541 research outputs found
Egypt's armed forces cement economic power: military business expansion impedes structural reforms
Since toppling President Mohamed Morsi in July 2013, the Egyptian military has successively expanded its civil economic activities. This development has attracted growing criticism, above all in the private sector. The government responded in October 2016 by announcing that the armed forces would diminish their economic role over the coming two to three years. But strong market positions, established privileges and historically ingrained structures make it unlikely that this will actually occur. Instead the economic activities of the armed forces, for example in the food, energy and construction sectors, will continue to shape the Egyptian economy. Realisation of the structural reforms Cairo agreed with the IMF in November 2016 is more than doubtful under these circumstances. Not least on those grounds, international donors should urge Egypt's leaders to curb the army's privileges. (author's abstract
Pretty Princess and Hurdling Heroes: A Content Analysis of Walt Disney Studio Movies
This study investigated the portrayal of active and passive behaviors of male and female characters in Walt Disney Studio original animated films. It was hypothesized that males would exhibit more active behaviors than their female counterparts and that females would exhibit more passive behaviors than their male counterparts. The results indicated that both of these hypotheses were supported. The study also found that the least likely interaction of male and female characters was when the male character was being passive and the female character was being active. The most likely was male characters performing active behaviors and female characters performing passive behaviors. There was also evidence discovered that newer Disney films portray female protagonists performing more active behaviors than older Disney films but male characters were not shown to have any differences in behaviors between older and newer films. There is also a discussion how these findings might affect the population viewing the results through cultivation theory and suggestions for further research on the subject
From Yemen war to joint army? Egyptian-Saudi differences over Arab military cooperation
"On 25 March 2015 a Saudi-led coalition of Arab states launched air strikes on Yemen to halt the advance of the Houthi movement. A few days later the summit of the Arab League decided to set up a joint Arab army. Nevertheless, the two most important Arab countries support opposing concepts for military cooperation: Egypt proposes institutionalised long-term military cooperation to increase its political weight in the region, while Saudi Arabia prefers ad hoc coalitions precisely in order to avoid long-term dependency on other countries, not least Egypt. However, the two events suggest that states in the region are stepping up military cooperation. Germany and the European Union should treat this development with scepticism. Experience shows that such collaborations tend to exacerbate rather than resolve regional conflicts." (Autorenreferat
Ägyptens Militär zementiert seine ökonomische Macht: die wirtschaftliche Expansion der Streitkräfte verhindert Strukturreformen im Land
Seit dem Sturz von Präsident Mohammed Mursi im Juli 2013 haben die ägyptischen Streitkräfte ihre Aktivitäten in der zivilen Wirtschaft des Landes sukzessive weiter ausgebaut. Vor allem im Privatsektor gibt es wachsende Kritik an dieser Entwicklung. Die ägyptische Führung reagierte darauf im Oktober 2016 mit der Ankündigung, das Militär werde seine ökonomische Rolle in den nächsten zwei bis drei Jahren reduzieren. Angesichts starker Marktpositionen, abgesicherter Privilegien und historisch gewachsener Strukturen ist jedoch unwahrscheinlich, dass dies tatsächlich geschieht. Vielmehr werden die Unternehmungen des Militärs, die sich unter anderem auf Versorgungs-, Energie- und Bausektor erstrecken, die ägyptische Wirtschaft auch in Zukunft prägen. Mehr als fraglich ist, ob sich unter diesen Umständen die Strukturreformen verwirklichen lassen, die Kairo im November 2016 mit dem IWF vereinbart hat. Nicht zuletzt deshalb sollten internationale Geber die ägyptische Führung dazu drängen, die Sonderrechte des Militärs zu reduzieren. (Autorenreferat
Vom Jemen-Krieg zur gemeinsamen Armee? Ägyptisch-saudische Differenzen über arabische Militärkooperation
"Am 25. März 2015 startete eine saudisch geführte Koalition arabischer Staaten Luftangriffe auf den Jemen, um den Vormarsch der Houthi-Bewegung zu stoppen. Wenige Tage später gaben die Teilnehmer des Gipfeltreffens der Arabischen Liga ihre Entscheidung bekannt, eine gemeinsame arabische Armee aufzustellen. Dabei vertreten die beiden wichtigsten arabischen Ländern gegensätzliche Konzepte militärischer Kooperation: Ägypten setzt auf eine langfristig ausgerichtete, institutionalisierte Militärzusammenarbeit, um größere politische Bedeutung in der Region zu gewinnen; Saudi-Arabien dagegen zieht Ad-hoc-Koalitionen vor, um langfristige Abhängigkeiten von anderen Ländern zu vermeiden, nicht zuletzt von Ägypten. Beide Ereignisse deuten darauf hin, dass die Staaten der Region militärisch vermehrt miteinander kooperieren. Deutschland und die EU sollten dieser Entwicklung mit Skepsis begegnen. Die bisherigen Erfahrungen zeigen, dass regionale Konflikte durch solche Kooperationen eher verschärft als gelöst wurden." (Autorenreferat
The case for neuregulin-1 as a clinical treatment for stroke
Ischemic stroke is the leading cause of serious long-term disability and the 5th leading cause of death in the United States. Revascularization of the occluded cerebral artery, either by thrombolysis or endovascular thrombectomy, is the only effective, clinically-approved stroke therapy. Several potentially neuroprotective agents, including glutamate antagonists, anti-inflammatory compounds and free radical scavenging agents were shown to be effective neuroprotectants in preclinical animal models of brain ischemia. However, these compounds did not demonstrate efficacy in clinical trials with human patients following stroke. Proposed reasons for the translational failure include an insufficient understanding on the cellular and molecular pathophysiology of ischemic stroke, lack of alignment between preclinical and clinical studies and inappropriate design of clinical trials based on the preclinical findings. Therefore, novel neuroprotective treatments must be developed based on a clearer understanding of the complex spatiotemporal mechanisms of ischemic stroke and with proper clinical trial design based on the preclinical findings from specific animal models of stroke. We and others have demonstrated the clinical potential for neuregulin-1 (NRG-1) in preclinical stroke studies. NRG-1 significantly reduced ischemia-induced neuronal death, neuroinflammation and oxidative stress in rodent stroke models with a therapeutic window of >13 h. Clinically, NRG-1 was shown to be safe in human patients and improved cardiac function in multisite phase II studies for heart failure. This review summarizes previous stroke clinical candidates and provides evidence that NRG-1 represents a novel, safe, neuroprotective strategy that has potential therapeutic value in treating individuals after acute ischemic stroke
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Neuroprotection by Exogenous and Endogenous Neuregulin-1 in Mouse Models of Focal Ischemic Stroke.
Identifying novel neuroprotectants that can halt or reverse the neurological effects of stroke is of interest to both clinicians and scientists. We and others previously showed the pre-clinical neuroprotective efficacy of neuregulin-1 (NRG-1) in rats following focal brain ischemia. In this study, we examined neuroprotection by exogenous and endogenous NRG-1 using a mouse model of ischemic stroke. C57BL6 mice were subjected to middle cerebral artery occlusion (MCAO) followed by reperfusion. NRG-1 or vehicle was infused intra-arterially (i.a.) or intravenously (i.v.) after MCAO and before the onset of reperfusion. NRG-1 treatment (16 μg/kg; i.a.) reduced cerebral cortical infarct volume by 72% in mice when delivered post-ischemia. NRG-1 also inhibited neuronal injury as measured by Fluoro Jade B labeling and rescued NeuN immunoreactivity in neurons. Neuroprotection by NRG-1 was also observed in mice when administered i.v. (100 μg/kg) in both male and female mice. We investigated whether endogenous NRG-1 was neuroprotective using male and female heterozygous NRG-1 knockout mice (NRG-1+/-) compared with wild-type mice (WT) littermates. NRG-1+/- and WT mice were subjected to MCAO for 45 min, and infarct size was measured 24 h following MCAO. NRG-1+/- mice displayed a sixfold increase in cortical infarct size compared with WT mice. These results demonstrate that NRG-1 treatment mitigates neuronal damage following cerebral ischemia. We further showed that reduced endogenous NRG-1 results in exacerbated neuronal injury in vivo. These findings suggest that NRG-1 represents a promising therapy to treat stroke in human patients
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Spontaneous Isomerization of Long-Lived Proteins Provides a Molecular Mechanism for the Lysosomal Failure Observed in Alzheimer's Disease.
Proteinaceous aggregation is a well-known observable in Alzheimer's disease (AD), but failure and storage of lysosomal bodies within neurons is equally ubiquitous and actually precedes bulk accumulation of extracellular amyloid plaque. In fact, AD shares many similarities with certain lysosomal storage disorders though establishing a biochemical connection has proven difficult. Herein, we demonstrate that isomerization and epimerization, which are spontaneous chemical modifications that occur in long-lived proteins, prevent digestion by the proteases in the lysosome (namely, the cathepsins). For example, isomerization of aspartic acid into l-isoAsp prevents digestion of the N-terminal portion of Aβ by cathepsin L, one of the most aggressive lysosomal proteases. Similar results were obtained after examination of various target peptides with a full series of cathepsins, including endo-, amino-, and carboxy-peptidases. In all cases peptide fragments too long for transporter recognition or release from the lysosome persisted after treatment, providing a mechanism for eventual lysosomal storage and bridging the gap between AD and lysosomal storage disorders. Additional experiments with microglial cells confirmed that isomerization disrupts proteolysis in active lysosomes. These results are easily rationalized in terms of protease active sites, which are engineered to precisely orient the peptide backbone and cannot accommodate the backbone shift caused by isoaspartic acid or side chain dislocation resulting from epimerization. Although Aβ is known to be isomerized and epimerized in plaques present in AD brains, we further establish that the rates of modification for aspartic acid in positions 1 and 7 are fast and could accrue prior to plaque formation. Spontaneous chemistry can therefore provide modified substrates capable of inducing gradual lysosomal failure, which may play an important role in the cascade of events leading to the disrupted proteostasis, amyloid formation, and tauopathies associated with AD
Pericytes contribute to airway remodeling in a mouse model of chronic allergic asthma
Myofibroblast accumulation, subepithelial fibrosis, and vascular remodeling are complicating features of chronic asthma, but the mechanisms are not clear. Platelet-derived growth factors (PDGFs) regulate the fate and function of various mesenchymal cells and have been implicated as mediators of lung fibrosis. However, it is not known whether PDGF-BB signaling via PDGFRβ, which is critical for the recruitment of pericytes to blood vessels, plays a role in airway remodeling in chronic asthma. In the present study, we used a selective PDGFRβ inhibitor (CP-673451) to investigate the role of PDGFRβ signaling in the development of airway remodeling and lung dysfunction in an established mouse model of house dust mite-induced chronic allergic asthma. Unexpectedly, we found that pharmacological inhibition of PDGFRβ signaling in the context of chronic aeroallergen exposure led to exacerbated lung dysfunction and airway smooth muscle thickening. Further studies revealed that the inflammatory response to aeroallergen challenge in mice was associated with decreased PDGF-BB expression and the loss of pericytes from the airway microvasculature. In parallel, cells positive for pericyte markers accumulated in the subepithelial region of chronically inflamed airways. This process was exacerbated in animals treated with CP-673451. The results indicate that perturbed PDGF-BB/PDGFRβ signaling and pericyte accumulation in the airway wall may contribute to airway remodeling in chronic allergic asthma
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