Citations

Background: Biomechanical studies support the use of suture tape reinforcement for limiting graft elongation and increasing strength in knee ligament reconstructions. Purpose: To compare posterior cruciate ligament (PCL) laxity, complication and reoperation rates, and patient-reported outcomes (PROs) after all-inside single-bundle PCL reconstruction (PCLR) with versus without independent suture tape reinforcement. Study Design: Cohort study; Level of evidence, 3. Methods: A retrospective cohort study of consecutive patients who underwent primary, all-inside allograft single-bundle PCLR with and without independent suture tape reinforcement at a single academic institution from 2012 to 2019. Medical records were reviewed for patient characteristics, additional injuries, and concomitant procedures. PRO scores (including the International Knee Documentation Committee [IKDC], Tegner activity scale, and Lysholm scores), bilateral comparison kneeling radiographs, and physical examination findings were collected at a minimum of 2 years postoperatively. Results: Included were 50 patients: 19 with suture tape reinforcement (mean age 30.6 ± 2.9 years) and 31 without suture tape reinforcement (control group; mean age 26.2 ± 1.6 years). One PCLR graft in the suture tape group failed. Posterior drawer examination revealed grade 1+ laxity in 4 of 19 (21%) of the suture tape cohort versus 6 of 31 (19%) of the control cohort ( P > .999). Bilateral kneeling radiographs showed similar side-to-side differences in laxity between the groups (suture tape vs control: mean, 1.9 ± 0.4 vs 2.6 ± 0.6 mm; P = .361). There were no statistically significant differences between the groups in postoperative IKDC (suture tape vs control: 79.3 vs 79.6; P = .779), Lysholm (87.5 vs 84.3; P = .828), or Tegner activity (5.6 vs 5.7; P = .562) scores. Conclusion: All-inside single-bundle PCLR with and without independent suture tape reinforcement demonstrated low rates of graft failure, complications, and reoperations, with satisfactory PROs at a minimum 2-year follow-up. Radiographic posterior tibial translation was comparable between the 2 groups.

Abstract Background Obesity is an established risk factor for colorectal cancer (CRC), but the evidence for the association is inconsistent across molecular subtypes of the disease. Methods We pooled data on body mass index (BMI), tumor microsatellite instability status, CpG island methylator phenotype status, BRAF and KRAS mutations, and Jass classification types for 11 872 CRC cases and 11 013 controls from 11 observational studies. We used multinomial logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) adjusted for covariables. Results Higher BMI was associated with increased CRC risk (OR per 5 kg/m2 = 1.18, 95% CI = 1.15 to 1.22). The positive association was stronger for men than women but similar across tumor subtypes defined by individual molecular markers. In analyses by Jass type, higher BMI was associated with elevated CRC risk for types 1-4 cases but not for type 5 CRC cases (considered familial-like/Lynch syndrome microsatellite instability-H, CpG island methylator phenotype-low or negative, BRAF-wild type, KRAS-wild type, OR = 1.04, 95% CI = 0.90 to 1.20). This pattern of associations for BMI and Jass types was consistent by sex and design of contributing studies (cohort or case-control). Conclusions In contrast to previous reports with fewer study participants, we found limited evidence of heterogeneity for the association between BMI and CRC risk according to molecular subtype, suggesting that obesity influences nearly all major pathways involved in colorectal carcinogenesis. The null association observed for the Jass type 5 suggests that BMI is not a risk factor for the development of CRC for individuals with Lynch syndrome.

Abstract The external globus pallidus (GPe) coordinates action-selection through GABAergic projections throughout the basal ganglia. GPe arkypallidal (arky) neurons project exclusively to the dorsal striatum, which regulates goal-directed and habitual reward-seeking. However, the role of GPe arky neurons in reward-seeking remains unknown. Here, we identified that a majority of arky neurons target the dorsolateral striatum (DLS). Using fiber photometry, we found that arky activities were higher during random interval (RI; habit) compared to random ratio (RR; goal) operant reward-seeking. Support vector machine analysis demonstrated that arky neuron activities have sufficient information to distinguish between RR and RI behavior. Genetic ablation of this arkyGPe◊DLS circuit facilitated a shift from goal-directed to habitual behavior. Conversely, chemogenetic activation reduced habitual seeking-behaviors, which was blocked by systemic D1R agonism. Our findings reveal a novel role of this arkyGPe◊DLS circuit in constraining habitual reward-seeking, which is relevant to addictive behaviors and other compulsive disorders.

NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Pediatric Aggressive Mature B-Cell Lymphomas include recommendations for the diagnosis and management of pediatric patients with primary mediastinal large B-cell lymphoma (PMBL) and sporadic variants of Burkitt lymphoma and diffuse large B-cell lymphoma. PMBL is now considered as a distinct entity arising from mature thymic B-cells accounting for 2% of mature B-cell lymphomas in children and adolescents. This discussion section includes the recommendations outlined in the NCCN Guidelines for the diagnosis and management of pediatric patients with PMBL.

Background: There is a dearth of knowledge on anterior shoulder instability in older patients. Purpose/Hypothesis: The purposes of this study were to describe the incidence and epidemiology, injury characteristics, and treatment and outcomes in patients ≥50 years old with first-time anterior shoulder instability. We also describe the historical trends in diagnosis and treatment. It was hypothesized that the rates of obtaining a magnetic resonance imaging (MRI) scan and surgical intervention have increased over the past 20 years. Study Design: Descriptive epidemiology study. Methods: An established geographic database was used to identify 179 patients older than 50 years who experienced new onset anterior shoulder instability between 1994 and 2016. Medical records were reviewed to obtain patient characteristics, imaging characteristics, and surgical treatment and outcomes, including recurrent instability. Comparative analysis was performed to identify differences between age groups. Mean follow-up time was 11 years. Results: The incidence of first-time anterior shoulder dislocation in our study population was 28.8 per 100,000 person-years, which is higher than previously reported. Full-thickness rotator cuff tears were found in 62% of the 66 patients who underwent MRI scans. Of all patients, 26% progressed to surgery at a mean time of 1.6 years after injury; 57% of all surgical procedures involved a rotator cuff repair, and 17% included anterior labral repair. All patients who underwent a labral repair also underwent concomitant rotator cuff repair. The rate of recurrent instability for the cohort was 15% at a median of 176 days after the initial instability event. There were no instances of recurrent instability after operative intervention. At an average of 7.5 years after the initial instability event, 14% of patients developed radiographic progression of glenohumeral arthritis. The rate of surgical intervention within 1 year of initial dislocation increased from 5.1% in 1994 to 1999 to 52% in 2015 to 2016. Conclusion: The incidence of first-time anterior shoulder instability in patients aged ≥50 years was 28.8 per 100,000 person-years. Full-thickness rotator cuff tears (62%) were the most common condition associated with anterior shoulder instability, followed by Hill-Sachs lesions (56%). The rate of recurrent instability for the entire cohort was 15%, with no instances of recurrent instability after operative intervention.

AbstractBackgroundDisruption of central circadian rhythms likely mediated by changes in microbiota and a decrease in gut-derived metabolites like short chain fatty acids (SCFAs) negatively impacts colonic barrier homeostasis. We aimed to explore the effects of isolated peripheral colonic circadian disruption on the colonic barrier in a mouse model of colitis and explore the mechanisms, including intestinal microbiota community structure and function.MethodsColon epithelial cell circadian rhythms were conditionally genetically disrupted in mice: TS4Cre-BMAL1lox (cBMAL1KO) with TS4Cre as control animals. Colitis was induced through 5 days of 2% dextran sulfate sodium (DSS). Disease activity index and intestinal barrier were assessed, as were fecal microbiota and metabolites.ResultsColitis symptoms were worse in mice with peripheral circadian disruption (cBMAL1KO). Specifically, the disease activity index and intestinal permeability were significantly higher in circadian-disrupted mice compared with control animals (TS4Cre) (P < .05). The worsening of colitis appears to be mediated, in part, through JAK (Janus kinase)-mediated STAT3 (signal transducer and activator of transcription 3), which was significantly elevated in circadian-disrupted (cBMAL1KO) mice treated with DSS (P < .05). Circadian-disrupted (cBMAL1KO) mice also had decreased SCFA metabolite concentrations and decreased relative abundances of SCFA-producing bacteria in their stool when compared with control animals (TS4Cre).ConclusionsDisruption of intestinal circadian rhythms in colonic epithelial cells promoted more severe colitis, increased inflammatory mediators (STAT3 [signal transducer and activator of transcription 3]), and decreased gut microbiota–derived SCFAs compared with DSS alone. Further investigation elucidating the molecular mechanisms behind these findings could provide novel circadian directed targets and strategies in the treatment of inflammatory bowel disease.

Background To standardize renal functional magnetic resonance imaging (MRI), it is important to understand the influence of side‐to‐side variation, regional variation within the organ, and hydration states in MRI and to search for variables that are not affected by those variations. Purpose To assess MRI‐based biomarkers for characterizing the kidney in healthy volunteers while considering variations in anatomic factors and hydration states. Study Type Prospective. Subjects Twenty‐five healthy volunteers (15 females and 10 males, median age 25 years). Field Strength/Sequence 3.0 T intravoxel incoherent motion diffusion‐weighted imaging, arterial spinning labeling imaging, blood oxygenation level dependent imaging, and three‐dimensional MR elastography. Assessment Functional variables were measured before and after water challenge. Regions of interest were manually drawn by two investigators (JC and ZZ, with 8‐ and 5‐year experiences in abdominal radiology) in the cortex, the medulla, and the entire kidney. The medulla/cortex ratio was calculated. Statistical Tests Paired t ‐test or Wilcoxon signed rank test; interobserver correlation coefficient; repeatability coefficients; Spearman's correlation; significance level: P < 0.05. Results Diffusion parameters were only subject to regional variation. R2*, RBF, and renal stiffness (RS) showed regional variation, side variation, and dependence on hydration states. For each side and hydration state, the cortex showed significantly higher standard apparent diffusion coefficient (sADC), higher true diffusion ( D ), lower R2*, and lower RS than the medulla. For each region at baseline, the left kidney showed significantly higher R2*, higher RS, and lower renal blood flow (RBF) than the right kidney. For each region and side, RS and RBF increased significantly while R2* decreased significantly after water intake. After introducing the intrinsic regional difference, significantly higher medulla/cortex ratio of RS remained after water intake except for RS@90 Hz in the right kidney. Data Conclusion Renal multiparametric MRI quantifications were affected by regional variation, side variation, and hydration states. Level of Evidence 2 Technical Efficacy Stage 1