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Find video protocols related to scientific articles indexed in Pubmed.
Kinesin spindle protein inhibitor SB743921 induces mitotic arrest and apoptosis and overcomes imatinib resistance of chronic myeloid leukemia cells.
Leuk. Lymphoma
PUBLISHED: 09-22-2014
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Inhibition of the cell mitotic pathway may provide a novel means for therapeutic intervention in chronic myeloid leukemia (CML). Kinesin spindle protein (KSP), a microtubule-associated motor protein which is essential for cell cycle progression, is overexpressed in bcr-abl+ CML cells. Retrovirus mediated bcr-abl transduction increases KSP expression in cord blood CD34 + cells. SB743921 is a selective KSP inhibitor which is being investigated in ongoing clinical trials for treatment of myeloma, leukemia and solid tumors. Treatment of CML cells with SB743921 resulted in reduced proliferation and colony forming cell (CFC) formation ability. SB743921 also actively blocked cell cycle progression, leading to apoptosis in both primary CML cells and cell lines. KSP inhibition sensitized CML cells to imatinib-induced apoptosis. Importantly, SB743921 inhibited the proliferation of various CML cells including T315I mutation-harboring cells. Furthermore, we demonstrated that SB743921 treatment suppressed ERK and AKT activity in CML cells. These data indicate that SB743921 may become a novel treatment agent for patients with CML.
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Ad5/48 hexon oncolytic virus expressing sTGF?RIIFc produces reduced hepatic and systemic toxicities and inhibits prostate cancer bone metastases.
Mol. Ther.
PUBLISHED: 03-21-2014
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We are interested in developing oncolytic adenoviruses for the treatment of prostate cancer (PCa) bone metastases. A key limitation of Adenovirus 5 (Ad5) is that upon systemic administration, it produces major liver and systemic toxicities. To address this issue, a chimaeric Ad5/48 adenovirus mHAd.sT?RFc was created. Seven hypervariable regions of Ad5 hexon present in Ad5-based Ad.sT?RFc expressing soluble transforming growth factor beta receptor II-Fc fusion protein (sTG?RIIFc), were replaced by those of Ad48. mHAd.sT?RFc, like Ad.sT?RFc, was replication competent in the human PCa cells, and produced high levels of sTG?RIIFc expression. Compared to Ad.sT?RFc, the systemic delivery of mHAd.sT?RFc in nude mice resulted in much reduced systemic toxicity, and reduced liver sequestration. Ad.sT?RFc produced significant liver necrosis, and increases in alanine transaminase, aspartate transaminase, lactate dehydrogenase, tumor necrosis factor-?, and interleukin-6 levels, while mHAd.sT?RFc produced much reduced responses of these markers. Intravenous delivery of Ad.sT?RFc or mHAd.sT?RFc (5 × 10(10) viral particles/mouse) in nude mice bearing PC-3-luc PCa bone metastases produced inhibition of bone metastases. Moreover, a larger dose of the mHAd.sT?RFc (4 × 10(11) viral particles /mouse) was also effective in inhibiting bone metastases. Thus, mHAd.sT?RFc could be developed for the treatment of PCa bone metastases.
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MicroRNAs: Novel Mechanism Involved in the Pathogenesis of Microwave Exposure on Rats' Hippocampus.
J. Mol. Neurosci.
PUBLISHED: 02-13-2014
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Microwave-induced adverse health outcomes have been gaining much attention in recent years. The hippocampus is sensitive and vulnerable to microwave exposure. Studies from our group and others showed that microwave-induced structural and functional injury of hippocampus, accompanied with alteration of gene and protein expression. It has been demonstrated that microRNAs (miRNAs) were involved in the physiological and pathological processes of brain. In this study, the miRNAs expression profiles of microwave-exposed hippocampus were detected by microarray analysis and verified by real-time polymerase chain reaction (PCR). At 7 days after 30 mW/cm(2) microwave exposure, the expression of 12 miRNAs increased, while other 70 miRNAs decreased in rats' hippocampus. However, most of miRNAs restored to normal levels at 14 days after exposure, only two upregulated miRNAs and 14 downregulated miRNAs were detected. Gene transcription, neuroprotection and receptors function related target genes were predicated by miRDB, miRbase and miRanda. Moreover, these differentially expressed miRNAs were involved in brain-related signaling pathways, such as synaptic vesicle cycle, long-term depression, calcium signaling and neurotrophin signaling pathways. In conclusion, we successfully characterized the miRNA profiles in microwave-exposed hippocampus, and that will be helpful to clarify the molecular mechanism and provide potential therapeutic targets.
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Cardiac-specific expression of the hepatocyte growth factor (HGF) under the control of a TnIc promoter confers a heart protective effect after myocardial infarction (MI).
Curr Gene Ther
PUBLISHED: 02-04-2014
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Uncontrolled therapeutic gene expression and neovascularization in non-specific tissues has lowered the safety of gene therapy. The aim of the study was to identify a cardiac-specific promoter to control target gene expression in heart tissue in vitro and in vivo.
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Beclin1 inhibition promotes autophagy and decreases gemcitabine-induced apoptosis in Miapaca2 pancreatic cancer cells.
Cancer Cell Int.
PUBLISHED: 03-07-2013
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Beclin1 is a well-known key regulator of autophagy, which is also a haploinsufficient tumor suppressor. Current studies revealed that down-regulation or monoallelic deletions of Beclin1 were frequently found in various cancers. The purpose of this study was to investigate the effects of Beclin1 inhibition on autophagy and Gemcitabine-induced apoptosis of pancreatic cancer cells.
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Permethrin exposure during puberty has the potential to enantioselectively induce reproductive toxicity in mice.
Environ Int
PUBLISHED: 05-19-2011
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Permethrin (PM), as a chiral pesticide, has two asymmetric centers, resulting in two pairs of enantiomers. In China, the commercial formulation of PM contains four enantiomers. The enantiomer-specific activity for endocrine disruption in mice remains unclear. In the present study, the four individual PM enantiomers were separated by preparative HPLC. Then, three week-old male ICR mice (after maternal ablactation) were orally administered (+)-cis, (-)-cis, (+)-trans, and (-)-trans-PM separately daily for 3 weeks at doses of 0, 25, 50 and 100 mg/kg/day, respectively. The results showed that 100 mg/kg of (+)-cis, (-)-cis and (-)-trans-PM treatments resulted in serious testicular histopathological damage, decreases in testis weight and serum testosterone (T) concentrations. Moreover, the transcription status of some key genes involved in cholesterol synthesis and transport as well as T synthesis in the testes were also influenced selectively by PM enantiomers, especially by the (+)-cis-PM. Additionally, peripheral benzodiazepine receptor (PBR) and 17?-hydroxysteroid dehydrogenase (17?-HSD) mRNA levels decreased significantly in the (+)-cis-PM group regardless of the administrated doses, while steroidogenic acute regulatory protein (StAR) levels were significantly down-regulated by (+)-cis and (-)-trans-PM. Moreover, significant differences were mainly found in HMG-CoA reductase, PBR, StAR and 17?-HSD mRNA levels between different enantiomers. Combined with the effects on physiology, histopathology and the expression of genes related to T synthesis, (+)-cis-PM showed the greatest endocrine disruption activities, (-)-cis and (-)-trans-PM were moderate, while (+)-trans-PM exhibited the lowest. These results suggested significant PM enantioselectivity in the reproductive toxicity of mice during puberty exposure.
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Cypermethrin exposure during puberty induces oxidative stress and endocrine disruption in male mice.
Chemosphere
PUBLISHED: 01-13-2011
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Cypermethrin (CYP) is one of the most common contaminants in the ecosystem. The effects of CYP exposure on the induction of oxidative stress and endocrine disruption were studied in adolescent male ICR mice. The hepatic activities of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) and total antioxidant capacity (T-AOC) increased significantly after 3 weeks (postnatal day 21-42) of oral administration of 20 mg kg(-1) CYP. In accordance with the enzyme activities, the mRNA levels for the genes encoding these antioxidant proteins, such as Sod1, Sod2, Gpx1 and Gpx2, were also up-regulated significantly in the 10 and 20 mg kg(-1) CYP treatment groups. Furthermore, we also found that the 3-week oral administration of CYP decreased transcription levels of key genes in pathways of cholesterol synthesis and transport and testosterone synthesis including HMG-CoA synthase, steroidogenic acute regulatory protein (StAR) and cytochrome P450 17?-hydroxysteroid dehydrogenase (P450 17? in the liver and testes. Serum testosterone levels also decreased significantly in mice after treatment with 20 mg kg(-1) CYP. Taken together, the results indicated that CYP can induce endocrine disruption in adolescent mice. The findings will be helpful in elucidating the mechanism of toxicity induced by CYP in adolescent mice.
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Effects of metolachlor on transcription of thyroid system-related genes in juvenile and adult Japanese medaka (Oryzias latipes).
Gen. Comp. Endocrinol.
PUBLISHED: 05-19-2010
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Metolachlor (MT) is one of the most important pesticides applied to corn and other crops for controlling broadleaf and grass weeds. However, the effects of MT on the thyroid system in fish remain to be elucidated. In the present experiment, transcription of genes related to the thyroid system, including thyrotropin releasing hormone (Trh), deiodinase 2 (Dio2), thyroid hormone receptor ? (Thr?), and thyroid hormone receptor ? (Thr?), were induced by MT in a sex-, developmental stage-, and tissue- specific manner when medaka were exposed to various concentrations of MT for 14 days. The transcriptional levels of the genes were only significantly altered in both juvenile and adult female medaka in response to MT exposure. And the lowest concentrations able to significantly induce transcription of the selected genes were 10 and 100 ?g/L in juvenile and adult female medaka, respectively. In adult female medaka, a significant up-regulation of these genes was detected only in the brain, with little or no effect in the liver. Furthermore, MT-induced (100 ?g/L) transcription of thyroid system-related genes was enhanced significantly in male juvenile medaka in the presence of estrogen (E2) (50 and 100 ng/L). Moreover, the mRNA levels of Thr? and Thr? in males increase with the combined treatments of 100 ?g/L MT and 100 ng/L E2. Dio2 increased when exposed to 100 ?g/L MT and 50 or 100 ng/L E2. The information obtained in the present study suggests that MT has the potential to influence several steps of the hypothalamus-pituitary-thyroid (HPT) axis homeostasis and to disrupt the thyroid system in medaka.
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Effects of adenovirus-mediated delivery of the human hepatocyte growth factor gene in experimental radiation-induced heart disease.
Int. J. Radiat. Oncol. Biol. Phys.
PUBLISHED: 04-15-2009
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Irradiation to the heart may lead to late cardiovascular complications. The purpose of this study was to investigate whether adenovirus-mediated delivery of the human hepatocyte growth factor gene could reduce post-irradiation damage of the rat heart and improve heart function.
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Protection against Radiation-induced Hematopoietic Damage in Bone Marrow by Hepatocyte Growth Factor Gene Transfer.
Int. J. Radiat. Biol.
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Abstract Purpose: To investigate whether adenovirus-mediated delivery of the human hepatocyte growth factor (HGF) gene could prevent radiation-induced hematopoietic damage. Materials and Methods: Thirty C57BL/6 mice were randomized into three groups, in which phosphate buffer saline (PBS), mock adenovirus vector (Ad-null) or adenovirus vector containing HGF (Ad-HGF) were injected into the tail vein of each group, respectively. After 48 hours, the mice received a single irradiation dose of 6.5 Gy (60)Co gamma rays. Blood samples were extracted via the tail vein at day 0, 4, 7, 10, 14, 21, 24 and 30 after irradiation, for red blood cell (RBC) and white blood cell (WBC) and cluster of differentiation4 (CD4)/cluster of differentiation8(CD8)ratio assessment. At weekly intervals following irradiation, serum erythropoietin (EPO), Interleukin-6 (IL-6) and Interferon-gamma (IFN-?) levels were measured using enzyme-linked immunosorbent assay (ELISA). On post-irradiation day 30, the mice were autopsied and erythroid burst-forming units (BFU-E) were evaluated. Results: Adenovirus-mediated HGF gene transfer could increase human HGF level in serum and have a significant elevation in RBC and WBC count. Ad-HGF increased EPO and IL-6 levels and prompted BFU-E formation. Ad-HGF decreased radiation-induced micronucleus frequency in the mouse bone marrow (BM). Most evidence of radiation-induced hematopoietic damage was observed morphologically in bone marrow specimen four weeks after irradiation. Ad-HGF protected against radiation-induced BM failure and increased survival. Finally, Ad-HGF increased the thymic index and enhanced immune function in the irradiated C57BL/6 mice. Conclusions: This is the first report to date that demonstrates the potential of HGF gene transfer to prevent radiation-induced hematopoietic damage.
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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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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.