Podcasts about cytotoxicity

In this episode of The Moss Report, Ben Moss and Dr. Ralph W. Moss explore the science and tradition behind ginger's role in cancer prevention and care. From leukemia stem cells to chemotherapy-induced nausea, ginger shows remarkable promise backed by real-world use and peer-reviewed research. Learn how to use roasted ginger powder, what sets ginger apart from turmeric, and why Dr. Moss believes it's a cornerstone of integrative cancer support. Products Mentioned Great Value Organic Turmeric Powder: https://amzn.to/4hZLT8K Frontier Organic Ginger Powder:  https://amzn.to/42rZsJE Garden of Life Golden Milk Powder: https://amzn.to/4ce9elW Gaia Herbs Golden Milk: https://amzn.to/42jSYvb Consumerlab Review of Ginger Products: https://www.consumerlab.com/reviews/ginger-supplement-review/ginger/?search=Ginger About Prof. Tsvee Lapidot https://bioforumconf.com/6th-international-meeting-of-the-israel-stem-cell-/820-prof-tsvee-lapidot About John Dick, PhD https://www.cdnmedhall.ca/laureates/johndick Important Links “A comprehensive self-help plan for cancer includes medicinal mushrooms. They are indispensable”. – Ralph W. Moss, PhD The Moss Method Mushroom Formula → https://mycolife.us For more information on cancer-fighting foods and supplements, please visit our website: https://www.themossreport.com Get The Moss Method Book →  https://www.amazon.com/gp/product/1881025799/ Moss Report Treatment Guides → https://themossreport.store/guides Dr. Moss' library of previous books → https://themossreport.store/books/ Explore Townsend Letter → https://www.townsendletter.com The deep dive 'Clinic Conversations' between Dr. Moss and Integrative Oncologists from around the world are available at → https://themossreport.com/doctors-clinics The Center for Integrative Oncology - https://www.intonc.org - is dedicated to exploring cancer care worldwide, bringing you in-depth reporting and insights through The Moss Report. As a 501(c)(3) nonprofit, the CIO relies on public support to continue this vital work. Please consider making a donation to help uncover and share current approaches and resources in cancer treatment. Cited Resources • Chueahongthong F, Tima S, Chiampanichayakul S, et al. Co-Treatments of Edible Curcumin from Turmeric Rhizomes and Chemotherapeutic Drugs on Cytotoxicity and FLT3 Protein Expression in Leukemic Stem Cells. Molecules. 2021 Sep 24;26(19):5785. doi: 10.3390/molecules26195785. PMID: 34641328; PMCID: PMC8510311. https://pubmed.ncbi.nlm.nih.gov/34641328 • Crichton M, Marshall S, Isenring E, et al. Effect of a Standardized Ginger Root Powder Regimen on Chemotherapy-Induced Nausea and Vomiting: A Multicenter, Double-Blind, Placebo-Controlled Randomized Trial. J Acad Nutr Diet. 2024 Mar;124(3):313-330.e6. doi: 10.1016/j.jand.2023.09.003. Epub 2023 Sep 10. PMID: 37699474. https://pubmed.ncbi.nlm.nih.gov/37699474 • Lapidot T, Sirard C, Vormoor J, et al. A cell initiating human acute myeloid leukaemia after transplantation into SCID mice. Nature. 1994 Feb 17;367(6464):645-8. doi: 10.1038/367645a0. PMID: 7509044. https://pubmed.ncbi.nlm.nih.gov/7509044 • Panyajai P, Viriyaadhammaa N, Chiampanichayakul S, et al. Anticancer and cancer preventive activities of shogaol and curcumin from Zingiberaceae family plants in KG-1a leukemic stem cells. BMC Complement Med Ther. 2025 Feb 28;25(1):87. doi: 10.1186/s12906-025-04829-7. PMID: 40022126; PMCID: PMC11869560. https://pubmed.ncbi.nlm.nih.gov/40022126 • Shidfar F, Rajab A, Rahideh T, et al. The effect of ginger (Zingiber officinale) on glycemic markers in patients with type 2 diabetes. J Complement Integr Med. 2015 Jun;12(2):165-70. doi: 10.1515/jcim-2014-0021. PMID: 25719344. https://pubmed.ncbi.nlm.nih.gov/25719344

BUFFALO, NY- June 5, 2024 – A new research paper was published in Oncotarget's Volume 15 on June 3, 2024, entitled, “Synergistic cytotoxicity of histone deacetylase and poly-ADP ribose polymerase inhibitors and decitabine in pancreatic cancer cells: Implications for novel therapy.” Histone deacetylase inhibitors (HDACi) can modulate the acetylation status of proteins, influencing the genomic instability exhibited by cancer cells. Poly (ADP ribose) polymerase (PARP) inhibitors (PARPi) have a direct effect on protein poly (ADP-ribosyl)ation, which is important for DNA repair. Decitabine is a nucleoside cytidine analogue, which when phosphorylated gets incorporated into the growing DNA strand, inhibiting methylation and inducing DNA damage by inactivating and trapping DNA methyltransferase on the DNA, thereby activating transcriptionally silenced DNA loci. In this new study, researchers Benigno C. Valdez, Apostolia M. Tsimberidou, Bin Yuan, Yago Nieto, Mehmet A. Baysal, Abhijit Chakraborty, Clark R. Andersen, and Borje S. Andersson from The University of Texas MD Anderson Cancer Center explored various combinations of HDACi and PARPi +/− decitabine (hypomethylating agent) in pancreatic cancer cell lines BxPC-3 and PL45 (wild-type BRCA1 and BRCA2) and Capan-1 (mutated BRCA2). “[...] we explored various combinations of HDACis and PARPis, with or without decitabine, in pancreatic cancer cell lines.” The combination of HDACi (panobinostat or vorinostat) with PARPi (talazoparib or olaparib) resulted in synergistic cytotoxicity in all cell lines tested. The addition of decitabine further increased the synergistic cytotoxicity noted with HDACi and PARPi, triggering apoptosis (evidenced by increased cleavage of caspase 3 and PARP1). The 3-drug combination treatments (vorinostat, talazoparib, and decitabine; vorinostat, olaparib, and decitabine; panobinostat, talazoparib, and decitabine; panobinostat, olaparib, and decitabine) induced more DNA damage (increased phosphorylation of histone 2AX) than the individual drugs and impaired the DNA repair pathways (decreased levels of ATM, BRCA1, and ATRX proteins). The 3-drug combinations also altered the epigenetic regulation of gene expression (NuRD complex subunits, reduced levels). “This is the first study to demonstrate synergistic interactions between the aforementioned agents in pancreatic cancer cell lines and provides preclinical data to design individualized therapeutic approaches with the potential to improve pancreatic cancer treatment outcomes.” DOI - https://doi.org/10.18632/oncotarget.28588 Correspondence to - Apostolia M. Tsimberidou - atsimber@mdanderson.org Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28588 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Joining me today is Jay Couey PhD, here to discuss the ongoing COVID-19 illusion, the many and varied dangers of the COVID injections, and the very serious risk of blindly following the consensus (scientific or otherwise) instead of considering all possibilities and coming to your own conclusions. We also review the overlap of nanotechnology with this conversation, focusing on the lipid nanoparticles within the injections, and discuss the possibility of there being more to these lipids than we have been told.  !function(r,u,m,b,l,e){r._Rumble=b,r[b]||(r[b]=function(){(r[b]._=r[b]._||[]).push(arguments);if(r[b]._.length==1){l=u.createElement(m),e=u.getElementsByTagName(m)[0],l.async=1,l.src="https://rumble.com/embedJS/u2q643"+(arguments[1].video?'.'+arguments[1].video:'')+"/?url="+encodeURIComponent(location.href)+"&args="+encodeURIComponent(JSON.stringify([].slice.apply(arguments))),e.parentNode.insertBefore(l,e)}})}(window, document, "script", "Rumble");   Rumble("play", {"video":"v4c2pcc","div":"rumble_v4c2pcc"}); Source Links: GigaohmBiological's Videos - Twitch (50) Gigaohm Biological Archive Gigaohm Biological (27)

  Join me for a summary of direct to print aligners. This lecture explores the application of a relatively new resin material which can be used for aligner fabrication, without the need of a 3D printed model. The lecture was given by Simon Graf who expertly compared the differences between conventional and direct to print aligners, as well as the clinical application of specific features of direct to print aligners.   Limitations of current aligner material: 1.         Only small undercuts 2.         Limited aligner thickness to sheet thickness / no selective thickness 3.         During the manufacturing process material can get thinner or thicker depending on heat distribution and stretch, 54% change in thickness of the aligner Lee 2022 4.         Plastic and resin waste, (122 million aligners and models in 2022 Slaymaker 2024) Advantages of direct to print aligners ·       Select thickness, 0.5-0.7mm, conventional aligners 0.75mm+ ·       Gingival margin ·       Dentist in charge of design, not company   Manufacturing steps of Direct to Print aligners (Tera Harz ‘Graphy') 1.         3D printing of resin aligner 2.         Centrifuge: Spin remove excess resin 3.         UV Light cure in Nitrogen chamber 4.         Washed twice, hot distilled water Characteristics of Direct to print aligners ·       Greater accuracy: (Zendura, Essix Ace and DTP were compared and DTP were 20-30% more accurate Koenig 2022) ·       Less with DTP (Hertan 2022) o   DTP 50% less still (2.59 Vs 5.26 N) o   DTP Less force as strain increases Shape memory effect ·       DTP Polymer chains crosslinked, not case in conventional aligners o   The shape recovers in DTP when strain is removed, which does not occur to the same degree in conventional aligners Lee 2022 o   Accelerated by placing in water Unknowns ·       How effective shape memory is remains unclear ·       Cytotoxicity – not enough data, although manufacturer protocols, lack of studies ·       Changing thickness, unclear how much of a difference in force it makes   Clinical points Teeth extrusion Lateral incisors ·       Difficult to do with conventional aligners, ·       Create ‘wedging' gingival pressure columns to squeeze the teeth to cause an extrusive force. Elastic Hooks without loss of force delivery on single tooth ·       Hook printed into aligner with DTP, instead of cut out which alters the force of the aligner instantly, maintain tooth control ·       Tip aligners and elastics: Still add attachment to tooth to prevent aligner displacing   Mandibular advancement ·       Problem of mandibular advancement with aligners o   Wings soft and not maintaining the AP position o   Hard block many breakages ·       DTP choice of thickness of block   Bite ramps Conventional bite ramps: limited length and often too short DTP no limit to size and thickness, and can be designed to not contact upper palatal surfaces, maintaining full tooth control    In the Transverse o   Palatal coverage can be added as feature, similar to a TPA o   Still being researched how much force can be delivered with palatal coverage   Concluding statement Enjoy the variability of direct printed aligners.   Contributions Contents: Abdallah Sharafeldin Edited and produced: Farooq Ahmed

⚡️⚡️⚡️در قسمت❌ پنجم ❌In-Sight طبق یک مقاله ی سال ۲۰۲۲ ،اثر سمانهای مختلف بر بافت اطراف ایمپلنت رو بررسی میکنیم.این مقاله مربوط به International journal of denristry هستش و کمک میکنه بهتون بتونید سمان مناسب برای رستوریشن ایمپلنتیتون رو‌انتخاب کنید.‼️‼️پادکست In-Sight مجموعه ای از پادکستهای کوتاهه که در اون ها ما بدون پرداختن به جزئیات ،خلاصه ی مقالات را مرور میکنیمپادکست In-Sight اپیزود میانی دنتکستهاستدکتر فواد شهابیان متخصص پروتز ،ایمپلنت زیباییاهواز کیانپارس061 3338 0090⚡️⚡️لینک ابسترکت مقاله❌❌ Hosted on Acast. See acast.com/privacy for more information.

References Front Immunol. 2023; 14: 1151166. Inflammation Research :official journal of the European Histamine Research Society 2018.1420-908X, Vol. 67, Issue 10. J Cell Sci. 2011 Dec 15; 124(24): 4147–4159. Hunter, R. and J. Garcia 1970. "Sugaree" https://music.youtube.com/watch?v=sxF9UJ-Rm0E&si=S4F0LvlFvUsTE1OO --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

Show Notes: Revisiting the Twilight Zone, the Matrix and the Days of Psychological/Biological Warfare during the implementation of the CCP stylized Draconian COVID RULES, Regulations and Mandates etc. in America and abroad. In this episode we enucleate and thoroughly go through the secret FDA document that has been withheld from the public. I also go through variegated shocking News headlines and global health news

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.28.551009v1?rss=1 Authors: Azevedo, L. P., Rios-Santos, F., Branco, C. B., Pressinotti, L. N., Reis, E. d. M., Filho, S. V., Martins, D. T. d. O., de Vasconcelos, L. G., Ferraz, R. H. d. S., Mesquita, F. V., Silva, W. d. A., Junior, P. T. d. S. Abstract: In previous studies, the oil extracted from the visceral fat of Caiman yacare (Daudin, 1802) demonstrated a wound-healing effect on the skin of Wistar rats. To enhance knowledge our about the mechanism underlying this effect, we analysed the oils toxicological potential in vitro. Cytotoxicity, genotoxicity, pro-oxidant, and antioxidant activities were evaluated in a V79-4 cell line. The oil was obtained using the Soxhlet method, and the proportions of the fatty acid profile was previously identified 43.74 % saturated and 34.65 % unsaturated fatty acids. Protocol 487 of the Organisation for Economic Co-operation and Development (OECD) was employed for cell line selection and concentrations. Cytotoxicity was determined using the MTT assay and clonogenic survival. Pro-oxidant and antioxidant activities were analysed using flow cytometry. Genotoxicity was evaluated using comet and micronucleus assays. The oil did not demonstrate cytotoxicity up to a concentration of 500 g/mL. At concentrations of 250 and 500 g/mL, the oil exerted a protective effect against oxidative stress and showed genotoxic effects only at the highest concentration (2000 g/mL). Like other oils of interest for human health, the oil extracted from the visceral fat of C. yacare demonstrated low toxicological potential in vitro. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.29.538801v1?rss=1 Authors: Lakkaraju, A. K., Tejero, O., Guixa-Gonzalez, R., De Cecco, E., Jungo, M., Tsai, C.-J., Mastromartino, R., Marino, J., Deupi, X., Hornemann, S., Schertler, G. F. X., Aguzzi, A. Abstract: Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.10.527989v1?rss=1 Authors: Carvalho, N. D., Rofatto, H. K., Villar, K. S., Magnelli, R. F., Mendonca, R. Z. Abstract: Brazil has a very large biological variety, which is an almost inexhaustible source of substances of pharmacological and biotechnological interest. Several studies have demonstrated the presence of bioactive peptides in insect hemolymph and their potential use as therapeutic agents. However, few data are available regarding molecules extracted from insects with anti-apoptotic action. The objective of this work was to identify and isolate proteins from the hemolymph of caterpillars of the Megalopygidae family with pharmacological and biotechnological interest. Two species of this family were studied, Podalia sp and Megalopyge albicolis. Cytotoxicity tests on Vero and Sf-9 cells revealed that the hemolymph of both caterpillars were cytotoxic only at concentrations greater than 5%v/v. In the anti-apoptotic activity assays, it was verified that the supplementation of cell cultures with only 1% of hemolymph v/v is sufficient to inhibit cell death by apoptosis induced by different inducers such as terbutyl, actinomycin D, hydrogen peroxide or even by nutrient depletion. For this study, cells were staining with trypan blue, crystal violet and fluorescent markers to cytoskeleton (actin and tubulin), mitochondria membrane electric potential (JC-1) and apoptosis marker (acridine orange and ethidium). The protein responsible for anti-apoptotic action was isolated through gel filtration chromatography, using an AKTA purifier high-resolution liquid chromatography system. The hemolymph was fractionated into 3 pools for Podalia sp and 6 pools for M. abicolis. In the antiapoptotic tests, semi purified hemolymph from both caterpillars showed anti-apoptotic effect in VERO and SF-9 cells, pre-treated with only 1% v/v of hemolymph and induced to death by different and apoptotic inductors. Was observed that the molecule with anti-apoptotic effect are present in pool 3 in both hemolymphs. This protector effect blocked and attenuated the disruption of the cytoskeleton (actin filaments), being that the protective effect also was observed on the integrity of the mitochondrial membrane of SF-9 cells pre-treated with both hemolymphs and treated with the apoptosis inducer Terbutil at concentrations of 25 to 100uM. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.13.511617v1?rss=1 Authors: Ok, M. T., Liu, J., Bliton, R. J., Hinesley, C. M., San Pedro, E. E. T., Breau, K. A., Gomez-Martinez, I., Burclaff, J., Magness, S. T. Abstract: Background & Aims: Clostridioides difficile (C. difficile) toxins A (TcdA) and B (TcdB) cause antibiotic-associated colitis and increase morbidity and mortality. Accurate in vitro models are necessary to detect early toxicity kinetics, investigate disease etiology, and develop pre-clinical models for new therapies. Properties of cancer cell lines and 3D organoids inherently limit these efforts. Here, we develop adult stem cell-derived monolayers of differentiated human colonic epithelium (hCE) with barrier function, investigate the impact of toxin application to apical/basal aspects of monolayers, and evaluate whether a leaky epithelial barrier enhances toxicity. Methods: Single-cell RNA-sequencing (scRNAseq) mapped C. difficile-relevant genes to cell lineages across the human gut. Transcriptomics informed timing of stem cell differentiation to achieve in vitro colonocyte maturation like that observed in vivo. Transepithelial electrical resistance (TEER) and fluorescent dextran permeability assays measured cytotoxicity as barrier loss post-toxin exposure. Leaky epithelial barriers were induced with diclofenac (DCF). Results: scRNAseq demonstrated broad and variable toxin receptor expression across the human gut lineages. Absorptive colonocytes displayed generally enhanced toxin receptor, Rho GTPase, and cell junction expression. 21-day differentiated Caco-2 cells remained immature whereas hCE monolayers were similar to mature colonocytes. hCE monolayers exhibited high barrier function after 1-day differentiation. Basal TcdA/B application to monolayers caused more toxicity and apoptosis than apical exposure. DCF induced leaky hCE monolayers and enhanced toxicity of TcdB exposure. Conclusions: hCE monolayers represent a physiologically relevant and sensitive culture system to evaluate impact of microbial toxins on gut epithelium, demonstrate uncoupled onset and magnitude of apical/basal toxicities with delayed apical toxicity, and highlight that leaky paracellular junctions enhance toxicity of apical TcdB exposure. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

References Mechanisms of Ageing and Development 2016. 156: 25-33 The Journal of Biological Chemistry 2018. 293: 2422-2437 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

In this episode, we review the high-yield topic of Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) from the Immunology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbulletsIn --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Dr. Stanley Lipkowitz and Dr. Yoshimi Endo Greer from the Women's Malignancies Branch at the National Cancer Institute discuss a research paper they co-authored that was published by Oncotarget in 2018, entitled, "ONC201 kills breast cancer cells in vitro by targeting mitochondria." DOI - https://doi.org/10.18632/oncotarget.24862 Correspondence to - lipkowis@mail.nih.gov Abstract We report a novel mechanism of action of ONC201 as a mitochondria-targeting drug in cancer cells. ONC201 was originally identified as a small molecule that induces transcription of TNF-related apoptosis-inducing ligand (TRAIL) and subsequently kills cancer cells by activating TRAIL death receptors. In this study, we examined ONC201 toxicity on multiple human breast and endometrial cancer cell lines. ONC201 attenuated cell viability in all cancer cell lines tested. Unexpectedly, ONC201 toxicity was not dependent on either TRAIL receptors nor caspases. Time-lapse live cell imaging revealed that ONC201 induces cell membrane ballooning followed by rupture, distinct from the morphology of cells undergoing apoptosis. Further investigation found that ONC201 induces phosphorylation of AMP-dependent kinase and ATP loss. Cytotoxicity and ATP depletion were significantly enhanced in the absence of glucose, suggesting that ONC201 targets mitochondrial respiration. Further analysis indicated that ONC201 indirectly inhibits mitochondrial respiration. Confocal and electron microscopic analysis demonstrated that ONC201 triggers mitochondrial structural damage and functional impairment. Moreover, ONC201 decreased mitochondrial DNA (mtDNA). RNAseq analysis revealed that ONC201 suppresses expression of multiple mtDNA-encoded genes and nuclear-encoded mitochondrial genes involved in oxidative phosphorylation and other mitochondrial functions. Importantly, fumarate hydratase deficient cancer cells and multiple cancer cell lines with reduced amounts of mtDNA were resistant to ONC201. These results indicate that cells not dependent on mitochondrial respiration are ONC201-resistant. Our data demonstrate that ONC201 kills cancer cells by disrupting mitochondrial function and further suggests that cancer cells that are dependent on glycolysis will be resistant to ONC201. Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.24862 Press release - https://www.oncotarget.com/index.php?journal=oncotarget&page=news&op=press&item=onc201-kills-breast-cancer-cells-in-vitro-by-targeting-mitochondria Keywords - ONC201, breast cancer, mitochondria About Oncotarget Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/OncotargetYouTube LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Oncotarget is published by Impact Journals, LLC: https://www.ImpactJournals.com Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

In this episode of RCA Radio, host Brandon Miller is joined by Dr. Matthew Jorgensen and Dr. Helin Räägel, Matt a board-certified toxicologist with a Ph.D. in chemistry and is Nelson Laboratory's Chemistry and Materials Scientist and Helin is Nelson Labs Senior Biocompatibility Expert with a Ph.D. in cell biology.Listen in as Matt and Helin help educate our listers about the world of pre-clinical testing/biocompatibility for medical devices by taking a deep dive into cytotoxicity testing of medical devices in this part of the Intro into Biocompatblity podcast series.About RCARegulatory Compliance Associates® Inc. (RCA) provides worldwide services to the following industries for resolution of compliance and regulatory challenges:PharmaceuticalBiologic & BiotechnologySterile compoundingMedical deviceWe understand the complexities of running a life science business and possess areas of expertise that include every facet of R&D, operations, regulatory affairs, quality, and manufacturing. We are used to working on the front lines and thriving in the scrutiny of FDA-and globally-regulated companies.As your partners, we can negotiate the potential minefield of regulatory, compliance, quality, and private equity due diligence with insight, hindsight, and the clear advantage of our unique expertise and experience.About Nelson LabsEvery year, hundreds of medical device, pharmaceutical, and tissue companies make Nelson Labs their testing laboratory of choice. For them, the decision is easy. Nelson Labs is a clear leader in the microbiology and analytical chemistry testing industry, offering more than 800 laboratory tests and employing more than 500 scientists and staff in state-of-the-art facilities. We are known for exceptional quality and rigorous testing standards, but it is our focus on the bigger picture that sets us apart. We look beyond test results and partner with you to achieve your long-term business goals — mitigating risk, being first to market, and succeeding with your customers.Companies choose Nelson Labs for our:Thought leaders and approachable experts. We give you direct access to industry authorities who understand your business and add value every step of the way.Customer-centric culture. We take the time to understand your vision. Your goals become our goals.Real-time project management tools and a dedicated client portal. We provide proactive information, keeping you informed and in control.Metric-driven testing processes. We're our own toughest customer, holding ourselves to goals exceeding 99% for things that matter most to you, like quality, turnaround time, and testing accuracy.Global compliance expertise and support. We act as a trusted advisor, helping you navigate the ever-changing compliance landscape.See how we can help you mitigate risk, be first to market, and succeed with your customers. 

Bulletproof Hygiene Podcast Episode 49 Hosts: Charissa Wood, RDH  & Brittany Simon, CRDH, BASDH Guest: Tracy Jacobs Key Takeaways: IntroductionStella LifeIntelligent Healing References: Summit Mighty Networks: Bulletproof Hygiene  Bulletproof Hygiene: The Guide For Finding Fulfillment Through Purposeful, Profitable Hygiene Stella Life Promo Code: 30OFFTJJProduct Specialist: Tracy Jacobs tjacobs@stellalife.com770-598-4755 Cytotoxicity and Gene Expression Changes of a Novel Homeopathic Antiseptic Oral Rinse in Comparison to Chlorhexidine in Gingival Fibroblasts VEGA Oral Recovery Care - Dental Healing Spray, Gel, Rinse-Stella Life – StellaLife Tweetables: We're here to help, not to hinder. Tracy Jacobs

ILC3 can contribute to the progression and aggravation of IBD's while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR− ILC3 or NCR+ ILC3 function NCR (natural cytotoxicity receptors), are type 1 transmembrane proteins of the immunoglobulin superfamily. Upon stimulation, NCR's mediate NK killing and release of IFNγ. They bind viral ligands such as hemagglutinins, neuraminidases, bacterial ligands, and cellular ligands related with auto immune diseases, tumour growth, and associated aging morbidity. References Experimental & Molecular Medicine volume 51, Article number: 80 (2019) Cell Death & Disease volume 10, Article number: 315 (2019) Front. Immunol., 28 September 2015 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika Vijay.In today's episode, I will be introducing Pharmacodyamics, definition, concept, and try to cover as one line statement, two line statement!!To begin with, today's little contemplation about Criticism, how big deal is it?, how important and wisely you can deal with it, is it really worth a panic? and much more!!And then as our topic proceeds, we will talk about the important drug actions like stimulation, depression, cytotoxicity, replacement, etc.And later I will cover important sites of drug action like Extracellular, Cellular and Intracellular!With these little but important concepts and knowledge bytes, I will be wrapping up with a great tip to be generous with praise and cautious with criticism, and pray and wow never to be trapped in either one!! For all the updates and latest episodes of my podcast, please visit www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine. It actually contains lot of updates about the medical sciences, drug information and my podcast updates also. You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!!You can access various links viahttps://linktr.ee/ispharmacologydifficult

Please comment by August 9, 2021 to tell HHS/WHO to please keep kratom legal worldwide. Politely share your kratom story here, make sure you get a confirmation email and tracking number, and under “What are you commenting about?” Select “International Government – I0037” https://www.federalregister.gov/documents/2021/07/23/2021-15685/international-drug-scheduling-convention-on-psychotropic-substances-single-convention-on-narcotic?fbclid=IwAR1jTz7JSte491H5eTQBwjrivN4Y60s1t-kIPc1iy9UvnjfY2kkwHNFuBvM Disclaimer: None of the content on this podcast or on KratomScience.com … Journal Club #23: Kratom alkaloid combo shown to help chemotherapy drug in killing cancer cells, more research needed Read More » The post Journal Club #23: Kratom alkaloid combo shown to help chemotherapy drug in killing cancer cells, more research needed first appeared on Kratom Science.

In this week's episode, Nathalie chats with Jean-François Tremblay start the conversation with  LL37 – a powerful antimicrobial peptide naturally synthesized in humans.  They then move on to a new hybrid peptide bringing Thymosin Alpha 1 and LL37 – designed to potentially mitigate the natural cytotoxic effects of LL37.   They then move on to the synthetic versions of the bioregulator peptides produced by CanLab and correct a commonly held misconception about proper dosing levels.  The good news is that Bioregulators just became a lot more affordable!  We then move on to GHK…and much much more!   Meet This Week's Guest Jean-Francois Tremblay is the owner of CanLab, a Montreal based company that specializes in synthesizing and manufacturing peptides. Jean-François Tremblay is a regular guest on this podcast.  Jean-Francois studied Exercise Physiology, Biochemistry, and Pharmacy at UQAM.  He has been researching (in theory and in practice) peptides and SARMS since the 90's and has been studying the theoretical basis of what peptides are and their practical applications in sports performance, anti-aging, and health in general.    Episode Sponsor:  drinkHRW.com To get the most out of any therapy it is crucial to address the foundations of health.  Molecular Hydrogen addresses  these foundations through its ability to help to manage reactive oxygen species (ROS), inflammation and improve metabolic balance.  I drink molecular hydrogen water every morning before anything else and have my clients do the same.  Anecdotally we have seen improvements in blood sugar control, pain from arthritis and even cognitive function in a Parkinson's patient.  Ongoing research is demonstrating the many ways that molecular hydrogen can support human health.     Use promo code Lonegvity10 to save 10% off your purchase at drinkHRW.com    Key Takeaways [03:35] Ll-37 can it possibly play a role in dealing with the current crisis? [07:13] Ll-37 to treat HIV… [08:00] Cytotoxicity (the dying of good cells) with ll-37. How can we mitigate that reaction? [09:08] Vitamin D levels and immunity; genetic variations that inhibit vitamin D conversion [11:23] How does air pollution effect health and natural ll-37 levels? [15:30] Ll-37/TA1 hybrid peptide.. What can it treat? Why does it work? [22:27] Dosing of ll-37/TA1 [28:00] Let's talk bioregulator peptides.. Synthetic vs natural? Oral vs injection? [33:15] Dosing of synthetic vs natural bioregulator peptides [41:00] Is Epitalon an anti-cancer compound? [43:23] Bioregulator peptides and their effects on other organs… [47:30] Thymosin beta 4's use in anti-aging and heart treatment... [51:00] Mots-C for energy and chronic fatigue.. [54:14] GHK and it's effect on genetics, skin and more… What is the best protocol for GHK?.. [60:01] Insulin pumps for peptides?.. Check out https://canlabsciences.com/ and use Promocode OSP15 for your purchase   Linkage: Study discussed re Human Cathelicidin (LL37) & Covid19 Insulin Pump   DISCLAIMER:  This podcast and the information presented are for informational purposes only and not intended to diagnose or treat disease.  Before making any changes to your nutrition or supplementation please check with your physician or health provider.  Most peptides are classified as research chemicals and are not intended for human use – this podcast in no way is promoting or endorsing the personal use of peptides beyond research purposes.

In this episode, our guests are joined my NAMSA’s Melissa Cadaret to discuss the ever-confusing cytotoxicity failure.  Manufacturers can have more questions created when encountering an unexpected cytotoxicity result and these podcast experts have seen thousands of various cytotoxicity results.  The information provided from a cytotoxicity test can be useful and stressful, so what do manufacturers need to know to navigate the cyto failure, whether expected or unexpected. “I would say we generally see some type of cytotoxicity failure weekly.” –Melissa Cadaret  “Cytotoxicity is not really an end point. It’s a screen.” – Sheri Krajewski-Bibins “It is what it is and it is what it’s not.” – Don Pohl “It’s the only biological effect listed as an overall screen for biocompatibility.” – Don Pohl “Things like copper, and antimicrobials really wreak havoc and contribute to a lot of cytotoxicity failures.  Some of your residues from your cleaning and in processing aspect are also a huge culprit.”  Melissa Cadaret  “It might have been expected.  You can get pretty good at predicting cytotoxicity.” – Don Pohl Discussion points include:  What does it mean when one receives a failed cyto result  What is the useful information you can gather from a cytotoxicity test What typical materials and devices may have problems with a cytotoxicity test What to do if you know your material is going to fail cyto

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.17.253591v1?rss=1 Authors: Fadilah, F., Andrajati, R., Arsianti, A., Paramita, R. I., Erlina, L., Yanuar, A. Abstract: Eugenol derivatives can inhibit BCL-2 in HT29 colorectal cancer cells. This study is aimed to acquiring new compounds of Eugenyl benzoate (2-methoxy-4-(prop-2-en-1-yl)phenyl benzoate) derivatives that can inhibit HT29 colorectal cancer cells. In this research, we used several chemical reactions to synthesize novel compounds, such as Esterification, Demethylation, Halohydrin, and Sharpless reaction. Cytotoxicity assays were performed to test the inhibitory activity of compounds against HT29 colon cancer cells. QSAR analysis were carried out to analyse the relationship of chemical structure of the novel compounds with their cytotoxic activity. Ten novel compounds were successfully synthesized and tested in vitro against the HT29 cell. The IC 50 of the novel compounds were between 26.56 {micro}mol/ml - 286.81 {micro}mol/ml which compound 4-[(2S)-2,3-dihydroxypropyl]-2-methoxyphenyl 2-hydroxybenzoate (9) showed as best active compound as BCL-2 inhibitors better than other synthesized compounds and Eugenol as well. QSAR analysis of the in vitro results gave a Log equation: 1/IC 50 = -0.865-0.210 (LogP) 2 + 1,264 (logP)-0.994 CMR (n = 10; r = 0.706; SE: 0.21; F = 0.497, sig = 7.86). The equation shows the log variable P and CMR affect IC 50 . The properties of hydrophobicity (log P) are more instrumental than the ones of steric (CMR). Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.13.249201v1?rss=1 Authors: Moharir, S. C., Raghawan, A. K., Swarup, G. Abstract: Optineurin (OPTN), a cytoplasmic adaptor protein involved in cargo selective autophagy of bacteria, damaged mitochondria and mutant protein aggregates, is frequently seen in pathological structures containing protein aggregates, associated with several neurodegenerative diseases. However, the function of OPTN in these protein aggregates is not known. Here, we have explored the role of OPTN in mutant protein aggregation and in cytoprotection from toxicity of mutant proteins. Mutant huntingtin (mHtt) and mutant ataxin-3 (mAtax-3) showed reduced formation of aggregates in Optn-/- mouse embryonic fibroblasts as compared with wild type cells. Co-expression of OPTN enhanced aggregate formation by mHtt and mAtax-3 in Optn-/- cells. C-terminal domain of OPTN (412-577 amino acids) was necessary and sufficient to promote aggregate formation by these mutant proteins. The E478G mutant of OPTN, defective in ubiquitin-binding and autophagy, was also able to promote aggregation of mHtt and mAtax-3. OPTN and its C-terminal domain form a complex with the chaperone HSP70 known to promote mutant protein aggregation. Overexpression of mHtt or mAtax-3 induced more cell death in Optn-/- cells compared with wild type cells. Importantly, compared to wild type cells, Optn-deficient cells having mHtt or mAtax-3 aggregates showed higher level of cell death in neuronal (N2A) and non-neuronal cells. Our results show that OPTN promotes formation of mutant huntingtin and mutant ataxin-3 aggregates, and this function of OPTN might be mediated through interaction with HSP70 chaperones. Our results also show that OPTN reduces cytotoxicity caused by these mutant protein aggregates. Copy rights belong to original authors. Visit the link for more info

In this episode, we'll look at the market for cell-based assays, including it's market size and growth opportunities, while also highlighting some data from a recent survey we conducted in 2019.

Cytotoxicity, sensitization and irritation, sometimes known as CSI, are three of the most common tests performed on medical devices. In this episode, our hosts discuss these tests, common pitfalls and how to address regulatory expectations

Kenya is set to begin open field trials of GMO cotton in March 2019, following the approval for national performance trials by the National Environment Management Authority (NEMA) in 2018. [In June 2018, it was reported that Kenya would start growing GMO cotton on a commercial basis in 2019.] This would make us the first in East Africa to grow GMOs in open fields, and fourth in Africa after South Africa, Burkina Faso and Sudan. BT cotton is among six crops that have been under confined field trials. The others are drought-tolerant maize, biofortified sorghum, viral resistant cassava, nutritionally enhanced cassava and gypsophila paniculata cut flowers. We’re joined by Anne Maina, co-ordinator of the Kenya Biodiversity Coalition, to discuss GMOs and food safety. Resources Kenya gears up for GMO cotton from next year Biotech maize field trials fail to get crop agency green light US seeks to push Kenya, other African countries to adopt GM crops Genetically modified Bt cotton not worth the hype Kenya soon to lift ban on production of genetically modified cotton, maize The future of cotton is not in genetically modified version Kenya rules out open trials on genetically modified crops Scientists say growing genetically-modified crop will revive local textile sector Why lifting GMO ban remains contentious despite attempts to introduce it in Kenya Feeding 9 Billion The biggest hurdle genetically engineered food faces isn’t science—it’s us Genetically Modified Foods: Breeding Uncertainty The Monsanto GMO Story: Adding a Fish Gene Into Tomatoes The GE Process Republished study: long-term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize Cytotoxicity on human cells of Cry1Ab and Cry1Ac Bt insecticidal toxins alone or with a glyphosate-based herbicide Genetically modified crops safety assessments: present limits and possible improvements Resource Guide to Organic Insect and Disease Management Kenya Apparel and Textile Industry: Diagnosis, Strategy and Action Plan How Monsanto’s GM cotton sowed trouble in Africa Burkina Faso calls time on Monsanto's GM cotton, demands $280m damages The Environmental Costs of Fast Fashion Fast fashion: Inside the fight to end the silence on waste Fast Fashion Is Killing People (Seriously!) Monsanto ordered to pay $289m as jury rules weedkiller caused man's cancer 'The world is against them': new era of cancer lawsuits threaten Monsanto The man who beat Monsanto: 'They have to pay for not being honest' Roundup weed killer lawsuit hits a snag, but Monsanto is not off the hook Integrated Pest Management (IPM) How to practice Integrated Pest Management? Biodiversity and Its Importance Episode 66: The Politics of Food in Nairobi Episode 78: Public Finance and the Right to Food [Part 1] Episode 79: Public Finance and the Right to Food [Part 2] Image Credit: Cornell Alliance for Science

Activation of immune cells is the all-important first step in mounting an immune response. Immune cell activation is a popular area of research because so much happens that is key to the downstream goal of fighting infection, cancer, and disease. There are many ways to measure immune cell activation, and they all have utility. Methods can be grouped into four main categories: Proliferation Assays, Cytokine Measurement, Surface Antigen Expression, and Cytotoxicity. In this webinar, we'll discuss specific assays in each of these categories, the joys and pitfalls of each assay, and recommendations on how to choose the best method. You will learn tips and strategies for successful assay development using the following methods: Proliferation: - 3H-Thymidine Uptake - Bromodeoxyuridine Uptake (BrdU) - ATP Luminescence - Fluorescent Dye Reduction (CFSE) Cytokine Measurement: - Multiplex vs. Single Cytokine - Choice of Cytokine (IFNg, TNFa, IL-6, IL-1?, etc.) - Kinetics of Cytokine Release Surface Antigen Expression: - CD69, CD25, PD-1, etc. - Combine with CFSE, Ki67 or BrdU - Kinetics are Important Cytotoxicity: - Two-Label Flow Cytometry - Calcein AM Dye Release - Luciferase Transduced Targets - Annexin V

Dina Morshedi, National Institute of Genetic Engineering and Biotechnology, Department of Industrial & Environmental Biotechnology, Tehran - IRAN. This seminar has been recorded at Area Science Park Trieste by ICGEB Trieste

After trauma, articular cartilage often does not heal due to incomplete bonding of the fractured surfaces. In this study we investigated the ability of chemical cross-linkers to facilitate bonding of articular cartilage, either alone or in combination with a pre-treatment with surface-degrading agents. Articular cartilage blocks were harvested from the femoropatellar groove of bovine calves. Two cartilage blocks, either after pre-treatment or without, were assembled in a custom-designed chamber in partial apposition and subjected to cross-linking treatment. Subsequently, bonding of cartilage was measured as adhesive strength, that is, the maximum force at rupture of bonded cartilage blocks divided by the overlap area. In a first approach, bonding was investigated after treatment with cross-linking reagents only, employing glutaraldehyde, 1-ethyl-3diaminopropyl-carbodiimide (EDC)/N-hydroxysuccinimide (NHS), genipin, or transglutaminase. Experiments were conducted with or without compression of the opposing surfaces. Compression during cross-linking strongly enhanced bonding, especially when applying EDC/NHS and glutaraldehyde. Therefore, all further experiments were performed under compressive conditions. Combinations of each of the four cross-linking agents with the degrading pretreatments, pepsin, trypsin, and guanidine, led to distinct improvements in bonding compared to the use of cross-linkers alone. The highest values of adhesive strength were achieved employing combinations of pepsin or guanidine with EDC/NHS, and guanidine with glutaraldehyde. The release of extracellular matrix components, that is, glycosaminoglycans and total collagen, from cartilage blocks after pre-treatment was measured, but could not be directly correlated to the determined adhesive strength. Cytotoxicity was determined for all substances employed, that is, surface degrading agents and cross-linkers, using the resazurin assay. Taking the favourable cell vitality after treatment with pepsin and EDC/NHS and the cytotoxic effects of guanidine and glutaraldehyde into account, the combination of pepsin and EDC/NHS appeared to be the most advantageous treatment in this study. In conclusion, bonding of articular cartilage blocks was achieved by chemical fixation of their surface components using cross-linking reagents. Application of compressive forces and prior modulation of surface structures enhanced cartilage bonding significantly. Enzymatic treatment in combination with cross-linkers may represent a promising addition to current techniques for articular cartilage repair.

Background/Aims: We investigated the effect of the peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist pioglitazone on growth and TRAIL-induced apoptosis in carcinoid cells. Methods: Carcinoid cells were incubated without and with pioglitazone. Effects on growth were examined by cell count and cell cycle analysis. p21(waf1/cip1) expression was determined by Western blotting. Cytotoxicity assay was performed by FACS analysis. Results: Pioglitazone suppressed the growth and induced apoptosis of carcinoid cells. Additionally, pioglitazone significantly enhanced carcinoid cell death induced by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). The enhancement of TRAIL-induced apoptosis was associated with an upregulation of cyclin-dependent kinase inhibitor p21(waf1/cip1) in pioglitazone-treated carcinoid cells. Importantly, overexpression of p21(waf1/cip1) in carcinoid cells by adenoviral gene transfer of p21 sensitized them to TRAIL-induced apoptosis. Conclusions: These results suggest that pioglitazone inhibits cell growth and sensitizes cells to TRAIL-induced apoptosis by induction of p21(waf1/cip1). Therefore, pioglitazone can be an effective therapeutic adjuvant for the treatment of carcinoid tumors. Copyright (C) 2001 S. Karger AG, Basel.

INFECTION of mice with viruses can generate cytotoxic T lymphocytes (CTL) which show restricted specificity for target cell lysis. Specific lysis requires that the virus used to prime the target cells must be of the same type as that used to sensitise the CTL, and that both target and CTL cells must express the same major histocompatability complex (MHC) gene product(s). The nature of the viral gene product(s) and their interaction with the MHC gene product(s) have been the subject of recent stud1−5. Previously we used Sendai virus to show that lysable target cells can be obtained using membrane vesicles which contain only the viral glycoproteins, indicating that these may be the specific viral gene products involved in target formation5. Sendai virus contains two glycoproteins—the haemagglutinin-neuraminidase (HANA) which promotes attachment of virus to cells and the fusion protein (F) which is involved in subsequent virus cell fusion7−9. Both activities are necessary for insertion of these viral glycoproteins into the plasma membrane of the cell10. In this letter we suggest that the insertion of the viral glycoproteins into the cell membrane is an essential step in target cell formation since we can show that virus containing an inactive fusion protein precursor (F0) cannot elicit T cell cytotoxicity unless the fusion activity is generated by proteolytic cleavage of the precursor. Sugamura et al. 6 have suggested that it is primarily the F glycoprotein of the Sendai virus envelope which is essential for the formation of the target antigen, as virus lacking the functional activities of F following trypsin digestion was inactive in priming target cells for T cell killing. However, we show that proteolytic inactivation of either of the two glycoproteins (F or HANA) of virus used to prime target cells will abolish the cytotoxic response.

CYTOTOXIC T cells lyse only those virus infected target cells in vitro which express, in addition to the viral antigen(s), those K or D region products of the major histocompati-bility complex (MHC) which were present during anti-viral sensitisation in vivo. This 'associative recogniton' by cytotoxic T cells could reflect the interaction of two T-cell receptors with specificity for target K or D gene products and independently for the viral antigen, or one receptor with specificity for virally altered K or D region products (see ref. 1 and refs therein). There are various ways that the MHC antigens could be altered, including 'modification from within', where the virus modifies host protein synthesis by interfering with transcription2, translation or post-translational glycosylation; or 'modification from without' where enzymic or chemical alteration of cell membrane proteins are induced by virus activity at the cell surface. In this report we show that inactivated Sendai virus or isolated Sendai virus envelopes can serve to modify a cell and make it a specific target for Sendai-immune T-cell killing, thus excluding the possibility of 'modification from within' in this system.

Thu, 1 Jan 1976 12:00:00 +0100 https://epub.ub.uni-muenchen.de/6776/1/6776.pdf Koszinowski, Ulrich H.; Ertl, H. ddc:610, Medizin

Tue, 1 Jan 1974 12:00:00 +0100 https://epub.ub.uni-muenchen.de/6977/1/Koszinowski_Ulrich_6977.pdf Volkmann, B.; Koszinowski, Ulrich H. ddc:610, Medizin

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.22.055152v1?rss=1 Authors: Pan, C.-Y., Lin, F.-Y., Kao, L.-S., Huang, C.-C., Liu, P.-S. Abstract: Zinc ions (Zn 2+ ) are important messenger molecules involved in various physiological functions. To maintain the homeostasis of cytosolic Zn 2+ concentration ([Zn 2+ ] c ), Zrt/Irt-related proteins (ZIPs) and Zn 2+ transporters (ZnTs) are the two families of proteins responsible for decreasing and increasing the [Zn 2+ ] c , respectively, by fluxing Zn 2+ across the membranes of the cell and intracellular compartments in opposite directions. Most studies focus on the cytotoxicity incurred by a high concentration of [Zn 2+ ] c and less investigate the [Zn 2+ ] c at physiological levels. Zinc oxide-nanoparticle (ZnO-NP) is blood brain barrier-permeable and elevates the [Zn 2+ ] c to different levels according to the concentrations of ZnO-NP applied. In this study, we mildly elevated the [Zn 2+ ] c by zinc oxide-nanoparticles (ZnO-NP) at concentrations below 1 mg/ml, which had little cytotoxicity, in cultured human neuroblastoma SH-SY5Y cells and characterized the importance of Zn 2+ transporters in 6-hydroxy dopamine (6-OHDA)-induced cell death. The results show that ZnO-NP at low concentrations elevated the [Zn 2+ ] c transiently in 6 hr, then declined gradually to a basal level in 24 hr. Knocking down the expression levels of ZnT 1 (mostly at the plasma membrane) and ZIP 8 (present in endosomes and lysosomes) increased and decreased the ZnO-NP-induced elevation of [Zn 2+ ] c , respectively. ZnO-NP treatment reduced the basal levels of reactive oxygen species and Bax/Bcl-2 mRNA ratios; in addition, ZnO-NP decreased the 6-OHDA-induced ROS production, p53 expression, and cell death. Therefore, mild elevations in [Zn 2+ ] c induced by ZnO-NP activate beneficial effects in reducing the 6-OHDA-induced cytotoxic effects. Therefore, brain-delivery of ZnO-NP can be regarded as a potential therapy for neurological disease. Copy rights belong to original authors. Visit the link for more info