scholarly journals Cytokine storm and histopathological findings in 60 cases of COVID-19-related death: from viral load research to immunohistochemical quantification of major players IL-1β, IL-6, IL-15 and TNF-α

2021 ◽  
Author(s):  
Paolo Frisoni ◽  
Margherita Neri ◽  
Stefano D’Errico ◽  
Letizia Alfieri ◽  
Diana Bonuccelli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Cells ◽  
Multiple Organ ◽  
Current Evidence ◽  
Control Group ◽  
Cytokine Storm ◽  
Tissue Localization ◽  
Tnf Α ◽  
Capillary Endothelial Cells ◽  
Inflammatory Cytokine Response

AbstractThis study involves the histological analysis of samples taken during autopsies in cases of COVID-19 related death to evaluate the inflammatory cytokine response and the tissue localization of the virus in various organs. In all the selected cases, SARS-CoV-2 RT-PCR on swabs collected from the upper (nasopharynx and oropharynx) and/or the lower respiratory (trachea and primary bronchi) tracts were positive. Tissue localization of SARS-CoV-2 was detected using antibodies against the nucleoprotein and the spike protein. Overall, we tested the hypothesis that the overexpression of proinflammatory cytokines plays an important role in the development of COVID-19-associated pneumonia by estimating the expression of multiple cytokines (IL-1β, IL-6, IL-10, IL-15, TNF-α, and MCP-1), inflammatory cells (CD4, CD8, CD20, and CD45), and fibrinogen. Immunohistochemical staining showed that endothelial cells expressed IL-1β in lung samples obtained from the COVID-19 group (p < 0.001). Similarly, alveolar capillary endothelial cells showed strong and diffuse immunoreactivity for IL-6 and IL-15 in the COVID-19 group (p < 0.001). TNF-α showed a higher immunoreactivity in the COVID-19 group than in the control group (p < 0.001). CD8 + T cells where more numerous in the lung samples obtained from the COVID-19 group (p < 0.001). Current evidence suggests that a cytokine storm is the major cause of acute respiratory distress syndrome (ARDS) and multiple organ failure and is consistently linked with fatal outcomes.

scholarly journals Characterization and tissue localization of zebrafish homologs of the human ABCB1 multidrug transporter

2021 ◽  
Author(s):  
Robert W. Robey ◽  
Andrea N. Robinson ◽  
Fatima Ali-Rahmani ◽  
Lyn M. Huff ◽  
Sabrina Lusvarghi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Multidrug Transporter ◽  
Glycoprotein P ◽  
Tissue Localization ◽  
Brain Vasculature ◽  
P Glycoprotein ◽  
Capillary Endothelial Cells ◽  
The Brain ◽  
Viable Model

ABSTRACTGiven its similarities with mammalian systems, the zebrafish has emerged as a potential model to study the blood-brain barrier (BBB). Capillary endothelial cells at the human BBB express high levels of P-glycoprotein (P-gp, encoded by the ABCB1 gene) and ABCG2 (encoded by the ABCG2 gene). However, little information has been available about ATP-binding cassette transporters expressed at the zebrafish BBB. In this study, we focus on the characterization and tissue localization of two genes that are similar to human ABCB1, zebrafish abcb4 and abcb5. Cytotoxicity assays with stably-transfected cell lines revealed that zebrafish Abcb5 cannot efficiently transport the substrates doxorubicin and mitoxantrone compared to human P-gp and zebrafish Abcb4. Additionally, zebrafish Abcb5 did not transport the fluorescent probes BODIPY-ethylenediamine or LDS 751, while they were readily transported by Abcb4 and P-gp. A high-throughput screen conducted with 90 human P-gp substrates confirmed that zebrafish Abcb4 has overlapping substrate specificity with P-gp. Basal ATPase activity of zebrafish Abcb4 and Abcb5 was comparable to that of human P-gp. In the brain vasculature, RNAscope probes to detect abcb4 colocalized with staining by the P-gp antibody C219, while abcb5 was not detected. Zebrafish abcb4 also colocalized with claudin-5 expression in brain endothelial cells. Abcb4 and Abcb5 had different tissue localizations in multiple zebrafish tissues, consistent with different functions. The data suggest that zebrafish Abcb4 most closely phenocopies P-gp and that the zebrafish may be a viable model to study the role of the multidrug transporter P-gp at the BBB.

Beneficial effects of rosmarinic acid against alcohol-induced hepatotoxicity in rats

2018 ◽  
Vol 96 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Parisa Hasanein ◽  
Rosa Seifi
Keyword(s):  
Rosmarinic Acid ◽  
Biological Activities ◽  
Inflammatory Cells ◽  
Liver Parenchyma ◽  
Serum Levels ◽  
Control Group ◽  
Ethanol Group ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Hepatic Lipid Peroxidation

Alcohol is a severe hepatotoxicant that causes a variety of liver disorders. Rosmarinic acid (RA), a natural phenol, shows some biological activities, including antioxidant and anti-inflammatory effects. We investigated the effects of RA (10 mg/kg) against ethanol-induced oxidative damage and hepatotoxicity in rats. Animals received ethanol (4 g/kg, i.g.) and (or) RA (10 mg/kg, i.g.) daily for 4 weeks. At the end of the treatment period, rats were weighed and use for biochemical, molecular, and histopathological examinations. Ethanol increased hepatic lipid peroxidation (P < 0.001) and decreased hepatic levels of reduced glutathione (P < 0.01), catalase (P < 0.05), and superoxide dismutase (P < 0.001) compared with control group. RA prevented the prooxidant and antioxidant imbalance induced by ethanol in liver. Furthermore, RA ameliorated the increased liver mass, serum levels of ALT, AST, LDH, TNF-α, and IL-6 in ethanol group. Necrosis and infiltration of inflammatory cells in liver parenchyma were attenuated by RA treatment. Our findings showed that RA prevents ethanol-induced oxidant/antioxidant imbalance and liver injury in an experimental model of ethanol-induced hepatotoxicity. Therefore, RA may be a good candidate to protect against ethanol-induced hepatotoxicity; this deserves consideration and further examination.

scholarly journals Both obesity-prone and obesity-resistant rats present delayed cutaneous wound healing

2011 ◽  
Vol 106 (4) ◽  
pp. 603-611 ◽  
Author(s):  
Adriana Paulino do Nascimento ◽  
Andréa Monte-Alto-Costa
Keyword(s):  
Wound Healing ◽  
Saturated Fat ◽  
Inflammatory Cells ◽  
Male Rats ◽  
Control Group ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Diet Induced Obesity ◽  
Tnf Α ◽  
Obesogenic Diet

Diet-induced overweight rats exhibit delayed cutaneous healing; however, when receiving an obesogenic diet, some rats are susceptible to developing the overweight phenotype, whereas others are resistant. We investigated cutaneous healing in diet-induced obesity (DIO)-prone and diet-resistant (DR) rats. Male rats were fed with a standard (control) or a high-saturated fat (30 % fat, w/w) diet for 20 weeks. Then, the experimental group was subdivided into DIO (n 17) and DR (n 16) groups. An excision lesion was made, and the animals were killed 7 or 14 d later. The average body weight was 29 and 25 % higher in the DIO group compared with the C and DR groups. Retroperitoneal fat was higher in the DIO group than in the control and DR groups (518 and 92 %) and was higher in the DR group than in the control group (223 %). The DIO group presented glucose intolerance, and both the DIO and DR groups presented delayed wound contraction (50 %) and re-epithelialisation (20 %). Compared with the DR group, the DIO group displayed higher amounts of inflammatory cells as well as higher levels of lipid peroxidation (P < 0·05). Myofibroblastic differentiation and vessel remodelling were delayed in both the DIO and DR groups. Nitrite levels were lower in the DIO group (340 % less) than in the DR group. TNF-α expression was increased in the DIO group (130 %) compared with the DR group. Our results showed that DIO as well as DR rats present delays in cutaneous wound healing, even though the DR group does not have an overweight phenotype.

Expression of p38 MAPK in Acute Lung Injury Induced by LPS in Mice

2014 ◽  
Vol 522-524 ◽  
pp. 332-336 ◽  
Author(s):  
Kai Xiu Qin ◽  
Yong Wang ◽  
Hua Gang Jian
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
P38 Mapk ◽  
Inflammatory Cells ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Control Group ◽  
Mitogen Activated Protein ◽  
Set Up

Objective To investigate the expression and roles of p38 mitogen-activated protein kinase (p38 MAPK) in LPS-induced acute lung injury (ALI) in mice. Methods The ALI mice models were set up by intraperineal injection of lipopolysaccharide (LPS). The expressions of p38 MAPK in lung tissues were detected by immunohistochemistry and Western-blot. Results The positive expressions of p38 MAPK distribute mainly in infiltrative inflammatory cells, epithelial cells and endothelial cells. And the level of expression of phosphated p38 MAPK in ALI group were higher obviously than that in the control group, and it reached a peak after two hours. Conclusion p38 MAPK signaling pathway was triggered by ALI induced by endotoxin.

The role of anti-endothelial cell antibodies in venous insufficiency

Phlebologie ◽  
2009 ◽  
Vol 38 (06) ◽  
pp. 263-266
Author(s):  
T. H. Akay ◽  
B. Bastürk ◽  
S. Özkan ◽  
S. Aslamaci ◽  
E. Aslim
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Chronic Venous Insufficiency ◽  
Venous Insufficiency ◽  
Varicose Veins ◽  
Duplex Ultrasound ◽  
Inflammatory Cells ◽  
Control Group ◽  
Antibody Complex ◽  
Antigen Antibody

SummaryIt is a hypothesis that autoimmune factors directed against endothelial cells play a role in developing venous insufficiency. We investigated the association between anti-endothelial cell antibodies (AECA) and the development of venous insufficiency and varicose veins. Patients, methods: 44 patients were evaluated with clinical examination and duplex ultrasound for diagnosing chronic venous insufficiency and varicose veins and 120 healthy volunteers were assigned as the control group without evidence of chronic venous insufficiency and varicose veins. All sera samples were analysed by using slides, each containing biochips coated with frozen sections of HUVEC (human umblical vein endothelial cells) and capillary-rich tissue such as skeletal muscle (Euroimmun, FB 1960–1005–2, Germany). If a positive reaction is obtained, specific antibodies of class IgA, IgG, IgM attach to the antigens. In a second step, the bound antibodies are stained with fluorescein labeled antihuman antibodies and visualised by fluorescence microscopy. Results: AECA was positive in 24 out of 44 patients (54.54%) and in 30 out of 120 volunteers (25%). We detected that anti HUVEC antibody occurred significantly more frequent in patients with chronic venous insufficiency or varicose veins: p = 0.0007, OR: 3.60 (1.65 < 7.92). Discussion: The presence of antibodies directed against the endothelial structure causes inflammatory cells of the immune system to move towards the location by both forming antigen-antibody complex and activating the complement system. Tissue damage may occur due to inflammation. In our study we have found a statistically significant relationship between antiendothelial cell antibodies and chronic venous insufficiency. Conclusion: Early diagnosis or prediction of venous insufficiency and/or varicose veins before the occurrence of symptoms may prevent the damage or even help to establish a prophylactic treatment.

scholarly journals Effects of IL-1β and TNF-α on the Expression of P311 in Vascular Endothelial Cells and Wound Healing in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Daijun Zhou ◽  
Tengfei Liu ◽  
Song Wang ◽  
Weifeng He ◽  
Wei Qian ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
Expression Levels ◽  
Relative Expression ◽  
Tnf Α

ObjectiveThis study aimed to define the role of interleukine-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the expression of P311 in vascular endothelial cells (VECs) and in wound healing.MethodsDAPI staining, a CCK-8 assay, cell migration assay, and an angiogenesis assay were used to assess the effects exerted by TNF-α and IL-1β at various concentrations on morphology, proliferation, migration, and angiogenesis of VECs. Western blot (WB) and reverse transcription-polymerase chain reaction (RT-PCR) models were employed to observe the effects exerted by proteins related to the nuclear factor-kappa B (NF-κB) signaling pathway and P311 mRNA expression. Bioinformatics analysis was performed on the binding sites of P311 and NF-κB. Finally, to investigate the effects of IL-1β and TNF-α on wound healing and the length of new epithelium in mice, we established a full-thickness wound defect model in mice. Immunohistochemistry was used to measure changes in P311, proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), CD31 (platelet endothelial cell adhesion molecule-1, PECAM-1/CD31), as well as other related proteins.ResultsWhen levels of TNF-α and IL-1β were both 20 ng/ml, their effects on cell proliferation, cytoskeleton protein expression, cell migration, and angiogenesis were the greatest (P &lt; 0.05). IL-1β and TNF-α at moderate concentrations effectively promoted P311 mRNA and p-NF-κB protein expression (P &lt; 0.05), while p-NF-K b protein expression was decreased (P &lt; 0.05). Luciferase assays showed that P311 expression was also relatively greater when stimulated at moderate concentrations (P &lt; 0.05), while relative expression was significantly lower when the p-NF-K b inhibitor CAPE was added (P &lt; 0.05). On 7-day wound healing rate comparison, the control, IL-1β, IL-1βab, TNF-α, and TNF-αab groups were 18, 37, 35, 39, and 36%, respectively, while control group + P311 siRNA was 31% (P &lt; 0.05). New epithelial length, granulation tissue thickness, and number of blood vessels trends were also the same. In the control group, P311 showed lower relative expression levels than the others (P &lt; 0.05). P311 relative expression levels trended as follows: control group &gt; IL-1βab &gt; IL-1β &gt; TNF-αab &gt; TNF-α (P &lt; 0.05).ConclusionWhen IL-1β and TNF-α concentrations are moderate, they effectively promote the proliferation, expression, migration, and angiogenesis of VECs, possibly by promoting the expression of the NF-K b pathway and thereby promoting the expression of P311. In vitro experiments on mice suggest that P311 effectively promotes wound healing, and its mechanism may be closely related to PCNA, CD31, and VEGF.

scholarly journals Yan-Hou-Qing formula attenuates ammonia-induced acute pharyngitis in rats via inhibition of NF-κB and COX-2

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Min Xu ◽  
Tian-Yong Hu ◽  
Dong-Cai Li ◽  
Li Ma ◽  
Hua Zhang ◽  
...  
Keyword(s):  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Control Group ◽  
Model Group ◽  
Rat Models ◽  
Acute Pharyngitis ◽  
Histopathologic Study ◽  
Tnf Α ◽  
Protein Expressions ◽  
Cox 2

Abstract Background Yan Hou Qing (YHQ) is a Chinese medicinal formula designed to alleviate sore throat symptoms, but underlying mechanism of YHQ treatment for pharyngitis is poorly defined up to now. Methods In this study, the modulation of YHQ on pharyngitis is investigated in ammonia-induced acute pharyngitis rat models. After treatment with YHQ or dexamethasone respectively for five consecutive days, all rats were sacrificed for biomolecular and histopathologic study. Protein expressions of MAPKs, NF-κB, COX-2 and 5-LOX in pharyngitis tissue were evaluated by western blot analysis and the levels of TNF-α, IL-6, prostaglandin (PG) E2, leukotrienes (LT)-B4 and LT-D4 in pharyngeal tissue were measured via ELISA assay. Evans blue (EB) dye exudation test was performed parallelly to assess the integrity of pharyngeal tissue. Results Compared with normal control group, EB dye exudation, and inflammatory cytokines in the model group were significantly increased, and the pharynx tissue was obviously infiltrated by inflammatory cells. YHQ treatment improved the inflammatory infiltrate in pharyngeal tissue, and reduced EB dye exudation in AP rat models. The up-regulated TNF-α and IL-6 in pharyngeal tissue of AP were significantly reduced by YHQ through inhibition of phosphorylation of p38, Erk and NF-κB. YHQ treatment also reversed the increased level of PGE2 through down-regulation of COX-2. Conclusions YHQ formula attenuated the pharyngitis related symptoms via suppression of COX-2 and phosphorylation of p38, Erk and NF-κB (p65).

Regulation of nicotine-induced apoptosis of pulmonary artery endothelial cells by treatment of N-acetylcysteine and vitamin E

2007 ◽  
Vol 26 (7) ◽  
pp. 595-602 ◽  
Author(s):  
R. Demiralay ◽  
N. Gürsan ◽  
H. Erdem
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vitamin E ◽  
Pulmonary Artery ◽  
Cell Apoptosis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Endothelial Cell Apoptosis ◽  
Antioxidant Agents ◽  
Tnf Α

This study investigated the frequency of apoptosis in rat pulmonary artery endothelial cells after intraperitoneal nicotine injection, examining the roles of the inflammatory markers myeloperoxidase (MPO), tumour necrosis factor alpha (TNF-α ), and vascular endothelial growth factor (VEGF) in nicotine-induced vascular damage and the protective effects of two known antioxidant agents, N-acetylcysteine (NAC) and vitamin E. Female Wistar rats were divided into four groups, each composed of nine rats: negative control group, positive control group, NACtreated group (500 mg/kg), and vitamin E-treated group (500 mg/kg). Nicotine was intraperitoneally injected at a dosage of 0.6 mg/kg for 21 days. Following nicotine injection, the antioxidants were administered orally; treatment was continued until the rats were killed. Lung tissue samples were stained with hematoxylin-eosin (H&E) for histopathological assessments. Apoptosis level in endothelial cells was determined by using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabelling) method. Staining of cytoplasmic TNF-α and VEGF in endothelial cells, and perivascular MPO activity were evaluated by immunohistochemistry. The treatments with NAC and vitamin E significantly reduced the rate of nicotine-induced endothelial cell apoptosis. NAC and vitamin E significantly reduced the increases in the local production of TNF-α and VEGF, and perivascular MPO activity. This findings suggest that NAC can be as effective as vitamin E in protecting against nicotine-induced endothelial cell apoptosis. Human & Experimental Toxicology (2007) 26: 595—602.

scholarly journals Inflammatory Markers in Primary Aldosteronism

2016 ◽  
pp. 229-237 ◽  
Author(s):  
Z. ŠOMLÓOVÁ ◽  
O. PETRÁK ◽  
J. ROSA ◽  
B. ŠTRAUCH ◽  
T. INDRA ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
High Frequency ◽  
Inflammatory Markers ◽  
Inflammatory Cells ◽  
Cardiovascular Complications ◽  
Control Group ◽  
Endocrine Hypertension ◽  
Tnf Α ◽  
Aldosterone Producing Adenoma ◽  
Cardiometabolic Profile

Primary aldosteronism (PA) is the most common cause of endocrine hypertension with a high frequency of cardiovascular complications. The unfavorable cardiometabolic profile may be due to aldosterone-mediated activation of inflammatory cells, circulatory cytokines and activation of collagen synthesis in the vessel wall. Aim of our study was to evaluate differences in the levels of hsCRP, IL-6, TNF-α and N-terminal propeptide of collagen I (PINP) in patients with PA and essential hypertension (EH) as a control group, and between the subtypes of PA (aldosterone producing adenoma – APA, idiopathic hyperaldosteronism – IHA). We studied 28 patients with PA (IHA – 10 patients, APA – 12 patients, 6 unclassified) and 28 matched patients with EH. There were no differences in the levels of inflammatory markers between the followed groups [EH vs. PA: TNF-α (5.09 [3.68-6.32] vs. 4.84 [3.62-6.50] pg/ml), IL-6 (0.94 [0.70-1.13] vs. 0.97 [0.71-1.28] pg/ml), hsCRP (0.53 [0.25-1.54] vs. 0.37 [0.31-0.61] mg/l), leukocytes (6.35±1.42 vs. 5.97±1.29 109 l); APA vs. IHA: TNF-α (4.54 [3.62-7.03] vs. 5.19 [4.23-5.27] pg/ml), IL-6 (0.96 [0.63-1.21] vs. 0.90 [0.65-1.06] pg/ml), hsCRP (0.34 [0.29-0.47] vs. 0.75 [0.36-1.11] mg/l), leukocytes (6.37±1.41 vs. 5.71±1.21 109 l)]. Significant differences in the levels of PINP between PA and EH group were observed (35.18 [28.46-41.16] vs. 45.21 [36.95-62.81] μg/l, p≤0.003). No differences in inflammatory markers were observed between the followed groups, we confirmed higher levels of PINP in patients with PA.

Inflammatory Cell Tissue Extravasation Pathways Can Be Regulated by Adherent Stem Cells by Inhibiting Selectin Ligand and Adhesion Receptor Expression On T Cells and Activated Endothelium.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3631-3631
Author(s):  
Wouter Van't Hof ◽  
Amy Raber ◽  
Juliana Woda ◽  
Nicholas Lehman ◽  
Rochelle Cutrone ◽  
...  
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Endothelial Cells ◽  
Stem Cell ◽  
Cell Surface ◽  
Inflammatory Cells ◽  
Employment Equity ◽  
Activated T Cells ◽  
Tnf Α ◽  
Equity Ownership

Abstract Abstract 3631 Poster Board III-567 MultiStem is an adult bone marrow derived stem cell product with immune-modulatory activity that falls within a class of adherent stem cell platforms emerging as modalities for allogeneic therapy for modulation of GVHD. Despite initial preclinical and clinical success there remains significant need for mechanistic understanding of stromal cell interaction with inflammatory cells, particularly relating to biodistribution and the microenvironments encountered after intravenous administration. Successful GVHD treatment or prophylaxis regimens will likely by optimized by a better appreciation of adherent stem cell interactions with GVHD initiating T cells in the tissue microenvironment or in secondary lymphoid tissues. In this study we evaluated interactions of MultiStem with activated peripheral blood cells as well as activated endothelial cells using in vitro co-culture systems that permit cross-talk via soluble factors. In co-culture experiments with activated T cells we observed that MultiStem strongly inhibits gene expression of Fut7, the enzyme responsible for expression of Lewis antigen (CD15s). The resultant lack of CD15s expression on the cell surface of activated T cells was shown to result in their reduced ability to bind to endothelium activated with TNFa, relative to T cells activated in the absence of MultiStem. Furthermore, we found that co-culture of MultiStem with endothelial cells prevents upregulation of E-selectin, V-CAM, and to a lesser degree, I-CAM, to the cell surface of endothelial cells upon activation with TNF-α or interleukin-1α. Inhibition of E-selectin expression by co-culture with MultiStem was not caused by increased cleavage of E-selectin from the cell surface. Instead, MultiStem modulates cell surface induction through decreasing transcription of V-CAM, E-selectin and ICAM. This reduction in cell surface adhesion molecule expression results in decreased neutrophil binding to endothelial cells compared with untreated controls. This activity does not appear to be common to all bone marrow derived adherent stem cells as mesenchymal stem cells (MSC) are unable to modulate V-CAM, E-selectin or I-CAM cell surface upregulation upon activation with TNF-α. These results suggest MSC and MultiStem have distinct secretion profiles. These novel observations indicate that, in addition to immunomodulation activity, MultiStem has unique potential to deter GVHD by impacting various arms of the extravasation process of GVHD pathology causing inflammatory cells. Disclosures: Van't Hof: Athersys: Employment, Equity Ownership. Raber:Athersys: Employment, Equity Ownership. Woda:Athersys: Employment, Equity Ownership. Lehman:Athersysa: Employment, Equity Ownership. Cutrone:Athersys: Employment. Ting:Athersys: Employment, Equity Ownership. Deans:Athersys: Employment, Equity Ownership.

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