Urban relatives ameliorate survival disparities for genitourinary cancer in rural patients.

INTRODUCTION: Patients living in rural areas have worse cancer-specific outcomes. This study examines the effect of family-based social capital on genitourinary cancer survival. We hypothesized that rural patients with urban relatives have improved survival relative to rural patients without urban family. METHODS: We examined rural and urban based Utah individuals diagnosed with genitourinary cancers between 1968 and 2018. Familial networks were determined using the Utah Population Database. Patients and relatives were classified as rural or urban based on 2010 rural-urban commuting area codes. Overall survival was analyzed using Cox proportional hazards models. RESULTS: We identified 24,746 patients with genitourinary cancer with a median follow-up of 8.72 years. Rural cancer patients without an urban relative had the worst outcomes with cancer-specific survival hazard ratios (HRs) at 5 and 10 years of 1.33 (95% CI 1.10-1.62) and 1.46 (95% CI 1.24-1.73), respectively relative to urban patients. Rural patients with urban first-degree relatives had improved survival with 5- and 10-year survival HRs of 1.21 (95% CI 1.06-1.40) and 1.16 (95% CI 1.03-1.31), respectively. CONCLUSIONS: Our findings suggest rural patients who have been diagnosed with a genitourinary cancer have improved survival when having relatives in urban centers relative to rural patients without urban relatives. Further research is needed to better understand the mechanisms through which having an urban family member contributes to improved cancer outcomes for rural patients. Better characterization of this affect may help inform policies to reduce urban-rural cancer disparities.

Cost and Utilization Outcomes in Huntsman at Home, a Novel Oncology Hospital at Home Program.

OBJECTIVES: In a real-world trial, we previously demonstrated that Huntsman at Home, a novel oncology hospital at home program, was associated with reduced health care utilization and costs. In this study, we sought to understand the impact of Huntsman at Home in specific patient subgroups defined by sex, age, area-level median income, Charlson Comorbidity Index, and current use of systemic anticancer therapy. DESIGN: Retrospective case-control study of the Huntsman Cancer Institute. Electronic Data Warehouse of patients enrolled in Huntsman at Home between August 2018 through October 2019 vs usual-care patients. SETTING AND PARTICIPANTS: A total of 169 patients admitted to Huntsman at Home compared with 198 usual-care patients. METHODS: Five dichotomous subgroups evaluated including sex (female vs male), age (≥65 vs <65), income (≥$78,735 vs <$78,735), Charlson Comorbidity Index (≥2 vs <2), and current systemic anticancer therapy use vs no current systemic anticancer therapy. Groups were compared with patients receiving usual care. Primary outcomes included 30-day costs, hospital length of stay, unplanned hospitalizations, and emergency room visits. RESULTS: Admission to Huntsman at Home was associated with an overall reduction across all 4 health care cost and utilization outcomes. Outcomes favoring admission to Huntsman at Home achieved statistical significance (P < .05) in at least 2 of the 4 outcomes for each subgroup studied. Of the subgroups that did not achieve statistically significant benefit from Huntsman at Home admission in some outcome categories, none of these subgroups favored usual care. CONCLUSIONS AND IMPLICATIONS: Admission to Huntsman at Home decreased utilization of unplanned health care and reduced costs across a wide spectrum of patient subgroups, suggesting overall consistent benefit from the service. Hospital at home models should be considered as a means by which the quality and efficiency of care can be maximized for patients with cancer.

Evaluating Therapeutic Activity of Galectin-1 in Sarcolemma Repair of Skeletal Muscle.

Galectin-1 is a small (14.5 kDa) multifunctional protein with cell-cell and cell-ECM adhesion due to interactions with the carbohydrate recognition domain (CRD). In two types of muscular dystrophies, this lectin protein has shown therapeutic properties, including positive regulation of skeletal muscle differentiation and regeneration. Both Duchenne and limb-girdle muscular dystrophy 2B (LGMD2B) are subtypes of muscular dystrophies characterized by deficient membrane repair, muscle weakness, and eventual loss of ambulation. This chapter explains confocal techniques such as laser injury, calcium imaging, and galectin-1 localization to examine the effects of galectin-1 on membrane repair in injured LGMD2B models.

Therapeutic Benefit of Galectin-1: Beyond Membrane Repair, a Multifaceted Approach to LGMD2B.

Two of the main pathologies characterizing dysferlinopathies are disrupted muscle membrane repair and chronic inflammation, which lead to symptoms of muscle weakness and wasting. Here, we used recombinant human Galectin-1 (rHsGal-1) as a therapeutic for LGMD2B mouse and human models. Various redox and multimerization states of Gal-1 show that rHsGal-1 is the most effective form in both increasing muscle repair and decreasing inflammation, due to its monomer-dimer equilibrium. Dose-response testing shows an effective 25-fold safety profile between 0.54 and 13.5 mg/kg rHsGal-1 in Bla/J mice. Mice treated weekly with rHsGal-1 showed downregulation of canonical NF-κB inflammation markers, decreased muscle fat deposition, upregulated anti-inflammatory cytokines, increased membrane repair, and increased functional movement compared to non-treated mice. Gal-1 treatment also resulted in a positive self-upregulation loop of increased endogenous Gal-1 expression independent of NF-κB activation. A similar reduction in disease pathologies in patient-derived human cells demonstrates the therapeutic potential of Gal-1 in LGMD2B patients.

Hidden dangers and updated labels on gastric balloons.

In recent years, intragastric balloons (IGBs) have emerged as an efficacious, nonsurgical modality to treat obesity. We present a case in which an IGB caused a gastric ulcer, only unearthed after the novel technique of deflation and early retrieval.

Treatment with galectin-1 improves myogenic potential and membrane repair in dysferlin-deficient models.

Limb-girdle muscular dystrophy type 2B (LGMD2B) is caused by mutations in the dysferlin gene, resulting in non-functional dysferlin, a key protein found in muscle membrane. Treatment options available for patients are chiefly palliative in nature and focus on maintaining ambulation. Our hypothesis is that galectin-1 (Gal-1), a soluble carbohydrate binding protein, increases membrane repair capacity and myogenic potential of dysferlin-deficient muscle cells and muscle fibers. To test this hypothesis, we used recombinant human galectin-1 (rHsGal-1) to treat dysferlin-deficient models. We show that rHsGal-1 treatments of 48 h-72 h promotes myogenic maturation as indicated through improvements in size, myotube alignment, myoblast migration, and membrane repair capacity in dysferlin-deficient myotubes and myofibers. Furthermore, increased membrane repair capacity of dysferlin-deficient myotubes, independent of increased myogenic maturation is apparent and co-localizes on the membrane of myotubes after a brief 10min treatment with labeled rHsGal-1. We show the carbohydrate recognition domain of Gal-1 is necessary for observed membrane repair. Improvements in membrane repair after only a 10 min rHsGal-1treatment suggest mechanical stabilization of the membrane due to interaction with glycosylated membrane bound, ECM or yet to be identified ligands through the CDR domain of Gal-1. rHsGal-1 shows calcium-independent membrane repair in dysferlin-deficient and wild-type myotubes and myofibers. Together our novel results reveal Gal-1 mediates disease pathologies through both changes in integral myogenic protein expression and mechanical membrane stabilization.