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#29029044   2017/10/13 Save this To Up

Enhanced killing of Escherichia coli using a combination of polyhexamethylene biguanide hydrochloride and 1-bromo-3-chloro-5,5- dimethylimidazolidine-2,4-dione.

The bactericidal activities of polyhexamethylene biguanide hydrochloride (PHMB), 1-bromo-3-chloro-5,5-dimethylimidazolidine-2,4-dione (BCDMH), and the combination of the two (designated as PB) were compared using Escherichia coli as the test organism. PB exhibited strong bactericidal activity: 10 mg/L PHMB combined with 8 mg/L BCDMH resulted in approximately 5.74 log10 reduction (LR), whereby 320 mg/L PHMB or 20 mg/L BCDMH was about 5.53 and 6.56 LR, respectively. Analyses using scanning electron microscopy, flow cytometry, and atomic absorption spectroscopy indicated that PB, PHMB, and BCDMH disrupted cell membranes and changed membrane structure and permeability, resulting in the leakage of intracellular soluble proteins and ions. PB exerted stronger effects on potassium and magnesium leakage, membrane potential, and permeability than BCDMH did. PB caused less protein leakage than PHMB did. These results suggest that at a relatively low concentration, PB exhibited good bactericidal activity and physiological effect on E. coli.

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17β-Acetoxy-2α-bromo-5 1-Acetyl-5-bromo-4-chloro 21-Acetoxy-9α-chloro-11 (6α,11β,16α)-21-(Acety 2-[(3S)-3-(Acetyloxy)-1-b (11β,16α,17α)-21-(Acet N-(4-Aminobutyl)-5-chloro N-(4-Aminobutyl)-5-chloro (1S,4R)-4-(2-Amino-6-chlo 1-[4-Amino-3-chloro-5-(tr N-(10-Aminodecyl)-5-chlor N-(2-Aminoethyl)-5-chloro

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#29029014   2017/10/13 Save this To Up

1,25-Dihydroxyvitamin D regulation of glutamine synthetase and glutamine metabolism in human mammary epithelial cells.

Genomic profiling has identified a subset of metabolic genes that are altered by 1,25-dihydroxyvitamin D (1,25D) in breast cells including GLUL, the gene that encodes glutamine synthetase (GS). Here, we explored the relevance of vitamin D modulation of GLUL and other metabolic genes in the context of glutamine utilization and dependence. We show that exposure of breast epithelial cells to glutamine deprivation or a GS inhibitor reduced growth and these effects were exacerbated by co-treatment with 1,25D. 1,25D down-regulation of GLUL was sufficient to reduce abundance and activity of GS. Flow cytometry demonstrated that glutamine deprivation induced S phase arrest, likely due to reduced availability of glutamine for DNA synthesis. In contrast, 1,25D induced GO/G1 arrest, indicating its effects are not solely due to reduced glutamine synthesis. Indeed, 1,25D also reduced expression of GLS1 and GLS2 genes which code for glutaminases that shunt glutamine into the TCA cycle. Consistent with reduced entry of glutamine into the TCA cycle, 1,25D inhibited glutamine oxidation and the metabolic response to exogenous glutamine as analyzed by Seahorse Extracellular Flux assays. Effects of 1,25D on GLUL/GS expression and glutamine oxidation were retained in HME cells that express SV-40 (HME-LT cells) but not in those that express SV-40 and oncogenic RAS (HME-PR cells). Furthermore, HME-PR cells exhibited glutamine-independence and expressed constitutively high levels of GLUL/GS which were unaffected by 1,25D. Collectively, this data suggests that 1,25D alters glutamine availability, dependence, and metabolism in non-transformed and pre-neoplastic mammary epithelial cells in association with cell cycle arrest.

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#29028842   2017/10/13 Save this To Up

In vitro investigation of head and neck cancer stem cell proportions and their changes following X-ray irradiation as a function of HPV status.

Some head and neck squamous cell carcinomas (HNSCC) have a distinct aetiology, which depends on the presence of oncogenic human papilloma virus (HPV). Also, HNSCC contains cancer stem cells (CSCs) that have greater radioresistance and capacity to change replication dynamics in response to irradiation compared to non-clonogenic cells. Since there is limited data on CSCs in HNSCC as a function of HPV status, better understanding of their radiobiology may enable improved treatment outcome.

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#29028806   2017/10/13 Save this To Up

A novel immunotoxin reveals a new role for CD321 in endothelial cells.

There are currently several antibody therapies that directly target tumors, and antibody-drug conjugates represent a novel moiety as next generation therapeutics. Here, we used a unique screening probe, DT3C, to identify functional antibodies that recognized surface molecules and functional epitopes, and which provided toxin delivery capability. Accordingly, we generated the 90G4 antibody, which induced DT3C-dependent cytotoxicity in endothelial cells. Molecular analysis revealed that 90G4 recognized CD321, a protein localized at tight junctions. Although CD321 plays a pivotal role in inflammation and lymphocyte trans-endothelial migration, little is known about its mechanism of action in endothelial cells. Targeting of CD321 by the 90G4 immunotoxin induced cell death. Moreover, 90G4 immunotoxin caused cytotoxicity primarily in migratory endothelial cells, but not in those forming sheets, suggesting a critical role for CD321 in tumor angiogenesis. We also found that hypoxia triggered redistribution of CD321 to a punctate localization on the basal side of cells, resulting in functional impairment of tight junctions and increased motility. Thus, our findings raise the intriguing possibility that endothelial CD321 presented cellular localization in tight junction as well as multifunctional dynamics in several conditions, leading to illuminate the importance of widely-expressed CD321 as a potential target for antitumor therapy.

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Human Internal Mammary Ar GFP Expressing Human Inte anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor ( Goat Anti-Human Endotheli GLP 1 ELISA Kit, Rat Gluc Glucagon ELISA KIT, Rat G Anti beta3 AR Human, Poly Cultrex In Vitro Angiogen

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#29028770   2017/10/13 Save this To Up

Expression and Clinical Correlations of Co-Stimulatory Molecules on Peripheral T Lymphocyte Subsets of Early-Stage Severe Sepsis: A Prospective Observational Study.

To investigate the expression and clinical correlations of co-stimulatory molecules on peripheral T cell subsets of severe sepsis (SS) patients.

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Multi organ carcinoma tis Multi organ carcinoma tis Pancreatic carcinoma and Multiple organs tumor and Tissue array of gastric d Multiple organ cancer tis Stomach adenocarcinoma wi Liver disease spectrum ti Liver carcinoma and norma Liver carcinoma and norma Liver carcinoma and norma Lung disease spectrum tis

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#29028628   2017/10/13 Save this To Up

Role of PDGF-BB in proliferation, differentiation and maintaining stem cell properties of PDL cells in vitro.

Platelet-derived growth factor-BB (PDGF-BB) is one of the most abundant growth factors in platelet derived products and has been shown to stimulate regeneration after tissue injury. There is a population of mesenchymal stem cells (MSC) in human periodontal ligament (PDL) which can contribute to tissue regeneration under appropriate conditions.

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#29028530   2017/10/13 Save this To Up

A pentanoic acid derivative targeting matrix metalloproteinase-2 (MMP-2) induces apoptosis in a chronic myeloid leukemia cell line.

Depending on our previous observations, some compounds of pentanoic acid were designed and synthesized. Characterization of the synthesized compounds was done by mass, NMR and IR spectroscopy as well as elemental analysis. Among the synthesized molecules, (2S)-5-oxo-2-[(nitrobenzene-4-yl sulfonyl) amino]-5-(pentylamino) pentanoic acid (Cpd 11) was found as a lead and potent inhibitor of matrix metalloproteinase-2 (MMP-2). Molecular modeling and enzyme inhibition studies were done to confirm the interaction or inhibitory potential of this compound. Thereafter, the biological screening was done through cytotoxicity, anti-invasion and apoptosis-related assays. Docking analysis revealed that Cpd 11 interacted with the target molecule MMP-2 and with MMP-9. However, enzyme inhibition assay showed 3-fold MMP-2 inhibition compared to MMP-9. Cytotoxicity assay showed the inhibitory potential of Cpd 11 against K562 cell line having IC50 value of 17.9 ± 0.01 μM after 48 h of incubation. The cell death was apoptotic in nature as revealed from the annexin V and sub-G1 cell cycle arrest assay. Besides this, Cpd 11 also exhibited dose dependent anti-invasive activity into K562 cell line. On the other hand, flow cytometry and western blot data revealed Cpd 11 induced downregulation of MMP-2 in K562 cell line after 48 h of incubation that might be linked with the anti-invasive and apoptotic activity furthermore. Therefore, the overall results validated each method and make this molecule as a potent MMP-2 inhibitor that blocked the invasion and could bring apoptosis at later stages in K562 cells sparing the normal ones.

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Mouse Anti-Human Matrix M Mouse Anti-Human Matrix M Mouse Anti-Human Matrix M Cell Meter™ Caspase 9 A Cultrex 24 Well BME Cell Cultrex 24 Well Laminin I Cultrex 24 Well Collagen Cultrex 24 Well Collagen α-Acetamino-α-carboxy-( 5-[4-(Aminomethyl)-3,5-di Apoptosis Phospho-Specifi Cell Cycle Control Phosph

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#29028094   2017/10/13 Save this To Up

Upregulation of miR-802 suppresses gastric cancer oncogenicity via targeting RAB23 expression.

The aberrant expression of microRNAs (miRNAs) has been observed in various types of cancer. Recently, miR-802 was found to play important role in tumor progression. However, the function of miR-802 in gastric cancer (GC) remains unknown. The aim of the present study was to investigate biological effects and underlying mechanisms of miR-802 in GC.

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#29028073   2017/10/13 Save this To Up

Polyphenol epigallocatechin-3-gallate alleviates high glucose-induced H9C2 cell damage through PI3K/Akt pathway.

The aim of this work was to study the protective effect of polyphenol epigallocatechin-3-gallate (EGCG) on high glucose-induced oxidative damage of H9C2 cells and to investigate the relationship between this effect and phosphatidyl inositol 3 kinase-serine/threonine kinase (P13K/Akt) signal transduction pathway.

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#29027985   2017/10/13 Save this To Up

Triterpenoids from Ocimum labiatum Activates Latent HIV-1 Expression In Vitro: Potential for Use in Adjuvant Therapy.

Latent HIV reservoirs in infected individuals prevent current treatment from eradicating infection. Treatment strategies against latency involve adjuvants for viral reactivation which exposes viral particles to antiretroviral drugs. In this study, the effect of novel triterpenoids isolated from Ocimum labiatum on HIV-1 expression was measured through HIV-1 p24 antigen capture in the U1 latency model of HIV-1 infection and in peripheral blood mononuclear cells (PBMCs) of infected patients on combination antiretroviral therapy (cART). The mechanism of viral reactivation was determined through the compound's effect on cytokine production, histone deacetylase (HDAC) inhibition, and protein kinase C (PKC) activation. Cytotoxicity of the triterpenoids was determined using a tetrazolium dye and flow cytometry. The isolated triterpene isomers, 3-hydroxy-4,6a,6b,11,12,14b-hexamethyl-1,2,3,4,6,6a,6b,7,8,8a,9,10,11,12,12a,14,14a,14b-octadecahydropicene-4,8a-dicarboxylic acid (HHODC), significantly (p < 0.05) induced HIV-1 expression in a dose-dependent manner in U1 cells at non-cytotoxic concentrations. HHODC also induced viral expression in PBMCs of HIV-1 infected patients on cART. In addition, the compound up-regulated the production of interleukin (IL)-2, IL-6, tumour necrosis factor (TNF)-α, and interferon (IFN)-γ but had no effect on HDAC and PKC activity, suggesting cytokine upregulation as being involved in latency activation. The observed in vitro reactivation of HIV-1 introduces the adjuvant potential of HHODC for the first time here.

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