25th International Congress of the European Association for Endoscopic Surgery (EAES) Frankfurt, Germany, 14-17 June 2017 : Oral Presentations

Introduction: Ouyang has recently proposed hiatal surface area (HSA) calculation by multiplanar multislice computer tomography (MDCT) scan as a useful tool for planning treatment of hiatus defects with hiatal hernia (HH), with or without gastroesophageal reflux (MRGE). Preoperative upper endoscopy or barium swallow cannot predict the HSA and pillars conditions. Aim to asses the efficacy of MDCT’s calculation of HSA for planning the best approach for the hiatal defects treatment. Methods: We retrospectively analyzed 25 patients, candidates to laparoscopic antireflux surgery as primary surgery or hiatus repair concomitant with or after bariatric surgery. Patients were analyzed preoperatively and after one-year follow-up by MDCT scan measurement of esophageal hiatus surface. Five normal patients were enrolled as control group. The HSA’s intraoperative calculation was performed after complete dissection of the area considered a triangle. Postoperative CT-scan was done after 12 months or any time reflux symptoms appeared. Results: (1) Mean HSA in control patients with no HH, no MRGE was cm2 and similar in non-complicated patients with previous LSG and cruroplasty. (2) Mean HSA in patients candidates to cruroplasty was 7.40 cm2. (3) Mean HSA in patients candidates to redo cruroplasty for recurrence was 10.11 cm2. Discussion. MDCT scan offer the possibility to obtain an objective measurement of the HSA and the correlation with endoscopic findings and symptoms. The preoperative information allow to discuss with patients the proper technique when a HSA[5 cm2 is detected. During the follow-up a correlation between symptoms and failure of cruroplasty can be assessed. Conclusions: MDCT scan seems to be an effective non-invasive method to plan hiatal defect treatment and to check during the follow-up the potential recurrence. Future research should correlate in larger series imaging data with intraoperative findings

Exact solution of Kerr black hole perturbations via CFT2 and instanton counting: Greybody factor, quasinormal modes, and Love numbers

We give explicit expressions for the finite frequency greybody factor, quasinormal modes, and Love numbers of Kerr black holes by computing the exact connection coefficients of the radial and angular parts of the Teukolsky equation. This is obtained by solving the connection problem of the confluent Heun equation in terms of the explicit expression of irregular Virasoro conformal blocks as sums over partitions via the Alday, Gaiotto, and Tachikawa correspondence. In the relevant approximation limits our results are in agreement with existing literature. The method we use can be extended to solve the linearized Einstein equation in other interesting gravitational backgrounds

Prolonged changes in hepatic mitochondrial activity and insulin sensitivity by high fructose intake in adolescent rats

Persistence of damage induced by unhealthy diets during youth has been little addressed. Therefore, we investigated the impact of a short‐term fructose‐rich diet on liver metabolic activity in adolescent rats and the putative persistence of alterations after removing fructose from the diet. Adolescent rats were fed a fructose‐rich diet for three weeks and then switched to a control diet for further three weeks. Body composition and energy balance were not affected by fructose‐rich diet, while increased body lipids and lipid gain were found after the rescue period. Switching to a control diet reversed the upregulation of plasma fructose, uric acid, lipocalin, and haptoglobin, while plasma triglycerides, alanine aminotransferase, lipopolysaccharide, and tumor necrosis factor alpha remained higher. Hepatic steatosis and ceramide were increased by fructose‐rich diet, but reversed by returning to a control diet, while altered hepatic response to insulin persisted. Liver fatty acid synthase and stearoyl‐CoA desaturase (SCD) activities were upregulated by fructose‐rich diet, and SCD activity remained higher after returning to the control diet. Fructose‐induced upregulation of complex II‐driven mitochondrial respiration, peroxisome proliferator‐activated receptor‐gamma coactivator 1 alpha, and peroxisome proliferator activated receptor α also persisted after switching to control diet. In conclusion, our results show prolonged fructose‐induced dysregulation of liver metabolic activity

Prolonged changes in hepatic mitochondrial activity and insulin sensitivity by high fructose intake in adolescent rats

Persistence of damage induced by unhealthy diets during youth has been little addressed. Therefore, we investigated the impact of a short-term fructose-rich diet on liver metabolic activity in adolescent rats and the putative persistence of alterations after removing fructose from the diet. Adolescent rats were fed a fructose-rich diet for three weeks and then switched to a control diet for further three weeks. Body composition and energy balance were not affected by fructose-rich diet, while increased body lipids and lipid gain were found after the rescue period. Switching to a control diet reversed the upregulation of plasma fructose, uric acid, lipocalin, and haptoglobin, while plasma triglycerides, alanine aminotransferase, lipopolysaccharide, and tumor necrosis factor alpha remained higher. Hepatic steatosis and ceramide were increased by fructose-rich diet, but reversed by returning to a control diet, while altered hepatic response to insulin persisted. Liver fatty acid synthase and stearoyl-CoA desaturase (SCD) activities were upregulated by fructose-rich diet, and SCD activity remained higher after returning to the control diet. Fructose-induced upregulation of complex II-driven mitochondrial respiration, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, and peroxisome proliferator activated receptor alpha also persisted after switching to control diet. In conclusion, our results show prolonged fructose-induced dysregulation of liver metabolic activity

Alterations in proton leak, oxidative status and uncoupling protein 3 content in skeletal muscle subsarcolemmal and intermyofibrillar mitochondria in old rats.

BACKGROUND: We considered of interest to evaluate how aging affects mitochondrial function in skeletal muscle. METHODS: We measured mitochondrial oxidative capacity and proton leak, together with lipid oxidative damage, superoxide dismutase specific activity and uncoupling protein 3 content, in subsarcolemmal and intermyofibrillar mitochondria from adult (six months) and old (two years) rats. Body composition, resting metabolic rate and plasma non esterified fatty acid levels were also assessed. RESULTS: Old rats displayed significantly higher body energy and lipids, while body proteins were significantly lower, compared to adult rats. In addition, plasma non esterified fatty acid levels were significantly higher, while resting metabolic rates were found to be significantly lower, in old rats compared to adult ones. Significantly lower oxidative capacities in whole tissue homogenates and in intermyofibrillar and subsarcolemmal mitochondria were found in old rats compared to adult ones. Subsarcolemmal and intermyofibrillar mitochondria from old rats exhibited a significantly lower proton leak rate, while oxidative damage was found to be significantly higher only in subsarcolemmal mitochondria. Mitochondrial superoxide dismutase specific activity was not significantly affected in old rats, while significantly higher content of uncoupling protein 3 was found in both mitochondrial populations from old rats compared to adult ones, although the magnitude of the increase was lower in subsarcolemmal than in intermyofibrillar mitochondria. CONCLUSIONS: The decrease in oxidative capacity and proton leak in intermyofibrillar and subsarcolemmal mitochondria could induce a decline in energy expenditure and thus contribute to the reduced resting metabolic rate found in old rats, while oxidative damage is present only in subsarcolemmal mitochondria