Platelet aggregation studies in canine cyclic hematopoiesis

Investigation of platelet function in dogs with cyclic hematopoiesis (OH) revealed a platelet aggregation disorder. Collagen-induced aggregation of CH dog platelets was significantly below normal, although normal aggregation in response to ADP was observed. The failure to aggregate in response to collagen was not influenced by platelet size. Aggregation was particularly low on days 2, 3, 4 and 14 of the 14-day neutrophil cycle which is typical of CH dogs. The lack of response to collagen suggests a defect in the arachidonic acid pathway of platelet metabolism since platelet-generated thromboxane B2 was significantly (~70%) below control levels. Platelets from dogs heterozygous for CH demonstrated moderately depressed responses to collagen which were intermediate between the values found for CH dog platelets and normal, mixed breed dog platelets. Not only does this work indicate a platelet defect in CH dogs, but this phenomenon may be useful as a genetic marker in identification of dogs heterozygous for the CH gene

Benefits of Implementing a Daily Safety Brief at the Baystate Children’s Hospital

https://scholarlycommons.libraryinfo.bhs.org/nurs_presentations2023/1008/thumbnail.jp

Developmental Genes Targeted for Epigenetic Variation between Twin-Twin Transfusion Syndrome Children

Background: Epigenetic mechanisms are thought to be critical in mediating the role of the intrauterine environment on lifelong health and disease. Twin-twin transfusion syndrome (TTTS) is a rare condition wherein fetuses share the placenta and develop vascular anastomoses, which allow blood to flow between the fetuses. The unequal flow results in reciprocal hypo- and hypervolemia in the affected twins, striking growth differences and physiologic adaptations in response to this significant stressor. The donor twin in the TTTS syndrome can be profoundly growth restricted and there is likely a nutritional imbalance between the twins. The consequences of TTTS on fetal programming are unknown. This condition can now be effectively treated through the use of fetal laparoscopic procedures, but the potential for lifelong morbidity related to this condition during development is apparent. As this condition and the resulting uteroplacental discordance can play a role in the epigenetic process, we sought to investigate the DNA methylation profiles of childhood survivors of TTTS (n = 14). We focused on differences in both global measures and genome-wide CpG specific DNA methylation between donor and recipient children in this pilot study in order to generate hypotheses for further research. Results: We identified significant hypomethylation of the LINE1 repetitive element in the peripheral blood of donor children and subtle variation in the genome-wide profiles of CpG specific methylation most prominent at CpG sites which are targets for polycomb group repressive complexes. Conclusions: These preliminary results suggest that coordinated epigenetic alterations result from the intrauterine environment experienced by infants with TTTS and may, at least in part, be responsible for downstream health conditions experienced by individuals surviving this condition

EGF regulates survivin stability through the Raf-1/ERK pathway in insulin-secreting pancreatic β-cells

<p>Abstract</p> <p>Background</p> <p>Postnatal expansion of the pancreatic β-cell mass is required to maintain glucose homeostasis immediately after birth. This β-cell expansion is regulated by multiple growth factors, including glucose, insulin, insulin-like growth factor (IGF-1) and epidermal growth factor (EGF). These mitogens signal through several downstream pathways (AKT, ERK, STAT3, and JNK) to regulate the survival and proliferation of β-cells. Survivin, an oncofetal protein with both pro-proliferative and anti-apoptotic properties, is a known transcriptional target of both IGF-1 and EGF in cancer cells. Here, we analyzed the effects of the β-cell mitogens IGF-1 and EGF on survivin regulation in the established pancreatic β-cell model cell lines, MIN6 and INS-1 and in primary mouse islets.</p> <p>Results</p> <p>In pancreatic β-cells, treatment with glucose, insulin, or EGF increased survivin protein levels at early time points. By contrast, no significant effects on survivin were observed following IGF-1 treatment. EGF-stimulated increases in survivin protein were abrogated in the presence of downstream inhibitors of the Raf-1/MEK/ERK pathway. EGF had no significant effect on <it>survivin </it>transcription however it prolonged the half-life of the survivin protein and stabilized survivin protein levels by inhibiting surviving ubiquitination.</p> <p>Conclusions</p> <p>This study defines a novel mechanism of survivin regulation by EGF through the Raf-1/MEK/ERK pathway in pancreatic β-cells, via prolongation of survivin protein half-life and inhibition of the ubiquitin-mediated proteasomal degradation pathway. This mechanism may be important for regulating β-cell expansion after birth.</p

Feasibility and Implementation of a Daily Safety Brief at a Children’s Hospital-in-a-hospital

Holistic and Nursing Scholarship Symposium Event Postershttps://scholarlycommons.libraryinfo.bhs.org/nurs_presentations/1005/thumbnail.jp

Benefits of Implementing a Daily Safety Brief at the Baystate Children’s Hospital

Nursing Scholarship Symposium Event Posters.https://scholarlycommons.libraryinfo.bhs.org/nurs_presentations/1001/thumbnail.jp