Habitat use, survival, and migration of a little-known East Asian endemic, the yellow-throated bunting Emberiza elegans.

Basic information on the ecology of species is key for their conservation. Here we study the ecology of the little-known yellow-throated bunting Emberiza elegans based on a multi-year study on its breeding grounds in the Russian Far East. For the first time in this species, we quantified breeding habitat parameters, calculated sex-specific apparent survival, and determined individual nonbreeding locations using light-level geolocation. We found that the habitat around song posts of male yellow-throated buntings is characterized by tree and shrub layers on richly littered moist ground. Habitat use overlaps with co-occurring Tristram's Buntings Emberiza tristrami and Black-faced Buntings E. spodocephala, but territories differ especially in tree cover and litter cover. Based on 4 years of color-ringing data of 72 individuals, we calculated an apparent survival rate of 36%, with higher survival estimates for male than for female yellow-throated buntings. We found no effect of carrying a geolocator on survival. We retrieved six geolocators from males. All birds migrated south-westward during autumn and spent the nonbreeding season at locations in China 700-1700 km away from their breeding sites. At least two individuals spent the boreal winter outside of the known range in northern or central China. Birds left the breeding area between early October and early November and returned between mid-March and mid-April. Our data on habitat use, survival rate, and migratory connectivity will help to assess threats to the populations of this enigmatic species, which might include habitat loss due to forest fires on the breeding grounds, and unsustainable harvest for consumption during the nonbreeding season.

A novel modular device for 3-D bone cell culture and non-destructive cell analysis.

Synthetic materials have emerged as bone substitutes for filling bone defects of critical sizes. Because bone healing requires a mechanically resistant matrix (scaffold) attractive to osteogenic cells and must allow revascularization for nutrient and oxygen supply, scaffold-based strategies focus on the further development of chemical and physical qualities of the material. Cellular ingrowth towards the scaffold center is critical; therefore selective information from inner regions, in particular from the central part, is essential. In this paper we introduce a novel modular in vitro system for three-dimensional (3-D) in vitro bone cell cultures. This 3-D system is developed exclusively for in vitro research purposes, with special emphasis on the geometrical scaffold design (pore size, pore design). The system is composed of a stack of titanium slices which are mounted on a clamp and which enable the separate monitoring of cell growth patterns on every single slice of the slide stack. In this way we are able to gain selective information about the regulation of the cell physiology in the inner part of the 3-D construct which can be used for the development of an optimized scaffold design for orthopedic implants.

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells.

BACKGROUND: Posterior capsule opacification is still the major complication in cataract surgery and is caused by migration and proliferation of residual lens epithelial cells. The challenge of a suitable therapy to inhibit capsule opacification is to specifically interfere with cellular mechanisms. Our approach using the T-calcium channel antagonist mibefradil is based on the hypothesis that this drug inhibits the signaling pathways mediated by cell adhesion. METHODS: The influence of mibefradil dihydrochloride was investigated on primary human lens epithelial cells (hLEC) from cataract surgery and on the human lens cell line HLE-B3. Apoptosis was quantitatively analyzed by flow cytometry (% increase of the sub-G1 peak), and verified by confocal microscopy (annexin V-biotin, TUNEL reaction). The membrane potential was detected by a membrane potential-sensitive dye. Integrin expression and proliferation were measured by flow cytometry. T-calcium channels in hLEC were verified by the whole-cell configuration of the patch-clamp technique. RESULTS: Mibefradil induced apoptosis in hLEC. Early signs of apoptosis were observed after only 4 h of incubation with mibefradil, accompanied by a significantly reduced cell area. Apoptosis correlated with inhibited integrin expression, reduced proliferation and the depolarization of the membrane potential. We could identify calcium channels of the T-type in our primary hLEC. CONCLUSIONS: We suggest that depolarization of the membrane potential and the inhibition of integrin expression leads to the loss of cell adhesion, which is the reason for the induction of apoptosis. Thus, mibefradil seems to be a suitable drug to prevent cell adhesion, migration and proliferation.