A systematic scoping review of health-promoting interventions for contact centre employees examined through a behaviour change wheel lens.

PURPOSE: Social determinants of health and poor working conditions contribute to excessive sickness absence and attrition in contact centre advisors. With no recent review conducted, the current scoping review is needed to investigate the volume, effectiveness, acceptability, and feasibility of health-promoting interventions for contact centre advisors. This will inform the adoption and implementation of evidence-based practice, and future research. METHODS: Searches conducted across four databases (MEDLINE, PsycInfo, CINAHL, Web of Science) and reference checking in February 2023 identified health-promoting interventions for contact centre advisors. Extracted and coded data from eligible interventions were systematically synthesised using the nine intervention functions of the Behaviour Change Wheel and behaviour change technique taxonomy. RESULTS: This scoping review identified a low number of high quality and peer-reviewed health-promoting intervention studies for contact centre advisors (28 studies since 2002). Most interventions were conducted in high-income countries with office-based advisors, predominantly using environmental restructuring and training strategies to improve health. Most interventions reported positive effectiveness results for the primary intended outcomes, which were broadly organised into: i) health behaviours (sedentary behaviour, physical activity, smoking); ii) physical health outcomes (musculoskeletal health, visual health, vocal health, sick building syndrome); iii) mental health outcomes (stress, job control, job satisfaction, wellbeing). Few interventions evaluated acceptability and feasibility. CONCLUSION: There is little evidence on the effectiveness, acceptability, and feasibility of health-promoting interventions for contact centre advisors. Evidence is especially needed in low-to-middle income countries, and for remote/hybrid, nightshift, older and disabled advisors.

Modeling the extracellular matrix in cell migration and morphogenesis: a guide for the curious biologist.

The extracellular matrix (ECM) is a highly complex structure through which biochemical and mechanical signals are transmitted. In processes of cell migration, the ECM also acts as a scaffold, providing structural support to cells as well as points of potential attachment. Although the ECM is a well-studied structure, its role in many biological processes remains difficult to investigate comprehensively due to its complexity and structural variation within an organism. In tandem with experiments, mathematical models are helpful in refining and testing hypotheses, generating predictions, and exploring conditions outside the scope of experiments. Such models can be combined and calibrated with in vivo and in vitro data to identify critical cell-ECM interactions that drive developmental and homeostatic processes, or the progression of diseases. In this review, we focus on mathematical and computational models of the ECM in processes such as cell migration including cancer metastasis, and in tissue structure and morphogenesis. By highlighting the predictive power of these models, we aim to help bridge the gap between experimental and computational approaches to studying the ECM and to provide guidance on selecting an appropriate model framework to complement corresponding experimental studies.

APC-driven actin nucleation powers collective cell dynamics in colorectal cancer cells.

Cell remodeling relies on dynamic rearrangements of cell contacts powered by the actin cytoskeleton. The tumor suppressor adenomatous polyposis coli (APC) nucleate actin filaments (F-actin) and localizes at cell junctions. Whether APC-driven actin nucleation acts in cell junction remodeling remains unknown. By combining bioimaging and genetic tools with artificial intelligence algorithms applied to colorectal cancer cell, we found that the APC-dependent actin pool contributes to sustaining levels of F-actin, as well as E-cadherin and occludin protein levels at cell junctions. Moreover, this activity preserved cell junction length and angle, as well as vertex motion and integrity. Loss of this F-actin pool led to larger cells with slow and random cell movement within a sheet. Our findings suggest that APC-driven actin nucleation promotes cell junction integrity and dynamics to facilitate collective cell remodeling and motility. This offers a new perspective to explore the relevance of APC-driven cytoskeletal function in gut morphogenesis.

Dinuclear Bis(1,2-diaryl-1,2-ethylenedithiolato)iron complexes: [FeIII2(L)4]n (n = 2-, 1-, 0, 1+).

The electronic structures of four members of the electron-transfer series [Fe2(1L)4]n (n = 2-, 1-, 0, 1+) have been elucidated in some detail by electronic absorption, IR, X-band electron paramagnetic resonance (EPR), and Mössbauer spectroscopies where (1L)(2-) represents the ligand 1,2-bis(4-tert-butylphenyl)-1,2-ethylenedithiolate(2-) and (1L*)- is its pi-radical monoanion. It is conclusively shown that all redox processes are ligand-centered and that high-valent iron(IV) is not accessible. The following complexes have been synthesized: [FeIII2(1L*)2(1L)2]0 (1), [FeIII2(2L*)2(2L)2].2CH2Cl2 (1') where (2L)(2-) is 1,2-bis(p-tolyl)-1,2-ethylenedithiolate(2-) and (2L*)- represents its pi-radical monoanion, [Cp2Co][FeIII2(1L*))(1L)3].4(toluene).0.5Et2O (2), and [Cp2Co]2[FeIII2(1L)4].2(toluene) (3). The crystal structures of 1' and 2 have been determined by single-crystal X-ray crystallography at 100 K. The ground states of complexes have been determined by temperature-dependent magnetic susceptibility measurements and EPR spectroscopy: 1' and 1 are diamagnetic (S(t) = 0); 2 (S(t) = 1/2); 3 (S(t) = 0); the monocation [Fe(III)2(1L*)3(1L)]+ possesses an S(t) = 1/2 ground state (S(t) = total spin ground state of dinuclear species). All species contain pairs of intermediate-spin ferric ions (S(Fe) = 3/2), which are strongly antiferromagnetically coupled (H = -2JS(1).S(2), where S1 = S2 = 3/2 and J = approximately -250 cm(-1)).