Childhood immunization appointment reminders and recalls: strengths, weaknesses and opportunities to increase vaccine coverage.

OBJECTIVES: Childhood immunization coverage has been shown to be greatly impacted by parental forgetfulness regarding immunizations and appointments. Evidence supports the use of reminders and recalls to overcome this barrier, which remind parents about upcoming immunization appointments and inform them once their child is overdue for an immunization. In this study, we sought to identify reminder/recall strategies used throughout a large Canadian province and determine the perceived strengths, weaknesses and areas of improvement of existing strategies. STUDY DESIGN AND METHODS: An environmental scan was performed in 2018 in two phases: (1) interviews with public health leaders from the five zones of Alberta and (2) an online survey of public health centres across the province. Data analysis occurred in 2018 and 2019. RESULTS: Commonly reported strengths of reminders and recalls included their ability to increase appointment attendance and remind parents about immunizations, respectively. A major identified weakness was their time-consuming/resource-intensive nature. Many participants believed reminder/recalls could be improved by modernizing delivery methods. Educational information or strategies to overcome language barriers were rarely incorporated into reminder/recall systems. CONCLUSIONS: There was support for incorporating text messaging and automation into reminder/recall systems while encouraging continued exploration of novel reminder/recall delivery methods. Tailoring reminder/recalls to the needs and preferences of target populations can maximize the effectiveness of these systems. This includes modernizing methods of delivery, addressing language barriers, providing educational information, and allotting some degree of flexibility to local level management of reminder/recalls.

Characterization of human larynx carcinoma cell lines HLaC'79 and HLaC'82: a common origin but diverged malignancies.

As part of a study on the relationship of tumour phenotype and behaviour, we have characterized two head and neck squamous cell carcinoma cell lines, derived from human laryngeal carcinomas and designated HLaC'79 and HLaC'82. Cytogenetic analysis revealed that HLaC'79 and HLaC'82 shared 10 major chromosome rearrangements indicating that the cell lines had a common origin. In the extremely complex chromosomal patterns, abnormalities were found in chromosomes 1, 3 (surplus 3q) and 5 (i(5p) x 2). Both cell lines displayed constitutive expression of vimentin and were capable of anchorage-independent growth in agarose gels. However, in spite of their common origin specific differences were found. Cells of HLaC'79 were spindle shaped and formed tumours in athymic mice. In contrast, cells of HLaC'82 had a compact morphology, contained less vimentin, were more contact inhibited and were not tumorigenic. These results indicate that malignant transformation in HLaC'82 was partially reversed.

Adhesion properties, intermediate filaments and malignant behaviour of head and neck squamous cell carcinoma cells in vitro.

This study compared phenotype and behaviour of seven head and neck squamous cell carcinoma (HNSCC) cell lines and normal epithelial cells. Indications were found that in HNSCC cells: 1) loss of the cell-cell adhesion molecule E-cadherin was correlated with loss of epithelioid cell morphology but not with loss of cell-cell cohesion; 2) reduced expression of the cell-cell adhesion molecule desmoglein was unrelated to cell shape or motility; 3) high expression of the cell-substrate adhesion molecule alpha 6 beta 4, a receptor for laminin, corresponded with epithelioid colony formation while, in our adhesion assay, low expression of alpha 6 beta 4 paradoxically coincided with an increased adhesion to laminin; 4) presence of vimentin intermediate filaments coincided with loss of anchorage dependency. We propose that by simultaneous downregulation of E-cadherin, replacement of alpha 6 beta 4 by an aberrant laminin receptor and co-expression of vimentin a malignant phenotype arises of spindle-shaped, motile, anchorage-independent HNSCC cells with enhanced laminin-binding capacity.