Behavioural syndrome in a solitary predator is independent of body size and growth rate.

Models explaining behavioural syndromes often focus on state-dependency, linking behavioural variation to individual differences in other phenotypic features. Empirical studies are, however, rare. Here, we tested for a size and growth-dependent stable behavioural syndrome in the juvenile-stages of a solitary apex predator (pike, Esox lucius), shown as repeatable foraging behaviour across risk. Pike swimming activity, latency to prey attack, number of successful and unsuccessful prey attacks was measured during the presence/absence of visual contact with a competitor or predator. Foraging behaviour across risks was considered an appropriate indicator of boldness in this solitary predator where a trade-off between foraging behaviour and threat avoidance has been reported. Support was found for a behavioural syndrome, where the rank order differences in the foraging behaviour between individuals were maintained across time and risk situation. However, individual behaviour was independent of body size and growth in conditions of high food availability, showing no evidence to support the state-dependent personality hypothesis. The importance of a combination of spatial and temporal environmental variation for generating growth differences is highlighted

Newly formed cystic lesions for the development of pneumomediastinum in Pneumocystis jirovecii pneumonia

<p>Abstract</p> <p>Background</p> <p><it>Pneumocystis jirovecii</it>, formerly named <it>Pneumocystis carinii</it>, is one of the most common opportunistic infections in human immunodeficiency virus (HIV)-infected patients.</p> <p>Case presentations</p> <p>We encountered two cases of spontaneous pneumomediastinum with subcutaneous emphysema in HIV-infected patients being treated for <it>Pneumocystis jirovecii </it>pneumonia with trimethoprim/sulfamethoxazole.</p> <p>Conclusion</p> <p>Clinicians should be aware that cystic lesions and bronchiectasis can develop in spite of trimethoprim/sulfamethoxazole treatment for <it>P. jirovecii </it>pneumonia. The newly formed bronchiectasis and cyst formation that were noted in follow up high resolution computed tomography (HRCT) but were not visible on HRCT at admission could be risk factors for the development of pneumothorax or pneumomediastinum with subcutaneous emphysema in HIV-patients.</p

Neurturin but not glial cell line-derived neurotrophic factor stimulates neuronal differentiation in NG108-15 cells

University of Liverpool, School of Biological Sciences International Symposium Celebrating 100 Years of Biochemistry in Liverpool and the U

Haemorrhagic transformation of ischaemic stroke: risk factors and prognostic implication

Poster presentationBackground: Haemorrhagic transformation (HT) complicating ischaemic stroke is associated with significant morbidities and mortality. The clinical implications of HT have not been explored locally. This study aimed to determine the risk factors and clinical implications of HT complicating cerebral infarction in the Hong Kong Chinese population. Methods: This was a retrospective case-control study of consecutive patients admitted to Queen Mary Hospital with acute ischaemic stroke (IS) between 1 January 2007 and 31 December 2011. HT was diagnosed with examination of repeated brain neuroimaging (computed tomography or magnetic resonance imaging) performed within 2 weeks of IS onset. Patients with IS without repeated neuroimaging within 2 weeks, and patients with transient ischaemic attack or intracranial haemorrhage were excluded. HT was classified according to the European-Australasian Acute Stroke Study (ECASS) II criteria. Poor clinical outcome was defined as mortality within 90 days or modified Rankin scale score >2 at completion of rehabilitation or around 90 days. Results: Of 718 patients recruited, 66 (9.2%) received intravenous (IV) thrombolysis and 117 (16.3%) developed HT—HI1, 12 (1.7%); HI2, 3 (0.42%); PH1, 46 (6.4%); PH2, 54 (7.5%); PH at remote site, 2 (0.28%). HT was independently predicted by IV thrombolytic therapy (odds ratio [OR]=2.86; 95% confidence interval [CI], 1.58-5.18), cardioembolic stroke (3.65; 2.23-5.97) and prior warfarin use (2.85; 1.27-6.39). At 90 days, 138 (19.2%) patients died. At completion of rehabilitation or around 90 days, 462 (64.3%) had poor outcome. The 90-day and 5-year mortality rates were significantly increased in patients with PH2 (hazard ratio=1.86; 95% CI, 1.07-3.24 and 1.53, 1.01-2.30, respectively). Multivariate analysis showed PH2 to be an independent predictor of poor outcome (OR=2.14; 95% CI, 1.04-4.40). Conclusion: IV thrombolytic therapy, cardioembolic stroke, and prior warfarin use were independent predictors of HT. PH2 was associated with increased risk of poor outcome at approximately 90 days and mortality at 5 years

Nesting problem using an immune-inspired optimization algorithm

Conference Theme: Unfolding the New Era of Business CollaborationSession D: Modeling and Optimization - D4-2: no. 22

Differential effects of glial cell line-derived neurotrophic factor and neurturin in RET/GFRα1-expressing cells

The c-ret protooncogene, RET, encodes a receptor tyrosine kinase. RET is activated by members of the glial cell line-derived neurotrophic factor (GDNF) family of ligands, which include GDNF, neurturin, artemin, and persephin. The ligands bind RET through GDNF family receptor α, termed GFRα1-4. Despite the importance of RET signaling in the development of the enteric nervous system and the kidney, the differential signaling mechanisms between RET ligands are poorly established. It has been suggested that signal specificity is achieved through binding of the ligand to its preferred GFRα. To compare the signaling profiles of GDNF and neurturin, we have identified a cell line, NG108-15, which endogenously expresses RET and GFRα1 but not GFRα2-4. Immunoblot data showed that GDNF caused a transient activation, whereas neurturin caused a sustained activation, of both p44/p42 MAP kinases and PLC-γ. Under serum starvation, NG108-15 cells differentiate and form neuntes. Neurturin but not GDNF stimulated neurite outgrowth, which could be blocked by the selective PLC inhibitor U73122. On the other hand, GDNF but not neurturin promoted cell survival, and this could be blocked by the p44/p42 MAP kinase inhibitor PD98059. Our findings not only show the differential signaling of GDNF and neurturin but also suggest that this can be achieved through binding to the same GFRα subtype, leading to distinct biological responses. © 2005 Wiley-Liss, Inc.link_to_subscribed_fulltex