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Find video protocols related to scientific articles indexed in Pubmed.
[Effect of tranilast on myocardial fibrosis in mice with viral myocarditis.]
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 11-20-2014
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To study the role of tranilast in the pathogenesis of myocardiac fibrosis in viral myocarditis.
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Angiotensin-Converting Enzyme Inhibitors and Amyotrophic Lateral Sclerosis Risk: A Total Population-Based Case-Control Study.
JAMA Neurol
PUBLISHED: 11-11-2014
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Although several studies have shown that use of angiotensin-converting enzyme inhibitors (ACEIs) potentially decreased amyotrophic lateral sclerosis (ALS) risk in animal models, to our knowledge, there has been no human study in the literature discussing this issue.
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Nidogen-1: a candidate biomarker for ovarian serous cancer.
Jpn. J. Clin. Oncol.
PUBLISHED: 11-08-2014
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Effective biomarkers for early detection of ovarian cancer are needed. Our study previously showed that basement membrane protein, nidogen-1 plasma level was significantly increased in ovarian cancer patients. This study aimed to examine the plasma levels of nidogen-1 in a large patient population to evaluate its effectiveness in ovarian serous carcinoma and expression in tumor tissues.
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Extendable blocking probe in reverse transcription for analysis of RNA variants with superior selectivity.
Nucleic Acids Res.
PUBLISHED: 11-08-2014
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Here we provide the first strategy to use a competitive Extendable Blocking Probe (ExBP) for allele-specific priming with superior selectivity at the stage of reverse transcription. In order to analyze highly similar RNA variants, a reverse-transcriptase primer whose sequence matches a specific variant selectively primes only that variant, whereas mismatch priming to the alternative variant is suppressed by virtue of hybridization and subsequent extension of the perfectly matched ExBP on that alternative variant template to form a cDNA-RNA hybrid. This hybrid will render the alternative RNA template unavailable for mismatch priming initiated by the specific primer in a hot-start protocol of reverse transcription when the temperature decreases to a level where such mismatch priming could occur. The ExBP-based reverse transcription assay detected BRAF and KRAS mutations in at least 1000-fold excess of wild-type RNA and detection was linear over a 4-log dynamic range. This novel strategy not only reveals the presence or absence of rare mutations with an exceptionally high selectivity, but also provides a convenient tool for accurate determination of RNA variants in different settings, such as quantification of allele-specific expression.
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Dendritic cells respond to nasopharygeal carcinoma cells through annexin A2-recognizing DC-SIGN.
Oncotarget
PUBLISHED: 11-06-2014
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Dendritic cells (DCs) play an essential role in immunity and are used in cancer immunotherapy. However, these cells can be tuned by tumors with immunosuppressive responses. DC-specific intercellular adhesion molecule 3-Grabbing Nonintegrin (DC-SIGN), a C-type lectin expressed on DCs, recognizes certain carbohydrate structures which can be found on cancer cells. Nasopharyngeal carcinoma (NPC) is an epithelial cell-derived malignant tumor, in which immune response remains unclear. This research is to reveal the molecular link on NPC cells that induces the immunosuppressive responses in DCs. In this article, we report identification of annexin A2 (ANXA2) on NPC cells as a ligand for DC-SIGN on DCs. N-linked mannose-rich glycan on ANXA2 may mediate the interaction. ANXA2 was abundantly expressed in NPC, and knockdown of ANXA2 suppressed NPC xenograft in mice, suggesting a crucial role of ANXA2 in NPC growth. Interaction with NPC cells caused DC-SIGN activation in DCs. Consequently DC maturation and the proinflammatory interleukin (IL)-12 production were inhibited, and the immunosuppressive IL-10 production was promoted. Blockage of either DC-SIGN or ANXA2 eliminated the production of IL-10 from DCs. This report suggests that suppression of ANXA2 at its expression or glycosylation on NPC may improve DC-mediated immunotherapy for the tumor.
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The effects of separating inferior alveolar neurovascular bundles on osteogenesis of tissue-engineered bone and vascularization.
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub
PUBLISHED: 11-04-2014
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To evaluate the effects of autologous blood vessels and nerves on vascularization.
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[Expressions of ROR?T; and FOXP3 and clinical significance in patients with oral lichen planus].
Shanghai Kou Qiang Yi Xue
PUBLISHED: 10-24-2014
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Oral lichen planus was considered as T cell mediated autoimmune disease affecting oral mucosa with unknown etiopathogenesis. Helper T lymphocytes played an important role in the pathogenesis of OLP. The purpose of this study was to investigate the possible role of Th17 and Treg cells in OLP lesions.
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Resveratrol suppresses TPA-induced matrix metalloproteinase-9 expression through the inhibition of MAPK pathways in oral cancer cells.
J. Oral Pathol. Med.
PUBLISHED: 10-21-2014
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Naturally occurring agents, such as resveratrol, have been determined to benefit health. Numerous studies have demonstrated that resveratrol has antioxidative, cardioprotective, and neuroprotective properties. However, the effect of resveratrol exerts on the metastasis of oral cancer cells remains unclear. In this study, we investigated the effect the anti-invasive activity of resveratrol on a human oral cancer cell line (SCC-9) in vitro and the underlying mechanisms.
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Long-term outcomes following sirolimus conversion after renal transplantation.
Immunol. Invest.
PUBLISHED: 10-09-2014
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Long-term outcomes following renal transplantation remain limited due to chronic progressive injury partly as a result of calcineurin inhibitor (CNI) toxicity. Thus, patients have been converted to non-CNI immunosuppressives despite the lack of evidence of long-term benefits from CNI free therapy. We now report our 10-year experience converting patients with well functioning transplants from CNI to sirolimus. We retrospectively analyzed outcomes of patients receiving continuous CNI based therapy (CNI, n?=?309) or who were switched to sirolimus within the first year of post-transplantation (CONV, n?=?54). The groups were similar for most recipient, graft and donor characteristics, however, diabetes was more common in the CNI group and statin use was more frequent in the CONV group. The average time to conversion was 7.2 months and the creatinine level at the time of switching was 1.4?mg/dl. Ten year graft and patient survival rates were equivalent in both groups. There were no differences in the causes of death or graft loss in both groups. Renal function was available for 5 years posttransplant and was no different between groups. Thus, there is no evidence that routinely switching patients with well functioning renal allografts to sirolimus from CNI based immunosuppression provides long-term benefit.
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Induction therapy in renal transplant recipients: a review.
Immunol. Invest.
PUBLISHED: 10-09-2014
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Transplant science has improved significantly over the last decade. Influenced by novel advancements, rejection rates and short-term graft losses diminished substantially. Induction therapy was shown to reduce rejection rates and improve short-term graft survival. In this article, we discuss the most commonly used induction agents and the choice of induction therapy in different renal transplant recipient subgroups. The medical literature as well as our own experience was used to prepare this review. At this time, induction therapy is commonly used in upwards of 80%, of renal transplant recipients. Depleting agents are the most frequently used agents and they account for more than 75% of all induction therapies in the United States. Currently, there is no consensus regarding the choice of induction therapy. The type of induction therapy is generally selected based on a comprehensive evaluation of the recipient and the donor's immunological risks, the risk of developing opportunistic infection and malignancy, recipient comorbidities, financial burden and the choice of maintenance immunosuppressive regimen.
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Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.
J. Cell Biol.
PUBLISHED: 10-01-2014
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DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein-interacting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Ku(-/-) mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847.
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Pathological changes in the maxillary sinus mucosae of patients with recurrent odontogenic maxillary sinusitis.
Pak J Med Sci
PUBLISHED: 09-17-2014
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To study the structural and functional changes of maxillary sinus mucosae of patients with odontogenic maxillary sinusitis, and to improve the therapeutic effects.
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Helicobacter pylori infection activates Src homology-2 domain-containing phosphatase 2 to suppress IFN-? signaling.
J. Immunol.
PUBLISHED: 09-15-2014
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Helicobacter pylori infection not only induces gastric inflammation but also increases the risk of gastric tumorigenesis. IFN-? has antimicrobial effects; however, H. pylori infection elevates IFN-?-mediated gastric inflammation and may suppress IFN-? signaling as a strategy to avoid immune destruction through an as-yet-unknown mechanism. This study was aimed at investigating the mechanism of H. pylori-induced IFN-? resistance. Postinfection of viable H. pylori decreased IFN-?-activated signal transducers and activators of transcription 1 and IFN regulatory factor 1 not only in human gastric epithelial MKN45 and AZ-521 but also in human monocytic U937 cells. H. pylori caused an increase in the C-terminal tyrosine phosphorylation of Src homology-2 domain-containing phosphatase (SHP) 2. Pharmacologically and genetically inhibiting SHP2 reversed H. pylori-induced IFN-? resistance. In contrast to a clinically isolated H. pylori strain HP238, the cytotoxin-associated gene A (CagA) isogenic mutant strain HP238(CagAm) failed to induce IFN-? resistance, indicating that CagA regulates this effect. Notably, HP238 and HP238(CagAm) differently caused SHP2 phosphorylation; however, imaging and biochemical analyses demonstrated CagA-mediated membrane-associated binding with phosphorylated SHP2. CagA-independent generation of reactive oxygen species (ROS) contributed to H. pylori-induced SHP2 phosphorylation; however, ROS/SHP2 mediated IFN-? resistance in a CagA-regulated manner. This finding not only provides an alternative mechanism for how CagA and ROS coregulate SHP2 activation but may also explain their roles in H. pylori-induced IFN-? resistance.
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Fast formation of superhydrophobic octadecylphosphonic acid (ODPA) coating for self-cleaning and oil/water separation.
Soft Matter
PUBLISHED: 09-02-2014
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A simple and fast method to prepare robust superhydrophobic octadecylphosphonic acid (ODPA) coating on oxidized copper mesh for self-cleaning and oil/water separation is reported here. The substrate of the copper mesh was first oxidized by simple immersion in an aqueous solution of 1.0 M NaOH and 0.05 M K2S2O8 at room temperature for 30 min, which was then covered with micro- and nanoscale Cu(OH)2 on the surface. Subsequently, the oxidized copper mesh was immersed in 2 × 10(-4) M octadecylphosphonic acid/tetrahydrofuran (ODPA/THF) solution, an ODPA coating formed on the oxidised copper mesh. The ODPA coating formation process takes place rapidly, almost in 1 second, which makes the as-prepared mesh exhibit superhydrophobicity with the water contact angle of approximately 158.9° and superoleophilicity with the oil contact angle of 0°. Moreover, the as-prepared mesh has self-cleaning effect and can be repeatedly used to efficiently separate a series of oil/water mixtures like gasoline/water and diesel/water. Interestingly, straightforward oxidation of a copper substrate produces a "water-removing" type oil/water separation mesh with underwater superoleophobicity, whereas ODPA coating on the oxidized copper mesh produces an "oil-removing" type oil/water separation mesh with superhydrophobicity and superoleophilicity. This interesting conversion results from a small amount of ODPA and takes place very rapidly.
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Macrophage migration inhibitory factor triggers chemotaxis of CD74+CXCR2+ NKT cells in chemically induced IFN-?-mediated skin inflammation.
J. Immunol.
PUBLISHED: 08-29-2014
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IFN-? mediates chemically induced skin inflammation; however, the mechanism by which IFN-?-producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-?-producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with the MIF antagonist (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-?(+) NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-? production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPA-induced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74(+)CXCR2(+) NKT cells for IFN-? production.
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[Efficacy of inhaled nitric oxide in premature infants with hypoxic respiratory failure].
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 08-21-2014
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To investigate the safety and efficacy of low-concentration inhaled nitric oxide (NO) in the treatment of hypoxic respiratory failure (HRF) among premature infants.
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Gene expression profiling in human lung development: an abundant resource for lung adenocarcinoma prognosis.
PLoS ONE
PUBLISHED: 08-20-2014
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A tumor can be viewed as a special "organ" that undergoes aberrant and poorly regulated organogenesis. Progress in cancer prognosis and therapy might be facilitated by re-examining distinctive processes that operate during normal development, to elucidate the intrinsic features of cancer that are significantly obscured by its heterogeneity. The global gene expression signatures of 44 human lung tissues at four development stages from Asian descent and 69 lung adenocarcinoma (ADC) tissue samples from ethnic Chinese patients were profiled using microarrays. All of the genes were classified into 27 distinct groups based on their expression patterns (named as PTN1 to PTN27) during the developmental process. In lung ADC, genes whose expression levels decreased steadily during lung development (genes in PTN1) generally had their expression reactivated, while those with uniformly increasing expression levels (genes in PTN27) had their expression suppressed. The genes in PTN1 contain many n-gene signatures that are of prognostic value for lung ADC. The prognostic relevance of a 12-gene demonstrator for patient survival was characterized in five cohorts of healthy and ADC patients [ADC_CICAMS (n = 69, p = 0.007), ADC_PNAS (n = 125, p = 0.0063), ADC_GSE13213 (n = 117, p = 0.0027), ADC_GSE8894 (n =? 2, p = 0.01), and ADC_NCI (n = 282, p = 0.045)] and in four groups of stage I patients [ADC_CICAMS (n = 22, p = 0.017), ADC_PNAS (n = 76, p = 0.018), ADC_GSE13213 (n = 79, p = 0.02), and ADC_qPCR (n = 62, p = 0.006)]. In conclusion, by comparison of gene expression profiles during human lung developmental process and lung ADC progression, we revealed that the genes with a uniformly decreasing expression pattern during lung development are of enormous prognostic value for lung ADC.
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Mercury ion responsive wettability and oil/water separation.
ACS Appl Mater Interfaces
PUBLISHED: 08-13-2014
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A novel Hg(2+) responsive oil/water separation mesh with poly(acrylic acid) hydrogel coating is reported. The mesh can separate oil and water because of the superhydrophilicity of the poly(acrylic acid) hydrogel coating on the mesh, and switch the wettability based on the chelation between Hg(2+) and poly(acrylic acid) . The reversible change in oil contact angle of as-prepared mesh is about 149° after immersion in Hg(2+) solution. This mesh is an ideal candidate for oil-polluted water purification, especially for water that contains Hg(2+) contaminant.
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The effect of calcium phosphate composite scaffolds on the osteogenic differentiation of rabbit dental pulp stem cells.
J Biomed Mater Res A
PUBLISHED: 08-07-2014
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The objective of this study is to compare the effects of the two calcium phosphate composite scaffolds on the attachment, proliferation, and osteogenic differentiation of rabbit dental pulp stem cells (DPSCs). One nano-hydroxyapatite/collagen/poly (l-lactide) (nHAC/PLA), imitating the composition and the micro-structure characteristics of the natural bone, was made by Beijing Allgens Medical Science & Technology Co., Ltd. (China). The other beta-tricalcium phosphate (?-TCP), being fully interoperability globular pore structure, was provided by Shanghai Bio-lu Biomaterials Co, Ltd. (China). We compared the absorption water rate and the protein adsorption rate of two scaffolds and the characterization of DPSCs cultured on the culture plate and both scaffolds under osteogenic differentiation media (ODM) treatment. The constructs were then implanted subcutaneously into the back of severely combined immunodeficient (SCID) mice for 8 and 12 weeks to compare their bone formation capacity. The results showed that the ODM-treated DPSCs expressed osteocalcin (OCN), bone sialoprotein (BSP), type I collagen (COLI) and osteopontin (OPN) by immunofluorescence staining. Positive alkaline phosphatase (ALP) staining, calcium deposition and calcium nodules were also observed on the ODM-treated DPSCs. The absorption water rate and protein adsorption rate of nHAC/PLA was significantly higher than ?-TCP. The initial attachment of DPSCs seeded onto nHAC/PLA was significantly higher than that onto ?-TCP; and the proliferation rate of the cells was also significantly higher than that of ?-TCP on 1, 3, and 7 days of cell culture. The ALP activity, calcium/phosphorus content and mineral formation of DPSCs?+??-TCP were significantly higher than DPSCs?+?nHAC/LA. When implanted into the back of SCID mice, nHAC/PLA alone had no new bone formation, newly formed mature bone and osteoid were only observed in ?-TCP alone, DPSCs?+?nHAC/PLA and DPSCs?+??-TCP, and this three groups displayed increased bone formation over the 12-week period. The percentage of total bone formation area had no difference between DPSCs?+??-TCP and DPSCs?+?nHAC/PLA at each time point, but the percentage of mature bone formation area of DPSCs?+??-TCP was significantly higher than that of DPSCs?+?nHAC/PLA. Our results demonstrated that the DPSCs on nHAC/PLA had a better proliferation, and that the DPSCs on ?-TCP had a more mineralization in vitro, much more newly formed mature bones in vivo were presented in DPSCs?+??-TCP group. These findings have provided a further knowledge that scaffold architecture has different influence on the attachment, proliferation and differentiation of cells. This study may provide insight into the clinical periodontal bone tissue repair with DPSCs?+??-TCP construct. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part, 2014.
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Predicting Subtypes of Thymic Epithelial Tumors Using CT: New Perspective based on a Comprehensive Analysis of 216 Patients.
Sci Rep
PUBLISHED: 07-31-2014
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It is highly necessary to identify low versus high risk thymic epithelial tumors (TETs) before operation to guide optimal treatment strategies. Current CT diagnostic parameters could not effectively achieve this goal. We evaluated three parameters of CT scan in a cohort of 216 TETs patients. Parameters of contrast enhancement, risk of aggressiveness, and nodule with fibrous septum were evaluated in low (A, AB) versus high risk (B1, B2, B3 and thymic carcinoma) TETs. Grade of contrast enhancement showed predictive value in classifying low and high risk TETs well. A maximal contrast-enhanced range of 25.5?HU could produce 78.8% sensitivity and 68.5% specificity in determining low risk subtypes. Additionally, risk of aggressiveness parameter was demonstrated to be associated with TETs subtype (r = 0.801, P < 0.001) and may add confidence in determining low versus high risk subtypes. Furthermore, multiple nodule with fibrous septum could suggest subtype AB. Findings from this study support role of studied parameters of CT manifestations in predicting the low and high risk stages of TETs. These findings provide empirical evidence for incorporating these parameters in clinical practice for identifying TETs stage before operation, if validated in additional studies.
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Annexin A2 in renal cell carcinoma: Expression, function, and prognostic significance.
Urol. Oncol.
PUBLISHED: 07-31-2014
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Renal cell carcinoma (RCC) is the most lethal genitourinary cancer and intrinsically resistant to chemotherapy, radiotherapy, and hormone therapy. Annexin A2 (Anxa2) is a calcium-dependent phospholipid-binding protein found on various cell types that plays multiple roles in regulating cellular functions. In RCC, Anxa2 expression was correlated with tumor differentiation, clinical outcomes, and the metastatic potential; however, the underlying mechanisms remain obscure. This study investigated the role of Anxa2 in regulating tumorigenesis of RCC.
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A facile solvent-manipulated mesh for reversible oil/water separation.
ACS Appl Mater Interfaces
PUBLISHED: 07-11-2014
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A controllable oil/water separation mesh has been successfully developed and easily manipulated by immersion in a stearic acid ethanol solution and tetrahydrofuran with a very short period of time. The superhydrophilic and underwater superoleophobic mesh is first obtained via a one-step chemical oxidation and subsequently converts to superhydrophobic after it is immersed in an ethanol solution of stearic acid for 5 min. The surface wettability is regained to superhydrophilic quickly by immersion in tetrahydrofuran for 5 min. More importantly, the reversible superhydrophobic-and-superhydrophilic switching can be repeated multiple times with almost no visible morphology variation. Therefore, this approach provides potential application in controllable oil/water separation and opens up new perspectives in manipulation of various metallic oxide substrates.
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Effects of dietary arginine supplementation on growth performance, flesh quality, muscle antioxidant capacity and antioxidant-related signalling molecule expression in young grass carp (Ctenopharyngodon idella).
Food Chem
PUBLISHED: 06-28-2014
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Growth performance, flesh quality, antioxidant status and antioxidant-related signalling molecule expression in the muscle of young grass carp, which were fed graded levels of arginine (6.9-24.5 g/kg diet) for eight weeks, were investigated. Muscle protein, lipid and nitric oxide contents, shear force, hydroxyproline concentration, and pH were significantly improved by appropriate arginine. Cooking loss, lactate content, cathepsins activities, malondialdehyde and protein carbonyl contents exhibited an opposite tendency. Additionally, optimum arginine significantly enhanced glutathione content and the activities and gene expression of copper/zinc superoxide dismutase, catalase and glutathione peroxidase in muscle. Moreover, the expression levels of glutamate-cysteine ligase, target of rapamycin, ribosome protein S6 kinase 1, casein kinase 2 and NF-E2-related factor 2 in muscle were significantly elevated by appropriate arginine. However, optimum arginine significantly decreased Kelch-like ECH-associated protein 1 mRNA levels in muscle. In conclusion, arginine improved the flesh quality and muscle antioxidant capacity and regulated antioxidant-related signalling molecule expression.
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New 6% hydroxyethyl starch 130/0.4 does not increase blood loss during major abdominal surgery - a randomized, controlled trial.
J. Formos. Med. Assoc.
PUBLISHED: 06-26-2014
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Ideal fluid management during surgery still poses a clinical dilemma gauging the benefits and adverse effects. This randomized controlled trial compared the tissue perfusion and coagulation profiles under clinically equivalent hydroxyethyl starch (HES 130/0.4) and lactated Ringer's solution (LR).
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[Effect of the peri-implantitis on the biological function of osteoblasts obtained from the mandibles].
Hua Xi Kou Qiang Yi Xue Za Zhi
PUBLISHED: 06-03-2014
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To study the effect of peri-implantitis inflammatory microenvironment on the biological function of jaw bone osteoblasts.
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Fast Track Ultrasound Protocol to Detect Acute Complications After Totally Implantable Venous Access Device Placement.
Ann. Surg. Oncol.
PUBLISHED: 06-02-2014
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The role of ultrasound examination in detection of postprocedure complications from totally implantable venous access devices (TIVAD) placement is still uncertain. In a cohort of 665 cancer outpatients, we assessed a quick ultrasound examination protocol in early detection of mechanical complications of catheterization.
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Endogenous NO upon estradiol-17? stimulation and NO donor differentially regulate mitochondrial S-nitrosylation in endothelial cells.
Endocrinology
PUBLISHED: 05-30-2014
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Adduction of a nitric oxide (NO) moiety (NO(•)) to cysteines termed as S-nitrosylation (SNO) has emerged as a crucial mechanism for NO signaling crucial for mediating the vascular effects of estrogens. Mitochondrion is a known vascular risk factor; however, the effects of estrogens on mitochondrial SNO are incompletely understood. In this study we determined the effects of estradiol-17? (E2?) on mitochondrial protein SNO in primary human umbilical vein endothelial cells and compared the mitochondrial nitroso-proteomes in E2?- and a NO donor S-nitrosoglutathione (GSNO)-treated cells using a proteomics approach. Treatment with 10 nM E2? and 1 mM GSNO for 30 minutes significantly increased the levels of mitochondrial SNO-proteins. Subcellular localization of SNO-proteins showed mitochondria as the major cellular organelle for protein SNO in response to E2? and GSNO. E2? stimulated mitochondrial endothelial nitric oxide synthase (eNOS) phosphorylation and mitochondrial protein SNO that was enhanced by overexpression of mitochondrion or Golgi, but not membrane targeting eNOS constructs. We identified 11, 32, and 54 SNO-proteins in the mitochondria from the untreated, E2?-, and GSNO-treated human umbilical vein endothelial cells, respectively. Comparisons of the nitroso-proteomes revealed that common and different mitochondrial SNO-proteins were affected by endogenous NO on E2? stimulation and exogenous NO from donor. These SNO-proteins were associated with various mitochondrial functions, including energy and redox regulation, transport, iron homeostasis, translation, mitochondrial morphology, and apoptosis, etc. Collectively, we conclude that estrogens rapidly stimulate protein SNO in endothelial mitochondria via mitochondrial eNOS, providing a mechanism for mediating the vascular effects of estrogens.
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The impaired intestinal mucosal immune system by valine deficiency for young grass carp (Ctenopharyngodon idella) is associated with decreasing immune status and regulating tight junction proteins transcript abundance in the intestine.
Fish Shellfish Immunol.
PUBLISHED: 05-19-2014
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This study investigated the effects of dietary valine on the growth, intestinal immune response, tight junction proteins transcript abundance and gene expression of immune-related signaling molecules in the intestine of young grass carp (Ctenopharyngodon idella). Six iso-nitrogenous diets containing graded levels of valine (4.3-19.1 g kg(-)(1) diet) were fed to the fish for 8 weeks. The results showed that percentage weight gain (PWG), feed intake and feed efficiency of fish were the lowest in fish fed the valine-deficient diet (P < 0.05). In addition, valine deficiency decreased lysozyme, acid phosphatase activities and complement 3 content in the intestine (P < 0.05), down-regulated mRNA levels of interleukin 10, transforming growth factor ?1, I?B? and target of rapamycin (TOR) (P < 0.05), and up-regulated tumor necrosis factor ?, interleukin 8 and nuclear factor ?B P65 (NF-?B P65) gene expression (P < 0.05). Additionally, valine deficiency significantly decreased transcript of Occludin, Claudin b, Claudin c, Claudin 3, and ZO-1 (P < 0.05), and improved Claudin 15 expression in the fish intestine (P < 0.05). However, valine did not have a significant effect on expression of Claudin 12 in the intestine of grass carp (P > 0.05). In conclusion, valine deficiency decreased fish growth and intestinal immune status, as well as regulated gene expression of tight junction proteins, NF-?B P65, I?B? and TOR in the fish intestine. Based on the quadratic regression analysis of lysozyme activity or PWG, the dietary valine requirement of young grass carp (268-679 g) were established to be 14.47 g kg(-1) diet (4.82 g 100 g(-1) CP) or 14.00 g kg(-1) diet (4.77 g 100 g(-1) CP), respectively.
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Role of p38 MAPK in enhanced human cancer cells killing by the combination of aspirin and ABT-737.
J. Cell. Mol. Med.
PUBLISHED: 05-16-2014
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Regular use of aspirin after diagnosis is associated with longer survival among patients with mutated-PIK3CA colorectal cancer, but not among patients with wild-type PIK3CA cancer. In this study, we showed that clinically achievable concentrations of aspirin and ABT-737 in combination could induce a synergistic growth arrest in several human PIK3CA wild-type cancer cells. In addition, our results also demonstrated that long-term combination treatment with aspirin and ABT-737 could synergistically induce apoptosis both in A549 and H1299 cells. In the meanwhile, short-term aspirin plus ABT-737 combination treatment induced a greater autophagic response than did either drug alone and the combination-induced autophagy switched from a cytoprotective signal to a death-promoting signal. Furthermore, we showed that p38 acted as a switch between two different types of cell death (autophagy and apoptosis) induced by aspirin plus ABT-737. Moreover, the increased anti-cancer efficacy of aspirin combined with ABT-737 was further validated in a human lung cancer A549 xenograft model. We hope that this synergy may contribute to failure of aspirin cancer therapy and ultimately lead to efficacious regimens for cancer therapy.
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Chemical constituents of Abies delavayi.
Phytochemistry
PUBLISHED: 05-12-2014
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Systematic phytochemical investigations on Abies delavayi afforded 110 compounds, including 49 terpenoids, 13 lignans, 20 flavonoids, three coumarins, and 25 other chemical constituents. By detailed analysis of one- and two-dimensional NMR spectroscopic and high-resolution mass spectrometric data, 10 previously unreported compounds were identified: they comprised three sesquiterpenoids, two diterpenoids, one triterpenoid, one monoterpenoid, one flavonoid, and two phenols. These 10 compounds and some previously known ones were subjected to two cytotoxic bioassays against three human tumor cell lines and NO production inhibition on RAW264.7 macrophages, respectively. (25R)-24,25-Dihydroabieslactone had the strongest cytotoxic activity against Colo-205 cells with an IC50 value of 19.0±3.7?g/mL. (+)-T-cadinol, 8,11,13-abietatrien-15-ol-18-yl acetate, 18-acetoxy-13-epi-manool, imperatorin, bergapten, and 5,7-O-dimethyl poriol exhibited weak inhibitory activity against LPS-induced NO production in RAW264.7 macrophages with IC50 values of approximately 50?g/mL.
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An increase in integrin-linked kinase non-canonically confers NF-¿B-mediated growth advantages to gastric cancer cells by activating ERK1/2.
Cell Commun. Signal
PUBLISHED: 05-07-2014
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BackgroundIncreased activity or expression of integrin-linked kinase (ILK), which regulates cell adhesion, migration, and proliferation, leads to oncogenesis. We identified the molecular basis for the regulation of ILK and its alternative role in conferring ERK1/2/NF-¿B-mediated growth advantages to gastric cancer cells.ResultsInhibiting ILK with short hairpin RNA or T315, a putative ILK inhibitor, abolished NF-¿B-mediated the growth in the human gastric cancer cells AGS, SNU-1, MKN45, and GES-1. ILK stimulated Ras activity to activate the c-Raf/MEK1/2/ERK1/2/ribosomal S6 kinase/inhibitor of ¿B¿/NF-¿B signaling by facilitating the formation of the IQ motif-containing GTPase-activating protein 1 (IQGAP1)¿Ras complex. Forced enzymatic ILK expression promoted cell growth by facilitating ERK1/2/NF-¿B signaling. PI3K activation or decreased PTEN expression prolonged ERK1/2 activation by protecting ILK from proteasome-mediated degradation. C-terminus of heat shock cognate 70 interacting protein, an HSP90-associated E3 ubiquitin ligase, mediated ILK ubiquitination to control PI3K- and HSP90-regulated ILK stabilization and signaling. In addition to cell growth, the identified pathway promoted cell migration and reduced the sensitivity of gastric cancer cells to the anticancer agents 5-fluorouracil and cisplatin. Additionally, exogenous administration of EGF as well as overexpression of EGFR triggered ILK- and IQGAP1-regulated ERK1/2/NF-¿B activation, cell growth, and migration.ConclusionAn increase in ILK non-canonically promotes ERK1/2/NF-¿B activation and leads to the growth of gastric cancer cells.
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Preparation and identification of transfer factor specific to Staphylococcus aureus in vitro.
Biotechnol. Appl. Biochem.
PUBLISHED: 05-07-2014
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The objective of the study was to explore the methods for preparing transfer factor specific to Staphylococcus aureus (SA-STF) in vitro. Under the optimum conditions, the spleen cells of rabbits were immunized with SA in vitro to prepare SA-STF, and the immune activities were identified with the phagocytosis and sterilization, skin delayed-type hypersensitivity, and immune protection tests. The concentration of polypeptide was 2.26 ± 0.27 mg/mL, and ribose was 0.684 ± 0.094 mg/mL. The phagocytosis and sterilization rates of the STF group were 70.9 ± 12.4% and 62.1 ± 12.2%, respectively, and compared with the non-specific transfer factor (NTF) group, there were no significant differences (P = 0.074 and 0.069, respectively). The skin was inflamed and marked nodules formed at the injection site in the mice of the STF group rather than the NTF and control groups. The survival rate of the STF-1 group was significantly higher than the survival rates of the STF-2 (P = 0.024) and NTF groups (P = 0.016). SA-STF was prepared and characterized successfully in vitro, and it probably is a biological candidate for therapy or adjuvant therapy for diseases caused by Staphylococcus aureus.
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Three-dimensional chemical imaging of skin using stimulated Raman scattering microscopy.
J Biomed Opt
PUBLISHED: 04-30-2014
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Stimulated Raman scattering (SRS) microscopy is used to generate structural and chemical three-dimensional images of native skin. We employed SRS microscopy to investigate the microanatomical features of skin and penetration of topically applied materials. Image depth stacks are collected at distinct wavelengths corresponding to vibrational modes of proteins, lipids, and water in the skin. We observed that corneocytes in stratum corneum are grouped together in clusters, 100 to 250 ?m in diameter, separated by 10- to 25-?m-wide microanatomical skin-folds called canyons. These canyons occasionally extend down to depths comparable to that of the dermal-epidermal junction below the flat surface regions in porcine and human skin. SRS imaging shows the distribution of chemical species within cell clusters and canyons. Water is predominately located within the cell clusters, and its concentration rapidly increases at the transition from stratum corneum to viable epidermis. Canyons do not contain detectable levels of water and are rich in lipid material. Oleic acid-d34 applied to the skin surface lines the canyons down to a depth of 50 ?m below the surface of the skin. This observation could have implications on the evaluation of penetration profiles of bioactive materials measured using traditional methods, such as tape-stripping.
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Copper exposure induces oxidative injury, disturbs the antioxidant system and changes the Nrf2/ARE (CuZnSOD) signaling in the fish brain: protective effects of myo-inositol.
Aquat. Toxicol.
PUBLISHED: 04-28-2014
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The brain is the center of the nervous system in all vertebrates, and homeostasis of the brain is crucial for fish survival. Copper (Cu) is essential for normal cellular processes in most eukaryotic organisms but is toxic in excess. Although Cu is indicated as a potent neurotoxicant, information regarding its threat to fish brain and underlying mechanisms is still scarce. In accordance, the objective of this study was to assess the effects and the potential mechanism of Cu toxicity by evaluating brain oxidative status, the enzymatic and mRNA levels of antioxidant genes, as well as the Nrf2/ARE signaling in the brain of fish after Cu exposure. The protective effects of myo-inositol (MI) against subsequent Cu exposure were also investigated. The results indicate that induction of oxidative stress by Cu is shown by increases in brain ROS production, lipid peroxidation and protein oxidation, which are accompanied by depletions of antioxidants, including total superoxide dismutase (T-SOD), CuZnSOD, glutathione-S-transferase (GST) and glutathione reductase (GR) activities and glutathione (GSH) content. Cu exposure increased the catalase (CAT) and glutathione peroxidase (GPx) activities. Further molecular results showed that Cu exposure up-regulated CuZnSOD, GPx1a and GR mRNA levels, suggesting an adaptive mechanism against stress. Moreover, Cu exposure increased fish brain Nrf2 nuclear accumulation and increased its ability of binding to ARE (CuZnSOD), which supported the increased CuZnSOD mRNA levels. In addition, Cu exposure caused increases of the expression of the Nrf2, Maf G1 (rather than Maf G2 gene) and PKCd genes, suggesting that de novo synthesis of those factors is required for the protracted induction of such antioxidant genes. However, the modulation of Keap1a (rather than Keap1b) of fish brain under Cu exposure might be used to turn off of the signaling cascade and avoid harmful effects. Interestingly, pre-treatment of fish with MI prevented the fish brain from Cu-induced oxidative damages mainly by increasing the GSH content and CuZnSOD and GST activities. Summarily, this study indicates that although Cu stimulates adaptive increases in the expression of some antioxidant enzyme genes through Nrf2/ARE signaling, it also induces oxidation and the depletion of most of antioxidant enzyme activities and GSH content due to the increase of ROS production, and MI protects the fish brain against Cu toxicity.
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Beta2-adrenergic agonist use and the risk of multiple sclerosis: a total population-based case-control study.
Mult. Scler.
PUBLISHED: 04-14-2014
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The aim of this study was to investigate whether the use of fenoterol, a beta2-adrenergic agonist, was associated with multiple sclerosis (MS) risk by conducting a total population-based case-control study in Taiwan.
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S-nitrosylation of Cofilin-1 Serves as a Novel Pathway for VEGF-stimulated Endothelial Cell Migration.
J. Cell. Physiol.
PUBLISHED: 04-11-2014
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Nitric oxide (NO) derived from endothelial NO synthase (eNOS) mediates vascular endothelial growth factor (VEGF)-stimulated endothelial cytoskeleton remodeling and migration; however, the underlying mechanisms are elusive. Covalent adduction of a NO moiety (NO(•) ) to cysteines called S-nitrosylation (SNO) is a key NO signaling pathway. The small actin-binding protein cofilin-1 (CFL1) is essential for actin cytoskeleton remodeling. We investigated whether S-nitrosylation regulates CFL1 function and endothelial cytoskeleton remodeling and migration upon VEGF stimulation. VEGF rapidly stimulated S-nitrosylation of CFL1, which was blocked by NO Synthase inhibition and eNOS knockdown by specific eNOS-siRNA. Cys80 and Cys139 were identified as the major SNO-sites in CFL1 by LC-MS/MS. The actin severing activity of recombinant SNO-mimetic CFL1 (C80/139A DMA-CFL1), but not SNO-deficient CFL1 (C80/139S DMS-CFL1), was significantly greater than that of wild-type CFL1 (wt-CFL1). When wt-CFL1 and its mutants were overexpressed in endothelial cells, basal actin bound wt-CFL1 was undetectable but significantly increased by VEGF; basal actin bound DMA-CFL1 was readily high and basal actin bound DMS-CFL1 was detectable but low, and both were unresponsive to VEGF. Treatment with VEGF significantly increased filamentous (F-) actin and filopodium formation and cell migration in endothelial cells. Overexpression of wt-CFL1 inhibited VEGF-induced F-actin formation. Overexpression of DMA but not DMS CFL1 decreased basal but not VEGF-stimulated F-actin formation. Overexpression of DMA but not DMS CFL1 suppressed VEGF-stimulated filopodium formation and migration in endothelial cells. Thus, S-nitrosylation of CFL1 provides a novel signaling pathway post-NO biosynthesis via eNOS-derived NO for endothelial cytoskeleton remodeling and migration upon VEGF stimulation. J. Cell. Biochem. © 2014 Wiley Periodicals, Inc.
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Projection target-specific action of nicotine in the caudal nucleus of the solitary tract.
J. Neurosci. Res.
PUBLISHED: 04-08-2014
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The brainstem nucleus of the solitary tract (NTS) is the key integrating relay in the central processing of sensory information from the thoracic and from most subdiaphragmatic viscera. Modulation of neuronal excitability and synaptic activity in the NTS by nicotinic agents can have potent effects on vital physiological functions, such as feeding, digestion, respiration, and blood circulation. Caudal NTS neurons demonstrate considerable heterogeneity in projection targets, synaptic properties, and expression of nicotinic acetylcholine receptors (nAChRs). However, despite its heterogeneity, the caudal NTS may contain discrete subsets of neurons with unique projection target-specific properties. To test this hypothesis, we used in vivo fluorescent tracing and ex vivo patch-clamp electrophysiology to evaluate responsiveness to nicotine of anatomically identified caudal NTS neurons that project to the hypothalamic paraventricular nucleus (PVN) and the brainstem caudal ventrolateral medulla (CVLM). The results of this study demonstrate that responsiveness to nicotine correlates with where the neurons project. Specifically, PVN-projecting caudal NTS neurons respond to nicotine only presynaptically (i.e., via activation of presynaptic nAChRs and potentiation of synaptic release of glutamate), suggesting indirect, glutamate-dependent effects of nicotine on the PVN-projecting NTS circuitry. By contrast, CVLM-projecting caudal NTS neurons exhibit only limited presynaptic, but dominant somatodendritic, responsiveness to nicotine, suggesting that the effects of nicotine on the CVLM-projecting NTS circuitry are direct and largely glutamate independent. Understanding the relationships among function-specific brainstem/hypothalamic neuronal networks, nuclei, and individual neurons could help develop therapies targeting identifiable neuronal circuits to offset impaired autonomic homeostasis.
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Oxidative damage repair by glutamine in fish enterocytes.
Fish Physiol. Biochem.
PUBLISHED: 04-04-2014
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Fish intestine is very sensitive to oxidative damage. Repair of damaged enterocytes may be involved to restore normal function of fish intestine. However, studies of fish enterocyte repair are scarce. The present study aimed to investigate the potential repair role of glutamine after a H2O2 challenge. In this study, fish enterocytes were post-treated with graded levels of glutamine (0, 4, 8, 12 and 20 mM of glutamine) after expose to 100 ?M H2O2. The basal control cells were kept in the glutamine-free minimum essential medium only. Results showed that the H2O2-induced decreases in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide optical density, alkaline phosphatase and Na(+), K(+)-ATPase activities were completely restored by subsequent glutamine treatments. In addition, cellular injury (lactate dehydrogenase), lipid peroxidation (malondialdehyde) and protein oxidation (protein carbonyls) caused by H2O2 were reversed by subsequent glutamine treatments. Furthermore, the H2O2-induced decreases in glutathione contents, glutathione reductase, superoxide dismutase and glutathione peroxidase activities were completely restored by subsequent glutamine treatments. In summary, the present study indicated that glutamine improved the repair activity in fish enterocytes after challenge with H2O2.
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Dietary tryptophan modulates intestinal immune response, barrier function, antioxidant status and gene expression of TOR and Nrf2 in young grass carp (Ctenopharyngodon idella).
Fish Shellfish Immunol.
PUBLISHED: 02-24-2014
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The present research evaluated the effects of dietary tryptophan (Trp) on growth performance, intestinal mucosal immune, barrier function and antioxidant capacity and gene expression of young grass carp (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of Trp at 0.7(control), 1.7, 3.1, 4.0, 5.2 and 6.1 g kg(-1) diet for 8 weeks. The results showed that Trp supplementation significantly enhanced the percent weight gain (PWG), feed intake and feed efficiency (P < 0.05), and decreased the plasma ammonia content (PAC) (P < 0.05). After the 8-week feeding trail, an environmental copper exposure trail was conducted for 4 days. Results from the copper exposure trail showed that dietary Trp enhanced the lysozyme, acid phosphatase activities and complement 3 contents in the intestine of young grass carp (P < 0.05). In addition, Trp supplementation increased the copper/zinc superoxide dismutase (SOD1), glutathione peroxidase (GPx) activities and glutathione contents (P < 0.05), and decreased the protein carbonyl and malondialdehyde contents (P < 0.05). Furthermore, the relative gene expression levels of interleukin 10, transforming growth factor-?1, occludin, zonula occludens 1, claudin-b, -c, and -3, SOD1, GPx and NF-E2-related factor 2 in the intestine were significantly up-regulated with increasing of dietary Trp up to a certain level (P < 0.05). Conversely, the mRNA levels of tumor necrosis factor ?, interleukin 8, target of rapamycin, Kelch-like-ECH-associated protein 1, claudin-12 and -15a in the intestine were significantly down-regulated by Trp (P < 0.05). Collectively, appropriate dietary Trp level improves fish growth, intestinal immune response, barrier function and antioxidant status, and regulated the mRNA levels of related signal molecules of young grass carp. Based on the quadratic regression analysis of the PWG and PAC, the dietary Trp requirement of young grass carp (287-699 g) was estimated to be 3.81 g kg(-1) diet (12.7 g kg(-1) protein) and 3.89 g kg(-1) diet (13.0 g kg(-1) protein), respectively.
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Activation of p38 MAPK-regulated Bcl-xL signaling increases survival against zoledronic acid-induced apoptosis in osteoclast precursors.
Bone
PUBLISHED: 02-24-2014
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The nitrogen-containing bisphosphonate zoledronic acid (ZA) induces apoptosis in osteoclasts and inhibits osteoclast-mediated bone resorption. It is widely used to treat osteoporosis. However, some patients are less responsive to ZA treatment, and the mechanisms of resistance are still unclear. Here, we identified that murine osteoclast precursors may develop resistance to ZA-induced apoptosis. These resistant cells survived the apoptotic effect of ZA following an increase in anti-apoptotic Bcl-xL. Pharmacologically inhibiting Bcl-xL facilitated ZA-induced apoptosis. Treatment with ZA activated p38 MAPK, increasing Bcl-xL expression and cell survival. Nuclear import of ?-catenin regulated by p38 MAPK determined Bcl-xL mRNA expression and cell survival in response to ZA. ZA also inactivated glycogen synthase kinase (GSK)-3?, a negative upstream regulator of ?-catenin, in a p38 MAPK-mediated manner. Synergistic pharmacological inhibition of p38 MAPK with ZA attenuated receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation and facilitated ZA-induced apoptosis. These results demonstrate that elevated Bcl-xL expression mediated by p38 MAPK-regulated GSK-3?/?-catenin signaling is required for cell survival of ZA-induced apoptosis in both osteoclast precursors and osteoclasts. Finally, we demonstrated that inhibiting p38 MAPK-mediated pathway enhanced ZA effect on increasing the bone mineral density of ovariectomized mice. This result suggests that targeting these pathways may represent a potential therapeutic strategy.
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Inhibiting glucosylceramide synthase facilitates the radiosensitizing effects of vinorelbine in lung adenocarcinoma cells.
Cancer Lett.
PUBLISHED: 02-11-2014
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The standard treatment regimen for patients diagnosed with non-small cell lung cancer (NSCLC) with locally advanced stage III disease is concurrent chemoradiotherapy (CCRT). This study investigated the molecular effects of vinca alkaloid vinorelbine (VNR)-based CCRT. We reviewed the records of 68 patients with stage III NSCLC: 42 patients received VNR-based CCRT, and 26 were treated with radiation alone. Human lung adenocarcinoma cells were used in this study to investigate the molecular effects of glucosylceramide synthase inhibition on VNR-based CCRT. There was response rate of 66.7% with CCRT, which was better than the response rate observed with radiation alone (30.8%; P<0.001). CCRT caused an increase in cell cycle arrest at G2/M phase accompanied by apoptosis. Oxidative c-Jun N-terminal kinase (JNK) activation was involved in the increased apoptosis levels but not the cell cycle arrest. CCRT also induced an increase in ceramide accompanied by a decrease in glucosylceramide that was positively correlated with the cytotoxic effects. Pharmacologically inhibiting glucosylceramide synthase facilitated VNR- and CCRT-induced apoptosis by promoting the JNK pathway. Inhibiting glucosylceramide synthase facilitates the radiosensitizing effects of VNR by promoting JNK-mediated apoptosis in lung adenocarcinoma cells.
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Annexin A2: its molecular regulation and cellular expression in cancer development.
Dis. Markers
PUBLISHED: 01-23-2014
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Annexin A2 (ANXA2) orchestrates multiple biologic processes and clinical associations, especially in cancer progression. The structure of ANXA2 affects its cellular localization and function. However, posttranslational modification and protease-mediated N-terminal cleavage also play critical roles in regulating ANXA2. ANXA2 expression levels vary among different types of cancers. With some cancers, ANXA2 can be used for the detection and diagnosis of cancer and for monitoring cancer progression. ANXA2 is also required for drug-resistance. This review discusses the feasibility of ANXA2 which is active in cancer development and can be a therapeutic target in cancer management.
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Rosiglitazone regulates anti-inflammation and growth inhibition via PTEN.
Biomed Res Int
PUBLISHED: 01-18-2014
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Peroxisome proliferator-activated receptor gamma (PPAR?) agonist has anti-inflammatory and anticancer properties. However, the mechanisms by which PPAR? agonist rosiglitazone interferes with inflammation and cancer via phosphatase and tensin homolog-(PTEN)-dependent pathway remain unclear. We found that lower doses (<25? ? M) of rosiglitazone significantly inhibited lipopolysaccharide-(LPS)-induced nitric oxide (NO) release (via inducible nitric oxide synthase, iNOS), prostaglandin E2 (PGE2) production (via cyclooxygenase-2, COX-2), and activation of Akt in RAW 264.7 murine macrophages. However, rosiglitazone did not inhibit the production of reactive oxygen species (ROS). In PTEN knockdown (shPTEN) cells exposed to LPS, rosiglitazone did not inhibit NO release, PGE2 production, and activation of Akt. These cells had elevated basal levels of iNOS, COX-2, and ROS. However, higher doses (25-100? ? M) of rosiglitazone, without LPS stimulation, did not block NO release and PGE2 productions, but they inhibited p38 MAPK phosphorylation and blocked ROS generation in shPTEN cells. In addition, rosiglitazone caused G1 arrest and reduced the number of cells in S?+?G2/M phase, leading to growth inhibition. These results indicate that the anti-inflammatory property of rosiglitazone is related to regulation of PTEN independent of inhibition on ROS production. However, rosiglitazone affected the dependence of PTEN-deficient cell growth on ROS.
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Phylogenetic analysis of STK gene family and Usp domain in maize.
Mol. Biol. Rep.
PUBLISHED: 01-11-2014
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Serine and threonine kinase STK1 and STK2 play an important regulatory role in the process of pollen development in maize. Six homologous sequences which were similar with STK1 and STK2 having more than 80 % similarity were found at NCBI, and they all belong to STK gene family. Phylogenetic analysis showed that STK family in maize might belong to RLK family. In STK family, gene duplication event was occurred during evolutionary process, and experienced purifying selection after gene duplication and the time of gene duplication was about 12 million years ago. The domains of STK family belongs to single transmembrane protein, which have intracellular conserved kinase catalytic domain and extracellular receptor domain on N-terminal. The evolution of intracellular selection was faster than extracellular selection, and positive selection or weak purifying selection play an important role. Analyzing its unique Usp domain we found that it was located between sensor domain at N-terminal and catalytic domain at C-terminal, which belongs to hydrophobic protein with several phosphorylation sites, acting on serine and threonine protein phosphorylation. The kinship of Usp domain in STK family was close to 35-like protein containing U-box domain, predicting that they might belong to the same family with a similar structure and function, so that we can predict the function of Usp domain in STK family.
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Reactive oxygen species-regulated glycogen synthase kinase-3? activation contributes to all-trans retinoic acid-induced apoptosis in granulocyte-differentiated HL60 cells.
Biochem. Pharmacol.
PUBLISHED: 01-06-2014
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All-trans retionic acid (ATRA) treatment confers disease remission in acute promyelocytic leukemia (APL) patients by inducing granulocytic differentiation, which is followed by cell apoptosis. Although glycogen synthase kinase (GSK)-3? is known to be required for spontaneous cell death in neutrophils, the requirement of GSK-3? activation for the apoptotic effects remains unknown. This question is addressed in the present study using a model of ATRA-induced granulocytic differentiation and apoptosis in APL HL60 cells. ATRA at a therapeutic concentration (1 ?M) induced granulocytic differentiation, followed by apoptosis. ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3?. Pharmacologically and genetically inhibiting GSK-3? effectively retarded ATRA-induced Mcl-1 degradation and apoptosis. Additional differentiation inducers, phorbol 12-myristate 13-acetate and dimethyl sulfoxide, also triggered GSK-3?-dependent apoptosis. Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3? activation and cell apoptosis. This study indicates that ROS initiate GSK-3?-dependent apoptosis in granulocyte-differentiated cells after long-term ATRA treatment.
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Injury Location and Mechanism for Complex Regional Pain Syndrome: A Nationwide Population-Based Case-Control Study in Taiwan.
Pain Pract
PUBLISHED: 01-03-2014
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Few studies have investigated the relationship between injury location, mechanism and their association with complex regional pain syndrome (CRPS). We conducted a nationwide database survey to explore this issue.
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Suprafenacine, an indazole-hydrazide agent, targets cancer cells through microtubule destabilization.
PLoS ONE
PUBLISHED: 01-01-2014
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Microtubules are a highly validated target in cancer therapy. However, the clinical development of tubulin binding agents (TBA) has been hampered by toxicity and chemoresistance issues and has necessitated the search for new TBAs. Here, we report the identification of a novel cell permeable, tubulin-destabilizing molecule - 4,5,6,7-tetrahydro-1H-indazole-3-carboxylic acid [1p-tolyl-meth-(E)-ylidene]-hydrazide (termed as Suprafenacine, SRF). SRF, identified by in silico screening of annotated chemical libraries, was shown to bind microtubules at the colchicine-binding site and inhibit polymerization. This led to G2/M cell cycle arrest and cell death via a mitochondria-mediated apoptotic pathway. Cell death was preceded by loss of mitochondrial membrane potential, JNK - mediated phosphorylation of Bcl-2 and Bad, and activation of caspase-3. Intriguingly, SRF was found to selectively inhibit cancer cell proliferation and was effective against drug-resistant cancer cells by virtue of its ability to bypass the multidrug resistance transporter P-glycoprotein. Taken together, our results suggest that SRF has potential as a chemotherapeutic agent for cancer treatment and provides an alternate scaffold for the development of improved anti-cancer agents.
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The IQD Gene Family in Soybean: Structure, Phylogeny, Evolution and Expression.
PLoS ONE
PUBLISHED: 01-01-2014
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Members of the plant-specific IQ67-domain (IQD) protein family are involved in plant development and the basal defense response. Although systematic characterization of this family has been carried out in Arabidopsis, tomato (Solanum lycopersicum), Brachypodium distachyon and rice (Oryza sativa), systematic analysis and expression profiling of this gene family in soybean (Glycine max) have not previously been reported. In this study, we identified and structurally characterized IQD genes in the soybean genome. A complete set of 67 soybean IQD genes (GmIQD1-67) was identified using Blast search tools, and the genes were clustered into four subfamilies (IQD I-IV) based on phylogeny. These soybean IQD genes are distributed unevenly across all 20 chromosomes, with 30 segmental duplication events, suggesting that segmental duplication has played a major role in the expansion of the soybean IQD gene family. Analysis of the Ka/Ks ratios showed that the duplicated genes of the GmIQD family primarily underwent purifying selection. Microsynteny was detected in most pairs: genes in clade 1-3 might be present in genome regions that were inverted, expanded or contracted after the divergence; most gene pairs in clade 4 showed high conservation with little rearrangement among these gene-residing regions. Of the soybean IQD genes examined, six were most highly expressed in young leaves, six in flowers, one in roots and two in nodules. Our qRT-PCR analysis of 24 soybean IQD III genes confirmed that these genes are regulated by MeJA stress. Our findings present a comprehensive overview of the soybean IQD gene family and provide insights into the evolution of this family. In addition, this work lays a solid foundation for further experiments aimed at determining the biological functions of soybean IQD genes in growth and development.
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Autophagy facilitates antibody-enhanced dengue virus infection in human pre-basophil/mast cells.
PLoS ONE
PUBLISHED: 01-01-2014
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Dengue virus (DENV) infection can cause severe hemorrhagic disease in humans. Although the pathogenic mechanisms underlying severe DENV disease remain unclear, one of the possible contributing factors is antibody-dependent enhancement (ADE) which occurs when sub-neutralizing antibodies derived from a previous DENV infection enhance viral infection through interaction between virus-antibody complexes and FcR-bearing cells, such as macrophages and basophil/mast cells. Although recent reports showed that DENV induces autophagy, the relationship between antibody-enhanced DENV infection and autophagy is not clear.
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The Alaris auditory evoked potential monitor as an indicator of seizure inducibility and duration during electroconvulsive therapy: an observational study.
BMC Anesthesiol
PUBLISHED: 01-01-2014
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Precise control of anesthetic depth during electroconvulsive therapy (ECT) is crucial because most intravenous anesthetics have anticonvulsant effects. In this study, we investigated the association between anesthetic depth measured by the Alaris auditory evoked potential index (AAI) and seizure inducibility and seizure duration during ECT.
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Protection against dengue virus infection in mice by administration of antibodies against modified nonstructural protein 1.
PLoS ONE
PUBLISHED: 01-01-2014
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Infection with dengue virus (DENV) may cause life-threatening disease with thrombocytopenia and vascular leakage which are related to dysfunction of platelets and endothelial cells. We previously showed that antibodies (Abs) against DENV nonstructural protein 1 (NS1) cross-react with human platelets and endothelial cells, leading to functional disturbances. Based on sequence homology analysis, the C-terminal region of DENV NS1 protein contains cross-reactive epitopes. For safety in vaccine development, the cross-reactive epitopes of DENV NS1 protein should be deleted or modified.
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[Analyzed the molecular interaction network of tumor suppressor gene 14-3-3 sigma in lung cancer cell based on stable isotope labeling by amino acids in cell culture technology].
Zhonghua Yu Fang Yi Xue Za Zhi
PUBLISHED: 11-20-2013
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To analysis the molecular interaction network of 14-3-3 sigma in non small cell lung cancer (NSCLC) cells.
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Bio-Inspired Anti-Oil-Fouling Chitosan-Coated Mesh for Oil/Water Separation Suitable for Broad pH Range and Hyper-Saline Environments.
ACS Appl Mater Interfaces
PUBLISHED: 11-11-2013
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Here, we report a bio-inspired chitosan (CS)-based mesh with high separation efficiency, oil-fouling repellency, and stability in a complex liquid environment. The surface of the CS coating maintains underwater superoleophobicity and low oil adhesion (<1 ?N) in pure water and hyper-saline solutions, and it can keep stable special wettability in broad pH range environments after the CS mesh is fully cross-linked with glutaraldehyde and then reduced by sodium borohydride to form a stable carbon-nitrogen single bond. The separation process is solely gravity-driven, and the mesh can separate a range of different oil/water mixtures with >99% separation efficiency in hyper-saline and broad pH range conditions. We envision that such a separation method will be useful in oil spill cleanup and industrial oily wastewater treatment in extreme environments.
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[Roles of cardiac mast cells and Toll-like receptor 4 in viral myocarditis among mice].
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 10-18-2013
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To investigate the role and significance of cardiac mast cells and Toll-like receptor 4 (TLR4) in the development and progression of viral myocarditis (VMC).
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[Assessment of prognostic and influencing factors in elderly patients with multiple organ dysfunction syndrome].
Zhonghua Yi Xue Za Zhi
PUBLISHED: 10-16-2013
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To preliminarily assess the prognosis of patients with multiple organ dysfunction syndrome (MODSE) and analyze their influencing factors.
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Defining the protein-protein interaction network of the human hippo pathway.
Mol. Cell Proteomics
PUBLISHED: 10-14-2013
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The Hippo pathway, which is conserved from Drosophila to mammals, has been recognized as a tumor suppressor signaling pathway governing cell proliferation and apoptosis, two key events involved in organ size control and tumorigenesis. Although several upstream regulators, the conserved kinase cascade and key downstream effectors including nuclear transcriptional factors have been defined, the global organization of this signaling pathway is not been fully understood. Thus, we conducted a proteomic analysis of human Hippo pathway, which revealed the involvement of an extensive protein-protein interaction network in this pathway. The mass spectrometry data were deposited to ProteomeXchange with identifier PXD000415. Our data suggest that 550 interactions within 343 unique protein components constitute the central protein-protein interaction landscape of human Hippo pathway. Our study provides a glimpse into the global organization of Hippo pathway, reveals previously unknown interactions within this pathway, and uncovers new potential components involved in the regulation of this pathway. Understanding these interactions will help us further dissect the Hippo signaling-pathway and extend our knowledge of organ size control.
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High-intensity emergency department visits increased in California, 2002-09.
Health Aff (Millwood)
PUBLISHED: 10-09-2013
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Increasing use of the emergency department (ED) is well documented, but little is known about the type and severity of ED visits or their distribution across safety-net and non-safety-net hospitals. We examined the rates of high-intensity ED visits--characterized by their use of advanced imaging, consultations with specialists, the evaluation of multiple systems, and highly complex medical decision making--by patients with a severe, potentially life-threatening illness in California from 2002 through 2009. Total annual ED visits increased by 25 percent, from 9.0 million to 11.3 million, but high-intensity ED visits nearly doubled, increasing 87 percent from 778,000 to 1.5 million per year. The percentage of ED visits with high-intensity care increased from 9 percent to 13 percent (a relative increase of 44 percent). Annual ED admissions increased by 39 percent overall; most of this increase was attributable to high-intensity ED admissions, which increased by 88 percent. Safety-net EDs experienced an increase in high-intensity visits of 157 percent, compared to an increase of 61 percent at non-safety-net EDs. These findings suggest a trend toward intensification of ED care, particularly at safety-net hospitals, whose patients may have limited access to care outside the ED.
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Size tunable fluorescent nano-graphite oxides: preparation and cell imaging applications.
Phys Chem Chem Phys
PUBLISHED: 10-08-2013
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Fluorescent nano-graphite oxides (NGO) with different size distribution were prepared via a one-pot hydrothermal route using ultrasmall graphite powder as starting material and subsequently separated using dialysis tubes with different molecular weight cutoff. The biomedical applications of these NGO for cell imaging were further investigated. Fourier transform infrared spectra demonstrated that many functional groups including the hydroxyl group, carboxyl group and epoxy group were present on NGO, which endowed them with good water solubility. These NGO showed size-dependent photoluminescence and excellent biocompatibility with A549 cells. As evidenced by laser scanning confocal microscopy images, NGO could be internalized by A549 cells and located in the cytoplasm. Given their good water solubility, size tunable photoluminescence and excellent biocompatibility, these NGO should be promising for bioimaging and various biomedical applications.
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The effects of dietary thiamin on oxidative damage and antioxidant defence of juvenile fish.
Fish Physiol. Biochem.
PUBLISHED: 10-03-2013
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The present study explored the effects of thiamin on antioxidant capacity of juvenile Jian carp (Cyprinus carpio var. Jian). In a 60-day feeding trial, a total of 1,050 juvenile Jian carp (8.20 ± 0.02 g) were fed graded levels of thiamin at 0.25, 0.48, 0.79, 1.06, 1.37, 1.63 and 2.65 mg thiamin kg(-1) diets. The results showed that malondialdehyde and protein carbonyl contents in serum, hepatopancreas, intestine and muscle were significantly decreased with increasing dietary thiamin levels (P < 0.05). Conversely, the anti-superoxide anion capacity and anti-hydroxyl radical capacity in serum, hepatopancreas, intestine and muscle were the lowest in fish fed the thiamin-unsupplemented diet. Meanwhile, the activities of catalase (CAT), glutathione peroxidase, glutathione S-transferase and glutathione reductase, and the contents of glutathione in serum, hepatopancreas, intestine and muscle were enhanced with increasing dietary thiamin levels (P < 0.05). Superoxide dismutase (SOD) activity in serum, hepatopancreas and intestine followed a similar trend as CAT (P < 0.05). However, SOD activity in muscle was not affected by dietary thiamin level (P > 0.05). The results indicated that thiamin could improve antioxidant defence and inhibit lipid peroxidation and protein oxidation of juvenile Jian carp.
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Blockade of reactive oxygen species and Akt activation is critical for anti-inflammation and growth inhibition of metformin in phosphatase and tensin homolog-deficient RAW264.7 cells.
Immunopharmacol Immunotoxicol
PUBLISHED: 09-20-2013
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Metformin is widely used for treatment of type 2 diabetes and has a potential application on the treatment of inflammation and cancer. Phosphatase and tensin homolog (PTEN) plays a critical role in cancer cell growth and inflammation; however, precise mechanisms remain unclear.
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[Identification and function analysis of pseudogenes].
Sheng Wu Gong Cheng Xue Bao
PUBLISHED: 09-10-2013
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Pseudogenes, which have long been described as "fossils", play a very important role in eukaryotic genomes. Recently, studies on the so called "junk gene" have attracted more attention. Far from being silent, pseudogenes participate in various biological activities, including being a part in the transcription process, or participating in the formation of small interfering RNA (siRNA) which regulated gene expression by means of the RNA-interference pathway. Recent studies have also shown that pseudogenes regulate tumor suppression through competing for the microRNA (miRNA) with their parent genes. However, a deeper understanding of function analysis of pseudogenes depends on the comprehensive and accurate identification. With the sequencing completion of many genomes and the innovation of bioinformatics tools, efficient and precise identification of pseudogenes have become available in a genome-wide scale. Our review focused particularly on the method of pseudogene identification, the mechanism of its regulatory roles and its potential to be applied in directed evolution. Besides, the promising research direction of pseudogenes was proposed.
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Dual-Scaled Porous Nitrocellulose Membranes with Underwater Superoleophobicity for Highly Efficient Oil/Water Separation.
Adv. Mater. Weinheim
PUBLISHED: 09-06-2013
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Large-area dual-scaled porous nitrocellulose (p-NC) membranes are fabricated by a facile, inexpensive and scalable perforating approach. These p-NC membranes show stable superhydrophilicity in air and underwater superoleophobicity. The p-NC membranes with intrinsic nanopores and array of microscale perforated pores could selectively and efficiently separate water from various oil/water mixtures with high efficiency (> 99%) rapidly.
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Dynamic behavioral strategies during sonar signal emission in roundleaf bats.
Physiol. Behav.
PUBLISHED: 08-30-2013
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For echolocating bats which emit biosonar pulses nasally, their nostrils are surrounded by fleshy appendages that diffract the outgoing ultrasonic waves. The posterior leaf, as a prominent part of the noseleaf, was mentioned in previous preliminary observations to move during flight in some species of bats, yet the detailed motion patterns and thus the possible functional role of the posterior leaf movement in biosonar systems remain unclear. In the current work, the motion of the posterior leaf of living pratts roundleaf bats has been investigated quantitatively. Temporal characterizations of the noseleaf movement and the ultrasonic pulse emission were performed by virtue of synchronized laser vibrometry and sound recording. The results showed that the posterior leaf tilted forwards and restored to original position within tens of milliseconds. Noseleaf motions were temporally correlated with the emitted ultrasonic pulses. The surfaces of the posterior leaf were moving in the anterior direction in most of the pulse duration. The bats were able to switch the motions on or off. From the comparison with the previously reported noseleaf dynamics in horseshoe bat, we find similar ratio sizes and displacements of the noseleaves compared to the used wavelengths, implying that similar behavioral strategies are utilized by species of bats and it may be applied to different components of the signal emitting apparatus. It suggests that the dynamic sensing principles may widely play a role in the biosonar systems and the investigation on time-variant mechanisms is of capital importance to understand the biosonar sensing strategies used by echolocating bats.
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Panton-Valentine Leukocidin Facilitates the Escape of Staphylococcus aureus From Human Keratinocyte Endosomes and Induces Apoptosis.
J. Infect. Dis.
PUBLISHED: 08-15-2013
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Skin and soft-tissue infections (SSTIs) caused by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) have emerged as major health problems throughout the world. Most SSTI CA-MRSA strains produce Panton-Valentine leukocidin (PVL), but its contribution to CA-MRSA pathogenesis is poorly defined. Here, we used an endemic PVL-positive SSTI-causing CA-MRSA strain from Taiwan, together with an isogenic PVL-knockout mutant (?pvl) and complemented PVL-positive derivative, to evaluate the role of PVL in the pathogenesis of CA-MRSA in the RHEK-1 human keratinocyte cell line and a rabbit skin infection model. We found that both PVL-positive CA-MRSA and isogenic ?pvl strains attached and were engulfed into endosomes of RHEK-1 cells within 1 hour following infection. However, by 2 hours after infection PVL-positive CA-MRSA more effectively disrupted endosomes, escaped into the cytoplasm, and replicated intracellularly. By 6 hours after infection, the PVL-positive strain caused significantly more caspase-dependent keratinocyte apoptosis than the isogenic ?pvl mutant. In the rabbit infection model, 1 week following infection the wild-type strain produced significantly more widespread lesions and cell apoptosis than the isogenic ?pvl mutant. These findings indicate that PVL is an important virulence factor that enables CA-MRSA to produce necrotizing skin infections by allowing the bacteria to escape from endosomes, replicate intracellularly, and induce apoptosis.
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Straightforward oxidation of a copper substrate produces an underwater superoleophobic mesh for oil/water separation.
Chemphyschem
PUBLISHED: 07-29-2013
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A superhydrophilic and underwater superoleophobic Cu(OH)2-covered mesh with micro- and nanoscale hierarchical composite structures is successfully fabricated through a one-step chemical oxidation of a smooth-copper mesh. Such mesh, without any further modification, can selectively separate water from oil/water mixtures with high separation efficiency, and possess excellent stability even after 60 uses. This method provides a simple, low-cost, and scalable strategy for the purification of oily wastewater.
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Anti-dengue virus nonstructural protein 1 antibodies cause NO-mediated endothelial cell apoptosis via ceramide-regulated glycogen synthase kinase-3? and NF-?B activation.
J. Immunol.
PUBLISHED: 07-12-2013
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Immunopathogenetic mechanisms of dengue virus (DENV) infection are involved in hemorrhagic syndrome resulting from thrombocytopenia, coagulopathy, and vasculopathy. We have proposed a mechanism of molecular mimicry in which Abs against DENV nonstructural protein 1 (NS1) cross-react with human endothelial cells and cause NF-?B-regulated immune activation and NO-mediated apoptosis. However, the signaling pathway leading to NF-?B activation after the binding of anti-DENV NS1 Abs to endothelial cells is unresolved. In this study, we found that anti-DENV NS1 Abs caused the formation of lipid raftlike structures, and that disrupting lipid raft formation by methyl-?-cyclodextrin decreased NO production and apoptosis. Treatment with anti-DENV NS1 Abs elevated ceramide generation in lipid rafts. Pharmacological inhibition of acid sphingomyelinase (aSMase) decreased anti-DENV NS1 Ab-mediated ceramide and NO production, as well as apoptosis. Exogenous ceramide treatment induced biogenesis of inducible NO synthase (iNOS)/NO and apoptosis through an NF-?B-regulated manner. Furthermore, activation of glycogen synthase kinase-3? (GSK-3?) was required for ceramide-induced NF-?B activation and iNOS expression. Notably, anti-DENV NS1 Abs caused GSK-3?-mediated NF-?B activation and iNOS expression, which were regulated by aSMase. Moreover, pharmacological inhibition of GSK-3? reduced hepatic endothelial cell apoptosis in mice passively administered anti-DENV NS1 Abs. These results suggest that anti-DENV NS1 Abs bind to the endothelial cell membrane and cause NO production and apoptosis via a mechanism involving the aSMase/ceramide/GSK-3?/NF-?B/iNOS/NO signaling pathway.
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Evident cognitive impairments in seemingly recovered patients after midazolam-based light sedation during diagnostic endoscopy.
J. Formos. Med. Assoc.
PUBLISHED: 06-11-2013
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Midazolam is a widely used sedative agent during colonoscopy, with cognitive toxicity. However, the potential cognitive hazard of midazolam-based light sedation has not been sufficiently examined. We aimed to examine the cognitive safety and vulnerability profile under midazolam light sedation, with a particular focus on individual variations.
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Autophagy facilitates cytokine-induced ICAM-1 expression.
Innate Immun
PUBLISHED: 06-10-2013
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ICAM-1 can be induced by inflammatory cytokines such as IFN-? and TNF-?. This study investigated whether autophagy regulates ICAM-1 given that autophagy facilitates signaling of these two cytokines. Exogenous IFN-? induced ICAM-1 in human lung epithelial A549 cells carrying wild type p53, a transcription factor reported for ICAM-1, but not in PC14PE6/AS2 (AS2) cells carrying mutated p53. However, IFN-? also induced ICAM-1 in A549 cells with short hairpin RNA-silenced p53. No changes in IFN-? receptor expression were observed in AS2 cells, but IFN-?-activated Jak2/STAT1/IFN regulatory factor 1 was markedly decreased. In AS2 cells, increased levels of reactive oxygen species induced the activation of Src homology domain-containing phosphatase 2 (SHP2), while SHP2 was essential for IFN-? resistance. AS2 cells showed autophagy resistance, and the manipulation of the autophagy pathway altered IFN-? resistance. Aberrant Bcl-2 expression and mammalian target of rapamycin activation contributed to both autophagy resistance and IFN-? resistance. Autophagy, but not p53, also modulated TNF-?-induced NF-?B activation and ICAM-1 expression. Inhibiting autophagy decreased the adhesion of human monocytic U937 cells to IFN-?-treated A549 cells. These results demonstrated that IFN-? and TNF-? induced ICAM-1 expression through a common pathway that was regulated by autophagy, but not p53.
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Diagnostic value of dynamics serum sCD163, sTREM-1, PCT, and CRP in differentiating sepsis, severity assessment, and prognostic prediction.
Mediators Inflamm.
PUBLISHED: 05-22-2013
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To describe the dynamics changes of sCD163, soluble serum triggering receptor expressed on myeloid cells-1 (sTREM-1), procalcitonin (PCT), and C-reactive protein (CRP) during the course of sepsis, as well as their outcome prediction.
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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.