Does surgeon or hospital volume influence outcome in dedicated colorectal units?-A Viennese perspective.

OBJECTIVE: A clear relationship between higher surgeon volume and improved outcomes has not been convincingly established in rectal cancer surgery. The aim of this study was to evaluate the impact of individual surgeon's caseload and hospital volume on perioperative outcome. METHODS: We retrospectively analyzed 336 consecutive patients undergoing oncological resection for rectal cancer at two Viennese hospitals between 1 January 2015 and 31 December 2020. The effect of baseline characteristics as well as surgeons' caseloads (low volume: 0-5 cases per year, high volume > 5 cases per year) on postoperative complication rates (Clavien-Dindo Classification groups of < 3 and ≥ 3) were evaluated. RESULTS: No differences in baseline characteristics were found between centers in terms of sex, smoking status, or comorbidities of patients. Interestingly, only 14.7% of surgeons met the criteria to be classified as high-volume surgeons, while accounting for 66.3% of all operations. There was a significant difference in outcomes depending on the treating center in univariate and multivariate binary logistic regression analysis (odds ratio (OR) = 2.403, p = 0.008). Open surgery was associated with lower complication rates than minimally invasive approaches in univariate analysis (OR = 0.417, p = 0.003, 95%CI = 0.232-0.739) but not multivariate analysis. This indicated that the center's policy rather than surgeon volume or mode of surgery impact on postoperative outcomes. CONCLUSION: Treating center standards impacted on outcome, while individual caseload of surgeons or mode of surgery did not independently affect complication rates in this analysis. The majority of rectal cancer resections are performed by a small number of surgeons in Viennese hospitals.

miRNA-132/212 Gene-Deletion Aggravates the Effect of Oxygen-Glucose Deprivation on Synaptic Functions in the Female Mouse Hippocampus.

Cerebral ischemia and its sequelae, which include memory impairment, constitute a leading cause of disability worldwide. Micro-RNAs (miRNA) are evolutionarily conserved short-length/noncoding RNA molecules recently implicated in adaptive/maladaptive neuronal responses to ischemia. Previous research independently implicated the miRNA-132/212 cluster in cholinergic signaling and synaptic transmission, and in adaptive/protective mechanisms of neuronal responses to hypoxia. However, the putative role of miRNA-132/212 in the response of synaptic transmission to ischemia remained unexplored. Using hippocampal slices from female miRNA-132/212 double-knockout mice in an established electrophysiological model of ischemia, we here describe that miRNA-132/212 gene-deletion aggravated the deleterious effect of repeated oxygen-glucose deprivation insults on synaptic transmission in the dentate gyrus, a brain region crucial for learning and memory functions. We also examined the effect of miRNA-132/212 gene-deletion on the expression of key mediators in cholinergic signaling that are implicated in both adaptive responses to ischemia and hippocampal neural signaling. miRNA-132/212 gene-deletion significantly altered hippocampal AChE and mAChR-M1, but not α7-nAChR or MeCP2 expression. The effects of miRNA-132/212 gene-deletion on hippocampal synaptic transmission and levels of cholinergic-signaling elements suggest the existence of a miRNA-132/212-dependent adaptive mechanism safeguarding the functional integrity of synaptic functions in the acute phase of cerebral ischemia.