Webinars

Series of 90-minute webinars, every 2-3 months, starting on Monday 11th January 2021

Dear Friends and Colleagues,

The 2021 EMBRN meeting scheduled for Utrecht has been postponed to the summer of 2022 due to COVID-19.

In the meantime, we would like to host a series of 90-minute webinars, every 2-3 months, with a keynote speaker and presentations from MSc, PhD students and postdoctoral researchers, who will be completing their studies, or other graduate students with very interesting results. This will give them a chance to present their results as there are currently no opportunities to present in person at scientific conferences.

We ask EMBRN members with junior researchers to select one person from their group to submit an abstract to the webinar that fit the theme of the research best (Title, Authors (Surname & initials), Affiliations, max. 100-200 words main text) for consideration to be included in the first webinar. Seven students will be selected to make presentations of 8 minutes each (plus 2 minutes Q&A). If many abstracts will be sent, the chance is that many will also unfortunately not be able to be selected. Please, do not be too disappointed if your abstract is not selected. We will provide an additional opportunity to present your work at our next EMBRN meeting in 2022.

The theme of the first webinar is Mast cells as targets for novel treatments (Chair: Prof. Marcus Maurer) - Date of webinar: Monday 11th January 2021 - successfully finished -

The theme of the second webinar is "From mast cell biology to mast cell-targeted treatments"
Date of webinar: March 3rd, 2021 - successfully finished -

The theme of the third webinar is "Mast cells in health and disease"
Date of webinar: May 3rd, 2021 - successfully finished -

The theme of the fourth webinar is "Basophils and Mast Cells in Health and Disease"
Date of webinar: September 27th, 2021 - successfully finished -

Further webinars are planned in May and June next year on “Mast Cell in health and disease” and “Mast cell functions in allergies and infectious diseases”. A separate call for these topics will be sent at a later date.

We look forward to your abstracts and hope, despite the difficult circumstances, that our webinars will provide a stimulating forum for presenting your research.

Announcement: Save the date!

Special Joint Webinar EMBRN - International Eosinophil Society on January 26th, 2022

Kind regards,

Francesca Levi-Schaffer & EMBRN Council

1st EMBRN Webinar: “Mast cells as targets for novel treatments”

Chair: Prof. Marcus Maurer

January 11, 2021: 17.00 – 18.30 CET

We thank the presenters of the first EMBRN webinar and all the participants. We are incredibly happy with the interest in this first webinar exceeding our expectations.

The recording is now available for everyone to watch here.

 

Agenda

Introduction

Aim and scope of the EMBRN webinars

Prof. Francesca Levi-Schaffer, EMBRN President (5 minutes)

Pharmacology & Experimental Therapeutics Unit, Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel

 

Keynote presentation

Mast cells as targets for novel treatments

Prof. Marcus Maurer, EMBRN Past President, webinar chair

(20-25 minutes)

Director of Research, Department of Dermatology and Allergy, Charité - Universitätsmedizin Berlin,

Germany

 

Selected oral presentations (6 min presentation and 4 min Q&A and discussion each)

  1. Chalatip CHOMPUNUD NA AYUDHYA (Philadelphia,PA, USA): Role of Tyrosine residues in MRGPRX2 on G protein and β-arrestin-mediated signaling in response to substance P
  2. Jessy ELST (Antwerp, Belgium): MRGPRX2 and immediate drug hypersensitivity: insights from cultured human mast cells
  3. Jiajun HE (Sichuan, China): Validation of a novel immunomodulatory compound for restoring tolerance
  4. Pier PUZZOVIO (Jerusalem, Israel): Revisiting the effect of cromolyn sodium on human and murine mast cells
  5. Willem ABMA (Stockholm, Sweden): Prostaglandin D2 inhibits mediator release and antigen induced bronchoconstriction in the guinea pig trachea by activation of DP1 receptors
  6. Deisy SEGURA-VILLALOBOS (Mexico City, Mexico): Cyclic hypoxia promotes a hyperresponsive phenotype to FcεRI crosslinking in mast cells

 

Brief summary, 2nd webinar announcement, farewell

2nd EMBRN Webinar: "From mast cell biology to mast cell-targeted treatments"
Chair: Prof. Francesca Levi-Schaffer
March 3rd, 2021: 09.00 – 10.30 CET

We thank the presenters of the first EMBRN webinar and all the participants. We are again incredibly happy with the interest in this webinar.

The recording is now available for everyone to watch here.

 

Agenda

Keynote presentation

From mast cell biology to mast cell-targeted treatments

Prof. Francesca Levi-Schaffer, EMBRN President (20-25 minutes)

Pharmacology & Experimental Therapeutics Unit, Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel

 

Selected oral presentations (6 min presentation and 4 min Q&A and discussion each)

  1. Sabin ACHARYA (Daejeon, Korea): Inotodiol ameliorates Th2 mediated airway inflammation by attenuating mast cell activities in a mouse model of asthma
  2. Eva CONDE (Paris, France): Anti-IgE vaccination prevents human IgE-mediated severe anaphylaxis in humanized mice
  3. Caterina IULIANO (Munich, Germany): Targeting mast-cell plasticity re-shapes the tumor microenvironment of melanoma
  4. Jielu LIU (Stockholm, Sweden): Distinct lipid mediator release and contraction by MRGPRX2 agonist and antigen in guinea pig trachea
  5. Vadym SULIMENKO (Prague, Czech Republic): Multifunctional fluorescently labeled polymer-coated GdF3 nanoparticles inhibit degranulation in rat basophilic leukemia (RBL) cells
  6. Roberta SULSENTI (Milan, Italy): Repurposing of the antiepileptic drug levetiracetam to restrain adenocarcinoma and neuroendocrine prostate cancer

 

Brief summary, next webinar announcement, farewell

 

Here you can find the abstracts of the webinar

3rd EMBRN Webinar: "Mast cells in health and disease"

Chair: Prof Francesca Levi-Schaffer

EMBRN President Pharmacology & Experimental Therapeutics Unit, Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel

May 3rd, 2021: 14.00 to 15.30 CET

Keynote presentation: "Tryptase, a marker of mast cells in health and disease"

Dr Joana Vitte, Associate Professor of Immunology, Aix-Marseille University, France

The recording is now available for everyone to watch here.

 

 

Agenda of the 3rd EMBRN webinar, May 3rd 2021, 2.00-3.30 pm CET

Introduction

Prof. Francesca Levi-Schaffer, EMBRN President
Pharmacology & Experimental Therapeutics Unit, Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel

Keynote presentation (15 min)

Dr. Joana Vitte (Marseille, Montpellier, France): Tryptase, a mast cell marker in health and disease
Associate Professor, Aix-Marseille University and IDESP Montpellier, France

Selected oral presentations (6 min presentation and 4 min Q&A and discussion each)

Simon P. Goldie (Southampton, Portsmouth, UK): Staphylococcus aureus within nasal mast cells as a driver of chronic rhinosinusitis: A role for simvastatin in disease management?

Anna-Karin Johnsson (Stockholm, Sweden): Characterization of lipid mediator release in IgE stimulated lung mast cells

Erika Haide Mendez Enriquez (Uppsala, Sweden): Mast cell-derived serotonin enhances methacholine-induced airway hyperresponsiveness in house dust mite-induced experimental asthma

Gunnar Nilsson (Stockholm, Sweden): Immunoprofiling reveals novel mast cell receptors and the continuous nature of human lung mast cell heterogeneity

Irit Shefler (Tel Aviv, Israel): Lung cancer-derived extracellular vesicles:  a possible mediator of mast cell activation in the tumor microenvironment

Pratibha Gaur (Jerusalem, Israel): Dexamethasone and CD300a activation display additive inhibitory effect on human and murine mast cell functions

Nyssa B. Samanas (Seattle, USA): Characterization of the mast cell surface proteome leads to the identification of CD98hc as a critical surface molecule for optimal mast cell function

Brief summary, 4th webinar announcement, farewell


Here you can find the abstracts of the webinar

Basophils and Mast Cells in Health and Disease, chairs:

Chairs: Didier G Ebo (University of Antwerpen, Belgium) and Bernhard F. Gibbs (University of Oldenburg, Germany)

September 27th, 2021: 10-11.30 Israel time, 9-10.30 am CEST (Berlin), 7-8.30 GMT

The recording is now available for everyone to watch here.

 

Agenda 4th webinar with all abstracts

4th EMBRN webinar: BASOPHILS AND MAST CELLS IN HEALTH AND DISEASE
September 27th 2021, 9.00-10.30 am CEST (Amsterdam, Berlin, Rome, Stockholm, Vienna)


Introduction (5 min)

Prof. Bernhard F. Gibbs, EMBRN Vice-President
Carl von Ossietzky University Oldenburg, Faculty for Medicine and Health Sciences, University Clinics for Dermatology, Oldenburg, Germany

Keynote presentation (20-25 min)

Prof. Didier G. Ebo (Antwerp and Ghent, Belgium): Flow assisted cellular allergy diagnostics: can mast cells beat basophils?
Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium; Department of Immunology, AZ Jan Palfijn Hospital Gent, Ghent, Belgium

Selected oral presentations (6 min presentation and 4 min Q&A and discussion each)

John Tchen (Paris, France)*
Mcpt8-CRE-tdT or “CTM8” mice: A new mouse model demonstrates that basophils have a non-redundant role in pristane-induced lupus-like disease development
William Worrall (Toulouse, France)* The anti-FcεRI antibody MAR-1 depletes basophils and cross-reacts with myeloid cells through its Fc portion.
Manuela Bratti (Paris, France)* Intracellular recycling compartment localized Insulin-Regulated Aminopeptidase (IRAP) controls FcR-mediated inflammatory diseases
Jessy Elst (Antwerp, Belgium)* The mast cell activation test in chlorhexidine allergy: a proof of concept
Yu-Wen Yeh (Hong Kong, China)* Wild mice and naturalized laboratory mice express lung parenchymal mast cells
Hadas Pahima (Jerusalem, Israel)* CD48 contributes to the IgE-dependent activation of murine mast cells

Brief summary, announcement, farewell


*Abstract included below (speakers bold)

Mcpt8-CRE-tdT or “CTM8” mice: A new mouse model demonstrates that basophils have a
non-redundant role in pristane-induced lupus-like disease development


John TCHEN1,2 Quentin SIMON1,2 Léa CHAPART1,2 Christophe PELLEFIGUES1,2 Hajime KARASUYAMA3 Kensuke MIYAKE3 Juan HIDALGO PAREJA4 Ulrich BLANK1,2 Marc BENHAMOU1,2 Eric DAUGAS1,2,5 Nicolas CHARLES1,2


1
Université de Paris, Centre de Recherche sur l’Inflammation, INSERM UMR1149, CNRS
ERL8252, Faculté de Médecine site Bichat, Paris, France
2 Université de Paris, Laboratoire d’Excellence Inflamex, Paris, France
3 Department of Immune Regulation, Graduate School of Medical and Dental Sciences,
Tokyo Medical and Dental University (TMDU), Tokyo, Japan
4 Universidad Autonoma de Barcelona, Facultad de Biociencias, Unidad de Fisiologia Animal
Bellaterra, Barcelona, Spain
5 Service de Néphrologie, Hôpital Bichat, Assistance Publique – Hôpitaux de Paris, Paris,
France

Tissue-specific mouse models are essential tools to decipher the role of each cell compartment and/or their expressed genes in the pathophysiology of diseases. Here, we describe a new knock-in mouse model allowing expressions of both the fluorescent protein tdTomato and the CRE recombinase specifically in the basophil compartment, under the control of the Mcpt8 gene. These “CTM8” mice did not show any abnormalities in their immune cell distribution nor in their basophil function. CTM8 mice allowed the identification of basophils by immunofluorescence and flow cytometry, and the basophil-specific CRE-mediated floxed gene deletion. Breeding of our CTM8 mice with the ROSA26flox-stop-DTA mice led to the generation of basophil-deficient mice with no detectable abnormalities in other cell compartments.
Basophils are involved in systemic lupus erythematous (SLE) pathophysiology by supporting and amplifying autoantibody production. Transient depletion of basophils through DT injection in Mcpt8DTR mice showed promising therapeutic effects on two distinct lupus-like mouse models (Lyn–/– and pristane-induced) and demonstrated the disease-amplifying role of basophils in these models. Here, constitutive basophil deficiency prevented pristane-induced lupus-like disease development by limiting autoantibody titers and renal damages, strongly suggesting that basophils have a non-redundant role in pristane-induced lupus-like disease induction and amplification. Moreover, we describe a new mouse model that will help to further decipher the role of basophils and their expressed genes in health and disease.


The anti-FcεRI antibody MAR-1 depletes basophils and cross-reacts with myeloid cells through its Fc portion

William Worrall a, #, Jasper Kamphuisa a, #, Julien Stackowiczb, c, Aurélie Mougela, Emilie Mauréa, Pierre Bruhnsb, Friederike Jönssonb, Laurent Guilleminaulta, d, Laurent L. Rebera, b

a Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), UMR 1291, University of Toulouse, INSERM, CNRS, Toulouse, France.
b Unit of Antibodies in Therapy and Pathology, Institut Pasteur, UMR 1222 INSERM, F-75015 Paris, France.
c Sorbonne University, ED394, F-75005 Paris, France.
d Department of Respiratory Medicine, University Hospital Centre of Toulouse, Toulouse, France.
#These authors contributed equally to this work.

MAR-1 is a monoclonal antibody used to stain mouse high-affinity IgE receptor FcεRI on basophils and mast cells. This clone is also used in vivo to deplete basophils and induce anaphylaxis. However, the use of MAR-1 has been controversial because this mAb can also bind the IgG receptors FcεRI and FcRIV. We have investigated the mechanisms of MAR-1’s interaction with FcRs, depletion of basophils and anaphylaxis. We found that MAR-1 stains mast cells and basophils and induces anaphylaxis through its interaction with FcεRI, independently of FcgRs. However, MAR-1 recognizes myeloid cells such as monocytes and macrophages in a FceRI-independent manner, by engaging FcgRs through its Fc portion. Indeed, an “Fc silent” recombinant version of MAR-1 only recognizes basophils and mast cells. Strikingly, basophil depletion was also mediated by the Fc portion of MAR-1, since the Fc silent MAR-1 was unable to deplete basophils. We propose that Fc silent MAR-1 should be preferred to assess FcεRI expression. However, this Fc silent format cannot be used for basophil depletion experiments.


Intracellular recycling compartment localized Insulin-Regulated Aminopeptidase (IRAP) controls FcR-mediated inflammatory diseases
Manuela Bratti1, Shamila Vibhushan1, Marc Benhamou1, Ulrich Blank1*#, Loredana Saveanu1* and Sanae Ben Mkaddem2*
1Université de Paris, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, Paris, France ; Laboratoire d'Excellence Inflamex, Paris, France.
2INSERM, U978, Bobigny, France 3Université Paris 13 Sorbonne Paris Nord, UFR SMBH, Bobigny, France
  * co-senior authors; # corresponding author

We investigated the role of Insulin-Regulated Amino Peptidase (IRAP) in IgE receptor (FcεRI) signaling by mast cells (MC). We confirmed that IRAP locates to an intracellular recycling compartment that rapidly recruits to the plasma membrane upon FcεRI stimulation. IRAP-/- versus WT MC exhibited a reduced ability to degranulate and release various chemokines and cytokines. Tyrosine-phosphorylation of several signaling effectors was diminished in IRAP-/- MC. Importantly, we identified Syk, a central tyrosine kinase downstream of FcεRI, as being less phosphorylated at the plasma membrane in IRAP-/- MC. In addition, pSHP-1S591, which positively regulates ITAM signaling, was decreased as well as further downstream events such as intracellular calcium increases. In vivo, IRAP-/- versus WT mice exhibited a less severe IgE-dependent passive systemic anaphylaxis. IgG-triggered active systemic anaphylaxis in humanized FcγRIIA transgenic mice was also reduced in the absence of IRAP and in vivo profiling confirmed decreased phosphorylation of Syk and SHP-1S591 in FcγRIIA-expressing neutrophils and monocytes. In a chronic model of autoimmune arthritis, disease development was reduced in IRAP-/- mice both in a FcγRIIA transgenic or WT background. Our findings support a role of IRAP-positive recycling compartments in FcR signaling, enhancing phosphorylation events at the plasma membrane and FcR-mediated inflammatory diseases.


The mast cell activation test in chlorhexidine allergy: a proof of concept

Jessy Elst1, Marie-Line M. van der Poorten1,2, Margaretha A. Faber1, Athina L. Van Gasse1,2, Lene H. Garvey4,5, Chris H. Bridts1, Leander P. De Puysseleyr1, Christel Mertens1, Margo M. Hagendorens1,2, Vito Sabato1,3, Didier G. Ebo1,3*

1 University of Antwerp, Faculty of Medicine and Health Sciences, Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Antwerp (Belgium) and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp (Belgium)
2 University of Antwerp, Faculty of Medicine and Health Sciences, Department of Paediatrics and the Infla-Med Centre of Excellence, Antwerp (Belgium) and Paediatrics, Antwerp University Hospital, Antwerp (Belgium)
3 Department of Immunology and Allergology, AZ Jan Palfijn Gent, Ghent, Belgium
4 Allergy Clinic, Department of Dermatology and Allergy, Gentofte Hospital, Denmark
5 Department of Clinical Medicine, University of Copenhagen, Denmark

Background: Conventional confirmatory testing for immediate drug hypersensitivity reactions (IDHRs) includes skin tests and quantification of drug-specific IgE antibodies (sIgE). However, these tests are not absolutely predictive for the clinical outcome and can yield false negative and false positive results.
Aim: To assess whether the mast cell activation test (MAT) could benefit diagnosis of chlorhexidine (CHX) IgE-mediated hypersensitivity.
Methods: Human mast cells (dMCs) were generated from CD34+ progenitor cells and sensitized with patients’ sera to become dMCIgE+ and subsequently incubated with CHX. We compared the outcome of the MAT with serum from patients with and without positive skin test and basophil activation test (BAT) to CHX.
Results: dMC sensitized with sera from patients with a positive skin test and BAT to CHX showed a dose-dependent degranulation upon stimulation with chlorhexidine, determined by upregulation of the degranulation marker CD63. In contrast, dMC sensitized with sera from patients with a negative skin test and BAT to chlorhexidine were unresponsive in the MAT.
Conclusion: The MAT can be used to diagnose IgE-dependent IDHRs. Besides, it shows potential to assess the clinical relevance of drug-sIgE antibodies in their ability to elicit MC degranulation and therefore discriminate between allergy, and merely sensitization.


Wild mice and naturalized laboratory mice express lung parenchymal mast cells
Yu-Wen Yeh1, Arka Sen Chaudhuri1, Ling Zhou2, Yu Fang2, Preben Boysen3, Zou Xiang1

1Department of Health Technology and Informatics, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong, China
2Center for Clinical Laboratory, Affiliated Hospital of Guizhou Medical University, Guiyang, China
3Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Oslo, Norway

Background: Conventional laboratory strains of mice profoundly lack lung parenchymal mast cells, which stands in clear contrast to the abundant presence of mast cells in human lungs. Ultra-hygienic specific pathogen-free (SPF) laboratory mice display reduced richness and complexity of microbiota. Accumulating evidence suggests that wild mice may be a more relevant model to mimic human immune responses. This project aimed to investigate the lung distribution of mast cells in free-living wild mice.
Results: Wild mice were trapped at Oslo, Norway and Hemtabad, India, and their mouse (Mus musculus) identity was confirmed by genotyping. Mast cells were identified at a substantial density in the lung parenchymal tissues of wild mice from both habitats using toluidine blue, tryptase and cKit staining. In contrast, lung mast cells were indeed absent in the conventional C57BL/6 or BALB/c strains of laboratory mice examined in parallel. Consistently, wild mice also expressed higher pulmonary levels of stem cell factor, a critical mast cell growth factor. Higher levels of histamine were recorded in the lung tissues of the wild mice. Having speculated that gut microbiota could have impacted the lung tissue residency of mast cells, we next bred C57BL/6 laboratory mice in a purposefully built, closed environment with bedding material obtained from the natural environment with wild rodent infestation in order to normalize the gut microbiota of these super clean SPF laboratory mice to that of the dirty wild mice. Interestingly, C57BL/6 mice born and spent their entire life in this environment developed lung mast cells at an appreciable density.
Conclusions: As wild populations of mice present various problems as a research tool (e.g., unreliable supply, large individual variation, etc.), our “naturalization” or “re-wilding” approach may provide a practical solution to the establishment of mouse models with constitutive lung mast cells, which may more closely mimic human asthma.


CD48 contributes to the IgE-dependent activation of murine mast cells

Pahima H
, Puzzovio PG, and Levi-Schaffer F

Pharmacology & Experimental Therapeutics Unit, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Israel

Background: CD48 is a glycosylphosphatidylinositol (GpI) receptor belonging to the SLAM family expressed on all the hematopoietic cells, including mast cells (MCs) in both mouse and human.  Being a GpI anchored receptor it lacks an intracellular domain molecule. Therefore, CD48 is considered to be a co-activating receptor rather than a bona fide activating receptor. We and others have previously shown its role in bacteria and bacterial toxins-driven MC activation.
Aim: To investigate the role of CD48 in IgE-dependent MC activation systems in vitro and in vivo.
Results: In vitro, IgE-dependent activation (IgE+anti-IgE or IgEanti-DNP+DNP) of CD48-/- bone marrow derived mast cells (BMMCs) resulted in reduced release of both beta-hexosaminidase and TNFα in comparison to WT BMMCs. As expected, a MC-dependent allergic peritonitis model (OVA / S.aureus enterotoxin B(SEB)) induced in Sash-MC deficient mice after i.p. reconstitution with CD48-/- BMMCs, displayed a decreased level of inflammation as measured by total cells and eosinophil numbers in the peritoneum, in comparison to Sash mice reconstituted with WT BMMCs. However in CD48-/- mice OVA/SEB allergic peritonitis induced a significant increase in the level of inflammation as measured in total peritoneal but not in eosinophil numbers.
Conclusion: CD48 has a clear activating/co-activating role on IgE- dependent activation as displayed specifically on MCs. This role is less evident if other cells participating in allergic inflammation are also deficient for this receptor possibly because of arising compensatory factors.


Login and installation

You received an invitation link to the zoom room as well as a meeting ID. A password is not needed. Click on the link and follow the instructions on the screen. zoom will install itself on your computer or, if it is already installed, open the corresponding meeting. If you have access to zoom yourself and would like to use it, open zoom, select “Join”, and enter the ID.
Please use your real name if you dial into the meeting. Our moderators must be able to identify you when you dial in so that they can connect you.

Location
When logging on, please make sure you are in a well illuminated room, ideally in front of a neutral white wall without any decorations. Please avoid patterned clothes.

Illumination
Use a light source in front of you. Make sure there are no shadows in the background and do not use any illumination from behind.

Camera
If your camera is still switched off, switch it on using the camera button. Please use a clean camera with a resolution of at least 720p. Choose the right space between you and the camera (at eye level). Use a laptop stand or even books to find the right angle.
Please refrain from using virtual backgrounds as there could be copyright concerns. If you are required to use a particular background for presentations, please let us know beforehand.

Audio
Please use a quiet room without echo when recording and eliminate every background noise from open windows or doors. Make sure you are using a wired headset.
The meeting will begin, and you will be requested to join via the computer audio. The system will first run a test. Check if you can hear the ringtone and confirm by clicking on “Yes”. If you do not hear any sound, please check if your volume is high enough or if you can select another output device (monitor with speakers, headphones, internal speakers, etc.)
Then check your microphone. The system will repeat your input with a time delay. If you don’t hear anything, change the input device if possible (built-in microphone, headset microphone, USB camera microphone, etc.).
You can switch your microphone on and off using the microphone button. Speak loudly and clearly to the camera.

Presenting
You will start the presentation from your computer. Open your presentation. Click on “Share screen” in the zoom window. You will then see an overview of your monitors in the first row.
Select the screen on which you can see your presentation. If you want to use multiple screens, check beforehand on which screen your presentation is presented in full screen. Zoom will show the screen number to be selected on the bottom left. If your presentation also includes audio content, select “Share computer sound”, otherwise please do not select this point.
Confirm by clicking on “Share”. Click on your presentation since it may have been set in the background, and briefly check if you can move forward. To return to the zoom menu, end your screen sharing by clicking on “Stop”.

Exiting the zoom session
You can exit the video conference only outside the screen sharing. To do this, click on “Exit meeting” on the bottom right in the video conference. If possible, please exit the meeting close to the end of your time slot.

Other information
If you call up other programmes during the video conference, you can also minimise zoom. zoom will now appear in a minimised window. To return to the full screen mode, move the mouse over the small window and select “Exit minimised video”.
Please close the programmes used parallelly or mute them.


Regardless of explicitly scheduled meetings, you can test the system requirements at any time on www.zoom.us/test.

Technical instruction

Joining a Zoom meeting

Here you will find a corresponding instruction:

https://support.zoom.us/hc/en-us/articles/201362193-Joining-a-meeting

Thanks to

Pharmacology & Pharmaceutical Sciences

Events & Meetings

Save the date!
Special Joint Webinar EMBRN - International Eosinophil Society on January 26th, 2022

Read more

Eosinophils and parasites: more than just effector cells

Summer IES webinar, held on June 30th (9:30-11:00 am ET, 3:30-5:00 pm...

Read more

Recordings

1st EMBRN Webinar: "Mast cells as targets for novel treatments"


2nd EMBRN Webinar: "From mast cell biology to mast cell-targeted treatments"


3rd EMBRN Webinar: "Mast cells in health and disease"


4th EMBRN Webinar: "Basophils and Mast Cells in Health and Disease"

Login

User login

Log in to access EMBRN experimental protocols, recent papers from the EMBRN lab and the updated member list.
Login

Our Partners

 

Sponsors

Your help is appreciated!

If you want to support our activities by donation or if you want to become a sponsor of EMBRN
please contact us.