Tuesday, 17 April 2018


An article published this year inSpringer Link using one of our products, PE Mouse anti-Human CD31, by our customers from Department of Pharmacology and Razi Drug Research Center, School of Medicine Iran, University of Medical Sciences Tehran, Iran, in the analysis of how Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes. Congrats and Thanks.


Summay:
Strategies based on mesenchymal stem cell (MSC) therapy for restoring injured articular cartilage are not effective enough in osteoarthritis (OA). Due to the enhanced inflammation and oxidative stress in OA microenvironment, differentiation of MSCs into chondrocytes would be impaired. This study aims to explore the effects of diallyl disulfide (DADS) on IL-1β-mediated inflammation and oxidative stress in human adipose derived mesenchymal stem cells (hADSCs) during chondrogenesis. MTT assay was employed to examine the effects of various concentrations of DADS on the viability of hADSCs at different time scales to obtain non-cytotoxic concentration range of DADS. The effects of DADS on IL-1β-induced intracellular ROS generation and lipid peroxidation were evaluated in hADSCs. Western blotting was used to analyze the protein expression levels of IκBα (np), IκBα (p), NF-κB (np) and NF-κB (p). Furthermore, the gene expression levels of antioxidant enzymes in hADSCs and chondrogenic markers at days 7, 14 and 21 of differentiation were measured using qRT-PCR. The results showed that addition of DADS significantly enhanced the mRNA expression levels of antioxidant enzymes as well as reduced ROS elevation, lipid peroxidation, IκBα activation and NF-κB nuclear translocation in hADSCs treated with IL-1β. In addition, DADS could significantly increase the expression levels of IL-1β-induced impaired chondrogenic marker genes in differentiated hADSCs. Treatment with DADS may provide an effective approach to prevent the pro-inflammatory cytokines and oxidative stress as catabolic causes of chondrocyte cell death and enhance the protective anabolic effects by promoting chondrogenesis associated gene expressions in hADSCs exposed to OA condition.

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PE Mouse anti-Human CD31


An article published this year inPlosOne using one of our products, 7AAD, by our customers from Department of Internal Medicine, AHEPA University Hospital, Aristotle University Medical School, Thessaloniki, Greece., in the analysis of how Prevalence and correlates of persistent intracellular HIV transcription in individuals on efavirenz versus atazanavir-based regimens: A prospective cohort study. Congrats and Thanks.


Summay:
Combination antiretroviral therapy(cART), albeit not curative, has improved substantially the morbidity and mortality of HIV disease through prolonged and sustained suppression of viral replication.[1] The establishment of HIV latency in a population of long lived memory CD4+ T cells is perceived as the major barrier for the eradication of HIV infection.[2] Several lines of evidence support the notion of persistent low level viral replication on cART at least in a subgroup of patients.[3–6] The importance of persistent HIV transcription(HIVpt) in patients on suppressive ART is unclear, but several studies suggest that biomarkers of HIVpt may be promising to assess residual viral replication.[7] There is limited evidence derived from raltegravir intensification studies that residual viral replication as evidenced by increases in 2-long terminal repeat circles may affect to a lesser extent patients on non-nucleoside transcriptase inhibitors(NNRTIs) versus protease inhibitors (PIs).[3,4] For drugs with steep dose-response curves such as PIs, small decreases in intracellular concentrations may diminish significantly the viral inhibition providing a plausible explanation for this observation.[8] Antiretroviral drugs may be substrates, inhibitors or inducers of ATP-binding cassette transporters(ABC transporters) which function as drug efflux pumps with possible implications for the intracellular concentrations of antiretrovirals.[9] In our prospective study, we used a method which combines immunophenotyping with ultrasensitive-FISH to detect unspliced HIV-1 gag-pol in relevant cell populations in order to compare HIVpt in virologically suppressed patients on efavirenz(EFV) or atazanavir/ritonavir (ATV/r) and a backbone of emtricitabine-tenofovir(FTC-TDF).[7,10,11] We followed prospectively our patient cohort for one year and investigated the impact of HIVpt on virological outcomes and CD4+ T-cell recovery. Finally, we tested for differences in the mRNA expression of two widely studied ABC transporters (P-glycoprotein, P-gp/ABCB1 and multidrug resistance-associated protein-1, MRP1/ABCC1) in peripheral blood mononuclear cells(PBMCs) between patients with and without HIVpt by treatment regimen.

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7AAD


An article published this year inIEEExplore Digital Library using one of our products, Propidium Iodide”, by our customers from Department of Advanced Energy, the University of Tokyo, Kashiwanoha, Kashiwa, Chiba, Japan., in the analysis of how Genotoxicity of tetrahydrofolic acid to hematopoietic stem and progenitor cells. Congrats and Thanks.


Summay:
Plasma irradiation of cancer is expected to activate a cancer-specific immune response; however, its long-term systemic effect in animal models has not been sufficiently investigated. In this study, the long-term systemic effect induced by plasma irradiation was examined using C57BL/6 mice inoculated with B16F10 melanoma. Melanoma tumors on the right hind legs of the mice were resected after treatment with nanosecond pulsed streamer discharge. The results showed that plasma treatment delayed the growth of recurrent tumors at the site of resection. In addition, plasma treatment delayed the growth of tumors re-inoculated at the non-irradiated site on the left leg of the mice after resection. Histological and single-cell analyses revealed that plasma had no direct effect on primary tumors, whereas it enhanced cytotoxic T cell infiltration into re-inoculated tumors. These results suggest that plasma treatment induces cancer-specific long-term immune memory in mice.

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Propidium Iodide


An article published this year in “ScienceDirect” using one of our products, “FITC AnnexinV”, by our customers from Laboratory of Tumor Molecular Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland, in the analysis of how Enantiomeric trans β-aryl-δ-iodo-γ-lactones derived from 2,5-dimethylbenzaldehyde induce apoptosis in canine lymphoma cell lines by downregulation of anti-apoptotic Bcl-2 family members Bcl-xL and Bcl-2. Congrats and Thanks.
 

Summay:
For many years, studies focused on developing new natural or synthetic compounds with antineoplastic activity have attracted the attention of researchers. An interesting group of such compounds seem to be those with both lactone moiety and an aromatic ring which, in addition to antimicrobial or antiviral activity, also exhibit antitumor properties. The study shows antitumor activity of two enantiomeric trans isomers of 5-(1-iodoethyl)-4-(2′,5′-dimethylphenyl)dihydrofuran-2-one. Our aim was to determine their antitumor activity manifested as an ability to induce apoptosis in selected canine cancer cell lines as well as to evaluate differences in their strength depending on the configuration of their stereogenic centers. The enantiomers (+)-(4R,5S,6R)-1 and (−)-(4S,5R,6S)-2 were found to induce classical caspase-dependent apoptosis through downregulation of the expression of anti-apoptotic proteins Bcl-xL and Bcl-2. Although the mechanism of apoptosis induction was the same for both enantiomers, they differed in their strength, as stronger antineoplastic activity in vitro was exhibited by isomer (+)-(4R,5S,6R)-1.


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FITC AnnexinV


An article published this year inScientific Reportsusing one of our products,Caspase3”, by our customers from Department of Cellular Biology and Immunology, IPBLN-CSIC, Granada, Spain in the analysis of howCD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism. Congrats and Thanks.


Summay:
In this study, we investigated the role of CD38 in a pristane-induced murine model of lupus. CD38-deficient (Cd38−/−) but not ART2-deficient (Art2−/−) mice developed less severe lupus compared to wild type (WT) mice, and their protective phenotype consisted of (i) decreased IFN-I-stimulated gene expression, (ii) decreased numbers of peritoneal CCR2hiLy6Chi inflammatory monocytes, TNF-α-producing Ly6G+ neutrophils and Ly6Clo monocytes /macrophages, (iii) decreased production of anti-single-stranded DNA and anti-nRNP autoantibodies, and (iv) ameliorated glomerulonephritis. Cd38−/− pristane-elicited peritoneal exudate cells had defective CCL2 and TNF-α secretion following TLR7 stimulation. However, Tnf-α and Cxcl12 gene expression in Cd38−/− bone marrow (BM) cells was intact, suggesting a CD38-independent TLR7/TNF-α/CXCL12 axis in the BM. Chemotactic responses of Cd38−/− Ly6Chi monocytes and Ly6G+ neutrophils were not impaired. However, Cd38−/− Ly6Chi monocytes and Ly6Clomonocytes/macrophages had defective apoptosis-mediated cell death. Importantly, mice lacking the cation channel TRPM2 (Trpm2−/−) exhibited very similar protection, with decreased numbers of PECs, and apoptotic Ly6Chi monocytes and Ly6Clo monocytes/macrophages compared to WT mice. These findings reveal a new role for CD38 in promoting aberrant inflammation and lupus-like autoimmunity via an apoptosis-driven mechanism. Furthermore, given the implications of CD38 in the activation of TRPM2, our data suggest that CD38 modulation of pristane-induced apoptosis is TRPM2-dependent.

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PURE - anti Human Anti Active Caspase-3

Thursday, 15 February 2018


An article published this year in European Journal of Medicinal Chemistry using some of our products, FITC Apoptosis Detection Kit” & “PI/RNASE Solution” by our customers present at the University of Coimbra, Portugal, in the analysis of how Advances on photodynamic therapy of melanoma through novel ring-fused 5,15-diphenylchlorins. Congrats and Thanks.


Summay:
The synthesis, photophysical behaviour and photosensitization ability of novel 4,5,6,7-tetrahydropyrazolo[1,5-a]pyridine-fused 5,15-diphenylchlorins against melanoma cells are described. All studied chlorins were found to be extremely active against melanoma cell lines A375 showing IC50 values below 20 nM. Furthermore, a dihydroxymethyl diphenylchlorin was identified as an excellent candidate to allow modulating of different types of cell death, apoptosis vs. necrosis, by varying its concentration. This can be explored as a tool to improve the effectiveness of PDT since inflammatory response resulting from necrotic cell death after PDT can activate the antitumor immune response with implications also regarding the vascular damage. This feature combined with very low cytotoxicity against human melanoma cells in the absence of light activation and against human fibroblast HFF-1 cells makes this chlorin a candidate of choice as a photosensitizer for PDT. A comprehensive photophysical investigation including the determination of quantum yields for fluorescence, singlet oxygen sensitization and internal conversion, lifetimes and rate constants of all the excited state deactivation processes has been undertaken.


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