Integrated magneto-optical traps on a chip using silicon pyramid structures

International audienceWe have integrated magneto-optical traps (MOTs) into an atom chip by etching pyramids into a silicon wafer. These have been used to trap atoms on the chip, directly from a room temperature vapor of rubidium. This new atom trapping method provides a simple way to integrate several atom sources on the same chip. It represents a substantial advance in atom chip technology and offers new possibilities for atom chip applications such as integrated single atom or photon sources and molecules on a chip

A measure of nature connectedness for children and adults: Validation, performance, and insights

With benefits to both human well-being and pro-nature conservation behaviors, nature connectedness is emerging as an important psychological construct for a sustainable future. The growing research and applied and policy-related interests require a straightforward measure of nature connectedness that is suitable for both children and adult populations. To establish the reliability of the new Nature Connection Index (NCI) three factor analyses were conducted. One was based on a large Monitor of Engagement with the Natural Environment (MENE) dataset for adults (n = 3568) with a replication from data sets collected online (n = 553), and a third used MENE data from children (n = 351). To validate the NCI as a measure for nature connectedness an online comparison study (n = 153) included the NCI alongside other established measures. The results showed that the NCI was a reliable and valid scale that offers a short, simple alternative to other measures of nature connectedness, particularly for populations including both children and adults, measured face to face or online. The utility of the NCI is also supported, with variations associated with various pro-environmental and pro-conservation behaviors observed, and importantly the NCI also revealed changes in nature connectedness across the lifespan.N/

Characteristics of integrated magneto-optical traps for atom chips

International audienceWe investigate the operation of pyramidal magneto-optical traps (MOTs) microfabricated in silicon. Measurements of the loading and loss rates give insight into the role of the nearby surface in the MOT dynamics. Studies of the fluorescence versus laser frequency and intensity allow us to develop a simple theory of operation. The number of 85Rb atoms trapped in the pyramid is approximately L6, where L . 6 is the size in mm. This follows quite naturally from the relation between capture velocity and size and differs from the L3.6 often used to describe larger MOTs. Our results constitute substantial progress towards fully integrated atomic physics experiments and devices

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to similar to 370,000 women, we identify 389 independent signals (P <5 x 10(-8)) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain similar to 7.4% of the population variance in age at menarche, corresponding to similar to 25% of the estimated heritability. We implicate similar to 250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project–imputed genotype data in up to ~370,000 women, we identify 389 independent signals (P < 5 × 10$^{−8}$) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain ~7.4% of the population variance in age at menarche, corresponding to ~25% of the estimated heritability. We implicate ~250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

The affective quality of human-natural environment relationships.

Using a psychometric methodology the present study explored the associations between natural environments and experiential feeling states. The effects of the frequency of participants' ( N = 90) experience of the natural environment and of the location of their childhood upbringing were also investigated. Ten natural environments mapped on to an orthogonal two-component experiential structure labeled Eudemonia (ostensibly positive feelings) and Apprehension (ostensibly negative feelings). Generally, the more natural environments tended to be associated with higher eudemonia and higher apprehension, the less natural environments with both lower eudemonia and lower apprehension. In line with expectations, participants from rural childhood locations, compared with urban participants, reported less Apprehension and participants with greater experience of the natural environment, compared with participants with less experience, reported greater Eudemonia and less Apprehension . Results are discussed in relation to environmental experiences and affective psychological well-being