Authigenic Mineral Texture in Submarine 1979 Basalt Drill Core, Surtsey Volcano, Iceland

Micrometer-scale maps of authigenic microstructures in submarine basaltic tuff from a 1979 Surtsey volcano, Iceland, drill core acquired 15 years after eruptions terminated describe the initial alteration of oceanic basalt in a low-temperature hydrothermal system. An integrative investigative approach uses synchrotron source X-ray microdiffraction, microfluoresence, micro-computed tomography, and scanning transmission electron microscopy coupled with Raman spectroscopy to create finely resolved spatial frameworks that record a continuum of alteration in glass and olivine. Microanalytical maps of vesicular and fractured lapilli in specimens from 157.1-, 137.9-, and 102.6-m depths and borehole temperatures of 83, 93.9, and 141.3 °C measured in 1980, respectively, describe the production of nanocrystalline clay mineral, zeolites, and Al-tobermorite in diverse microenvironments. Irregular alteration fronts at 157.1-m depth resemble microchannels associated with biological activity in older basalts. By contrast, linear microstructures with little resemblance to previously described alteration features have nanocrystalline clay mineral (nontronite) and zeolite (amicite) texture. The crystallographic preferred orientation rotates around an axis parallel to the linear feature. Raman spectra indicating degraded and poorly ordered carbonaceous matter of possible biological origin are associated with nanocrystalline clay mineral in a crystallographically oriented linear microstructure in altered olivine at 102.6 m and with subcircular nanoscale cavities in altered glass at 137.9-m depth. Although evidence for biotic processes is inconclusive, the integrated analyses describe the complex organization of previously unrecognized mineral texture in very young basalt. They provide a foundational mineralogical reference for longitudinal, time-lapse characterizations of palagonitized basalt in oceanic environments

Mosquito Biodiversity Patterns Around Urban Environments in South-Central Okinawa Island, Japan

Okinawa is the largest, most urbanized, and densely populated island in the Ryukyus Archipelago, where mosquito species diversity has been thoroughly studied. However, the south-central Okinawa mosquito fauna has been relatively poorly studied. Here, we present results from a mosquito faunal survey in urban environments of Nishihara city, south-central Okinawa. Mosquitoes were sampled biweekly, from April 2007 to March 2008, at 3 different environments: a forest preserve, an animal farm, and a water reservoir. We employed 4 mosquito collection methods: 1) oviposition traps; 2) light traps; 3) sweep nets; and 4) larval surveys of tree holes, leaf axils, and artificial water containers. We collected a total of 568 adults and 10,270 larvae belonging to 6 genera and 13 species, including 6 species of medical importance: Aedes albopictus, Armigeres subalbatus, Anopheles Hyrcanus group, Culex bitaeniorhynchus, Cx. quinquefasciatus, and Cx. tritaeniorhynchus. Mosquito species composition was similar to data from previous studies in Okinawa Island. The flattening of the species accumulation curve suggests that our diversity sampling was exhaustive with light and oviposition traps, as well as the coincidence between the species richness we found in the field and estimates from the Chao2 index, a theoretical estimator of species richness based on species abundance. This study highlights the importance of combining several sampling techniques to properly characterize regional mosquito fauna and to monitor changes in the presence of mosquito species

The RING-CH ligase K5 antagonizes restriction of KSHV and HIV-1 particle release by mediating ubiquitin-dependent endosomal degradation of tetherin

Tetherin (CD317/BST2) is an interferon-induced membrane protein that inhibits the release of diverse enveloped viral particles. Several mammalian viruses have evolved countermeasures that inactivate tetherin, with the prototype being the HIV-1 Vpu protein. Here we show that the human herpesvirus Kaposi's sarcoma-associated herpesvirus (KSHV) is sensitive to tetherin restriction and its activity is counteracted by the KSHV encoded RING-CH E3 ubiquitin ligase K5. Tetherin expression in KSHV-infected cells inhibits viral particle release, as does depletion of K5 protein using RNA interference. K5 induces a species-specific downregulation of human tetherin from the cell surface followed by its endosomal degradation. We show that K5 targets a single lysine (K18) in the cytoplasmic tail of tetherin for ubiquitination, leading to relocalization of tetherin to CD63-positive endosomal compartments. Tetherin degradation is dependent on ESCRT-mediated endosomal sorting, but does not require a tyrosine-based sorting signal in the tetherin cytoplasmic tail. Importantly, we also show that the ability of K5 to substitute for Vpu in HIV-1 release is entirely dependent on K18 and the RING-CH domain of K5. By contrast, while Vpu induces ubiquitination of tetherin cytoplasmic tail lysine residues, mutation of these positions has no effect on its antagonism of tetherin function, and residual tetherin is associated with the trans-Golgi network (TGN) in Vpu-expressing cells. Taken together our results demonstrate that K5 is a mechanistically distinct viral countermeasure to tetherin-mediated restriction, and that herpesvirus particle release is sensitive to this mode of antiviral inhibition

Prevalence of self-reported finger deformations and occupational risk factors among professional cooks: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Previous studies have pointed out that the school lunch workers in Japan are suffering from work-related disorders including finger deformations. The purpose of this study was to investigate the prevalence of self-reported finger deformations and the association with job-related risk factors.</p> <p>Methods</p> <p>A cross-sectional questionnaire study of 5,719 subjects (response rate: 81%, 982 men and 4,737 women) was undertaken during September 2003 to February 2004.</p> <p>Results</p> <p>Finger deformations were found among 11.7% of the men and 35.6% of the women studied, with significant differences among sex, age and sex-age groups. For both men and women the pattern of finger deformations across the hand was similar for the right and the left hand. For women, the deformations were found in about 10% of the distal interphalangeal joints of all fingers. Based on multiple logistic regression analyses, the factors female sex, age, the number of cooked lunches per cook and cooking activities were independently associated with the prevalence of finger deformations. High prevalence odds ratios were found for those frequently carrying or using tools by hands such as delivering containers, distributing meals, preparing dishes, washing equipment, cutting and stirring foods.</p> <p>Conclusions</p> <p>Among the school lunch workers studied, women had a higher prevalence of finger deformations on all joints of both hands. Various cooking tasks were associated with the prevalence of finger deformations. The results suggest that improvements in working conditions are important for preventing work-related disorders such as finger deformations.</p

Bmi1 Confers Resistance to Oxidative Stress on Hematopoietic Stem Cells

The polycomb-group (PcG) proteins function as general regulators of stem cells. We previously reported that retrovirus-mediated overexpression of Bmi1, a gene encoding a core component of polycomb repressive complex (PRC) 1, maintained self-renewing hematopoietic stem cells (HSCs) during long-term culture. However, the effects of overexpression of Bmi1 on HSCs in vivo remained to be precisely addressed.In this study, we generated a mouse line where Bmi1 can be conditionally overexpressed under the control of the endogenous Rosa26 promoter in a hematopoietic cell-specific fashion (Tie2-Cre;R26Stop(FL)Bmi1). Although overexpression of Bmi1 did not significantly affect steady state hematopoiesis, it promoted expansion of functional HSCs during ex vivo culture and efficiently protected HSCs against loss of self-renewal capacity during serial transplantation. Overexpression of Bmi1 had no effect on DNA damage response triggered by ionizing radiation. In contrast, Tie2-Cre;R26Stop(FL)Bmi1 HSCs under oxidative stress maintained a multipotent state and generally tolerated oxidative stress better than the control. Unexpectedly, overexpression of Bmi1 had no impact on the level of intracellular reactive oxygen species (ROS).Our findings demonstrate that overexpression of Bmi1 confers resistance to stresses, particularly oxidative stress, onto HSCs. This thereby enhances their regenerative capacity and suggests that Bmi1 is located downstream of ROS signaling and negatively regulated by it

CD1d-Expressing Breast Cancer Cells Modulate NKT Cell-Mediated Antitumor Immunity in a Murine Model of Breast Cancer Metastasis

Tumor tolerance and immune suppression remain formidable obstacles to the efficacy of immunotherapies that harness the immune system to eradicate breast cancer. A novel syngeneic mouse model of breast cancer metastasis was developed in our lab to investigate mechanisms of immune regulation of breast cancer. Comparative analysis of low-metastatic vs. highly metastatic tumor cells isolated from these mice revealed several important genetic alterations related to immune control of cancer, including a significant downregulation of cd1d1 in the highly metastatic tumor cells. The cd1d1 gene in mice encodes the MHC class I-like molecule CD1d, which presents glycolipid antigens to a specialized subset of T cells known as natural killer T (NKT) cells. We hypothesize that breast cancer cells, through downregulation of CD1d and subsequent evasion of NKT-mediated antitumor immunity, gain increased potential for metastatic tumor progression.In this study, we demonstrate in a mouse model of breast cancer metastasis that tumor downregulation of CD1d inhibits iNKT-mediated antitumor immunity and promotes metastatic breast cancer progression in a CD1d-dependent manner in vitro and in vivo. Using NKT-deficient transgenic mouse models, we demonstrate important differences between type I and type II NKT cells in their ability to regulate antitumor immunity of CD1d-expressing breast tumors.The results of this study emphasize the importance of determining the CD1d expression status of the tumor when tailoring NKT-based immunotherapies for the prevention and treatment of metastatic breast cancer

SOX2 Co-Occupies Distal Enhancer Elements with Distinct POU Factors in ESCs and NPCs to Specify Cell State

SOX2 is a master regulator of both pluripotent embryonic stem cells (ESCs) and multipotent neural progenitor cells (NPCs); however, we currently lack a detailed understanding of how SOX2 controls these distinct stem cell populations. Here we show by genome-wide analysis that, while SOX2 bound to a distinct set of gene promoters in ESCs and NPCs, the majority of regions coincided with unique distal enhancer elements, important cis-acting regulators of tissue-specific gene expression programs. Notably, SOX2 bound the same consensus DNA motif in both cell types, suggesting that additional factors contribute to target specificity. We found that, similar to its association with OCT4 (Pou5f1) in ESCs, the related POU family member BRN2 (Pou3f2) co-occupied a large set of putative distal enhancers with SOX2 in NPCs. Forced expression of BRN2 in ESCs led to functional recruitment of SOX2 to a subset of NPC-specific targets and to precocious differentiation toward a neural-like state. Further analysis of the bound sequences revealed differences in the distances of SOX and POU peaks in the two cell types and identified motifs for additional transcription factors. Together, these data suggest that SOX2 controls a larger network of genes than previously anticipated through binding of distal enhancers and that transitions in POU partner factors may control tissue-specific transcriptional programs. Our findings have important implications for understanding lineage specification and somatic cell reprogramming, where SOX2, OCT4, and BRN2 have been shown to be key factors

Human cellular restriction factors that target HIV-1 replication

Recent findings have highlighted roles played by innate cellular factors in restricting intracellular viral replication. In this review, we discuss in brief the activities of apolipoprotein B mRNA-editing enzyme 3G (APOBEC3G), bone marrow stromal cell antigen 2 (BST-2), cyclophilin A, tripartite motif protein 5 alpha (Trim5α), and cellular microRNAs as examples of host restriction factors that target HIV-1. We point to countermeasures encoded by HIV-1 for moderating the potency of these cellular restriction functions