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Purpose To (1) evaluate the efficacy of surgery for arthrofibrosis (AF), as measured by preoperative and postoperative range of motion (ROM), and (2) evaluate patient‐reported outcomes at mid‐ to long‐term follow‐up. Methods We performed a retrospective review of a prospectively collected database including patients who sustained multiligamentous knee injuries (MLKIs) managed surgically, sustained loss of ROM after surgical intervention, and underwent subsequent lysis of adhesions (LOA) and/or manipulation under anesthesia (MUA). Loss of ROM was defined as clinically symptomatic loss of terminal extension (flexion deformity) and/or flexion compared with the contralateral side. Results In total, 12 patients (6 male and 6 female patients; age, 36.0 ± 8.7 years; body mass index, 36.3 ± 8.7) met the inclusion criteria and underwent LOA and/or MUA at a mean of 14 ± 27 months (median, 4.0 months; interquartile range, 3.5‐9.3 months) after MLKI surgery. Prior to AF intervention, patients showed mean flexion of 75.9° ± 36.0° (range, 30°‐129°), mean extension of 3.2° ± 5.2° (range, 0°‐12°), and a mean arc of motion of 72.7° ± 34.1° (range, 30°‐117°). At a mean follow‐up of 7.0 ± 3.9 years (range, 2.4‐16.6 years) after AF intervention, patients showed a significant increase in knee flexion of 49° ( P = .003), a significant increase in arc of motion of 51° ( P = .002), and an increase in extension of 3° ( P = .086). The mean final International Knee Documentation Committee score was 59.5 ± 23.9; Lysholm score, 72.1 ± 20.6; Tegner activity scale score, 5.6 ± 2.8; visual analog scale score at rest, 1.0 ± 1.6; and visual analog scale score with use, 3.3 ± 2.5. At final follow‐up, 2 patients (17%) had undergone conversion to total knee arthroplasty (TKA) at 10.3 and 24.8 years after MLKI surgery. Of the 10 patients who did not go on to TKA, 9 (90%) reported that they were satisfied or very satisfied with their AF knee surgery. Conclusions At mid‐term follow‐up, LOA and/or MUA for symptomatic AF after multiligamentous knee surgery results in high rates of patient satisfaction and improved knee ROM and pain scores, as well as durable and satisfactory functional outcomes in patients not undergoing TKA. Level of Evidence Level IV, therapeutic case series.

Abstract We examined the individual prognostic contribution of absolute neutrophil (ANC), lymphocyte (ALC), and monocyte (AMC) counts, on overall (OS), leukemia‐free (LFS), and myelofibrosis‐free (MFFS) survival in essential thrombocythemia (ET). Informative cases ( N = 598; median age 59 years; females 62%) were retrospectively accrued from a Mayo Clinic database: JAK2 59%, CALR 27%, triple‐negative 11%, and MPL 3%; international prognostic scoring system for ET (IPSET) risk high 21%, intermediate 42%, and low 37%; 7% (37/515) had abnormal karyotype and 10% (21/205) adverse mutations ( SF3B1/SRSF2/U2AF1/TP53 ). At median 8.4 years, 163 (27%) deaths, 71 (12%) fibrotic, and 20 (3%) leukemic transformations were recorded. Multivariable analysis resulted in HR (95% CI) of 16.5 (9.9–27.4) for age > 70 years, 3.7 (2.3–6.0) for age 50–70 years, 2.4 (1.7–3.3) for ANC ≥8 × 10 9 /L, and 1.9 (1.4–2.6) for ALC <1.7 × 10 9 /L. The corresponding HR‐based scores were 4, 2, 1, and 1, resulting in an new 4‐tiered AgeAncAlc (AAA; triple A) risk model: high (5–6 points; median survival 8 years; HR 30.1, 95% CI 17.6–54), intermediate‐2 (4 points; median 13.5 years; HR 12.7, 95% CI 7.1–23.0), intermediate‐1 (2–3 points; median 20.7 years; HR 3.8, 95% CI 2.3–6.4) and low (0–1 points; median 47 years). The AAA model (Akaike Information Criterion [AIC] 621) performed better than IPSET (AIC 647) and was subsequently validated by an external University of Florence ET cohort ( N = 485). None of the AAA variables predicted LFS while ALC <1.7 × 10 9 /L was associated with inferior MFFS ( p = .01). Adverse mutations ( p < .01) and karyotype ( p < .01) displayed additional prognostic value without disqualifying the prognostic integrity of the AAA model. This study proposes a simple and globally applicable survival model for ET, which can be used as a platform for further molecular refinement. This study also suggests a potential role for immune‐related biomarkers, as a prognostic tool in myeloproliferative neoplasms.

The objective of this article is to review the evidence of abnormal gastrointestinal (GI) tract motor functions in the context of disorders of gut–brain interaction (DGBI). These include abnormalities of oesophageal motility, gastric emptying, gastric accommodation, colonic transit, colonic motility, colonic volume and rectal evacuation. For each section regarding GI motor dysfunction, the article describes the preferred methods and the documented motor dysfunctions in DGBI based on those methods. The predominantly non-invasive measurements of gut motility as well as therapeutic interventions directed to abnormalities of motility suggest that such measurements are to be considered in patients with DGBI not responding to first-line approaches to behavioural or empirical dietary or pharmacological treatment.

Neurological disorders and type 2 diabetes mellitus (T2DM) are deeply intertwined. For example, autonomic neuropathy contributes to the development of T2DM and continued unmanaged T2DM causes further progression of nerve damage. Increasing glycemic control has been shown to prevent the onset and progression of diabetic autonomic neuropathies. Neuromodulation consisting of combined stimulation of celiac vagal fibers innervating the pancreas with concurrent electrical blockade of neuronal hepatic vagal fibers innervating the liver has been shown to increase glycemic control in animal models of T2DM. The present study demonstrated that the neuromodulation reversed glucose intolerance in alloxan-treated swine in both pre- and overt stages of T2DM. This was demonstrated by improved performance on oral glucose tolerance tests (OGTTs), as assessed by area under the curve (AUC). In prediabetic swine (fasting plasma glucose (FPG) range: 101–119 mg/dL) the median AUC decreased from 31.9 AUs (IQR = 28.6, 35.5) to 15.9 AUs (IQR = 15.1, 18.3) p = 0.004. In diabetic swine (FPG range: 133–207 mg/dL) the median AUC decreased from 54.2 AUs (IQR = 41.5, 56.6) to 16.0 AUs (IQR = 15.4, 21.5) p = 0.003. This neuromodulation technique may offer a new treatment for T2DM and reverse glycemic dysregulation at multiple states of T2DM involved in diabetic neuropathy including at its development and during progression.

Transplant pathology plays a critical role in ensuring that transplanted organs function properly and the immune systems of the recipients do not reject them. To improve outcomes for transplant recipients, accurate diagnosis and timely treatment are essential. Recent advances in artificial intelligence (AI)-empowered digital pathology could help monitor allograft rejection and weaning of immunosuppressive drugs. To explore the role of AI in transplant pathology, we conducted a systematic search of electronic databases from January 2010 to April 2023. The PRISMA checklist was used as a guide for screening article titles, abstracts, and full texts, and we selected articles that met our inclusion criteria. Through this search, we identified 68 articles from multiple databases. After careful screening, only 14 articles were included based on title and abstract. Our review focuses on the AI approaches applied to four transplant organs: heart, lungs, liver, and kidneys. Specifically, we found that several deep learning-based AI models have been developed to analyze digital pathology slides of biopsy specimens from transplant organs. The use of AI models could improve clinicians’ decision-making capabilities and reduce diagnostic variability. In conclusion, our review highlights the advancements and limitations of AI in transplant pathology. We believe that these AI technologies have the potential to significantly improve transplant outcomes and pave the way for future advancements in this field.

This commentary offers the reader an alternative to mentoring through the use of PODCASTS. By providing the listener with an understanding of the challenges and opportunities for self-reflection and sharing of experiences by the interviewees, we are impacting the listener attitudes and future goals through lessons learned.

Abstract This manuscript describes a novel approach for treating patients with long‐term sequelae from hemoglobin Evans (Hb Evans). After instituting conservative therapies for approximately 2 years, our patient's symptoms continually worsened. Therefore, we performed red blood cell exchange (RBCx) to reduce his Hb Evans percentage and his co‐existing elevation of methemoglobin. Our assumptions of clinical benefit were based on our collective experience performing RBCx for patients with sickle cell disease. After the first exchange, pre‐ and post‐laboratory results supported our approach and the patient experienced marked improvement in his clinical signs and symptoms. This report provides preliminary proof of principle for the use of RBCx to treat Hb Evans and other non‐Hb S hemoglobinopathies.

Background: Normative changes in right ventricular (RV) structure and function have not been characterized in the context of treatment-associated functional recovery (RV functional recovery [RVFnRec]). The aim of this study is to assess the clinical relevance of a proposed RVFnRec definition. Methods: We evaluated 63 incident patients with pulmonary arterial hypertension by right heart catheterization and cardiac magnetic resonance imaging at diagnosis and cardiac magnetic resonance imaging and invasive cardiopulmonary exercise testing following treatment (≈11 months). Sex, age, ethnicity matched healthy control subjects (n=62) with 1-time cardiac magnetic resonance imaging and noninvasive cardiopulmonary exercise testing were recruited from the PVDOMICS (Redefining Pulmonary Hypertension through Pulmonary Vascular Disease Phenomics) project. We examined therapeutic cardiac magnetic resonance imaging changes relative to the evidence-based peak oxygen consumption (VO 2peak )>15 mL/(kg·min) to define RVFnRec by receiver operating curve analysis. Afterload was measured as mean pulmonary artery pressure, resistance, compliance, and elastance. Results: A drop in RV end-diastolic volume of −15 mL best defined RVFnRec (area under the curve, 0.87; P =0.0001) and neared upper 95% CI RV end-diastolic volume of controls. This cutoff was met by 22 out of 63 (35%) patients which was reinforced by freedom from clinical worsening, RVFnRec 1 out of 21 (5%) versus no RVFnRec 17 out of 42, 40% (log-rank P =0.006). A therapy-associated increase of 0.8 mL/mm Hg in compliance had the best predictive value of RVFnRec (area under the curve, 0.76; [95% CI, 0.64–0.88]; P =0.001). RVFnRec patients had greater increases in stroke volume, and cardiac output at exercise. Conclusions: RVFnRec defined by RV end-diastolic volume therapeutic decrease of −15 mL predicts exercise capacity, freedom from clinical worsening, and nears normalization. A therapeutic improvement of compliance is superior to other measures of afterload in predicting RVFnRec. RVFnRec is also associated with increased RV output reserve at exercise.

LINKED CONTENTThis article is linked to Ravi et al and Uchida & Dougan papers. To view these articles, visit https://doi.org/10.1111/apt.16180 and https://doi.org/10.1111/apt.16205