| 1. |
|
|
| 2. |
- Gatenholm, Birgitta, 1986, et al.
(författare)
-
Collagen 2A Type B Induction after 3D Bioprinting Chondrocytes In Situ into Osteoarthritic Chondral Tibial Lesion.
- 2021
-
Ingår i: Cartilage. - : SAGE Publications. - 1947-6043 .- 1947-6035. ; 13:2 (Suppl.)
-
Tidskriftsartikel (refereegranskat)abstract
- Large cartilage defects and osteoarthritis (OA) cause cartilage loss and remain a therapeutic challenge. Three-dimensional (3D) bioprinting with autologous cells using a computer-aided design (CAD) model generated from 3D imaging has the potential to reconstruct patient-specific features that match an articular joint lesion.To scan a human OA tibial plateau with a cartilage defect, retrieved after total knee arthroplasty, following clinical imaging techniques were used: (1) computed tomography (CT), (2) magnetic resonance imaging (MRI), and (3) a 3D scanner. From such a scan, a CAD file was obtained to generate G-code to control 3D bioprinting in situ directly into the tibial plateau lesion.Highest resolution was obtained using the 3D scanner (2.77 times more points/mm2 than CT), and of the 3 devices tested, only the 3D scanner was able to detect the actual OA defect area. Human chondrocytes included in 3D bioprinted constructs produced extracellular matrix and formed cartilage tissue fragments after 2 weeks of differentiation and high levels of a mature splice version of collagen type II (Col IIA type B), characteristic of native articular cartilage and aggrecan (ACAN). Chondrocytes had a mean viability of 81% in prints after day 5 of differentiation toward cartilage and similar viability was detected in control 3D pellet differentiation of chondrocytes (mean viability 72%).Articular cartilage can be formed in 3D bioprints. Thus, this 3D bioprinting system with chondrocytes simulating a patient-specific 3D model provides an attractive strategy for future treatments of cartilage defects or early OA.
|
|
| 3. |
- Jönelid, Birgitta, et al.
(författare)
-
Screening of biomarkers for prediction of multisite artery disease in patients with recent myocardial infarction
- 2021
-
Ingår i: Scandinavian Journal of Clinical and Laboratory Investigation. - : Taylor & Francis. - 0036-5513 .- 1502-7686. ; 81:5, s. 353-360
-
Tidskriftsartikel (refereegranskat)abstract
- A few studies have examined biomarkers in patients with myocardial infarction (MI) and peripheral artery disease (PAD), i.e. multisite artery disease (MSAD). The aim of the study was firstly, to associate biomarkers with the occurrence of PAD/MSAD and secondly, if those can, in addition to clinical characteristics, identify MI patients with MSAD.In two prospectively observational studies including unselected patients with recent MI, PAD was defined as an abnormal ankle-brachial index (ABI) score (1.4). The proximity extension assay (PEA) technique was used, simultaneously analyzing 92 biomarkers with association to cardiovascular disease. Biomarkers were tested for univariate associations with PAD. Random forest was used to identify biomarkers with a higher association to PAD. The additional discriminatory accuracy of adding biomarkers to clinical characteristics was analyzed by the c-statistics. Nine biomarkers were identified as significantly associated with MSAD/PAD in the primary patient cohort, analyzed early after the MI. In the prediction analysis, six biomarkers were identified associated with PAD. Three of these; Tumor necrosis factor receptor (TNFR-1), Tumor necrosis factor receptor 2 (TNFR-2) and Growth Differentiation Factor 15 (GDF-15) improved c-statistics when added to clinical characteristics from 0.683 (95% CI 0.610-0.756) to 0.715 (95% CI 0.645-0.784) in the primary patient cohort with a similar result, 0.729 (95% CI 0.687-0.770) to 0.752 (95% CI 0.771-0.792) in the secondary patient cohort. Biomarkers associated with inflammatory pathways are associated with MSAD in MI patients. Three biomarkers of 92; TNFR-1, TNFR-2 and GDF-15, in this exploratory added information in the prediction of MSAD and emphasis the importance of further studies.
|
|
