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Find video protocols related to scientific articles indexed in Pubmed.
Antimicrobial susceptibility and molecular typing of salmonella agona isolated from humans and other sources.
Foodborne Pathog. Dis.
PUBLISHED: 10-31-2014
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Abstract Salmonella enterica serotype Agona (Salmonella Agona) has been among the top 10 serotypes that cause human diarrheal diseases in China. A total of 95 Salmonella Agona (67 from humans, and 28 from animals, food of animal origins, and environmental sources) recovered in Shanghai, China from 2005 to 2011 were subjected to antimicrobial susceptibility testing and molecular subtyping using pulsed-field gel electrophoresis (PFGE). Approximately 68.4% of the Salmonella Agona isolates were pansusceptible to 15 antimicrobial agents tested, and 4 isolates (4.21%) were resistant to at least 3 antimicrobials. PFGE analysis resulted in 41 unique patterns, of which 4 major PFGE patterns (X3, X4, X5, and X6) were grouped together at 96.1% similarity. Isolates of the four patterns included those from food (pork, beef, and chicken) and humans. Our findings showed that the same clones of Salmonella Agona were recovered from human patients and food, and that food of animal origin was potentially a major vehicle of Salmonella Agona in human salmonellosis in Shanghai.
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Astragaloside IV alleviates early brain injury following experimental subarachnoid hemorrhage in rats.
Int J Med Sci
PUBLISHED: 08-08-2014
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Astragaloside IV, one of the main effective components isolated from Astragalus membranaceus, has multiple neuroprotective properties, while the effects of astragaloside IV on the attenuation of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) and its possible mechanisms are unknown. In the present study, we aimed to determine whether astragaloside IV could inhibit oxidative stress, reduce neuronal apoptosis, and improve neurological deficits after experimental SAH in rats. Rats (n=68) were randomly divided into the following groups: Sham group, SAH group, SAH+vehicle group, and SAH+astragaloside IV group. Astragaloside IV or an equal volume of vehicle was administered at 1 h and 6 h after SAH, all the rats were subsequently sacrificed at 24 h after SAH. Mortality, neurological scores, and brain edema were assessed, biochemical tests and histological studies were also performed at that point. SAH induced an increase in the malondialdehyde (MDA) level, neuronal apoptosis, cleaved caspase 3, brain edema and decreased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Astragaloside IV treatment reversed these changes and improved neurobehavioral outcomes of SAH rats. Our findings suggested that astragaloside IV may alleviate EBI after SAH through antioxidative and anti-apoptotic effects.
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Molecular profiling and computational network analysis of TAZ-mediated mammary tumorigenesis identifies actionable therapeutic targets.
Oncotarget
PUBLISHED: 08-07-2014
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Triple-negative breast cancer (TNBC) accounts for approximately 15-20% of all breast cancer (BC) cases and contributes disproportionately to BC mortality. TAZ, a key transducer of the Hippo pathway, has recently been demonstrated to confer breast cancer stem cell (CSC) traits. However, TAZ target genes and the underlying transcriptional regulatory pathways responsible for the CSC phenomenon remain unknown. Here, we demonstrate that the oncogenic activity of TAZ is essential for propagation of the malignant phenotype. We further show that constitutively active TAZ tumor-derived cells exhibit unique tumor-initiating properties, including increased self-renewal and metastatic seeding potential, acquired chemotherapy resistance and the ability to efficiently regenerate tumor formation in vivo. Combined digital RNA expression analysis and computational network approaches identify several signaling pathways that distinguish breast cancer tumor-initiating cells (T-ICs) from bulk tumor cells. We demonstrate the utility of this approach by repositioning the small molecule tyrosine kinase inhibitor, Dasatinib, which selectively targets T-ICs and inhibits TNBC growth in vivo.
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Enhancement of Autophagy by Histone Deacetylase Inhibitor Trichostatin A Ameliorates Neuronal Apoptosis After Subarachnoid Hemorrhage in Rats.
Mol. Neurobiol.
PUBLISHED: 08-06-2014
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Trichostatin A (TSA), a pan-histone deacetylase inhibitor, exerts multiple neuroprotective properties. This study aims to examine whether TSA could enhance autophagy, thereby reduce neuronal apoptosis and ultimately attenuate early brain injury (EBI) following subarachnoid hemorrhage (SAH). SAH was performed through endovascular perforation method, and mortality, neurological score, and brain water content were evaluated at 24 h after surgery. Western blot were used for quantification of acetylated histone H3, LC3-II, LC3-I, Beclin-1, cytochrome c, Bax, and cleaved caspase-3 expression. Immunofluorescence was performed for colocalization of Beclin-1 and neuronal nuclei (NeuN). Apoptotic cell death of neurons was quantified with double staining of terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling (TUNEL) and NeuN. The autophagy inhibitor 3-methyladenine (3-MA) was used to manipulate the proposed pathway. Our results demonstrated that TSA reduced brain edema and alleviated neurological deficits at 24 h after SAH. TSA significantly increased acetylated histone H3, the LC3-II/LC3-I ratio, and Beclin-1 while decreased Bax and cleaved caspase-3 in the cortex. Beclin-1 and NeuN, TUNEL, and NeuN, respectively, were colocalized in cortical cells. Neuronal apoptosis in the ipsilateral basal cortex was significantly inhibited after TSA treatment. Conversely, 3-MA reversed the beneficial effects of TSA. These results proposed that TSA administration enhanced autophagy, which contributes to alleviation of neuronal apoptosis, improvement of neurological function, and attenuation of EBI following SAH.
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Methylation status of promoter 1 region of GDNF gene in human glioma cells.
Int J Clin Exp Med
PUBLISHED: 07-15-2014
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This study aimed to investigate the methylation status of promoter 1 region of glial cell line-derived neurotrophic factor (GDNF) in human glioma cells and to explore the effect of GDNF methylation on the expression of GDNF in glioma.
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PTPN14 forms a complex with Kibra and LATS1 proteins and negatively regulates the YAP oncogenic function.
J. Biol. Chem.
PUBLISHED: 07-14-2014
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The Hippo signaling pathway regulates cellular proliferation and survival, thus exerting profound effects on normal cell fate and tumorigenesis. Pivotal effectors of this pathway are YAP/TAZ, transcriptional co-activators whose dysfunction contributes to epithelial-to-mesenchymal transition and malignant transformation. Therefore, it is of great importance to decipher the mechanisms underlying the regulations of YAP/TAZ at various levels. Here we report that non-receptor tyrosine phosphatase 14 (PTPN14) interacts with the Kibra protein. The interaction between PTPN14 and Kibra is through the PPXY domain of PTPN14 and WW domain of Kibra. PTPN14 and Kibra can induce the LATS1 activation independently and cooperatively. Interestingly, activation of LATS1 by PTPN14 is dependent on the C terminus of PTPN14 and independent of the upstream mammalian STE20-like kinase (MST) proteins. Furthermore, we demonstrate that PTPN14 increases the LAST1 protein stability. Last, overexpression of Kibra rescues the increased cell migration and aberrant three-dimensional morphogenesis induced by knockdown of PTPN14, and this rescue is mediated through the activation of the upstream LATS1 kinase and subsequent cytoplasmic sequestration of YAP. In summary, our results indicate a potential regulatory role of PTPN14 in the Hippo pathway and demonstrate another layer of regulation in the YAP oncogenic function.
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Robust deep network with maximum correntropy criterion for seizure detection.
Biomed Res Int
PUBLISHED: 07-06-2014
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Effective seizure detection from long-term EEG is highly important for seizure diagnosis. Existing methods usually design the feature and classifier individually, while little work has been done for the simultaneous optimization of the two parts. This work proposes a deep network to jointly learn a feature and a classifier so that they could help each other to make the whole system optimal. To deal with the challenge of the impulsive noises and outliers caused by EMG artifacts in EEG signals, we formulate a robust stacked autoencoder (R-SAE) as a part of the network to learn an effective feature. In R-SAE, the maximum correntropy criterion (MCC) is proposed to reduce the effect of noise/outliers. Unlike the mean square error (MSE), the output of the new kernel MCC increases more slowly than that of MSE when the input goes away from the center. Thus, the effect of those noises/outliers positioned far away from the center can be suppressed. The proposed method is evaluated on six patients of 33.6 hours of scalp EEG data. Our method achieves a sensitivity of 100% and a specificity of 99%, which is promising for clinical applications.
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Crosstalk Between Macroautophagy and Chaperone-Mediated Autophagy: Implications for the Treatment of Neurological Diseases.
Mol. Neurobiol.
PUBLISHED: 07-02-2014
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Macroautophagy and chaperone-mediated autophagy (CMA) are two important subtypes of autophagy that play a critical role in cellular quality control under physiological and pathological conditions. Despite the marked differences between these two autophagic pathways, macroautophagy and CMA are intimately connected with each other during the autophagy-lysosomal degradation process, in particular, in the setting of neurological illness. Macroautophagy serves as a backup mechanism to removal of malfunctioning proteins (i.e., aberrant ?-synuclein) from the cytoplasm when CMA is compromised, and vice versa. The molecular mechanisms underlying the conversation between macroautophagy and CMA are being clarified. Herein, we survey current overviews concentrating on the complex interactions between macroautophagy and CMA, and present therapeutic potentials through utilization and manipulation of macroautophagy-CMA crosstalk in the treatment of neurological diseases.
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Comparison of carotid artery endarterectomy and carotid artery stenting in patients with atherosclerotic carotid stenosis.
J Craniofac Surg
PUBLISHED: 06-10-2014
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The choice of carotid artery endarterectomy (CEA) or carotid artery stenting (CAS), as surgical and interventional treatment of atherosclerotic carotid stenosis, respectively, has been controversial in decades, especially for asymptomatic patients with carotid stenosis. Age and the diameter of impaired carotid artery might be 2 important factors to decide whether CEA or CAS should be performed. Besides, contrast-enhanced ultrasound (CEUS) has been confirmed as an effective method to predict the risk of stroke by classifying the carotid plaque into 4 grades. The role of CEUS in the choice of CEA or CAS still remains unclear.
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Functionalization of biomass carbonaceous aerogels: selective preparation of MnO2@CA composites for supercapacitors.
ACS Appl Mater Interfaces
PUBLISHED: 06-06-2014
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Functionalized porous carbon materials with hierarchical structure and developed porosity coming from natural and renewable biomass have been attracting tremendous attention recently. In this work, we present a facile and scalable method to synthesize MnO2 loaded carbonaceous aerogel (MnO2@CA) composites via the hydrothermal carbonaceous (HTC) process. We employ two reaction systems of the mixed metal ion precursors to study the optimal selective adsorption and further reaction of MnO2 precursor on CA. Our experimental results show that the system containing KMnO4 and Na2S2O3·5H2O exhibits better electrochemical properties compared with the reaction system of MnSO4·H2O and (NH4)2S2O8. For the former, the obtained MnO2@CA displays the specific capacitance of 123.5 F·g(-1). The enhanced supercapacitance of MnO2@CA nanocomposites could be ascribed to both electrochemical contributions of the loaded MnO2 nanoparticles and the porous structure of three-dimensional carbonaceous aerogels. This study not only indicates that it is vital for the reaction systems to match with porous carbonaceous materials, but also offers a new fabrication strategy to prepare lightweight and high-performance materials that can be used in energy storage devices.
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Mass spectrometric analysis of cerebrospinal fluid protein for glioma and its clinical application.
Contemp Oncol (Pozn)
PUBLISHED: 06-03-2014
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To establish and evaluate the fingerprint diagnostic models of cerebrospinal protein profile in glioma with surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) and bioinformatics analysis, in order to seek new tumor markers.
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Emergence and prevalence of non-H2S-producing Salmonella enterica serovar Senftenberg isolates belonging to novel sequence type 1751 in China.
J. Clin. Microbiol.
PUBLISHED: 05-14-2014
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Salmonella enterica serovar Senftenberg is a common nontyphoidal Salmonella serotype which causes human Salmonella infections worldwide. In this study, 182 S. Senftenberg isolates, including 17 atypical non-hydrogen sulfide (H2S)-producing isolates, were detected in China from 2005 to 2011. The microbiological and genetic characteristics of the non-H2S-producing and selected H2S-producing isolates were determined by using pulsed-field gel electrophoresis (PFGE), multilocus sequence typing (MLST), and clustered regularly interspaced short palindromic repeat (CRISPR) analysis. The phs operons were amplified and sequenced. The 17 non-H2S-producing and 36 H2S-producing isolates belonged to 7 sequence types (STs), including 3 new STs, ST1751, ST1757, and ST1758. Fourteen of the 17 non-H2S-producing isolates belonged to ST1751 and had very similar PFGE patterns. All 17 non-H2S-producing isolates had a nonsense mutation at position 1621 of phsA. H2S-producing and non-H2S-producing S. Senftenberg isolates were isolated from the same stool sample from three patients; isolates from the same patients displayed the same antimicrobial susceptibility, ST, and PFGE pattern but could be discriminated based on CRISPR spacers. Non-H2S-producing S. Senftenberg isolates belonging to ST1751 have been prevalent in Shanghai, China. It is possible that these emerging organisms will disseminate further, because they are difficult to detect. Thus, we should strengthen the surveillance for the spread of this atypical S. Senftenberg variant.
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Association of osteopontin expression with the prognosis of glioma patient: a meta-analysis.
Tumour Biol.
PUBLISHED: 04-10-2014
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So far, several studies on the association between osteopontin (OPN) expression and glioma have been performed, but the conclusion still was not clear. The aim of the present meta-analysis was to determine the relationship between OPN expression and prognosis of patients with glioma. The electronic database was searched for articles on the association between OPN expression and glioma until 31 January 2014. Odds ratios (OR) and the relative risks with 95 % CI were utilized to analyze the qualitative data in retrospective studies and prospective studies, respectively. The standardized mean difference and the corresponding 95 % CI were used for analyzing the studies with quantitative data. Heterogeneity of all included studies was assessed using Cochrane's Q test and I (2) measurement. The publication bias was examined by the Egger test. Sixteen cohort studies (854 patients) on OPN expression and gliomas prognosis were included in the present meta-analysis. It was found that OPN expression was significantly higher in patients with high-grade glioma than in patients with low-grade glioma (? (2)?=?8.38, I (2) ?=?16.6 %, P?=?0.300), and the expression of OPN increased with glioma grade. The combined data showed the correlation between high OPN expression and tumor reoccurrence (OR?=?18.61, 95 % CI?=?6.34-54.67, P?=?0.405). In addition, the results of the pooled analysis indicated that OPN expression was significantly related to overall survival (HR?=?1.83; 95 % CI?=?1.36-2.46). In conclusion, OPN may be a biomarker for predicting the prognosis of gliomas.
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Biofilm formation in Haemophilus parasuis: relationship with antibiotic resistance, serotype and genetic typing.
Res. Vet. Sci.
PUBLISHED: 03-26-2014
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Biofilms are surface-associated microbial communities, which are encased in self-synthesized extracellular environment. Biofilm formation may trigger drug resistance and inflammation, resulting in persistent infections. Haemophilus parasuis is the etiological agent of a systemic disease, Glässer's disease, characterized by fibrinous polyserositis, arthritis and meningitis in pigs. The purpose of this study was to examine the correlation between biofilm and antibiotic resistance among the clinical isolates of H. parasuis. In the present study, we tested biofilm-forming ability of 110 H. parasuis isolates from various farms using polystyrene microtiter plate assays. Seventy-three isolates of H. parasuis (66.4%) showed biofilm formation and most of them performed weak biofilm-forming ability (38/73). All isolates were tested for antimicrobial susceptibility to 18 antimicrobial agents by the broth microdilution method. H. parasuis isolates showed very high resistance (>90%) to sulfanilamide, nalidixic acid, and trimethoprim. Resistance to eight antibiotics such as penicillin (41.1% vs 8.1%), ampicillin (31.5% vs 8.1%), amoxicillin (28.8% vs 5.4%), gentamicin (46.6% vs 24.3%), cefazolin (19.2% vs 2.7%), doxycycline (19.2% vs 8.1%), cefotaxime (11% vs 2.7%), and cefaclor (13.7% vs 5.4%) was comparatively higher among biofilm producers than non-biofilm producers. Pulsed-field gel electrophoresis (PFGE) analyses could distinguish various isolates. Our data indicated that H. parasuis field isolates were able to form biofilms in vitro. In addition, biofilm positive strains had positive correlation with resistance to ?-lactams antibiotics. Thus, biofilm formation may play important roles during H. parasuis infections.
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Distortion of memory V?2 ?? T cells contributes to immune dysfunction in chronic HIV infection.
Cell. Mol. Immunol.
PUBLISHED: 03-09-2014
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?? T cells play important roles in innate immunity as the first-line of defense against infectious diseases. Human immunodeficiency virus (HIV) infection disrupts the balance between V?1 T cells and V?2 T cells and causes dysfunction among ?? T cells. However, the biological mechanisms and clinical consequences of this disruption require further investigation. In this study, we performed a comprehensive analysis of phenotype and function of memory ?? T cells in cohorts of Chinese individuals with HIV infection. We found a dynamic change in memory V?2 ?? T cells, skewed toward an activated and terminally differentiated effector memory phenotype TEMRA V?2 ?? T cell, which may account for the dysfunction of V?2 ?? T cells in HIV disease. In addition, we found that IL-17-producing ?? T cells were significantly increased in HIV-infected patients with fast disease progression and positively correlated with HLA-DR(+) ?? T cells and CD38(+)HLA-DR(+) ?? T cells. This suggests the IL-17 signaling pathway is involved in ?? T-cell activation and HIV pathogenesis. Our findings provide novel insights into the role of V?2 T cells during HIV pathogenesis and represent a sound basis on which to consider immune therapies with these cells.Cellular & Molecular Immunology advance online publication, 15 September 2014; doi:10.1038/cmi.2014.77.
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Anterior corpus callosotomy combined with anterior temporal resection with amygdalohippocampectomy: outcome in a patient with congenital bilateral perisylvian syndrome.
Turk Neurosurg
PUBLISHED: 02-19-2014
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Congenital bilateral perisylvian syndrome (CBPS) is characterized by epilepsy, cognitive deficits, pseudobulbar palsy and diplegia of the facial, pharyngeal and masticatory muscles. Epilepsy has been described in nearly 90% of affected patients. The epilepsy is usually severe and pharmacoresistant in about 55 percent of CBPS patients. Until now, only 12 cases of surgical treatment on CBPS have been reported; the surgical treatment is usually corpus callosotomy. In this paper, we describe a previously unreported combination of anterior corpus callosotomy plus anterior temporal lobectomy with amygdalohippocampectomy for a patient with CBPS, resulting in a satisfactory clinical outcome. Based on this case, we suggest that palliative focal resective surgery combined with anterior corpus callosotomy should be considered when a predominance of the epileptiform discharges suggests focal onset in patients with CBPS. Meanwhile, the clinical decision to adopt this combination surgery must be based on a thorough pre-surgical evaluation, and should take into account the clinical, radiological, and EEG features.
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Botch is a ?-glutamyl cyclotransferase that deglycinates and antagonizes Notch.
Cell Rep
PUBLISHED: 02-12-2014
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Botch promotes embryonic neurogenesis by inhibiting the initial S1 furin-like cleavage step of Notch maturation. The biochemical process by which Botch inhibits Notch maturation is not known. Here, we show that Botch has ?-glutamyl cyclotransferase (GGCT) activity that deglycinates Notch, which prevents the S1 furin-like cleavage. Moreover, Notch is monoglycinated on the ?-glutamyl carbon of glutamate 1,669. The deglycinase activity of Botch is required for inhibition of Notch signaling both in vitro and in vivo. When the ?-glutamyl-glycine at position 1,669 of Notch is degylcinated, it is replaced by 5-oxy-proline. These results reveal that Botch regulates Notch signaling through deglycination and identify a posttranslational modification of Notch that plays an important role in neurogenesis.
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Whole-genome sequencing identifies genomic heterogeneity at a nucleotide and chromosomal level in bladder cancer.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 01-27-2014
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Using complete genome analysis, we sequenced five bladder tumors accrued from patients with muscle-invasive transitional cell carcinoma of the urinary bladder (TCC-UB) and identified a spectrum of genomic aberrations. In three tumors, complex genotype changes were noted. All three had tumor protein p53 mutations and a relatively large number of single-nucleotide variants (SNVs; average of 11.2 per megabase), structural variants (SVs; average of 46), or both. This group was best characterized by chromothripsis and the presence of subclonal populations of neoplastic cells or intratumoral mutational heterogeneity. Here, we provide evidence that the process of chromothripsis in TCC-UB is mediated by nonhomologous end-joining using kilobase, rather than megabase, fragments of DNA, which we refer to as "stitchers," to repair this process. We postulate that a potential unifying theme among tumors with the more complex genotype group is a defective replication-licensing complex. A second group (two bladder tumors) had no chromothripsis, and a simpler genotype, WT tumor protein p53, had relatively few SNVs (average of 5.9 per megabase) and only a single SV. There was no evidence of a subclonal population of neoplastic cells. In this group, we used a preclinical model of bladder carcinoma cell lines to study a unique SV (translocation and amplification) of the gene glutamate receptor ionotropic N-methyl D-aspertate as a potential new therapeutic target in bladder cancer.
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Valproic acid: a new candidate of therapeutic application for the acute central nervous system injuries.
Neurochem. Res.
PUBLISHED: 01-15-2014
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Acute central nervous system (CNS) injuries, including stroke, traumatic brain injury (TBI), and spinal cord injury (SCI), are common causes of human disabilities and deaths, but the pathophysiology of these diseases is not fully elucidated and, thus, effective pharmacotherapies are still lacking. Valproic acid (VPA), an inhibitor of histone deacetylation, is mainly used to treat epilepsy and bipolar disorder with few complications. Recently, the neuroprotective effects of VPA have been demonstrated in several models of acute CNS injuries, such as stroke, TBI, and SCI. VPA protects the brain from injury progression via anti-inflammatory, anti-apoptotic, and neurotrophic effects. In this review, we focus on the emerging neuroprotective properties of VPA and explore the underlying mechanisms. In particular, we discuss several potential related factors in VPA research and present the opportunity to administer VPA as a novel neuropective agent.
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Antimicrobial resistance of Shigella spp. from humans in Shanghai, China, 2004-2011.
Diagn. Microbiol. Infect. Dis.
PUBLISHED: 01-07-2014
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A retrospective study conducted on patients with diarrhea in Shanghai, China from 2004-2011, indicated that of 77,600 samples collected, 1,635 (2.1%) tested positive for Shigella. Species isolated included S. sonnei (1,066, 65.1%), S. flexneri (569, 34.7%), and S. boydii (3, 0.2%). Most of the Shigella isolates were found to be resistant to streptomycin (98.7%), trimethoprim (98.0%), ampicillin (92.1%), and nalidixic acid (91.7%). Additionally, many isolates were resistant to tetracycline (86.9%), trimethoprim + sulfamethoxazole (80.1%), sulfisoxazole (76.8%) and gentamicin (55.5%). Approximately 80% of the isolates were resistant to at least eight antimicrobial agents, 14% to at least ten antimicrobials tested and 10 isolates to fourteen antimicrobials, including sulfonamides, fluoroquinolones, tetracyclines, aminoglycosides and ?-lactamases. Importantly, co-resistance to fluoroquinolones and the third- and fourth-generation cephalosporins was also identified. The high levels of resistance to antimicrobial agents commonly used in clinical medicine presents a great challenge to treating patients with shigellosis.
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Global Characterization of Differential Gene Expression Profiles in Mouse V?1+ and V?4+ ?? T Cells.
PLoS ONE
PUBLISHED: 01-01-2014
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Peripheral ?? T cells in mice are classified into two major subpopulations, V?1+ and V?4+, based on the composition of T cell receptors. However, their intrinsic differences remain unclear. In this study, we analyzed gene expression profiles of the two subsets using Illumina HiSeq 2000 Sequencer. We identified 1995 transcripts related to the activation of V?1+ ?? T cells, and 2158 transcripts related to the activation of V?4+ ?? T cells. We identified 24 transcripts differentially expressed between the two subsets in resting condition, and 20 after PMA/Ionomycin treatment. We found that both cell types maintained phenotypes producing IFN-?, TNF-?, TGF-? and IL-10. However, V?1+ ?? T cells produced more Th2 type cytokines, such as IL-4 and IL-5, while V?4+ ?? T cells preferentially produced IL-17. Our study provides a comprehensive gene expression profile of mouse peripheral V?1+ and V?4+ ?? T cells that describes the inherent differences between them.
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Caspases: a molecular switch node in the crosstalk between autophagy and apoptosis.
Int. J. Biol. Sci.
PUBLISHED: 01-01-2014
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Autophagy and apoptosis are two important catabolic processes contributing to the maintenance of cellular and tissue homeostasis. Autophagy controls the turnover of protein aggregates and damaged organelles within cells, while apoptosis is the principal mechanism by which unwanted cells are dismantled and eliminated from organisms. Despite marked differences between these two pathways, they are highly interconnected in determining the fate of cells. Intriguingly, caspases, the primary drivers of apoptotic cell death, play a critical role in mediating the complex crosstalk between autophagy and apoptosis. Pro-apoptotic signals can converge to activate caspases to execute apoptotic cell death. In addition, activated caspases can degrade autophagy proteins (i.e., Beclin-1, Atg5, and Atg7) to shut down the autophagic response. Moreover, caspases can convert pro-autophagic proteins into pro-apoptotic proteints to trigger apoptotic cell death instead. It is clear that caspases are important in both apoptosis and autophagy, thus a detailed deciphering of the role of caspases in these two processes is still required to clarify the functional relationship between them. In this article, we provide a current overview of caspases in its interplay between autophagy and apoptosis. We emphasized that defining the role of caspases in autophagy-apoptosis crosstalk will provide a framework for more precise manipulation of these two processes during cell death.
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Neuroprotective effect of hydrogen-rich saline against neurologic damage and apoptosis in early brain injury following subarachnoid hemorrhage: possible role of the Akt/GSK3? signaling pathway.
PLoS ONE
PUBLISHED: 01-01-2014
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Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3? signaling pathway.
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Relationship between enhanced intensity of contrast enhanced ultrasound and microvessel density of aortic atherosclerostic plaque in rabbit model.
PLoS ONE
PUBLISHED: 01-01-2014
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The aim of this study was to evaluate the relationship between enhanced intensity of contrast enhanced ultrasound and microvessel density of aortic atherosclerotic plaque in rabbit model. The abdominal aortas of thirty-six male New Zealand rabbits were damaged by balloon expansion and the animals were then fed a high fat diet for 12 weeks. Twenty-seven plaques on the near aortic wall were detected using conventional ultrasound examination. The maximum thickness of each plaque was recorded. CEUS was performed on these 27 plaques and the time-intensity curves (TICs) were analyzed offline. Using the quantitative ACQ software, features such as the arrival time (AT), time to peak (TTP), baseline intensity (BI), peak intensity (PI) and enhanced intensity (EI) (EI?=?PI-BI) were assessed. Inter- and intra-observer agreement of EI were assessed using the Bland-Altman test. After CEUS examination, the rabbits were sacrificed for pathological examination and CD34 monoclonal antibody immunohistochemical detection. Microvessel density (MVD) was counted under the microscope. The relationship between indexes of CEUS and the level of MVD was analyzed. There was a good positive linear correlation between EI and MVD (??=?0. 854, P<0. 001), the intraclass correlations for inter- and intra-observer agreement for EI were 0.73 and 0.82 respectively, suggesting that EI may be act as a useful index for plaque risk stratification in animal models.
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Role of P2X purinoceptor 7 in neurogenic pulmonary edema after subarachnoid hemorrhage in rats.
PLoS ONE
PUBLISHED: 01-01-2014
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Neurogenic pulmonary edema (NPE) is an acute and serious complication after subarachnoid hemorrhage (SAH) with high mortality. The present study aimed to test the therapeutic potential of brilliant blue G (BBG), a selective P2X purinoceptor 7 (P2X7R) antagonist, on NPE in a rat SAH model.
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6p22.3 amplification as a biomarker and potential therapeutic target of advanced stage bladder cancer.
Oncotarget
PUBLISHED: 11-16-2013
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Genetic and epigenetic alterations have been identified as to contribute directly or indirectly to the generation of transitional cell carcinoma of the urinary bladder (TCC-UB). In a comparative fashion much less is known about copy number alterations in TCC-UB, but it appears that amplification of chromosome 6p22 is one of the most frequent changes. Using fluorescence in situ hybridization (FISH) analyses, we evaluated chromosomal 6p22 amplification in a large cohort of bladder cancer patients with complete surgical staging and outcome data. We have also used shRNA knockdown candidate oncogenes in the cell based study. We found that amplification of chromosome 6p22.3 is significantly associated with the muscle-invasive transitional cell carcinoma of the urinary bladder (TCC-UB) (22%) in contrast to superficial TCC-UB (9%) (p=7.2-04). The rate of 6p22.3 amplification in pN>1 patients (32%) is more than twice that in pN0 (16%) patients (p=0.05). Interestingly, we found that 6p22.3 amplification is as twice as high (p=0.0201) in African American (AA) than European American (EA) TCC-UB patients. Moreover, we showed that the expression of some candidate genes (E2F3, CDKAL1 and Sox4) in the 6p22.3 region is highly correlated with the chromosomal amplification. In particular, knockdown of E2F3 inhibits cell proliferation in a 6p22.3-dependent manner, whereas knockdown of CDKAL1 and Sox4 has no effect on cell proliferation. Using gene expression profiling, we further identified some common as well as distinctive subset targets of the E2F3 family members. In summary, our data indicate that E2F3 is a key regulator of cell proliferation in a subset of bladder cancer and the 6p22.3 amplicon is a biomarker of aggressive phenotype in this tumor type.
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Comparison between routine and improved decompressive craniectomy on patients with malignant cerebral artery infarction without traumatic brain injury.
J Craniofac Surg
PUBLISHED: 11-14-2013
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Malignant cerebral artery infarction is one kind of ischemic stroke with high mortality. The aim of this study was to analyze comparatively the preoperative and postoperative clinical data as well as the prognostic factors in these patients who underwent improved decompressive craniectomy or routine decompressive craniectomy.
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Interplay between different magnetisms in Cr-doped topological insulators.
ACS Nano
PUBLISHED: 09-30-2013
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Breaking the time-reversal-symmetry of topological insulators through magnetic doping has led to exotic physical discoveries. Here, we report the gate-dependent magneto-transport measurements on the Cr-doped (BixSb1-x)2Te3 thin films. With effective top-gate modulations, we demonstrate the presence of both the hole-mediated RKKY coupling and carrier-independent van Vleck magnetism in the magnetic TI systems. Most importantly, by varying the Cr doping concentrations from 2% to 20%, we unveil the interplay between the two magnetic orders and establish the valid approach to either enhance or suppress each individual contribution. The electric-field-controlled ferromagnetisms identified in the Cr-doped TI materials will serve as the fundamental step to further explore the TRS-breaking TI systems, and it may also help to expand the functionality of TI-based device for spintronics applications.
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P2X7 Receptor Antagonism Inhibits p38 Mitogen-Activated Protein Kinase Activation and Ameliorates Neuronal Apoptosis After Subarachnoid Hemorrhage in Rats.
Crit. Care Med.
PUBLISHED: 08-22-2013
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Brilliant blue G, a selective P2X7 receptor antagonist, exhibits neuroprotective properties. This study examined whether brilliant blue G treatment ameliorates early brain injury after experimental subarachnoid hemorrhage, specifically via inhibiting p38 mitogen-activated protein kinase-related proapoptotic pathways.
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Innate immune cell-derived microparticles facilitate hepatocarcinoma metastasis by transferring integrin ?(M)?? to tumor cells.
J. Immunol.
PUBLISHED: 08-16-2013
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Mechanisms by which tumor cells metastasize to distant organs still remain enigmatic. Immune cells have been assumed to be the root of metastasis by their fusing with tumor cells. This fusion theory, although interpreting tumor metastasis analogically and intriguingly, is arguable to date. We show in this study an alternative explanation by immune cell-derived microparticles (MPs). Upon stimulation by PMA or tumor cell-derived supernatants, immune cells released membrane-based MPs, which were taken up by H22 tumor cells, leading to tumor cell migration in vitro and metastasis in vivo. The underlying molecular basis was involved in integrin ?(M)?? (CD11b/CD18), which could be effectively relayed from stimulated innate immune cells to MPs, then to tumor cells. Blocking either CD11b or CD18 led to significant decreases in MP-mediated tumor cell metastasis. This MP-mediated transfer of immune phenotype to tumor cells might also occur in vivo. These findings suggest that tumor cells may usurp innate immune cell phenotypes via MP pathway for their metastasis, providing new insight into tumor metastatic mechanism.
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Controversies and evolving new mechanisms in subarachnoid hemorrhage.
Prog. Neurobiol.
PUBLISHED: 08-09-2013
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Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms "early brain injury" and "delayed brain injury" are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications.
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Vav1-phospholipase C-?1 (Vav1-PLC-?1) pathway initiated by T cell antigen receptor (TCR??) activation is required to overcome inhibition by ubiquitin ligase Cbl-b during ??T cell cytotoxicity.
J. Biol. Chem.
PUBLISHED: 07-29-2013
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T cell antigen receptor ?? (TCR??) and natural killer group 2, member D (NKG2D) are two crucial receptors for ??T cell cytotoxicity. Compelling evidences suggest that ??T cell cytotoxicity is TCR??-dependent and can be co-stimulated by NKG2D. However, the molecular mechanism of underlying TCR??-dependent activation of ??T cells remains unclear. In this study we demonstrated that TCR?? but not NKG2D engagement induced lytic granule polarization and promoted ??T cell cytotoxicity. TCR?? activation alone was sufficient to trigger Vav1-dependent phospholipase C-?1 signaling, resulting in lytic granule polarization and effective killing, whereas NKG2D engagement alone failed to trigger cytotoxicity-related signaling to overcome the inhibitory effect of Cbl-b; therefore, NKG2D engagement alone could not induce effective killing. However, NKG2D ligation augmented the activation of ??T cell cytotoxicity through the Vav1-phospholipase C-?1 pathway. Vav1 overexpression or Cbl-b knockdown not only enhanced TCR?? activation-initiated killing but also enabled NKG2D activation alone to induce ??T cell cytotoxicity. Taken together, our results suggest that the activation of ??T cell cytotoxicity requires a strong activation signal to overcome the inhibitory effect of Cbl-b. Our finding provides new insights into the molecular mechanisms underlying the initiation of ??T cell cytotoxicity and likely implications for optimizing ??T cell-based cancer immunotherapy.
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Dynamic Chromatin Modification Sustains Epithelial-Mesenchymal Transition following Inducible Expression of Snail-1.
Cell Rep
PUBLISHED: 06-25-2013
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Epithelial-mesenchymal transition (EMT) is thought to contribute to cancer metastasis, but its underlying mechanisms are not well understood. To define early steps in this cellular transformation, we analyzed human mammary epithelial cells with tightly regulated expression of Snail-1, a master regulator of EMT. After Snail-1 induction, epithelial markers were repressed within 6 hr, and mesenchymal genes were induced at 24 hr. Snail-1 binding to its target promoters was transient (6-48 hr) despite continued protein expression, and it was followed by both transient and long-lasting chromatin changes. Pharmacological inhibition of selected histone acetylation and demethylation pathways suppressed the induction as well as the maintenance of Snail-1-mediated EMT. Thus, EMT involves an epigenetic switch that may be prevented or reversed with the use of small-molecule inhibitors of chromatin modifiers.
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Rapid identification and differentiation of non-O157 Shiga toxin-producing Escherichia coli using polymerase chain reaction coupled to electrospray ionization mass spectrometry.
Foodborne Pathog. Dis.
PUBLISHED: 06-14-2013
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A polymerase chain reaction (PCR)-mass spectroscopy assay was developed to identify non-O157 Shiga toxin-producing Escherichia coli (STEC) with Plex-ID biosensor system, a platform identifying short PCR amplicons by specific base compositions. This assay simultaneously amplifies five fragments of two housekeeping genes, two subunits of stx2 gene, and four other virulence genes of STEC. A total of 164 well-characterized STEC isolates were examined with the assay to build a DNA base composition database. Another panel of 108 diverse STEC isolates was tested with the established database to evaluate the assays identification capability. Among the 108 isolates, the assay specificity was 100% for three (stx1, eae, and aggA) out of five tested virulence genes, but 99% for stx2 and 96% for hlyA, respectively. Main stx1/stx2 subtypes and multiple alleles of stx1/stx2 could be differentiated. The assay successfully identified several clinically significant serotypes, including O91:H14, O103:H25, O145:H28/NM, O113:H21, and O104:H4. Meanwhile, it was able to group isolates with different levels of pathogenic potential. The results suggest that this high-throughput method may be useful in clinical and regulatory laboratories for STEC identification, particularly strains with increased pathogenic potential.
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Polycomb repressive complex PRC2 regulates Xenopus retina development downstream of Wnt/?-catenin signaling.
Development
PUBLISHED: 06-05-2013
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The histone methyltransferase complex PRC2 controls key steps in developmental transitions and cell fate choices; however, its roles in vertebrate eye development remain unknown. Here, we report that in Xenopus, PRC2 regulates the progression of retinal progenitors from proliferation to differentiation. We show that the PRC2 core components are enriched in retinal progenitors and downregulated in differentiated cells. Knockdown of the PRC2 core component Ezh2 leads to reduced retinal progenitor proliferation, in part due to upregulation of the Cdk inhibitor p15(Ink4b). In addition, although PRC2 knockdown does not alter eye patterning, retinal progenitor gene expression or expression of the neural competence factor Sox2, it does cause suppression of proneural bHLH gene expression, indicating that PRC2 is crucial for the initiation of neural differentiation in the retina. Consistent with this, knocking down or blocking PRC2 function constrains the generation of most retinal neural cell types and promotes a Müller glial cell fate decision. We also show that Wnt/?-catenin signaling acting through the receptor Frizzled 5, but independent of Sox2, regulates expression of key PRC2 subunits in the developing retina. This is consistent with a role for this pathway in coordinating proliferation and the transition to neurogenesis in the Xenopus retina. Our data establish PRC2 as a regulator of proliferation and differentiation during eye development.
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Whole-Genome Sequences of Four Salmonella enterica Serotype Newport Strains from Humans.
Genome Announc
PUBLISHED: 05-11-2013
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Salmonellosis contributes significantly to the public health burden globally. Salmonella enterica serotype Newport is among Salmonella serotypes most associated with food-borne illness in the United States and China. It was thought to be polyphyletic and to contain different lineages. We report draft genomes of four S. Newport strains isolated from humans in China.
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Regulatory T cell in stroke: a new paradigm for immune regulation.
Clin. Dev. Immunol.
PUBLISHED: 04-30-2013
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Stroke is a common, debilitating trauma that has an incompletely elucidated pathophysiology and lacks an effective therapy. FoxP3(+)CD25(+)CD4(+) regulatory T cells (Tregs) suppress a variety of normal physiological and pathological immune responses via several pathways, such as inhibitory cytokine secretion, direct cytolysis induction, and antigen-presenting cell functional modulation. FoxP3(+)CD25(+)CD4(+) Tregs are involved in a variety of central nervous system diseases and injuries, including axonal injury, neurodegenerative diseases, and stroke. Specifically, FoxP3(+)CD25(+)CD4(+) Tregs exert neuroprotective effects in acute experimental stroke models. These beneficial effects, however, are difficult to elucidate. In this review, we summarized evidence of FoxP3(+)CD25(+)CD4(+) Tregs as potentially important immunomodulators in stroke pathogenesis and highlight further investigations for possible immunotherapeutic strategies by modulating the quantity and/or functional effects of FoxP3(+)CD25(+)CD4(+) Tregs in stroke patients.
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The cytotoxic effect of ?-elemene against malignant glioma is enhanced by base-excision repair inhibitor methoxyamine.
J. Neurooncol.
PUBLISHED: 04-27-2013
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This study investigated the effects of ?-elemene + methoxyamine, a DNA base-excision repair inhibitor, on the inhibition of glioma growth. We treated C6 and SHG44 glioma cells with ?-elemene and methoxyamine individually or in combinations, and subsequently analyzed cellular survivals by MTT assay. Comet assay, ?-H2AX focus formation assay and Western-blot were performed to investigate whether the observed cytotoxicity was associates with DNA damages. Finally, a xenograft tumor model was established in nude mice with C6 cells to analyze in vivo tumor inhibition effects of ?-elemene, which was followed by determination of the expression of anti-apoptotic protein Bcl-2 via immunohistochemistry staining. Results showed that ?-elemene could significantly inhibit the growth of glioma cells in a dose- and time-dependent manner. The combination of methoxyamine with ?-elemene could result in a greater extent of DNA injuries in vitro. Furthermore, in vivo tumors exhibited a marked shrinkage in volume in ?-elemene + methoxyamine treatment group. Immunohistochemistry analysis of the tumor tissues showed a distinctive decrease in Bcl-2 staining in ?-elemene (56 %) and ?-elemene + methoxyamine (36 %) groups when compared with the negative control (77 %). In conclusion, ?-elemene exhibits a significant cytotoxic effect against glioma cells both in vitro and in vivo, which is likely to be mediated by its potential to damage tumor cell DNA and activate apoptotic pathway. Such growth inhibition effect of ?-elemene could be potentiated by methoxyamine co-administration. Therefore, a combination of the two agents as a novel chemotherapeutic option for glioma merits further investigations.
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Over-expression of regulator of G protein signaling 5 promotes tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma cells.
J Surg Oncol
PUBLISHED: 04-17-2013
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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. The regulator of G-protein signaling 5 (RGS5) has been reported to be highly expressed in some malignant tumors. However, its expression and role in HCC has not been reported.
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P2X7R/cryopyrin inflammasome axis inhibition reduces neuroinflammation after SAH.
Neurobiol. Dis.
PUBLISHED: 03-18-2013
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Neuroinflammation contributes to the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Cytotoxic events following SAH, such as extracellular accumulation of adenosine triphosphate (ATP), may activate the P2X purinoceptor 7 (P2X7R)/cryopyrin inflammasome axis, thus inducing the proinflammatory cytokine IL-1?/IL-18 secretion. We therefore hypothesized that inhibition of P2X7R/cryopyrin inflammasome axis would ameliorate neuroinflammation after SAH. In the present study, SAH was induced by the endovascular perforation in rats. Small interfering RNAs (siRNAs) of P2X7R or cryopyrin were administered intracerebroventricularly 24h before SAH. Brilliant blue G (BBG), a non-competitive antagonist of P2X7R, was administered intraperitoneally 30min following SAH. Post-assessments including SAH severity score, neurobehavioral test, brain water content, Western blot and immunofluorescence, were performed. Administration of P2X7R and cryopyrin siRNA as well as pharmacologic blockade of P2X7R by BBG ameliorated neurological deficits and brain edema at 24h following SAH. Inhibition of P2X7R/cryopyrin inflammasome axis suppressed caspase-1 activation, which subsequently decreased maturation of IL-1?/IL-18. To investigate the link between P2X7R and cryopyrin inflammasome in vivo, Benzoylbenzoyl-ATP (BzATP), a P2X7R agonist, was given to lipopolysaccharide (LPS) primed naive rats with scramble or cryopyrin siRNAs. In LPS-primed naive rats, BzATP induced caspase-1 activation and mature IL-1? release were neutralized by cryopyrin siRNA. Thus, the P2X7R/cryopyrin inflammasome axis may contribute to neuroinflammation via activation of caspase-1 and thereafter mature IL-1?/IL-18 production following SAH. Therapeutic interventions targeting P2X7R/cryopyrin pathway may be a novel approach to ameliorate EBI following SAH.
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Low-frequency stimulation inhibits epileptogenesis by modulating the early network of the limbic system as evaluated in amygdala kindling model.
Brain Struct Funct
PUBLISHED: 02-02-2013
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Low-frequency stimulation (LFS) is emerging as a new option for the treatment of epilepsy. The present study was designed to determine whether there is a crucial period for the treatment of epileptogenesis with LFS. LFS was delivered at different time-points to evaluate its anti-epileptogenic effect on amygdala-kindling rats. (18)F-fluorodeoxyglucose small-animal positron-emission tomography (microPET) and multi-channel EEG recording (MER) were used to investigate the dynamics of brain networks during epileptogenesis and LFS treatment. Interestingly, LFS delivered in the first 7 days significantly retarded the progression of behavioral seizure stages and shortened the afterdischarge duration (ADD), LFS delivered throughout the whole process resulted in similar effects. However, if LFS was delivered at the beginning of seizure stage 2 or 3 (5 ± 0.3 days during kindling acquisition), it had no anti-epileptogenic effect and even prolonged the ADD and enhanced synchronization of the EEGs. MicroPET study revealed a notable hypometabolism in the amygdala, piriform cortex, entorhinal cortex and other regions in the limbic system during the period from seizure stage 0 to stage 2 or 3. The glucose metabolism in those regions was specifically increased by LFS. MER further verified that an early network of afterdischarge spread was formed in those brain regions during kindling acquisition. Thus, we provided direct evidence that modulation of the early network in the limbic system is crucial for the anti-epileptogenic effect of LFS in amygdaloid-kindling rats.
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Early and late postoperative seizure outcome in 97 patients with supratentorial meningioma and preoperative seizures: a retrospective study.
J. Neurooncol.
PUBLISHED: 01-07-2013
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We identified factors associated with early and late postoperative seizure control in patients with supratentorial meningioma plus preoperative seizures. In this retrospective study, univariate analysis and multivariate logistic regression analysis compared 24 clinical variables according to the occurrence of early (?1 week) or late (>1 week) postoperative seizures. Sixty-two of 97 patients (63.9 %) were seizure free for the entire postoperative follow-up period (29.5 ± 11.8 months), while 13 patients (13.4 %) still had frequent seizures at the end of follow-up. Fourteen of 97 patients (14.4 %) experienced early postoperative seizures, and emergence of new postoperative neurological deficits was the only significant risk factor (odds ratio = 7.377). Thirty-three patients (34.0 %) experienced late postoperative seizures at some time during follow-up, including 12 of 14 patients with early postoperative seizures. Associated risk factors for late postoperative seizures included tumor progression (odds ratio = 7.012) and new permanent postoperative neurological deficits (odds ratio = 4.327). Occurrence of postoperative seizures in patients with supratentorial meningioma and preoperative seizure was associated with new postoperative neurological deficits. Reduced cerebral or vascular injury during surgery may lead to fewer postoperative neurological deficits and better seizure outcome.
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Draft Genome Sequences of Three Salmonella enterica Serotype Agona Strains from China.
Genome Announc
PUBLISHED: 01-07-2013
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Salmonellosis has been one of the major contributors to the global public health burden. Salmonella enterica serotype Agona has ranked among the top 10 and top 20 most frequent Salmonella serotypes isolated from human sources in China and the United States, respectively. We report draft genomes of three S. Agona strains from China.
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A novel respiratory rate estimation method for sound-based wearable monitoring systems.
Conf Proc IEEE Eng Med Biol Soc
PUBLISHED: 08-29-2011
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The respiratory rate is a vital sign that can provide important information about the health of a patient, especially that of the respiratory system. The aim of this study is to develop a simple method that can be applied in wearable systems to monitor the respiratory rate automatically and continuously over extended periods of time. In this paper, a novel respiratory rate estimation method is presented to achieve this target. The proposed method has been evaluated in both the open-source data as well as the local-hospital data, and the results are encouraging. The findings of this study revealed strong linear correlation to the reference respiratory rate. The correlation coefficients for the open-source data and the in-hospital data are 0.99 and 0.96 respectively. The standard deviation of the estimation error is less than 7% for both types of data.
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A case of McCune-Albright syndrome associated with pituitary GH adenoma: therapeutic process and autopsy.
J. Pediatr. Endocrinol. Metab.
PUBLISHED: 08-10-2011
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McCune-Albright syndrome (MAS) is a clinical syndrome with low incidence, and its concurrence with pituitary GH adenoma is rare. Little of the history, treatment and outcome has been studied.
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Serum resistance in Haemophilus parasuis SC096 strain requires outer membrane protein P2 expression.
FEMS Microbiol. Lett.
PUBLISHED: 07-25-2011
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Haemophilus parasuis outer membrane protein P2 (OmpP2), the most abundant protein in the outer membrane, has been identified as an antigenic protein and a potential virulence factor. To study the precise function of OmpP2, an ompP2-deficient mutant (?ompP2) of a H. parasuis serovar 4 clinical strain SC096 was constructed by a modified natural transformation system. Compared with the wild-type SC096 strain, the ?ompP2 mutant showed a pronounced growth defect and exhibited significantly greater sensitivity to the bactericidal action of porcine and rabbit sera, whereas the complemented strain could restore the growth and serum resistance phenotypes. The results indicated that H. parasuis OmpP2 from SC096 strain is an important surface protein involved in serum resistance.
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Antimicrobial susceptibility and PFGE genotyping of Haemophilus parasuis isolates from pigs in South China (2008-2010).
J. Vet. Med. Sci.
PUBLISHED: 04-04-2011
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H. parasuis isolates (n=112) from pigs were tested for antimicrobial susceptibility against 23 antimicrobial agents by the disk diffusion method. All isolates were sensitive to Florfenico and most strains were sensitive to Cefotaxime (103/112; 92%), Ceftazidime (99/112; 88.4%), Chloramphenicol (90/112; 80.4%) and Gentamicin (85/112; 75.9%). High resistance levels to Nalidixic acid (84.8%), TMP (67.9%) and Trimethoprim+Sulfamethoxazole (58%) were observed. Genomic DNA extracted from 52 isolates resistant to at least seven antimicrobial agents was analyzed by PFGE and 46 distinct PFGE patterns identified. Diverse variation was observed between the drug-resistant H. parasuis isolates examined, suggesting that resistance traits were acquired independently by the respective isolates.
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The AAA+ ATPase Thorase regulates AMPA receptor-dependent synaptic plasticity and behavior.
Cell
PUBLISHED: 03-07-2011
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The synaptic insertion or removal of AMPA receptors (AMPAR) plays critical roles in the regulation of synaptic activity reflected in the expression of long-term potentiation (LTP) and long-term depression (LTD). The cellular events underlying this important process in learning and memory are still being revealed. Here we describe and characterize the AAA+ ATPase Thorase, which regulates the expression of surface AMPAR. In an ATPase-dependent manner Thorase mediates the internalization of AMPAR by disassembling the AMPAR-GRIP1 complex. Following genetic deletion of Thorase, the internalization of AMPAR is substantially reduced, leading to increased amplitudes of miniature excitatory postsynaptic currents, enhancement of LTP, and elimination of LTD. These molecular events are expressed as deficits in learning and memory in Thorase null mice. This study identifies an AAA+ ATPase that plays a critical role in regulating the surface expression of AMPAR and thereby regulates synaptic plasticity and learning and memory.
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Molecular characterization of fluoroquinolone resistance in Haemophilus parasuis isolated from pigs in South China.
J. Antimicrob. Chemother.
PUBLISHED: 01-07-2011
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To perform molecular characterization of fluoroquinolone-resistant Haemophilus parasuis isolated from South China.
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An approach to the bis-oxazole macrocycle of diazonamides.
Org. Lett.
PUBLISHED: 12-21-2010
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A convergent approach to a macrocyclic compound embodying the complete "eastern" quadrant of diazonamides is described. The opening sequence in this work relies on an oxazole-forming reaction devised earlier in this group, while a late step involves a Robinson-Gabriel cyclization of an amidoketone to form a second oxazole.
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A new technique for management of intercavernous sinus bleeding with titanium clips in transsphenoidal surgery.
Neurol India
PUBLISHED: 12-15-2010
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Venous bleeding induced by intercavernous sinus injury during sellar dural opening is a challenging intraoperative complication and is difficult to treat in transsphenoidal surgery. To date, few studies concerning the management of intercavernous sinus bleeding have been reported.
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A genome-wide RNAi screen identifies multiple RSK-dependent regulators of cell migration.
Genes Dev.
PUBLISHED: 11-09-2010
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To define the functional pathways regulating epithelial cell migration, we performed a genome-wide RNAi screen using 55,000 pooled lentiviral shRNAs targeting ?11,000 genes, selecting for transduced cells with increased motility. A stringent validation protocol generated a set of 31 genes representing diverse pathways whose knockdown dramatically enhances cellular migration. Some of these pathways share features of epithelial-to-mesenchymal transition (EMT), and together they implicate key regulators of transcription, cellular signaling, and metabolism, as well as novel modulators of cellular trafficking, such as DLG5. In delineating downstream pathways mediating these migration phenotypes, we observed universal activation of ERKs and a profound dependence on their RSK effectors. Pharmacological inhibition of RSK dramatically suppresses epithelial cell migration induced by knockdown of all 31 genes, suggesting that convergence of diverse migratory pathways on this kinase may provide a therapeutic opportunity in disorders of cell migration, including cancer metastasis.
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Synthesis of 5-amino-oxazole-4-carboxylates from alpha-chloroglycinates.
Org. Lett.
PUBLISHED: 08-12-2010
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Aluminum-based Lewis acids are effective promoters of the condensation of alpha-chloroglycinates with isonitriles or with cyanide ion, leading to the formation of 5-amino-oxazoles.
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A simple method to analyze the similarity of biological sequences based on the fuzzy theory.
J. Theor. Biol.
PUBLISHED: 04-01-2010
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In this paper, we propose a simple method to analyze the similarity of biological sequences. By taking the average contents of biological sequences and their information entropies as the variables, the fuzzy method is used to cluster them. From the results of application, it finds that the method is relatively easy and rapid. Unlike other methods such as the graphical representation methods, which is usually very complex to compute some invariants of matric derived from graphical representation, our method pays more attention to the information of biological sequences themselves. Especially with the help of the software (SPSS), it seems to be very convenient. Therefore, it may be used to study the new biological sequences such as their evolution relationship and structures.
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Development of an oxazole conjunctive reagent and application to the total synthesis of siphonazoles.
J. Org. Chem.
PUBLISHED: 12-03-2009
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The preparation of 4-carbethoxy-5-methyl-2-(phenylsulfonyl)methyloxazole and its use in the elaboration of more complex oxazoles are described. A total synthesis of the unique natural products siphonazoles A and B, illustrates an application of this building block. A discussion of the biological activity of the siphonazoles is also presented.
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Prevalence and functional analysis of sequence variants in the ATR checkpoint mediator Claspin.
Mol. Cancer Res.
PUBLISHED: 09-08-2009
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Mutational inactivation of genes controlling the DNA-damage response contributes to cancer susceptibility within families and within the general population as well as to sporadic tumorigenesis. Claspin (CLSPN) encodes a recently recognized mediator protein essential for the ATR and CHK1-dependent checkpoint elicited by replicative stress or the presence of ssDNA. Here, we describe a study to determine whether mutational disruption of CLSPN contributes to cancer susceptibility and sporadic tumorigenesis. We resequenced CLSPN from the germline of selected cancer families with a history of breast cancer (n = 25) or a multicancer phenotype (n = 46) as well as from a panel of sporadic cancer cell lines (n = 52) derived from a variety of tumor types. Eight nonsynonymous variants, including a recurrent mutation, were identified from the germline of two cancer-prone individuals and five cancer cell lines of breast, ovarian, and hematopoietic origin. None of the variants was present within population controls. In contrast, mutations were rare within genes encoding the CLSPN-interacting protein ATR and its binding partner ATRIP. One variant of CLSPN, encoding the I783S missense mutation, was defective in its ability to mediate CHK1 phosphorylation following DNA damage and was unable to rescue sensitivity to replicative stress in CLSPN-depleted cells. Taken together, these observations raise the possibility that CLSPN may encode a component of the DNA-damage response pathway that is targeted by mutations in human cancers, suggesting the need for larger population-based studies to investigate whether CLSPN variants contribute to cancer susceptibility.
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A developmentally regulated inducer of EMT, LBX1, contributes to breast cancer progression.
Genes Dev.
PUBLISHED: 08-05-2009
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Epithelial-to-mesenchymal transition (EMT) plays an important role during normal embryogenesis, and it has been implicated in cancer invasion and metastasis. Here, we report that Ladybird homeobox 1 (LBX1), a developmentally regulated homeobox gene, directs expression of the known EMT inducers ZEB1, ZEB2, Snail1, and transforming growth factor beta2 (TGFB2). In mammary epithelial cells, overexpression of LBX1 leads to morphological transformation, expression of mesenchymal markers, enhanced cell migration, increased CD44(high)/CD24(low) progenitor cell population, and tumorigenic cooperation with known oncogenes. In human breast cancer, LBX1 is up-regulated in the unfavorable estrogen receptor (ER)/progesterone (PR)/HER2 triple-negative basal-like subtype. Thus, aberrant expression of LBX1 may lead to the activation of a developmentally regulated EMT pathway in human breast cancer.
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YAP-dependent induction of amphiregulin identifies a non-cell-autonomous component of the Hippo pathway.
Nat. Cell Biol.
PUBLISHED: 07-14-2009
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The Hippo signalling pathway regulates cellular proliferation and survival, thus has profound effects on normal cell fate and tumorigenesis. The pivotal effector of this pathway is YAP (yes-associated protein), a transcriptional co-activator amplified in mouse and human cancers, where it promotes epithelial to mesenchymal transition (EMT) and malignant transformation. So far, studies of YAP target genes have focused on cell-autonomous mediators; here we show that YAP-expressing MCF10A breast epithelial cells enhance the proliferation of neighbouring untransfected cells, implicating a non-cell-autonomous mechanism. We identify the gene for the epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) as a transcriptional target of YAP, whose induction contributes to YAP-mediated cell proliferation and migration, but not EMT. Knockdown of AREG or addition of an EGFR kinase inhibitor abrogates the proliferative effects of YAP expression. Suppression of the negative YAP regulators LATS1 and 2 (large tumour suppressor 1 and 2) is sufficient to induce AREG expression, consistent with physiological regulation of AREG by the Hippo pathway. Genetic interaction between the Drosophila YAP orthologue Yorkie and Egfr signalling components supports the link between these two highly conserved signalling pathways. Thus, YAP-dependent secretion of AREG indicates that activation of EGFR signalling is an important non-cell-autonomous effector of the Hippo pathway, which has implications for the regulation of both physiological and malignant cell proliferation.
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A new dynamic device for low-dimensional materials testing.
Rev Sci Instrum
PUBLISHED: 06-25-2009
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As the geometrical size of low-dimensional materials decreases to micro- or nanoscale, the traditional dynamic loading system cannot be used anymore to measure the dynamic mechanical property. In this study, a new dynamic loading system was developed. A piezoelectric transducer actuator was used for displacement loading, and a mechanical lever was designed to amplify the displacement load. Finite element method simulation and validation experiments were conducted to analyze the strength and function of the mechanical lever. As an application test, a sample from an aluminum film was investigated using the system. The success of the experiment, as shown by the results, demonstrated the feasibility of the system for low-dimensional materials study.
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Shifts in replication timing actively affect histone acetylation during nucleosome reassembly.
Mol. Cell
PUBLISHED: 05-28-2009
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The entire genome is replicated in a programmed manner, with specific regions undergoing DNA synthesis at different times in S phase. Active genes generally replicate in early S phase, while repressed genes replicate late, and for some loci this process is developmentally regulated. Using a nuclear microinjection system, we demonstrate that DNA sequences originally packaged into nucleosomes containing deacetylated histones during late S become reassembled with acetylated histones after undergoing replication in early S. Conversely, a change from early to late replication timing is accompanied by repackaging into nucleosomes containing deacetylated histones. This is carried out by differential cell-cycle-controlled acetylation and deacetylation of histones H3 and H4. These studies provide strong evidence that switches in replication timing may play a role in the regulation of nucleosome structure during development.
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Study of magnetic dynamic properties for magnetic cluster and quantum dots with hexagonal array.
J Nanosci Nanotechnol
PUBLISHED: 05-16-2009
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Based on the Monte-Carlo simulation, magnetic dynamic properties of magnetic clusters and quasi two-dimensional quantum dots with hexagonal lattice arrays have been calculated. It has been found that the saturation fields for the cluster and quantum dot increase with increasing dipolar interaction. However, hysteresis loops of the quantum dots are different from those in clusters. Hysteresis behavior of quantum dot array is associated closely with the radius of quantum dot and the distance between quantum dots. The calculated results are consistent with experimental results. Finally, the step effect of hysteresis loops has been explained by the competition roles among the configurational anisotropy energy, Zeeman energy and thermal energy.
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The tumor suppressor WTX shuttles to the nucleus and modulates WT1 activity.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 05-04-2009
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WTX encodes a tumor suppressor gene inactivated in Wilms tumor and recently implicated in WNT signaling through enhancement of cytoplasmic beta-catenin (CTNNB1) degradation. Here, we report that WTX translocates to the nucleus, a property that is modified by an endogenous splicing variant and is modulated by a nuclear export inhibitor. WTX is present in distinct subnuclear structures and co-localizes with the paraspeckle marker p54NRB/NONO, suggesting a role in transcriptional regulation. Notably, WTX binds WT1, another Wilms tumor suppressor and stem cell marker that encodes a zinc-finger transcription factor, and enhances WT1-mediated transcription of Amphiregulin, an endogenous target gene. Together, these observations suggest a role for WTX in nuclear pathways implicated in the transcriptional regulation of cellular differentiation programs.
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Total synthesis of siphonazoles by the use of a conjunctive oxazole building block.
Org. Lett.
PUBLISHED: 04-29-2009
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The preparation of 4-carbethoxy-5-methyl-2-(phenylsulfonyl)methyloxazole and its use in the elaboration of more complex oxazoles are described. A total synthesis of the unique natural products, siphonazoles A and B, illustrates an application of the new building block.
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Edaravone reduces brain oedema and attenuates cell death after intracerebral haemorrhage in mice.
Brain Inj
PUBLISHED: 03-31-2009
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Edaravone, a potent scavenger of hydroxyl radicals, has been used to treat acute cerebral ischemia, but its effects on intracerebral haemorrhage (ICH) are unknown. The present study tried to understand the effects of edaravone on ICH in mice.
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A novel method to analyze the similarity of biological sequences.
J. Biomol. Struct. Dyn.
PUBLISHED: 02-25-2009
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In this paper, we propose a new method based on the 2-D graphical representation to analyze the similarity of biological sequences and classify the protein secondary structure sequences. Instead of computing some characteristics from the distance matrix, the average area surrounded by the curve and X axis is computed as a new invariant. The new method is tested on two sets: the coding sequences of 30 mitochondrial genes from NCBI and 12 protein secondary structure sequences. The similarity/disimilarity and phylogenetic tree (dendrogram) of these sequences verify the validity of our method.
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Concentration polarization of high-density lipoprotein and its relation with shear stress in an in vitro model.
J. Biomed. Biotechnol.
PUBLISHED: 02-09-2009
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The purpose of this study was to determine the concentration polarization of high-density lipoprotein (HDL) at the surface of the carotid artery under conditions of steady flow and to establish its relationship with shear stress using an in vitro vascular simulation model of carotid bifurcation. Shear stress, HDL concentration at the surface, and the ratio of HDL concentration at the surface to concentration in bulk flow were measured at different locations within the model under high-speed (1.451 m/s) and low-speed (0.559 m/s) flow. HDL showed concentration polarization at the surface of the carotid artery model, particularly in the internal carotid artery sinus. With decreasing flow velocity, the shear stress at the surface also decreased, and HDL concentration polarization increased. The concentration polarization of HDL was negatively and strongly correlated with shear stress at both low- (r = -0.872, P < .001) and high-speed flow (r = -0.592, P = .0018).
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Molecular basis of CD4 repression by the Swi/Snf-like BAF chromatin remodeling complex.
Eur. J. Immunol.
PUBLISHED: 01-31-2009
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The Brg1/Brm-associated factor (BAF) chromatin remodeling complex directly binds the CD4 silencer and is essential for CD4 repression during T-cell development, because deletion of the ATPase subunit Brg1 or a dominant negative mutant of BAF57 each impairs CD4 repression in early thymocytes. Paradoxically, BAF57 is dispensable for remodeling nucleosomes in vitro or for binding of the BAF complex to the CD4 silencer in vivo. Thus, it is unclear whether BAF57-dependent CD4 repression involves chromatin remodeling and, if so, how the remodeling translates into CD4 repression. Here we show that nucleosomes at the CD4 silencer occupy multiple translational frames. BAF57 dominant negative mutant does not alter these frames, but reduces the accessibility of the entire silencer without affecting the flanking regions, concomitant with localized accumulation of linker histone H1 and eviction of Runx1, a key repressor of CD4 transcription that directly binds the CD4 silencer. Our data indicate that precise nucleosome positioning is not critical for the CD4 silencer function and that BAF57 participates in remodeling H1-containing chromatin at the CD4 silencer, which enables Runx1 to access the silencer and repress CD4. In addition to BAF57, multiple other subunits in the BAF complex are also dispensable for chromatin remodelling in vitro. Our data suggest that these subunits could also help remodel chromatin at a step after the recruitment of the BAF complex to target genes.
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Pesticide exposure and suicidal ideation in rural communities in Zhejiang province, China.
Bull. World Health Organ.
PUBLISHED: 01-23-2009
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To investigate the association between pesticide exposure and suicidal ideation in rural areas of China.
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Efficient epileptic seizure detection by a combined IMF-VoE feature.
Conf Proc IEEE Eng Med Biol Soc
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Automatic seizure detection from the electroen-cephalogram (EEG) plays an important role in an on-demand closed-loop therapeutic system. A new feature, called IMF-VoE, is proposed to predict the occurrence of seizures. The IMF-VoE feature combines three intrinsic mode functions (IMFs) from the empirical mode decomposition of a EEG signal and the variance of the range between the upper and lower envelopes (VoE) of the signal. These multiple cues encode the intrinsic characteristics of seizure states, thus are able to distinguish them from the background. The feature is tested on 80.4 hours of EEG data with 10 seizures of 4 patients. The sensitivity of 100% is obtained with a low false detection rate of 0.16 per hour. Average time delays are 19.4s, 13.2s, and 10.7s at the false detection rates of 0.16 per hour, 0.27 per hour, and 0.41 per hour respectively, when different thresholds are used. The result is competitive among recent studies. In addition, since the IMF-VoE is compact, the detection system is of high computational efficiency and able to run in real time.
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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.