The three-body recombination of a condensed Bose gas near a Feshbach resonance

In this paper, we study the three-body recombination rate of a homogeneous dilute Bose gas with a Feshbach resonance at zero temperature. The ground state and excitations of this system are obtained. The three-body recombination in the ground state is due to the break-up of an atom pair in the quantum depletion and the formation of a molecule by an atom from the broken pair and an atom from the condensate. The rate of this process is in good agreement with the experiment on $^{23}$Na in a wide range of magnetic fields.Comment: 10 pages, 2 figures, to be published in Phys. Rev.

Validation of the Italian version of the Revised Prenatal Coping Inventory (NuPCI) and its correlations with pregnancy-specific stress

Background: Pregnancy is a period of happiness but also of physical and psychological changes that can lead to distress. Functional coping strategies can reduce the pregnancy specific-stress. This study aimed to assess the psychometric properties of the Revised Prenatal Coping Inventory (NuPCI) in an Italian sample and to investigate how coping strategies were associated with pregnancy-specific stress. Methods: In this cross-sectional study, low-risk pregnant women (N = 211) were assessed with NuPCI, NuPDQ (Revised-Prenatal Distress Questionnaire), Brief-COPE (Coping Orientation to the Problems Experienced), and STAI (State-Trait Anxiety Inventory). The reliability of NuPCI was evaluated by assessing its internal consistency and factor structure (with a Confirmatory Factor Analysis, CFA). The concurrent validity between NuPCI and Brief-COPE and NuPDQ and STAI was investigated. Lastly, the relationship between NuPCI and NuPDQ was analyzed, as well as the ability of these scales to predict Apgar score at birth. Results: Internal consistency of NuPCI scales was good for Planning-Preparation (\u251C=0.84) and Spiritual-Positive Coping (\u251C=0.81) scales, acceptable for Avoidance (\u251C=0.76) scale. Moreover, the original three-factor structure was confirmed using a CFA with 29 of the 32 items (\u3c72374 = 618.06; RMSEA = 0.056, 95% confidence interval: [0.048, 0.063]); CFI = 0.920; and TLI = 0.913). Statistically significant correlations between NuPCI scales and Brief-COPE subscales ranged between r = + 0.217 and r = + 0.624; also, NuPDQ score was positively correlated with STAI scales (State scale: r = + 0.539; Trait scale: r = + 0.462). Concurrent validity was confirmed reporting that NuPDQ score was predicted by NuPCI scores (R2 = 0.423, p < 0.001), positively by Avoidance (\u3b2=+0.572) and Planning-Preparation (\u3b2=+0.215) and negatively by Spiritual-Positive Coping (\u3b2=-0.132). Finally, considering the stress, the effect of the Avoidance and Spiritual-Positive Coping scores respectively in decreasing (+ 155%) and increasing (+ 16%) the Apgar score became stronger. Conclusions: Italian NuPCI has sound psychometric properties and it is a useful coping measure. NuPDQ showed also a good validity. Our results may suggest a significant role for coping strategies, particularly in modulating the condition of the newborn at birth

A novel ubiquitin mark at the N-terminal tail of histone H2As targeted by RNF168 ubiquitin ligase

Ubiquitination of histones plays a critical role in the regulation of several processes within the nucleus, including maintenance of genome stability and transcriptional regulation. The only known ubiquitination site on histones is represented by a conserved Lys residue located at the C terminus of the protein. Here, we describe a novel ubiquitin mark at the N-terminal tail of histone H2As consisting of two Lys residues at positions 13 and 15 (K13/K15). This "bidentate" site is a target of the DNA damage response (DDR) ubiquitin ligases RNF8 and RNF168. Histone mutants lacking the K13/K15 site impair RNF168- and DNA damage-dependent ubiquitination. Conversely, inactivation of the canonical C-terminal site prevents the constitutive monoubiquitination of histone H2As but does not abolish the ubiquitination induced by RNF168. A ubiquitination-defective mutant is obtained by inactivating both the N- and the C-terminal sites, suggesting that these are unique, non-redundant acceptors of ubiquitination on histone H2As. This unprecedented result implies that RNF168 generates a qualitatively different Ub mark on chromatin

Structural Transformation of the Tandem Ubiquitin-Interacting Motifs in Ataxin-3 and Their Cooperative Interactions with Ubiquitin Chains

The ubiquitin-interacting motif (UIM) is a short peptide with dual function of binding ubiquitin (Ub) and promoting ubiquitination. We elucidated the structures and dynamics of the tandem UIMs of ataxin-3 (AT3-UIM12) both in free and Ub-bound forms. The solution structure of free AT3-UIM12 consists of two α-helices and a flexible linker, whereas that of the Ub-bound form is much more compact with hydrophobic contacts between the two helices. NMR dynamics indicates that the flexible linker becomes rigid when AT3-UIM12 binds with Ub. Isothermal titration calorimetry and NMR titration demonstrate that AT3-UIM12 binds diUb with two distinct affinities, and the linker plays a critical role in association of the two helices in diUb binding. These results provide an implication that the tandem UIM12 interacts with Ub or diUb in a cooperative manner through an allosteric effect and dynamics change of the linker region, which might be related to its recognitions with various Ub chains and ubiquitinated substrates

Ubiquitin Phosphorylation at Thr12 Modulates the DNA Damage Response. Walser et al

Modification of ubiquitin by phosphorylation is a new and largely unexplored concept in the field. Here we found that ubiquitin phosphorylation at Thr12 (pUbT12) represents a novel histone mark, H2AK15pUbT12, which regulates the DNA damage response by inhibiting 53BP1-mediated DNA repair. Detectable as chromatin modification on H2AK15ub, pUbT12 accumulates in nuclear foci and is increased upon DNA damage. Mutating Thr12 prevents the removal of ubiquitin from H2AK15ub by USP51 deubiquitinating enzyme, leading to a pronounced accumulation of ubiquitinated chromatin. Chromatin modified by pUbT12 is inaccessible to 53BP1, but permissive to the homologous recombination (HR) proteins RNF169, RAD51 and BRCA1/BARD1 complex. Phosphorylation of ubiquitin at Thr12 in the chromatin context is a new histone mark – H2AK15pUbT12 – that regulates the DDR by hampering the activity of 53BP1 at damaged chromosomes

Histone ubiquitination by the DNA damage response is required for efficient DNA replication in unperturbed S-phase. Schmid et al.

Aiming at better understanding the role of non-canonical ubiquitin-mediated events in the control of DNA replication, we made quite relevant observations on the role of key DNA damage response factors – ATM/RNF8/RNF168/53BP1 – in ensuring complete and accurate DNA replication. In a nutshell, we found that the histone ubiquitin ligase RNF168 associates with PCNA at a subset of replication factories and is required for proper DNA replication in unperturbed S phase. RNF168-deficient cells show accumulation of reversed forks and reduced fork speed, which relies on MRE11-dependent reversed fork processing. These replication phenotypes are shared with other key DDR factors, ATM, RNF8 and 53BP1, and are recapitulated in cells derived from patients affected by the RIDDLE and Ataxia Telangiectasia syndromes, caused by loss of RNF168 and ATM, respectively. RNF168-deficient cells show defects in replicating a prototype of difficult-to-replicate regions, i.e. expanded GAA repeats, previously shown to induce transient fork slowing and remodelling. These replication defects are associated with detectable chromosome abnormalities in mitosis