Interdisciplinary team work is a complex process in which different types of staff work together to share expertise, knowledge, and skills to impact on patient care. Despite increasing emphasis on interdisciplinary team work over the past decade, in particular the growth of interdisciplinary education [1], there is little evidence as to the most effective way of delivering interdisciplinary team work [2]. This difficulty is compounded by the multifactorial nature of team work, which comprises the skill mix, setting of care, service organisation, individual relationships and management structures.
The systematic review, reported and published in full in the main study report [31], first considered quantitative studies; in particular randomised controlled trials (RCTs) published and unpublished between 1994 and 2009, that evaluated the process and outcomes of different interprofessional staffing models. Reference lists associated with the identified reports and articles were also searched for additional studies. Results were limited to English language articles in recognition of the importance of cultural factors in team work, and issues relating to differences in terminology (for example, multi-, inter-, trans- and cross- disciplinary working). A total of 153 studies, including 11 systematic reviews or meta-analysis, were reviewed and analysed; however, only 101 were usable based on the supporting level of contextual detail. Data on team effectiveness was extracted along with details on team processes, coordination, and leadership; all elements identified as important in the earlier concept analysis of the interdisciplinary team [18].
X Factor 241 Cbr Download Sites
Previous studies have shown that heterochronic miRNAs regulate a number of targets, including hbl-1, lin-14, and lin-28 [10]. HBL-1 is a zinc-finger transcription factor that critically mediates embryogenesis [11], and that controls developmental timing during post-embryonic development [9]. LIN-14 is a novel class of transcription factor [12] that is initially expressed at high levels in hypodermal blast cells in newly hatched L1 animals but at lower levels by the L2 stage [13]. LIN-28 is a conserved RNA-binding protein that controls the maturation of let-7 miRNA [5, 14,15,16]. Hypomorphic and null alleles of lin-14 and hbl-1 cause an increase whereas lin-28 mutants cause a decrease in the overall number of seam cells [9, 17, 18].
In addition to heterochronic miRNAs and their targets, seam cell division is also regulated by the divergent WNT asymmetry pathway, whose components include the β-catenins WRM-1 and SYS-1, the NEMO-like kinase (NLK) LIT-1, and the T-cell factor/lymphoid enhancer factor (TCF/LEF) POP-1 [18, 19]. Removal of POP-1 activity causes seam cells to divide symmetrically, and thereby leads to an increase in their number. Conversely, since LIT-1 normally forms a complex with WRM-1 to phosphorylate and thus stimulate POP-1 export from the nucleus, disrupting WRM-1 and/or LIT-1 activity reduces the number of seam cells [19]. Similarly, the ratio of nuclear POP-1/SYS-1 activity affects the fate of daughter cells, such that those with lower POP-1 (and hence comparatively higher SYS-1) levels retain their seam cell fate, whereas those with higher POP-1 (and hence comparatively lower SYS-1) levels differentiate [20,21,22,23]. Genetic studies have also shown that WNT asymmetry pathway components interact with heterochronic genes to control seam cell development [17, 18].
We induced RNAi-mediated silencing to examine interactions between pry-1 and WNT asymmetry pathway components during seam cell development. The fates of seam cell daughters are specified by the nuclear levels of POP-1 that are high in the anterior cell (hypodermal fate) and low in the posterior cell (seam cell fate) [19, 32] (Fig. 5a). The results of our experiments revealed that knockdowns of wrm-1 or lit-1 suppresses the pry-1(mu38) seam cell phenotype (Fig. 5b), likely because PRY-1 promotes asymmetric division by negatively regulating both of these factors in anterior daughter cells (Fig. 5a). This is consistent with PRY-1 being localized to the anterior cortex of dividing seam cells [23]. A similar genetic interaction between pry-1, wrm-1, and lit-1 was previously reported to occur during the asymmetric division of embryonic EMS cells [33]. 2ff7e9595c
Comments