The effect of letter writing on a long-term care resident with loneliness.

Older adults living in long term care (LTC) facilities may experience increased isolation and loneliness. This was compounded with the Coronavirus Disease 2019 (COVID-19) pandemic. Loneliness and isolation increase the risk for physical, psychological, and social decline. This case report discusses the effect of a letter writing initiative on feelings of loneliness and connection in a long-term care resident. Personalized care is the standard in the long-term care setting and letter writing between two people can contribute to personalized meaningful care as evidenced by the example provided. Further research is needed to explore social connection and loneliness and methods to combat these issues with a personalized approach for different populations within LTC facilities.

Promoting Connection in the Faith Community Through Letter Writing.

ABSTRACT: Faith community nurses can reduce loneliness and provide connection for homebound members of faith communities through promotion of letter writing. Undergraduate nursing students who were matched with members of their own faith community wrote letters to older adults for 10 weeks as a community service-learning project. Data from the UCLA Loneliness Scale pre- and post-intervention showed reduced loneliness and greater connection among recipients of the letters.

Exploring Alternate Visions of Caring in a World of Social Distancing.

Compounded by the COVID-19 pandemic, both loneliness and isolation are a growing concern for the older adult population. An intergenerational holistic exchange, Cardinals CARE (Cardinals, Adopt, Residents for Engagement), was developed as a way to connect older adults in long-term care facilities (LTCFs) with nursing students while demonstrating the meeting of student service learning outcomes. Students shared correspondence with residents in LTCFs for a 10-week period, sending mail weekly in the form of letters, artwork, crafts, an appropriate joke, or anything to encourage engagement. Jean Watson's Theory of Transpersonal Caring was used as a framework for the project. Students (n = 109) participating in the program provided interaction with 734 residents in 11 LTCFs in 3 counties. Students utilized reflective journaling to demonstrate the meeting of service learning outcomes and described the power of connection and the opportunity to provide holistic care. A result of the project was the intergenerational connectedness showcasing the reciprocal nature of the CARE project. Further research is needed to build an evidence base for the use of such interaction to promote connection and combat loneliness.

Improving nursing students' confidence in caring for persons with dementia.

BACKGROUND: Nursing students need experiences providing patient centered care for persons with dementia. METHODS: Students were provided with a voluntary opportunity to complete an online educational module that focused on caring for persons with dementia. Dementia knowledge was measured with the Alzheimer Dementia and Knowledge Scale and confidence was assessed with the Sense of Competence in Dementia Care Staff Scale. RESULTS: Data suggested that students developed an increased confidence in caring for persons with dementia after the education. Key to person centered care, students demonstrated an increased ability to sustain person hood and build relationships. CONCLUSIONS: The growing complexity and needs of persons with dementia in various practice settings requires a nursing workforce able to apply clinical reasoning and provide person centered care. Further studies are needed exploring the effects of online educational opportunities on learning outcomes and clinical reasoning to build confidence in caring for persons with dementia.

Faith Community Nursing: Identifying and Combating Social Isolation and Loneliness in Older Adults.

ABSTRACT: The number of older adults worldwide is growing; the incidence of social isolation and loneliness among this population is also increasing. Social isolation and loneliness can have significant physical, mental, and spiritual impacts. Faith community nurses are in an optimal position to identify and intervene to help faith communities reduce the social isolation and loneliness among community-dwelling older adults. Risk factors and tools to identify both circumstances are discussed along with interventions and a case study.

Experiential Service Learning: Building skills and sensitivity with Kolb's learning theory.

Preparing a healthcare workforce able to respond to the growing complexity of health issues facing older adults is a critical issue for interprofessional educators. Students are in need of experiences promoting confidence and skill in communicating with older adults with cognitive issues. Student emotional and cognitive responses to an interprofessional Music and Memory® project in long term care facilities were evaluated. Forty-eight students met with assigned adults weekly to develop personalized music playlists and complete a journal entry. Student participants demonstrated improved interpersonal connections, enhanced professional skills, and increased empathy toward clients. Results are explored within the context of Kolb's Learning Theory and application of the evaluation outcomes for interprofessional education.

Using Personalized Music Playlists for Patients With Dementia as a Teaching Innovation.

Nursing students need innovative educational approaches to bridge generational and cultural differences and improve communication skills with patients who are cognitively impaired. An individualized music and memory intervention for older adults with dementia and communication issues was implemented. A review of weekly student journals provided information regarding the use of the approach as an alternative therapy and benefit for students. The usefulness of the music and memory program as an innovative learning tool has widespread applicability to various health care settings.

A subclass of acylated anti-inflammatory mediators usurp Toll-like receptor 2 to inhibit neutrophil recruitment through peroxisome proliferator-activated receptor gamma.

Toll-like receptors are host sentinel receptors that signal the presence of infectious nonself and initiate protective immunity. One of the primary immune defense mechanisms is the recruitment of neutrophils from the bloodstream into the infected tissue. Although neutrophils are important in host defense, they can also be responsible for damaging pathologies associated with excessive inflammation. Here, we report that the di-acylated TLR2 ligand lipoteichoic acid can directly inhibit neutrophil recruitment in vivo. This discovery allowed us to test the concept that conventional proinflammatory TLR2 ligands can be made to act as inhibitors through specific structural modifications. Indeed, lipopeptide TLR2 ligands, when modified at their acyl chains to contain linoleate, lose their capacity to induce inflammation and yield ligands that can directly inhibit the in vivo neutrophil recruitment initiated by a wide range of proinflammatory stimuli. The inhibitory capacity of LTA and these modified ligands requires the expression of TLR2, but is independent of the TLR2 signaling adaptor, MyD88. Instead, this inhibitory effect requires functional activity of the fatty acid and nuclear hormone receptor peroxisome proliferator-activated receptor γ (PPARγ). Therefore, these data support a model in TLR2 biology where structural modifications of these ligands can profoundly influence host-microbial interactions. These inhibitory TLR2 ligands also have broader implications with respect to their potential use in various inflammatory disease settings.

Endothelial LSP1 is involved in endothelial dome formation, minimizing vascular permeability changes during neutrophil transmigration in vivo.

The endothelium actively participates in neutrophil migration out of the vasculature via dynamic, cytoskeleton-dependent rearrangements leading to the formation of transmigratory cups in vitro, and to domes that completely surround the leukocyte in vivo. Leukocyte-specific protein 1 (LSP1), an F-actin-binding protein recently shown to be in the endothelium, is critical for effective transmigration, although the mechanism has remained elusive. Herein we show that endothelial LSP1 is expressed in the nucleus and cytosol of resting endothelial cells and associates with the cytoskeleton upon endothelial activation. Two-photon microscopy revealed that endothelial LSP1 was crucial for the formation of endothelial domes in vivo in response to neutrophil chemokine keratinocyte-derived chemokine (KC) as well as in response to endogenously produced chemokines stimulated by cytokines (tumor necrosis factor α [TNFα] or interleukin-1ß [IL-1ß]). Endothelial domes were significantly reduced in Lsp1(-/-) compared with wild-type (WT) mice. Lsp1(-/-) animals not only showed impaired neutrophil emigration after KC and TNFα stimulation, but also had disproportionate increases in vascular permeability. We demonstrate that endothelial LSP1 is recruited to the cytoskeleton in inflammation and plays an important role in forming endothelial domes thereby regulating neutrophil transendothelial migration. The permeability data may underscore the physiologic relevance of domes and the role for LSP1 in endothelial barrier integrity.

Utilizing a Learning Management System to Provide Nursing Professional Development.

The provider unit involved in this project was based in a university setting within a school of nursing and serves both the university nursing faculty and nurses within the community. To support effective online content design principles, usability, a connection to the content, and a method for participants to provide sound feedback, a nurse planner for the unit and an instructional designer in the university collaborated to transition nursing professional development activities to an online format utilizing a learning management system. Virtual learning is viable and a potentially effective option to provide interactive and innovative professional development.

An Educational Intervention to Decrease the Number of Emergency Incidents of Restraint and Seclusion on a Behavioral Health Unit.

BACKGROUND: The objective of this study was to implement an educational intervention on an inpatient, behavioral health care unit with the goal of reducing the number of crisis interventions of seclusion or restraint. METHOD: A quasi-experimental pretest and posttest design using De-escalate Anyone, Anywhere, Anytime training was employed with a focus of an increased understanding of a range of de-escalation techniques to use instead of restraint and seclusion. RESULTS: A convenience sample of 21 mental health employees participated in the training. The rates of restraint declined from a mean of 6 preintervention to 2 postintervention. The number of seclusions on the designated unit declined from a mean of 4.33 preintervention to a mean of 1.667 postintervention. CONCLUSION: These data suggest that an educational intervention to increase the knowledge of direct care staff in a broad range of de-escalation techniques resulted in a reduction in the use of restraint and seclusion. Ongoing training for nursing staff may reassure them of the efficacy of alternative methods for dealing with aggressive patients. [J Contin Educ Nurs. 2022;53(2):70-76.].

The phytochemical piceatannol induces the loss of CBL and CBL-associated proteins.

Piceatannol is a naturally occurring bioactive stilbene with documented antileukemic properties. It has been extensively used as a Syk-selective protein tyrosine kinase inhibitor for the study of various signaling pathways. Herein, we show that the hydroxystilbene, piceatannol, and related catechol ring-containing compounds are able to induce the loss of the Cbl family of proteins. Normal cellular Cbl-regulatory mechanisms were not involved in this process. Screening of a small library of piceatannol-like compounds indicated that aromaticity and a catechol ring were required for the induction of Cbl loss. Further examination of these two chemical properties showed that the oxidative conversion of the catechol ring of piceatannol into a highly reactive O-benzoquinone was the cause of piceatannol-induced Cbl loss. Characterization of the Cbl selectivity of piceatannol-induced protein loss revealed that this compound was also able to induce the functional loss of specific Cbl-associated proteins involved in signaling pathways commonly associated with cancer. This work uncovers a new, piceatannol-dependent effect and shows a novel way in which this phenomenon can be exploited to inhibit disease-associated signaling pathways.

Immune cell Toll-like receptor 4 is required for cardiac myocyte impairment during endotoxemia.

The aim of this study was to investigate the importance of Toll-like receptor 4 (TLR4) signaling on cardiac myocytes versus immune cells in lipopolysaccharide (LPS)-induced cardiac dysfunction. Cardiac myocytes isolated from LPS-treated C57Bl/6 mice showed reduced shortening and calcium transients as compared with myocytes from untreated mice. In addition, LPS-treated C57Bl/6 mice showed impaired cardiac mitochondrial function, including reduced respiration and reduced time of induction of permeability transition. All of the aforementioned cardiac dysfunction was dependent on TLR4, because LPS-treated TLR4-deficient mice did not have reduced myocyte shortening or mitochondrial dysfunction. To evaluate the role of cardiac myocyte versus leukocyte TLR4, LPS was injected into chimeric mice with TLR4-positive leukocytes and TLR4-deficient myocytes. These mice showed reduced myocyte shortening in response to LPS. Myocytes from chimeric mice with TLR4-deficient leukocytes and TLR4-positive myocytes had no response to LPS. In addition, isolated myocytes from C57Bl/6 mice subsequently treated with LPS and serum for various times did not have reduced shortening, despite the presence of TLR4 mRNA and protein, as determined by reverse-transcription polymerase chain reaction and fluorescent-activated cell sorting. In fact, cardiac myocytes had equivalent amounts of TLR4 as endothelium; however, only the latter is responsive to LPS. Furthermore, signaling pathways downstream of TLR4 were not activated during direct LPS treatment of myocytes. In conclusion, TLR4 on leukocytes, and not on cardiac myocytes, is important for cardiac myocyte impairment during endotoxemia.

Stimulation of the murine Uchl1 gene promoter by the B-Myb transcription factor.

It has been reported that human lung cancers frequently overexpress both the ubiquitous cell cycle transcription factor B-myb and the ubiquitin carboxyterminal hydrolase UCHL1, an enzyme whose expression is normally limited to neurons and neuroendocrine cells in the lung. A possible explanation for the co-expression of these markers is that Uchl1 is subject to transcriptional regulation by B-Myb, and in tumors the ectopic expression of UCHL1 is a direct consequence of B-Myb overexpression. We have tested this hypothesis in the mouse model system by cloning the murine Uchl1 promoter and analyzing its regulation by murine B-Myb. Expression of a luciferase reporter gene driven by the Uchl1 promoter was induced by cotransfected B-Myb, but induction was not dependent on the presence of a myb consensus binding site identified in the promoter region. B-Myb induction was dependent on the context of the Uchl1 TATA box, as has been reported for other genes. Transgenic mice expressing a truncated, constitutively active form of B-Myb in the lung epithelium showed elevated expression of UCHL1 protein. We conclude that B-Myb can stimulate expression of the Uchl1 both in cultured cells and in vivo.

Lipoteichoic acid induces unique inflammatory responses when compared to other toll-like receptor 2 ligands.

Toll-like receptors (TLRs) recognize evolutionarily-conserved molecular patterns originating from invading microbes. In this study, we were interested in determining if microbial ligands, which use distinct TLR2-containing receptor complexes, represent unique signals to the cell and can thereby stimulate unique cellular responses. Using the TLR2 ligands, R-FSL1, S-FSL1, Pam2CSK4, Pam3CSK4, and lipoteichoic acid (LTA), we demonstrate that these ligands activate NF-kappaB and MAP Kinase pathways with ligand-specific differential kinetics in murine macrophages. Most strikingly, LTA stimulation of these pathways was substantially delayed when compared with the other TLR2 ligands. These kinetics differences were associated with a delay in the LTA-induced expression of a subset of genes as compared with another TLR2 ligand, R-FSL1. However, this did not translate to overall differences in gene expression patterns four hours following stimulation with different TLR2 ligands. We extended this study to evaluate the in vivo responses to distinct TLR2 ligands using a murine model of acute inflammation, which employs intravital microscopy to monitor leukocyte recruitment into the cremaster muscle. We found that, although R-FSL1, S-FSL1, Pam2CSK4, and Pam3CSK4 were all able to stimulate robust leukocyte recruitment in vivo, LTA remained functionally inert in this in vivo model. Therefore distinct TLR2 ligands elicit unique cellular responses, as evidenced by differences in the kinetic profiles of signaling and gene expression responses in vitro, as well as the physiologically relevant differences in the in vivo responses to these ligands.

Mice that exclusively express TLR4 on endothelial cells can efficiently clear a lethal systemic Gram-negative bacterial infection.

Recognition of LPS by TLR4 on immune sentinel cells such as macrophages is thought to be key to the recruitment of neutrophils to sites of infection with Gram-negative bacteria. To explore whether endothelial TLR4 plays a role in this process, we engineered and imaged mice that expressed TLR4 exclusively on endothelium (known herein as EndotheliumTLR4 mice). Local administration of LPS into tissue induced comparable neutrophil recruitment in EndotheliumTLR4 and wild-type mice. Following systemic LPS or intraperitoneal E. coli administration, most neutrophils were sequestered in the lungs of wild-type mice and did not accumulate at primary sites of infection. In contrast, EndotheliumTLR4 mice showed reduced pulmonary capillary neutrophil sequestration over the first 24 hours; as a result, they mobilized neutrophils to primary sites of infection, cleared bacteria, and resisted a dose of E. coli that killed 50% of wild-type mice in the first 48 hours. In fact, the only defect we detected in EndotheliumTLR4 mice was a failure to accumulate neutrophils in the lungs following intratracheal administration of LPS; this response required TLR4 on bone marrow-derived immune cells. Therefore, endothelial TLR4 functions as the primary intravascular sentinel system for detection of bacteria, whereas bone marrow-derived immune cells are critical for pathogen detection at barrier sites. Nonendothelial TLR4 contributes to failure to accumulate neutrophils at primary infection sites in a disseminated systemic infection.