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  • 1
    Online Resource
    Online Resource
    Seminal CD38 is a pivotal regulator for fetomaternal tolerance
    Proceedings of the National Academy of Sciences ; 2015
    In:  Proceedings of the National Academy of Sciences Vol. 112, No. 5 ( 2015-02-03), p. 1559-1564
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 112, No. 5 ( 2015-02-03), p. 1559-1564
    Abstract: A successful pregnancy depends on a complex process that establishes fetomaternal tolerance. Seminal plasma is known to induce maternal immune tolerance to paternal alloantigens, but the seminal factors that regulate maternal immunity have yet to be characterized. Here, we show that a soluble form of CD38 (sCD38) released from seminal vesicles to the seminal plasma plays a crucial role in inducing tolerogenic dendritic cells and CD4 + forkhead box P3 + (Foxp3 + ) regulatory T cells (Tregs), thereby enhancing maternal immune tolerance and protecting the semiallogeneic fetus from resorption. The abortion rate in BALB/c females mated with C57BL/6 Cd38 −/− males was high compared with that in females mated with Cd38 +/+ males, and this was associated with a reduced proportion of Tregs within the CD4 + T-cell pool. Direct intravaginal injection of sCD38 to CBA/J pregnant mice at preimplantation increased Tregs and pregnancy rates in mice under abortive sonic stress from 48 h after mating until euthanasia. Thus, sCD38 released from seminal vesicles to the seminal plasma acts as an immunoregulatory factor to protect semiallogeneic fetuses from maternal immune responses.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1413493112
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2015
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  • 2
    Online Resource
    Online Resource
    Metastable hexagonal close-packed palladium hydride in liquid cell TEM
    Springer Science and Business Media LLC ; 2022
    In:  Nature Vol. 603, No. 7902 ( 2022-03-24), p. 631-636
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 603, No. 7902 ( 2022-03-24), p. 631-636
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/s41586-021-04391-5
    RVK:
    TA 1000
    RVK:
    UA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
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  • 3
    Online Resource
    Online Resource
    Targeted knockout of a chemokine-like gene increases anxiety and fear responses
    Proceedings of the National Academy of Sciences ; 2018
    In:  Proceedings of the National Academy of Sciences Vol. 115, No. 5 ( 2018-01-30)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 115, No. 5 ( 2018-01-30)
    Abstract: Emotional responses, such as fear and anxiety, are fundamentally important behavioral phenomena with strong fitness components in most animal species. Anxiety-related disorders continue to represent a major unmet medical need in our society, mostly because we still do not fully understand the mechanisms of these diseases. Animal models may speed up discovery of these mechanisms. The zebrafish is a highly promising model organism in this field. Here, we report the identification of a chemokine-like gene family, samdori ( sam ), and present functional characterization of one of its members, sam2 . We show exclusive mRNA expression of s am2 in the CNS, predominantly in the dorsal habenula, telencephalon, and hypothalamus. We found knockout (KO) zebrafish to exhibit altered anxiety-related responses in the tank, scototaxis and shoaling assays, and increased crh mRNA expression in their hypothalamus compared with wild-type fish. To investigate generalizability of our findings to mammals, we developed a Sam2 KO mouse and compared it to wild-type littermates. Consistent with zebrafish findings, homozygous KO mice exhibited signs of elevated anxiety. We also found bath application of purified SAM2 protein to increase inhibitory postsynaptic transmission onto CRH neurons of the paraventricular nucleus. Finally, we identified a human homolog of SAM2 , and were able to refine a candidate gene region encompassing SAM2 , among 21 annotated genes, which is associated with intellectual disability and autism spectrum disorder in the 12q14.1 deletion syndrome. Taken together, these results suggest a crucial and evolutionarily conserved role of sam2 in regulating mechanisms associated with anxiety.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1707663115
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2018
    detail.hit.zdb_id: 209104-5
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    SSG: 11
    SSG: 12
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  • 4
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    Online Resource
    DMNQ S‐64 Induces Apoptosis via Caspase Activation and Cyclooxygenase‐2 Inhibition in Human Nonsmall Lung Cancer Cells
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1095, No. 1 ( 2007-01), p. 7-18
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1095, No. 1 ( 2007-01), p. 7-18
    Abstract: Abstract :  Shikonin has been reported to induce apoptosis and inhibit angiogenesis in vivo and in vitro . 6‐(1‐propoxyiminoalkyl)‐5,8‐dimethoxyoxy 1,4‐naphtoquinone S‐64 (DMNQ S‐64) was synthesized as a shikonin derivative. In this article, the underlying apoptotic mechanism of DMNQ S‐64 was examined. DMNQ S‐64 exerted cytotoxicity against A549 lung carcinoma cells with IC 50 of 27.3 μM. Apoptotic bodies were observed in DMNQ S‐64‐treated A549 cells by 4′‐6‐diamidino‐2‐phenylindole (DAPI) staining assay. DMNQ S‐64 also increased sub‐G1 DNA portion in a concentration‐dependent manner by flow cytometric analysis. Western blotting has revealed that DMNQ S‐64 effectively activates the expression of caspase 8, 9, and 3, cleaves poly (ADP‐ribose) polymerase, and increases the ratio of Bax/Bcl‐2. Furthermore, cytochrome c was released in a concentration‐dependent manner by DMNQ S‐64. Similarly, DMNQ S‐64 significantly increased caspase 3 activity by enzyme‐linked immunosorbent assay (ELISA). It also significantly inhibited the level of prostaglandin E2 (PGE 2 ) by ELISA and downregulated the expression of cyclooxygenase‐2 (COX‐2) in a concentration‐dependent manner. Taken together, DMNQ S‐64 may exhibit cytotoxicity against A549 cells via caspase activation and COX‐2 inhibition.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.002
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
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    SSG: 11
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  • 5
    Online Resource
    Online Resource
    Conversion of Th2 memory cells into Foxp3 + regulatory T cells suppressing Th2-mediated allergic asthma
    Proceedings of the National Academy of Sciences ; 2010
    In:  Proceedings of the National Academy of Sciences Vol. 107, No. 19 ( 2010-05-11), p. 8742-8747
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 107, No. 19 ( 2010-05-11), p. 8742-8747
    Abstract: Genetic and epigenetic programming of T helper (Th) cell subsets during their polarization from naive Th cells establishes long-lived memory Th cells that stably maintain their lineage signatures. However, whether memory Th cells can be redifferentiated into another Th lineage is unclear. In this study, we show that Ag-specific memory Th cells were redifferentiated into Foxp3 + T cells by TGF-β when stimulated in the presence of all-trans retinoic acid and rapamycin. The “converted” Foxp3 + T cells that were derived from Th2 memory cells down-regulated GATA-3 and IRF4 and produced little IL-4, IL-5, and IL-13. Instead, the converted Foxp3 + T cells suppressed the proliferation and cytokine production of Th2 memory cells. More importantly, the converted Foxp3 + T cells efficiently accumulated in the airways and significantly suppressed Th2 memory cell-mediated airway hyperreactivity, eosinophilia, and allergen-specific IgE production. Our findings reveal the plasticity of Th2 memory cells and provide a strategy for adoptive immunotherapy for the treatment of allergic diseases.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0911756107
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2010
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    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Integrative functional genomic analysis of human brain development and neuropsychiatric risks
    American Association for the Advancement of Science (AAAS) ; 2018
    In:  Science Vol. 362, No. 6420 ( 2018-12-14)
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 362, No. 6420 ( 2018-12-14)
    Abstract: To broaden our understanding of human neurodevelopment, we profiled transcriptomic and epigenomic landscapes across brain regions and/or cell types for the entire span of prenatal and postnatal development. Integrative analysis revealed temporal, regional, sex, and cell type–specific dynamics. We observed a global transcriptomic cup-shaped pattern, characterized by a late fetal transition associated with sharply decreased regional differences and changes in cellular composition and maturation, followed by a reversal in childhood-adolescence, and accompanied by epigenomic reorganizations. Analysis of gene coexpression modules revealed relationships with epigenomic regulation and neurodevelopmental processes. Genes with genetic associations to brain-based traits and neuropsychiatric disorders (including MEF2C , SATB2 , SOX5 , TCF4 , and TSHZ3 ) converged in a small number of modules and distinct cell types, revealing insights into neurodevelopment and the genomic basis of neuropsychiatric risks.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aat7615
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2018
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    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 7
    Online Resource
    Online Resource
    Mitochondria‐Based Model for Fetal Origin of Adult Disease and Insulin Resistance
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1042, No. 1 ( 2005-05), p. 1-18
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1042, No. 1 ( 2005-05), p. 1-18
    Abstract: A bstract : Insulin resistance has been recognized as the fundamental underlying metabolic defect in the pathogenesis of metabolic syndrome, a clustering of cardiovascular risk factors such as diabetes, hypertension, dyslipidemia, and obesity. Recent studies established that mitochondrial dysfunction is involved in insulin resistance in general and fetal origin of this state in particular. Because genes are the fundamental molecular basis of inheritance—and thus the cornerstones of evolution—a model explaining insulin resistance is based at the gene level at best. Since a certain mtDNA polymorphism, 16189T 〉 C, is associated with insulin resistance, mtDNA has to be a basic component of the gene‐based model. We developed a mitochondria‐based model that explains insulin resistance in terms of quantitative and qualitative change of the mitochondrion and its DNA. This model can accommodate several important hypotheses, such as thrifty genotype hypothesis, thrifty phenotype hypothesis, fetal insulin hypothesis, contribution of metabolic imprinting by epigenetic changes, and many other features associated with insulin resistance. We will discuss mechanisms that indicate why the perturbed initial condition of mitochondrial function should lead to the reduced insulin sensitivity.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1338.001
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
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    SSG: 11
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