Patients receiving in-center hemodialysis (HD) spend 9–12 hours per week in the clinical environment, making the physical setting an important contributor to emotional well-being. Depression is common in HD and is associated with decreased quality of life, higher hospitalization rates, and increased mortality. This quality improvement study evaluated whether patient-selected wall art was associated with improved mood in two distinct HD units at the Greater Los Angeles Veterans Affairs Medical Center. Patients completed anonymous pre- and post-intervention questionnaires assessing mood with PHQ screening items, environmental satisfaction, and artwork preferences. Based on patient selections, eight pieces of artwork were installed in each unit, and identical surveys were redistributed after artwork installation. Because the responses were de-identified and unmatched, pre- and post-intervention data were analyzed as independent samples using descriptive statistics. Twenty-nine patients completed the pre-intervention survey and twelve completed the post-intervention survey. Mean PHQ-9 scores decreased from 7.28 to 6.50 and PHQ-2 positivity decreased from 24.1% to 16.7%, representing an 11% relative reduction in symptom severity and a 31% reduction in positive depression screens. Patients also expressed strong enthusiasm for the artwork. Patient-selected wall art may offer a low-cost, patient-centered, and scalable strategy to improve the psychosocial experience of chronic dialysis care.

The gut microbiome is an area of growing interest in inflammatory diseases, including rheumatoid arthritis (RA). Dysbiosis has been suggested to increase inflammation and contribute to immune dysfunction in RA. Paraoxonase-1 (PON1) is an HDL-associated enzyme that metabolizes pro-inflammatory oxidized lipids and prevents the development of atherosclerosis. Our previous studies showed that overexpression of the human PON1 gene in mice correlates with reduced inflammatory arthritic activity. However, the relationship between PON1 genotype and activity with gut dysbiosis during the onset of murine inflammatory arthritis has not been studied. K/BxN serum transfer to C57BL6 mice was used as an arthritic model in wild type (WT) and PON1 human transgene (PON1Tg) mice. Fecal samples were collected and sent to Transnetyx for shotgun sequencing. Microbial populations were then analyzed using MaAsLin3, adonis2, and linear mixed models. Prior to the induction of RA, differential taxa analysis revealed 80 significantly altered taxa in the microbial composition of PON1Tg mice compared to WT mice. Following RA induction, there were no differences in the microbiome of PON1Tg mice compared to WT mice. Alterations in various functional pathways were also determined. These results suggest that the gut microbiome may contribute to the protective role of PON1, warranting further studies into its role in RA progression.

This abstract has been withheld from publication.

Periprosthetic joint infection (PJI) is a severe complication of total joint arthroplasty, causing bone loss, implant failure, and is associated with higher 5-year mortality than many common cancers. No pharmacologic therapies exist to prevent PJI-associated osteolysis. Intermittent parathyroid hormone (iPTH), an FDA-approved anabolic agent that stimulates osteoblast activity and bone formation, has not been evaluated in the context of infection-induced bone loss. We hypothesized that iPTH treatment would preserve periprosthetic bone integrity during active infection. Using a bioluminescent S. aureus strain, a predominant pathogen in PJI, 38 male C57BL/6 mice were randomized into six groups: sterile+saline, sterile+iPTH, infected+saline, infected+iPTH, infected+vancomycin, or infected+iPTH+vancomycin. In our established murine model of post-arthroplasty knee infection, animals underwent surgery with bacterial inoculation or sterile control and received iPTH or saline 3×/week for 8 weeks. Ex vivo micro-CT demonstrated that infection significantly reduced bone volume fraction (BV/TV), while vancomycin alone did not prevent bone loss. However, iPTH-treated mice maintained BV/TV comparable to sterile controls, and combined iPTH and vancomycin yielded the greatest bone preservation. Bioluminescent imaging confirmed similar bacterial burdens across groups, thus iPTH does not impair bacterial clearance. Combined iPTH and antibiotic therapy may benefit patients undergoing revision or nonsurgical candidates on suppressive therapy.

Surgery is the primary potentially curative treatment for soft tissue sarcoma (STS), yet incomplete resection is associated with poor outcomes. Our prior clinical studies have shown that patients who underwent an initial macroscopically incomplete resection (R2) had significantly worse survival, even when a complete resection was later achieved. Here, we hypothesized that incomplete resection may inadvertently trigger a “regime shift," pushing the tumor microenvironment (TME) towards an immunosuppressive rather than immune-active state. Using our murine sarcoma model, we found that R2 surgery increased recruitment of myeloid-derived suppressor cells (MDSCs), reduced the function of intratumoral CD8 T cells, and promoted the progression of residual disease. Notably, analysis of post-surgical tumor samples revealed elevated levels of pro-inflammatory cytokines, such as TNFα, which have been shown in other malignancies to drive MDSC accumulation, enhance their survival, and suppress their functions in the TME. To define the role of TNFα, we will treat R2 mice with an anti-TNFα antibody perioperatively and characterize the immune landscape, specifically MDSC, after surgery. To increase CD8 T cell functions, we will combine our treatment plan with anti-PD-1 blockade. Our goal is to reverse this immunosuppressive shift, followed by surgery; restore anti-tumor immunity; and improve control of residual disease.