Nurturing the Human Dimension in Digital and Medical Spaces Through Pedagogy of Care - a Case of Creative Enquiry.

The COVID-19 pandemic ushered in digital learning experiences to front and centre of medical education in disruptive ways. As the pandemic subsides students and educators sigh in relief, longing to move away from the loneliness and disconnection and back to the norms of face-to-face learning and consulting. In the field of medical education however, the need for digital education has exponentially increased over the decade with strong evidence for future growth. We face the pressure of increasing student numbers on clinical placement and some students now desire or even need hybrid options for the flexibility of time, place, and pace. There is persistent criticism that digital education lacks human connection. This paper argues, however, that it is possible and vital to humanise the virtual learning experience, though particular attention needs to be given to digital pedagogy and relational aspects of learning and teaching. Drawing on Noddings' pedagogies of care and her theoretical model, we unpack one case-study of a medical education elective course that transitioned online during the pandemic. The aim of this paper is to engage medical educators with the pedagogy of care and relational pedagogy literature, which are currently almost absent from the medical education literature, as applied to the digital education realm. Core themes include modelling care and connection, enabling dialogue, inviting student engagement and practice in caring for each other and supporting the deeper work of being present themselves and confirming each other. Limitations and implications for future research will also be explored.

Systemic treatment of anti-CD4CD25 T cell monoclonal antibody exacerbates sialoadenitis in submandibular glands during the early life in lupus-prone female NZB x NZWF mice.

BACKGROUND: The maintenance mechanisms of peripheral tolerance by CD4(+)CD25(+) T cells before the development of sialoadenitis in secondary Sjögren's syndrome (sSS) are not well understood. The aim of the present study is to examine the effect of reduction of CD4(+)CD25(+) T cells on the development of sialoadenitis during the early life in female NZB x NZWF(1) (B/WF(1)) mice, a model for human sSS. METHODS: Female B/WF(1) mice at 3 days after birth were treated with either anti-mouse CD4(+)CD25(+) T cells rat IgG(1) monoclonal antibody (mAb) or Rat IgG(1)(control). At 25 weeks of age, autoantibodies against nucleus and cytoplasm of ductal epithelial and myoepithelial cells, and histpathology of submandibular glands were examined in the mAb-treated and control groups. Also the development of anti-Ro/SS-A antibodies was examined until 25 weeks of age in both groups. RESULTS: The mAb-treated group showed severe lesions with the development of autoantibodies compared to the control group. CONCLUSIONS: The present results suggest that peripheral CD4(+)CD25(+) T cells may, at least in part, contribute to down-regulate the development of sialoadenitis in submandibular glands of lupus-prone female B/WF(1) mice during their early life.

Ultrastructure of myoepithelial cells as a target cell in sialoadenitis of submandibular glands of lupus-prone female NZBxNZWF1 mice.

The changes of myoepithelial cells of sialoadenitis in submandibular glands in lupus-prone female NZB x NZWF1 (B/WF1) mice, a model for human secondary Sjögren's syndrome (sSS), were examined ultrastructurally. Inflammatory foci consisting of mainly lymphoid cells (lymphocytes and plasma cells) in the interlobular interstitium began to develop from 18 weeks of ages, and those were found within acini from the age of 25 weeks. These were paralleled with the production of anti-double-stranded deoxyribonucleic acid and anti-Ro/SS-A antibodies with age. Infiltrated lymphoid cells consisted of CD4+ T cells and Ig+ (or IgG2a+) cells. Electron microscopy revealed destruction of myoepithelial cells with lysis of basement membranes contacted with either lymphocytes or plasma cells. These led to the destruction (degeneration and necrosis) of the epithelium in striated and intercalated ducts and acinar epithelium. Further destruction of those cells occurred by the invasion of lymphocytes into the epithelial layers. Small numbers of apoptotic myoepithelium and duct epithelium from the age of 25 to 36 weeks and an increase of those cells in survived mice at 44 weeks of age were observed. The present study suggests that the myoepithelium may be one of the target cells and that the destruction of myoepithelial cells by infiltrated lymphoid cells may precede the destruction of acinar ducts and epithelium in sialoadenitis in sSS.

Elimination of CD4(+)CD25(+) T cell accelerates the development of glomerulonephritis during the preactive phase in autoimmune-prone female NZB x NZW F mice.

The role of CD4(+)CD25+ T cell in glomerulonephritis (GN) development during the preactive phase was investigated in autoimmune-prone female NZB x NZW F1 (B/WF1) mice. The administration of anti-mouse CD25+ T-cell monoclonal antibody (PC61.5) 3 days after birth induced the development of GN with an increase in IgG2a antinuclear antibody, productions of IL-6 and IFN-gamma, whereas TGF-beta1 production decreased, compared to untreated control mice. The present study results suggest that CD4(+)CD25+ T cells may, at least in part, downregulate the development of GN during the preactive phase in B/WF1 mice.