Barriers and enablers for dental care among dentate home-based older New Zealanders who receive living support.

OBJECTIVE: To explore the structural, social and individual barriers to, and facilitators for, accessing dental services and remaining dentate, among a purposive sample of dentate home-based older people who receive living support (HBOPWRLS). BACKGROUND: Studies on the oral health of older people have largely been quantitative, while fewer studies have specifically explored the dental service utilisation patterns of dentate HBOPWRLS, especially in New Zealand. MATERIALS AND METHOD: In early 2019, semi-structured interviews were conducted with a purposive sample of 40 dentate HBOPWRLS from one region of New Zealand. A parallel coding and thematic analysis of the interview data was conducted, based on the constant comparative method. RESULTS: Barriers to accessing dental services included the cost of dental treatment, negotiating transport issues, social isolation, traumatic childhood dental experiences, lack of role modelling for good oral health and hygiene, self-ageing and drawing upon discourses of older people, and health conditions impacting on mobility and access to oral health care. Facilitators for accessing dental services included having a support network, parental role models, healthy diet, knowledge of the link between oral and general health, dental clearances for surgery, not wanting dentures and having a strong dislike of them, and agency to resist dentists' advice to have a full extraction. CONCLUSION: The expense of dental care is a major barrier to HBOPWRLS accessing dental services at a life stage of reduced income. Strategies for boosting dental service access among socially isolated older people need further exploration.

Some orthodontists' experiences of volunteering for a community orthodontic initiative.

INTRODUCTION: In society, dental professionals, including orthodontists, are often viewed as being solely motivated by money. Nevertheless, numerous orthodontists volunteer for community initiatives where they provide free or heavily subsidized treatment for underserved populations. This study explores the motivations of a group of New Zealand orthodontists who volunteered for one of these initiatives, Wish For A Smile (WFAS), as well as the high and low points of this work. METHODS: Qualitative telephone interviews were conducted with 11 orthodontists who volunteer for WFAS. An inductive data analysis of the data was undertaken and a descriptive qualitative method was chosen. RESULTS: Most participants volunteered for WFAS because they desired to give back to the community. High points of their voluntary work were seeing patients' self-esteem, happiness, and future life chances increase as a result of treatment. Low points included seeing the challenging life circumstances of some WFAS patients and treating some adolescents who appeared not to qualify. A number of participants said WFAS patients were more grateful and cooperative than fee-paying patients, whereas others reported the opposite. CONCLUSIONS: There are many reasons why orthodontists volunteer for orthodontic community initiatives, although many may be motivated by a sense of social responsibility to give back to the community.

Leuko-polymersomes.

Polymersomes are vesicles whose membranes are comprised of self-assembled amphiphilic block co-polymers. Synthetic control of block co-polymer chemistry provides an advantageous diversity of polymersome functions, ranging from tunable materials strength, superior encaspulation of hydrophobic and hydrophilic drugs and optical dyes, and facile functionalization. We have exploited polymersome tunability to make leuko-polymersomes: polymersomes with the adhesive properties of leukocytes. By functionalizing the terminal groups on the outer shell of the vesicle with biotin, we have used modular avidin-biotin chemistry to attach adhesion ligands that mimic the two critical adhesion pathways that leukocytes utilize to achieve adhesion in the fast fluid flow of blood vessels--selectins and integrins. We demonstrate that adhesion is specific and is supported at hydrodynamic flow rates at which leukocytes adhere. We envision the use of such particles for monitoring or treating inflammation, cancer and cardiovascular disease.

Neutrophil traction stresses are concentrated in the uropod during migration.

We find that in contrast to strongly adherent, slow moving cells such as fibroblasts, neutrophils exert contractile stresses largely in the rear of the cell (uropod) relative to the direction of motion. Rather than the leading edge pulling the cell, the rear is both anchoring the cell and the area in which the contractile forces are concentrated. These tractions rapidly reorient themselves during a turn, on a timescale of seconds to minutes, and their repositioning precedes and sets the direction of motion during a turn. We find the total average root mean-squared traction force to be 28+/-10 nN during chemokinesis, and 67+/-10 nN during chemotaxis. We hypothesize that the contraction forces in the back of the neutrophil not only break uropodial adhesive contacts but also create a rearward squeezing contractility, as seen in amoeboid or amoeboidlike cells and the formation of blebs in cells, causing a flow of intracellular material to the fluidlike lamellipod. Our findings suggest an entirely new model of neutrophil locomotion.

Interplay between shear stress and adhesion on neutrophil locomotion.

Leukocyte locomotion over the lumen of inflamed endothelial cells is a critical step, following firm adhesion, in the inflammatory response. Once firmly adherent, the cell will spread and will either undergo diapedesis through individual vascular endothelial cells or will migrate to tight junctions before extravasating to the site of injury or infection. Little is known about the mechanisms of neutrophil spreading or locomotion, or how motility is affected by the physical environment. We performed a systematic study to investigate the effect of the type of adhesive ligand and shear stress on neutrophil motility by employing a parallel-plate flow chamber with reconstituted protein surfaces of E-selectin, E-selectin/PECAM-1, and E-selectin/ICAM-1. We find that the level and type of adhesive ligand and the shear rate are intertwined in affecting several metrics of migration, such as the migration velocity, random motility, index of migration, and the percentage of cells moving in the direction of flow. On surfaces with high levels of PECAM-1, there is a near doubling in random motility at a shear rate of 180 s(-1) compared to the motility in the absence of flow. On surfaces with ICAM-1, neutrophil random motility exhibits a weaker response to shear rate, decreasing slightly when shear rate is increased from static conditions to 180 s(-1), and is only slightly higher at 1000 s(-1) than in the absence of flow. The random motility increases with increasing surface concentrations of E-selectin and PECAM-1 under static and flow conditions. Our findings illustrate that the endothelium may regulate neutrophil migration in postcapillary venules through the presentation of various adhesion ligands at sites of inflammation.

I-domain of lymphocyte function-associated antigen-1 mediates rolling of polystyrene particles on ICAM-1 under flow.

In their active state, beta(2)-integrins, such as LFA-1, mediate the firm arrest of leukocytes by binding intercellular adhesion molecules (ICAMs) expressed on endothelium. Although the primary function of LFA-1 is assumed to be the ability to mediate firm adhesion, recent work has shown that LFA-1 can contribute to cell tethering and rolling under hydrodynamic flow, a role previously largely attributed to the selectins. The inserted (I) domain of LFA-1 has recently been crystallized in the wild-type (wt) and locked-open conformations and has been shown to, respectively, support rolling and firm adhesion under flow when expressed in alpha(L)beta(2) heterodimers or as isolated domains on cells. Here, we report results from cell-free adhesion assays where wt I-domain-coated polystyrene particles were allowed to interact with ICAM-1-coated surfaces in shear flow. We show that wt I-domain can independently mediate the capture of particles from flow and support their rolling on ICAM-1 surfaces in a manner similar to how carbohydrate-selectin interactions mediate rolling. Adhesion is specific and blocked by appropriate antibodies. We also show that the rolling velocity of I-domain-coated particles depends on the wall shear stress in flow chamber, I-domain site density on microsphere surfaces, and ICAM-1 site density on substrate surfaces. Furthermore, we show that rolling is less sensitive to wall shear stress and ICAM-1 substrate density at high density of I-domain on the microsphere surface. Computer simulations using adhesive dynamics can recreate bead rolling dynamics and show that the mechanochemical properties of ICAM-1-I-domain interactions are similar to those of carbohydrate-selectin interactions. Understanding the biophysics of adhesion mediated by the I-domain of LFA-1 can elucidate the complex roles this integrin plays in leukocyte adhesion in inflammation.

PSGL-1 derived from human neutrophils is a high-efficiency ligand for endothelium-expressed E-selectin under flow.

P-selectin glycoprotein ligand-1 (PSGL-1) has been proposed as an important tethering ligand for E-selectin and is expressed at a modest level on human leukocytes. Sialyl Lewis x (sLe(x))-like glycans bind to E-selectin and are expressed at a relatively high level on circulating leukocytes. It is unclear whether PSGL-1 has unique biochemical attributes that contribute to its role as an E-selectin ligand. To probe this issue, we conjugated microspheres with either sLe(x) or PSGL-1 purified from myeloid cells (neutrophils and HL-60) and compared their adhesion to endothelial expressed E-selectin under defined shear conditions. We found that both sLe(x) and PSGL-1 microspheres adhere to 4 h of IL-1beta-activated human umbilical vein endothelial cells predominantly through E-selectin. Analysis of the adhesion revealed that the rate of initial tethering of the PSGL-1 microspheres to E-selectin was significantly greater than the rate of initial tethering of the sLe(x) microspheres despite the fact that the sLe(x) microspheres tested had higher ligand densities than the PSGL-1 microspheres. We also found that pretreatment of the PSGL-1 or sLe(x) microspheres with HECA-452 had no significant effect on initial tethering to E-selectin. These results support the hypotheses that 1) PSGL-1 is a high-efficiency tethering ligand for E-selectin, 2) ligand biochemistry can significantly influence initial tethering to E-selectin, and 3) PSGL-1 tethering to E-selectin can occur via non-HECA-452 reactive epitopes.