173 research outputs found
Relative deprivation and inequalities in social and political activism
In this paper we analyse whether relative deprivation has divergent effects on different types of social and political action. We expect that it will depress volunteering with parties as well as different types of conventional political participation more generally while stimulating volunteering with anti-cuts organisations and engagement in various kinds of protest activism. There is little research into how relative deprivation impacts on different types of social and political action from the wide range of activities available to citizens in contemporary democracies as well as into how this relationship might vary based on the wider economic context. While many studies construct scales, we examine participation in specific activities and associations, such as parties or anti-cuts organisations, voting, contacting, demonstrating and striking to show that deprivation has divergent effects that depart from what is traditionally argued. We apply random effects models with cross-level interactions utilizing an original cross-national European dataset collected in 2015 (N = 17,667) within a collaborative funded-project. We show that a negative economic context has a mobilizing effect by both increasing the stimulating effect of relative deprivation on protest activism as well as by closing or reversing the gap between resource-poor and resource-rich groups for volunteering with parties and voting
Role of mitochondrial raft-like microdomains in the regulation of cell apoptosis
Lipid rafts are envisaged as lateral assemblies of specific lipids and proteins that dissociate and associate rapidly and form functional clusters in cell membranes. These structural platforms are not confined to the plasma membrane; indeed lipid microdomains are similarly formed at subcellular organelles, which include endoplasmic reticulum, Golgi and mitochondria, named raft-like microdomains. In addition, some components of raft-like microdomains are present within ER-mitochondria associated membranes. This review is focused on the role of mitochondrial raft-like microdomains in the regulation of cell apoptosis, since these microdomains may represent preferential sites where key reactions take place, regulating mitochondria hyperpolarization, fission-associated changes, megapore formation and release of apoptogenic factors. These structural platforms appear to modulate cytoplasmic pathways switching cell fate towards cell survival or death. Main insights on this issue derive from some pathological conditions in which alterations of microdomains structure or function can lead to severe alterations of cell activity and life span. In the light of the role played by raft-like microdomains to integrate apoptotic signals and in regulating mitochondrial dynamics, it is conceivable that these membrane structures may play a role in the mitochondrial alterations observed in some of the most common human neurodegenerative diseases, such as Amyotrophic lateral sclerosis, Huntington's chorea and prion-related diseases. These findings introduce an additional task for identifying new molecular target(s) of pharmacological agents in these pathologies
Initial load-to-failure and failure analysis in single- and double-row repair techniques for rotator cuff repair
WNT signalling in prostate cancer
Genome sequencing and gene expression analyses of prostate tumours have highlighted the potential importance of genetic and epigenetic changes observed in WNT signalling pathway components in prostate tumours-particularly in the development of castration-resistant prostate cancer. WNT signalling is also important in the prostate tumour microenvironment, in which WNT proteins secreted by the tumour stroma promote resistance to therapy, and in prostate cancer stem or progenitor cells, in which WNT-β-catenin signals promote self-renewal or expansion. Preclinical studies have demonstrated the potential of inhibitors that target WNT receptor complexes at the cell membrane or that block the interaction of β-catenin with lymphoid enhancer-binding factor 1 and the androgen receptor, in preventing prostate cancer progression. Some WNT signalling inhibitors are in phase I trials, but they have yet to be tested in patients with prostate cancer
Branch ligatures and blood aspiration for post-traumatic superficial temporal artery pseudoaneurysm: surgical technique
The aim of this study is to report a new minimally invasive technique of superficial temporal artery (STA) pseudoaneurysm treatment. Several surgical options have been employed to treat STA pseudoaneurysms. To address this rare condition, the employed techniques are ligation and excision of the aneurysm, endovascular coil embolization or percutaneous ultrasound-guided thrombin injection. Between techniques no significant differences are reported in terms of outcomes. The decision to adopt a technique depends on STA pseudoaneurysm morphology and surgeon preference. In the present report, STA pseudoaneurysm afferent and efferent branches were identified by ultrasound in a 92-year-old female. Under local anaesthesia, these branches were ligated through small skin incisions. STA pseudoaneurysm decompression was obtained by an 'over the needle aspiration'. A compressive dressing was left in space for 48 h
Specificity and heregulin regulation of Ebp1 (ErbB3 binding protein 1) mediated repression of androgen receptor signalling
Although ErbB receptors have been implicated in the progression of prostate cancer, little is known about proteins that may mediate their interactions with the androgen receptor (AR). Ebp1, a protein cloned via its association with the ErbB3 receptor, binds the AR and inhibits androgen-regulated transactivation of wild-type AR in COS cells. As the complement of coregulators in different cells are important for AR activity, we determined the effect of Ebp1 on AR function in prostate cancer cell lines. In addition, we examined the regulation of Ebp1 function by the ErbB3/4 ligand heregulin (HRG). In this study, we demonstrate, using several natural AR-regulated promoters, that Ebp1 repressed transcriptional activation of wild-type AR in prostate cancer cell lines. Downregulation of Ebp1 expression in LNCaP cells using siRNA resulted in activation of AR in the absence of androgen. Ebp1 associated with ErbB3 in LNCaP cells in the absence of HRG, but HRG induced the dissociation of Ebp1 from ErbB3. In contrast, HRG treatment enhanced both the association of Ebp1 with AR and also the ability of Ebp1 to repress AR transactivation. These studies suggest that Ebp1 is an AR corepressor whose biological activity can be regulated by the ErbB3 ligand, HRG
Tendon–bone contact pressure and biomechanical evaluation of a modified suture-bridge technique for rotator cuff repair
The aim of the study was to evaluate the time-zero mechanical and footprint properties of a suture-bridge technique for rotator cuff repair in an animal model. Thirty fresh-frozen sheep shoulders were randomly assigned among three investigation groups: (1) cyclic loading, (2) load-to-failure testing, and (3) tendon–bone interface contact pressure measurement. Shoulders were cyclically loaded from 10 to 180 N and displacement to gap formation of 5- and 10-mm at the repair site. Cycles to failure were determined. Additionally, the ultimate tensile strength and stiffness were verified along with the mode of failure. The average contact pressure and pressure pattern were investigated using a pressure-sensitive film system. All of the specimens resisted against 3,000 cycles and none of them reached a gap formation of 10 mm. The number of cycles to 5-mm gap formation was 2,884.5 ± 96.8 cycles. The ultimate tensile strength was 565.8 ± 17.8 N and stiffness was 173.7 ± 9.9 N/mm. The entire specimen presented a unique mode of failure as it is well known in using high strength sutures by pulling them through the tendon. We observed a mean contact pressure of 1.19 ± 0.03 MPa, applied on the footprint area. The fundamental results of our study support the use of a suture-bridge technique for optimising the conditions of the healing biology of a reconstructed rotator cuff tendon. Nevertheless, an individual estimation has to be done if using the suture-bridge technique clinically. Further investigation is necessary to evaluate the cell biological healing process in order to achieve further sufficient advancements in rotator cuff repair
Viewing Loved Faces Inhibits Defense Reactions: A Health-Promotion Mechanism?
We have known for decades that social support is associated with positive health outcomes. And yet, the neurophysiological mechanisms underlying this association remain poorly understood. The link between social support and positive health outcomes is likely to depend on the neurophysiological regulatory mechanisms underlying reward and defensive reactions. The present study examines the hypothesis that emotional social support (love) provides safety cues that activate the appetitive reward system and simultaneously inhibit defense reactions. Using the startle probe paradigm, 54 undergraduate students (24 men) viewed black and white photographs of loved (romantic partner, father, mother, and best friend), neutral (unknown), and unpleasant (mutilated) faces. Eye–blink startle, zygomatic major activity, heart rate, and skin conductance responses to the faces, together with subjective ratings of valence, arousal, and dominance, were obtained. Viewing loved faces induced a marked inhibition of the eye-blink startle response accompanied by a pattern of zygomatic, heart rate, skin conductance, and subjective changes indicative of an intense positive emotional response. Effects were similar for men and women, but the startle inhibition and the zygomatic response were larger in female participants. A comparison between the faces of the romantic partner and the parent who shares the partner’s gender further suggests that this effect is not attributable to familiarity or arousal. We conclude that this inhibitory capacity may contribute to the health benefits associated with social support.This research was funded by grant P07-SEJ-02964 from Junta de Andalucía (Spain)
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