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In the era of managed care, evidence-based practice, and short term, solution focused interventions, clinicians in agency based settings generally do not have the luxury of long-term contact with bereaved children. Although a substantial, yet controversial, literature argues that children cannot fully resolve early loss until adulthood, limited attention is given to how children's understandings of early loss shift as their cognitive capacities mature. This article argues the emotional experience of grief shifts: 1) as children grapple with both normative life changes and the tasks of mourning, and 2) as their cognitive and emotional development allow them to understand and question aspects of their deceased parent's life and death in new ways. This article will present an overview of longitudinal and cross-sectional research on the long-term impact of childhood grief. We then suggest the ways bereaved children and adolescents revisit and reintegrate the loss of a parent as their emotional, moral, and cognitive capacities mature and as normative ego-centrism and magical thinking decline. To demonstrate these ideas, we draw on the case of a parentally bereaved boy and his family presenting across agency-based and private-practice work over the course of 14 years. This case suggests the need for coordinated care for children who are moving beyond the initial trauma of parental loss into various stages of grief and reintegration. While the loss of a parent is permanent and unchanging, the process is not: it is part of the child's ongoing experience. (Worden, 1996, p. 16).

We report the second known case of acute angle-closure glaucoma from vitreous prolapse after neodymium:YAG (Nd:YAG) laser posterior capsulotomy in a patient with a posterior chamber intraocular lens (IOL). This is the first reported case to result in corneal decompensation that required penetrating keratoplasty. The rare complication of vitreous prolapse was unusual in this patient because of the presence of a posterior chamber IOL, a small 4.0 mm capsulotomy opening, and low (26 mJ) Nd:YAG laser energy.

Dephosphorylation by the Ca2+/calmodulin-dependent phosphatase calcineurin has been suggested as an important mechanism of Ca2+-dependent inactivation of voltage-gated Ca2+ channels. We have tested whether calcineurin plays a role in the inactivation process of two types of high-voltage-activated Ca2+ channels (L and N type) widely expressed in the central nervous system, using the immunosuppressive drug FK506 (tacrolimus), which inhibits calcineurin after binding to intracellular FK506 binding proteins. Inactivation of L- and N-type Ca2+ channels was studied in a rat pituitary tumor cell line (GH3) and chicken dorsal root ganglion neurons, respectively. With the use of antisera directed against the calcineurin subunit B and the 12,000 mol. wt binding protein, we show that both proteins are present in the cytoplasm of GH3 cells and chicken dorsal root ganglion neurons. Ionic currents through voltage-gated Ca2+ channels were investigated in the perforated-patch and whole-cell configurations of the patch-clamp technique. The inactivation of L- as well as N-type Ca2+ currents could be well fitted with a bi-exponential function. Inactivation was largely reduced when Ba2+ substituted for extracellular Ca2+ or when the Ca2+ chelator EGTA was present intracellularly, indicating that both types of Ca2+ currents exhibited Ca2+-dependent inactivation. Extracellular (perforated-patch configuration) or intracellular (whole-cell configuration) application of FK506 to inactivate calcineurin had no effect on the amplitude and time-course of Ca2+ channel current inactivation of either L- or N-type Ca2+ channels. In addition, we found that recovery from inactivation and rundown of N-type Ca2+ channel currents were not affected by FK506. Our results provide direct evidence that the calcium-dependent enzyme calcineurin is not involved in the inactivation process of the two Ca2+ channel types which are important for neuronal functioning, such as gene expression and transmitter release.

Three "brittle" diabetic patients were given constant subcutaneous insulin infusion with a portable battery-driven pump, and their plasma glucose and hemoglobin A1 were measured at frequent intervals during inpatient or outpatient periods. Mean plasma glucose decreased significantly in all inhospital patients and remained significantly less than before pump therapy in two of three as outpatients during the 8--12 wk of follow-ups; however, complete normalization of glucose metabolism was not accomplished in any. All three demonstrated a progressive decline in hemoglobin A1 levels to normal or near-normal values. The need for long-term studies of open loop infusion systems in a research setting before their adaptation to routine care is emphasized.