Comparison of robotic versus laparoscopic right colectomy node retrieval in the obese population.

Data are scarce comparing robotic and laparoscopic colectomy node retrieval based on body mass index or age. With differences in anastomosis, mobilization, and ligation between these approaches, obese and/or elderly patients undergoing robotic surgery may have differences in node yield compared to laparoscopy. A retrospective review was conducted between four institutions from February 1, 2019 through August 1, 2021, during which 144 right colectomies were performed. Benign pathology, open colectomies, and conversions to open were excluded. All included surgeons had at least five patients to ensure experience. The population was categorized by a robotic or laparoscopic approach. Records were reviewed focusing on age, body mass index, surgical approach, anastomosis, pathology, and node count. The node count was then compared by body mass index and age between the robotic or laparoscopic approach to identify differences. After applied exclusions and outlier analysis, our final sample consisted of 80 patients. Both body mass index and age were significant, (p = 0.002 and p = 0.005, respectively). Body mass index ≤ 25.0 and age < 60 years old had higher average node counts. These variables interacted, (p = 0.003); those with both < 60 years old and body mass index ≤ 25 showed the greatest number of nodes (36.9). Laparoscopy yielded more nodes in ≥ 60 years old than robotics (27.4 verses 20.9), though this was not significant (p = 0.68). Node retrieval in overweight and obese patients did not differ between approaches (p = 0.48). Both body mass index and age influence the number of nodes that can be extracted in right hemicolectomies by experienced surgeons.

Predominant expression of Alzheimer's disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts.

BACKGROUND: Genome-wide association studies have identified BIN1 within the second most significant susceptibility locus in late-onset Alzheimer's disease (AD). BIN1 undergoes complex alternative splicing to generate multiple isoforms with diverse functions in multiple cellular processes including endocytosis and membrane remodeling. An increase in BIN1 expression in AD and an interaction between BIN1 and Tau have been reported. However, disparate descriptions of BIN1 expression and localization in the brain previously reported in the literature and the lack of clarity on brain BIN1 isoforms present formidable challenges to our understanding of how genetic variants in BIN1 increase the risk for AD. METHODS: In this study, we analyzed BIN1 mRNA and protein levels in human brain samples from individuals with or without AD. In addition, we characterized the BIN1 expression and isoform diversity in human and rodent tissue by immunohistochemistry and immunoblotting using a panel of BIN1 antibodies. RESULTS: Here, we report on BIN1 isoform diversity in the human brain and document alterations in the levels of select BIN1 isoforms in individuals with AD. In addition, we report striking BIN1 localization to white matter tracts in rodent and the human brain, and document that the large majority of BIN1 is expressed in mature oligodendrocytes whereas neuronal BIN1 represents a minor fraction. This predominant non-neuronal BIN1 localization contrasts with the strict neuronal expression and presynaptic localization of the BIN1 paralog, Amphiphysin 1. We also observe upregulation of BIN1 at the onset of postnatal myelination in the brain and during differentiation of cultured oligodendrocytes. Finally, we document that the loss of BIN1 significantly correlates with the extent of demyelination in multiple sclerosis lesions. CONCLUSION: Our study provides new insights into the brain distribution and cellular expression of an important risk factor associated with late-onset AD. We propose that efforts to define how genetic variants in BIN1 elevate the risk for AD would behoove to consider BIN1 function in the context of its main expression in mature oligodendrocytes and the potential for a role of BIN1 in the membrane remodeling that accompanies the process of myelination.