Adventist Hinsdale Hospital

This paper describes a novel application and evaluation of programmable networking in High-Energy Physics (HEP): a complete parser for the custom packet format used by Fermilab’s DUNE experiment. Notably, this parser is implemented on a Tofino programmable network switch and evaluated on the FABRIC testbed by using network traffic generated by the ICEBERG DUNE prototype. The parsed network traffic consists of Jumbo Ethernet frames that contain digitizations of sensor readings from ICEBERG’s detector.

<h2>Abstract</h2> There has been recent increased interest in intramedullary fibular nails for the treatment of fibular fractures. While most publications highlight the clinical outcomes and decreased complication rates associated with fibular nails in comparison to their plate and screw counterparts, no studies to date have discussed the intramedually anatomy of the distal fibula as it pertains to fibular nailing. We retrospectively reviewed 197 tibial/fibular CT scans. Measurements of the intramedullary canal were taken at set points (180 mm, 130 mm from the fibular tip, the isthmus, and the widest portion of the fibula) in both the coronal and sagittal planes. 43 CT scans met inclusion criteria. The average width of the isthmus was 4.21 ± 1.08 mm (range, 2.19-7.33 mm) in the coronal plane and 5.27 ± 1.40 mm (range, 1.7-7.91 mm) in the sagittal plane. The average width of the fibula at 130 mm from the distal tip of the fibula was 5.18 ± 1.15 mm (range, 2.46-8.31 mm) in the coronal plane and 6.41 ± 1.45 mm (range, 2.88-9.89 mm) in the sagittal plane. 180 mm from the distal tip of the fibula, the average diameter was 5.77 ± 1.49 mm (range, 3.02-10.2 mm) and 7.18 ± 1.66 mm (range, 2.42-10.42 mm), for the coronal and sagittal planes, respectively. This is the first study of its kind to provide important insight into the distal fibula's intramedullary anatomy, specifically as it pertains to fibular nails. <h3>Level of Evidence</h3> 3

LBA5515 Background: Batiraxcept is an Fc-fusion protein engineered to have a 200-fold higher affinity than wild-type AXL for its activating ligand GAS6. Batiraxcept sequesters GAS6 and inhibits its interaction with AXL. The Phase 1b study demonstrated safety with batiraxcept in combination with paclitaxel. Methods: This was a global, placebo-controlled, double-blind, phase III trial (ClinicalTrials.gov identifier: NCT04729608). Patients with PROC were randomly assigned 1:1 to receive intravenous batiraxcept every 2 weeks (D1, 15 every 28 days) with once-a-week IV paclitaxel (D1, 8, 15 every 28 days) or placebo with paclitaxel until disease progression. The primary endpoint was progression-free survival as assessed by investigator-assessed progression-free survival and secondary endpoint was overall survival. The randomization was stratified by platinum-free interval (&lt; 3 months, 3 to 6 months), prior lines (1 to 2, 3 to 4), and prior bevacizumab status (yes, no). Exploratory endpoints include objective response rate, duration of response, quality of life, clinical benefit rate, and pharmacokinetic and pharmacodynamic profile. Results: A total of 366 participants were randomly assigned, and analysis was performed based on intent-to-treat. There were 183 participants who had prior bevacizumab and 177 with no prior bevacizumab. Median PFS (mPFS) was 5.13 months in the batiraxcept + paclitaxel arm and 5.49 months in the control paclitaxel arm, hazard ratio (HR) 1.29 (CI, 1.01 to 1.64; p=0.98). Median OS with batiraxcept + paclitaxel was 14.29 months versus 14.39 months, HR 1.06 (CI 0.77 to 1.46; p=0.64). Objective response rates (ORRs) per RECIST 1.1 were similar in both arms: 25.1% with batiraxcept + paclitaxel versus 26.2% with control paclitaxel arm. An exploratory analysis of the 304 evaluable tumors found that 61 (20%) of tumors had high AXL expression by immunohistochemistry (IHC). In participants with high tumor AXL expression, median PFS was 5.78 months in the batiraxcept + paclitaxel arm and 3.71 months in the control paclitaxel arm, HR 0.55 (CI, 0.31 to 0.98; p=0.042). For high AXL expressing tumors, median OS was 17.8 months in the batiraxcept + paclitaxel cohort and 8.11 months in the paclitaxel cohort, HR 0.32 (CI, 0.14 to 0.73; p=0.006). Conclusions: The addition of batiraxcept to paclitaxel did not improve PFS or OS. However, in AXL high tumors, the PFS and OS were higher in participants who received batiraxcept with paclitaxel compared to paclitaxel alone. Clinical trial information: NCT04729608 .

Introduction/BackgroundIn the phase 3 RUBY trial (NCT03981796) of patients with primary advanced or recurrent endometrial cancer (pA/rEC), dostarlimab+carboplatin-paclitaxel significantly improved progression-free survival (PFS) versus carboplatin-paclitaxel alone in the mismatch repair deficient/microsatellite instability-high (dMMR/MSI-H) and overall populations with a statistically significant and clinically meaningful benefit in the overall population. Here we report on PFS2-PFS1 (defined as time from disease progression to the date of progression on the first subsequent anticancer therapy following study treatment or death by any cause) in the RUBY trial.Methodology>Patients with pA/rEC were randomised 1:1 to dostarlimab+carboplatin-paclitaxel or placebo+carboplatin-paclitaxel Q3W (6 cycles) followed by dostarlimab or placebo monotherapy Q6W ≤3 years or disease progression. PFS2-PFS1 was a post hoc analysis in all populations.ResultsOf 494 patients randomized (245 dostarlimab+carboplatin-paclitaxel; 249 placebo+carboplatin-paclitaxel), 118 were dMMR/MSI-H (53 dostarlimab+carboplatin-paclitaxel; 65 placebo+carboplatin-paclitaxel). In the dMMR/MSI-H population, median PFS2-PFS1 was longer in the dostarlimab+carboplatin-paclitaxel arm (17.7 vs 10.5 months; HR, 0.77; figure 1). In the mismatch repair proficient/microsatellite stable (MMRp/MSS) population, median PFS2-PFS1 was numerically higher (7.9 vs 7.1 months; HR, 0.82) favouring dostarlimab+carboplatin-paclitaxel; notably, the survival curves progressively separate after approximately 3 months and remain separated. Median PFS2-PFS1 in the overall population was also numerically higher with dostarlimab+carboplatin-paclitaxel (7.9 vs 7.3 months; HR, 0.82). 462 Figure 1ConclusionIn the RUBY trial of patients with pA/rEC, longer PFS2-PFS1 in the dMMR/MSI-H population suggests that patients continue to derive benefit from dostarlimab treatment following disease progression. In the MMRp/MSS population, the early and progressive separation of the KM curves suggest that the PFS1 benefit of immunotherapy+carboplatin-paclitaxel may translate into better long-term outcomes, including PFS2 and eventually overall survival. Overall, these results suggest that the sequencing of dostarlimab+carboplatin-paclitaxel as 1L treatment provides benefit beyond PFS1 into PFS2. This provides further support for dostarlimab+carboplatin-paclitaxel as standard-of-care in pA/rEC.DisclosuresThis study (NCT03981796) was sponsored by GSK, Waltham, MA, USA.Third-party medical writing support: Writing and editorial support, funded and coordinated by GSK (Waltham, MA, USA), was provided by Shannon Morgan-Pelosi, PhD, and Jennifer Robertson, PhD, of Ashfield MedComms, an Inizio company.COI: Dr McCourt reports personal royalties <$200 annually from UpToDate; and personal honoraria of $200 from the Washington University OB/Gyn annual symposium.Dr Shahin reports institutional grants from AstraZeneca, GSK, and Merck; honoraria from AstraZeneca, GSK, Merck, and Seagen; expert testimony fees from Robindon & Havens PSC, Lexington KY; advisory board fees from Seagen; and board member for Unite for Her.Dr Kristeleit reports Grants from Clovis and MSD; honoraria and consultancy fees from Basilea Pharmaceutica, MSD, AstraZeneca, Clovis, Eisai, Incyte, and Pharmamar; and personal fees from GSK.Dr Willmott reports speakers’ bureau fees from Astra Zeneca, Eisai, Immunogen, Merck, and Seagen, and advisory board fees from AstraZeneca, Immunogen, and Seagen.Dr Barlin reports participation on the FLORA and XPORT steering committees, participation in advisory boards for AstraZeneca, Clovis, Mersana, OncoC4, and Immunogen, and participation in speaker’s bureaus for AstraZeneca and Merck.Dr Gilbert reports institutional grants from Alkermes, AstraZeneca, Clovis, Esperas, ImmunoGen Inc, IMV, Karyopharm, Merck Sharp & Dohme, Mersana, Novocure GmbH, OncoQuest Pharmaceuticals, Pfizer, Roche, and Tesaro; consulting fees from Merck; and honoraria from Alkermes, AstraZeneca, Eisai, Eisai-Merck, and GSK.Dr Cloven reports participation in advisory boards for GSK, Kartos, Novita, Takeda, Toray, Umoja, and Zentalis.Dr Bjørge reports grants/research support from AstraZeneca, honoraria/consulting fees from Onsanger, and participation in a company-sponsored speakers’ bureau for MSD.Dr Black reports institutional grant fees from GSK; fees for being a member of GOG Partners Investigational Council; and medical director/owner of Trials365, LLC.Dr Mathews reports institutional research funding from AvengeBio Astellas Pharma, AstraZeneca, Deciphera, EMD Serono, Genentech, Genmab, GSK, Merck, Moderna, The National Cancer Institute, Regeneron, Seagen, and Syros.Dr Powell reports grants/research support from GSK and honoraria/consultation fees from AstraZeneca, Clovis Oncology, Eisai, GSK, Immunogen, and Merck. Dr Gilbert reports institutional grants from Alkermes, GSK, Immunogen Inc, Karyopharm, Merck Sharp & Dohme, Pfizer, Roche, and Tesaro and honoraria/consultation fees from Alkermes, Eisai, Eisai-Merck, GSK, Merck, and Novocure.Dr Mirza reports institutional research grants from Allarity, Apexigen, AstraZeneca, Boehringer Ingelheim, Clovis, GSK, Novartis, and Ultimovacs; trial chair for Deciphera, Mersana, and NuvationBio; invited speaker for AstraZeneca, GenMab, GSK, Mersana, Seagen, and Takeda; a member of board of directors and holds stocks and shares for Karyopharm and Sera Prognostics.Drs Gold, Landrum, Ronzino, Sharma, Wymenga, and Zub have nothing disclose.Drs Antony and Stevens are employees of GSK.

Arthritis of the first metatarsophalangeal (MTP) joint, hallux rigid, is a common and disabling source of foot pain in the adult population. Hallux rigidus is characterized by diseased cartilage and large, periarticular osteophytes that result in a stiff, painful joint. Activity modification, sensible shoes, orthotics, anti-inflammatory medications and occasional intra-articular steroid injections can be attempted to alleviate the discomfort associated with hallux rigidus. A number of surgical options exist for the treatment of recalcitrant hallux rigidus. Cheilectomy is a useful treatment for dorsal impingement pain seen in mild hallux rigidus. A new polyvinyl alcohol hemi-arthroplasty implant has shown promising early and midterm results in the treatment of advanced hallux rigidus; however, arthrodesis of the first MTP joint remains the gold standard treatment for advanced hallux rigidus because of unpredictable outcomes after early-generation joint replacement implants.