«Even though we only demonstrated the technique
with model membranes and single cells, this technique is translatable to biological tissue,» said Brasselet.
Not exact matches
The researchers have also developed an analogous
model that works for calcium interactions
with phospholipids at the cell
membrane.
Here, we present experiments using a reconstituted fusion system that suggest a simple
model in which the complexin accessory helix forms an alternative four - helix bundle
with the target - SNARE near the
membrane, preventing the vesicle - SNARE from completing its zippering.
Interactions of these proteins
with the outer
membrane in vivo and in vitro are well known, allowing for direct comparisons
with the synthetic
model.
The researchers began by creating large
membrane models with embedded and dyed channel proteins; they then put them on a glass surface and measured them using a single - molecule measuring method known as fluorescence correlation spectroscopy.
Modeling revealed that tilting of the PHDs to conform
with membrane deformations creates the low - energy pathway for hemifission.
Using whole - cell path clamp, both dSPNs and iSPNs from Q175 6 - month old mice showed elevated
membrane resistance and reduced rheobase current, consistent
with previous reports of SPN hyperexcitability in mouse
models of HD.
The Evaluation of a Biphasic Osteochondral Implant Coupled
with an Electrospun
Membrane in a Large Animal
Model.
With this series of protocols the BCL allows construction of backbone
models for large and
membrane proteins from the primary sequence.
In particular, an experimental study on the permeability of prebiotic vesicle
membranes composed of binary lipid mixtures allows us to construct a semi-empirical
model where protocells are able to reproduce and undergo an evolutionary process based on their coupling
with an internal chemistry that supports lipid synthesis.
For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together
with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal
membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat
model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain,
with the significant exception of its use in the treatment of convulsion diseases.