Love in the Time of COVID: Perceived Partner Responsiveness Buffers People from Lower Relationship Quality Associated with COVID-Related Stressors

External stressors can erode relationship quality, though little is known about what can mitigate these effects. We examined whether COVID-related stressors were associated with lower relationship quality, and whether perceived partner responsiveness—the extent to which people believe their partner understands, validates, and cares for them—buffers these effects. When people in relationships reported more COVID-related stressors they reported poorer relationship quality at the onset of the pandemic (N = 3,593 from 57 countries) and over the subsequent three months (N = 1,125). At the onset of the pandemic, most associations were buffered by perceived partner responsiveness, such that people who perceived their partners to be low in responsiveness reported poorer relationship quality when they experienced COVID-related stressors, but these associations were reduced among people who perceived their partners to be highly responsive. In some cases, these associations were buffered over the ensuing weeks of the pandemic

Gender gaps in urban mobility

Abstract Mobile phone data have been extensively used to study urban mobility. However, studies based on gender-disaggregated large-scale data are still lacking, limiting our understanding of gendered aspects of urban mobility and our ability to design policies for gender equality. Here we study urban mobility from a gendered perspective, combining commercial and open datasets for the city of Santiago, Chile. We analyze call detail records for a large cohort of anonymized mobile phone users and reveal a gender gap in mobility: women visit fewer unique locations than men, and distribute their time less equally among such locations. Mapping this mobility gap over administrative divisions, we observe that a wider gap is associated with lower income and lack of public and private transportation options. Our results uncover a complex interplay between gendered mobility patterns, socio-economic factors and urban affordances, calling for further research and providing insights for policymakers and urban planners

Some illustrative examples of permutability of fuzzy operators and fuzzy relations

Composition of fuzzy operators often appears and it is natural to ask when the order of composition does not change the result. In previous papers, we characterized permutability in the case of fuzzy consequence operators and fuzzy interior operators. We also showed the connection between the permutability of the fuzzy relations and the permutability of their induced fuzzy operators. In this work we present some examples of permutability and non permutability of fuzzy operators and fuzzy relations in order to illustrate these results

Testing the Homogeneity of Type Ia Supernovae in the Near-Infrared for Accurate Distance Estimations

Type Ia Supernovae (SNe Ia) have been extensively used as standardisable candles in the optical for several decades. However, SNe Ia have shown to be more homogeneous in the near-infrared (NIR), where the effect of dust extinction is also attenuated. In this work, we explore the possibility of using a low number of NIR observations for accurate distance estimations, given the homogeneity at these wavelengths. We found that one epoch in $J$ and/or $H$ band, plus good $gr$-band coverage, gives an accurate estimation of peak magnitudes in $J$ ($J_{max}$) and $H$ ($H_{max}$) bands. The use of a single NIR epoch only introduces an additional scatter of $\sim0.05$ mag for epochs around the time of $B$-band peak magnitude ($T_{max}$). We also tested the effect of optical cadence and signal-to-noise ratio (S/N) in the estimation of $T_{max}$ and its uncertainty propagation to the NIR peak magnitudes. Both cadence and S/N have a similar contribution, where we constrained the introduced scatter of each to $<0.02$ mag in $J_{max}$ and $<0.01$ in $H_{max}$. However, these effects are expected to be negligible, provided the data quality is comparable to that obtained for observations of nearby SNe ($z\lesssim0.1$). The effect of S/N in the NIR was tested as well. For SNe Ia at $0.08<z\lesssim0.1$, NIR observations with better S/N than that found in the CSP sample is necessary to constrain the introduced scatter to a minimum ($\lesssim0.05$ mag). These results provide confidence for our FLOWS project that aims in using SNe Ia with public ZTF optical light curves and few NIR epochs to map out the peculiar velocity field of the local Universe. This will allow us to determine the distribution of dark matter in our own supercluster, Laniakea, and test the standard cosmological model by measuring the growth rate of structures, parameterised by $fD$, and the Hubble-Lema\^itre constant, $H_0$.Comment: Accepted in A&

The Glial Regenerative Response to Central Nervous System Injury Is Enabled by Pros-Notch and Pros-NFκB Feedback

Organisms are structurally robust, as cells accommodate changes preserving structural integrity and function. The molecular mechanisms underlying structural robustness and plasticity are poorly understood, but can be investigated by probing how cells respond to injury. Injury to the CNS induces proliferation of enwrapping glia, leading to axonal re-enwrapment and partial functional recovery. This glial regenerative response is found across species, and may reflect a common underlying genetic mechanism. Here, we show that injury to the Drosophila larval CNS induces glial proliferation, and we uncover a gene network controlling this response. It consists of the mutual maintenance between the cell cycle inhibitor Prospero (Pros) and the cell cycle activators Notch and NFκB. Together they maintain glia in the brink of dividing, they enable glial proliferation following injury, and subsequently they exert negative feedback on cell division restoring cell cycle arrest. Pros also promotes glial differentiation, resolving vacuolization, enabling debris clearance and axonal enwrapment. Disruption of this gene network prevents repair and induces tumourigenesis. Using wound area measurements across genotypes and time-lapse recordings we show that when glial proliferation and glial differentiation are abolished, both the size of the glial wound and neuropile vacuolization increase. When glial proliferation and differentiation are enabled, glial wound size decreases and injury-induced apoptosis and vacuolization are prevented. The uncovered gene network promotes regeneration of the glial lesion and neuropile repair. In the unharmed animal, it is most likely a homeostatic mechanism for structural robustness. This gene network may be of relevance to mammalian glia to promote repair upon CNS injury or disease

Functional Interactions between the erupted/tsg101 Growth Suppressor Gene and the DaPKC and rbf1 Genes in Drosophila Imaginal Disc Tumors

BACKGROUND: The Drosophila gene erupted (ept) encodes the fly homolog of human Tumor Susceptibility Gene-101 (TSG101), which functions as part of the conserved ESCRT-1 complex to facilitate the movement of cargoes through the endolysosomal pathway. Loss of ept or other genes that encode components of the endocytic machinery (e.g. synatxin7/avalanche, rab5, and vps25) produces disorganized overgrowth of imaginal disc tissue. Excess cell division is postulated to be a primary cause of these 'neoplastic' phenotypes, but the autonomous effect of these mutations on cell cycle control has not been examined. PRINCIPAL FINDINGS: Here we show that disc cells lacking ept function display an altered cell cycle profile indicative of deregulated progression through the G1-to-S phase transition and express reduced levels of the tumor suppressor ortholog and G1/S inhibitor Rbf1. Genetic reductions of the Drosophila aPKC kinase (DaPKC), which has been shown to promote tumor growth in other fly tumor models, prevent both the ept neoplastic phenotype and the reduction in Rbf1 levels that otherwise occurs in clones of ept mutant cells; this effect is coincident with changes in localization of Notch and Crumbs, two proteins whose sorting is altered in ept mutant cells. The effect on Rbf1 can also be blocked by removal of the gamma-secretase component presenilin, suggesting that cleavage of a gamma-secretase target influences Rbf1 levels in ept mutant cells. Expression of exogenous rbf1 completely ablates ept mutant eye tissues but only mildly affects the development of discs composed of cells with wild type ept. CONCLUSIONS: Together, these data show that loss of ept alters nuclear cell cycle control in developing imaginal discs and identify the DaPKC, presenilin, and rbf1 genes as modifiers of molecular and cellular phenotypes that result from loss of ept

Antagonistic Regulation of Apoptosis and Differentiation by the Cut Transcription Factor Represents a Tumor-Suppressing Mechanism in Drosophila

Apoptosis is essential to prevent oncogenic transformation by triggering self-destruction of harmful cells, including those unable to differentiate. However, the mechanisms linking impaired cell differentiation and apoptosis during development and disease are not well understood. Here we report that the Drosophila transcription factor Cut coordinately controls differentiation and repression of apoptosis via direct regulation of the pro-apoptotic gene reaper. We also demonstrate that this regulatory circuit acts in diverse cell lineages to remove uncommitted precursor cells in status nascendi and thereby interferes with their potential to develop into cancer cells. Consistent with the role of Cut homologues in controlling cell death in vertebrates, we find repression of apoptosis regulators by Cux1 in human cancer cells. Finally, we present evidence that suggests that other lineage-restricted specification factors employ a similar mechanism to put the brakes on the oncogenic process

SETDB1 Is Involved in Postembryonic DNA Methylation and Gene Silencing in Drosophila

DNA methylation is fundamental for the stability and activity of genomes. Drosophila melanogaster and vertebrates establish a global DNA methylation pattern of their genome during early embryogenesis. Large-scale analyses of DNA methylation patterns have uncovered revealed that DNA methylation patterns are dynamic rather than static and change in a gene-specific fashion during development and in diseased cells. However, the factors and mechanisms involved in dynamic, postembryonic DNA methylation remain unclear. Methylation of lysine 9 in histone H3 (H3-K9) by members of the Su(var)3–9 family of histone methyltransferases (HMTs) triggers embryonic DNA methylation in Arthropods and Chordates. Here, we demonstrate that Drosophila SETDB1 (dSETDB1) can mediate DNA methylation and silencing of genes and retrotransposons. We found that dSETDB1 tri-methylates H3-K9 and binds methylated CpA motifs. Tri-methylation of H3-K9 by dSETDB1 mediates recruitment of DNA methyltransferase 2 (Dnmt2) and Su(var)205, the Drosophila ortholog of mammalian “Heterochromatin Protein 1”, to target genes for dSETDB1. By enlisting Dnmt2 and Su(var)205, dSETDB1 triggers DNA methylation and silencing of genes and retrotransposons in Drosophila cells. DSETDB1 is involved in postembryonic DNA methylation and silencing of Rt1b{} retrotransposons and the tumor suppressor gene retinoblastoma family protein 1 (Rb) in imaginal discs. Collectively, our findings implicate dSETDB1 in postembryonic DNA methylation, provide a model for silencing of the tumor suppressor Rb, and uncover a role for cell type-specific DNA methylation in Drosophila development

Highly Differentiated, Resting Gn-Specific Memory CD8+ T Cells Persist Years after Infection by Andes Hantavirus

In man, infection with South American Andes virus (ANDV) causes hantavirus cardiopulmonary syndrome (HCPS). HCPS due to ANDV is endemic in Southern Chile and much of Argentina and increasing numbers of cases are reported all over South America. A case-fatality rate of about 36% together with the absence of successful antiviral therapies urge the development of a vaccine. Although T-cell responses were shown to be critically involved in immunity to hantaviruses in mouse models, no data are available on the magnitude, specificity and longevity of ANDV-specific memory T-cell responses in patients. Using sets of overlapping peptides in IFN-γ ELISPOT assays, we herein show in 78 Chilean convalescent patients that Gn-derived epitopes were immunodominant as compared to those from the N- and Gc-proteins. Furthermore, while the relative contribution of the N-specific response significantly declined over time, Gn-specific responses remained readily detectable ex vivo up to 13 years after the acute infection. Tetramer analysis further showed that up to 16.8% of all circulating CD3+CD8+ T cells were specific for the single HLA-B*3501-restricted epitope Gn465–473 years after the acute infection. Remarkably, Gn465–473–specific cells readily secreted IFN-γ, granzyme B and TNF-α but not IL-2 upon stimulation and showed a ‘revertant’ CD45RA+CD27−CD28−CCR7−CD127− effector memory phenotype, thereby resembling a phenotype seen in other latent virus infections. Most intriguingly, titers of neutralizing antibodies increased over time in 10/17 individuals months to years after the acute infection and independently of whether they were residents of endemic areas or not. Thus, our data suggest intrinsic, latent antigenic stimulation of Gn-specific T-cells. However, it remains a major task for future studies to proof this hypothesis by determination of viral antigen in convalescent patients. Furthermore, it remains to be seen whether Gn-specific T cells are critical for viral control and protective immunity. If so, Gn-derived immunodominant epitopes could be of high value for future ANDV vaccines