Based on QTL-seq analysis using the F2 population obtained from a cross between ‘Nipponbare’ and the IL, we detected two novel loci qCSS3 and qCSS9 (QTL for the Control of Seed Shattering in rice on chromosomes 3 and 9), which were found to be involved in the difference in seed-shattering degree between ‘Nipponbare’ and W630. Then, we further focused on qCSS3 in order to understand its potential role on the loss of seed shattering. The candidate region of qCSS3 was found to be located within a 526-kb region using substitution mapping analysis. Interestingly, the qCSS3 candidate region partially overlaps the selective sweep detected for Japonica but not for Indica rice cultivars, suggesting that this region harbours the mutation at a novel seed-shattering locus specifically selected for non-seed-shattering behaviour in Japonica cultivars

Clinical and Immunopathological Features of Moyamoya Disease

Background: Moyamoya disease (MMD) is a cerebrovascular disease characterized by progressive stenosis or occlusion of the terminal portion of internal carotid arteries and the formation of a vascular network at the base of the brain. The pathogenesis of MMD is still unclear. Methodology/Principal Findings: We retrospectively analyzed clinical data for 65 consecutive patients with MMD in our institutions and evaluated the histopathological and immunohistochemical findings of intracranial vessels from 3 patients. The onset age distribution was found to have 1 peak at 40–49 year-old age group, no significant difference was observed in the female-to-male ratio (F/M = 1.2). Intracranial hemorrhage was the predominant disease type (75%). Positive family history was observed in 4.6 % of patients. Histopathological findings were a narrowed lumen due to intimal fibrous thickening without significant inflammatory cell infiltration, and the internal elastic lamina was markedly tortuous and stratified. All 3 autopsy cases showed vacuolar degeneration in the cerebrovascular smooth muscle cells. Immunohistochemical study showed the migration of smooth muscle cells in the thickened intima, and aberrant expression of IgG and S100A4 protein in vascular smooth muscle cells. The Complement C3 immunoreactivity was negative. Conclusion/Significance: This study indicated that aberrant expression of IgG and S100A4 protein in intracranial vascular wall of MMD patients, which suggested that immune-related factors may be involved in the functional and morphologica

Endothelial Progenitor Cell Number and Colony-forming Capacity in Overweight and Obese Adults

OBJECTIVE: To investigate whether adiposity influences endothelial progenitor cell (EPC) number and colony-forming capacity.DESIGN: Cross-sectional study of normal weight, overweight and obese adult humans.PARTICIPANTS: Sixty-seven sedentary adults (aged 45-65 years): 25 normal weight (body mass index (BMI) or=30 kg/m(2); 18 males/6 females). All participants were non-smokers and free of overt cardiometabolic disease.MEASUREMENTS: Peripheral blood samples were collected and circulating EPC number was assessed by flow cytometry. Putative EPCs were defined as CD45(-)/CD34(+)/VEGFR-2(+)/CD133(+) or CD45(-)/CD34(+) cells. EPC colony-forming capacity was measured in vitro using a colony-forming unit (CFU) assay.RESULTS: Number of circulating putative EPCs (either CD45(-)/CD34(+)/VEGFR-2(+)/CD133(+) or CD45(-)/CD34(+) cells) was lower (P\u3c0.05) in obese (0.0007±0.0001%; 0.050±0.006%) compared with overweight (0.0016±0.0004%; 0.089±0.019%) and normal weight (0.0015±0.0003%; 0.082±0.008%) adults. There were no differences in EPC number between the overweight and normal weight groups. EPC colony-formation was significantly less in the obese (6±1) and overweight (4±1) compared with normal weight (9±2) adults.CONCLUSION: These results indicate that: (1) the number of circulating EPCs is lower in obese compared with overweight and normal weight adults; and (2) EPC colony-forming capacity is blunted in overweight and obese adults compared with normal weight adults. Impairments in EPC number and function may contribute to adiposity-related cardiovascular risk

Arrhythmogenic mechanisms in the isolated perfused hypokalaemic murine heart

AIM: Hypokalaemia is associated with a lethal form of ventricular tachycardia (VT), torsade de pointes, through pathophysiological mechanisms requiring clarification. METHODS: Left ventricular endocardial and epicardial monophasic action potentials were compared in isolated mouse hearts paced from the right ventricular epicardium perfused with hypokalaemic (3 and 4 mm [K(+)](o)) solutions. Corresponding K(+) currents were compared in whole-cell patch-clamped epicardial and endocardial myocytes. RESULTS: Hypokalaemia prolonged epicardial action potential durations (APD) from mean APD(90)s of 37.2 ± 1.7 ms (n = 7) to 58.4 ± 4.1 ms (n =7) and 66.7 ± 2.1 ms (n = 11) at 5.2, 4 and 3 mm [K(+)](o) respectively. Endocardial APD(90)s correspondingly increased from 51.6 ± 1.9 ms (n = 7) to 62.8 ± 2.8 ms (n = 7) and 62.9 ± 5.9 ms (n = 11) giving reductions in endocardial–epicardial differences, ΔAPD(90), from 14.4 ± 2.6 to 4.4 ± 5.0 and −3.4 ± 6.0 ms respectively. Early afterdepolarizations (EADs) occurred in epicardia in three of seven spontaneously beating hearts at 4 mm [K(+)](o) with triggered beats followed by episodes of non-sustained VT in nine of 11 preparations at 3 mm. Programmed electrical stimulation never induced arrhythmic events in preparations perfused with normokalemic solutions yet induced VT in two of seven and nine of 11 preparations at 4 and 3 mm [K(+)](o) respectively. Early outward K(+) current correspondingly fell from 73.46 ± 8.45 to 61.16±6.14 pA/pF in isolated epicardial but not endocardial myocytes (n = 9) (3 mm [K(+)](o)). CONCLUSIONS: Hypokalaemic mouse hearts recapitulate the clinical arrhythmogenic phenotype, demonstrating EADs and triggered beats that might initiate VT on the one hand and reduced transmural dispersion of repolarization reflected in ΔAPD(90) suggesting arrhythmogenic substrate on the other

Dependence of adsorption-induced structural transition on framework structure of porous coordination polymers

Porous coordination polymers (PCPs) with soft frameworks show a gate phenomenon consisting of an abrupt structural transition induced by adsorption of guest molecules. To understand the dependence of the gating behavior on the host framework structure, we conduct grand canonical Monte Carlo simulations and a free-energy analysis of a simplified model of a stacked-layer PCP. The interlayer width of the rigid layers composing the simplified model can be changed by guest adsorption and by varying the initial interlayer width h 0, which is controlled by the length of pillars between the layers. We introduce three types of gating behavior, one-step gating, filling and gating, and double gating, which depend on three parameters: the initial interlayer width h 0; the interaction parameter ɛ ss, which determines the host–guest framework interaction as well as the inter-framework interaction; and the elastic modulus of the framework, which depends on the stiffness of the pillars. We show that the one-step gating and the filling and gating behaviors depend strongly on h 0 rather than on ɛ ss, and thus a transformation from filling and gating to double gating can be achieved by reducing the stiffness of the host framework. This study should be a guideline for controlling the gating pressure of PCPs by modifying their chemical components