Gravitational Collapse in Turbulent Molecular Clouds. I. Gasdynamical Turbulence

Observed molecular clouds often appear to have very low star formation efficiencies and lifetimes an order of magnitude longer than their free-fall times. Their support is attributed to the random supersonic motions observed in them. We study the support of molecular clouds against gravitational collapse by supersonic, gas dynamical turbulence using direct numerical simulation. Computations with two different algorithms are compared: a particle-based, Lagrangian method (SPH), and a grid-based, Eulerian, second-order method (ZEUS). The effects of both algorithm and resolution can be studied with this method. We find that, under typical molecular cloud conditions, global collapse can indeed be prevented, but density enhancements caused by strong shocks nevertheless become gravitationally unstable and collapse into dense cores and, presumably, stars. The occurance and efficiency of local collapse decreases as the driving wave length decreases and the driving strength increases. It appears that local collapse can only be prevented entirely with unrealistically short wave length driving, but observed core formation rates can be reproduced with more realistic driving. At high collapse rates, cores are formed on short time scales in coherent structures with high efficiency, while at low collapse rates they are scattered randomly throughout the region and exhibit considerable age spread. We suggest that this naturally explains the observed distinction between isolated and clustered star formation.Comment: Minor revisions in response to referee, thirteen figures, accepted to Astrophys.

p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia

We gratefully acknowledge L. Sen-Martín, J. Alegre-Cebollada (CNIC, Madrid) and L. Carrier (University Medical Center HamburgEppendorf and DZHK, Hamburg) for the cMyBP3-C KO cardiac tissue; D. Roiz-Valle and C. López-Otín (IUOPA; Universidad de Oviedo, Oviedo) for the LmnaG609G/G609G cardiac tissue; and R. J. Davis for the MKK6 KO mice. We thank G. Giovinazzo and the CNIC Pluripotent Cell Technology Unit (CNIC, Madrid) for the hiPSCs. We thank S. Bartlett and F. Chanut (CNIC, Madrid) for English editing, and R. R. Mondragon (University of Michigan, Ann Arbor) for technical support. We are grateful to R. J. Davis (University of Massachusetts Chan Medical School, Worcester), A. Padmanabhan (University of California, San Francisco) and M. Costa and C. López-Otín (IUOPA; Universidad de Oviedo, Oviedo) for critical reading of the manuscript. We thank the staf at the CNIC Genomics and Bioinformatics Units for technical support and help with data analysis and A. C. Silva for help with figure editing and design. This work was funded by a CNIC Intramural Project Severo Ochoa (Expediente 12- 2016 IGP) to G.S. and J.J. G.S. is supported by the following projects: PMP21/00057 IMPACT-2021, funded by the Instituto de Salud Carlos III (ISCIII), and PDC2021-121147-I00 and PID2019-104399RB-I00, funded by MCIN/AEI/10.13039/501100011033—all funded by the European Union (FEDER/FSE); ‘Una manera de hacer Europa’/‘El FSE invierte en tu futuro’/Next Generation EU and co-funded by the European Union/Plan de Recuperación, Transformación y Resiliencia (PRTR). R.R.B. is a fellow of the FPU Program (FPU17/03847). B.G.T. was a fellow of the FPI Severo Ochoa CNIC Program (SVP‐2013‐067639) and an American Heart Association Postdoctoral Fellow (18POST34080175). The following grants provided additional funding: Instituto de Salud Carlos III, PDC2021-121147-I00 Convocatoria: Proyectos Prueba de Concepto 2021 Ministerio de Ciencia e Innovación and PID2022-138525OB-I00 Ministerio de Ciencia e Innovación; US National Heart, Lung, and Blood Institute (R01 grant HL122352); Fondos FEDER, Madrid, Spain, and Fundación Bancaria ‘La Caixa (project HR19/52160013) to J.J.; American Heart Association Postdoctoral Fellowship 14POST17820005 to D.P.B.; and MICINN PGC2018-097019-B-I00, ISCIII-SGEFI/ERDF (PRB3-IPT17/0019, ProteoRed), the Fundació Marató TV3 (grant 122/C/2015) and ‘la Caixa’ Banking Foundation (project code HR17- 00247) to J.V. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN) and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S, funded by MICIN/AEI/10.13039/501100011033).S

Multi-technical approach for the characterization of polychrome decorative surfaces at Spanish Mission Churches in Nueva Vizcaya (Chihuahua, Mexico)

An interdisciplinary and multi-institutional group of science and art conservation specialists has provided new insight into the painting materials used in the polychrome walls and wooden ceilings in four seventeenth century Spanish colonial churches of Nueva Vizcaya (Chihuahua, Mexico). A multi-analytical study of the decorative surfaces was performed in situ using spectroscopic approaches (XRF, FORS), False Colour Infrared Reflectography–IRFC, as well as micro sampling (ATR-FTIR, LM, GC/MS). A survey of natural resources and study (ATR-FTIR, LM) was carried out to elucidate the natural occurrence of a select number of materials in the surrounding areas of the churches. The present paper presents a multi-analytical study and characterization of green, red-orange and black colour pigments and binders selected from the decorative surfaces. The aim of this study is to highlight relationships between local materials and those from the original polychrome ceilings, in order to understand the material and technological influences that converged in the Spanish colonial architecture of northern Mexico

MPK6, sphinganine and the \u3ci\u3eLCB2a\u3c/i\u3e gene from serine palmitoyltransferase are required in the signaling pathway that mediates cell death induced by long chain bases in \u3ci\u3eArabidopsis\u3c/i\u3e

• Long chain bases (LCBs) are sphingolipid intermediates acting as second messengers in programmed cell death (PCD) in plants. Most of the molecular and cellular features of this signaling function remain unknown. • We induced PCD conditions in Arabidopsis thaliana seedlings and analyzed LCB accumulation kinetics, cell ultrastructure and phenotypes in serine palmitoyltransferase (spt), mitogen-activated protein kinase (mpk), mitogenactivated protein phosphatase (mkp1) and lcb-hydroxylase (sbh) mutants. • The lcb2a-1 mutant was unable to mount an effective PCD in response to fumonisin B1 (FB1), revealing that the LCB2a gene is essential for the induction of PCD. The accumulation kinetics of LCBs in wild-type (WT) and lcb2a-1 plants and reconstitution experiments with sphinganine indicated that this LCB was primarily responsible for PCD elicitation. The resistance of the null mpk6 mutant to manifest PCD on FB1 and sphinganine addition and the failure to show resistance on pathogen infection and MPK6 activation by FB1 and LCBs indicated that MPK6 mediates PCD downstream of LCBs. • This work describes MPK6 as a novel transducer in the pathway leading to LCBinduced PCD in Arabidopsis, and reveals that sphinganine and the LCB2a gene are required in a PCD process that operates as one of the more effective strategies used as defense against pathogens in plants

Dengue illness impacts daily human mobility patterns in Iquitos, Peru

Background Human mobility plays a central role in shaping pathogen transmission by generating spatial and/or individual variability in potential pathogen-transmitting contacts. Recent research has shown that symptomatic infection can influence human mobility and pathogen transmission dynamics. Better understanding the complex relationship between symptom severity, infectiousness, and human mobility requires quantification of movement patterns throughout infectiousness. For dengue virus (DENV), human infectiousness peaks 0–2 days after symptom onset, making it paramount to understand human movement patterns from the beginning of illness. Methodology and principal findings Through community-based febrile surveillance and RT-PCR assays, we identified a cohort of DENV+ residents of the city of Iquitos, Peru (n = 63). Using retrospective interviews, we measured the movements of these individuals when healthy and during each day of symptomatic illness. The most dramatic changes in mobility occurred during the first three days after symptom onset; individuals visited significantly fewer locations (Wilcoxon test, p = 0.017) and spent significantly more time at home (Wilcoxon test, p = 0.005), compared to when healthy. By 7–9 days after symptom onset, mobility measures had returned to healthy levels. Throughout an individual’s symptomatic period, the day of illness and their subjective sense of well-being were the most significant predictors for the number of locations and houses they visited. Conclusions/Significance Our study is one of the first to collect and analyze human mobility data at a daily scale during symptomatic infection. Accounting for the observed changes in human mobility throughout illness will improve understanding of the impact of disease on DENV transmission dynamics and the interpretation of public health-based surveillance data

The impact of dengue illness on social distancing and caregiving behavior

Background Human mobility among residential locations can drive dengue virus (DENV) transmission dynamics. Recently, it was shown that individuals with symptomatic DENV infection exhibit significant changes in their mobility patterns, spending more time at home during illness. This change in mobility is predicted to increase the risk of acquiring infection for those living with or visiting the ill individual. It has yet to be considered, however, whether social contacts are also changing their mobility, either by socially distancing themselves from the infectious individual or increasing contact to help care for them. Social, or physical, distancing and caregiving could have diverse yet important impacts on DENV transmission dynamics; therefore, it is necessary to better understand the nature and frequency of these behaviors including their effect on mobility. Methodology and principal findings Through community-based febrile illness surveillance and RT-PCR infection confirmation, 67 DENV positive (DENV+) residents were identified in the city of Iquitos, Peru. Using retrospective interviews, data were collected on visitors and home-based care received during the illness. While 15% of participants lost visitors during their illness, 22% gained visitors; overall, 32% of all individuals (particularly females) received visitors while symptomatic. Caregiving was common (90%), particularly caring by housemates (91%) and caring for children (98%). Twenty-eight percent of caregivers changed their behavior enough to have their work (and, likely, mobility patterns) affected. This was significantly more likely when caring for individuals with low “health-related quality of well-being” during illness (Fisher’s Exact, p = 0.01). Conclusions/Significance Our study demonstrates that social contacts of individuals with dengue modify their patterns of visitation and caregiving. The observed mobility changes could impact a susceptible individual’s exposure to virus or a presymptomatic/clinically inapparent individual’s contribution to onward transmission. Accounting for changes in social contact mobility is imperative in order to get a more accurate understanding of DENV transmission

Highlights from the Pierre Auger Observatory

The Pierre Auger Observatory is the world's largest cosmic ray observatory. Our current exposure reaches nearly 40,000 km$^2$ str and provides us with an unprecedented quality data set. The performance and stability of the detectors and their enhancements are described. Data analyses have led to a number of major breakthroughs. Among these we discuss the energy spectrum and the searches for large-scale anisotropies. We present analyses of our X$_{max}$ data and show how it can be interpreted in terms of mass composition. We also describe some new analyses that extract mass sensitive parameters from the 100% duty cycle SD data. A coherent interpretation of all these recent results opens new directions. The consequences regarding the cosmic ray composition and the properties of UHECR sources are briefly discussed.Comment: 9 pages, 12 figures, talk given at the 33rd International Cosmic Ray Conference, Rio de Janeiro 201

IFN-γ signaling, with the synergistic contribution of TNF-α, mediates cell specific microglial and astroglial activation in experimental models of Parkinson's disease

To through light on the mechanisms underlying the stimulation and persistence of glial cell activation in Parkinsonism, we investigate the function of IFN-γ and TNF-α in experimental models of Parkinson's disease and analyze their relation with local glial cell activation. It was found that IFN-γ and TNF-α remained higher over the years in the serum and CNS of chronic Parkinsonian macaques than in untreated animals, accompanied by sustained glial activation (microglia and astroglia) in the substantia nigra pars compacta. Importantly, Parkinsonian monkeys showed persistent and increasing levels of IFN-γR signaling in both microglial and astroglial cells. In addition, experiments performed in IFN-γ and TNF-α KO mice treated with MPTP revealed that, even before dopaminergic cell death can be observed, the presence of IFN-γ and TNF-α is crucial for microglial and astroglial activation, and, together, they have an important synergistic role. Both cytokines were necessary for the full level of activation to be attained in both microglial and astroglial cells. These results demonstrate that IFN-γ signaling, together with the contribution of TNF-α, have a critical and cell-specific role in stimulating and maintaining glial cell activation in Parkinsonism

Anisotropy and chemical composition of ultra-high energy cosmic rays using arrival directions measured by the Pierre Auger Observatory

The Pierre Auger Collaboration has reported evidence for anisotropy in the distribution of arrival directions of the cosmic rays with energies $E>E_{th}=5.5\times 10^{19}$ eV. These show a correlation with the distribution of nearby extragalactic objects, including an apparent excess around the direction of Centaurus A. If the particles responsible for these excesses at $E>E_{th}$ are heavy nuclei with charge $Z$, the proton component of the sources should lead to excesses in the same regions at energies $E/Z$. We here report the lack of anisotropies in these directions at energies above $E_{th}/Z$ (for illustrative values of $Z=6,\ 13,\ 26$). If the anisotropies above $E_{th}$ are due to nuclei with charge $Z$, and under reasonable assumptions about the acceleration process, these observations imply stringent constraints on the allowed proton fraction at the lower energies

p38γ and p38δ regulate postnatal cardiac metabolism through glycogen synthase 1

During the first weeks of postnatal heart development, cardiomyocytes undergo a major adaptive metabolic shift from glycolytic energy production to fatty acid oxidation. This metabolic change is contemporaneous to the up-regulation and activation of the p38γ and p38δ stress-activated protein kinases in the heart. We demonstrate that p38γ/δ contribute to the early postnatal cardiac metabolic switch through inhibitory phosphorylation of glycogen synthase 1 (GYS1) and glycogen metabolism inactivation. Premature induction of p38γ/δ activation in cardiomyocytes of newborn mice results in an early GYS1 phosphorylation and inhibition of cardiac glycogen production, triggering an early metabolic shift that induces a deficit in cardiomyocyte fuel supply, leading to whole-body metabolic deregulation and maladaptive cardiac pathogenesis. Notably, the adverse effects of forced premature cardiac p38γ/δ activation in neonate mice are prevented by maternal diet supplementation of fatty acids during pregnancy and lactation. These results suggest that diet interventions have a potential for treating human cardiac genetic diseases that affect heart metabolism.G.S. is a YIP EMBO member. B.G.T. was a fellow of the FPI Severo Ochoa CNIC program (SVP-2013-067639) and currently is funded by the AHA-CHF (AHA award number: 818798). V.M.R. is a FPI fellow (BES-2014-069332) and A.M.S. is a fellow of the FPI Severo Ochoa CNIC program (BES-2016-077635). This work was funded by the following grants: to G.S.: funding from the EFSD/Lilly European Diabetes Research Programme Dr Sabio, from Spanish Ministry of Science, Innovation and Universities (MINECO-FEDER SAF2016-79126-R and PID2019-104399RB-I00), Comunidad de Madrid (IMMUNOTHERCAN-CM S2010/BMD-2326 and B2017/BMD-3733) and Fundación Jesús Serra; to P.A.: Ayudas para apoyar grupos de investigación del sistema Universitario Vasco (IT971-16 to P.A.), MCIU/AEI/FEDER, funding from Spanish Ministry of Science, Innovation and Universities (RTI2018-095134-B-100); Excellence Network Grant from MICIU/AEI (SAF2016-81975-REDT and 2018-PN188) to PA and GS; to J.V.: funding from Spanish Ministry of Science, Innovation and Universities (PGC2018-097019-B-I00), the Instituto de Salud Carlos III (Fondo de Investigación Sanitaria grant PRB3 (PT17/0019/0003- ISCIII-SGEFI / ERDF, ProteoRed), and “la Caixa” Banking Foundation (project code HR17-00247); to J.P.B.: funding from Spanish Ministry of Science, Innovation and Universities (PID2019-105699RB-I00, RED2018‐102576‐T) and Escalera de Excelencia (CLU-2017-03); to J.A.E.: funding from Spanish Ministry of Science, Innovation and Universities MINECO (RED2018-102576-T, RTI2018-099357-B-I00), CIBERFES (CB16/10/00282), and HFSP (RGP0016/2018). RAP (XPC/BBV1602 and MIN/RYC1102). The CNIC is supported by the Ministry of Science, Innovation and Universities and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript