Publications by authors named "Eric Sleeper"

Objectives: To assess the frequency and recognition of abnormal nutritional status and elevated admitting blood pressure (BP) in hospitalized children.

Study Design: From children aged 3 to 18 years who were hospitalized during 4 months of 2005 (n = 1143), a stratified sample of paper-based medical records were reviewed for demographics, anthropometric and BP measurements and interpretations, care related to nutrition and BP, and discharge diagnoses. Records of 317 of 337 (94%) selected patients were reviewed, and data from 277 of these patients (records with weight and height documented) were analyzed. US references were applied to assign body mass index and BP percentiles. Data were weighted to account for sampling.

Results: A total of 51% of subjects were Medicaid/self-pay, with a median age of 9.1 years; and 20% of subjects were obese (14% overweight, 58% healthy weight, 8% underweight). Body mass index was plotted/calculated for 35% of subjects. Six percent of subjects had BP >99th percentile + 5 mm Hg (18% BP 95th to < or =99th percentile + 5 mm Hg). A nutrition referral was documented for 61% of subjects who were underweight and 39% of subjects who were obese. BP concerns were documented for 26% of subjects with BP >99th percentile + 5 mm Hg.

Conclusions: Many pediatric inpatients had abnormal nutritional status or elevated BP. Systems to improve interpretation of these measures, which are commonly obtained in pediatric hospital settings, are needed.

Despite an increasing interest in neural stem cell (NSC) research, relatively little is known about the biochemical regulation of cell death pathways in these cells. We demonstrate here, using murine-derived multipotent C17.2 NSCs, that cells undergo mitochondria-mediated cell death in response to apoptotic stimuli such as oxidative stress induced by 2,3-dimethoxy-1,4-naphthoquinone (DMNQ). In particular, treated cells exhibited apoptotic features, including Bax translocation, cytochrome c release, activation of caspase-9 and -3, chromatin condensation and DNA fragmentation. Although C17.2 cells possess the Fas receptor and express procaspase-8, agonistic Fas mAb treatment failed to induce apoptosis. Fas treatment activated the extracellular signal-regulated protein kinase (ERK) pathway, which may have an antiapoptotic as well as a growth stimulating role. Combined, our findings indicate that while NSCs are sensitive to cytotoxic stimuli that involve an engagement of mitochondria, Fas treatment does not induce death and may have an alternative role.