An article published this year in “Virus Research” using one of our products, “CF-BlueTM Mouse Anti-Human CD3”, by our customers from the Department of Medical and Clinical Microbiology, Faculty of Medicine, Near East University, Nicosia, Cyprus,  in the analysis of The role of Treg population in pathogenesis of Crimean Congo hemorrhagic fever. Congrats and Thanks.

Summay:

Crimean-Congo hemorrhagic fever (CCHF) is a severe human infection caused by CCHF virus (CCHFV). Today, although the literature on CCHF pathogenesis is still limited, it is thought to be associated with immunosuppression in the early phase of infection followed by pro-inflammatory immune response that may lead to fatal outcomes. The aim of this study is to investigate the role of regulatory T-cells (T_reg cells) in the pathogenesis of CCHFV.

Peripheral blood mononuclear cell samples collected from 14 acute CCHF patients with mild disease course and 13 healthy subjects were included in this study. T_reg expression and functional levels were analyzed by flow cytometry. T_reg cells were identified as CD4+CD25 + CD127dim cells, and their functional levels were compared by measuring their ability to suppress CD69 and CD154 expression by activated T-cells.

The flow cytometry analysis revealed that total T-cell and helper T-cell levels did not vary between the two groups. In contrast, CCHF patients displayed higher T_reg cell levels but lower T_reg suppressive activities when compared with control subjects.

This is the first study on the involvement of T_reg cells in CCHF pathogenesis. Our results indicate that even though T_reg cell levels are elevated during acute phase of CCHF infection, not all generated T_reg cells has immunosuppressive capacity, and therefore may not represent ‘true’ T_reg cell population. Future studies on the intrinsic mechanisms responsible for the reduced T_reg inhibitory activities are required for further enlightening the CCHF pathogenesis, especially in the acute phase of the disease.

Fig. 1. Gating strategy used to sort CD25 + CD127dim Treg cells in CD4 + T-cell population. Following the identification of lymphocytes by forward and size scatter, Treg cells were selected as CD25 + CD127dim cells in the CD3 + CD4 + cell population. The gating strategy resulted in purity of more than %90.

Reference:

https://www.sciencedirect.com/science/article/pii/S0168170218301175#!

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CF-BlueTM Mouse Anti-Human CD3

http://www.immunostep.com/human-antibodies/3779-cd3.html?search_query=3CFB&results=2

An article published this year in “Clinical Cancer Research” using one of our products, “MitoStep + FITC Apoptosis Detection Kit”, by our customers from the Cancer Research Center-IBMCC (USAL-CSIC), Salamanca, Spain and the Hematology Department, University Hospital of Salamanca, SpainU,  in the analysis of how Amiloride, an old diuretic drug, is a potential therapeutic agent for multiple myeloma. Congrats and Thanks.

Summay:

Amiloride-induced apoptosis was observed in a broad panel of MM cell lines and in a xenograft mouse model. Moreover, amiloride also had a synergistic effect when combined with dexamethasone, melphalan, lenalidomide and pomalidomide. RNA-Seq experiments showed that amiloride not only significantly altered the level of transcript isoforms and alternative splicing events, but also deregulated the spliceosomal machinery. Additionally, disruption of the splicing machinery in immunofluorescence studies was associated with the inhibition of myeloma cell viability after amiloride exposure. Although amiloride was able to induce apoptosis in myeloma cells lacking p53 expression, activation of p53 signaling was observed in wild-type and mutated TP53 cells after amiloride exposure. On the other hand, we did not find a significant systemic toxicity in mice treated with amiloride.

Figure. Amiloride induces apoptosis, activates caspases and deregulates mitochondrial potential in MM cell lines. H929, JJN3 and KMS12-BM cells were treated with increasing concentrations of amiloride for 24 h. (A) The induction of apoptosis was Research. Downloaded from clincancerres.aacrjournals.org on August 9, 2017. © 2017 American Association for Cancer Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on August 8, 2017; DOI: 10.1158/1078-0432.CCR-17-0678 28 analyzed by flow cytometry after annexin-V/PI staining. (B) Mitochondrial membrane depolarization was examined by flow cytometry after DilC1(5) staining. (C) The activity of caspase 8, caspase 9 and caspase 3/7 was analyzed by luminescent caspase assays. Results are expressed as the mean ± SD of three independent experiments. Statistically significant differences between untreated and treated cell lines are represented as **p < 0.01 and *p < 0.05 (Student's t-test). 

Reference:

https://www.researchgate.net/profile/Ramon_Garcia-Sanz/publication/319012932_Amiloride_an_old_diuretic_drug_is_a_potential_therapeutic_agent_for_multiple_myeloma/links/59c948c6a6fdcc451d545a92/Amiloride-an-old-diuretic-drug-is-a-potential-therapeutic-agent-for-multiple-myeloma.pdf

Product link:

MitoStep + FITC Apoptosis Detection Kit

http://www.immunostep.com/apoptosis/3739-kmaf-100t.html

An article published this year in “Journal of Colloid and Interface Science” using one of our products, “FITC Apoptosis Detection Kit”, by our customers from the University of Zaragoza, Spain, in the analysis of how Controlled release of bupivacaine using hybrid thermoresponsive nanoparticles activated via photothermal heating. Congrats and Thanks.

Summay:

Near-infrared (NIR) responsive nanoparticles are of great interest in the biomedical field as antennas for photothermal therapy and also as triggers for on-demand drug delivery. The present work reports the preparation of hollow gold nanoparticles (HGNPs) with plasmonic absorption in the NIR region covalently bound to a thermoresponsive polymeric shell that can be used as an on-demand drug delivery system for the release of analgesic drugs. The photothermal heating induced by the nanoparticles is able to produce the collapse of the polymeric shell thus generating the release of the local anesthetic bupivacaine in a spatiotemporally controlled way. Those HGNPs contain a 10 wt.% of polymer and present excellent reversible heating under NIR light excitation. Bupivacaine released at physiological temperature (37 °C) showed a pseudo-zero order release that could be spatiotemporally modified on-demand after applying several pulses of light/temperature above and below the lower critical solution temperature (LCST) of the polymeric shell. Furthermore, the nanomaterials obtained did not displayed detrimental effects on four mammalian cell lines at doses up to 0.2 mg/mL. From the results obtained it can be concluded than this type of hybrid thermoresponsive nanoparticle can be used as an externally activated on-demand drug delivery system.

Reference:

https://www.sciencedirect.com/science/article/pii/S0021979718303631

Product link:

FITC Apoptosis Detection Kit

http://www.immunostep.com/apoptosis/3727-anxvkf-100t.html

An article published this year in “Springer 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.

Reference:

https://link.springer.com/article/10.1007/s00441-018-2825-y

Product link:

PE Mouse anti-Human CD31

http://www.immunostep.com/human-antibodies/2627-cd31.html?search_query=Cd31&results=21

An article published this year in “PlosOne” 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.

Reference:

https://search.proquest.com/docview/2013606597/fulltextPDF/C96A64A8424A468CPQ/1?accountid=17252

Product link:

7AAD

http://www.immunostep.com/solutions-buffers-chemicals/3871-7aad-solution.html?search_query=7AAD&results=1

An article published this year in “IEEExplore 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.

Reference:

https://ieeexplore.ieee.org/abstract/document/8303765/

Product link:

Propidium Iodide

http://www.immunostep.com/solutions-buffers-chemicals/3872-pi-solution.html?search_query=PI&results=52