Patients Who Have Limited English Proficiency Have Decreased Utilization of Revision Surgeries After Hip and Knee Arthroplasty.

BACKGROUND: While racial and ethnic disparities are well documented in access to total joint arthroplasty (TJA), little is known about the association between having limited English proficiency (LEP) and postoperative care access. This study seeks to correlate LEP status with rates of revision surgery after hip and knee arthroplasty. METHODS: This was a retrospective cohort study of patients aged ≥ 18 years who underwent either total hip or total knee arthroplasty between January 2013 and December 2021 at a single academic medical center. The predictor variable was English proficiency status, where LEP was defined as having a primary language that was not English. Multivariable regressions controlling for potential demographic and clinical confounders were used to calculate adjusted odds ratios of undergoing revision surgery within 1 and 2 years after primary arthroplasty for patients who have LEP, compared to English proficient patients. RESULTS: A total of 7,985 hip and knee arthroplasty surgeries were included in the analysis. There were 577 (7.2%) patients who were classified as having LEP. Patients who have LEP were less likely to undergo revision surgeries within 1 year (1.4% versus 3.2%, P = .01) and 2 years (1.7% versus 3.9%, P = .006) of primary TJA. Patients who have LEP had adjusted odds ratios of 0.45 (confidence interval: 0.22-0.92, P = .03) and 0.44 (confidence interval: 0.23-0.85, P = .01) of receiving revision surgery within 1 and 2 years, respectively. CONCLUSION: Patients who have LEP, compared to English proficient patients, were less likely to undergo revision surgeries at the same institution up to 2 years after hip and knee arthroplasty. These findings suggest that patients who have LEP may face barriers in accessing postoperative care.

Lifting the Digital Curtain: Utilizing Social Media to Promote Health Content and Engage with Asian Populations.

BACKGROUND/AIMS: To understand how social media can be used to improve Asian subgroup engagement in a research registry. METHODS: A 10-week social media campaign was implemented with the goal of increasing the percentage of Asian participants in the Stanford Research Registry - platforms utilized include Facebook, Instagram, and Twitter through the Stanford Center for Asian Health Research and Education accounts. Participant data was disaggregated by race and ethnicity in order to better understand the diversity among Asian subgroups. RESULTS: The percentage of Asian participants increased from 14.3% at baseline to 23.8% at the end of the campaign (525 Asian identifying individuals to 1,871). The greatest increase occurred during the general outreach phase which utilized all channels of outreach available. Frequencies of some ethnicities, such as Japanese, Korean, and Vietnamese, were higher in the Multi-Ethnic and/or Multi-Racial categories compared to their corresponding monoethnic groups. CONCLUSIONS: Social media is a powerful tool that can be leveraged for targeted recruitment - in this study we see how it can increase diversity amongst research participants and potentially be used as an effective tool for information dissemination. This work can be expanded in the future by examining other social media platforms more targeted toward Asian populations, and more thorough disaggregation to fully understand the diversity present in the Asian population.

Insulin-stimulated endoproteolytic TUG cleavage links energy expenditure with glucose uptake.

TUG tethering proteins bind and sequester GLUT4 glucose transporters intracellularly, and insulin stimulates TUG cleavage to translocate GLUT4 to the cell surface and increase glucose uptake. This effect of insulin is independent of phosphatidylinositol 3-kinase, and its physiological relevance remains uncertain. Here we show that this TUG cleavage pathway regulates both insulin-stimulated glucose uptake in muscle and organism-level energy expenditure. Using mice with muscle-specific Tug (Aspscr1)-knockout and muscle-specific constitutive TUG cleavage, we show that, after GLUT4 release, the TUG C-terminal cleavage product enters the nucleus, binds peroxisome proliferator-activated receptor (PPAR)γ and its coactivator PGC-1α and regulates gene expression to promote lipid oxidation and thermogenesis. This pathway acts in muscle and adipose cells to upregulate sarcolipin and uncoupling protein 1 (UCP1), respectively. The PPARγ2 Pro12Ala polymorphism, which reduces diabetes risk, enhances TUG binding. The ATE1 arginyltransferase, which mediates a specific protein degradation pathway and controls thermogenesis, regulates the stability of the TUG product. We conclude that insulin-stimulated TUG cleavage coordinates whole-body energy expenditure with glucose uptake, that this mechanism might contribute to the thermic effect of food and that its attenuation could promote obesity.

GLUT4 Storage Vesicles: Specialized Organelles for Regulated Trafficking.

Fat and muscle cells contain a specialized, intracellular organelle known as the GLUT4 storage vesicle (GSV). Insulin stimulation mobilizes GSVs, so that these vesicles fuse at the cell surface and insert GLUT4 glucose transporters into the plasma membrane. This example is likely one instance of a broader paradigm for regulated, non-secretory exocytosis, in which intracellular vesicles are translocated in response to diverse extracellular stimuli. GSVs have been studied extensively, yet these vesicles remain enigmatic. Data support the view that in unstimulated cells, GSVs are present as a pool of preformed small vesicles, which are distinct from endosomes and other membrane-bound organelles. In adipocytes, GSVs contain specific cargoes including GLUT4, IRAP, LRP1, and sortilin. They are formed by membrane budding, involving sortilin and probably CHC22 clathrin in humans, but the donor compartment from which these vesicles form remains uncertain. In unstimulated cells, GSVs are trapped by TUG proteins near the endoplasmic reticulum - Golgi intermediate compartment (ERGIC). Insulin signals through two main pathways to mobilize these vesicles. Signaling by the Akt kinase modulates Rab GTPases to target the GSVs to the cell surface. Signaling by the Rho-family GTPase TC10α stimulates Usp25m-mediated TUG cleavage to liberate the vesicles from the Golgi. Cleavage produces a ubiquitin-like protein modifier, TUGUL, that links the GSVs to KIF5B kinesin motors to promote their movement to the cell surface. In obesity, attenuation of these processes results in insulin resistance and contributes to type 2 diabetes and may simultaneously contribute to hypertension and dyslipidemia in the metabolic syndrome.