Channelling of hydrothermal fluids during the accretion and evolution of the upper oceanic crust: Sr isotope evidence from ODP Hole 1256D

ODP Hole 1256D in the eastern equatorial Pacific is the first penetration of a complete section of fast spread ocean crust down to the dike-gabbro transition, and only the second borehole to sample in situ sheeted dikes after DSDP Hole 504B. Here a high spatial resolution record of whole rock and mineral strontium isotopic compositions from Site 1256 is combined with core observations and downhole wireline geophysical measurements to determine the extent of basalt-hydrothermal fluid reaction and to identify fluid pathways at different levels in the upper ocean crust.The volcanic sequence at Site 1256 is dominated by sheet and massive lava flows but the Sr isotope profile shows only limited exchange with seawater. However, the upper margins of two anomalously thick (>25 m) massive flow sequences are strongly hydrothermally altered with elevated Sr isotope ratios and appear to be conduits of lateral low-temperature off-axis fluid flow. Elsewhere in the lavas, high 87Sr/86Sr are restricted to breccia horizons. Mineralised hyaloclastic breccias in the Lava-Dike Transition are strongly altered to Mg-saponite, silica and pyrite, indicating alteration by mixed seawater and cooled hydrothermal fluids. In the Sheeted Dike Complex 87Sr/86Sr ratios are pervasively shifted towards hydrothermal fluid values (~0.705). Dike chilled margins display secondary mineral assemblages formed during both axial recharge and discharge and have higher 87Sr/86Sr than dike cores, indicating preferential fluid flow along dike margins. Localised increases in 87Sr/86Sr in the Dike-Gabbro Transition indicates the channelling of fluids along the sub-horizontal intrusive boundaries of the 25 to 50 m-thick gabbroic intrusions, with only minor increases in 87Sr/86Sr within the cores of the gabbro bodies.When compared to the pillow lava-dominated section from Hole 504B, the Sr isotope measurements from Site 1256 suggest that the extent of hydrothermal circulation in the upper ocean crust may be strongly dependent on the eruption style. Sheet and massive flow dominated lava sequences typical of fast spreading ridges may experience relatively restricted circulation, but there may be much more widespread circulation through pillow lava-dominated sections. In addition, the Hole 1256D sheeted dikes display a much greater extent of Sr-isotopic exchange compared to dikes from Hole 504B. Because seawater-derived hydrothermal fluids must transit the dikes during their evolution to black smoker-type fluids, the different Sr-isotope profiles for Holes 504B and 1256D suggest there are significant variations in mid-ocean ridge hydrothermal systems at fast and intermediate spreading ridges, which may impact geochemical cycles of elements mobilised by fluid-rock exchange at different temperatures

BAAV Transcytosis Requires an Interaction with β-1-4 Linked- Glucosamine and gp96

Cell surface carbohydrates play an important role in virus entry and intracellular trafficking. Bovine Adeno-Associated Virus (BAAV) uses plasma membrane gangliosides for transduction and infection. In addition, independent of the infectious pathway, BAAV also has the ability to pass through barrier epithelia and endothelia using a transcytosis pathway dependent upon the presence of cell surface carbohydrates. Thus, in order to better define the carbohydrate interactions that are necessary for BAAV infection or transcytosis, a glycan microarray composed of both natural and synthetic carbohydrates was probed with HA-tagged BAAV particles. This identified chitotriose, a trimer of β-1-4-linked N-acetyl glucosamine, as having an interaction with BAAV. Competition experiments showed that the BAAV interaction with this carbohydrate is not necessary for infection but is instead important in the transcytosis pathway. The β-1-4-linked N-acetyl glucosamine modification has been reported on gp96, a glycoprotein involved in the transcytosis of bacteria and toxins. Significantly, immunoprecipitation and competition experiments with an anti-gp96 antibody and a soluble form of gp96, respectively, showed this glycoprotein can also interact with BAAV to serve as a receptor for its transcytosis

Deficient inhibition in alcohol-dependence: let's consider the role of the motor system!

Impaired inhibitory control contributes to the development, maintenance, and relapse of alcohol-dependence, but the neural correlates of this deficit are still unclear. Because inhibitory control has been labeled as an executive function, most studies have focused on prefrontal areas, overlooking the contribution of more "primary" structures, such as the motor system. Yet, appropriate neural inhibition of the motor output pathway has emerged as a central aspect of healthy behavior. Here, we tested the hypothesis that this motor inhibition is altered in alcohol-dependence. Neural inhibitory measures of motor activity were obtained in 20 detoxified alcohol-dependent (AD) patients and 20 matched healthy subjects, using a standard transcranial magnetic stimulation procedure whereby motor-evoked potentials (MEPs) are elicited in a choice reaction time task. Moreover, behavioral inhibition and trait impulsivity were evaluated in all participants. Finally, the relapse status of patients was assessed 1 year after the experiment. As expected, AD patients displayed poorer behavioral inhibition and higher trait impulsivity than controls. More importantly, the MEP data revealed a considerable shortage of neural motor inhibition in AD patients. Interestingly, this neural defect was strongest in the patients who ended up relapsing during the year following the experiment. Our data suggest a strong motor component in the neural correlates of altered inhibitory control in AD patients. They also highlight an intriguing relationship with relapse and the perspective of a new biomarker to follow strategies aiming at reducing relapse in AD patients

Acquired antibody responses against Plasmodium vivax infection vary with host genotype for duffy antigen receptor for chemokines (DARC).

BACKGROUND: Polymorphism of the Duffy Antigen Receptor for Chemokines (DARC) is associated with susceptibility to and the severity of Plasmodium vivax malaria in humans. P. vivax uses DARC to invade erythrocytes. Individuals lacking DARC are 'resistant' to P. vivax erythrocytic infection. However, susceptibility to P. vivax in DARC+ individuals is reported to vary between specific DARC genotypes. We hypothesized that the natural acquisition of antibodies to P. vivax blood stages may vary with the host genotype and the level of DARC expression. Furthermore, high parasitemia has been reported to effect the acquisition of immunity against pre-erythrocytic parasites. We investigated the correlation between host DARC genotypes and the frequency and magnitude of antibodies against P. vivax erythrocytic stage antigens. METHODOLOGY/FINDINGS: We assessed the frequencies and magnitudes of antibody responses against P. vivax and P. falciparum sporozoite and erythrocytic antigens in Colombian donors from malaria-endemic regions. The frequency and level of naturally-acquired antibodies against the P. vivax erythrocytic antigens merozoite surface protein 1 (PvMSP1) and Duffy binding protein (PvDBP) varied with the host DARC genotypes. Donors with one negative allele (FY*B/FY*Bnull and FY*A/FY*Bnull) were more likely to have anti-PvMSP1 and anti-PvDBP antibodies than those with two positive alleles (FY*B/FY*B and FY*A/FY*B). The lower IgG3 and IgG1 components of the total IgG response may account for the decreased responses to P. vivax erythrocytic antigens with FY*A/FY*B and FY*B/FY*B genotypes. No such association was detected with P. falciparum erythrocytic antigens, which does not use DARC for erythrocyte invasion. CONCLUSION/SIGNIFICANCE: Individuals with higher DARC expression, which is associated with higher susceptibility to P. vivax infection, exhibited low frequencies and magnitudes of P. vivax blood-stage specific antibody responses. This may indicate that one of the primary mechanisms by which P. vivax evades host immunity is through DARC indirectly down-regulating humoral responses against erythrocytic invasion and development