Warning You have reached the maximum number of saved studies Listing a study does not mean it has been evaluated by the U. Federal Government. Read our disclaimer for details. Last Update Posted : February 16, Study Description. The purpose of this study is to examine the impact of ascorbic acid vitamin c and zinc gluconate in reducing duration of symptoms in patients diagnosed with coronavirus disease COVID Patients above the age of 18 who present to the Cleveland Clinic outpatient testing and receive a positive test for COVID will be invited to participate.
Detailed Description:. FDA Resources. Arms and Interventions. Readily available marketed open label ascorbic acid. Readily available marketed open label zinc gluconate. Readily available marketed open label ascorbic acid and zinc gluconate. Standard of care medications only as prescribed by patient's physician. Outcome Measures. Primary Outcome Measures : Symptom Reduction [ Time Frame: 28 days ] Number of days to reach a 50 percent reduction in the cumulative symptom score with each symptom evaluated on a scale.
Differences in hospitalization events between the study arms. Differences in severity of symptoms between study arms. Differences in number of patients who were prescribed adjunctive medications for their diagnosis between study arms.
Differences in number of patients in study arms who experienced side effects from the supplements. Eligibility Criteria. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision.
Also, considering that H3N2 influenza virus shows a good circulation in humans and pigs as well as a slow antigenic drift in swine 14 , we believe that the antigenic divergence between human and swine influenza virus might be increased. Therefore, our results shown in Fig. To clarify the underlying mechanisms on the survival by the presence of the sufficient amounts vitamin C in the mice, we examined the viral titers in the lung of each experimental group.
As shown in Fig. This provides the importance of the vitamin C concentration at the initial stage of influenza virus infection. That is to say, damages through the replication of influenza viruses can be effectively prevented, when vitamin C concentration is sufficiently high at the initial stage of viral infection.
If it is insufficient, however, the pathogenesis of influenza virus could not be prevented. And then the survival of mice was monitored for 7 days after virus inoculation. This result proves that vitamin C is an essential factor for the production of anti-vital immune response during the early phase of virus infection through the production of type I IFNs.
The phosphorylation of signal transducers and activators of transcription STATs is the critical signaling process after the dimerization of its receptors, when type I IFNs are increased 17 , Results are representative of three independent experiments and each performed in triplicates. The defects on the production of type I IFNs followed by the activation of STATs are closely related to the inflammatory responses due to the failure of controlling virus replication at the initial stage of its infection At the same time, the infiltration of inflammatory cells into the lung is increased approximately 2.
And then the excessive inflammatory responses were occurred by the in vivo challenge of concanamycin A D After centrifugation of BAL fluids, the numbers of infiltrated immune cells into the lung upon influenza A virus infection of in the presence or absence of vitamin C were counted under microscope.
Therefore, it might be possible that the maintaining sufficient levels of vitamin C in the plasma by the continuous uptake through the diet or supplement could effectively prevent in vivo pathogenesis of influenza virus at the initial stage of viral infection.
The illness and mortality of mice were then monitored daily for 7 day. After 1 day of IAV, blood was collected from the intra-orbital plexus with a heparinized capillary tube. Total cell numbers per BAL was determined by counting under the microscope.
Unpaired two-tailed t test was used to compare the two groups WT vs. Statistical tests were carried out using GraphPad InStat version 5. The authors have no financial conflict of interest. National Center for Biotechnology Information , U. Journal List Immune Netw v. Immune Netw. Published online Apr Find articles by Yejin Kim.
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Corresponding author: Jeffrey I. Copyright notice. The publisher's final edited version of this article is available at Leuk Lymphoma. See other articles in PMC that cite the published article. Abstract Ascorbic acid has been shown to kill various cancer cell lines at pharmacologic concentrations. Keywords: Ascorbic acid, Epstein Barr virus, Burkitt, lymphoma, reactive oxygen species, bortezomib.
Reagents Ascorbic acid and bovine liver catalase were obtained from Sigma-Aldrich St. Combination Studies Combination studies were performed and analyzed as previously described [ 25 ]. Measurement of Ascorbic Acid Levels in Plasma Peripheral blood was collected in heparinized tubes from animals injected either i.
Open in a separate window. Figure 1. Table I EC50s for EBV-positive and negative B cell lines treated with ascorbic acid Each value represents the average of four experiments that were performed in triplicate as well as the SD for the data. Figure 2. Figure 3. Caspase 3 cleavage is not induced by ascorbic acid Cells were treated with 2 mM ascorbic acid for 8, 24, or 48 hr, lysates were prepared and analyzed by immunoblotting with anti-caspase 3 antibodies.
Figure 4. Q-VD, a general caspase inhibitor, does not protect from ascorbic acid-induced cell death A. Figure 5. Ascorbic acid does not induce EBV lytic reactivation Cells were treated with 2 mM ascorbic acid for 8, 24, or 48 hr, and lysates were analyzed by immunoblotting with an anti-BZLF-1 antibody.
Ascorbic Acid Induces Production of ROS Catalase is a powerful antioxidant and scavenger of hydrogen peroxide which previously was shown to be protective against ascorbic acid-induced cell death caused by the production of ROS [ 19 ]. Figure 6. Figure 7. Ascorbic acid is antagonistic to bortezomib based on isobologram plots of lymphoma cell lines A. Figure 8. Ascorbic acid inhibits the activity of bortezomib even when treatment with ascorbic acid is delayed A.
Figure 9. Ascorbic acid does not increase survival of SCID mice inoculated intraperitoneally i. Ascorbic acid does not prolong survival or affect the size of masses in SCID mice inoculated subcutaneously s. Mice inoculated intraperitoneally i. Cohen JI. Epstein-Barr Virus Infection. N Engl J Med. Current understanding of the role of Epstein-Barr virus in lymphomagenesis and therapeutic approaches to EBV-associated lymphomas. Leukemia and Lymphoma.
Gastric carcinoma: monoclonal epithelial malignant cells expressing Epstein-Barr virus latent infection protein. Transcriptional analysis of Epstein-Barr virus gene expression in EBV-positive gastric carcinoma: unique viral latency in the tumour cells. Br J Cancer. Expression of Epstein-Barr virus latent gene products in tumour cells of Hodgkin's disease. Clonal proliferations of cells infected with Epstein-Barr virus in preinvasive lesions related to nasopharyngeal carcinoma.
Nasal NK- and T-cell lymphomas share the same type of Epstein-Barr virus latency as nasopharyngeal carcinoma and Hodgkin's disease. Int J Cancer. J Virol. Epstein-Barr virus lymphoproliferative disease associated with acquired immunodeficiency. Medicine Baltimore ; 70 2 — Epstein-Barr virus latent and replicative gene expression in post-transplant lymphoproliferative disorders and AIDS-related non-Hodgkin's lymphomas.
Ann Oncol. Epstein-Barr virus-latent gene expression and tumor cell phenotype in acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma. Correlation of lymphoma phenotype with three distinct patterns of viral latency. Am J Pathol. Epstein-Barr virus induces an oxidative stress during the early stages of infection in B lymphocytes, epithelial, and lymphoblastoid cell lines.
Mol Cell Biochem. Free Radic Biol Med. Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a pro-drug to deliver hydrogen peroxide to tissues.
Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Proceedings of the National Academy of Sciences.
Verrax J, Calderon PB. Pharmacologic concentrations of ascorbate are achieved by parenteral administration and exhibit antitumoral effects. High-dose vitamin C ascorbic acid therapy in the treatment of patients with advanced cancer.
Anticancer Res. Vitamin C: a concentration-function approach yields pharmacology and therapeutic discoveries. Adv Nutr. Phase I evaluation of intravenous ascorbic acid in combination with gemcitabine and erlotinib in patients with metastatic pancreatic cancer. PLoS One. Tubacin kills epstein-barr virus EBV -Burkitt lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis. J Biol Chem. Chou TC, Talalay P. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors.
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