Background In the context of the COVID-19 pandemic and social distancing rules, access to in-person training activities had temporarily been interrupted, speeding up the implementation of telesimulation for minimally invasive surgery (MIS) essential skills training (T-ESTM, Telesimulation - Essential Skills Training Module) in our center. The aim of this study was to explore the effectiveness of T-ESTM. Methods T-ESTM was scheduled into 2 sessions of 3 hours through the Zoom® virtual meeting platform. The academic lectures, the tutorials for box-trainer set-up and 7 performance tasks were accessed through an online campus previous to the remote encounter for personalized guidance and debriefing. Initial (pre-telementoring) and final (post 6-hour telementoring) assessment scoring as well as timing for Task 2 (circle-cutting pattern), 3 (extracorporeal Roeder knot) and 5 (intracorporeal Square knot) were registered. Results 61 participants were recruited. The mean age was 31±5 years. 65% were surgical residents. 48% performed low complexity procedures. 52% had previous experience with simulation training. In Task 2, there was a 21% improvement in the final score obtained, as well as a significant decrease in time of 33%; in Task 3, there was an increase of 39% in the scoring and a decrease of 49% in the timing; and in Task 5, participants improved their technique a 30% and decreased the performance time a 47%. All the differences were statistically significant. Discussion Our data support T-ESTM as a reproducible and effective educational tool for remote MIS essential skills hands-on training.

It has been known for many years that plasma and tissues contain a variety of enzymes capable of metabolizing kinins. The aim of the present study was to evaluate, by means of functional studies in a capacitance vessel such as the human umbilical vein (HUV), the possible role played by the metallopeptidases angiotensin-converting enzyme (ACE), neutral endopeptidase (NEP), and aminopeptidase M (APM) as an inactivating pathway of the B(1) receptor endogenous agonist des-Arg(10)-kallidin (DAKD). In HUV rings with and without endothelium, concentration-response curves (CRCs) to DAKD were determined after a 300-min incubation period, and enzymatic inhibitors were added to the organ baths 30 min before construction of the CRC. Presence of endothelial layer was confirmed by histological studies. There was a significant leftward shift observed in control HUV rings devoid of endothelium compared with intact tissues. Exposure to 1 microM captopril (ACE inhibitor) potentiated DAKD-elicited vasoconstrictor responses in HUV rings with endothelium while no such effect was observed in tissues devoid of endothelium. Application of 10 microM amastatin (APM inhibitor) induced a leftward shift of DAKD-elicited contractile responses in HUV with and without endothelium. On the other hand, 10 microM phosphoramidon (NEP inhibitor) showed no potentiating effect in HUV rings either with or without endothelium. However, under concurrent inhibition of ACE, NEP and APM, there was a higher potentiation of DAKD-elicited contractile responses compared with the effect observed with combined inhibition of ACE and APM. Moreover, when we evaluated contractile responses induced by Sar(0)-D-Phe(8)-des-Arg(9)-BK (a metabolically protected B(1) receptor agonist), no potentiating effect was observed under triple enzymatic inhibition. In conclusion, in the present study for the first time, we demonstrated in a capacitance vessel, HUV, that metallopeptidases ACE, NEP and APM represent a relevant functional inactivation pathway of DAKD.

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