Influence of Health Insurance Types on Clinical Cancer Care Accessibility and Quality Using <i>All of Us</i> Database

Background and Objectives: Cancer, as the second leading cause of death in the United States, poses a huge healthcare burden. Barriers to access to advanced therapies influence the outcome of cancer treatment. In this study, we examined whether insurance types affect the quality of cancer clinical care. Materials and Methods: Data for 13,340 cancer patients with Purchased or Medicaid insurance from the All of Us database were collected for this study. The chi-squared test of proportions was employed to determine the significance of patient cohort characteristics and the accessibility of healthcare services between the Purchased and Medicaid insurance groups. Results: Cancer patients who are African American, with lower socioeconomic status, or with lower educational attainment are more likely to be insured by Medicaid. An analysis of the survey questions demonstrated the relationship between income and education level and insurance type, as Medicaid cancer patients were less likely to receive primary care and specialist physician access and more likely to request lower-cost medications. Conclusions: The inequities of the US healthcare system are observed for cancer patient care; access to physicians and medications is highly varied and dependent on insurance types. Socioeconomic factors further influence insurance types, generating a significant impact on the overall clinical care quality for cancer patients that eventually determines treatment outcomes and the quality of life

Introduction of a Novel Sequential Approach to the Ponte Osteotomy to Minimize Spinal Canal Exposure

Ponte osteotomy is an increasingly popular technique for multiplanar correction of adolescent idiopathic scoliosis. Prior cadaveric studies have suggested that sequential posterior spinal releases increase spinal flexibility. Here we introduce a novel technique involving a sequential approach to the Ponte osteotomy that minimizes spinal canal exposure. One fresh-frozen adult human cadaveric thoracic spine specimen with 4 cm of ribs was divided into three sections (T1–T5, T6–T9, T10–L1) and mounted for biomechanical testing. Each segment was loaded with five Newton meters under four conditions: baseline inferior facetectomy with supra/interspinous ligament release, superior articular process (SAP) osteotomy in situ, spinous process (SP) osteotomy in situ, and complete posterior column osteotomy with SP/SAP excision and ligamentum flavum release (PCO). Compared to baseline, in situ SAP osteotomy alone provided 3.5%, 7.6%, and 7.2% increase in flexion/extension, lateral bending, and axial rotation, respectively. In situ SP osteotomy increased flexion/extension, lateral bending, and axial rotation by 15%, 18%, and 10.3%, respectively. PCO increased flexion/extension, lateral bending, and axial rotation by 19.6%, 28.3%, and 12.2%, respectively. Our report introduces a novel approach where incremental increases in range of motion can be achieved with minimal spinal canal exposure and demonstrates feasibility in a cadaveric model.</jats:p

PI5P4Ks drive metabolic homeostasis through peroxisome-mitochondria interplay.

PI5P4Ks are a class of phosphoinositide kinases that phosphorylate PI-5-P to PI-4,5-P2. Distinct localization of phosphoinositides is fundamental for a multitude of cellular functions. Here, we identify a role for peroxisomal PI-4,5-P2 generated by the PI5P4Ks in maintaining energy balance. We demonstrate that PI-4,5-P2 regulates peroxisomal fatty acid oxidation by mediating trafficking of lipid droplets to peroxisomes, which is essential for sustaining mitochondrial metabolism. Using fluorescent-tagged lipids and metabolite tracing, we show that loss of the PI5P4Ks significantly impairs lipid uptake and β-oxidation in the mitochondria. Further, loss of PI5P4Ks results in dramatic alterations in mitochondrial structural and functional integrity, which under nutrient deprivation is further exacerbated, causing cell death. Notably, inhibition of the PI5P4Ks in cancer cells and mouse tumor models leads to decreased cell viability and tumor growth, respectively. Together, these studies reveal an unexplored role for PI5P4Ks in preserving metabolic homeostasis, which is necessary for tumorigenesis