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As institutions strive to improve teaching and learning for all, educators must consider equitable instruction. This includes equitable distributions of authority and agency among students. The authors define distribution of authority as shared opportunities for decision-making in enacting mathematical tasks and agency as the power to carry out these self-made decisions. Equitable distributions of authority and agency can be enhanced in mathematics public sensemaking classrooms where students participate in discourse as active members of the classroom. In public sensemaking classrooms, students understand and acknowledge one another's ideas, present and revise arguments, and take risks by sharing ideas. This study investigates one group of students and how they positioned one another during mathematical groupwork in a public sensemaking classroom as well as how the positioning impacted the distribution of agency and authority. At the time of data collection, the students attended a school for grades 6-12 situated in an urban public school that focuses largely on preparing students for careers in the health sciences and other health-related fields. Data was collected as video footage and analyzed using a priori codes. Analyses indicate that one student replicates the role of teacher by redistributing authority and agency back to other students through self-removal. This is contrasted with other motivations for self-removal while doing mathematics in a team. The findings inform researchers and classroom teachers of potential metacognitive awareness of equity between students, positioning patterns that may occur during collaborative groupwork, and the effectiveness of public sensemaking classrooms on distributing authority and agency equitably during groupwork.

Aims: Veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) is a life‐saving procedure for supporting patients with cardiogenic shock after cardiac surgery. This work aimed to analyse the impact of changes in blood lactate levels on the survival of patients on post‐cardiotomy ECMO (PC‐ECMO) and whether lactate clearance (LC) performs better than absolute lactate levels. Methods and Results: We retrospectively analysed the data of adult patients who received PC‐ECMO at our centre between 2016 and 2022. The primary outcome was the in‐hospital mortality rate. Arterial lactate levels were measured at ECMO initiation, peak and 12 and 24 h after VA‐ECMO support. LC was calculated at 12 and 24 h. Out of 2368 patients who received cardiac surgeries, 152 (median age, 48 years; 57.9% of them were men) received PC‐ECMO. Of them, 48 (31.6%) survived and were discharged, while 104 (68.4%) died during the index hospitalization. Non‐survivors had higher frequencies of atrial fibrillation (41.35% vs. 12.5%, P < 0.001), chronic kidney disease (26.9% vs. 6.3%, P = 0.004), prolonged cardiopulmonary bypass (237 vs. 192 min, P = 0.016) and aortic cross‐clamping times (160 vs. 124 min, P = 0.04) than survivors. Non‐survivors had a significantly higher median Sequential Organ Failure Assessment (SOFA) score at ECMO initiation (13.5 vs. 9, P < 0.001) and a lower median Survival After Veno‐arterial ECMO (SAVE) score (−3 vs. 3, P < 0.001) with higher SAVE classes (P < 0.001) than survivors. After 12 h of VA‐ECMO support, the blood lactate level was negatively correlated with LC in survivors (r = −0.755, P < 0.001) and non‐survivors (r = −0.601, P < 0.001). After 24 h, the same negative correlation was identified between survivors (r = −0.764, P < 0.001) and non‐survivors (r = −0.847, P < 0.001). Blood lactate levels measured at 12 h to determine hospital mortality [>8.2 mmol/L, area under the receiver operating characteristic curve (AUROC): 0.868] and 24 h (>2.6 mmol/L, AUROC: 0.896) had the best performance, followed by LC‐T12 (<21.94%, AUROC: 0.807), LC‐T24 (<40.3%, AUROC: 0.839) and peak blood lactate (>14.35 mmol/L, AUROC: 0.828). The initial pre‐ECMO blood lactate (>6.25 mmol/L, AUROC: 0.731) had an acceptable ability to discriminate mortality but was less than the following measurements and clearance. Kaplan–Meier curves demonstrated that LC of <21.94% at T12 h and <40.3% at T24 h was associated with decreased survival (log‐rank P < 0.001). Cox proportional hazards regression analysis for mortality revealed that LC of <21.94% at T12 h had an adjusted hazard ratio (HR) of 2.73 [95% confidence interval (CI): 1.64–5.762, P < 0.001] and LC of <40.3% at T24 h had an adjusted HR of 1.98 (95% CI: 1.46–4.173, P < 0.001). The predictors of hospital mortality after PC‐ECMO were the lactate level at 12 h [odds ratio (OR): 1.67, 95% CI: 1.121–2.181, P = 0.001], initial SOFA score (OR: 1.593, 95% CI: 1.15–2.73, P < 0.001), initial blood lactate (OR: 1.21, 95% CI: 1.016–1.721, P = 0.032) and atrial fibrillation (OR: 6.17, 95% CI: 2.37–57.214, P = 0.003). Bivariate models using lactate levels and clearance at the same points revealed that blood lactate levels performed better than the clearance percentage. Conclusions: Serial measurements of arterial blood lactate and LC help in obtaining early prognostic guidance in adult patients supported by VA‐ECMO after cardiac surgery. Absolute lactate levels, compared with LC at the same time points, demonstrated better performance in differentiating mortality. [ABSTRACT FROM AUTHOR]

RationaleConsideration of lung transplantation in patients with systemic sclerosis (SSc) remains guarded, often due to the concern for esophageal dysfunction and the associated potential for allograft injury and suboptimal post-lung transplantation outcomes.ObjectivesThe purpose of this study was to systematically report our single-center experience regarding lung transplantation in the setting of SSc, with a particular focus on esophageal dysfunction.MethodsWe retrospectively reviewed all lung transplants at our center from January 1, 2000 through August 31, 2012 (n = 562), comparing the SSc group (n = 35) to the following lung transplant diagnostic subsets: all non-SSc (n = 527), non-SSc diffuse fibrotic lung disease (n = 264), and a non-SSc matched group (n = 109). We evaluated post-lung transplant outcomes, including survival, primary graft dysfunction, acute rejection, bronchiolitis obliterans syndrome, and microbiology of respiratory isolates. In addition, we defined severe esophageal dysfunction using esophageal manometry and esophageal morphometry criteria on the basis of chest computed tomography images. For patients with SSc referred for lung transplant but subsequently denied (n = 36), we queried the reason(s) for denial with respect to the concern for esophageal dysfunction.Measurements and main resultsThe 1-, 3-, and 5-year post-lung transplant survival for SSc was 94, 77, and 70%, respectively, and similar to the other groups. The remaining post-lung transplant outcomes evaluated were also similar between SSc and the other groups. Approximately 60% of the SSc group had severe esophageal dysfunction. Pre-lung transplant chest computed tomography imaging demonstrated significantly abnormal esophageal morphometry for SSc when compared with the matched group. Importantly, esophageal dysfunction was the sole reason for lung transplant denial in a single case.ConclusionsRelative to other lung transplant indications, our SSc group experienced comparable survival, primary graft dysfunction, acute rejection, bronchiolitis obliterans syndrome, and microbiology of respiratory isolates, despite the high prevalence of severe esophageal dysfunction. Esophageal dysfunction rarely precluded active listing for lung transplantation.

Aim: Giant colorectal polyps (≥3 cm) can be managed by endoscopic excision or surgical resection. There has been a shift to endoscopic submucosal dissection (ESD) for the treatment of such lesions as the expertise in advanced therapeutic endoscopy develops. This study aims to compare the outcome and safety profile of ESD against surgical resection for patients with giant colorectal polyps. Methods: We performed a retrospective review on patients with giant colorectal polyps removed by either ESD or surgery over a 10‐year period (from May 2010 to September 2020) in a regional hospital in Hong Kong. Propensity score matching was performed based on patient demographics and polyp characteristics. Outcomes including polyp histology, complication rates, length of hospital stay, and re‐admission rates were analysed. Results: Fifty‐one patients (ESD group: 34, surgery group: 17) were included in the analysis. The mean polyp diameter was 3.35 cm (ESD group) and 3.53 cm (surgery group). The median procedure time was comparable (160 vs 167 min; P =.251) and the most common polyp histological type was tubulovillous adenoma (44.1% vs 47.1%; P =.130) for both groups. A shorter median length of stay (1 day vs 6 days; P =.028) and lower re‐admission rate (0% vs 5.9%; P <.001) were observed in the ESD group, whereas a higher major complication rate (Clavien–Dindo classification grade IIIa or above; 2.9% vs 11.7%; P =.013) was observed in the surgery group. Conclusions: ESD is a safe and effective treatment for giant colonic polyps with ESD size ≥3 cm. It has the advantage of lower complication rates, shorter length of hospital stays, and lower re‐admission rates compared with surgical resection. [ABSTRACT FROM AUTHOR]

Background Colorectal cancer (CRC) is the third highest incidence cancer and is the leading cause of cancer mortality worldwide. Metastasis to distal organ is the major cause of cancer mortality. However, the underlying genetic factors are unclear. This study aimed to identify metastasis-relevant genes and pathways for better management of metastasis-prone patients. Methods A case-case genome-wide association study comprising 2677 sporadic Chinese CRC cases (1282 metastasis-positive vs 1395 metastasis-negative) was performed using the Human SNP6 microarray platform and analysed with the correlation/trend test based on the additive model. SNP variants with association testing -log10 p value =5 were imported into Functional Mapping and Annotation (FUMA) for functional annotation. Results Glycolysis was uncovered as the top hallmark gene set. Transcripts from two of the five genes profiled, hematopoietic substrate 1 associated protein X 1 (HAX1) and hyaluronan-mediatedmotility receptor (HMMR), were significantly upregulated in the metastasis-positive tumours. In contrast to disease-risk variants, HAX1 appeared to act synergistically with HMMR in significantly impacting metastasis-free survival. Examining the subtype datasets with FUMA and Ingenuity Pathway Analysis (IPA) identified distinct pathways demonstrating sexual dimorphism in CRC metastasis. Conclusions Combining genome-wide association testing with in silico functional annotation and wet-bench validation identified metastasis-relevant genes that could serve as features to develop subtype-specific metastasis-risk signatures for tailored management of patients with stage I-III CRC. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is the third highest incidence cancer and a leading cause of cancer mortality worldwide. To date, chemotherapeutic treatment of advanced CRC that has metastasized has a dismayed success rate of less than 30%. Further, most (80%) sporadic CRCs are microsatellite-stable and are refractory to immune checkpoint blockade therapy. KRAS is a gatekeeper gene in colorectal tumorigenesis. Nevertheless, KRAS is 'undruggable' due to its structure. Thus, focus has been diverted to develop small molecule inhibitors for its downstream effector such as ERK/MAPK. Despite intense research efforts for the past few decades, no small molecule inhibitor has been in clinical use for CRC. Antibody targeting KRAS itself is an attractive alternative. We developed a transient ex vivo patient-derived matched mucosa-tumor primary culture to assess whether anti-KRAS antibody can be internalized to bind and inactivate KRAS. We showed that anti-KRAS antibody can enter live mucosa-tumor cells and specifically aggregate KRAS in the cytoplasm, thus hindering its translocation to the inner plasma membrane. The mis-localization of KRAS reduces KRAS dwelling time at the site where it tethers to activate downstream effectors. We previously showed that expression of SOX9 was KRAS-mutation-dependent and possibly a better effector than ERK in CRC. Herein, we showed that anti-KRAS antibody treated tumor cells have less intense SOX9 cytoplasmic and nuclear staining compared to untreated cells. Our results demonstrated that internalized anti-KRAS antibody inhibits KRAS function in tumor. With an efficient intracellular antibody delivery system, this can be further developed as combinatorial therapeutics for CRC and other KRAS-driven cancers. [ABSTRACT FROM AUTHOR]

Background: The optimal interval between completion of neoadjuvant chemoradiotherapy and surgery in rectal adenocarcinoma was controversial. Aim: To study the impact of standard versus extended time interval for surgery after neoadjuvant chemoradiotherapy in relation to the surgical outcomes in locally advanced rectal cancer. Method: Retrospective review on consecutive patients with rectal adenocarcinoma completed long course neoadjuvant chemoradiation and surgery in New Territories West cluster, Hong Kong. Patients were divided into three groups according to time interval before surgery: group A (<12 weeks), group B (13–15 weeks) and group C (>15 weeks). Primary outcome was overall recurrence, including local and distant recurrence. Secondary outcomes included surgical morbidities, complete pathological responses and 5‐year survival. Results: A total of 107 patients were recruited between January 2010 and December 2014. The waiting period had no impact on medical and surgical complications, pathological complete response (pCR), and downstaging effect. Intensive care unit (ICU) admission, and permanent stoma rate were significantly increased with waiting period more than 15 weeks. The 2‐year and 5‐year overall recurrence rate, 5‐year disease‐free and overall survival were similar among the three groups. Time interval of surgery more than 15 weeks had six times higher risk of 5‐year overall recurrence in multivariable logistic regression analysis. Conclusion: Interval of surgery more than 12 weeks after completion of long course neoadjuvant chemoradiotherapy did not improve oncological outcomes. [ABSTRACT FROM AUTHOR]