Citations

Introduction: Golf is a widely played recreational sport, but degenerative osteoarthritis in older adults can limit participation and performance. This study prospectively evaluates recreational golfers’ performance metrics of play, and clinical outcomes before and after total knee arthroplasty (TKA). Methods: A prospective cohort of 10 recreational golfers undergoing primary TKA were assessed at a professional golf performance center preoperatively and at 3 months, and 1-year postoperatively. The mean age was 72 years, 90% were men, and 50% underwent TKA on the lead leg. . Participants averaged 67 rounds in the year prior to surgery, maintained a handicap index (HCP) of 18. Golf performance metrics (driver and 7-iron), force-plate biomechanics, return-to-play timing, quality of play, and Knee Injury and Osteoarthritis Outcome Score, Junior (KOOS-JR) were analyzed using descriptive statistics. Results: At 1-year postoperatively, the mean changes in driver and 7-iron swing speed (+1.3 and -1.5 miles per hour (mph), respectively, 95% CI: -5, 4.7), ball speed (+3.5 and -2.6 mph, 95% CI: -12.9, 12.3), carry distance (-0.8 and +6.2 yards, 95% CI: -17.7, 17.1), maximum torque (+43 and +85 pounds per foot (lbs/ft), 95% CI: -30, 259), and vertical force (+93 and +119 lbs/ft, 95% CI: -175, 412). All patients returned to full golf rounds playing a mean 8 (SD: +5.7) and 44 (SD: +29.7) rounds by 3- and 12-months, respectively, with no change in HCP (P = 0.9). The KOOS-JR significantly improved (57 to 80, P = 0.01). Conclusion: Recreational golfers safely returned to play after TKA with no significant changes in swing performance or handicap, while patient-reported outcomes improved. These findings suggest TKA enables resumption of golf without compromising performance.

Abstract Background Central nervous system (CNS) involvement by mycosis fungoides (MF) is an uncommon but serious manifestation of advanced disease. Large-cell transformation (LCT) is associated with aggressive clinical behavior and increased risk of extracutaneous dissemination; however, CNS involvement remains rare and is infrequently confirmed by molecular studies. Case Presentation: We report a 77-year-old man with a 13-year history of MF who presented with progressive generalized weakness, gait instability, and weight loss. Brain magnetic resonance imaging demonstrated multiple bilateral enhancing intraparenchymal lesions concerning for primary CNS lymphoma. Cerebrospinal fluid cytology and flow cytometry were nondiagnostic. Stereotactic biopsy of a right frontal lesion revealed diffuse infiltration of brain parenchyma by large atypical lymphoid cells with a predominantly perivascular distribution. By immunohistochemistry, the lymphocytes express CD3, TCRβF1, CD30, and demonstrate diffuse p53 overexpression, complete loss of p16, and a high proliferative index (70–80%). Comparison with a prior skin biopsy which showed typical MF morphology with limited CD30 expression (< 10% of atypical lymphocytes). Polymerase chain reaction–based T-cell receptor gene rearrangement studies performed on both CNS and skin specimens demonstrated similar clonal rearrangements, confirming CNS dissemination of the original MF clone with large-cell transformation. Discussion CNS involvement in MF is rare and may occur years after the initial diagnosis, particularly in the setting of transformation. This case highlights several important features, including multifocal intraparenchymal CNS disease, nondiagnostic cerebrospinal fluid studies, and molecular confirmation of clonal relatedness between skin and CNS lesions. These findings underscore the limitations of cerebrospinal fluid-based diagnostic studies and emphasize the importance of tissue biopsy and molecular analysis in establishing the diagnosis. Conclusion We describe a rare case of MF with large-cell transformation presenting as multifocal intraparenchymal CNS disease. Molecular demonstration of identical T-cell receptor rearrangements in skin and brain lesions provided definitive evidence of metastatic dissemination. Recognition of this rare complication is essential, as new neurologic symptoms in patients with MF should prompt evaluation for CNS involvement regardless of the extent of active cutaneous disease.

ABSTRACT Problem Patients with threatened preterm labor (PTL) are treated with antibiotics, corticosteroids, and magnesium sulfate to mitigate infection, promote fetal lung maturation, provide fetal neuroprotection and overall minimize the impact of prematurity on the neonate. However, the effect of these drugs on the placental inflammatory profile is unknown even though these are given systemically and reach the placenta. We evaluated their action in an ex vivo model of placental inflammation. Method of Study Placental explants from uncomplicated pregnancies were exposed to lipopolysaccharide (LPS) ± azithromycin, betamethasone, and/or magnesium sulfate. Production (lysate) and secretion (supernatant) of pro‐ and anti‐inflammatory cytokines were assessed by ELISA. Results Both pro‐ and anti‐inflammatory cytokines were increased by LPS versus untreated. Azithromycin, or magnesium sulfate did not alter the inflammatory profile by themselves nor when added at the same time or 24 h after LPS. Betamethasone decreased both pro‐ and anti‐inflammatory cytokines only when administered at the same time as LPS, without any effects if delayed. Conclusions Therapeutic interventions classically used for preterm labor (PTL) do not impact the placental inflammatory profile by themselves or in the context of an ex vivo placental explants model of LPS‐induced inflammation, except for betamethasone when administered concurrently with LPS.