15 research outputs found
Optical Coherence Tomography Features of POEMS Syndrome and Castleman Disease-associated Papillopathy
Cephalopods in neuroscience: regulations, research and the 3Rs
Cephalopods have been utilised in neurosci- ence research for more than 100 years particularly because of their phenotypic plasticity, complex and centralised nervous system, tractability for studies of learning and cellular mechanisms of memory (e.g. long-term potentia- tion) and anatomical features facilitating physiological studies (e.g. squid giant axon and synapse). On 1 January 2013, research using any of the about 700 extant species of ‘‘live cephalopods’’ became regulated within the European Union by Directive 2010/63/EU on the ‘‘Protection of Animals used for Scientific Purposes’’, giving cephalopods the same EU legal protection as previously afforded only to vertebrates. The Directive has a number of implications, particularly for neuroscience research. These include: (1) projects will need justification, authorisation from local competent authorities, and be subject to review including a harm-benefit assessment and adherence to the 3Rs princi- ples (Replacement, Refinement and Reduction). (2) To support project evaluation and compliance with the new EU law, guidelines specific to cephalopods will need to be developed, covering capture, transport, handling, housing, care, maintenance, health monitoring, humane anaesthesia, analgesia and euthanasia. (3) Objective criteria need to be developed to identify signs of pain, suffering, distress and lasting harm particularly in the context of their induction by an experimental procedure. Despite diversity of views existing on some of these topics, this paper reviews the above topics and describes the approaches being taken by the cephalopod research community (represented by the authorship) to produce ‘‘guidelines’’ and the potential contribution of neuroscience research to cephalopod welfare
Intramedullary Subependymoma Occupying the Right Half of the Thoracic Spinal Cord. Case Report.
Incumbents' Defense Strategies: A Comparison of Deterrence and Shakeout Strategy Based on Evolutionary Game Theory
Analyses of Sox-B and Sox-E Family Genes in the Cephalopod Sepia officinalis: Revealing the Conserved and the Unusual
Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis
Angiogenesis, the formation of new vessels, is found in Multiple Sclerosis (MS) demyelinating lesions following
Vascular Endothelial Growth Factor (VEGF) release and the production of several other angiogenic molecules. The
increased energy demand of inflammatory cuffs and damaged neural cells explains the strong angiogenic response
in plaques and surrounding white matter. An angiogenic response has also been documented in an experimental
model of MS, experimental allergic encephalomyelitis (EAE), where blood
–
brain barrier disruption and vascular
remodelling appeared in a pre-symptomatic disease phase. In both MS and EAE, VEGF acts as a pro-inflammatory
factor in the early phase but its reduced responsivity in the late phase can disrupt neuroregenerative attempts, since
VEGF naturally enhances neuron resistance to injury and regulates
neural progenitor proliferation, migration, differentiation
and oligodendrocyte precursor cell (OPC) survival and migrati
on to demyelinated lesions. An
giogenesis, neurogenesis and
oligodendroglia maturation are closely intertwined in the neurovascular niches of the subventricular zone, one of the
preferential locations of inflammatory lesions in MS, and in all the other temporary vascular niches where the mutual
fostering of angiogenesis and OPC maturation occurs. Angiogenesis, induced either by CNS inflammation or by hypoxic
stimuli related to neurovascular uncoupling, appears to be ineffective in chronic MS due to a counterbalancing effect
of vasoconstrictive mechanisms determined by the reduced axonal activity, astrocyte dysfunction, microglia secretion
of free radical species and mitochondrial abnormalities. Thus, angiogenesis, that supplies several trophic factors, should
be promoted in therapeutic neuroregeneration efforts to combat the progressive, degenerative phase of MS