Decreasing Nurses' Anxiety About Pediatric End-of-Life Care With Simulation.

BACKGROUND: Caring for pediatric patients at the end of life (EOL) can lead to anxiety and burnout for critical care nurses. New graduate nurses (NGNs) often report receiving inadequate education related to EOL care and then enter the workforce with limited clinical experience in caring for patients at EOL. A quality improvement project at a pediatric academic hospital sought to determine whether a simulation-based educational program for NGNs working in critical care could reduce anxiety about EOL care. METHOD: Eight NGNs participated in a case study and simulation-based educational program that encompassed topics such as communication, symptom management, postmortem care, and support for the family at EOL. Anxiety was measured pre- and postprogram with the Spielberger State-Trait Anxiety Inventory (STAI©). RESULTS: Anxiety levels after participation in the EOL educational program decreased by 24.1% from preprogram levels. CONCLUSION: Providing NGNs in critical care with a case- and simulation-based EOL educational program can reduce anxiety levels and potentially decrease caregiver burnout. [J Contin Educ Nurs. 2023;54(12):574-580.].

Changing the Culture of Pediatric Palliative Care at the Bedside.

The benefits of palliative care services have been widely documented; however, many organizations are unable to financially support the number of professionals needed to meet the growing demand. Nurses receive minimal training in palliative care, and the resulting knowledge gap can lead to a lack of confidence when providing the essential aspects of palliative care. Recognizing the needs of patients and staff, one organization created a Palliative Care Champions Program to support and educate bedside staff. The Champions received initial and ongoing education, allowing them to function as liaisons to the Palliative Care Team while providing education and mentorship to staff. A program evaluation tool measuring Champion comfort and confidence in the provision of palliative care has shown positive results. Champions reported an increase in confidence in their ability to identify appropriate consults and mentor staff, as well as an increase in comfort in being considered an expert in palliative care. Consults to the Palliative Care service increased by 28% within the first 12 months of program implementation. The Palliative Care Champions Program framework can be easily adapted to fit the needs of other organizations.

Health-related outcomes of adverse childhood experiences in Texas, 2002.

INTRODUCTION: We assessed the prevalence of 7 childhood adversities (psychological, physical, and sexual abuse; household mental illness; household substance abuse; maternal battery; and incarceration of a household member) and the associations of those adversities with health outcomes. METHODS: Using data from 5,378 people who responded to the 2002 Texas Behavioral Risk Factor Surveillance System survey (which included questions about childhood adversity), we created 4 groups: no childhood abuse or household dysfunction, childhood abuse only, household dysfunction only, and both childhood abuse and household dysfunction. We examined groups by sociodemographic variables and the association with current smoking, obesity, and self-rated health. RESULTS: Among adult respondents, 46% reported at least 1 childhood adversity. Reports of both household dysfunction and abuse were significantly lower for college graduates than for people with less education. For those with both abuse and household dysfunction, the odds of current smoking were 1.9 and for obesity were 1.3. Compared to people without childhood adversities, people who experienced childhood adversities more frequently reported having fair or poor general health status. CONCLUSION: Childhood adversities are common among Texas adults. People with childhood adversities are more likely to be socioeconomically disadvantaged, less educated, and have difficulties maintaining employment in adulthood compared to people with no adversities. Moreover, childhood adversities appear to be associated with health problems such as current smoking, obesity, and poor or fair general health among Texas adults.

Galectin 3 induces a distinctive pattern of cytokine and chemokine production in rheumatoid synovial fibroblasts via selective signaling pathways.

OBJECTIVE: High expression of galectin 3 at sites of joint destruction in rheumatoid arthritis (RA) suggests that galectin 3 plays a role in RA pathogenesis. Previous studies have demonstrated the effects of galectins on immune cells, such as lymphocytes and macrophages. This study was undertaken to investigate the hypothesis that galectin 3 induces proinflammatory effects in RA by modulating the pattern of cytokine and chemokine production in synovial fibroblasts. METHODS: Matched samples of RA synovial and skin fibroblasts were pretreated with galectin 3 or tumor necrosis factor alpha (TNFalpha), and the levels of a panel of cytokines, chemokines, and matrix metalloproteinases (MMPs) were determined using enzyme-linked immunosorbent assays and multiplex assays. Specific inhibitors were used to dissect signaling pathways, which were confirmed by Western blotting and NF-kappaB activation assay. RESULTS: Galectin 3 induced secretion of interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor, CXCL8, and MMP-3 in both synovial and skin fibroblasts. By contrast, galectin 3-induced secretion of TNFalpha, CCL2, CCL3, and CCL5 was significantly greater in synovial fibroblasts than in skin fibroblasts. TNFalpha blockade ruled out autocrine TNFalpha-stimulated induction of chemokines. The MAPKs p38, JNK, and ERK were necessary for IL-6 production, but phosphatidylinositol 3-kinase (PI 3-kinase) was required for selective CCL5 induction. NF-kappaB activation was required for production of both IL-6 and CCL5. CONCLUSION: Our findings indicate that galectin 3 promotes proinflammatory cytokine secretion by tissue fibroblasts. However, galectin 3 induces the production of mononuclear cell-recruiting chemokines uniquely from synovial fibroblasts, but not matched skin fibroblasts, via a PI 3-kinase signaling pathway. These data provide further evidence of the role of synovial fibroblasts in regulating the pattern and persistence of the inflammatory infiltrate in RA and suggest a new and important functional consequence of the observed high expression of galectin 3 in the rheumatoid synovium.

Cardiac glucose utilization in mice with mutated alpha- and beta-thyroid hormone receptors.

Abnormal thyroid function is usually associated with altered cardiac function. Mutations in the thyroid hormone (TH)-binding region of the TH beta-receptor (TRbeta) that eliminate its TH-binding ability lead to the thyroid hormone resistance syndrome (RTH) in humans, which is characterized by high blood TH levels, goiter, hyperactivity, and tachycardia. Mice with "knock-in" mutations in the TH alpha-receptor (TRalpha) or TRbeta that remove their TH-binding ability have been developed, and those with the mutated TRbeta (TRbeta(PV/PV)) appear to provide a model for RTH. These two types of mutants show different effects on cerebral energy metabolism, e.g., negligible change in glucose utilization (CMR(Glc)) in TRbeta(PV/PV) mice and markedly reduced CMR(Glc), like that found in cretinous rats, in the mice (TRalpha(PV/+)) with the knock-in mutation of the TRalpha gene. Studies in knockout mice have indicated that the TRalpha may also influence heart rate. Because mutations in both receptor genes appear to affect some parameters of cardiac function and because cardiac functional activity and energy metabolism are linked, we measured heart glucose utilization (HMR(Glc)) in both the TRbeta(PV/PV) and TRalpha(PV/+) mutants. Compared with values in normal wild-type mice, HMR(Glc) was reduced (-77 to -95%) in TRalpha(PV/+) mutants and increased (87 to 340%) in TRbeta(PV/PV) mutants, the degree depending on the region of the heart. Thus the TRalpha(PV/+) and TRbeta(PV/PV) mutations lead, respectively, to opposite effects on energy metabolism in the heart that are consistent with the bradycardia seen in hypothyroidism and the tachycardia associated with hyperthyroidism and RTH.

A common ABCC2 promoter polymorphism is not a determinant of the risk of spina bifida.

BACKGROUND: There is compelling evidence that the risk of spina bifida, a malformation of the caudal neural tube, is associated with maternal and/or embryonic disturbances in folate/homocysteine metabolism. Hence, functional variants of genes that influence folate/homocysteine metabolism constitute a biologically plausible group of candidate risk factors for spina bifida and other neural tube defects. One such candidate is ABCC2, the gene encoding ABCC2, (a.k.a. canalicular multispecific organic anion transporter [cMOAT], multidrug resistance related protein 2 [MRP2]), a member of the ABC transporter family that effluxes natural folates and anti-folate drugs such as methotrexate. METHODS: The association between the risk of spina bifida and both the maternal and embryonic ABCC2 C(-24)T genotype was evaluated by using the transmission disequilibrium test and log-linear modeling. RESULTS: These analyses provided no evidence that the risk of spina bifida was significantly related to either the maternal or embryonic ABCC2 C(-24)T genotype. CONCLUSIONS: The results of the present analyses suggest that the C(-24)T variant of the ABCC2 gene is not a major determinant of spina bifida risk.

p53-dependent induction of serine proteases in irradiated mouse colon.

Tumor suppressor p53 induces apoptosis through the transactivation of target genes. Previous work has shown that p53-dependent gene expression changes in response to ionizing radiation are tissue specific. To determine critical p53 target genes in the colon, we irradiated wild-type and p53-null mice and examined the global p53 gene expression patterns in response to ionizing radiation. Microarray analysis using the Affymetrix MOE430A genechip showed that many of the genes that increased in a p53-dependent manner are serine proteases (e.g., elastase, trypsin) and other proteases (e.g., carboxypeptidases). Reverse transcription polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blots were used to validate microarray results on trypsin 4, carboxypeptidase A1, and elastase-2, three genes that have potential p53-binding elements. Further study of tissue specific mediators of p53-dependent responses such as serine proteases will greatly increase understanding of in vivo p53-dependent pathways within the colon triggered by ionizing radiation.

Functional activation of cerebral metabolism in mice with mutated thyroid hormone nuclear receptors.

Neonatal hypothyroidism impairs structural maturation in the brain and results in diminished electrical activities and energy metabolism. We recently found that glucose utilization (CMR(glc)) is markedly depressed throughout the brain in mice with targeted mutations in thyroid hormone receptor alpha1 (TR alpha 1), but not TR beta. Previous studies had shown that CMR(glc) increases linearly with spike frequency in the afferent pathways to synapse-rich regions in neuropil, but not in neuronal cell bodies. To determine whether the decreased CMR(glc) in mutant TR alpha 1(PV/+) mice reflected lesser synaptic density or reduced functional activity in existing synapses, we stimulated vibrissae unilaterally and measured CMR(glc) bilaterally in four stations of the whisker-to-barrel cortex pathway. Baseline CMR(glc) (unstimulated side) was markedly lower in all four stations in the TR alpha 1(PV/+) mutants than in wild-type controls, even though Northern blot and immunohistochemical examinations showed normal Na(+),K(+)-adenosine triphosphatase expression and neuronal differentiation. Despite the lower baseline CMR(glc), however, vibrissal stimulation evoked percent increases in CMR(glc) in the TR alpha 1(PV/+) mutants that were as great as those in wild-type mice. These results indicate that in the TR alpha 1(PV/+) mutants there it is a reduction in synaptic density that is responsible for the decrease in CMR(glc), but functionality of existing synapses is retained.