African swine fever virus (ASFV) is highly contagious and can cause lethal disease in pigs. ASFV is primarily replicated in the cytoplasm of pig macrophages, which is oxidative and caused constant damage to ASFV genome. ASFV AP endonuclease (AsfvAP) catalyzes DNA cleavage reaction at the abasic site and is a key enzyme of ASFV base excision repair (BER) system. Although it plays an essential role in ASFV survival in host cells, the basis underlying substrate binding and cleavage by AsfvAP remains unclear. Here, we reported the structural and functional studies of AsfvAP, showing that AsfvAP adopts a novel DNA-binding mode distinct from other APs. AsfvAP possesses many unique structural features, including one narrower nucleotide-binding pocket at the active site, the C16-C20 disulfide bond-containing region, and histidine-rich loop. As indicated by our mutagenesis, in vitro binding and cleavage assays, these features are important for AsfvAP to suit the acidic and oxidative environment. Owing to their functional importance, these unique features could serve as targets for designing small molecule inhibitors that could disrupt the repair process of ASFV genome and help fight against this deadly virus in the future. © The Author(s) 2020.N1-methyladenosine (m1A) is one of the important post-transcriptional modifications in RNA and plays an important role in promoting translation or decay of m1A-methylated messenger RNA (mRNA), but the "reader" protein and the exact biological role of m1A remain to be determined. Here, we identified that nine potential m1A "reader" proteins including YTH domain family and heterogeneous nuclear ribonucleoprotein by mass spectrometry, and among them, YTH domain-containing protein 3 (YTHDF3), could bind directly to m1A-carrying RNA. Dovitinib YTHDF3 was then identified to negatively regulate invasion and migration of trophoblast. Mechanistically, we found that the m1A "reader" YTHDF3 bound to certain m1A-methylated transcripts, such as insulin-like growth factor 1 receptor (IGF1R), with the combination of iCLIP-seq (individual-nucleotide resolution ultraviolet crosslinking and immunoprecipitation high-throughput sequencing) and m1A-seq. Furthermore, YTHDF3 could promote IGF1R mRNA degradation and thus inhibit IGF1R protein expression along with its downstream matrix metallopeptidase 9 signaling pathway, consequently decreasing migration and invasion of trophoblast. Thus, we demonstrated that YTHDF3 as an m1A reader decreased invasion and migration of trophoblast by inhibiting IGF1R expression. Our study outlines a new m1A epigenetic way to regulate the trophoblast activity, which suggests a novel therapeutic target for trophoblast-associated pregnancy disorders. © The Author(s) 2020.Skin aging is driven by intrinsic and extrinsic factors impacting on skin functionality with progressive age. One factor of this multifaceted process is cellular senescence, as it has recently been identified to contribute to a declining tissue functionality in old age. In the skin, senescent cells have been found to markedly accumulate with age, and thus might impact directly on skin characteristics. Especially the switch from young, extracellular matrix-building fibroblasts to a senescence-associated secretory phenotype (SASP) could alter the microenvironment in the skin drastically and therefore promote skin aging. In order to study the influence of senescence in human skin, 3D organotypic cultures are a well-suited model system. However, only few "aged" skin- equivalent (SE) models are available, requiring complex and long-term experimental setups. Here, we adapted a previously published full-thickness SE model by seeding increasing ratios of stress-induced premature senescent versus normal fibroblasts into the collagen matrix, terming these SE "senoskin". Immunohistochemistry stainings revealed a shift in the balance between proliferation (Ki67) and differentiation (Keratin 10 and Filaggrin) of keratinocytes within our senoskin equivalents, as well as partial impairment of skin barrier function and changed surface properties. Monitoring of cytokine levels of known SASP factors confirmedly showed an upregulation in 2D cultures of senescent cells and at the time of seeding into the skin equivalent. Surprisingly, we find a blunted response of cytokines in the senoskin equivalent over time during 3D differentiation. © The Author(s) 2020.Context Seventy-five percent of incarcerated women are of reproductive age, most of whom are at-risk for unintended pregnancy. Women who are incarcerated come disproportionately from socioeconomically disadvantaged backgrounds and often lack access to desired reproductive health care. While the carceral system provides a unique opportunity to fill this gap, a better understanding of the contraceptive needs, desires, and plans of incarcerated women is needed to optimize health care provision within the carceral system. A review of current contraceptive services available to women inmates may both identify model care programs and shed light on areas for improvement. Evidence acquisition PubMed electronic database used to identify relevant articles published between January 1975 and September 2019 using a systematic review method. Results Twenty-five articles met the inclusion criteria and answered four key questions surrounding contraception in the carceral system. Most articles (48%) represented scientific research. Other publications identified by this review were expert commentaries, policy briefings, guidance and recommendations reports, and law and bioethics reviews. Conclusions Incarcerated women desire access to standard and emergency contraception from carceral health care systems. Knowledgeable family planning practitioners providing patient-centered and trauma-informed care and public health interventions linking newly released inmates to community clinics can help alleviate inmates' concerns regarding initiating desired contraception while incarcerated. © The Author(s) 2020.MIRAGE syndrome is a recently identified disorder characterized by myelodysplasia, infection, restriction of growth, adrenal hypoplasia, genital phenotypes, and enteropathy. It is caused by a gain-of-function variant in the SAMD9 gene, but there is limited knowledge regarding the genotype-phenotype correlation. We herein report a Japanese patient with MIRAGE syndrome carrying a novel de novo heterozygous missense variant in the SAMD9 gene (c.4435 G > T; p.Ala1479Ser). © The Author(s) 2020.