Not exact matches
Our technological expertise ranges from the
most fundamental approaches to study
membrane transport in lymphocytes and dendritic cells (subcellular compartmentalization, intravital microscopy, phagosomal functions), the systematic analysis of gene expression and it regulation (RNAseq, Chip Seq, proteomics) and physiological and pathological immune responses (mouse
models for cancer immunity, immunomodulation / vaccination, human clinical studies in cancer).
«Both the neuronal and average human
membrane models — arguably the
most compositionally complex plasma
membrane lipid
models to date — showed non-ideal lateral lipid mixing at different length and time scales, demonstrating the inherent complexity of biological
membranes.»
Dmitry: as the paper itself notes, the
most likely mechanism for the ability of hydroxypropyl - β - cyclodextrin to lower Aβ burden in the mouse
model is AD finding is by normalizing
membrane cholesterol content and reducing the appearance of abnormal cathepsin D - positive lysosomes, leading to reduced beta - secretase cleavage of APP and an upregulation of genes involved in cholesterol trafficking and Aβ clearance.
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.