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Find video protocols related to scientific articles indexed in Pubmed.
[Pro731Ser mutation in the ?-myosin heavy chain and hypertrophic cardiomyopathy in a Chinese pedigree].
Zhonghua Xin Xue Guan Bing Za Zhi
PUBLISHED: 10-21-2014
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To identify the casual mutation of a Chinese pedigree with hypertrophic cardiomyopathy (HCM), and to analyze the genotype-phenotype relationship.
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Malignant effects of multiple rare variants in sarcomere genes on the prognosis of patients with hypertrophic cardiomyopathy.
Eur. J. Heart Fail.
PUBLISHED: 07-31-2014
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Although genetic testing has been recommended in patients with hypertrophic cardiomyopathy (HCM) in current clinical practice, its utility in prognostic prediction remains to be ascertained. We assessed the dosage effect of rare variants in sarcomere genes on the long-term outcomes of HCM.
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MiR-451 is decreased in hypertrophic cardiomyopathy and regulates autophagy by targeting TSC1.
J. Cell. Mol. Med.
PUBLISHED: 04-09-2014
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The molecular mechanisms that drive the development of cardiac hypertrophy in hypertrophic cardiomyopathy (HCM) remain elusive. Accumulated evidence suggests that microRNAs are essential regulators of cardiac remodelling. We have been suggested that microRNAs could play a role in the process of HCM. To uncover which microRNAs were changed in their expression, microRNA microarrays were performed on heart tissue from HCM patients (n = 7) and from healthy donors (n = 5). Among the 13 microRNAs that were differentially expressed in HCM, miR-451 was the most down-regulated. Ectopic overexpression of miR-451 in neonatal rat cardiomyocytes (NRCM) decreased the cell size, whereas knockdown of endogenous miR-451 increased the cell surface area. Luciferase reporter assay analyses demonstrated that tuberous sclerosis complex 1 (TSC1) was a direct target of miR-451. Overexpression of miR-451 in both HeLa cells and NRCM suppressed the expression of TSC1. Furthermore, TSC1 was significantly up-regulated in HCM myocardia, which correlated with the decreased levels of miR-451. As TSC1 is a known positive regulator of autophagy, we examined the role of miR-451 in the regulation of autophagy. Overexpression of miR-451 in vitro inhibited the formation of the autophagosome. Conversely, miR-451 knockdown accelerated autophagosome formation. Consistently, an increased number of autophagosomes was observed in HCM myocardia, accompanied by up-regulated autophagy markers, and the lipidated form of LC3 and Beclin-1. Taken together, our findings indicate that miR-451 regulates cardiac hypertrophy and cardiac autophagy by targeting TSC1. The down-regulation of miR-451 may contribute to the development of HCM and may be a potential therapeutic target for this disease.
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Rare variants in genes encoding MuRF1 and MuRF2 are modifiers of hypertrophic cardiomyopathy.
Int J Mol Sci
PUBLISHED: 03-07-2014
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Modifier genes contribute to the diverse clinical manifestations of hypertrophic cardiomyopathy (HCM), but are still largely unknown. Muscle ring finger (MuRF) proteins are a class of muscle-specific ubiquitin E3-ligases that appear to modulate cardiac mass and function by regulating the ubiquitin-proteasome system. In this study we screened all the three members of the MuRF family, MuRF1, MuRF2 and MuRF3, in 594 unrelated HCM patients and 307 healthy controls by targeted resequencing. Identified rare variants were confirmed by capillary Sanger sequencing. The prevalence of rare variants in both MuRF1 and MuRF2 in HCM patients was higher than that in control subjects (MuRF1 13/594 (2.2%) vs. 1/307 (0.3%), p = 0.04; MuRF2 22/594 (3.7%) vs. 2/307 (0.7%); p = 0.007). Patients with rare variants in MuRF1 or MuRF2 were younger (p = 0.04) and had greater maximum left ventricular wall thickness (p = 0.006) than those without such variants. Mutations in genes encoding sarcomere proteins were present in 19 (55.9%) of the 34 HCM patients with rare variants in MuRF1 and MuRF2. These data strongly supported that rare variants in MuRF1 and MuRF2 are associated with higher penetrance and more severe clinical manifestations of HCM. The findings suggest that dysregulation of the ubiquitin-proteasome system contributes to the pathogenesis of HCM.
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PIN architecture for ultrasensitive organic thin film photoconductors.
Sci Rep
PUBLISHED: 02-18-2014
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Organic thin film photoconductors (OTFPs) are expected to have wide applications in the field of optical communications, artificial vision and biomedical sensing due to their great advantages of high flexibility and low-cost large-area fabrication. However, their performances are not satisfactory at present: the value of responsivity (R), the parameter that measures the sensitivity of a photoconductor to light, is below 1 AW(-1). We believe such poor performance is resulted from an intrinsic self-limited effect of present bare blend based device structure. Here we designed a PIN architecture for OTFPs, the PIN device exhibits a significantly improved high R value of 96.5 AW(-1). The PIN architecture and the performance the PIN device shows here should represent an important step in the development of OTFPs.
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High-performance flexible ultraviolet photoconductors based on solution-processed ultrathin ZnO/Au nanoparticle composite films.
Sci Rep
PUBLISHED: 02-07-2014
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Transparent ultraviolet (UV) ZnO thin film photoconductors are expected to have great applications in environmental monitoring, large-area displays, and optical communications, and they have drawn enormous interests in recent years. However, at present their performances are not satisfactory: the responsivity R (a parameter characterizing the sensitivity of the device to light) is not high (<1.0 × 10(3)?AW(-1)), and the transparency T is not high either (<80%). Realizing high R and high T remains a big challenge today. In this paper, by employing solution-processed ultrathin ZnO/Au nanoparticle composite films, R as high as 1.51 × 10(5)?AW(-1) and T of over 90% are achieved. High values for detectivity D* and linear dynamic range LDR are also obtained, which are 2.05 × 10(15) Jones and 60?dB, respectively. Moreover, such high-performance devices can be fabricated on flexible PET (polyethylene terephthalate) substrates.
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A low prevalence of sarcomeric gene variants in a Chinese cohort with left ventricular non-compaction.
Heart Vessels
PUBLISHED: 01-04-2014
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Left ventricular non-compaction (LVNC) is genetically heterogeneous. It has been previously shown that LVNC is associated with defects in TAZ, DNTA, LDB3, YWHAE, MIB1, PRDM16, and sarcomeric genes. This study was aimed to investigate sarcomeric gene mutations in a Chinese population with LVNC. From 2004 to 2010, 57 unrelated Chinese patients with LVNC were recruited at Fuwai Hospital, Beijing, China. Detailed clinical evaluation was performed on the probands and available family members. DNA samples isolated from the peripheral blood of the index cases were screened for 10 sarcomeric genes, including MYH7, MYBPC3, MYL2, MYL3, MYH6, TNNC1, TNNT2, TNNI3, TPM1, and ACTC1. Seven heterozygous mutations (6 missense and 1 deletion) were identified in 7 (12 %) of the patients. These mutations were distributed among 4 genes, 4 in MYH7, and 1 each in ACTC1, TNNT2, and TPM1. Six of the mutations were novel and another one was reported previously. All mutations affected conserved amino acid residues and were predicted to alter the structure of the proteins by in silico analysis. No significant difference was observed between mutation-positive and mutation-negative patients with respect to clinical characteristics at baseline and mortality during follow-up. In conclusion, our study indicates that sarcomeric gene mutations are uncommon causes of LVNC in Chinese patients and genetic background of the disease may be divergent among the different races.
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Female sex is associated with worse prognosis in patients with hypertrophic cardiomyopathy in China.
PLoS ONE
PUBLISHED: 01-01-2014
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Sex plays an important role in the clinical expression and prognosis of various cardiovascular diseases. This study was designed to observe the effects of sex on hypertrophic cardiomyopathy (HCM).
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Correlation of ventricular arrhythmias with genotype in arrhythmogenic right ventricular cardiomyopathy.
Circ Cardiovasc Genet
PUBLISHED: 10-14-2013
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Background- Although mutations of several genes are associated with arrhythmogenic right ventricular cardiomyopathy (ARVC), the exact correlation between genotype and ventricular arrhythmia features remains unclear. This study was aimed to examine the possible association of the 9 known genes of ARVC with clinical and electrophysiological characteristics. Methods and Results- Ninety subjects diagnosed with ARVC who underwent electrophysiological study were recruited for screening the 9 known ARVC-causing genes. A total of 53 mutations were identified in 57 (63%) subjects. Mutation carriers had more frequent clinical ventricular tachycardia (VT; 89% versus 55%; P<0.001) and negative T waves in V1 to V3 (61% versus 33%; P=0.016). Subjects with plakophilin-2 (PKP2) mutations also had more frequent VT than those without mutations in PKP2. Comparison between subjects with multiple and single mutations showed that syncope occurred more often in the former group (58% versus 24%; P=0.018). VT was significantly more often induced in mutation carriers compared with noncarriers (75% versus 39%; P=0.001), as well as in PKP2 mutation carriers compared with subjects without PKP2 mutations (80% versus 48%; P=0.002). Induced VT with a rate ?200 bpm was more often documented in mutation carriers (88% versus 54%; P=0.013), as well as in PKP2 mutation carriers (91% versus 67%; P=0.041). Conclusions- Pathogenic gene mutations were found in nearly two thirds of subjects diagnosed with ARVC. Mutation carriers, especially PKP2, had a higher proportion of a history of VT and more inducible fast VT.
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Optoelectronic properties of a fullerene derivative containing adamantane group.
ACS Appl Mater Interfaces
PUBLISHED: 09-27-2013
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A fullerene derivative linked with an adamantane cage, [6,6]-phenyl-C61-butyric acid 1-adamantane methyl ester (PC61BAd), has been designed and synthesized. Systematic investigations on its organic field effect performance, photovoltaic properties, and corresponding thermal stability have been made. In OFET device, the electron mobility (?e) of PC61BAd was found to reach a value as high as 0.01 cm(2)/V·s with a high on-off (Ion/Ioff) ratio of 4.9 × 10(6) that is useful for logic device applications. In the organic photovoltaic devices of P3HT:PC61BAd, the power conversion efficiency (PCE) was found to reach 3.31 % in the optimized device. More importantly, the active layer of P3HT:PC61BAd was found to exhibit superior thermal stability over that of P3HT:PC61BM. After heating at 150 °C for 20 h, the P3HT:PC61BAd device still showed a PCE of 2.44 %, demonstrating the applicability of PC61BAd as an acceptor material for the preparation of thermally stable organic solar cells. X-ray diffraction and atomic force microscopy were employed to probe the structure and morphology of PC61BAd and to rationalize its performance as an organic electronic material.
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Indan-C60: from a crystalline molecule to photovoltaic application.
Chem. Commun. (Camb.)
PUBLISHED: 09-16-2013
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Crystalline Indan-C60 and its photovoltaic application were studied. Microsheets and aloe-like micro-nano superstructures can be assembled from Indan-C60. Indan-PC61BM derived from Indan-C60 was further investigated as an acceptor for OPV devices, which shows a higher Voc, FF, and PCE than those obtained using PC61BM.
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Association between the cytotoxic T-lymphocyte antigen 4 +49A/G polymorphism and bladder cancer risk.
Tumour Biol.
PUBLISHED: 08-13-2013
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Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a potent immunoregulatory molecule that suppresses antitumor response by downregulating T cell activation. The most studied CTLA-4 +49A/G polymorphism has been associated with various cancers risks. However, little is known about the association between CTLA-4 +49A/G polymorphism and bladder cancer risk. A hospital-based case-control study was conducted in 300 patients with bladder cancer and 300 healthy controls matched with age and sex. The CTLA-4 +49A/G polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism. Patients with bladder cancer had a significantly lower frequency of CTLA-4 +49GG genotype [odds ratio (OR)?=?0.44, 95 % confidence interval (CI)?=?0.23, 0.85; P?=?0.01] and G allele (OR?=?0.73, 95 % CI?=?0.56, 0.96; P?=?0.02) than healthy controls. When stratifying by the stage, grade, and histological type of bladder cancer, we found no statistical association. This is the first study to highlight the significant association between CTLA-4 +49A/G polymorphism and bladder cancer risk. Additional studies are needed to confirm this finding.
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Isolated left ventricular noncompaction: clinical profile and prognosis in 106 adult patients.
Heart Vessels
PUBLISHED: 06-09-2013
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This study was undertaken to evaluate the clinical course of isolated left ventricular noncompaction (ILVNC) and to identify the predictors for adverse outcomes in an adult cohort with ILVNC. Between March 2003 and April 2012, 106 adult patients diagnosed with ILVNC at Fuwai Hospital were included in this study. The medical history, electrocardiograms, and echocardiograms of these patients were retrospectively analyzed by chart review. Of these patients, 64 (60 %) were in New York Heart Association (NYHA) functional class III/IV and 84 (79 %) had systolic dysfunction (left ventricular ejection fraction (LVEF) <50 %). During a follow-up of 2.9 ± 2.1 years, 28 (26 %) patients died or underwent heart transplantation. The annual incidence of death or transplantation was 9.1 %. The determinants of death or heart transplantation included NYHA functional class III/IV (hazard ratio (HR) 4.52; 95 % confidence interval (CI) 1.57-13.04; P = 0.005), decreased left ventricular ejection fraction (HR 0.94; 95 % CI 0.90-0.97; P = 0.001), dilated left ventricular end-diastolic diameter (HR, 1.06; 95 % CI, 1.02-1.09; P = 0.001), increased left atrial diameter (HR 1.08; 95 % CI 1.03-1.14; P = 0.001), reduced systolic blood pressure (HR 0.96; 95 % CI 0.94-0.99; P = 0.003), the presence of pulmonary hypertension (HR 3.50; 95 % CI 1.63-7.51; P = 0.001), and right bundle branch block (HR 7.79; 95 % CI 2.56-23.76; P < 0.001). In conclusion, this study demonstrates that ILVNC is related to a high incidence of death or heart transplantation. Advanced heart failure, a dilated left heart with systolic dysfunction, reduced systolic blood pressure, pulmonary hypertension, and right bundle branch block predict adverse outcomes of ILVNC.
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Fill factor in organic solar cells.
Phys Chem Chem Phys
PUBLISHED: 05-07-2013
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The fill factor (FF) is an important parameter that determines the power conversion efficiency of an organic solar cell. There are several factors that can significantly influence FF, and these factors interact with each other very intricately. Due to this reason, a deep understanding of FF is quite difficult. Based on the three fundamental elements in the solar cell equivalent circuit, namely series resistance, shunt resistance and diode, we reviews the research progress in understanding on FF in organic solar cells. Physics lying behind the often-observed undesirable S-shaped J-V curves is also summarized. This paper aims to give a brief and comprehensive summary on FF from a fundamental point of view.
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TNNI3K, a cardiac-specific kinase, promotes physiological cardiac hypertrophy in transgenic mice.
PLoS ONE
PUBLISHED: 02-06-2013
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Protein kinase plays an essential role in controlling cardiac growth and hypertrophic remodeling. The cardiac troponin I-interacting kinase (TNNI3K), a novel cardiac specific kinase, is associated with cardiomyocyte hypertrophy. However, the precise function of TNNI3K in regulating cardiac remodeling has remained controversial.
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Clinical profile and prognostic significance of atrial fibrillation in hypertrophic cardiomyopathy.
Cardiology
PUBLISHED: 01-29-2013
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The clinical outcomes of hypertrophic cardiomyopathy (HCM) are largely unpredictable. This study aimed to investigate the relationship between atrial fibrillation (AF) and its prognostic implications in Chinese patients with HCM.
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Synthesis of novel acceptor molecules of mono- and multiadduct fullerene derivatives for improving photovoltaic performance.
ACS Appl Mater Interfaces
PUBLISHED: 01-18-2013
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We have successfully synthesized and separated a series of tert-butyl 4-C(61)-benzoate (t-BCB) organofullerenes, including monoadduct, diadduct, and triadduct compounds, and investigated their photophysics, electrochemistry, thermal properties, and high-performance liquid chromatography analysis. The photovoltaic devices were fabricated based on monoadduct, diadduct, and triadduct products, and the devices based on them exhibited power conversion efficiencies of 2.43%, 0.48%, and 1.68%, respectively. This was the first time to study the dependent relationship on the device performance and the different isomer numbers.
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Multiple gene mutations, not the type of mutation, are the modifier of left ventricle hypertrophy in patients with hypertrophic cardiomyopathy.
Mol. Biol. Rep.
PUBLISHED: 01-03-2013
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Genotype-phenotype correlation of hypertrophic cardiomyopathy (HCM) has been challenging because of the genetic and clinical heterogeneity. To determine the mutation profile of Chinese patients with HCM and to correlate genotypes with phenotypes, we performed a systematic mutation screening of the eight most commonly mutated genes encoding sarcomere proteins in 200 unrelated Chinese adult patients using direct DNA sequencing. A total of 98 mutations were identified in 102 mutation carriers. The frequency of mutations in MYH7, MYBPC3, TNNT2 and TNNI3 was 26.0, 18.0, 4.0 and 3.5 % respectively. Among the 200 genotyped HCM patients, 83 harbored a single mutation, and 19 (9.5 %) harbored multiple mutations. The number of mutations was positively correlated with the maximum wall thickness. We found that neither particular gene nor specific mutation was correlated to clinical phenotype. In summary, the frequency of multiple mutations was greater in Chinese HCM patients than in the Caucasian population. Multiple mutations in sarcomere protein may be a risk factor for left ventricular wall thickness.
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Autosomal recessive transmission of MYBPC3 mutation results in malignant phenotype of hypertrophic cardiomyopathy.
PLoS ONE
PUBLISHED: 01-01-2013
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Hypertrophic cardiomyopathy (HCM) due to mutations in genes encoding sarcomere proteins is most commonly inherited as an autosomal dominant trait. Since nearly 50% of HCM cases occur in the absence of a family history, a recessive inheritance pattern may be involved.
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Inverse association of plasma level of high-density lipoprotein cholesterol with intracerebral hemorrhage.
J. Lipid Res.
PUBLISHED: 06-16-2011
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This study aimed to investigate whether plasma levels of HDL cholesterol (HDL-C) were associated with the risk of intracerebral hemorrhage (ICH). Plasma HDL-C was determined via enzymatic methods, and ICH was ascertained via medical history, physical examination, and brain imaging (computed tomography or magnetic resonance imaging). The multivariable logistic regression model was used to calculate the odds ratios (OR) and 95% confidence intervals (CI) of ICH according to levels of plasma cholesterol. A total of 170 patients with ICH were identified from 6,046 participants. After adjustment for conventional cardiovascular risk factors, the OR was 2.06 (95% CI, 1.25-3.12; P < 0.01) for participants in the first tertile of HDL-C levels (<1.38 mmol/l) and 1.13 (95% CI, 0.72-1.78; P = 0.59) for participants in the second tertile (1.38-1.64 mmol/l), compared with participants in the third tertile (??1.65 mmol/l). Subgroup analysis indicated that the detrimental effects of HDL-C were more significant in men and lean participants than in their corresponding controls, independent of hypertension. The results presented herein indicate that low plasma HDL-C (<1.38 mmol/l) may be associated with risk of ICH.
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Mutations in NEXN, a Z-disc gene, are associated with hypertrophic cardiomyopathy.
Am. J. Hum. Genet.
PUBLISHED: 06-05-2010
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Hypertrophic cardiomyopathy (HCM), the most common inherited cardiac disorder, is characterized by increased ventricular wall thickness that cannot be explained by underlying conditions, cadiomyocyte hypertrophy and disarray, and increased myocardial fibrosis. In as many as 50% of HCM cases, the genetic cause remains unknown, suggesting that more genes may be involved. Nexilin, encoded by NEXN, is a cardiac Z-disc protein recently identified as a crucial protein that functions to protect cardiac Z-discs from forces generated within the sarcomere. We screened NEXN in 121 unrelated HCM patients who did not carry any mutation in eight genes commonly mutated in myofilament disease. Two missense mutations, c.391C>G (p.Q131E) and c.835C>T (p.R279C), were identified in exons 5 and 8 of NEXN, respectively, in two probands. Each of the two mutations segregated with the HCM phenotype in the family and was absent in 384 control chromosomes. In silico analysis revealed that both of the mutations affect highly conserved amino acid residues, which are predicted to be functionally deleterious. Cellular transfection studies showed that the two mutations resulted in local accumulations of nexilin and that the expressed fragment of actin-binding domain containing p.Q131E completely lost the ability to bind F-actin in C2C12 cells. Coimmunoprecipitation assay indicated that the p.Q131E mutation decreased the binding of full-length NEXN to ?-actin and abolished the interaction between the fragment of actin-binding domain and ?-actin. Therefore, the mutations in NEXN that we describe here may further expand the knowledge of Z-disc genes in the pathogenesis of HCM.
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Association of putative functional variants in the PLAU gene and the PLAUR gene with myocardial infarction.
Clin. Sci.
PUBLISHED: 06-04-2010
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uPA (urokinase-plasminogen activator) and its receptor (uPAR) have been implicated in a broad spectrum of pathophysiological processes, including fibrinolysis, proteolysis, inflammation, atherogenesis and plaque destabilization, all of which are involved in the pathogenesis of MI (myocardial infarction). We hypothesized that putative functional genetic variation in the two genes encoding uPA and uPAR (PLAU and PLAUR respectively) might influence the susceptibility to MI. We genotyped rs4065 [3-UTR (untranslated region) *141C>T) and rs2227564 (Pro141Leu) in the PLAU gene as well as rs344781 (-516T>C) in the PLAUR gene in 633 MI patients and 1237 gender- and age-matched control subjects. Our results showed that the T allele of rs4065 was significantly associated with an increased risk of MI, with an adjusted OR (odds ratio) of 1.38 [95% CI (confidence interval), 1.07-1.78; P=0.012) under the dominant model, 1.4 (95% CI, 1.12-1.75; P=0.003) under the additive model and 2.5 (95% CI, 1.15-5.41; P=0.02) under the recessive model. The findings were then replicated in another independent case-control study including 545 MI patients and 597 control subjects. In conclusion, our results suggest that rs4065 might be a previously unknown genetic risk factor for MI in the Chinese Han population.
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Functional haplotypes of the hTERT gene, leukocyte telomere length shortening, and the risk of peripheral arterial disease.
PLoS ONE
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The development of peripheral arterial disease (PAD) is heterogeneous even in the presence of similar risk factors. Our aim was to determine whether inter-individual differences in leukocyte telomere length contribute to the susceptibility of PAD.
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MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.
J. Cell. Biochem.
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Cardiac hypertrophy has been known as an independent predictor for cardiovascular morbidity and mortality. Molecular mechanisms underlying the development of heart failure remain elusive. Recently, microRNAs (miRs) have been established as important regulators in cardiac hypertrophy. Here, we reported miR-221 was up-regulated in both transverse aortic constricted mice and patients with hypertrophic cardiomyopathy (HCM). Forced expression of miR-221 by transfection of miR-221 mimics increased myocyte cell size and induced the re-expression of fetal genes, which were inhibited by the knockdown of endogenous miR-221 in cardiomyocytes. The TargetScan algorithm-based prediction identified that p27, a cardiac hypertrophic suppressor, is the putative target of miR-221, which was confirmed by luciferase assay and Western blotting. In conclusion, our results demonstrated that miR-221 regulated cardiomyocyte hypertrophy probably through down-regulation of p27, suggesting that miR-221 may be a new intervention target for cardiac hypertrophy.
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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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