JoVE Visualize What is visualize?
Stop Reading. Start Watching.
Advanced Search
Stop Reading. Start Watching.
Regular Search
Find video protocols related to scientific articles indexed in Pubmed.
Earlier evidence of spheno-occipital synchondrosis fusion correlates with severity of midface hypoplasia in patients with syndromic craniosynostosis.
Plast. Reconstr. Surg.
PUBLISHED: 08-28-2014
Show Abstract
Hide Abstract
The spheno-occipital synchondrosis is an important driver of facial and cranial base growth. The current study characterizes its fusion in patients with Apert, Crouzon, and Pfeiffer syndromes and correlates early fusion with the presence, and degree, of midface hypoplasia.
Related JoVE Video
Treatment of large calvarial defects with bone transport osteogenesis: a preclinical sheep model.
J Craniofac Surg
PUBLISHED: 08-15-2014
Show Abstract
Hide Abstract
Bone transport osteogenesis (BTO), distraction of a free portion of bone across a defect, offers an autologous solution to large cranial defects that may allow treatment without permanent hardware implantation. This study establishes a sheep model to evaluate the feasibility and distraction kinetics of BTO.
Related JoVE Video
New brain infarcts on magnetic resonance imaging after coronary artery bypass graft surgery: lesion patterns, mechanism, and predictors.
Ann. Neurol.
PUBLISHED: 08-11-2014
Show Abstract
Hide Abstract
New brain infarcts after coronary artery bypass graft (CABG) are markedly more frequent than clinically evident stroke and have been proposed as a surrogate marker of postprocedural stroke. We sought to investigate the lesion patterns, mechanisms, and predictors of new brain infarction after CABG surgery.
Related JoVE Video
Sustained delivery of rhBMP-2 by means of poly(lactic-co-glycolic acid) microspheres: cranial bone regeneration without heterotopic ossification or craniosynostosis.
Plast. Reconstr. Surg.
PUBLISHED: 03-14-2014
Show Abstract
Hide Abstract
Commercially available recombinant human bone morphogenetic protein 2 (rhBMP2) has demonstrated efficacy in bone regeneration, but not without significant side effects. The authors used rhBMP2 encapsulated in poly(lactic-co-glycolic acid) (PLGA) microspheres placed in a rabbit cranial defect model to test whether low-dose, sustained delivery can effectively induce bone regeneration.
Related JoVE Video
Diagnostic and prognostic value of multimodal MRI in transient ischemic attack.
Int J Stroke
PUBLISHED: 07-15-2013
Show Abstract
Hide Abstract
The clinical diagnosis of transient ischemic attack is highly subjective, and the risk prediction after transient ischemic attack using the clinical parameters still remains unsatisfactory.
Related JoVE Video
Outcomes after Tissue Plasminogen Activator Administration under the Drip and Ship Paradigm May Differ According to the Regional Stroke Care System.
J Stroke Cerebrovasc Dis
PUBLISHED: 06-09-2013
Show Abstract
Hide Abstract
The drip and ship paradigm for stroke patients enhances the rate of using intravenous tissue plasminogen activator (IVT) in community hospitals. The safety and outcomes of patients treated with IVT for acute ischemic stroke (AIS) under the drip and ship paradigm were compared with patients directly treated at a comprehensive stroke center in the Busan metropolitan area of Korea. This was a retrospective study of patients with AIS treated with IVT between January 2009 and January 2012. Information on patients baseline characteristics, neuroimaging, symptomatic intracerebral hemorrhage (sICH), and outcome 90 days after using IVT was obtained from our stroke registry. We surveyed stroke neurologists regarding their pattern of post-thrombolysis care. During the observation periods, we selected 317 patients using IVT. Among these, 239 patients received IVT at our stroke center, and 78 were treated at 21 community hospitals under the drip and ship paradigm. Initial neurologic deficits and the size of ischemic lesions on magnetic resonance imaging were much more severe in patients treated with IVT under the drip and ship paradigm compared with patients treated at our comprehensive stroke center. The prevalence of a poor outcome (modified Rankin Scale score 3-6) 90 days after IVT was much higher in patients treated with the drip and ship paradigm than in those treated at our comprehensive stroke center. Regarding the occurrence of sICH, there was no significant difference between the 2 groups. The clinical characteristics and outcomes after using IVT under the drip and ship paradigm may differ greatly among stroke care systems.
Related JoVE Video
IGF-1-mediated osteoblastic niche expansion enhances long-term hematopoietic stem cell engraftment after murine bone marrow transplantation.
Stem Cells
PUBLISHED: 03-24-2013
Show Abstract
Hide Abstract
The efficiency of hematopoietic stem cell (HSC) engraftment after bone marrow (BM) transplantation depends largely on the capacity of the marrow microenvironment to accept the transplanted cells. While radioablation of BM damages osteoblastic stem cell niches, little is known about their restoration and mechanisms governing their receptivity to engraft transplanted HSCs. We previously reported rapid restoration and profound expansion of the marrow endosteal microenvironment in response to marrow radioablation. Here, we show that this reorganization represents proliferation of mature endosteal osteoblasts which seem to arise from a small subset of high-proliferative, relatively radio-resistant endosteal cells. Multiple layers of osteoblasts form along the endosteal surface within 48 hours after total body irradiation, concomitant with a peak in marrow cytokine expression. This niche reorganization fosters homing of the transplanted hematopoietic cells to the host marrow space and engraftment of long-term-HSC. Inhibition of insulin-like growth factor (IGF)-1-receptor tyrosine kinase signaling abrogates endosteal osteoblast proliferation and donor HSC engraftment, suggesting that the cytokine IGF-1 is a crucial mediator of endosteal niche reorganization and consequently donor HSC engraftment. Further understanding of this novel mechanism of IGF-1-dependent osteoblastic niche expansion and HSC engraftment may yield clinical applications for improving engraftment efficiency after clinical HSC transplantation.
Related JoVE Video
Ischemic stroke in patients with cancer: Is it different from usual strokes?
Int J Stroke
PUBLISHED: 02-13-2013
Show Abstract
Hide Abstract
It remains unclear whether the characteristics of ischemic stroke in patients with cancer (ISC) differ from usual ischemic strokes (non-ISC). Although a small number of studies have been conducted to characterize ISC, the status of cancer has rarely been considered seriously.
Related JoVE Video
The Muenke syndrome mutation (FgfR3P244R) causes cranial base shortening associated with growth plate dysfunction and premature perichondrial ossification in murine basicranial synchondroses.
Dev. Dyn.
PUBLISHED: 10-22-2011
Show Abstract
Hide Abstract
Muenke syndrome caused by the FGFR3(P250R) mutation is an autosomal dominant disorder mostly identified with coronal suture synostosis, but it also presents with other craniofacial phenotypes that include mild to moderate midface hypoplasia. The Muenke syndrome mutation is thought to dysregulate intramembranous ossification at the cranial suture without disturbing endochondral bone formation in the skull. We show in this study that knock-in mice harboring the mutation responsible for the Muenke syndrome (FgfR3(P244R)) display postnatal shortening of the cranial base along with synchondrosis growth plate dysfunction characterized by loss of resting, proliferating and hypertrophic chondrocyte zones and decreased Ihh expression. Furthermore, premature conversion of resting chondrocytes along the perichondrium into prehypertrophic chondrocytes leads to perichondrial bony bridge formation, effectively terminating the postnatal growth of the cranial base. Thus, we conclude that the Muenke syndrome mutation disturbs endochondral and perichondrial ossification in the cranial base, explaining the midface hypoplasia in patients.
Related JoVE Video
Engineering of a periodontal ligament construct: cell and fibre alignment induced by shear stress.
J. Clin. Periodontol.
PUBLISHED: 08-16-2011
Show Abstract
Hide Abstract
We report an in vitro technique to establish alignment of collagen fibres and cells within a three-dimensional tissue equivalent that mimics the natural periodontal ligament (PDL) using a novel custom-designed bioreactor.
Related JoVE Video
Efficacy and safety of combination antiplatelet therapies in patients with symptomatic intracranial atherosclerotic stenosis.
Stroke
PUBLISHED: 07-28-2011
Show Abstract
Hide Abstract
An optimal strategy for management of symptomatic intracranial atherosclerotic stenosis (ICAS) has not yet been established. We compared the efficacy of 2 combinations of antiplatelets, aspirin plus cilostazol (cilostazol group) verus aspirin plus clopidogrel (clopidogrel group), on the progression of ICAS, which is known to be associated with clinical stroke recurrence.
Related JoVE Video
Diversity of single small subcortical infarctions according to infarct location and parent artery disease: analysis of indicators for small vessel disease and atherosclerosis.
Stroke
PUBLISHED: 10-21-2010
Show Abstract
Hide Abstract
Single small subcortical infarctions (SSSIs), so-called lacunae, are typically caused by lipohyalinosis of a perforator artery. However, SSSIs can be caused by underlying large parent arterial disease or microatheroma of the proximal portion of a perforator artery. We sought to investigate whether indicators for small vessel disease (SVD) and atherosclerosis in patients with SSSI differ according to lesion location and the presence of parent artery disease.
Related JoVE Video
Metopic craniosynostosis due to mutations in GLI3: A novel association.
Am. J. Med. Genet. A
PUBLISHED: 06-29-2010
Show Abstract
Hide Abstract
We report on the novel association of trigonocephaly and polysyndactyly in two unrelated patients due to mutations within the last third (exon 14) and first third (exon 6) of the GLI3 gene, respectively. GLI3 acts as a downstream mediator of the Sonic hedgehog signal-transduction pathway which is essential for early development; and plays a role in cell growth, specialization, and patterning of structures such as the brain and limbs. GLI3 mutations have been identified in patients with Pallister-Hall, Grieg cephalopolysyndactyly syndrome (GCPS), postaxial polydactyly type A1, preaxial polydactyly type IV, and in one patient with acrocallosal syndrome (ACLS). Furthermore, deletions including the GLI3 gene have been reported in patients with features of GCPS and ACLS. To date, trigonocephaly has not been associated with abnormalities of GLI3 and craniosynostosis is not a feature of GCPS. However, Hootnick and Holmes reported on a father with polysyndactyly and son with trigonocephaly, polysyndactyly, and agenesis of the corpus callosum, considered GCPS thereafter. Guzzetta et al. subsequently described a patient with trigonocephaly, polysyndactyly, and agenesis of the corpus callosum postulating a diagnosis of GCPS, later considered ACLS. In retrospect, these two patients, evaluated prior to mutational analysis, and our patients, with confirmed mutations, likely fall within the GLI3 morphopathy spectrum and may provide a bridge to better understanding those patients with overlapping features of GCPS and ACLS. Based on this observation, we suggest GLI3 studies in patients presenting with this constellation of findings, specifically metopic craniosynostosis with polysyndactyly, in order to provide appropriate medical management and genetic counseling.
Related JoVE Video
Dura in the pathogenesis of syndromic craniosynostosis: fibroblast growth factor receptor 2 mutations in dural cells promote osteogenic proliferation and differentiation of osteoblasts.
J Craniofac Surg
PUBLISHED: 05-22-2010
Show Abstract
Hide Abstract
Mutations in fibroblast growth factor receptor 2 (FGFR2), a transmembrane receptor expressed in suture mesenchyme, osteogenic fronts, and dura, have been implicated in the etiopathogenesis of craniosynostosis syndromes. The C278F- and P253R-FGFR2 mutations result in Crouzon and Apert syndromes, respectively. The dura mater plays a critical role in the formation and maintenance of cranial sutures. However, its role in syndromic craniosynostosis remains unclear. This study examines the influence of FGFR2 mutations in dural cells on osteoblast proliferation and differentiation. Primary cultures of dural cells and osteoblasts were established, and adenoviral-FGFR2 constructs were prepared by subcloning mutant (C278F and P253R) FGFR2 constructs into adenovirus. Dural cells were infected with adenovirus, and dural protein expression was confirmed by immunostaining. Infected dural cells were cocultured with osteoblasts using a transwell system for 7 days. Dural cells infected with null adenovirus served as the negative control. In separate cultures, osteoblasts were directly infected with the adenoviral-FGFR2 constructs. Osteoblast proliferation was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and differentiation was analyzed by alkaline phosphatase assay, histochemical staining, and gene expression studies. Osteoblasts directly infected with the Crouzon (C278F-FGFR2) mutation demonstrated an increase in cell proliferation (P < 0.05). Osteoblasts directly infected with the Apert (P253R-FGFR2) mutation demonstrated an increase in alkaline phosphatase activity. In coculture experiments, osteoblasts cocultured with Crouzon-transformed dural cells demonstrated increased cell proliferation (P < 0.05), whereas osteoblasts cocultured with Apert-transformed dural cells showed an increase in alkaline phosphatase activity (P < 0.05). In addition, osteogenic gene expression (alkaline phosphatase, osteopontin, and runx2) were up-regulated in osteoblasts cocultured with Apert-expressing dural cells. These experiments suggest that FGFR2 mutations in dural cells alter normal dural signaling. Apert mutations promote osteodifferentiation, whereas Crouzon mutations result in enhanced cell proliferation. These mutations may induce craniosynostosis in part through the influence of mutation-induced constitutive signaling in the dura, with subsequent enhancement of dural-mediated osteogenesis.
Related JoVE Video
New cerebral lesions on T2*-weighted gradient-echo imaging after cardiac valve surgery.
Cerebrovasc. Dis.
PUBLISHED: 04-16-2010
Show Abstract
Hide Abstract
It is well known that silent ischemic brain lesions on diffusion-weighted imaging (DWI) commonly occur after various interventional procedures or surgeries. However, to our knowledge, postoperative new lesions on T2*-weighted gradient-echo imaging (GRE) have never been explored.
Related JoVE Video
Novel ANKH mutation in a patient with sporadic craniometaphyseal dysplasia.
Am. J. Med. Genet. A
PUBLISHED: 02-27-2010
Show Abstract
Hide Abstract
Craniometaphyseal dysplasia is caused by mutations in ANKH (ankylosis, progressive homolog [mouse]) in the majority of cases, and all of the reported mutations are single amino acid changes. Genomic DNA from an affected patient, his biological parents, and a sibling was amplified and ANKH was sequenced. The affected patient had a complex heterozygous mutation in exon 7 (c.936T > C, c.938C > G, c.942_953delTGGTTGACGGAA), predicting p.Try290Gln and p.Trp292_Glu295del. We studied the effect of the predicted mutation on the subcellular distribution of ANKH protein. Immunofluorescent labeling of COS-7 cells transduced with normal or mutant Ank (murine progressive ankylosis), showed that normal Ank localized to both the plasma membrane and cytoplasm, whereas mutant Ank was detected only in the cytoplasmic compartment. We propose that this craniometaphyseal dysplasia mutation causes a loss of ANKH protein expression and activity in the plasma membrane as a result of aberrant intracellular protein trafficking.
Related JoVE Video
Related JoVE Video
Mesenchymal progenitors residing close to the bone surface are functionally distinct from those in the central bone marrow.
Bone
Show Abstract
Hide Abstract
Long bone is an anatomically complicated tissue with trabecular-rich metaphyses at two ends and cortical-rich diaphysis at the center. The traditional flushing method isolates only mesenchymal progenitor cells from the central region of long bones and these cells are distant from the bone surface. We propose that mesenchymal progenitors residing in endosteal bone marrow that is close to the sites of bone formation, such as trabecular bone and endosteum, behave differently from those in the central bone marrow. In this report, we separately isolated endosteal bone marrow using a unique enzymatic digestion approach and demonstrated that it contained a much higher frequency of mesenchymal progenitors than the central bone marrow. Endosteal mesenchymal progenitors express common mesenchymal stem cell markers and are capable of multi-lineage differentiation. However, we found that mesenchymal progenitors isolated from different anatomical regions of the marrow did exhibit important functional differences. Compared with their central marrow counterparts, endosteal mesenchymal progenitors have superior proliferative ability with reduced expression of cell cycle inhibitors. They showed greater immunosuppressive activity in culture and in a mouse model of inflammatory bowel disease. Aging is a major contributing factor for trabecular bone loss. We found that old mice have a dramatically decreased number of endosteal mesenchymal progenitors compared with young mice. Parathyroid hormone (PTH) treatment potently stimulates bone formation. A single PTH injection greatly increased the number of endosteal mesenchymal progenitors, particularly those located at the metaphyseal bone, but had no effect on their central counterparts. In summary, endosteal mesenchymal progenitors are more metabolically active and relevant to physiological bone formation than central mesenchymal progenitors. Hence, they represent a biologically important target for future mesenchymal stem cell studies.
Related JoVE Video
Risk factors and stroke mechanisms in atherosclerotic stroke: intracranial compared with extracranial and anterior compared with posterior circulation disease.
Stroke
Show Abstract
Hide Abstract
The aim of this study was to investigate differences in risk factors and stroke mechanisms between intracranial atherosclerosis (ICAS) and extracranial atherosclerosis (ECAS) and between anterior and posterior circulation atherosclerosis.
Related JoVE Video
Intra-amniotic transient transduction of the periderm with a viral vector encoding TGF?3 prevents cleft palate in Tgf?3(-/-) mouse embryos.
Mol. Ther.
Show Abstract
Hide Abstract
Cleft palate is a developmental defect resulting from the failure of embryonic palatal shelves to fuse with each other at a critical time. Immediately before and during palatal fusion (E13-E15 in mice), transforming growth factor ?3 (TGF?3) is expressed in the palatal shelf medial edge epithelium (MEE) and plays a pivotal role in palatal fusion. Using Tgf?3(-/-) mice, which display complete penetrance of the cleft palate phenotype, we tested the hypothesis that intra-amniotic gene transfer could be used to prevent cleft palate formation by restoring palatal midline epithelial function. An adenoviral vector encoding Tgf?3 was microinjected into the amniotic sacs of mouse embryos at successive developmental stages. Transduced Tgf?3(-/-) fetuses showed efficient recovery of palatal fusion with mesenchymal confluence following injection at E12.5 (100%), E13.5 (100%), E14.5 (82%), and E15.5 (75%). Viral vectors injected into the amniotic sac transduced the most superficial and transient peridermal cell layer but not underlying basal epithelial cells. TGF?3 transduction of the peridermdal cell layer was sufficient to induce adhesion, fusion, and disappearance of the palatal shelf MEE in a cell nonautonomous manner. We propose that intra-amniotic gene transfer approaches have therapeutic potential to prevent cleft palate in utero, especially those resulting from palatal midline epithelial dysfunction.
Related JoVE Video
Differential closure of the spheno-occipital synchondrosis in syndromic craniosynostosis.
Plast. Reconstr. Surg.
Show Abstract
Hide Abstract
The spheno-occipital synchondrosis is a driver of cranial base and facial growth. Its premature fusion has been associated with midface hypoplasia in animal models. The authors reviewed computed tomographic scans of patients with Apert and Muenke syndrome, craniosynostosis syndromes with midface hypoplasia, to assess premature fusion of the spheno-occipital synchondrosis when compared with normal controls.
Related JoVE Video
Biomarkers and location of atherosclerosis: matrix metalloproteinase-2 may be related to intracranial atherosclerosis.
Atherosclerosis
Show Abstract
Hide Abstract
Various biomarkers are linked with the pathophysiology of atherosclerosis. We hypothesized that these factors may be associated with the location and burden of cerebral atherosclerosis.
Related JoVE Video
Moyamoya disease-related versus primary intracerebral hemorrhage: [corrected] location and outcomes are different.
Stroke
Show Abstract
Hide Abstract
The purpose of our study was to compare lesion location between moyamoya disease-related intracerebral hemorrhage (MMD-ICH) and primary intracerebral hemorrhage (P-ICH).
Related JoVE Video

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.