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Article ; Online: Matrix metalloproteinases in coronary artery disease and myocardial infarction.

Bräuninger, Hanna / Krüger, Saskia / Bacmeister, Lucas / Nyström, Alexander / Eyerich, Kilian / Westermann, Dirk / Lindner, Diana

Basic research in cardiology

2023 Volume 118, Issue 1, Page(s) 18

Abstract: Cardiovascular diseases (CVDs) remain the leading cause of death worldwide. Most cardiovascular deaths are caused by ischaemic heart diseases such as myocardial infarction (MI). Hereby atherosclerosis in the coronary arteries often precedes disease ... ...

Abstract	Cardiovascular diseases (CVDs) remain the leading cause of death worldwide. Most cardiovascular deaths are caused by ischaemic heart diseases such as myocardial infarction (MI). Hereby atherosclerosis in the coronary arteries often precedes disease manifestation. Since tissue remodelling plays an important role in the development and progression of atherosclerosis as well as in outcome after MI, regulation of matrix metalloproteinases (MMPs) as the major ECM-degrading enzymes with diverse other functions is crucial. Here, we provide an overview of the expression profiles of MMPs in coronary artery and left ventricular tissue using publicly available data from whole tissue to single-cell resolution. To approach an association between MMP expression and the development and outcome of CVDs, we further review studies investigating polymorphisms in MMP genes since polymorphisms are known to have an impact on gene expression. This review therefore aims to shed light on the role of MMPs in atherosclerosis and MI by summarizing current knowledge from publically available datasets, human studies, and analyses of polymorphisms up to preclinical and clinical trials of pharmacological MMP inhibition.
MeSH term(s)	Humans ; Coronary Artery Disease/genetics ; Myocardial Infarction/genetics ; Myocardial Ischemia ; Atherosclerosis ; Matrix Metalloproteinases
Chemical Substances	Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2023-05-09
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-023-00987-2
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Article ; Online: Location, Dissection, and Analysis of the Murine Stellate Ganglion.

Scherschel, Katharina / Bräuninger, Hanna / Glufke, Klara / Jungen, Christiane / Klöcker, Nikolaj / Meyer, Christian

Journal of visualized experiments : JoVE

2020 , Issue 166

Abstract: The autonomic nervous system is a substantial driver of cardiac electrophysiology. Especially the role of its sympathetic branch is an ongoing matter of investigation in the pathophysiology of ventricular arrhythmias (VA). Neurons in the stellate ganglia ...

Abstract	The autonomic nervous system is a substantial driver of cardiac electrophysiology. Especially the role of its sympathetic branch is an ongoing matter of investigation in the pathophysiology of ventricular arrhythmias (VA). Neurons in the stellate ganglia (SG) - bilateral star-shaped structures of the sympathetic chain - are an important component of the sympathetic infrastructure. The SG are a recognized target for treatment via cardiac sympathetic denervation in patients with therapy-refractory VA. While neuronal remodeling and glial activation in the SG have been described in patients with VA, the underlying cellular and molecular processes that potentially precede the onset of arrhythmia are only insufficiently understood and should be elucidated to improve autonomic modulation. Mouse models allow us to study sympathetic neuronal remodeling, but identification of the murine SG is challenging for the inexperienced investigator. Thus, in-depth cellular and molecular biological studies of the murine SG are lacking for many common cardiac diseases. Here, we describe a basic repertoire for dissecting and studying the SG in adult mice for analyses at RNA level (RNA isolation for gene expression analyses, in situ hybridization), protein level (immunofluorescent whole mount staining), and cellular level (basic morphology, cell size measurement). We present potential solutions to overcome challenges in the preparation technique, and how to improve staining via quenching of autofluorescence. This allows for the visualization of neurons as well as glial cells via established markers in order to determine cell composition and remodeling processes. The methods presented here allow characterizing the SG to gain further information on autonomic dysfunction in mice prone to VA and can be complemented by additional techniques investigating neuronal and glial components of the autonomic nervous system in the heart.
MeSH term(s)	Animals ; Arrhythmias, Cardiac/physiopathology ; Dissection ; Female ; Humans ; Imaging, Three-Dimensional ; Immunohistochemistry ; In Situ Hybridization ; Male ; Mice, Inbred C57BL ; Stellate Ganglion/anatomy & histology ; Stellate Ganglion/metabolism ; Stellate Ganglion/physiopathology
Language	English
Publishing date	2020-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/62026
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Article ; Online: Human cardiac organoids to model COVID-19 cytokine storm induced cardiac injuries.

Arhontoulis, Dimitrios C / Kerr, Charles M / Richards, Dylan / Tjen, Kelsey / Hyams, Nathaniel / Jones, Jefferey A / Deleon-Pennell, Kristine / Menick, Donald / Bräuninger, Hanna / Lindner, Diana / Westermann, Dirk / Mei, Ying

Journal of tissue engineering and regenerative medicine

2022 Volume 16, Issue 9, Page(s) 799–811

Abstract: Acute cardiac injuries occur in 20%-25% of hospitalized COVID-19 patients. Herein, we demonstrate that human cardiac organoids (hCOs) are a viable platform to model the cardiac injuries caused by COVID-19 hyperinflammation. As IL-1β is an upstream ... ...

Abstract	Acute cardiac injuries occur in 20%-25% of hospitalized COVID-19 patients. Herein, we demonstrate that human cardiac organoids (hCOs) are a viable platform to model the cardiac injuries caused by COVID-19 hyperinflammation. As IL-1β is an upstream cytokine and a core COVID-19 signature cytokine, it was used to stimulate hCOs to induce the release of a milieu of proinflammatory cytokines that mirror the profile of COVID-19 cytokine storm. The IL-1β treated hCOs recapitulated transcriptomic, structural, and functional signatures of COVID-19 hearts. The comparison of IL-1β treated hCOs with cardiac tissue from COVID-19 autopsies illustrated the critical roles of hyper-inflammation in COVID-19 cardiac insults and indicated the cardioprotective effects of endothelium. The IL-1β treated hCOs thus provide a defined and robust model to assess the efficacy and potential side effects of immunomodulatory drugs, as well as the reversibility of COVID-19 cardiac injuries at baseline and simulated exercise conditions.
MeSH term(s)	COVID-19/complications ; Cytokine Release Syndrome/virology ; Cytokines/metabolism ; Heart Diseases/virology ; Humans ; Models, Biological ; Organoids
Chemical Substances	Cytokines
Language	English
Publishing date	2022-06-11
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2316155-3
ISSN	1932-7005 ; 1932-6254
ISSN (online)	1932-7005
ISSN	1932-6254
DOI	10.1002/term.3327
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Article: Location, dissection, and analysis of the murine stellate ganglion

Scherschel, Katharina / Bräuninger, Hanna / Glufke, Klara / Jungen, Christiane / Klöcker, Nikolaj / Meyer, Christian

Journal of visualized experiments. 2020 Dec. 22, , no. 166

2020

Abstract	The autonomic nervous system is a substantial driver of cardiac electrophysiology. Especially the role of its sympathetic branch is an ongoing matter of investigation in the pathophysiology of ventricular arrhythmias (VA). Neurons in the stellate ganglia (SG) – bilateral star-shaped structures of the sympathetic chain – are an important component of the sympathetic infrastructure. The SG are a recognized target for treatment via cardiac sympathetic denervation in patients with therapy-refractory VA. While neuronal remodeling and glial activation in the SG have been described in patients with VA, the underlying cellular and molecular processes that potentially precede the onset of arrhythmia are only insufficiently understood and should be elucidated to improve autonomic modulation. Mouse models allow us to study sympathetic neuronal remodeling, but identification of the murine SG is challenging for the inexperienced investigator. Thus, in-depth cellular and molecular biological studies of the murine SG are lacking for many common cardiac diseases. Here, we describe a basic repertoire for dissecting and studying the SG in adult mice for analyses at RNA level (RNA isolation for gene expression analyses, in situ hybridization), protein level (immunofluorescent whole mount staining), and cellular level (basic morphology, cell size measurement). We present potential solutions to overcome challenges in the preparation technique, and how to improve staining via quenching of autofluorescence. This allows for the visualization of neurons as well as glial cells via established markers in order to determine cell composition and remodeling processes. The methods presented here allow characterizing the SG to gain further information on autonomic dysfunction in mice prone to VA and can be complemented by additional techniques investigating neuronal and glial components of the autonomic nervous system in the heart.
Keywords	RNA ; adults ; arrhythmia ; autonomic nervous system ; dissection ; electrophysiology ; ganglia ; gene expression ; heart ; hybridization ; infrastructure ; mice ; neurons ; pathophysiology ; protein content
Language	English
Dates of publication	2020-1222
Size	p. e62026.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/62026
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cytokine-Mediated Alterations of Human Cardiac Fibroblast's Secretome.

Bräuninger, Hanna / Thottakara, Tilo / Schön, Jacob / Voss, Svenja / Dhople, Vishnu / Warnke, Svenja / Scherschel, Katharina / Schrage, Benedikt / Kirchhof, Paulus / Blankenberg, Stefan / Völker, Uwe / Westermann, Dirk / Hammer, Elke / Lindner, Diana

International journal of molecular sciences

2021 Volume 22, Issue 22

Abstract: Fibroblasts contribute to approximately 20% of the non-cardiomyocytic cells in the heart. They play important roles in the myocardial adaption to stretch, inflammation, and other pathophysiological conditions. Fibroblasts are a major source of ... ...

Abstract	Fibroblasts contribute to approximately 20% of the non-cardiomyocytic cells in the heart. They play important roles in the myocardial adaption to stretch, inflammation, and other pathophysiological conditions. Fibroblasts are a major source of extracellular matrix (ECM) proteins whose production is regulated by cytokines, such as TNF-α or TGF-β. The resulting myocardial fibrosis is a hallmark of pathological remodeling in dilated cardiomyopathy (DCM). Therefore, in the present study, the secretome and corresponding transcriptome of human cardiac fibroblasts from patients with DCM was investigated under normal conditions and after TNF-α or TGF-β stimulation. Secreted proteins were quantified via mass spectrometry and expression of genes coding for secreted proteins was analyzed via Affymetrix Transcriptome Profiling. Thus, we provide comprehensive proteome and transcriptome data on the human cardiac fibroblast's secretome. In the secretome of quiescent fibroblasts, 58% of the protein amount belonged to the ECM fraction. Interestingly, cytokines were responsible for 5% of the total protein amount in the secretome and up to 10% in the corresponding transcriptome. Furthermore, cytokine gene expression and secretion were upregulated upon TNF-α stimulation, while collagen secretion levels were elevated after TGF-β treatment. These results suggest that myocardial fibroblasts contribute to pro-fibrotic and to inflammatory processes in response to extracellular stimuli.
MeSH term(s)	Cardiomyopathy, Dilated/genetics ; Cardiomyopathy, Dilated/metabolism ; Cardiomyopathy, Dilated/pathology ; Cells, Cultured ; Collagen/genetics ; Collagen/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Cytokines/pharmacology ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Microscopy, Fluorescence ; Myocardium/cytology ; Myocardium/metabolism ; Oligonucleotide Array Sequence Analysis ; Secretome/drug effects ; Secretome/metabolism ; Tandem Mass Spectrometry ; Transcriptome/drug effects ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/pharmacology ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Cytokines ; Transforming Growth Factor beta ; Tumor Necrosis Factor-alpha ; Collagen (9007-34-5)
Language	English
Publishing date	2021-11-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222212262
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Article ; Online: Characterization of the HCN Interaction Partner TRIP8b/PEX5R in the Intracardiac Nervous System of TRIP8b-Deficient and Wild-Type Mice.

Scherschel, Katharina / Bräuninger, Hanna / Mölders, Andrea / Erlenhardt, Nadine / Amin, Ehsan / Jungen, Christiane / Pape, Ulrike / Lindner, Diana / Chetkovich, Dane M / Klöcker, Nikolaj / Meyer, Christian

International journal of molecular sciences

2021 Volume 22, Issue 9

Abstract: The tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b/PEX5R) is an interaction partner and auxiliary subunit of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, which are key for rhythm generation in the brain and ... ...

Abstract	The tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b/PEX5R) is an interaction partner and auxiliary subunit of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, which are key for rhythm generation in the brain and in the heart. Since TRIP8b is expressed in central neurons but not in cardiomyocytes, the TRIP8b-HCN interaction has been studied intensely in the brain, but is deemed irrelevant in the cardiac conduction system. Still, to date, TRIP8b has not been studied in the intrinsic cardiac nervous system (ICNS), a neuronal network located within epicardial fat pads. In vitro electrophysiological studies revealed that TRIP8b-deficient mouse hearts exhibit increased atrial refractory and atrioventricular nodal refractory periods, compared to hearts of wild-type littermates. Meanwhile, heart rate, sino-nodal recovery time, and ventricular refractory period did not differ between genotypes. Trip8b mRNA was detected in the ICNS by quantitative polymerase chain reaction. RNAscope in situ hybridization confirmed Trip8b localization in neuronal somata and nerve fibers. Additionally, we found a very low amount of mRNAs in the sinus node and atrioventricular node, most likely attributable to the delicate fibers innervating the conduction system. In contrast, TRIP8b protein was not detectable. Our data suggest that TRIP8b in the ICNS may play a role in the modulation of atrial electrophysiology beyond HCN-mediated sino-nodal control of the heart.
MeSH term(s)	Animals ; Gene Deletion ; Gene Expression ; Heart/physiology ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism ; Peroxins/genetics ; Peroxins/metabolism ; Protein Interaction Maps ; RNA, Messenger/genetics
Chemical Substances	Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Membrane Proteins ; Peroxins ; Pex5l protein, mouse ; RNA, Messenger
Language	English
Publishing date	2021-04-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22094772
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Article ; Online: Characterization of the HCN Interaction Partner TRIP8b/PEX5R in the Intracardiac Nervous System of TRIP8b-Deficient and Wild-Type Mice

Katharina Scherschel / Hanna Bräuninger / Andrea Mölders / Nadine Erlenhardt / Ehsan Amin / Christiane Jungen / Ulrike Pape / Diana Lindner / Dane M. Chetkovich / Nikolaj Klöcker / Christian Meyer

International Journal of Molecular Sciences, Vol 22, Iss 4772, p

2021 Volume 4772

Abstract	The tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b/PEX5R) is an interaction partner and auxiliary subunit of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, which are key for rhythm generation in the brain and in the heart. Since TRIP8b is expressed in central neurons but not in cardiomyocytes, the TRIP8b-HCN interaction has been studied intensely in the brain, but is deemed irrelevant in the cardiac conduction system. Still, to date, TRIP8b has not been studied in the intrinsic cardiac nervous system (ICNS), a neuronal network located within epicardial fat pads. In vitro electrophysiological studies revealed that TRIP8b-deficient mouse hearts exhibit increased atrial refractory and atrioventricular nodal refractory periods, compared to hearts of wild-type littermates. Meanwhile, heart rate, sino-nodal recovery time, and ventricular refractory period did not differ between genotypes. Trip8b mRNA was detected in the ICNS by quantitative polymerase chain reaction. RNAscope in situ hybridization confirmed Trip8b localization in neuronal somata and nerve fibers. Additionally, we found a very low amount of mRNAs in the sinus node and atrioventricular node, most likely attributable to the delicate fibers innervating the conduction system. In contrast, TRIP8b protein was not detectable. Our data suggest that TRIP8b in the ICNS may play a role in the modulation of atrial electrophysiology beyond HCN-mediated sino-nodal control of the heart.
Keywords	autonomic nervous system ; TRIP8b ; HCN channels ; cardiac electrophysiology ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases.

Lindner, Diana / Fitzek, Antonia / Bräuninger, Hanna / Aleshcheva, Ganna / Edler, Caroline / Meissner, Kira / Scherschel, Katharina / Kirchhof, Paulus / Escher, Felicitas / Schultheiss, Heinz-Peter / Blankenberg, Stefan / Püschel, Klaus / Westermann, Dirk

JAMA cardiology

2020 Volume 5, Issue 11, Page(s) 1281–1285

Abstract: Importance: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can be documented in various tissues, but the frequency of cardiac involvement as well as possible consequences are unknown.: Objective: To evaluate the presence of SARS-CoV-2 ... ...

Abstract	Importance: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can be documented in various tissues, but the frequency of cardiac involvement as well as possible consequences are unknown. Objective: To evaluate the presence of SARS-CoV-2 in the myocardial tissue from autopsy cases and to document a possible cardiac response to that infection. Design, setting, and participants: This cohort study used data from consecutive autopsy cases from Germany between April 8 and April 18, 2020. All patients had tested positive for SARS-CoV-2 in pharyngeal swab tests. Exposures: Patients who died of coronavirus disease 2019. Main outcomes and measures: Incidence of SARS-CoV-2 positivity in cardiac tissue as well as CD3+, CD45+, and CD68+ cells in the myocardium and gene expression of tumor necrosis growth factor α, interferon γ, chemokine ligand 5, as well as interleukin-6, -8, and -18. Results: Cardiac tissue from 39 consecutive autopsy cases were included. The median (interquartile range) age of patients was 85 (78-89) years, and 23 (59.0%) were women. SARS-CoV-2 could be documented in 24 of 39 patients (61.5%). Viral load above 1000 copies per μg RNA could be documented in 16 of 39 patients (41.0%). A cytokine response panel consisting of 6 proinflammatory genes was increased in those 16 patients compared with 15 patients without any SARS-CoV-2 in the heart. Comparison of 15 patients without cardiac infection with 16 patients with more than 1000 copies revealed no inflammatory cell infiltrates or differences in leukocyte numbers per high power field. Conclusions and relevance: In this analysis of autopsy cases, viral presence within the myocardium could be documented. While a response to this infection could be reported in cases with higher virus load vs no virus infection, this was not associated with an influx of inflammatory cells. Future investigations should focus on evaluating the long-term consequences of this cardiac involvement.
MeSH term(s)	Aged ; Aged, 80 and over ; Autopsy/methods ; COVID-19/complications ; COVID-19/diagnosis ; COVID-19/epidemiology ; COVID-19/virology ; Cardiovascular Infections/etiology ; Cardiovascular Infections/metabolism ; Cardiovascular Infections/virology ; Chemokines/metabolism ; Cohort Studies ; Female ; Germany/epidemiology ; Humans ; Incidence ; Interferon-gamma/metabolism ; Interleukin-18/metabolism ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Male ; Myocarditis/etiology ; Myocarditis/metabolism ; Myocarditis/virology ; Myocardium/immunology ; Myocardium/metabolism ; Pandemics ; Peptide Fragments/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/isolation & purification ; Tumor Necrosis Factor-alpha/metabolism ; Viral Load/statistics & numerical data
Chemical Substances	Chemokines ; Interleukin-18 ; Interleukin-6 ; Interleukin-8 ; Peptide Fragments ; Tumor Necrosis Factor-alpha ; interferon gamma (1-39) ; Interferon-gamma (82115-62-6)
Keywords	covid19
Language	English
Publishing date	2020-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2380-6591
ISSN (online)	2380-6591
DOI	10.1001/jamacardio.2020.3551
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Article ; Online: Cytokine-mediated alterations of human cardiac fibroblast’s secretome

2021

Abstract: Fibroblasts contribute to approximately 20% of the non-cardiomyocytic cells in the heart. They play important roles in the myocardial adaption to stretch, inflammation, and other patho-physiological conditions. Fibroblasts are a major source of ... ...

Abstract	Fibroblasts contribute to approximately 20% of the non-cardiomyocytic cells in the heart. They play important roles in the myocardial adaption to stretch, inflammation, and other patho-physiological conditions. Fibroblasts are a major source of extracellular matrix (ECM) proteins whose production is regulated by cytokines, such as TNF-α or TGF-β. The resulting myocardial fibrosis is a hallmark of pathological remodeling in dilated cardiomyopathy (DCM). Therefore, in the present study, the secretome and corresponding transcriptome of human cardiac fibroblasts from patients with DCM was investigated under normal conditions and after TNF-α or TGF-β stim-ulation. Secreted proteins were quantified via mass spectrometry and expression of genes coding for secreted proteins was analyzed via Affymetrix Transcriptome Profiling. Thus, we provide com-prehensive proteome and transcriptome data on the human cardiac fibroblast’s secretome. In the secretome of quiescent fibroblasts, 58% of the protein amount belonged to the ECM fraction. Inter-estingly, cytokines were responsible for 5% of the total protein amount in the secretome and up to 10% in the corresponding transcriptome. Furthermore, cytokine gene expression and secretion were upregulated upon TNF-α stimulation, while collagen secretion levels were elevated after TGF-β treatment. These results suggest that myocardial fibroblasts contribute to pro-fibrotic and to inflammatory processes in response to extracellular stimuli.
Keywords	Text ; ddc:570 ; Affymetrix ; Cardiac fibroblast ; Cytokine ; Mass spectrometry ; Proteome ; Secretome ; TGF-β ; TNF-α ; Transcriptome
Subject code	610
Language	English
Publishing date	2021-11-12
Publishing country	de
Document type	Article ; Online
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Article ; Online: Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases

JAMA Cardiology ; ISSN 2380-6583

2020

Keywords	covid19
Language	English
Publisher	American Medical Association (AMA)
Publishing country	us
Document type	Article ; Online
DOI	10.1001/jamacardio.2020.3551
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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