The findings of this study suggest that isometric hip muscle strength might not be a predisposing factor for the development of PFDS.
This is the first study to examine VMO size in PFPS patients by MRI. Patients with patellofemoral problems exhibited atrophy of the VMO. Although it is not clear whether this atrophy is a result or a cause of PFPS, the results of this study do show that atrophy of the VMO is a contributing factor in PFPS. Longitudinal, prospective studies are needed to establish the cause-effect relation of VMO atrophy and PFPS.
Patients with a greater quadriceps muscle size, lower eccentric knee strength, and less pain have a better short-term functional outcome after conservative treatment for PFP.
This study prospectively investigates whether catastrophizing thinking is associated with length of hospital stay after total knee arthroplasty. Forty-three patients who underwent primary total knee arthroplasty were included in this study. Prior to their operation all patients were asked to complete the pain catastrophizing scale, and a Western Ontario McMaster Universities Osteoarthritis index. A multiple regression analysis identified pain catastrophizing thinking and age as predictors of hospital stay after total knee arthroplasty. Patients with a higher degree of pain catastrophizing prior to the total knee arthroplasty and those with a higher age have a significantly greater risk for a longer hospital stay. Therefore, the results of this study indicate that the pre-operative level of pain catastrophizing in patients determine, in combination with other variables, the length and inter-individual variation in hospital stay after total knee arthroplasty. Reducing catastrophizing thinking about pain through cognitive-behavioral techniques is likely to reduce levels of fear after total knee arthroplasty. As a result, pain and function immediately post-operative might improve, leading to a decrease in length of hospital stay. Although during the last decades the duration of hospital stay is significantly reduced, this study shows that this can be improved when taking into account the contribution of psychological factors such as pain catastrophizing.
We constructed chimeric receptors wherein the extracellular domain of the erythropoietin receptor (EpoR) was fused to the transmembrane and intracellular domains of the interferon (IFN) type I receptor subunits, IFNaR1 or IFNaR2-2. Transfection into 2fTGH and Tyk2-deficient 11,1 cells showed that EpoR/IFNaR2-2 alone was able to transduce a signal upon stimulation with erythropoietin (Epo), as judged by induction of the interferon type I-inducible 6-16 promoter. In contrast, protection against infection with encephalomyocarditis virus or vesicular stomatitis virus was reduced or absent, respectively. To further investigate the role of IFNaR1 in the induction of an antiviral state, we analyzed the Epo-versus IFN␣-induced transcription of a set of genes, involved in antiviral protection. Up to 24 h after stimulation with Epo or IFN␣, comparable transcription of the p56, dsRNA-dependent protein kinase, 2-5A synthetase, and MxA genes was seen. However, at later time points, only in the case of Epo induction, a sharp decrease of mRNA levels was observed. Western blotting analysis of dsRNA-dependent protein kinase showed a similar pattern at the protein level. Taken together, our results imply a role for IFNaR1 in the induction of sustained mRNA and protein levels that are likely required for optimal antiviral activity.It is generally accepted that activation of a cell by a cytokine is initiated by ligand-induced clustering of receptor subunits, which can occur as di-, tri-, or higher order oligomers, involving identical or related subunits. With the exception of the heptamembrane-spanning receptors, members from the hematopoietin/IFN, 1 tumor necrosis factor/nerve growth factor, and tyrosine kinase receptor families are all activated by this mechanism of cytokine-driven multimerization. Ligand binding to the first receptor component induces the association with additional receptor subunits eventually resulting in an increase of affinity for the ligand (1, 2). Alternatively, preformed receptor complexes may also exist on the cell membrane (3). Interferons belong to the class I cytokine family and are divided into type I interferons (at least 14 IFN␣ subtypes, IFN, IFN, and the bovine embryonic IFN) that have antiviral, cytostatic, and hematopoietic activities on many cell types, and the type II interferon or IFN␥ that is also involved in many immune functions. Both types of interferons bind to distinct receptors that belong to the class I cytokine receptors. The interferon type I receptor (IFNaR) is composed of two subunits, IFNaR1 and IFNaR2-2. As a result of alternative splicing, subtypes of the latter subunit do also exist: a cytoplasmic truncated transmembrane form (IFNaR2-1) and a soluble form (IFNaR2-3) (4 -8).A large body of evidence has shown that the class I cytokine receptors make use of associated kinases (JAKs) to start intracellular tyrosine phosphorylation, resulting in the activation of the so-called Stat proteins. This JAK/Stat pathway is essential for transcription of many of the cytokine-inducible ge...
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