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Find video protocols related to scientific articles indexed in Pubmed.
Limited duration of complete remission on ruxolitinib in myeloid neoplasms with PCM1-JAK2 and BCR-JAK2 fusion genes.
Ann. Hematol.
PUBLISHED: 09-11-2014
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Rearrangements of chromosome band 9p24 are known to be associated with JAK2 fusion genes, e.g., t(8;9)(p22;p24) with a PCM1-JAK2 and t(9;22)(p24;q11) with a BCR-JAK2 fusion gene, respectively. In association with myeloid neoplasms, the clinical course is aggressive, and in absence of effective conventional treatment options, long-term remission is usually only observed after allogeneic stem cell transplantation (ASCT). With the discovery of inhibitors of the JAK2 tyrosine kinase and based on encouraging in vitro and in vivo data, we treated two male patients with myeloid neoplasms and a PCM1-JAK2 or a BCR-JAK2 fusion gene, respectively, with the JAK1/JAK2 inhibitor ruxolitinib. After 12 months of treatment, both patients achieved a complete clinical, hematologic, and cytogenetic response. Non-hematologic toxicity was only grade 1 while no hematologic toxicity was observed. However, remission in both patients was only short-term, with relapse occurring after 18 and 24 months, respectively, making ASCT indispensable in both cases. This data highlight (1) the ongoing importance of cytogenetic analysis for the diagnostic work-up of myeloid neoplasms as it may guide targeted therapy and (2) remission under ruxolitinib may only be short-termed in JAK2 fusion genes but it may be an important bridging therapy prior to ASCT.
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Activity-induced dendrite and dendritic spine development in human amyloid precursor protein transgenic mice.
Int. J. Dev. Neurosci.
PUBLISHED: 01-10-2011
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The amyloid precursor protein is essential for proper neuronal function but an imbalance in processing or metabolism or its overexpression lead to severe malfunction of the brain. The present study focused on dendritic morphology of hippocampal neurons in mice overexpressing the wild-type human amyloid precursor protein (hAPP). In addition, we examined whether enhanced physical activity may affect hAPP-related morphological changes. Overexpression of hAPP resulted in significant enlargement of dendrites, especially within the basal dendritic field but had no effect on spine density. Enhanced physical activity only moderately potentiated hAPP induced changes in dendritic size. Physical activity dependent increases in spine density were, however, augmented by hAPP overexpression. The results suggest that enhanced levels of wild-type hAPP do not result in degenerative changes of neuronal morphology, but rather promote dendritic growth.
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Constitutively enhanced p21Ras activity amplifies dendritic remodeling of hippocampal neurons during physical activity.
Int. J. Dev. Neurosci.
PUBLISHED: 02-24-2009
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In the present study we show that overexpression of constitutively active Ras amplifies the dendritic remodeling observed when animals were allowed to be physically active. The monomeric G-protein Ras is a key molecular trigger of distinct signal transduction pathways that play an important role in proper functioning of neurons. Our previous studies on Ras-transgenic synRas mice have demonstrated a considerable impact of Ras on dendritic growth, extension and synaptic connectivity of neurons. Voluntary access to a running wheel resulted in enlargement of hippocampal pyramidal cell dendrites in wild-type mice as expected. However, constitutively elevated Ras activity further enhanced dendritic growth and branching especially of apical arbors. The resultant dendritic surface gain was paralleled by a significant increase in dendritic spine density. Since Ras is crucially involved in signaling and cascades of neurotrophins that are elevated after physical activity, these results strongly suggest an important role of Ras in dendritic dynamics during induced neuronal remodeling.
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Deprivation-induced dendritic shrinkage might be oppositely affected by the expression of wild-type and mutated human amyloid precursor protein.
J. Neurosci. Res.
PUBLISHED: 01-27-2009
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The physiological role of the amyloid precursor protein (APP) and its proteolytic fragments in the brain is associated with neuronal survival, neurite outgrowth, synaptic formation, and neuronal plasticity. However, malregulation of APP processing leads to disordered balance of fragments, which may results in opposite, degenerative neuronal effects. In the present study, we analyzed in vivo effects of the expression of wild-type or mutated human APP on afferent deprivation-induced changes of dendritic morphology. After vibrissectomy, expression of wild-type human APP prevented diameter shrinkage of dendritic segments as well as dendritic rarefaction of apical arbors. In contrast, mutant human APP expression exacerbated degenerative changes of deprived barrel neurons. Degradation of apical arbors was especially pronounced. Results demonstrate for the first time opposite effects of the expression of wild-type and mutated human APP on deprivation-induced dendritic restructuring in vivo.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.