Acquisition of Noun Plurals among Early Sequential Russian-Hebrew Speaking Bilinguals: A Longitudinal Multiple Case Study

Abstract The focus of the present study was the trajectory of the acquisition of noun pluralization in Hebrew as a window into the development of inflectional morphology among early sequential Russian-Hebrew speaking bilinguals. Our participants were six early sequential bilingual children between 36 and 42 months of age at the beginning of the study, who acquired Russian (L1) at home and at preschool within a 'first language first approach' and whose age at the onset of their acquisition of Hebrew (L2) was about 3 years. We investigated both qualitative and quantitative features of noun pluralization in Hebrew (L2) acquisition in order to determine (1) whether early sequential bilingual children are delayed or accelerated in this domain; (2) whether they show similar or different patterns of errors in comparison to the L1 children; and (3) at what age sequential bilingual children acquire regular versus irregular noun plural forms compared with the L1 children. We relied on a multi-faceted longitudinal analysis of noun pluralization, examining both correct and incorrect production-in structured elicitations as well as in (semi-) spontaneous interactions. Comparing our data to those collected for Hebrew L1 speakers, the results for monolinguals and early sequential bilinguals show a striking similarity with respect to the development of pluralization. These findings suggest that the accelerated rate of ESBs' L2 pluralization mechanism provides evidence of the linguistic maturation hypothesis

Obstetric anesthesia services in Israel snapshot (OASIS) study: A 72 hour cross-sectional observational study of workforce supply and demand

BACKGROUND: We planned an observational study to assess obstetric anesthesia services nationwide. We aimed to assess the effect of the anesthesia workload/workforce ratio on quality and safety outcomes of obstetric anesthesia care. METHODS: Observers prospectively collected data from labor units over 72 h (Wednesday, Thursday and Friday). Independent variables were workload (WL) and workforce (WF). WL was assessed by the Obstetric Anesthesia Activity Index (OAAI), which is the estimated time in a 24-h period spent on epidurals and all cesarean deliveries. Workforce (WF) was assessed by the number of anesthesiologists dedicated to the labor ward per week. Dependent variables were the time until anesthesiologist arrival for epidural (quality measure) and the occurrence of general anesthesia for urgent Cesarean section, CS, (safety measure). This census included vaginal deliveries and unscheduled (but not elective) CS. RESULTS: Data on 575 deliveries are from 12 maternity units only, primarily because a major hospital chain chose not to participate; eight other hospitals lacked institutional review board approval. The epidural response rate was 94.4%; 321 of 340 parturients who requested epidural analgesia (EA) received it. Of the 19 women who requested EA but gave birth without it, 14 (77%) were due to late arrival of the anesthesiologist. Median waiting times for anesthesiologist arrival ranged from 5 to 28 min. The OAAI varied from 4.6 to 25.1 and WF ranged from 0 to 2 per shift. Request rates for EA in hospitals serving predominantly orthodox Jewish communities and in peripheral hospitals were similar to those of the entire sample. More than a fifth (13/62; 21%) of the unscheduled CS received general anesthesia, and of these almost a quarter (3/13; 23%) were attributed to delayed anesthesiologist arrival. CONCLUSIONS: Inadequate WF allocations may impair quality and safety outcomes in obstetric anesthesia services. OAAI is a better predictor of WL than delivery numbers alone, especially concerning WF shortage. To assess the quality and safety of anesthetic services to labor units nationally, observational data on workforce, workload, and clinical outcomes should be collected prospectively in all labor units in Israel

Group G Streptococcal Bacteremia in Jerusalem

Recurrent group G Steptococcus bacteremia, associated with lymphatic disorders and possibly emm stG840.0, is described

Phosphorylation of the Drosophila melanogaster RNA–Binding Protein HOW by MAPK/ERK Enhances Its Dimerization and Activity

Drosophila melanogaster Held Out Wings (HOW) is a conserved RNA–binding protein (RBP) belonging to the STAR family, whose closest mammalian ortholog Quaking (QKI) has been implicated in embryonic development and nervous system myelination. The HOW RBP modulates a variety of developmental processes by controlling mRNA levels and the splicing profile of multiple key regulatory genes; however, mechanisms regulating its activity in tissues have yet to be elucidated. Here, we link receptor tyrosine kinase (RTK) signaling to the regulation of QKI subfamily of STAR proteins, by showing that HOW undergoes phosphorylation by MAPK/ERK. Importantly, we show that this modification facilitates HOW dimerization and potentiates its ability to bind RNA and regulate its levels. Employing an antibody that specifically recognizes phosphorylated HOW, we show that HOW is phosphorylated in embryonic muscles and heart cardioblasts in vivo, thus documenting for the first time Serine/Threonine (Ser/Thr) phosphorylation of a STAR protein in the context of an intact organism. We also identify the sallimus/D-titin (sls) gene as a novel muscle target of HOW–mediated negative regulation and further show that this regulation is phosphorylation-dependent, underscoring the physiological relevance of this modification. Importantly, we demonstrate that HOW Thr phosphorylation is reduced following muscle-specific knock down of Drosophila MAPK rolled and that, correspondingly, Sls is elevated in these muscles, similarly to the HOW RNAi effect. Taken together, our results provide a coherent mechanism of differential HOW activation; MAPK/ERK-dependent phosphorylation of HOW promotes the formation of HOW dimers and thus enhances its activity in controlling mRNA levels of key muscle-specific genes. Hence, our findings bridge between MAPK/ERK signaling and RNA regulation in developing muscles

HOW(L) is phosphorylated <i>in vitro</i> and in S2R+ cells by MAPK/ERK on one or more TP sites.

<p>A. ERK2 phosphorylates HOW <i>in vitro</i>. HOW(L)^WT and HOW(L)^TTAA (phospho mutant) constructs were <i>in vitro</i> translated (using S³⁵ labeling) and incubated with activated ERK2. The reaction was resolved on an SDS gel. The left part of the panel (lanes 1–4) shows phosphorylation of the Yan (Aop) protein as a control. HOW(L)^WT protein, but not the HOW(L)^TTAA mutant (lanes 7–8) exhibits a molecular weight shift of a fraction of the protein when incubated with the kinase (lane 5) relative to HOW without the kinase (lane 6). B. HOW(L), but not HOW(S), is phosphorylated in S2R+ cells. HOW proteins were immunoprecipitated using an anti-HOW antibody and reacted with anti-pTP (top panel) and anti-HOW (middle panel) antibodies. HOW proteins in the crude extract are shown in the bottom panel. From the left: HOW(S)^WT, HOW(L)^WT and HOW(L)^TTAA. C. Treatment with the MAPKK/MEK inhibitor U0126 decreases HOW phosphorylation. HOW proteins were immunoprecipitated with an anti-HOW antibody from cells transfected with <i>how(l)^WT</i> treated (or not) with U0126, or with <i>how(l)^TTAA</i> and reacted with anti-pTP antibody (top panel) or with anti-HOW antibody (2^nd from the top). The crude extract was reacted with anti-pERK antibody (2^nd from the bottom), to confirm the extent of U0126 inhibition, and anti-Actin (bottom panel) as a loading control. C′. Quantification of the reduction of phosphorylation following treatment with U0126. For each sample, the ratio between the pTP band measurement and the total HOW band was calculated, and normalized to the HOW(L)^WT (non-treated sample) ratio. Results shown are the average of three experiments; error bars indicate SEM. Following U0126 treatment, HOW phosphorylation was reduced to 0.47±0.07 relative to non-treated cells (P = 0.0021, unpaired t-test, n = 3). D. Same as in C, except cells were treated with TPA/PMA. A representative experiment is presented. D′. Quantification of three TPA treatment experiments, in which HOW phosphorylation was increased by 1.28±0.06 (P = 0.0076, unpaired t-test, n = 3).</p