Robotically assisted single-site transabdominal preperitoneal hernia repair is safe and effective. The absence of clinical evidence of recurrence or neuralgia is encouraging and should promote further study.

Background and objectivesAlthough high spinal anesthesia (HSA) has been used in cardiac surgery, the technique has not yet been widely accepted. This retrospective study was designed to investigate the impact of HSA technique on fast-track strategy in cardiac surgery.MethodsElective cardiac surgery cases (n=1025) were divided into two groups: cases with HSA combined with general anesthesia (GA) (HSA group, n=188) and cases with GA only (GA group, n=837). In the HSA group, bupivacaine and morphine were intrathecally administered immediately before GA was induced. Outcomes included fast-track extubation (less than 6 hours), extubation in the operating room, fast-track discharge from the intensive care unit (ICU) (less than 48 hours) and hospital (less than 7 days).ResultsIn the HSA group, 60.1% were extubated in less than 6 hours after ICU admission, as compared with 39.9% in the GA group (p<0.001). In the HSA group, 33.0% were extubated in the operating room, as compared with 4.4% in the GA group (p<0.001). LOS in the ICU was less than 48 hours in 67.6% in the HSA group, as compared with 57.2% of those in the GA group (p=0.033). LOS in the hospital was less than 7 days in 63.3% in the HSA group, as compared with 53.5% in the GA group (p=0.084).ConclusionsHSA technique combined with GA in cardiac surgery increased the rate of fast-track extubation (less than 6 hours) when compared with GA only.

Marine nitrogen (N2) fixation was historically considered to be absent or reduced in nitrate (NO3−) rich environments. This is commonly attributed to the lower energetic cost of NO3− uptake compared to diazotrophy in oxic environments. This paradigm often contributes to making inferences about diazotroph distribution and activity in the ocean, and is also often used in biogeochemical ocean models. To assess the general validity of this paradigm beyond the traditionally used model organism Trichodesmium spp., we grew cultures of the unicellular cyanobacterium Crocosphaera watsonii WH8501 long term in medium containing replete concentrations of NO3−. NO3− uptake was measured in comparison to N2 fixation to assess the cultures’ nitrogen source preferences. We further measured culture growth rate, cell stoichiometry, and carbon fixation rate to determine if the presence of NO3− had any effect on cell metabolism. We found that uptake of NO3− by this strain of Crocosphaera was minimal in comparison to other N sources (~2–4% of total uptake). Furthermore, availability of NO3− did not statistically alter N2 fixation rate nor any aspect of cell physiology or metabolism measured (cellular growth rate, cell stoichiometry, cell size, nitrogen fixation rate, nitrogenase activity) in comparison to a NO3− free control culture. These results demonstrate the capability of a marine diazotroph to fix nitrogen and grow independently of NO3−. This lack of sensitivity of diazotrophy to NO3− suggests that assumptions often made about, and model formulations of, N2 fixation should be reconsidered.

Introduction: The left (LV) and right (RV) ventricles are intrinsically linked directly via shared myofiber and an interventricular septum and indirectly via a closed loop hemodynamic circuit [1], a phenomenon known as ventricular interdependence. While this interdependence has been investigated for over a century [1], the individual contributions of these elements require further investigation and quantification, particularly in heart failure (HF). To address this, we performed in silico experiments that quantify the influence of specific contributors individually to elucidate the effects of LV diastolic dysfunction (DD) and systolic dysfunction (SD) on RV function and vice versa. We hypothesize that our simulations will capture interventricular interactions in HF and RV compensation in LV dysfunction. Materials and Methods: We developed a 6-compartment cardiovascular model that includes a 2-compartment biventricular heart model [2] encapsulated in a simple extensible pericardium [3] and a 4-compartment electrical circuit analog-based circulation model. The ventricles are based on the TriSeg model [2], which approximates the RV and LV free walls and septum as semispherical, thick-walled segments. Active and passive cardiac myofiber mechanics, geometry, and mechanical ventricular interdependence are used to calculate biventricular pressures and volumes. We use nominally healthy values for a 70 kg person for all model parameters. To simulate SD, we reduce active contractile function in the myofiber mechanics model, and for DD, we increase passive myofiber stiffness. Systolic and diastolic function are assessed by the end-systolic pressure-volume relationship (ESPVR) and end-diastolic pressure-volume relationship (EDPVR), respectively, over a range of filling volumes. Results: Acute LV SD affects neither RV systolic function nor RV diastolic function. Similarly, acute LV DD affects neither RV systolic function nor RV diastolic function. In contrast, both RV SD and RV DD impair LV filling and cause moderate LV DD with a maintained LV EF. Particularly in RV SD, the slope of the LV EDPVR is increased compared to the healthy case, suggesting LV stiffening. Note, this apparent LV stiffening is not due to either wall thickening or changes in LV passive mechanics but instead due to ventricular interactions and septal bowing. In addition, with increasing LV dysfunction the cardiac power (area of the pressure-volume loop) decreased while the RV cardiac power increased, suggesting RV compensation to maintain a healthy cardiac output. Conclusions: We observed that three dysfunction simulations (LV DD, RV SD, and RV DD) exhibit phenotypes seen in HFpEF (LV DD and EF > 50%), suggesting multiple modes of HF in HFpEF, which is consistent with and may help explain the clinical heterogeneity of HFpEF. With more refined and specific diagnostic categories of HFpEF, more targeted treatments can be developed, which will likely improv outcomes in this disease state. NIH R01HL154624 (NCC and DAB), NIH T32HL116270 (SMK), and NIH T32HL00785322 (EBR) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.