Baby O and the Withdrawal of Life-Sustaining Medical Treatment in the Devastated Neonate: A Review of Clinical, Ethical, and Legal Issues.

The discontinuation of life sustaining medical treatment (LSMT) in severely and permanently impaired neonates, especially artificial nutrition and hydration (ANH) is subject to uncertainty and controversy. Definitive clinical guidelines are lacking, clinical research is limited, ethical disagreement is commonplace, and while case and statutory law provide legal underpinning for the practice in defined circumstances, uncertainty in this realm likely influences clinical practice. We use the case of a neurologically devastated neonate to highlight and review these arenas, and show how, using available legal, ethical, and clinical standards and practice, the case of Baby O was resolved, and to underline the need for further research in neonatal palliative care.

Dysregulation of cell-to-cell connectivity and stomatal patterning by loss-of-function mutation in Arabidopsis chorus (glucan synthase-like 8).

Patterning of stomata, valves on the plant epidermis, requires the orchestrated actions of signaling components and cell-fate determinants. To understand the regulation of stomatal patterning, we performed a genetic screen using a background that partially lacks stomatal signaling receptors. Here, we report the isolation and characterization of chorus (chor), which confers excessive proliferation of stomatal-lineage cells mediated by SPEECHLESS (SPCH). chor breaks redundancy among three ERECTA family genes and strongly enhances stomatal patterning defects caused by loss-of-function in TOO MANY MOUTHS. chor seedlings also exhibit incomplete cytokinesis and growth defects, including disruptions in root tissue patterning and root hair cell morphogenesis. CHOR encodes a putative callose synthase, GLUCAN SYNTHASE-LIKE 8 (GSL8), that is required for callose deposition at the cell plate, cell wall and plasmodesmata. Consistently, symplastic macromolecular diffusion between epidermal cells is significantly increased in chor, and proteins that do not normally move cell-to-cell, including a fluorescent protein-tagged SPCH, diffuse to neighboring cells. Such a phenotype is not a general trait caused by cytokinesis defects. Our findings suggest that the restriction of symplastic movement might be an essential step for the proper segregation of cell-fate determinants during stomatal development.