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Find video protocols related to scientific articles indexed in Pubmed.
Shock absorbing function study on denucleated intervertebral disc with or without hydrogel injection through static and dynamic biomechanical tests in vitro.
Biomed Res Int
PUBLISHED: 04-13-2014
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Hydrogel injection has been recently proposed as a novel therapy for disc degenerative diseases, with the potential to restore the spine motion and the intervertebral disc height. However, it remains unknown whether the new technique could also maintain the shock absorbing property of the treated intervertebral disc. In this study, 18 porcine lumbar bone-disc-bone specimens were collected and randomly divided into three groups: the normal with intact intervertebral discs, the mimic for the injection of disulfide cross-linked hyaluronan hydrogels following discectomy, and the control disc with discectomy only. In the static compression test, specimens in the mimic group exhibited displacements similar to those in the normal discs, whereas the control group showed a significantly larger displacement range in the first two steps (P < 0.05). With the frequency increasing, all specimens generally displayed an increasing storage modulus, decreasing loss modulus, and tan?. At any frequency point, the control group exhibited the largest value in all the three parameters among three groups while the normal group was the lowest, with the mimic group being mostly close to the normal group. Therefore, the hydrogel injection into the intervertebral discs greatly restored their shock absorbing function, suggesting that the technique could serve as an effective approach to maintaining biomechanical properties of the degenerative intervertebral disc.
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CD146 as a new marker for an increased chondroprogenitor cell sub-population in the later stages of osteoarthritis.
J. Orthop. Res.
PUBLISHED: 02-17-2014
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Cartilage-derived mesenchymal stem cells (MSCs) have been isolated with different methods. In this study lateral and medial femoral condyles were respectively collected from patients with late-stage osteoarthritis during the total knee arthroplasty. After digestion of the cartilage tissues with type II collagenase and analysis by fluorescence-activated cell sorting (FACS) with CD146, a chondroprogenitor cell sub-population were isolated and purified. The expression of other MSC-associated markers in the CD146(+) chondroprogenitors was analyzed by flow cytometry. Multi-lineage differentiation capacity of CD146(+) chondroprogenitors was compared with that of unsorted chondrocytes and adipose-derived MSCs (ADMSCs). Higher percentage of CD146(+) chondroprogenitors isolated from the medial femoral condyles was observed than that from the lateral. CD146(+) chondroprogenitors expressed high levels of MSC-specific surface antigens, and showed higher chondrogenesis capacity than ADMSCs and unsorted chondrocytes in a 3D cell pellet culture model. Thus CD146 might be a new cell surface marker for cartilage progenitor cell population in the late-stage osteoarthritis. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.
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HP1? mediates defective heterochromatin repair and accelerates senescence in Zmpste24-deficient cells.
Cell Cycle
PUBLISHED: 02-14-2014
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Heterochromatin protein 1 (HP1) interacts with various proteins, including lamins, to play versatile functions within nuclei, such as chromatin remodeling and DNA repair. Accumulation of prelamin A leads to misshapen nuclei, heterochromatin disorganization, genomic instability, and premature aging in Zmpste24-null mice. Here, we investigated the effects of prelamin A on HP1? homeostasis, subcellular distribution, phosphorylation, and their contribution to accelerated senescence in mouse embryonic fibroblasts (MEFs) derived from Zmpste24(-/-) mice. The results showed that the level of HP1? was significantly increased in Zmpste24(-/-) cells. Although prelamin A interacted with HP1? in a manner similar to lamin A, HP1? associated with the nuclease-resistant nuclear matrix fraction was remarkably increased in Zmpste24(-/-) MEFs compared with that in wild-type littermate controls. In wild-type cells, HP1? was phosphorylated at Thr50, and the phosphorylation was maximized around 30 min, gradually dispersed 2 h after DNA damage induced by camptothecin. However, the peak of HP1? phosphorylation was significantly compromised and appeared until 2 h, which is correlated with the delayed maximal formation of ?-H2AX foci in Zmpste24(-/-) MEFs. Furthermore, knocking down HP1? by siRNA alleviated the delayed DNA damage response and accelerated senescence in Zmpste24(-/-) MEFs, evidenced by the rescue of the delayed ?-H2AX foci formation, downregulation of p16, and reduction of senescence-associated ?-galactosidase activity. Taken together, these findings establish a functional link between prelamin A, HP1?, chromatin remodeling, DNA repair, and early senescence in Zmpste24-deficient mice, suggesting a potential therapeutic strategy for laminopathy-based premature aging via the intervention of HP1?.
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Transplantation of induced pluripotent stem cells improves functional recovery in Huntington's disease rat model.
PLoS ONE
PUBLISHED: 01-01-2014
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The purpose of this study was to determine the functional recovery of the transplanted induced pluripotent stem cells in a rat model of Huntington's disease with use of 18F-FDG microPET/CT imaging.
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Development of a lentivirus vector-based assay for non-destructive monitoring of cell fusion activity.
PLoS ONE
PUBLISHED: 01-01-2014
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Cell-to-cell fusion can be quantified by endowing acceptor and donor cells with latent reporter genes/proteins and activators of these genes/proteins, respectively. One way to accomplish this goal is by using a bipartite lentivirus vector (LV)-based cell fusion assay system in which the cellular fusion partners are transduced with a flippase-activatable Photinus pyralis luciferase (PpLuc) expression unit (acceptor cells) or with a recombinant gene encoding FLPeNLS+, a nuclear-targeted and molecularly evolved version of flippase (donor cells). Fusion of both cell populations will lead to the FLPe-dependent generation of a functional PpLuc gene. PpLuc activity is typically measured in cell lysates, precluding consecutive analysis of one cell culture. Therefore, in this study the PpLuc-coding sequence was replaced by that of Gaussia princeps luciferase (GpLuc), a secretory protein allowing repeated analysis of the same cell culture. In myotubes the spread of FLPeNLS+ may be limited due to its nuclear localization signal (NLS) causing low signal outputs. To test this hypothesis, myoblasts were transduced with LVs encoding either FLPeNLS+ or an NLS-less version of FLPe (FLPeNLS-) and subsequently co-cultured in different ratios with myoblasts containing the FLPe-activatable GpLuc expression cassette. At different times after induction of cell-to-cell fusion the GpLuc activity in the culture medium was determined. FLPeNLS+ and FLPeNLS- both activated the latent GpLuc gene but when the percentage of FLPe-expressing myoblasts was limiting, FLPeNLS+ generally yielded slightly higher signals than FLPeNLS- while at low acceptor-to-donor cell ratios FLPeNLS- was usually superior. The ability of FLPeNLS+ to spread through myofibers and to induce reporter gene expression is thus not limited by its NLS. However, at high FLPe concentrations the presence of the NLS negatively affected reporter gene expression. In summary, a rapid and simple chemiluminescence assay for quantifying cell-to-cell fusion progression based on GpLuc has been developed.
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EPO promotes bone repair through enhanced cartilaginous callus formation and angiogenesis.
PLoS ONE
PUBLISHED: 01-01-2014
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Erythropoietin (EPO)/erythropoietin receptor (EPOR) signaling is involved in the development and regeneration of several non-hematopoietic tissues including the skeleton. EPO is identified as a downstream target of the hypoxia inducible factor-? (HIF-?) pathway. It is shown that EPO exerts a positive role in bone repair, however, the underlying cellular and molecular mechanisms remain unclear. In the present study we show that EPO and EPOR are expressed in the proliferating, pre-hypertrophic and hypertrophic zone of the developing mouse growth plates as well as in the cartilaginous callus of the healing bone. The proliferation rate of chondrocytes is increased under EPO treatment, while this effect is decreased following siRNA mediated knockdown of EPOR in chondrocytes. EPO treatment increases biosynthesis of proteoglycan, accompanied by up-regulation of chondrogenic marker genes including SOX9, SOX5, SOX6, collagen type 2, and aggrecan. The effects are inhibited by knockdown of EPOR. Blockage of the endogenous EPO in chondrocytes also impaired the chondrogenic differentiation. In addition, EPO promotes metatarsal endothelial sprouting in vitro. This coincides with the in vivo data that local delivery of EPO increases vascularity at the mid-stage of bone healing (day 14). In a mouse femoral fracture model, EPO promotes cartilaginous callus formation at days 7 and 14, and enhances bone healing at day 28 indexed by improved X-ray score and micro-CT analysis of microstructure of new bone regenerates, which results in improved biomechanical properties. Our results indicate that EPO enhances chondrogenic and angiogenic responses during bone repair. EPO's function on chondrocyte proliferation and differentiation is at least partially mediated by its receptor EPOR. EPO may serve as a therapeutic agent to facilitate skeletal regeneration.
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Intervention timing of strontium treatment on estrogen depletion-induced osteoporosis in rats: Bone microstructure and mechanics.
J. Orthop. Res.
PUBLISHED: 10-11-2013
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To evaluate the effect of intervention timing of Sr treatment on trabecular bone microstructure and mechanics.
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Coupling of small leucine-rich proteoglycans to hypoxic survival of a progenitor cell-like subpopulation in Rhesus Macaque intervertebral disc.
Biomaterials
PUBLISHED: 04-24-2013
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Degeneration of the intervertebral disc (IVD) is a major spinal disorder that associates with neck and back pain. Recent studies of clinical samples and animal models for IVD degeneration have identified cells with multi-potency in the IVD. However, IVD tissue-specific progenitor cells and their niche components are not clear, although degenerated IVD-derived cells possess in vitro characteristics of mesenchymal stromal cell (MSCs). Here, we firstly identified the tissue-specific intervertebral disc progenitor cells (DPCs) from healthy Rhesus monkey and report the niche components modulated the survival of DPCs under hypoxia. DPCs possess clonogenicity, multipotency and retain differentiation potential after extended expansion in vitro and in vivo. In particular, the nucleus pulposus-derived DPCs are sensitive to low oxygen tension and undergo apoptosis under hypoxic conditions due to their inability to induce/stabilize hypoxia-inducible factors (HIF). The presence of small leucine-rich proteoglycans (SLRP), biglycan or decorin, can reduce the susceptibility of DPCs to hypoxia-induced apoptosis via promoting the activation/stabilization of HIF-1? and HIF-2?. As IVD is avascular, we propose SLRPs are niche components of DPCs in IVD homeostasis, providing new insights in progenitor cell biology and niche factors under a hypoxic microenvironment.
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Developmental definition of MSCs: new insights into pending questions.
Cell Reprogram
PUBLISHED: 09-15-2011
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Mesenchymal stem cells (MSCs) are a rare heterogeneous population of multipotent cells that can be isolated from many different adult and fetal tissues. They exhibit the capacity to give rise to cells of multiple lineages and are defined by their phenotype and functional properties, such as spindle-shaped morphology, adherence to plastic, immune response modulation capacity, and multilineage differentiation potential. Accordingly, MSCs have a wide range of promising applications in the treatment of autoimmune diseases, tissue repair, and regeneration. Recent studies have shed some light on the exact identity and native distribution of MSCs, whereas controversial results are still being reported, indicating the need for further review on their definition and origin. In this article, we summarize the important progress and describe some of our own relevant work on the developmental definition of MSCs.
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Cis-regulatory functions of overlapping HIF-1alpha/E-box/AP-1-like sequences of CD164.
BMC Mol. Biol.
PUBLISHED: 08-09-2011
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CD164 (also known as MGC-24v or endolyn) is a sialomucin which has been suggested to participate in regulating the proliferation, cell adhesion and differentiation of hematopoietic stem and progenitor cells. CD164 is also involved in the development of cancer. The functions of cis-regulatory elements of CD164 remain relatively unknown.
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Osteoprotegerin deficiency attenuates strontium-mediated inhibition of osteoclastogenesis and bone resorption.
J. Bone Miner. Res.
PUBLISHED: 05-26-2011
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Strontium (Sr) exerts an anabolic and antiresorptive effect on bone, but the mechanism remains unknown. Osteoprotegerin (OPG) expressed by osteoblasts plays an important role in regulating bone homeostasis by inhibiting osteoclastogenesis and bone resorption. This study aims at evaluating the role of OPG in Sr-mediated inhibition of osteoclastogenesis and bone resorption. Six-week-old Opg knockout (KO) male mice and their wild-type (WT) littermates were treated orally with vehicle (Veh) or Sr compound (4 mmol/kg) daily for 8 weeks. Bone mass and microstructure in the lumbar spine (L(4)) and proximal tibia were analyzed with micro-computed tomography (µCT). Bone remodeling was evaluated with serum biochemical analysis and static and dynamic bone histomorphometry. Osteoclast differentiation potential and gene expression were analyzed in bone marrow cells. The findings demonstrate that Sr compound treatment results in greater bone volume and trabecular number than Veh treatment in WT mice. The anabolic response of trabecular bone to Sr treatment is attenuated in KO mice. Although Sr treatment significantly decreases in vitro osteoclastogenesis and bone resorption in WT mice, these effects are attenuated in KO mice. Furthermore, Sr treatment profoundly increases Opg gene expression in the tibias and OPG protein levels in the sera of WT mice. This study concludes that the inhibition of osteoclastogenesis and bone resorption is possibly associated with OPG upregulation by Sr treatment.
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Stem cell-based approaches for intervertebral disc regeneration.
Curr Stem Cell Res Ther
PUBLISHED: 05-21-2011
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Degeneration of the intervertebral disc is an age-related progressive process considered to be the major cause of a series of spine disorders, such as low-back pain that affects the majority of adult population and causes a huge loss of time from work and medical expenses. Numerous regenerative approaches are being developed with the aim to halt or reverse degeneration, including intradiscal administration of nucleus pulposus cells and mesenchymal stem cells and anabolic growth factors. Each of the currently proposed approaches, however, has exhibited certain limitations or shortcomings, largely due to our limited understanding on the cell biology, turnover mechanisms of the intervertebral disc as well as the etiology of disc degeneration. Intervertebral disc, particularly the central nucleus pulposus, is the largest enclosed and avascular tissue in the body and owes a microenvironment under high mechanical and osmotic pressures, at severely hypoxia, and with very limited nutrient supply. In order to achieve an optimal outcome of new regenerative therapies in such a harsh circumstance, identifying and characterizing endogenous regenerative properties of normal and degenerate intervertebral disc, including stem/progenitor cells themselves and extracellular factors located within the stem cell niche, may provide effective insights into selecting the most suitable cell sources and improving or rebuilding the microenvironment favorable for endogenous or transplanted stem cells.
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Evaluation of cell tracking effects for transplanted mesenchymal stem cells with jetPEI/Gd-DTPA complexes in animal models of hemorrhagic spinal cord injury.
Brain Res.
PUBLISHED: 02-20-2011
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Cell tracking using iron oxide nanoparticles has been well established in MRI. However, in experimental rat models, the intrinsic iron signal derived from erythrocytes masks the labeled cells. The research evaluated a clinically applied Gd-DTPA for T1-weighted positive enhancement for cell tracking in spinal cord injury (SCI) rat models. MSCs were labeled with jetPEI/Gd-DTPA particles to evaluate the transfection efficiency by MRI in vitro. Differentiation assays were carried out to evaluate the differentiation ability of Gd-DTPA-labeled MSCs. The Gd-DTPA-labeled MSCs were transplanted to rat SCI model and monitored by MRI in vivo. Fluorescence images were taken to confirm the MRI results. Behavior test was assessed with Basso, Beattie, and Bresnahan (BBB) scoring in 6weeks after cell transplantation. The Gd-labeled MSCs showed a significant increase in signal intensity in T1-weighted images. After local transplantation, Gd-DTPA-labeled MSCs could be detected in SCI rat models by the persistent T1-weighted positive enhancement from 3 to 14days. Under electronic microscope, Gd-DTPA/jetPEI complexes were mostly observed in cytoplasm. Fluorescence microscopy examination showed that the Gd-labeled MSCs survived and distributed within the injured spinal cord until 2weeks. The Gd-labeled MSCs were identified and tracked with MRI by cross and sagittal sections. The BBB scores of the rats with labeled MSCs transplantation were significantly higher than those of control rats. Our results demonstrated that Gd-DTPA is appropriate for cell tracking in rat model of SCI, indicating that an efficient and nontoxic label method with Gd-DTPA could properly track MSCs in hemorrhage animal models.
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In vivo anabolic effect of strontium on trabecular bone was associated with increased osteoblastogenesis of bone marrow stromal cells.
J. Orthop. Res.
PUBLISHED: 03-03-2010
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In vitro studies have demonstrated that strontium (Sr) could increase osteogenic differentiation of bone marrow stromal cells (BMSCs). We investigated the in vivo effect of Sr on BMSCs. Thirty-six female rats were randomly divided into the following groups: sham operated and treated with either vehicle (Sham + Veh) or Sr compound (Sham + Sr) and ovariectomized and treated with either vehicle (OVX + Veh) or Sr compound (OVX + Sr). Vehicle and Sr were orally administrated daily starting immediately after the surgery and continuing for 12 weeks. The anabolic effect of Sr on trabecular bone was determined at the structural and tissue level by microCT and histomorphometry, respectively. Colony formation assays demonstrated that BMSCs exhibited higher osteogenic colony but lower adipogenic colony in Sr-treated versus Veh-treated OVX rats. The mRNA level of osteogenic genes was higher, while the mRNA level of adipogenic genes was lower in BMSCs from Sr-treated versus Veh-treated Sham and OVX rats. The effect of Sr on rat BMSCs was reproducible in human BMSCs. Taken together, this study suggests that the anabolic effect of Sr on normal or osteoporotic bones is associated with increased osteoblastic differentiation of BMSCs.
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Strontium promotes osteogenic differentiation of mesenchymal stem cells through the Ras/MAPK signaling pathway.
Cell. Physiol. Biochem.
PUBLISHED: 02-18-2009
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Strontium ralenate is a new anti-osteoporosis agent. The cellular and molecular mechanism underlying the anabolic effect of strontium on bone remains to be elucidated. Osteoblasts, the main bone forming cells are known to be derived from bone marrow mesenchymal stem cells (MSCs). The present study therefore aimed to investigate the possible effects of strontium on MSCs and signaling pathways possibly involved. It was firstly demonstrated that strontium treatment significantly increased osteoblast-related gene expression and alkaline phosphatase (ALP) of osteogenic-differentiating MSCs. Accompanying the enhanced osteogenic differentiation, the increased phosphorylation of mitogen-activated protein kinase (MAPK) ERK1/2 and p38 was detected in strontium-treated MSCs. PD98059 and SB203580, selective inhibitors of ERK1/2 kinase and p38, attenuated the effect of strontium on osteogenesis. Furthermore, it was demonstrated that Rat Sarcoma viral oncogene homolog (RAS), an upstream regulator of ERK1/2 and p38, was activated by strontium treatment and siRNA-mediated Ras knockdown inhibited strontium-stimulated expression of osteogenic markers. Finally, the transcriptional activity and phosphorylation level of Runx2 was significantly increased in response to strontium treatment in MSCs. PD98059 and Ras siRNA inhibited the effect of strontium on Runx2 activation. Taken together, these results indicated that strontium can promote osteogenic differentiation of MSCs through activating the Ras/MAPK signaling pathway and the downstream transcription factor Runx2.
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[Expression of CXC chemokine receptor 4 in muscle satellite cells of muscle injury tissues].
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi
PUBLISHED: 02-06-2009
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To observe the expressions of CXC chemokine receptor 4 (CXCR4) in muscle satellite cells in situ of normal and cardiotoxin-intoxicated muscle tissues so as to further investigate the molecular mechanism involving in muscle regeneration such as progressing muscular dystrophy (PMD) for seeking the way to cure muscle retrogression.
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Intrinsic properties of mesemchymal stem cells from human bone marrow, umbilical cord and umbilical cord blood comparing the different sources of MSC.
Curr Stem Cell Res Ther
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The past decade has witnessed numerous publications on mesenchymal stem cells (MSC), which have great potential in regenerative medicine. MSC from various types of origins exhibit different characteristics, which may relate to the maintenance role of MSC in that specific source. Reports have emerged that among the most widely investigated sources, umbilical cord (UC) or umbilical cord blood (UCB) derived MSC throw advantages over bone marrow (BM) derived MSC due to their close to fetal origin. Here the methodologies used to separate MSC from UC or UCB, and the intrinsic properties, including proliferation capacity, multipotency, cytokine profile, cell surface protein expression and gene expression, between UC, UCB and BM derived MSC, are discussed in details, though may not in a full picture, for the first time.
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Inhibiting CD164 expression in colon cancer cell line HCT116 leads to reduced cancer cell proliferation, mobility, and metastasis in vitro and in vivo.
Cancer Invest.
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CD164 (Endolyn) is a sialomucin, which has been found to play roles in regulating proliferation, adhesion, and differentiation of hematopoietic stem cells. Possible association of CD164 with solid cancer development remains unknown.
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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.

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

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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.