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Finite element method-based hemming simula-
tions are prone to high setup effort and computational time,
leading to delays in industrial product development. In this
study, we propose a layer-based surrogate model using graph
convolutional network (GCN) to predict stress distribution
through the sheet metal thickness. The inputs comprise
material properties, geometric and process parameters. The
model is then trained on stress tensors derived from the end
of hemming simulations generated with varied geometries
and thicknesses. Using the trained GCN model, stress distri-
butions are predicted with nearly 90% accuracy on and near
the surface, where tension and compression usually domi-
nate, indicating a clear geometric influence there. With a
reduction in computation time of over 99%, these results
indicate a practical surrogate for hemming simulations and
motivate future work on enhanced nodal features and model
generalization.
Die Hauptziele im Teilvorhaben des Verbundpartners OTH Regensburg innerhalb des Projektes MyReha-Digital waren (1) die Entwicklung von Funktionsparametern, welche basierend auf biomechanischen und physiotherapeutischen Analysen eine Einschätzung des individuellen Rehabilitationsfortschrittes zulassen und fortschrittbezogen Übungen zuordnen sowie (2) die Erstellung eines phasenbasierten Übungskatalogs. Weitere Aufgabenstellungen umfassten Mitverantwortung für die Patienten-App (Konzeption, Gestaltung, Umsetzung), Beteiligung bei der Fertigstellung eines Demonstrators sowie bei der Durchführung und Evaluation einer frühen klinischen Anwendungsbeobachtung des Rehabilitationssystem.
Collagen IX is indispensable for timely maturation of cartilage during fracture repair in mice
(2007)
Fracture repair recapitulates in adult organisms the sequence of cell biological events of endochondral ossification during skeletal development and growth. After initial inflammation and deposition of granulation tissue, a cartilaginous callus is formed which, subsequently, is remodeled into bone. In part, bone formation is influenced also by the properties of the extracellular matrix of the cartilaginous callus. Deletion of individual macromolecular components can alter extracellular matrix suprastructures, and hence stability and organization of mesenchymal tissues. Here, we took advantage of the collagen IX knockout mouse model to better understand the role of this collagen for organization, differentiation and maturation of a cartilaginous template during formation of new bone. Although a seemingly crucial component of cartilage fibrits is missing, collagen IX-deficient mice develop normally, but are predisposed to premature joint cartilage degeneration. However, we show here that lack of collagen IX alters the time course of callus differentiation during bone fracture healing. The maturation of cartilage matrix was delayed in collagen IX-deficient mice calli as judged by collagen X expression during the repair phase and the total amount of cartilage matrix was reduced. Entering the remodeling phase of fracture healing, Col9a1(-/-) calli retained a larger percentage of cartilage matrix than in wild type indicating also a delayed formation of new bone. We concluded that endochondral bone formation can occur in collagen IX knockout mice but is impaired under conditions of stress, such as the repair of an unfixed fractured long bone. (c) 2006 Elsevier B.V./International Society of Matrix Biology. All rights reserved.
For a large part, skeletal development, growth, and repair occur by endochondral ossification which comprises an orderly sequence of consecutive steps of proliferation and late differentiation of chondrocytes. After vascular invasion into hypertrophic cartilage, the tissue is remodelled into bone. At all stages, the process is under tight environmental control exerted by a combination of regulators, including nutritional supply and signalling through growth factors, hormones, and cell-matrix-interactions. Therefore, genetic elimination of collagen IX, a stabilizing component of the periphery of thin cartilage fibrils, is expected to compromise extracellular matrix properties and, hence, the chondrocyte environment required for normal cartilage development and homeostasis. Here, we have shown that growth plate cartilage morphology is markedly disturbed in mice lacking collagen X Abnormalities were most prominent in late proliferative, pre-hypertrophic, and hypertrophic zones whereas restin and early proliferative zones were less affected. In central epiphyseal regions of long bones, newborn animals show grossly abnormal areas with strongly reduced cell numbers, irregular distribution of glycosaminoglycans in the extracellular matrix, and a profoundly disturbed columnar arrangement of chondrocytes with an irregular beta(1) integrin immunostaining. As a result, all long bones are shorter and broader in newborn Col9al-/- mice. Remarkably, these abnormalities are attenuated in adult mice, but the number of cells per area still is too low due to reduced cell proliferation. (c) 2008 Elsevier B.V./International Society of Matrix Biology. All rights reserved.
Collagen XVI is integrated tissue-dependently into distinct fibrillar aggregates, such as D-banded cartilage fibrils and fibrillin-1-containing microfibrils. In skin, the distribution of collagen XVI overlaps that of the collagen-binding integrins alpha 1 beta 1 and alpha 2 beta 1. Basal layer keratinocytes express integrin alpha 2 beta 1, whereas integrin alpha 1 beta 1 occurs in smooth muscle cells surrounding blood vessels, in hair follicles, and on adipocytes. Cells bearing the integrins alpha 1 beta 1 and alpha 2 beta 1 attach and spread on recombinant collagen XVI. Furthermore, collagen XVI induces the recruitment of these integrins into focal adhesion plaques, a principal step in integrin signaling. Of potential physiological relevance, these integrin-collagen XVI interactions may connect cells with specialized fibrils, thus contributing to the organization of fibrillar and cellular components within connective tissues. In cell-free binding assays, collagen XVI is more avidly bound by alpha 1 beta 1 integrin than by alpha 2 beta 1 integrin. Both integrins interact with collagen XVI via the A domain of their alpha subunits. A tryptic collagen XVI fragment comprising the collagenous domains 1 - 3 is recognized by alpha 1 beta 1 integrin. Electron microscopy of complexes of alpha 1 beta 1 integrin with this tryptic collagen XVI fragment or with full-length collagen XVI revealed a unique alpha 1 beta 1 integrin-binding site within collagen XVI located close to its C-terminal end.
In Crohn's disease (CD) the stress-shield of intestinal subepithelial myofibroblasts (ISEMF) provided by intact tissue is disturbed due to inflammation and thus, cells start with remodelling activities. This is characterized by increased numbers of collagen-producing ISEMF causing an uncontrolled, irreversible wound-healing response to the chronic inflammation of the gastrointestinal tract. Reconstitution of the original ECM leads ISEMF to exit this cycle. In contrast, during fibrosis, ISEMF persist. It is known that ISEMF produce and deposit collagen types I, III, IV and V; however synthesis and the role of fibrillar peripheral molecules like collagen type XVI have not been addressed yet. Here, we have analyzed the distribution of collagen XVI in the normal and inflamed bowel wall, its gene and protein expression by ISEMF of different inflammation stages, the cell-matrix interactions in different phases of the inflammatory process and their effect on cell spreading, proliferation and migration. Collagen XVI is deposited in the submucosa of the intestinal wall where it co-localizes with fibrillin-1 and integrin alpha 1. ISEMF reveal increasing gene and protein expression of collagen XVI concurrent to increasing inflammation. ISEMF reveal more mature focal adhesion contacts when seeded on collagen XVI resulting in an extensive cell spreading. This involves recruitment of alpha 1 beta 1 integrin, which shows increased cell surface expression on ISEMF in late stages of inflammation. We assume that collagen XVI promotes persistence of ISEMF in the normal and, even stronger in the inflamed bowel wall by stabilizing focal adhesion contacts via cell-matrix interaction preferentially through recruitment of alpha 1 beta 1 integrin into the tips of the focal adhesion contacts. (C) 2009 Elsevier B.V. All rights reserved.
This study investigated whether etoricoxib (COX-II blocker) has a superior efficacy of preventing heterotopic ossification (HO) after total hip arthroplasty (THA) compared to diclofenac (non-selective NSAID). One hundred patients were included (50 in each group) in this single centre, prospective, double-blinded, randomized, controlled trial. Etoricoxib (90 mg) was administered once and diclofenac (75 mg) twice per day for a perioperative period of nine days. The incidence of HO was evaluated on radiographs of the pelvis six months after surgery. Eighty nine of 100 (89 %) patients could be analysed. The overall HO incidence was 37.8 %. There was no significant difference between both study groups. Twelve patients (27.3 %) of the DIC group and 13 patients (28.9 %) of the ETO group showed Brooker grade I ossifications. Five patients (11.4 %) of the DIC and four patients of the ETO (8.9 %) group showed grade II HO formations. No class III or IV HO formations occured in both groups. Ad hoc analysis detected a negative correlation between HO incidence and limited abduction and internal rotation of the hip. Etoricoxib and diclofenac are equally effective for oral HO prophylaxis after primary cementless THA when given for nine peri-operative days to ensure a full recovery and high patient satisfaction.
Individual physiological knee kinematics are highly variable in normal knees and are altered following cruciate-substituting (PS) and cruciate-retaining (CR) total knee arthroplasty (TKA). We wanted to know whether knee kinematics are different choosing two different knee designs, CR and PS TKA, during surgery using computer navigation. For this purpose, 60 consecutive TKA were randomised, receiving either CR (37 patients) or PS TKA (23 patients). All patients underwent computer navigation, and kinematics were assessed prior to making any cuts or releases and after implantation. Outcome measures were relative rotation between femur and tibia, measured medial and lateral gaps and medial and lateral condylar lift-off. We were not able to demonstrate a significant difference in femoral external rotation between either group prior to implantation (7.9A degrees CR vs. 7.4A degrees PS) or after implantation (9.0A degrees CR vs. 11.3A degrees PS), both groups showed femoral roll-back. It significantly increased pre- to postoperatively in PS TKA. In the CR group both gaps increased, the change of the medial gap was significantly attributable to medial release. In the PS group both gaps increased and the change of the medial and of the lateral gap was significant. Condylar lift-off was observed in the CR group during 20A degrees and 60A degrees of flexion. This study did not reveal significant differences in navigation-based knee kinematics between CR and PS implants. Femoral roll-back was observed in both implant designs, but significantly increased pre- to postoperatively in PS TKA. A slight midflexion instability was observed in CR TKA. Intra-operative computer navigation can measure knee kinematics during surgery before and after TKR implantation and may assist surgeons to optimise knee kinematics or identify abnormal knee kinematics that could be corrected with ligament releases to improve the functional result of a TKR, whether it is a CR or PS design. Our intra-operative finding needs to be confirmed using fluoroscopic or radiographic 3D matching after complete recovery from surgery.
Background: Although the relationship between posture and back pain is still under debate, the potential role of body alignment highlights the importance of postural assessment in the health sector. Despite growing concern about musculoskeletal issues, there remains a lack of consensus on effective methods for detecting postural anomalies.
Methods: This observational study compared postural assessments conducted by orthopedic specialists with those obtained through rasterstereographical spine scans using the DIERS formetric system. Fifty-four children from the third grade (mean age 9.4 years) underwent both assessments, allowing for a comprehensive examination of orthopedic abnormalities. Statistical analysis, including McNemar tests, was employed to compare the results of the assessments and evaluate potential discrepancies.
Results: The comparison between the orthopedic examination and the DIERS scan revealed significant differences in assessing trunk imbalance (p?<?0.001), thoracic kyphosis (p?<?0.001), and lumbar lordosis (p?<?0.001). Additionally, the study identified a high prevalence of orthopedic abnormalities, with 79.6% of the examined children exhibiting at least one issue in the orthopedic visual assessment.
Conclusions: The study highlights the divergence between orthopedic evaluations and DIERS scans, emphasizing the challenges in achieving consistent postural assessments. The static analysis provided by the DIERS system, which quantifies posture in angles and distances, contrasts with the dynamic, functionality-focused approach of orthopedic examinations. The findings raise questions about the practicality and significance of integrating rasterstereography into routine pediatric orthopedic practice. The results underscore the complexity of postural evaluations and advocate for a comprehensive approach to address the multifaceted nature of back health in children.