Dynamic spin response of a strongly interacting Fermi gas

We present an experimental investigation of the dynamic spin response of a strongly interacting Fermi gas using Bragg spectroscopy. By varying the detuning of the Bragg lasers, we show that it is possible to measure the response in the spin and density channels separately. At low Bragg energies, the spin response is suppressed due to pairing, whereas the density response is enhanced. These experiments provide the first independent measurements of the spin-parallel and spin-antiparallel dynamic and static structure factors and open the way to a complete study of the structure factors at any momentum. At high momentum the spin-antiparallel dynamic structure factor displays a universal high frequency tail, proportional to $\omega^{-5/2}$, where $\hbar \omega$ is the probe energy.Comment: Replaced with final versio

Cellular aspect ratio and cell division mechanics underlie the patterning of cell progeny in diverse mammalian epithelia.

Cell division is essential to expand, shape, and replenish epithelia. In the adult small intestine, cells from a common progenitor intermix with other lineages, whereas cell progeny in many other epithelia form contiguous patches. The mechanisms that generate these distinct patterns of progeny are poorly understood. Using light sheet and confocal imaging of intestinal organoids, we show that lineages intersperse during cytokinesis, when elongated interphase cells insert between apically displaced daughters. Reducing the cellular aspect ratio to minimize the height difference between interphase and mitotic cells disrupts interspersion, producing contiguous patches. Cellular aspect ratio is similarly a key parameter for division-coupled interspersion in the early mouse embryo, suggesting that this physical mechanism for patterning progeny may pertain to many mammalian epithelia. Our results reveal that the process of cytokinesis in elongated mammalian epithelia allows lineages to intermix and that cellular aspect ratio is a critical modulator of the progeny pattern

Comparative Genomics of Two Sequential <i>Candida glabrata</i> Clinical Isolates.

&lt;i&gt;Candida glabrata&lt;/i&gt; is an important fungal pathogen which develops rapid antifungal resistance in treated patients. It is known that azole treatments lead to antifungal resistance in this fungal species and that multidrug efflux transporters are involved in this process. Specific mutations in the transcriptional regulator &lt;i&gt;PDR1&lt;/i&gt; result in upregulation of the transporters. In addition, we showed that the &lt;i&gt;PDR1&lt;/i&gt; mutations can contribute to enhance virulence in animal models. In this study, we were interested to compare genomes of two specific &lt;i&gt;C. glabrata&lt;/i&gt; -related isolates, one of which was azole susceptible (DSY562) while the other was azole resistant (DSY565). DSY565 contained a &lt;i&gt;PDR1&lt;/i&gt; mutation (L280F) and was isolated after a time-lapse of 50 d of azole therapy. We expected that genome comparisons between both isolates could reveal additional mutations reflecting host adaptation or even additional resistance mechanisms. The PacBio technology used here yielded 14 major contigs (sizes 0.18-1.6 Mb) and mitochondrial genomes from both DSY562 and DSY565 isolates that were highly similar to each other. Comparisons of the clinical genomes with the published CBS138 genome indicated important genome rearrangements, but not between the clinical strains. Among the unique features, several retrotransposons were identified in the genomes of the investigated clinical isolates. DSY562 and DSY565 each contained a large set of adhesin-like genes (101 and 107, respectively), which exceed by far the number of reported adhesins (63) in the CBS138 genome. Comparison between DSY562 and DSY565 yielded 17 nonsynonymous SNPs (among which the was the expected &lt;i&gt;PDR1&lt;/i&gt; mutation) as well as small size indels in coding regions (11) but mainly in adhesin-like genes. The genomes contained a DNA mismatch repair allele of &lt;i&gt;MSH2&lt;/i&gt; known to be involved in the so-called hyper-mutator phenotype of this yeast species and the number of accumulated mutations between both clinical isolates is consistent with the presence of a &lt;i&gt;MSH2&lt;/i&gt; defect. In conclusion, this study is the first to compare genomes of &lt;i&gt;C. glabrata&lt;/i&gt; sequential clinical isolates using the PacBio technology as an approach. The genomes of these isolates taken in the same patient at two different time points exhibited limited variations, even if submitted to the host pressure

Molecular requirements for actin-based lamella formation in Drosophila S2 cells

Cell migration occurs through the protrusion of the actin-enriched lamella. Here, we investigated the effects of RNAi depletion of ∼90 proteins implicated in actin function on lamella formation in Drosophila S2 cells. Similar to in vitro reconstitution studies of actin-based Listeria movement, we find that lamellae formation requires a relatively small set of proteins that participate in actin nucleation (Arp2/3 and SCAR), barbed end capping (capping protein), filament depolymerization (cofilin and Aip1), and actin monomer binding (profilin and cyclase-associated protein). Lamellae are initiated by parallel and partially redundant signaling pathways involving Rac GTPases and the adaptor protein Nck, which stimulate SCAR, an Arp2/3 activator. We also show that RNAi of three proteins (kette, Abi, and Sra-1) known to copurify with and inhibit SCAR in vitro leads to SCAR degradation, revealing a novel function of this protein complex in SCAR stability. Our results have identified an essential set of proteins involved in actin dynamics during lamella formation in Drosophila S2 cells

Interventions for improving clinical outcomes and health-related quality-of-life for people living with skeletal dysplasias: an evidence gap map

Purpose: Skeletal dysplasias are rare genetic disorders that are characterized by abnormal development of bone and cartilage. There are multiple medical and non-medical treatments for specific symptoms of skeletal dysplasias e.g. pain, as well as corrective surgical procedures to improve physical functioning. The aim of this paper was to develop an evidence-gap map of treatment options for skeletal dysplasias, and their impact on patient outcomes. Methods: We conducted an evidence-gap map to identify the available evidence on the impact of treatment options on people with skeletal dysplasias on clinical outcomes (such as increase in height), and dimensions of health-related quality of life. A structured search strategy was applied to five databases. Two reviewers independently assessed articles for inclusion in two stages: titles and abstracts (stage 1), and full text of studies retained at stage 2. Results: 58 studies fulfilled our inclusion criteria. The included studies covered 12 types of skeletal dysplasia that are non-lethal with severe limb deformities that could result in significant pain and numerous orthopaedic interventions. Most studies reported on the effect of surgical interventions (n = 40, 69%), followed by the effect of treatments on dimensions of health quality-of-life (n = 4, 6.8%) and psychosocial functioning (n = 8, 13.8%). Conclusion: Most studies reported on clinical outcomes from surgery for people living with Achondroplasia. Consequently, there are gaps in the literature on the full range of treatment options (including no active treatment), outcomes and the lived experience of people living with other skeletal dysplasias. More research is warranted to examine the impact of treatments on health-related quality-of-life of people living with skeletal dysplasias, including their relatives to enable them to make preference- and valued based decisions about treatment