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#29049961   2017/10/19 Save this To Up

Smartphone app-based/portable sensor for the detection of fluoro-surfactant PFOA.

We developed a smartphone app-based monitoring tool for the detection of anionic surfactants (AS), including perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS). Akin to the methylene blue active substances (MBAS), liquid-phase extraction (LPE) is employed to extract the hydrophobic ion-pair of dye (ethyl violet)-AS to an organic phase (ethyl acetate). The colour (RGB) of the organic phase is read using a smartphone camera with the help of a reading kit. The value of RGB is carefully corrected and linked to the concentration of ASs with a standard deviation of <10% in the 10-1000 ppb (part per billion) range. In order to avoid the interference arising from inorganic anions (such as those found in tap water and groundwater), the water sample is pre-treated either by solid-phase extraction (SPE), which takes ∼30 min, or by dual liquid-phase extraction (dual-LPE, developed by us), which takes ∼5 min. In the latter case, the organic phase of the first LPE (equilibrium with water sample) is transferred and subjected to a second LPE (equilibrium with Milli-Q water) to remove any potential background interference. In the meantime, SPE can also pre-concentrate ASs at 100-1000 times (in volume) to benefit the sensitivity. Consequently, our smartphone app can detect PFOA spiked in tap/groundwater with an LOD of 10 ppb (∼12 nM, dual-LPE of ∼5 min), or 0.5 ppb (∼1.2 nM, SPE of ∼3 h), suggesting that it has the potential to succeed as a pre-screening tool for on-site application and in common laboratory tests.

2279 related Products with: Smartphone app-based/portable sensor for the detection of fluoro-surfactant PFOA.

MarkerGeneTM Fluorescent Formaldehyde Detection Ki 2 Fluoro 5 formylphenylbo Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media Cellufine Formyl Media Formalin Solution (20%) Formalin Solution (20%) Formalin Solution (20%) Formalin (10% Neutral Bu

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#29048685   2017/10/19 Save this To Up

miR-504 promotes tumour growth and metastasis in human osteosarcoma by targeting TP53INP1.

An increasing number of studies have demonstrated that microRNAs participate in the development of osteosarcoma by acting as tumour suppressor or tumour-promoting genes. We investigated the role of miR-504 in the growth and metastasis of osteosarcoma. The expression of miR-504 in clinical osteosarcoma samples was higher than that in the adjacent normal tissue and correlated with tumour size and clinical stage. Tumour protein p53-inducible nuclear protein 1 (TP53INP1) was downregulated in the clinical osteosarcoma samples compared with the adjacent normal tissues and was consistently correlated with the clinical stage. The results of dual-luciferase reporter assay and western blot analysis demonstrated that the TP53INP1 gene is a direct target of miR-504. Altogether, the Cell Counting Kit-8 (CCK-8), the colony formation, the flow cytometry and the Transwell assay results demonstrated that miR-504 promoted osteosarcoma cell growth and metastasis in vitro. P73, P21, Bax, cleaved-caspase-3 and secreted protein acidic and rich in cysteine (SPARC) were associated with the suppressive role of miR-504/TP53INP1. The overexpression of miR-504 in osteosarcoma xenografts enhanced the tumour growth and increased the metastatic burden. Collectively, these results revealed that TP53INP1 is a target gene of miR-504 and that miR-504 enhances osteosarcoma growth and promotes distant metastases by targeting TP53INP1. Thus, miR-504/TP53INP1 may be associated with osteosarcoma size and clinical stage.

2327 related Products with: miR-504 promotes tumour growth and metastasis in human osteosarcoma by targeting TP53INP1.

Human Insulin-like Growth Human Insulin-like Growth Growth Factor (Human) Ant Human normal bone and ost Goat Anti-Human Fibroblas Human Insulin-like Growth Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Epidermal Growth Factor ( Epidermal Growth Factor ( Epidermal Growth Factor ( Epidermal Growth Factor (

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#29048682   2017/10/19 Save this To Up

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153.

Malignant glioma, the most common intracranial primary tumor, is characterized by increased angiogenesis. Accumulating evidence has shown that long non-coding RNAs (lncRNAs) play an important role in a variety of biological behaviors of tumors. However, the role of lncRNAs in the regulation of glioma vascular endothelial cell function remains to be investigated. To simulate the glioma microenvironment, we applied glioma conditioned medium (GCM) to human cerebral microvascular endothelial cells (hCMECs). In the present study, the lncRNA SNHG15 was found to be highly expressed in glioma vascular endothelial cells. Cell Counting Kit-8 (CCK-8), migration and tube formation assays demonstrated that knockdown of SNHG15 inhibited glioma vascular endothelial cell proliferation, migration and tube formation in vitro. Furthermore, knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis. Bioinformatics software and dual-luciferase system analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153. Additionally, the present study showed that miR-153 targeted the 3'‑untranslated region of VEGFA and Cdc42 and downregulated their expression. In conclusion, knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation. Therefore, SNHG15 and miR-153 are new potential therapeutic targets for anti-angiogenesis treatment of glioma.

2608 related Products with: SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153.

Human Brain Microvascular GFP Expressing Human Brai Human Dermal Lymphatic Mi GFP Expressing Human Derm Human Glomerular Microvas GFP Expressing Human Glom RFP Expressing Human Glom Human Dermal Microvascula Human Pancreatic Microvas Human Retinal Microvascul GFP Expressing Human Reti RFP Expressing Human Reti

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#29048677   2017/10/19 Save this To Up

MicroRNA-154 as a prognostic factor in bladder cancer inhibits cellular malignancy by targeting RSF1 and RUNX2.

Recent studies have demonstrated that microRNA-154 (miR-154) is involved in tumorigenesis, progression, invasion and metastasis in several types of human cancer. However, whether it plays a role in bladder cancer (BC) is unclear. The aim of the present study was to determine miR-154 levels in human BC tissues and investigate the correlation between miR-154 levels and clinicopathological characteristics as well as patient outcome. Using RT-qPCR, we found that the expression levels of miR-154 were significantly lower in BC tissues compared to adjacent normal tissues. We also demonstrated that downregulation of miR-154 was associated with advanced clinicopathological features and worse prognoses for patients with BC. Using a variety of integrated approaches, we demonstrated that both runt-related transcription factor 2 (RUNX2) and remodeling and spacing factor 1 (RSF1) were miR-154 targets. Notably, there was an inverse correlation between RSF1, RUNX2 and miR-154 expression in BC tissues. The biological functions of miR-154 were examined in vitro using Cell Counting Kit-8 (CCK-8), wound healing, and Transwell assays with T24 human bladder carcinoma cells transfected with miR-154 mimics or negative controls. These assays demonstrated that miR-154 significantly suppressed proliferation, migration and invasion of T24 cells (P<0.05). Furthermore, overexpression of RSF1 and RUNX2 rescued miR-154-induced inhibition of these aggressive behaviors. Our results indicated that miR-154, and its downstream targets RSF1 and RUNX2, are promising options for future BC therapies.

2510 related Products with: MicroRNA-154 as a prognostic factor in bladder cancer inhibits cellular malignancy by targeting RSF1 and RUNX2.

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#29048665   2017/10/19 Save this To Up

TGX-221 inhibits proliferation and induces apoptosis in human glioblastoma cells.

Glioblastoma is the most common type of primary brain tumor in adults, with high mortality and morbidity rates. More effective therapeutic strategies are imperative. Previous studies have shown that the known p110-β-selective inhibitor TGX-221 blocks the activation of PKB/Akt in PTEN-deficient cells. We treated U87 and U251 glioblastoma cells with TGX-221 to determine the effect of TGX-221. We performed a Cell Counting Kit-8 (CCK-8) test, EDU staining and cell cycle distribution analysis and found that TGX-221 inhibited glioblastoma cell proliferation. Next, the effect of TGX-221 on cell apoptosis was investigated using flow cytometry. These results demonstrated that TGX-221 induced apoptosis in glioblastoma cells. Moreover, migration and invasion assays revealed that TGX-221 inhibited human glioblastoma cell migration and invasion. Collectively, our study revealed that TGX-221 could inhibit proliferation and induce apoptosis in glioblastoma cells.

1809 related Products with: TGX-221 inhibits proliferation and induces apoptosis in human glioblastoma cells.

Epidermal Growth Factor ( Epidermal Growth Factor ( Macrophage Colony Stimula Macrophage Colony Stimula Apoptosis (Human) Antibod Apoptosis (Human) Antibod Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Rabbit Anti-Human Apoptos Anti C Reactive Protein A

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#29048660   2017/10/19 Save this To Up

Canonical and non-canonical WNT signaling in cancer stem cells and their niches: Cellular heterogeneity, omics reprogramming, targeted therapy and tumor plasticity (Review).

Cancer stem cells (CSCs), which have the potential for self-renewal, differentiation and de-differentiation, undergo epigenetic, epithelial-mesenchymal, immunological and metabolic reprogramming to adapt to the tumor microenvironment and survive host defense or therapeutic insults. Intra-tumor heterogeneity and cancer-cell plasticity give rise to therapeutic resistance and recurrence through clonal replacement and reactivation of dormant CSCs, respectively. WNT signaling cascades cross-talk with the FGF, Notch, Hedgehog and TGFβ/BMP signaling cascades and regulate expression of functional CSC markers, such as CD44, CD133 (PROM1), EPCAM and LGR5 (GPR49). Aberrant canonical and non-canonical WNT signaling in human malignancies, including breast, colorectal, gastric, lung, ovary, pancreatic, prostate and uterine cancers, leukemia and melanoma, are involved in CSC survival, bulk-tumor expansion and invasion/metastasis. WNT signaling-targeted therapeutics, such as anti-FZD1/2/5/7/8 monoclonal antibody (mAb) (vantictumab), anti-LGR5 antibody-drug conjugate (ADC) (mAb-mc-vc-PAB-MMAE), anti-PTK7 ADC (PF-06647020), anti-ROR1 mAb (cirmtuzumab), anti-RSPO3 mAb (rosmantuzumab), small-molecule porcupine inhibitors (ETC-159, WNT-C59 and WNT974), tankyrase inhibitors (AZ1366, G007-LK, NVP-TNKS656 and XAV939) and β-catenin inhibitors (BC2059, CWP232228, ICG-001 and PRI-724), are in clinical trials or preclinical studies for the treatment of patients with WNT-driven cancers. WNT signaling-targeted therapeutics are applicable for combination therapy with BCR-ABL, EGFR, FLT3, KIT or RET inhibitors to treat a subset of tyrosine kinase-driven cancers because WNT and tyrosine kinase signaling cascades converge to β-catenin for the maintenance and expansion of CSCs. WNT signaling-targeted therapeutics might also be applicable for combination therapy with immune checkpoint blockers, such as atezolizumab, avelumab, durvalumab, ipilimumab, nivolumab and pembrolizumab, to treat cancers with immune evasion, although the context-dependent effects of WNT signaling on immunity should be carefully assessed. Omics monitoring, such as genome sequencing and transcriptome tests, immunohistochemical analyses on PD-L1 (CD274), PD-1 (PDCD1), ROR1 and nuclear β-catenin and organoid-based drug screening, is necessary to determine the appropriate WNT signaling-targeted therapeutics for cancer patients.

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Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Macrophage Colony Stimula Macrophage Colony Stimula Androgen Receptor (Ab 650 Wnt Signaling Pathway TCF AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac

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#29048645   2017/10/19 Save this To Up

Establishment and characterization of human osteosarcoma cells resistant to pyropheophorbide-α methyl ester-mediated photodynamic therapy.

The present study was performed to establish and characterize new human osteosarcoma cell lines resistant to pyropheophorbide-α methyl ester‑mediated photodynamic therapy (MPPa-PDT). MPPa-PDT-resistant cells are isolated from the human osteosarcoma MG63 and HOS cell lines and two resistant populations were finally acquired, including MG63/PDT and HOS/PDT. Cell Counting Kit-8 (CCK-8) assay was used to determine the MPPa-PDT, cisplatin (CDDP) resistance and proliferation of MG63, MG63/PDT, HOS and HOS/PDT cells. The intracellular ROS were analyzed using DCFH-DA staining. The colony formation, invasion and migration of parental and resistant cells were compared. FCM was employed to examine the cell cycle distribution, the apoptosis rate and the proportion of CD133+ cells. The fluorescence intensity of intracellular MPPa was observed by fluorescence microscopy and quantified using microplate reader. The protein levels were assessed by western blotting (WB). Compared with two parental cells, MG63/PDT and HOS/PDT were 1.67- and 1.61-fold resistant to MPPa-PDT, respectively, and also exhibited the resistance to CDDP. FCM assays confirmed that both MG63/PDT and HOS/PDT cells treated with MPPa-PDT displayed a significantly lower apoptosis rate in comparison with their corresponding parental cells. The expression of apoptosis-related proteins (i.e. cleaved-caspase 3 and cleaved‑PARP), intracellular ROS and the antioxidant proteins (HO-1 and SOD1) in MG63/PDT and HOS/PDT cells was also lower than that in parental cells. Both MG63/PDT and HOS/PDT cells exhibited changes in proliferation, photosensitizer absorption, colony formation, invasion, migration and the cell cycle distribution as compared to MG63 and HOS cells, respectively. Compared to MG63 and HOS cells, both resistant cell lines had a higher expression of CD133, survivin, Bcl-xL, Bcl-2, MRP1, MDR1 and ABCG2, but a lower expression of Bax. The present study successfully established two resistant human osteosarcoma cell lines which are valuable to explore the resistance-related mechanisms and the approaches to overcome resistance.

1238 related Products with: Establishment and characterization of human osteosarcoma cells resistant to pyropheophorbide-α methyl ester-mediated photodynamic therapy.

(αR)-Acetyloxybenzenebut (αS,βS)-β-[(2-Aminophe Human Tonsil Microvascula N alpha 4 Tosyl L arginin Anti C Reactive Protein A Epidermal Growth Factor ( Epidermal Growth Factor ( Histone H3 (Tri-Methyl-Ly Histone H3 (Di-Methyl-Lys Goat Anti-Human DNA Methy Rabbit Anti-Human Androge Rabbit Anti-Human Androge

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#29048615   2017/10/19 Save this To Up

Overexpression of RAB34 correlates with poor prognosis and tumor progression in hepatocellular carcinoma.

RAB34, a protein belonging to the RAB family, is involved in protein transport, repositioning of lysosomes and activation of micropinocytosis. However, few studies have reported its function in human epithelial cancers. Immunohistochemistry (IHC) and western blotting were used to detect expression of RAB34 at the tissue and cell levels. Cell Counting Kit-8 (CCK-8), EDU assay and flow cytometry were used for analyzing cell proliferation. Transwell and scratch wound healing assays were used for assessing cell migration ability. Western blotting was used for detecting expression of E-cadherin and N-cadherin. In the present study, we found that both DNA copy and protein level of RAB34 were upregulating in human hepatocellular carcinoma (HCC) tissues when compared with that in adjacent tissues. Analysis of the correlation between RAB34 expression and clinicopathological features showed that patients with overexpression of RAB34 consistently had large tumor size, vessel invasion and poor tumor grade. Furthermore, overall survival analysis showed that patients with upregulated expression of RAB34 were associated with poor prognosis. Moreover, cell function experiments showed that suppression of RAB34 led to a lower proliferation rate and migration ability. In addition, this phenomenon may be attributed to cell cycle phase G1 arrest and mesenchymal-epithelial transition under condition of RAB34 suppression. The present study demonstrated that RAB34 plays an important role in the initiation and progression of HCC. Our results suggest a new therapeutic target for the clinical treatment of HCC.

1283 related Products with: Overexpression of RAB34 correlates with poor prognosis and tumor progression in hepatocellular carcinoma.

Liver hepatocellular carc Liver cancer (hepatocellu Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Normal liver and hepatoce Multi organ carcinoma tis Multi organ carcinoma tis Pancreatic carcinoma and Multiple organs tumor and Liver carcinoma and norma

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#29048509   2017/10/19 Save this To Up

Plasma But Not Cerebrospinal Fluid Interleukin 7 and Interleukin 5 Levels Pre-Antiretroviral Therapy Commencement Predict Cryptococcosis-Associated Immune Reconstitution Inflammatory Syndrome.

Patients with human immunodeficiency virus/AIDS-associated cryptococcal meningitis (CM) frequently experience clinical deterioration, known as cryptococcosis-associated immune reconstitution inflammatory syndrome (C-IRIS), upon initiation of antiretroviral therapy (ART). The immunological mechanisms underlying C-IRIS are incompletely defined and no reliable predictive biomarkers exist. We investigated whether plasma or cerebrospinal fluid (CSF) levels of cytokines and chemokines predicted C-IRIS and are potential predictive biomarkers.

2492 related Products with: Plasma But Not Cerebrospinal Fluid Interleukin 7 and Interleukin 5 Levels Pre-Antiretroviral Therapy Commencement Predict Cryptococcosis-Associated Immune Reconstitution Inflammatory Syndrome.

CELLKINES Natural Human I Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-17E (IL Human Interleukin-17F IL- Human Interleukin-17AF He Human Interleukin-29 IL-2 Human Interleukin-17A IL- Rat Anti-Mouse Interleuki Mouse Anti-Human Interleu Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki

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#29048112   2017/10/19 Save this To Up

How we diagnose and treat systemic mastocytosis in adults.

Rapid advances in the understanding of the molecular biology, data from translational and clinical trials, and retrospective analyses has influenced the diagnosis and treatment of systemic mastocytosis (SM). Many options have existed for the symptomatic management of SM patients, but recent evolution in regards to the molecular underpinnings of this disease and our ability to distinguish clonal mastocytosis from mast cell activation syndrome has changed our treatment paradigm and opened new opportunities for understanding genetic risk, transformation to mast cell leukaemia, and treatment choices. Key to this change has been the discovery of the KIT mutation and the use of next generation sequencing to evaluate for co-existing molecular mutations that may define the disease course. Careful diagnosis, judicious symptom management and close surveillance of those who may have yet undiagnosed disease is paramount in providing optimal management. In this article, we review the diagnosis and provide a paradigm for the management of SM patients.

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Caspase-5 Inhibitor Z-WEH Caspase-5 Inhibitor Z-WEH Caspase 5 Inhibitor Z WEH Caspase 5 Inhibitor Z WEH Caspase-5 Inhibitor Z-WEH Caspase-5 Inhibitor Z-WEH Caspase 5 Inhibitor Z WEH Caspase 5 Inhibitor Z WEH GLP 2 ELISA Kit, Rat Prog PARP Treated Protein Cont T-2 Toxin Mycotoxins ELIS Zearalenone Mycotoxins EL

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