Dynamics of adolescents' smartphone use and well-being are positive but ephemeral

Well-being and smartphone use are thought to influence each other. However, previous studies mainly focused on one direction (looking at the effects of smartphone use on well-being) and considered between-person effects, with self-reported measures of smartphone use. By using 2548 assessments of well-being and trace data of smartphone use collected for 45 consecutive days in 82 adolescent participants (M$_{age}$ = 13.47, SD$_{age}$ = 1.62, 54% females), the present study disentangled the reciprocal and individual dynamics of well-being and smartphone use. Hierarchical Bayesian Continuous Time Dynamic Models were used to estimate how a change in frequency and duration of smartphone use predicted a later change in well-being, and vice versa. Results revealed that (i) when participants used the smartphone frequently and for a longer period, they also reported higher levels of well-being; (ii) well-being positively predicted subsequent duration of smartphone use; (iii) usage patterns and system dynamics showed heterogeneity, with many subjects showing reciprocal effects close to zero; finally, (iv) changes in well-being tend to persist longer than changes in the frequency and duration of smartphone use

Nef does not contribute to replication differences between R5 pre-AIDS and AIDS HIV-1 clones from patient ACH142

AIDS-associated, CCR5-tropic (R5) HIV-1 clones, isolated from a patient that never developed CXCR4-tropic HIV-1, replicate to a greater extent and cause greater cytopathic effects than R5 HIV-1 clones isolated before the onset of AIDS. Previously, we showed that HIV-1 Env substantially contributed to the enhanced replication of an AIDS clone. In order to determine if Nef makes a similar contribution, we cloned and phenotypically analyzed nef genes from a series of patient ACH142 derived R5 HIV-1 clones. The AIDS-associated Nef contains a series of residues found in Nef proteins from progressors [1]. In contrast to other reports [1-3], this AIDS-associated Nef downmodulated MHC-I to a greater extent and CD4 less than pre-AIDS Nef proteins. Additionally, all Nef proteins enhanced infectivity similarly in a single round of replication. Combined with our previous study, these data show that evolution of the HIV-1 env gene, but not the nef gene, within patient ACH142 significantly contributed to the enhanced replication and cytopathic effects of the AIDS-associated R5 HIV-1 clone

Imaging Flaws under Insulation Using a Squid Magnetometer

Superconducting QUantum Interference Devices (SQUID) are the most sensitive instruments known for the measurement of magnetic fields. An all niobium two-hole homemade SQUID can easily achieve sensitivities of 10-4 Ф0/√Hz (Ф0 = 2.07 × 10-15 Wb). Our complete system has a sensitivity of 50 × 10-15 Tesla √Hz, and more sophisticated systems can reach sensitivities one order of magnitude higher. Due to its high sensitivity, and to the advent of high temperature superconductivity, SQUID systems presents new opportunities for its use in nondestructive evaluation of electrically conducting and ferromagnetic structures, mainly when the area to be inspected is difficult to be reached

First determination of the one-proton induced Non-Mesonic Weak Decay width of p-shell {\Lambda}-Hypernuclei

Previous studies of proton and neutron spectra from Non-Mesonic Weak Decay of eight Lambda-Hypernuclei (A = 5-16) have been revisited. New values of the ratio of the two-nucleon and the one-proton induced decay widths, Gamma_2N/Gamma_p, are obtained from single proton spectra, Gamma_2N/Gamma_p = 0.50 +/- 0.24, and from neutron and proton coincidence spectra, Gamma_2N/Gamma_p = 0.36 +/- 0.14stat +0.05sys -0.04sys , in full agreement with previously published ones. With these values, a method is developed to extract the one-proton induced decay width in units of the free Lambda decay width, Gamma_p/Gamma_Lambda, without resorting to Intra Nuclear Cascade models but by exploiting only experimental data, under the assumption of a linear dependence on A of the Final State Interaction contribution. This is the first systematic determination ever done and it agrees within the errors with recent theoretical calculations.Comment: 16 pages, 3 figures, 2 table

A Dominant, Recombination-Defective Allele of Dmc1 Causing Male-Specific Sterility

DMC1 is a meiosis-specific homolog of bacterial RecA and eukaryotic RAD51 that can catalyze homologous DNA strand invasion and D-loop formation in vitro. DMC1-deficient mice and yeast are sterile due to defective meiotic recombination and chromosome synapsis. The authors identified a male dominant sterile allele of Dmc1, Dmc1(Mei11), encoding a missense mutation in the L2 DNA binding domain that abolishes strand invasion activity. Meiosis in male heterozygotes arrests in pachynema, characterized by incomplete chromosome synapsis and no crossing-over. Young heterozygous females have normal litter sizes despite having a decreased oocyte pool, a high incidence of meiosis I abnormalities, and susceptibility to premature ovarian failure. Dmc1(Mei11) exposes a sex difference in recombination in that a significant portion of female oocytes can compensate for DMC1 deficiency to undergo crossing-over and complete gametogenesis. Importantly, these data demonstrate that dominant alleles of meiosis genes can arise and propagate in populations, causing infertility and other reproductive consequences due to meiotic prophase I defects

HIPK2 and extrachromosomal histone H2B are separately recruited by Aurora-B for cytokinesis

Cytokinesis, the final phase of cell division, is necessary to form two distinct daughter cells with correct distribution of genomic and cytoplasmic materials. Its failure provokes genetically unstable states, such as tetraploidization and polyploidization, which can contribute to tumorigenesis. Aurora-B kinase controls multiple cytokinetic events, from chromosome condensation to abscission when the midbody is severed. We have previously shown that HIPK2, a kinase involved in DNA damage response and development, localizes at the midbody and contributes to abscission by phosphorylating extrachromosomal histone H2B at Ser14. Of relevance, HIPK2-defective cells do not phosphorylate H2B and do not successfully complete cytokinesis leading to accumulation of binucleated cells, chromosomal instability, and increased tumorigenicity. However, how HIPK2 and H2B are recruited to the midbody during cytokinesis is still unknown. Here, we show that regardless of their direct (H2B) and indirect (HIPK2) binding of chromosomal DNA, both H2B and HIPK2 localize at the midbody independently of nucleic acids. Instead, by using mitotic kinase-specific inhibitors in a spatio-temporal regulated manner, we found that Aurora-B kinase activity is required to recruit both HIPK2 and H2B to the midbody. Molecular characterization showed that Aurora-B directly binds and phosphorylates H2B at Ser32 while indirectly recruits HIPK2 through the central spindle components MgcRacGAP and PRC1. Thus, among different cytokinetic functions, Aurora-B separately recruits HIPK2 and H2B to the midbody and these activities contribute to faithful cytokinesis