Hip muscle weakness in patients with symptomatic femoroacetabular impingement

SummaryObjectiveFemoroacetabular impingement (FAI) is a pathomechanical process, which may cause hip pain, disability and early development of hip osteoarthritis (OA) in young and active adults. Patients with FAI experience functional disability during dynamic weight-bearing activities, which could originate from weakness of the hip muscles. The objective of this study was to compare hip muscle strength between patients with symptomatic FAI and healthy controls. It was hypothesized that patients would present overall hip muscle weakness compared to controls.MethodsA total of 22 FAI patients and 22 controls matched for gender, age, and body mass participated in the study. We evaluated isometric maximal voluntary contraction (MVC) strength of all hip muscle groups using hand-held and isokinetic dynamometry, and electromyographic (EMG) activity of the rectus femoris (RF) and tensor fasciae latae (TFL) muscles during active flexion of the hip.ResultsFAI patients had significantly lower MVC strength than controls for hip adduction (28%), flexion (26%), external rotation (18%) and abduction (11%). TFL EMG activity was significantly lower in FAI patients compared with controls (P=0.048), while RF EMG activity did not differ significantly between the two groups (P=0.056).ConclusionsPatients with symptomatic FAI presented muscle weakness for all hip muscle groups, except for internal rotators and extensors. Based on EMG recordings, it was demonstrated that patients with symptomatic FAI have a reduced ability to activate TFL muscle during hip flexion. These findings provide orthopedic surgeons with objective information about the amount and specificity of hip muscle weakness in patients with FAI. Future research should investigate the relationship between hip muscle weakness, functional disability and overuse injury risks, as well as the effects of hip muscle strengthening on clinical outcomes in individuals with symptomatic FAI

Project Opti-Milk: Optimisation and Comparison of High Yield and Low Input Milk Production Strategies on Pilot Farms in the Lowlands of Switzerland

Compared to other European countries milk production costs in Switzerland are high. Therefore Swiss milk producers must drastically reduce their costs. The high yield strategy (HY) and the full grazing (FG) or low-cost strategy appear most promising, at least for the lowland regions. Although the basic knowledge is available for both strategies, they have been applied very little in Switzerland in a consistent and optimised form

NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions.

NLRC5 is a transcriptional regulator of MHC class I (MHCI), which maintains high MHCI expression particularly in T cells. Recent evidence highlights an important NK-T-cell crosstalk, raising the question on whether NLRC5 specifically modulates this interaction. Here we show that NK cells from Nlrc5-deficient mice exhibit moderate alterations in inhibitory receptor expression and responsiveness. Interestingly, NLRC5 expression in T cells is required to protect them from NK-cell-mediated elimination upon inflammation. Using T-cell-specific Nlrc5-deficient mice, we show that NK cells surprisingly break tolerance even towards 'self' Nlrc5-deficient T cells under inflammatory conditions. Furthermore, during chronic LCMV infection, the total CD8(+) T-cell population is severely decreased in these mice, a phenotype reverted by NK-cell depletion. These findings strongly suggest that endogenous T cells with low MHCI expression become NK-cell targets, having thus important implications for T-cell responses in naturally or therapeutically induced inflammatory conditions

Coherent control of polariton parametric scattering in semiconductor microcavities

In a pump-probe experiment, we have been able to control, with phase-locked probe pulses, the ultrafast nonlinear optical emission of a semiconductor microcavity, arising from polariton parametric amplification. This evidences the coherence of the polariton population near k = 0, even for delays much longer than the pulse width. The control of a large population at k = 0 is possible although the probe pulses are much weaker than the large polarization they control. With rising pump power the dynamics of the scattering get faster. Just above threshold the parametric scattering process shows unexpected long coherence times, whereas when pump power is risen the contrast decays due to a significant pump reservoir depletion. The weak pulses at normal incidence control the whole angular emission pattern of the microcavity

Festchrift: A Collection of Essays on Architectural History

A collection of essays on architectural history prepared by the Northern Pacific Coast Chapter Society of Architectural Historians dedicated to Professor Marion Dean Ross, chapter founder, on the occasion of his 65th birthday

Transcriptional Upregulation of NLRC5 by Radiation Drives STING- and Interferon-Independent MHC-I Expression on Cancer Cells and T Cell Cytotoxicity.

Radiation therapy has been shown to enhance the efficacy of various T cell-targeted immunotherapies that improve antigen-specific T cell expansion, T regulatory cell depletion, or effector T cell function. Additionally, radiation therapy has been proposed as a means to recruit T cells to the treatment site and modulate cancer cells as effector T cell targets. The significance of these features remains unclear. We set out to determine, in checkpoint inhibitor resistant models, which components of radiation are primarily responsible for overcoming this resistance. In order to model the vaccination effect of radiation, we used a Listeria monocytogenes based vaccine to generate a large population of tumor antigen specific T cells but found that the presence of cells with cytotoxic capacity was unable to replicate the efficacy of radiation with combination checkpoint blockade. Instead, we demonstrated that a major role of radiation was to increase the susceptibility of surviving cancer cells to CD8+ T cell-mediated control through enhanced MHC-I expression. We observed a novel mechanism of genetic induction of MHC-I in cancer cells through upregulation of the MHC-I transactivator NLRC5. These data support the critical role of local modulation of tumors by radiation to improve tumor control with combination immunotherapy

TRIM27 Negatively Regulates NOD2 by Ubiquitination and Proteasomal Degradation

NOD2, the nucleotide-binding domain and leucine-rich repeat containing gene family (NLR) member 2 is involved in mediating antimicrobial responses. Dysfunctional NOD2 activity can lead to severe inflammatory disorders, but the regulation of NOD2 is still poorly understood. Recently, proteins of the tripartite motif (TRIM) protein family have emerged as regulators of innate immune responses by acting as E3 ubiquitin ligases. We identified TRIM27 as a new specific binding partner for NOD2. We show that NOD2 physically interacts with TRIM27 via the nucleotide-binding domain, and that NOD2 activation enhances this interaction. Dependent on functional TRIM27, ectopically expressed NOD2 is ubiquitinated with K48-linked ubiquitin chains followed by proteasomal degradation. Accordingly, TRIM27 affects NOD2-mediated pro-inflammatory responses. NOD2 mutations are linked to susceptibility to Crohns disease. We found that TRIM27 expression is increased in Crohns disease patients, underscoring a physiological role of TRIM27 in regulating NOD2 signaling. In HeLa cells, TRIM27 is partially localized in the nucleus. We revealed that ectopically expressed NOD2 can shuttle to the nucleus in a Walker A dependent manner, suggesting that NOD2 and TRIM27 might functionally cooperate in the nucleus. We conclude that TRIM27 negatively regulates NOD2-mediated signaling by degradation of NOD2 and suggest that TRIM27 could be a new target for therapeutic intervention in NOD2-associated diseases.Funding Agencies|German Research Foundation (DFG)|SFB670-NG01|Swedish Society of Medicine||Regional Research Council of South-East Sweden (FORSS)||Swedish Research Council division of Medicine||Gustav V 90th anniversary foundation||Italian Telethon Foundation||DFG|SE 1122/2-1|</p

The SIB Swiss Institute of Bioinformatics' resources: focus on curated databases

The SIB Swiss Institute of Bioinformatics (www.isb-sib.ch) provides world-class bioinformatics databases, software tools, services and training to the international life science community in academia and industry. These solutions allow life scientists to turn the exponentially growing amount of data into knowledge. Here, we provide an overview of SIB's resources and competence areas, with a strong focus on curated databases and SIB's most popular and widely used resources. In particular, SIB's Bioinformatics resource portal ExPASy features over 150 resources, including UniProtKB/Swiss-Prot, ENZYME, PROSITE, neXtProt, STRING, UniCarbKB, SugarBindDB, SwissRegulon, EPD, arrayMap, Bgee, SWISS-MODEL Repository, OMA, OrthoDB and other databases, which are briefly described in this article