Sleep Apnea is Not an Obstacle for Outpatient Hip and Knee Arthroplasty.

BACKGROUND: Up to 25% of patients requiring hip or knee arthroplasty have sleep apnea (SA), and these patients have historically been excluded from outpatient programs. The objectives of this study were to evaluate same-day discharge failure as well as 30-day complications, readmissions, and unexpected visits. METHODS: A retrospective case-control study comparing patients who have and do not have SA matched for age, sex and arthroplasty type (total hip arthroplasty, total knee arthroplasty, unicompartimental knee arthroplasty) who underwent primary outpatient surgery between February 2019 and December 2022 in 2 academic hospitals was conducted. Cases with mild SA, moderate SA with a body mass index (BMI) <35, and SA of all severity treated by continuous positive airway pressure machines were eligible. There were 156 patients included (78 cases). Complications were assessed according to the Clavien-Dindo Classification and the Comprehensive Complication Index. Continuous variables were evaluated by Student's T or Mann-Whitney tests, while categorical data were analyzed by Chi-square or Fisher tests. Univariate analyses were performed to determine discharge failure risk factors. RESULTS: There were 6 cases (7.7%) and 5 controls (6.4%) who failed to be discharged on surgery day (P = .754), with postoperative hypoxemia (6, [3.8%]) and apnea periods (3, [1.9%]) being the most common causes. Higher BMI (odds ratio = 1.19, P = .013) and general anesthesia (odds ratio = 11.97, P = .004) were found to be risk factors for discharge failure. No difference was observed on 30-day readmissions (P = .497), unexpected visits (P = 1.000), and complications on the Clavien-Dindo Classification (P > .269) and Comprehensive Complication Index (P > .334) scales. CONCLUSIONS: Selected patients who have SA can safely undergo outpatient hip or knee arthroplasty. Higher BMI and general anesthesia increased the odds of same-day discharge failure. LEVEL OF EVIDENCE: Level III, Case-control Study.

Prognostic Factors of Function in Nonoperatively Treated Radial Head Fractures: A Prospective Cohort Study.

OBJECTIVES: To identify patient-related factors and fracture characteristics influencing the functional outcomes of nonoperatively treated radial head fractures and to determine function at 1 year. DESIGN: Prospective cohort study. SETTING: Academic Level 1 trauma center. PATIENTS/PARTICIPANTS: Consecutive isolated radial head fractures fitting the inclusion criteria between May 2013 and July 2016. INTERVENTION: Nonoperative treatment of isolated radial head fractures. OUTCOME MEASUREMENTS: Logistic regressions between potential prognostic factors and function assessed with the Mayo Elbow Performance Score (MEPS), the Disabilities of the Arm, Shoulder, and Hand (DASH) score, and range of motion at 1.5-3-6-12 months. RESULTS: One hundred fourteen patients were included (78% Mason I [OTA/AO 2R1B1], 20% Mason II [OTA/AO 2R1B3], and 2% Mason III [OTA/AO 2R1C3]). Mean MEPS and DASH score at the last follow-up were excellent [96.4 ± 7.6 and 3.7 ± 8.6] with, respectively, 79.8% and 92.7% of satisfactory results. Depressive symptoms at injury baseline (Quick Inventory of Depressive Symptomatology > 5) are a constant predictor of unsatisfactory function (MEPS <90 or DASH >17]). Older age and female sex were all linked to worse function at the first follow-ups ( P < 0.05), whereas lower socioeconomic class and receiving financial compensations were associated to unsatisfactory function at 1 year ( P < 0.05). CONCLUSIONS: Although most nonoperatively treated radial head fractures heal with excellent function, some patients still exhibit unsatisfactory results at 1 year. Symptoms of depression at injury baseline are a constant and significant predictor of unsatisfactory function. Early detection of depressive symptoms would allow for interventions that may optimize function. LEVEL OF EVIDENCE: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

Smoking status impacts treatment efficacy in smoke-induced lung inflammation: A pre-clinical study.

Rationale: Smoking status and smoking history remain poorly accounted for as variables that could affect the efficacy of new drugs being tested in chronic obstructive pulmonary disease (COPD) patients. As a proof of concept, we used a pre-clinical model of cigarette smoke (CS) exposure to compare the impact of treatment during active CS exposure or during the cessation period on the anti-inflammatory effects IL-1α signaling blockade. Methods: Mice were exposed to CS for 2 weeks, followed by a 1-week cessation, then acutely re-exposed for 2 days. Mice were treated with an anti-IL-1α antibody either during CS exposure or during cessation and inflammatory outcomes were assessed. Results: We found that mice re-exposed to CS displayed reduced neutrophil counts and cytokine levels in the bronchoalveolar lavage (BAL) compared to mice exposed only acutely. Moreover, we found that treatment with an anti-IL-1α antibody during the initial CS exposure delayed inflammatory processes and interfered with pulmonary adaptation, leading to rebound pulmonary neutrophilia, increased BAL cytokine secretion (CCL2) and upregulated Mmp12 expression. Conversely, administration of anti-IL-1α during cessation had the opposite effect, improving BAL neutrophilia, decreasing CCL2 levels and reducing Mmp12 expression. Discussion: These results suggest that pulmonary adaptation to CS exposure dampens inflammation and blocking IL-1α signaling during CS exposure delays the inflammatory response. More importantly, the same treatment administered during cessation hastens the return to pulmonary inflammatory homeostasis, strongly suggesting that smoking status and treatment timing should be considered when testing new biologics in COPD.

Glycerol contained in vaping liquids affects the liver and aspects of energy homeostasis in a sex-dependent manner.

Vaping is increasingly popular among the young and adult population. Vaping liquids contained in electronic cigarettes (e-cigarettes) are mainly composed of propylene glycol and glycerol, to which nicotine and flavors are added. Among several biological processes, glycerol is a metabolic substrate used for lipid synthesis in fed state as well as glucose synthesis in fasting state. We aimed to investigate the effects of glycerol e-cigarette aerosol exposure on the aspects of glycerol and glucose homeostasis. Adult and young male and female mice were exposed to e-cigarette aerosols with glycerol as vaping liquid using an established whole-body exposure system. Mice were exposed acutely (single 2-h exposure) or chronically (2 h/day, 5 days/week for 9 weeks). Circulating glycerol and glucose levels were assessed and glycerol as well as glucose tolerance tests were performed. The liver was also investigated to assess changes in the histology, lipid content, inflammation, and stress markers. Lung functions were also assessed as well as hepatic mRNA expression of genes controlling the circadian rhythm. Acute exposure to glycerol aerosols generated by an e-cigarette increased circulating glycerol levels in female mice. Increased hepatic triglyceride and phosphatidylcholine concentrations were observed in female mice with no increase in circulating alanine aminotransferase or evidence of inflammation, fibrosis, or endoplasmic reticulum stress. Chronic exposure to glycerol e-cigarette aerosols mildly impacted glucose tolerance test in young female and male mice. Fasting glycerol, glucose, and insulin remained unchanged. Increased pulmonary resistance was observed in young male mice. Taken together, this study shows that the glycerol contained in vaping liquids can affect the liver as well as the aspects of glucose and glycerol homeostasis. Additional work is required to translate these observations to humans and determine the biological and potential pathological impacts of these findings.

Control of adipogenic commitment by a STAT3-VSTM2A axis.

White adipose tissue (WAT) is a dynamic organ that plays crucial roles in controlling metabolic homeostasis. During development and periods of energy excess, adipose progenitors are recruited and differentiate into adipocytes to promote lipid storage capability. The identity of adipose progenitors and the signals that promote their recruitment are still incompletely characterized. We have recently identified V-set and transmembrane domain-containing protein 2A (VSTM2A) as a novel protein enriched in preadipocytes that amplifies adipogenic commitment. Despite the emerging role of VSTM2A in promoting adipogenesis, the molecular mechanisms regulating Vstm2a expression in preadipocytes are still unknown. To define the molecular mechanisms controlling Vstm2a expression, we have treated preadipocytes with an array of compounds capable of modulating established regulators of adipogenesis. Here, we report that Vstm2a expression is positively regulated by PI3K/mTOR and cAMP-dependent signaling pathways and repressed by the MAPK pathway and the glucocorticoid receptor. By integrating the impact of all the molecules tested, we identified signal transducer and activator of transcription 3 (STAT3) as a novel downstream transcription factor affecting Vstm2a expression. We show that activation of STAT3 increased Vstm2a expression, whereas its inhibition repressed this process. In mice, we found that STAT3 phosphorylation is elevated in the early phases of WAT development, an effect that strongly associates with Vstm2a expression. Our findings identify STAT3 as a key transcription factor regulating Vstm2a expression in preadipocytes.NEW & NOTEWORTHY cAMP-dependent and PI3K-mTOR signaling pathways promote the expression of Vstm2a. STAT3 is a key transcription factor that controls Vstm2a expression in preadipocytes. STAT3 is activated in the early phases of WAT development, an effect that strongly associates with Vstm2a expression.

Apolipoprotein C-I reduces cholesteryl esters selective uptake from LDL and HDL by binding to HepG2 cells and lipoproteins.

Plasma cholesterol from low- and high-density lipoproteins (LDL and HDL) are cleared from the circulation by specific receptors that either totally degrade lipoproteins as the LDL receptor or selectively take up their cholesteryl esters (CE) like the scavenger receptor class B type I (SR-BI). The aim of the present study was to define the effect of apoC-I on the uptake of LDL and HDL(3) by HepG2 cells. In experiments conducted with exogenously added purified apoC-I, no significant effect was observed on lipoprotein-protein association and degradation; however, LDL- and HDL(3)-CE selective uptake was significantly reduced in a dose-dependent manner. This study also shows that apoC-I has the ability to associate with HepG2 cells and with LDL and HDL(3). Moreover, pre-incubation of HepG2 cells with apoC-I reduces HDL(3)-CE selective uptake and pre-incubation of LDL and HDL(3) with apoC-I decreases their CE selective uptake by HepG2 cells. Thus, apoC-I can accomplish its inhibitory effect on SR-BI activity by either binding to SR-BI or lipoproteins. We conclude that by reducing hepatic lipoprotein-CE selective uptake, apoC-I has an atherogenic character.