Danube University Krems

About: Danube University Krems is a education organization based out in Krems, Niederösterreich, Austria. It is known for research contribution in the topics: Stroke & Population. The organization has 498 authors who have published 1572 publications receiving 68797 citations.

Systematic dysphagia screening and dietary modifications to reduce stroke-associated pneumonia rates in a stroke-unit.

Abstract: Background and purpose While formal screening for dysphagia following acute stroke is strongly recommended, there is little evidence on how multi-consistency screening and dietary modifications affect the rate of stroke-associated pneumonia (SAP). This observational study reports which factors affect formal screening on a stroke-unit and how dietary recommendations relate to SAP. Method Analyses from a database including 1394 patients admitted with acute stroke at our stroke-unit in Austria between 2012 and 2014. Dietary modifications were performed following the recommendations from the Gugging Swallowing Screen (GUSS). Patients evaluated with GUSS were compared to the unscreened patients. Results Overall, 993 (71.2%) patients were screened with GUSS; of these 50 (5.0%) developed SAP. In the 401 unscreened patients, the SAP rate was similar: 22 (5.5%). Multivariable analysis showed that either mild to very mild strokes or very severe strokes were less likely to undergo formal screening. Older age, pre-existing disability, history of hypertension, atrial fibrillation, stroke severity, cardiological and neurological complications, nasogastric tubes, and intubation were significant markers for SAP. Out of 216 patients, 30 (13.9%) developed SAP in spite of receiving nil per mouth (NPO). Conclusion The routine use of GUSS is less often applied in either mild strokes or very severe strokes. While most patients with high risk of SAP were identified by GUSS and assigned to NPO, dietary modifications could not prevent SAP in 1 of 7 cases. Other causes of SAP such as silent aspiration, bacteraemia or central breathing disturbances should be considered.

Long-Term Outcomes of a Multimodal Day-Clinic Treatment for Chronic Pain under the Conditions of Routine Care.

Abstract: Chronic pain has high prevalence rates and is one of the top causes of years lived with disability. The aim of the present study was to evaluate the long-term effects of a multimodal day-clinic treatment for chronic pain. The sample included 183 chronic pain patients (114 females and 69 males; 53.3 ± 9.8 years) who participated in a four-week multimodal day-clinic treatment for chronic pain. The patients’ average current pain intensity (NRS), sensory and affective pain (Pain Perception Scale), and depression and anxiety (HADS) were assessed at pre- and posttreatment, as well as at three follow-ups (one month, six months, and twelve months after completion of the treatment). Multilevel models for discontinuous change were performed to evaluate the change of the outcome variables. Improvements from pretreatment to posttreatment and from pretreatment to all follow-ups emerged for pain intensity (NRS; 0.54 ≤ d ≤ 0.74), affective pain (Pain Perception Scale; 0.24 ≤ d ≤ 0.47), depression (HADS; 0.38 ≤ d ≤ 0.53), and anxiety (HADS; 0.26 ≤ d ≤ 0.43) (all ). Sensory pain as assessed with the Pain Perception Scale did not show any significant change. Patients suffering from chronic pain benefited from the multimodal pain treatment up to twelve months after completion of the treatment.

Platelet-rich plasma supports proliferation and redifferentiation of chondrocytes during in vitro expansion

Abstract: Articular cartilage regeneration is insufficient to restore sports injuries or defects that can occur from trauma. Treatment options for cartilage repair include autologous chondrocyte implantation (ACI) by isolation, expansion, and reimplantation of healthy donor chondrocytes. Chondrocyte expansion onto 2D substrates leads to dedifferentiation and loss of the cellular phenotype. We aimed to overcome the state of dedifferentiation by biochemical stimuli with platelet derivatives such as platelet rich plasma (PRP) and hyper acute serum (HAS) to achieve sufficient cell numbers in combination with variable oxygen tension. Human articular chondrocytes from osteoarthritic (OA) cartilage chondrocytes were switched from 10% FCS supplementation to either 10% PRP or 10% HAS after initial passaging for further experiments under normoxic (20%O2) or hypoxic (1%O2) conditions. An XTT assay measured the effect of PRP or HAS on the cell proliferation at 3, 6 and 9 days. The chondrogenic redifferentiation potential of dedifferentiated chondrocytes was determined with RT-qPCR for markers of expression for type II collagen (COL2A1), type I collagen (COL1A1) and matrix metalloproteinases MMP3, MMP13 at 24hrs and 72hrs. Measured protein levels of 100% PRP or HAS by multiplex quantification revealed bFGF, G-CSF, PDGF was significantly higher in PRP than in HAS (p<0.05) but LEPTIN levels did not differ. The quantified protein levels did not differ when isolated from same donors at a different time. Chondrocyte proliferation indicated that supplementation of 10% HAS enhanced the proliferation rate compared to 10% PRP or 10% FCS at 6 and 9 days significantly (p<0.05). mRNA levels for expression of COL1A1 were significantly downregulated (p<0.05) when cultured with 10% PRP than 10% HAS or 10% FCS under normoxic/hypoxic conditions. COL2A1 was significantly upregulated (p<0.05) in PRP than 10% HAS or 10% FCS. MMP3 expression was downregulated after 72hrs under all conditions. MMP13 was upregulated with 10% PRP at both 24 and 72 hrs but significantly downregulated under hypoxia (1%O2) for all circumstances. While HAS has its effect on chondrocyte proliferation, PRP enhances both proliferation and redifferentiation of dedifferentiated chondrocytes. PRP can replace standard usage of FCS for chondrogenic priming and expansion as implications for clinical use such as ACI procedures.

Extracellular Purine Metabolism Is the Switchboard of Immunosuppressive Macrophages and a Novel Target to Treat Diseases With Macrophage Imbalances.

Abstract: If misregulated, macrophage (Mϕ)-T cell interactions can drive chronic inflammation thereby causing diseases, such as rheumatoid arthritis (RA). We report that in a proinflammatory environment, granulocyte-Mϕ (GM-CSF)- and Mϕ colony-stimulating factor (M-CSF)-dependent Mϕs have dichotomous effects on T cell activity. While GM-CSF-dependent Mϕs show a highly stimulatory activity typical for M1 Mϕs, M-CSF-dependent Mϕs, marked by folate receptor β (FRβ), adopt an immunosuppressive M2 phenotype. We find the latter to be caused by the purinergic pathway that directs release of extracellular ATP and its conversion to immunosuppressive adenosine by co-expressed CD39 and CD73. Since we observed a misbalance between immunosuppressive and immunostimulatory Mϕs in human and murine arthritic joints, we devised a new strategy for RA treatment based on targeted delivery of a novel methotrexate (MTX) formulation to the immunosuppressive FRβ+CD39+CD73+ Mϕs, which boosts adenosine production and curtails the dominance of proinflammatory Mϕs. In contrast to untargeted MTX, this approach leads to potent alleviation of inflammation in the murine arthritis model. In conclusion, we define the Mϕ extracellular purine metabolism as a novel checkpoint in Mϕ cell fate decision-making and an attractive target to control pathological Mϕs in immune-mediated diseases.