Paediatric teams in front of childhood obesity: A qualitative study within the STOP project.

INTRODUCTION: Understanding the underlying factors that influence the approach to overweight and obesity in children is basic to best support families searching a solution to this important public health problem. OBJECTIVE: To assess attitudes and feelings of paediatric staff in addressing overweight and childhood obesity to parents, exploring perceived barriers and facilitators, for an effective care. PARTICIPANTS AND METHOD: Qualitative study by means of individual semi-structured questionnaires of paediatric staff (paediatricians and paediatrician nurses; n = 57; 68% female) of primary health care centres and hospitals in Mallorca. Thematic analysis was done. RESULTS: Three themes emerged from the data: "Parents' attitude in childhood obesity" (sub-themes "The conscience of parents", "The parents ask for help"), "Paediatric staff and childhood obesity" (sub-themes "Approaching to the problem: The interview with parents", "Looking together for the solution"), and "System barriers" (sub-themes "Improving teamwork and health policy", "Family participation in addressing childhood obesity"). CONCLUSIONS: Paediatric staffs know how to treat childhood obesity, but demand training on motivation. Effectivity on therapy of childhood obesity will be obtained after parents/carers recognize the problem and establish a trustful relationship with paediatric staff. The health system is still a barrier to the activity of paediatric personnel.

Human CD22 Inhibits Murine B Cell Receptor Activation in a Human CD22 Transgenic Mouse Model.

CD22, a sialic acid-binding Ig-type lectin (Siglec) family member, is an inhibitory coreceptor of the BCR with established roles in health and disease. The restricted expression pattern of CD22 on B cells and most B cell lymphomas has made CD22 a therapeutic target for B cell-mediated diseases. Models to better understand how in vivo targeting of CD22 translates to human disease are needed. In this article, we report the development of a transgenic mouse expressing human CD22 (hCD22) in B cells and assess its ability to functionally substitute for murine CD22 (mCD22) for regulation of BCR signaling, Ab responses, homing, and tolerance. Expression of hCD22 on transgenic murine B cells is comparable to expression on human primary B cells, and it colocalizes with mCD22 on the cell surface. Murine B cells expressing only hCD22 have identical calcium (Ca2+) flux responses to anti-IgM as mCD22-expressing wild-type B cells. Furthermore, hCD22 transgenic mice on an mCD22-/- background have restored levels of marginal zone B cells and Ab responses compared with deficiencies observed in CD22-/- mice. Consistent with these observations, hCD22 transgenic mice develop normal humoral responses in a peanut allergy oral sensitization model. Homing of B cells to Peyer's patches was partially rescued by expression of hCD22 compared with CD22-/- B cells, although not to wild-type levels. Notably, Siglec-engaging antigenic liposomes formulated with an hCD22 ligand were shown to prevent B cell activation, increase cell death, and induce tolerance in vivo. This hCD22 transgenic mouse will be a valuable model for investigating the function of hCD22 and preclinical studies targeting hCD22.