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1.
BJS Open ; 4(6): 1100-1108, 2020 Dec 02.
Article in English | MEDLINE | ID: mdl-33052038

ABSTRACT

BACKGROUND: Minimally invasive surgery is the standard technique for many operations. Laparoscopic training has a long learning curve. Robotic solutions may shorten the training pathway. The aim of this study was to compare laparoscopic with robotic training in surgical trainees and medical students. METHODS: Surgical trainees (ST group) were randomized to receive 6 h of robotic or laparoscopic simulation training. They then performed three surgical tasks in cadaveric specimens. Medical students (MS group) had 2 h of robotic or laparoscopic simulation training followed by one surgical task. The Global Rating Scale (GRS) score (maximum 30), number of suture errors, and time to complete each procedure were recorded. RESULTS: The median GRS score for the ST group was better for each procedure after robotic training compared with laparoscopic training (total GRS score: 27·00 (i.q.r. 22·25-28·33) versus 18·00 (16·50-19·04) respectively, P < 0·001; 10 participants in each arm). The ST group made fewer errors in robotic than in laparoscopic tasks, for both continuous (7·00 (4·75-9·63) versus 22·25 (20·75-25·25); P < 0·001) and interrupted (8·25 (6·38-10·13) versus 29·50 (23·75-31·50); P < 0·001) sutures. For the MS group, the robotic group completed 8·67 interrupted sutures with 15·50 errors in 40 min, compared with only 3·50 sutures with 40·00 errors in the laparoscopic group (P < 0·001) (10 participants in each arm). Fatigue and physical comfort levels were better after robotic compared with laparoscopic operating for both groups (P < 0·001). CONCLUSION: The acquisition of surgical skills in surgical trainees and the surgically naive takes less time with a robotic compared with a laparoscopic platform.

2.
Orthopade ; 48(4): 315-321, 2019 Apr.
Article in German | MEDLINE | ID: mdl-30868208

ABSTRACT

BACKGROUND: Instability is a common cause of failure in primary and, especially, revision total hip arthroplasty. The reasons for instability include implant malpositioning, impingement, inadequate offset reconstruction, and gluteal insufficiency. Impingement following THA and revision THA is divided into prosthetic and bony impingement, and in addition to instability also causes pain in the area of the hip joint. Offset reconstruction during revision THA is of particular biomechanical importance, since insufficient reconstruction leads not only to instability and pain but also to dislocation. Abductor deficiency often occurs after revision THA and leads to a change in gait pattern, instability and pain. AIM: Current diagnostic and treatment procedures for instability, impingement, insufficient offset reconstruction and abductor deficiency after THA and revision THA are summarized. RESULTS AND DISCUSSION: Diagnosis of an instable THA and painful THA includes patient history, physical examination and medical imaging. Thus, in almost all cases, the cause can be determined and treated. Dislocation after primary THA in the early postoperative period can often be treated conservatively if accurate component placement is observed, while a late-onset and recurrent dislocation after primary and revision THA usually needs surgical procedures. To avoid bony and prosthetic THA impingement intraoperative control is absolutely necessary. If possible, the offset reconstruction is based on the condition of the native hip joint and can be achieved by using modular prostheses, neck adapters and different head lengths. Abductor deficiency also occurs frequently after revision THA and can be treated surgically if severe clinical symptoms and fatty degeneration of the abductors have been diagnosed.


Subject(s)
Arthroplasty, Replacement, Hip , Hip Prosthesis , Joint Dislocations , Hip Joint , Humans , Prosthesis Failure , Reoperation
3.
Oncogene ; 36(22): 3094-3103, 2017 06 01.
Article in English | MEDLINE | ID: mdl-27941872

ABSTRACT

The mechanisms of initiation of pancreatic ductal adenocarcinoma (PDAC) are still largely unknown. In the present study, we analysed the role of anterior gradient-2 (AGR2) in the earliest stages of pancreatic neoplasia. Immunohistochemical analysis of chronic pancreatitis (CP) and peritumoral areas in PDAC tissues showed that AGR2 was present in tubular complexes (TC) and early pancreatic intraepithelial neoplasia (PanINs). Moreover, AGR2 was also found in discrete subpopulations of non-transformed cells neighbouring these pre-neoplastic lesions. In primary cells derived from human patient-derived xenograft (PDX) model, flow-cytometry revealed that AGR2 was overexpressed in pancreatic cancer stem cells (CSC) compared with non-stem cancer cells. In LSL-KrasG12D;Pdx1-Cre (KC) mouse model Agr2 induction preceded the formation of pre-neoplastic lesions and their development was largely inhibited by Agr2 deletion in engineered LSL-KrasG12D;Pdx1-Cre; Agr2-/- mice. In vitro, AGR2 expression was stimulated by tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeostasis. The unfolded protein response proteins GRP78, ATF6 and XBP1s were found expressed in CP and PDAC peritumoral tissues, but in contrast to AGR2, their expression was switched off during TC and PanIN formation. Real-time PCR and ELISA analyses showed that ER stress induced a pro-inflammatory phenotype in pancreatic normal, cancer and stellate cells. Moreover, AGR2 expression was inducible by paracrine transfer of ER stress and pro-inflammation between different pancreatic cell types. Our findings demonstrate that AGR2 induced in ER-stressed and inflammatory pre-neoplastic pancreas is a potential marker of cancer progenitor cells with an important functional role in PDAC initiation.


Subject(s)
Carcinoma, Pancreatic Ductal/pathology , Endoplasmic Reticulum Stress/physiology , Mucoproteins/metabolism , Pancreatic Neoplasms/pathology , Animals , Carcinoma, Pancreatic Ductal/genetics , Carcinoma, Pancreatic Ductal/metabolism , Cell Transformation, Neoplastic/genetics , Cell Transformation, Neoplastic/metabolism , Cell Transformation, Neoplastic/pathology , Disease Models, Animal , Endoplasmic Reticulum Chaperone BiP , Humans , Mice , Mucoproteins/biosynthesis , Mucoproteins/deficiency , Mucoproteins/genetics , Oncogene Proteins , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/metabolism , Proto-Oncogene Proteins p21(ras)/genetics , Proto-Oncogene Proteins p21(ras)/metabolism
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