Fosterskov2073

In contrast to unstretched cells, stretched fibroblasts showed elongation of stress fibers, cell and cytoskeletal alignment perpendicular to strain direction, less rounded cell nuclei, increased numbers of focal adhesions, proliferation, amplified CXN43, and main ECM component expression in both cultures. The applied cyclic stretch protocol evoked an anabolic response and enhanced tendon-related marker expression in ACL-derived fibroblasts emigrating from 3D spheroids and seems also promising to support in future tissue formation in ACL scaffolds seeded in vitro with spheroids.

Fixed orthodontic appliances impair oral hygiene increasing the risk of non-cavitated lesions (NCLs) and tooth decay. The aim of this study was to compare the outcomes of fluoride and xylitol varnishes in preventing NCLs during comprehensive orthodontic treatment.

The sample comprised 55 volunteers from 15 to 20 years of age under orthodontic treatment that were randomly divided into three groups Fluoride Group (FG; n=17), Xylitol Group (XG; n=19), and Placebo Group (PG; n=19). The patients in each group received two applications of the following varnishes Duraphat

(5% NaF), 20% xylitol, and placebo (no F/Xylitol) in the three groups, respectively. The varnishes were applied in the first appointment (T0) and 3 months later (T1). Clinical examinations were carried out at T0 and 6 months after (T2) using the ICDAS index and the QLF system (fluorescence difference). The intergroup comparisons were performed by ANOVA/Tukey's or Kruskal-Wallis/Dunn's tests (P<0.05).

There was no significant intergroup difference regarding ICDAS index changes from T0 to T2. Fluoride varnish produced significantly greater increase in fluorescence of NCLs (mean change of -0.65 +0.78 and -0.56 +0.83, for maxilla and mandible, respectively) in comparison to the other groups. The majority of non-cavitated lesions improved in the fluoride and xylitol varnish groups.

Fluoride varnish produced significantly greater increase in enamel fluorescence compared to xylitol and placebo varnishes. In short term, both fluoride and xylitol varnishes produced remineralization of NCLs in orthodontic patients.

Non-cavitated lesions can be effectively controlled in high-risk orthodontic patients by means of fluoride varnishes.

ReBEC Identifier RBR-6mdxfq; Date of Register March 19th, 2020. Retrospectively Registered.

ReBEC Identifier RBR-6mdxfq; Date of Register March 19th, 2020. Retrospectively Registered.

The current standard treatment for external rectal prolapse and symptomatic high-grade internal rectal prolapse is surgical correction with minimally invasive ventral mesh rectopexy using either laparoscopy or robotic assistance. This study examines the number of procedures needed to complete the learning curve for robot-assisted ventral mesh rectopexy (RVMR) and reach adequate performance.

A retrospective analysis of all primary RVMR from 2011 to 2019 performed in a tertiary pelvic floor clinic by two colorectal surgeons (A and B) was performed. Wnt inhibitor Both surgeons had previous experience with laparoscopic rectopexy, but no robotic experience. Skin-to-skin operating times (OT) were assessed using LC-CUSUM analyses. Intraoperative and postoperative complications were analyzed using CUSUM analyses.

A total of 182 (surgeon A) and 91 (surgeon B) RVMRs were performed in total. There were no relevant differences in patient characteristics between the two surgeons. Median OT was 75min (range 46-155; surgeon A) and 90min (range 63-139; surgeon B). The learning curve regarding OT was completed after 36 procedures for surgeon A and 55 procedures for surgeon B. Both before and after completion of the learning curve, intraoperative and postoperative complication rates remained below a predefined acceptable level of performance.

36 to 55 procedures are required to complete the learning curve for RVMR. The implementation of robotic surgery does not inflict any additional risks on patients at the beginning of a surgeon's learning curve.

36 to 55 procedures are required to complete the learning curve for RVMR. The implementation of robotic surgery does not inflict any additional risks on patients at the beginning of a surgeon's learning curve.

Patients who received endoscopic resection (ER) for early gastric cancer (EGC) or high-grade dysplasia (HGD) are at high risk for the subsequent development of metachronous gastric cancer (MGC). This study aims to compare the detection rate and stage of MGC between biannual and annual endoscopic surveillance after ER of EGC or HGD.

From September 2009 to August 2019, 859 patients who underwent ER for the treatment of EGC or HGD were analyzed, retrospectively. Patients received endoscopic surveillance twice a year (high-intensity group) or annually (low-intensity group) for 3years.

A total of 521 patients were enrolled in this study (267 patients in the high-intensity group and 254 patients in the low-intensity group). During a mean follow-up of 5.3 ± 1.6years, MGCs were found in 27 patients (16.9%) in the high-intensity group and 18 patients (7.1%) in the low-intensity group (P = 0.219). In patients with moderate to severe atrophy (Kimura-Takemoto grade C3 ~ O3), detection rates of MGC during 3years from were 8.4% (16/191) and 2.2% (4/186), respectively (P = 0.007). Forty-four patients who received treatment for MGC, including endoscopic or surgical resection, were stage IA. Only one patient in the low-intensity group was diagnosed as stage IIIA advanced gastric cancer.

There was no significant difference in the detection rate of MGC between biannual and annual endoscopic surveillance after ER of EGC or HGD. However, biannual surveillance showed a higher detection rate during the first 3years, especially for patients with moderate to severe gastric atrophy.

There was no significant difference in the detection rate of MGC between biannual and annual endoscopic surveillance after ER of EGC or HGD. However, biannual surveillance showed a higher detection rate during the first 3 years, especially for patients with moderate to severe gastric atrophy.