A New Extraction System for Extremely Low Level 14C in Meteorites.

第3回極域科学シンポジウム/第35回南極隕石シンポジウム 11月29日（木） 国立国語研究所 2階講

Developing Ultra Small-Scale Radiocarbon Sample Measurement at the University of Tokyo

From the 20th International Radiocarbon Conference held in Kona, Hawaii, USA, May 31-June 3, 2009.We have developed accelerator mass spectrometry (AMS) measurement techniques for ultra small-size samples ranging from 0.01 to 0.10 mg C with a new type of MC-SNICS ion source system. We can generate 4 times higher ion beam current intensity for ultra-small samples by optimization of graphite position in the target holder with the new ionizer geometry. CO2 gas graphitized in the newly developed vacuum line is pressed to a depth of 1.5 mm from the front of the target holder. This is much deeper than the previous position at 0.35 mm depth. We measured 12C4+ beam currents generated by small standards and ion beam currents (15-30 mu-A) from the targets in optimized position, lasting 20 min for 0.01 mg C and 65 min for 0.10 mg C. We observed that the measured 14C/12C ratios are unaffected by the difference of ion beam currents ranging from 5 to 30 mu-A, enabling measurement of ultra-small samples with high precision. Examination of the background samples revealed 1.1 mu-g of modern and 1 mu-g of dead carbon contaminations during target graphite preparation. We make corrections for the contamination from both the modern and background components. Reduction of the contamination is necessary for conducting more accurate measurement.The Radiocarbon archives are made available by Radiocarbon and the University of Arizona Libraries. Contact [email protected] for further information.Migrated from OJS platform February 202

Modern and possible paleotsunami deposits in Samenoura, Sanriku Coast, and their relation to tsunami source mechanisms

Samenoura is situated in the bay head of a small inlet on the Pacific coast of Oshika Peninsula, one of the nearest places to the epicenter of the 2011 Tohoku-oki Earthquake. According to the Joint Survey Group, wave heights were measured at more than 20 m near the coastline. This area was severely damaged as a result of both co-seismic subsidence and tsunami inundation. We carried out field surveys of the Tohoku-oki and paleotsunami deposits at Samenoura in March, May and October 2013. Sandy deposits laid down by the Tohoku-oki tsunami were up to 20 cm thick at locations with an elevation greater than 10 m, and were several cm thick within the forest higher up. The tsunami deposit also contained numerous shell fragments and foraminifera. Although some possible sources of the tsunami deposits can be attributed to narrow sandy beaches near the study area, the deposition of such a thick sandy deposit is more or less enigmatic, considering the steep Ria-type coastal topography.Using a gouge auger and geoslicer, we found at least two sand layers intercalated within muddy sediments. A volcanic ash layer, which corresponds to the AD 915 Towada-a tephra, was also identified from a horizon between these sand layers. The underlying sand layer was most probably laid down by the 869 Jogan earthquake tsunami, one of the large-scale events known to have affected the region. Previous studies of the Jogan tsunami have proposed several possible source models that involve an interplate thrust earthquake. Given that the local bathymetry and topography of Samenoura Bay may be sensitive to the waveform of a large-scale tsunami, paleotsunami deposits found from this area may be the key to determining the source mechanisms of events on the Sanriku Coast.In this presentation, the possible correlation of the sandy deposits with known paleotsunami events based on detailed radiocarbon dating is discussed. The hydrodynamic character and processes of tsunami sediment erosion and deposition in Samenoura Bay are analyzed using numerical modeling of both interplate and outer-rise earthquake scenarios.Copyright on Japan Geoscience Union Meeting, 2014

The undatables : Quantifying uncertainty in a highly expanded Late Glacial-Holocene sediment sequence recovered from the deepest Baltic Sea basin-IODP Site M0063

Laminated, organic-rich silts and clays with high dissolved gas content characterize sediments at IODP Site M0063 in the Landsort Deep, which at 459 m is the deepest basin in the Baltic Sea. Cores recovered from Hole M0063A experienced significant expansion as gas was released during the recovery process, resulting in high sediment loss. Therefore, during operations at subsequent holes, penetration was reduced to 2 m per 3.3 m core, permitting expansion into 1.3 m of initially empty liner. Fully filled liners were recovered from Holes B through E, indicating that the length of recovered intervals exceeded the penetrated distance by a factor of > 1.5. A typical down-core logarithmic trend in gamma density profiles, with anomalously low-density values within the upper similar to 1 m of each core, suggests that expansion primarily occurred in this upper interval. Thus, we suggest that a simple linear correction is inappropriate. This interpretation is supported by anisotropy of magnetic susceptibility data that indicate vertical stretching in the upper similar to 1.5 m of expanded cores. Based on the mean gamma density profiles of cores from Holes M0063C and D, we obtain an expansion function that is used to adjust the depth of each core to conform to its known penetration. The variance in these profiles allows for quantification of uncertainty in the adjusted depth scale. Using a number of bulk C-14 dates, we explore how the presence of multiple carbon source pathways leads to poorly constrained radiocarbon reservoir age variability that significantly affects age and sedimentation rate calculations.Peer reviewe

Identification of the Microsporidian Encephalitozoon cuniculi as a New Target of the IFNγ-Inducible IRG Resistance System

The IRG system of IFNγ-inducible GTPases constitutes a powerful resistance mechanism in mice against Toxoplasma gondii and two Chlamydia strains but not against many other bacteria and protozoa. Why only T. gondii and Chlamydia? We hypothesized that unusual features of the entry mechanisms and intracellular replicative niches of these two organisms, neither of which resembles a phagosome, might hint at a common principle. We examined another unicellular parasitic organism of mammals, member of an early-diverging group of Fungi, that bypasses the phagocytic mechanism when it enters the host cell: the microsporidian Encephalitozoon cuniculi. Consistent with the known susceptibility of IFNγ-deficient mice to E. cuniculi infection, we found that IFNγ treatment suppresses meront development and spore formation in mouse fibroblasts in vitro, and that this effect is mediated by IRG proteins. The process resembles that previously described in T. gondii and Chlamydia resistance. Effector (GKS subfamily) IRG proteins accumulate at the parasitophorous vacuole of E. cuniculi and the meronts are eliminated. The suppression of E. cuniculi growth by IFNγ is completely reversed in cells lacking regulatory (GMS subfamily) IRG proteins, cells that effectively lack all IRG function. In addition IFNγ-induced cells infected with E. cuniculi die by necrosis as previously shown for IFNγ-induced cells resisting T. gondii infection. Thus the IRG resistance system provides cell-autonomous immunity to specific parasites from three kingdoms of life: protozoa, bacteria and fungi. The phylogenetic divergence of the three organisms whose vacuoles are now known to be involved in IRG-mediated immunity and the non-phagosomal character of the vacuoles themselves strongly suggests that the IRG system is triggered not by the presence of specific parasite components but rather by absence of specific host components on the vacuolar membrane.Grants from the Deutsche Forschungsgemeinschaft: SFB635, 670, 680, SPP1399

IFN-γ-Inducible Irga6 Mediates Host Resistance against Chlamydia trachomatis via Autophagy

Chlamydial infection of the host cell induces Gamma interferon (IFNγ), a central immunoprotector for humans and mice. The primary defense against Chlamydia infection in the mouse involves the IFNγ-inducible family of IRG proteins; however, the precise mechanisms mediating the pathogen's elimination are unknown. In this study, we identify Irga6 as an important resistance factor against C. trachomatis, but not C. muridarum, infection in IFNγ-stimulated mouse embryonic fibroblasts (MEFs). We show that Irga6, Irgd, Irgm2 and Irgm3 accumulate at bacterial inclusions in MEFs upon stimulation with IFNγ, whereas Irgb6 colocalized in the presence or absence of the cytokine. This accumulation triggers a rerouting of bacterial inclusions to autophagosomes that subsequently fuse to lysosomes for elimination. Autophagy-deficient Atg5−/− MEFs and lysosomal acidification impaired cells surrender to infection. Irgm2, Irgm3 and Irgd still localize to inclusions in IFNγ-induced Atg5−/− cells, but Irga6 localization is disrupted indicating its pivotal role in pathogen resistance. Irga6-deficient (Irga6−/−) MEFs, in which chlamydial growth is enhanced, do not respond to IFNγ even though Irgb6, Irgd, Irgm2 and Irgm3 still localize to inclusions. Taken together, we identify Irga6 as a necessary factor in conferring host resistance by remodelling a classically nonfusogenic intracellular pathogen to stimulate fusion with autophagosomes, thereby rerouting the intruder to the lysosomal compartment for destruction

Adhesion Molecules Associated with Female Genital Tract Infection

Altres ajuts: Marie Curie Career Integration Grant i una beca Fundació Dexeus Salut de la DonaEfforts to develop vaccines that can elicit mucosal immune responses in the female genital tract against sexually transmitted infections have been hampered by an inability to measure immune responses in these tissues. The differential expression of adhesion molecules is known to confer site-dependent homing of circulating effector T cells to mucosal tissues. Specific homing molecules have been defined that can be measured in blood as surrogate markers of local immunity (e.g. α4β7 for gut). Here we analyzed the expression pattern of adhesion molecules by circulating effector T cells following mucosal infection of the female genital tract in mice and during a symptomatic episode of vaginosis in women. While CCR2, CCR5, CXCR6 and CD11c were preferentially expressed in a mouse model of Chlamydia infection, only CCR5 and CD11c were clearly expressed by effector T cells during bacterial vaginosis in women. Other homing molecules previously suggested as required for homing to the genital mucosa such as α4β1 and α4β7 were also differentially expressed in these patients. However, CD11c expression, an integrin chain rarely analyzed in the context of T cell immunity, was the most consistently elevated in all activated effector CD8+ T cell subsets analyzed. This molecule was also induced after systemic infection in mice, suggesting that CD11c is not exclusive of genital tract infection. Still, its increase in response to genital tract disorders may represent a novel surrogate marker of mucosal immunity in women, and warrants further exploration for diagnostic and therapeutic purposes

Compensatory T Cell Responses in IRG-Deficient Mice Prevent Sustained Chlamydia trachomatis Infections

The obligate intracellular pathogen Chlamydia trachomatis is the most common cause of bacterial sexually transmitted diseases in the United States. In women C. trachomatis can establish persistent genital infections that lead to pelvic inflammatory disease and sterility. In contrast to natural infections in humans, experimentally induced infections with C. trachomatis in mice are rapidly cleared. The cytokine interferon-γ (IFNγ) plays a critical role in the clearance of C. trachomatis infections in mice. Because IFNγ induces an antimicrobial defense system in mice but not in humans that is composed of a large family of Immunity Related GTPases (IRGs), we questioned whether mice deficient in IRG immunity would develop persistent infections with C. trachomatis as observed in human patients. We found that IRG-deficient Irgm1/m3(-/-) mice transiently develop high bacterial burden post intrauterine infection, but subsequently clear the infection more efficiently than wildtype mice. We show that the delayed but highly effective clearance of intrauterine C. trachomatis infections in Irgm1/m3(-/-) mice is dependent on an exacerbated CD4+ T cell response. These findings indicate that the absence of the predominant murine innate effector mechanism restricting C. trachomatis growth inside epithelial cells results in a compensatory adaptive immune response, which is at least in part driven by CD4+ T cells and prevents the establishment of a persistent infection in mice

Loss of the interferon-γ-inducible regulatory immunity-related GTPase (IRG), Irgm1, causes activation of effector IRG proteins on lysosomes, damaging lysosomal function and predicting the dramatic susceptibility of Irgm1-deficient mice to infection

The interferon-γ (IFN-γ)-inducible immunity-related GTPase (IRG), Irgm1, plays an essential role in restraining activation of the IRG pathogen resistance system. However, the loss of Irgm1 in mice also causes a dramatic but unexplained susceptibility phenotype upon infection with a variety of pathogens, including many not normally controlled by the IRG system. This phenotype is associated with lymphopenia, hemopoietic collapse, and death of the mouse.Deutscher Akademischer Austausch Dienst (DAAD); International Graduate School in Development Health and Disease (IGS-DHD); Deutsche For-schungsgemeinschaft (SFBs 635, 670, 680); Max-Planck-Gesellschaft (Max Planck Fellowship)