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Article ; Online: Teletherapy, AAC & COVID-19: the experiences of speech language pathologists providing teletherapy during a global pandemic.

Nader, Danielle T / Erickson, Karen A

Augmentative and alternative communication (Baltimore, Md. : 1985)

2023 Volume 39, Issue 3, Page(s) 146–156

Abstract: The COVID-19 pandemic required many speech-language pathologists (SLPs) to transition to teletherapy service delivery. This study was designed to explore the experiences and perceptions of SLPs who made this transition with children with disabilities who ...

Abstract	The COVID-19 pandemic required many speech-language pathologists (SLPs) to transition to teletherapy service delivery. This study was designed to explore the experiences and perceptions of SLPs who made this transition with children with disabilities who used aided augmentative and alternative communication (AAC). Semi-structured interviews were conducted virtually with 10 SLPs who provided regular teletherapy services to children who used AAC during but not before the pandemic. Interview transcripts were analyzed thematically using immersion, reduction, and constant comparison to understand SLP experiences and perceptions individually and across the group. Results reveal that despite the challenges faced transitioning to teletherapy, there were benefits. Furthermore, many of the participating SLPs developed successful strategies and solutions for the challenges they faced. Participants in this study highlighted the unique and important role that caregivers and parents played in the success of the teletherapy they provided. This study suggests that SLPs, caregivers, and children demonstrated resilience in the face of a large-scale, unforeseen change. SLPs consistently reported the ability to maintain continuity of care during a stressful transition period, while meeting the unique needs of the children who used AAC they served.
MeSH term(s)	Child ; Humans ; Communication Disorders ; Pandemics ; Pathologists ; Speech ; Speech-Language Pathology ; Communication Aids for Disabled ; COVID-19
Language	English
Publishing date	2023-01-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2068579-8
ISSN	1477-3848 ; 0743-4618
ISSN (online)	1477-3848
ISSN	0743-4618
DOI	10.1080/07434618.2022.2159871
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Molecular Cross-Talk between Integrins and Cadherins Leads to a Loss of Vascular Barrier Integrity during SARS-CoV-2 Infection.

Nader, Danielle / Kerrigan, Steve W

Viruses

2022 Volume 14, Issue 5

Abstract: The vascular barrier is heavily injured following SARS-CoV-2 infection and contributes enormously to life-threatening complications in COVID-19. This endothelial dysfunction is associated with the phlogistic phenomenon of cytokine storms, thrombotic ... ...

Abstract	The vascular barrier is heavily injured following SARS-CoV-2 infection and contributes enormously to life-threatening complications in COVID-19. This endothelial dysfunction is associated with the phlogistic phenomenon of cytokine storms, thrombotic complications, abnormal coagulation, hypoxemia, and multiple organ failure. The mechanisms surrounding COVID-19 associated endotheliitis have been widely attributed to ACE2-mediated pathways. However, integrins are emerging as possible receptor candidates for SARS-CoV-2, and their complex intracellular signaling events are essential for maintaining endothelial homeostasis. Here, we showed that the spike protein of SARS-CoV-2 depends on its RGD motif to drive barrier dysregulation by hijacking integrin αVβ3, expressed on human endothelial cells. This triggers the redistribution and internalization of major junction protein VE-Cadherin which leads to the barrier disruption phenotype. Both extracellular and intracellular inhibitors of integrin αVβ3 prevented these effects, similarly to the RGD-cyclic peptide compound Cilengitide, which suggests that the spike protein-through its RGD motif-binds to αVβ3 and elicits vascular leakage events. These findings support integrins as an additional receptor for SARS-CoV-2, particularly as integrin engagement can elucidate many of the adverse endothelial dysfunction events that stem from COVID-19.
MeSH term(s)	COVID-19 ; Cadherins ; Endothelial Cells/metabolism ; Humans ; Integrin alphaVbeta3 ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/metabolism
Chemical Substances	Cadherins ; Integrin alphaVbeta3 ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-04-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14050891
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Article ; Online: Vascular dysregulation following SARS-CoV-2 infection involves integrin signaling through a VE-Cadherin mediated pathway

Nader, Danielle / Kerrigan, Steve

bioRxiv

Abstract	The vascular barrier is heavily injured following SARS-CoV-2 infection and contributes enormously to life-threatening complications in COVID-19. This endothelial dysfunction is associated with the phlogistic phenomenon of cytokine storms, thrombotic complications, abnormal coagulation, hypoxemia, and multiple organ failure. The mechanisms surrounding COVID-19 associated endotheliitis have been widely attributed to ACE2-mediated pathways. However, integrins have emerged as possible receptor candidates for SARS-CoV-2, and their complex intracellular signaling events are essential for maintaining endothelial homeostasis. Here, we showed that the spike protein of SARS-CoV-2 depends on its RGD motif to drive barrier dysregulation through hijacking integrin αVβ3. This triggers the redistribution and internalization of major junction protein VE-Cadherin which leads to the barrier disruption phenotype. Both extracellular and intracellular inhibitors of integrin αVβ3 prevented these effects, similarly to the RGD-cyclic peptide compound Cilengitide, which suggests that the spike protein – through its RGD motif – binds to αVβ3 and elicits vascular leakage events. These findings support integrins as an additional receptor for SARS-CoV-2, particularly as integrin engagement can elucidate many of the adverse endothelial dysfunction events that stem from COVID-19.
Keywords	covid19
Language	English
Publishing date	2022-03-15
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.03.15.484274
Database	COVID19

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Article ; Online: A new perspective in sepsis treatment: could RGD-dependent integrins be novel targets?

Nader, Danielle / Curley, Gerard F / Kerrigan, Steven W

Drug discovery today

2020 Volume 25, Issue 12, Page(s) 2317–2325

Abstract: Sepsis is a life-threatening condition caused by the response of the body to an infection, and has recently been regarded as a global health priority because of the lack of effective treatments available. Vascular endothelial cells have a crucial role in ...

Abstract	Sepsis is a life-threatening condition caused by the response of the body to an infection, and has recently been regarded as a global health priority because of the lack of effective treatments available. Vascular endothelial cells have a crucial role in sepsis and are believed to be a major target of pathogens during the early stages of infection. Accumulating evidence suggests that common sepsis pathogens, including bacteria, fungi, and viruses, all contain a critical integrin recognition motif, Arg-Gly-Asp (RGD), in their major cell wall-exposed proteins that might act as ligands to crosslink to vascular endothelial cells, triggering systemic dysregulation resulting in sepsis. In this review, we discuss the potential of anti-integrin therapy in the treatment of sepsis and septic shock.
MeSH term(s)	Bacterial Infections/drug therapy ; Humans ; Integrins/antagonists & inhibitors ; Mycoses/drug therapy ; Oligopeptides/antagonists & inhibitors ; Sepsis/drug therapy ; Virus Diseases/drug therapy
Chemical Substances	Integrins ; Oligopeptides ; arginyl-glycyl-aspartic acid (78VO7F77PN)
Keywords	covid19
Language	English
Publishing date	2020-10-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2020.09.038
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Article ; Online: SARS-CoV-2 uses major endothelial integrin αvβ3 to cause vascular dysregulation in-vitro during COVID-19.

Nader, Danielle / Fletcher, Nicola / Curley, Gerard F / Kerrigan, Steven W

PloS one

2021 Volume 16, Issue 6, Page(s) e0253347

Abstract: The unprecedented global COVID-19 pandemic has prompted a desperate international effort to accelerate the development of anti-viral candidates. For unknown reasons, COVID-19 infections are associated with adverse cardiovascular complications, ... ...

Abstract	The unprecedented global COVID-19 pandemic has prompted a desperate international effort to accelerate the development of anti-viral candidates. For unknown reasons, COVID-19 infections are associated with adverse cardiovascular complications, implicating that vascular endothelial cells are essential in viral propagation. The etiological pathogen, SARS-CoV-2, has a higher reproductive number and infection rate than its predecessors, indicating it possesses novel characteristics that infers enhanced transmissibility. A unique K403R spike protein substitution encodes an Arg-Gly-Asp (RGD) motif, introducing a potential role for RGD-binding host integrins. Integrin αVβ3 is widely expressed across the host, particularly in the endothelium, which acts as the final barrier before microbial entry into the bloodstream. This mutagenesis creates an additional binding site, which may be sufficient to increase SARS-CoV-2 pathogenicity. Here, we investigate how SARS-CoV-2 passes from the epithelium to endothelium, the effects of αVβ3 antagonist, Cilengitide, on viral adhesion, vasculature permeability and leakage, and also report on a simulated interaction between the viral and host protein in-silico.
MeSH term(s)	Antigens, CD/metabolism ; Binding Sites ; COVID-19/metabolism ; COVID-19/physiopathology ; Caco-2 Cells ; Cadherins/metabolism ; Computer Simulation ; Endothelium, Vascular/cytology ; Endothelium, Vascular/physiopathology ; Endothelium, Vascular/virology ; Host-Pathogen Interactions/drug effects ; Humans ; Integrin alphaVbeta3/chemistry ; Integrin alphaVbeta3/metabolism ; Models, Molecular ; Mutation ; Permeability ; SARS-CoV-2/drug effects ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism ; SARS-CoV-2/pathogenicity ; Snake Venoms/pharmacology ; Spike Glycoprotein, Coronavirus/chemistry ; Spike Glycoprotein, Coronavirus/metabolism ; Virus Internalization
Chemical Substances	Antigens, CD ; Cadherins ; Integrin alphaVbeta3 ; Snake Venoms ; Spike Glycoprotein, Coronavirus ; cadherin 5 ; Cilengitide (4EDF46E4GI)
Language	English
Publishing date	2021-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0253347
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Article ; Online: Integrins as Therapeutic Targets for SARS-CoV-2.

Gressett, Timothy E / Nader, Danielle / Robles, Juan Pablo / Buranda, Tione / Kerrigan, Steven W / Bix, Gregory

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 892323

MeSH term(s)	Angiotensin-Converting Enzyme 2 ; Antiviral Agents ; Humans ; Integrins ; SARS-CoV-2 ; COVID-19 Drug Treatment
Chemical Substances	Antiviral Agents ; Integrins ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2022-04-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.892323
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Article: Targeting Internalized

Nader, Danielle / Yousef, Fajer / Kavanagh, Nicola / Ryan, Benedict K / Kerrigan, Steven W

Antibiotics (Basel, Switzerland)

2021 Volume 10, Issue 5

Abstract: The bacterial ... ...

Abstract	The bacterial pathogen
Language	English
Publishing date	2021-05-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2681345-2
ISSN	2079-6382
ISSN	2079-6382
DOI	10.3390/antibiotics10050581
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Article ; Online: Human endothelial cell-derived exosomal microRNA-99a/b drives a sustained inflammatory response during sepsis by inhibiting mTOR expression.

Fitzpatrick, Glenn / Nader, Danielle / Watkin, Rebecca / McCoy, Claire E / Curley, Gerard F / Kerrigan, Steven W

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 854126

Abstract: The pathophysiology of sepsis and its accompanying hyper-inflammatory response are key events that lead to multi-organ failure and death. A growing body of literature now suggests that the vascular endothelium plays a critical role in driving early ... ...

Abstract	The pathophysiology of sepsis and its accompanying hyper-inflammatory response are key events that lead to multi-organ failure and death. A growing body of literature now suggests that the vascular endothelium plays a critical role in driving early events of sepsis progression. In this study, we demonstrate how endothelial-derived exosomes contribute to a successive pro-inflammatory phenotype of monocytes. Exosomes isolated from
MeSH term(s)	Endothelial Cells/metabolism ; Exosomes/metabolism ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Sepsis/genetics ; Sepsis/metabolism ; Sepsis/pathology ; Staphylococcus aureus/genetics ; TOR Serine-Threonine Kinases/genetics
Chemical Substances	MIRN99 microRNA, human ; MicroRNAs ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-08-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.854126
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A dual-receptor mechanism between integrins and ACE2 widens SARS-CoV-2 tissue tropism

Nader, Danielle / Gressett, Timothy E / Hossen, Md Lokman / Chapagain, Prem P / Kerrigan, Steven W. / Bix, Gregory

bioRxiv

Abstract: In addition to the ACE2 receptor, SARS-CoV-2 binds to integrins to gain host cell entry and trigger pro-inflammatory integrin-mediated signalling cascades. Integrins, therefore, are likely candidates for a dual-receptor mechanism with ACE2 to explain the ...

Abstract	In addition to the ACE2 receptor, SARS-CoV-2 binds to integrins to gain host cell entry and trigger pro-inflammatory integrin-mediated signalling cascades. Integrins, therefore, are likely candidates for a dual-receptor mechanism with ACE2 to explain the increased infectivity seen in SARS-CoV-2 models. As integrins are primarily expressed in vasculature and persistent vasculopathy is seen in COVID-19, examining the role of endothelial integrin involvement is crucial in uncovering the pathophysiology of SARS-CoV-2.
Keywords	covid19
Language	English
Publishing date	2022-01-03
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.01.02.474028
Database	COVID19

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