Mark Willcox

Prof. Mark Willcox

University of New South Wales (UNSW) Sydney, Australia
orcid

Research Focus & Metrics

Academic Career Length

42Years (1985-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 July 2017 in The Ocular Surface
Verified
Journal Article
Closed access
Mark WillcoxMark Willcox
Mark Willcox
PAPablo Argüeso
Pablo Argüeso
Georgi GeorgievGeorgi Georgiev
Georgi Georgiev
JHJuha M. Holopainen
Juha M. Holopainen
GLGordon Laurie
Gordon Laurie
Lyndon JonesLyndon Jones
Lyndon Jones

1 October 2017 in The Ocular Surface
Verified
Journal Article
Open access
Jennifer P CraigJennifer P Craig
Jennifer P Craig
JNJ. Daniel Nelson
J. Daniel Nelson
DADimitri T. Azar
Dimitri T. Azar
CBCarlos Belmonte
Carlos Belmonte
ABAnthony J. Bron
Anthony J. Bron
DSDavid A. Sullivan
David A. Sullivan
This article presents an Executive Summary of the conclusions and recommendations of the 10-chapter TFOS DEWS II report. The entire TFOS DEWS II report was published in the July 2017 issue of The Ocular Surface. A downloadable version of the document and additional material, including videos of diagnostic and management techniques, are available on the TFOS website: www.TearFilm.org.

1 January 2010 in Nutrition & Metabolism
Verified
Journal Article
Open access
PDF file
JFJudith Flanagan
Judith Flanagan
PSPeter A Simmons
Peter A Simmons
JVJoseph Vehige
Joseph Vehige
Mark WillcoxMark Willcox
Mark Willcox
QGQian Garrett
Qian Garrett
Carnitine is a conditionally essential nutrient that plays a vital role in energy production and fatty acid metabolism. Vegetarians possess a greater bioavailability than meat eaters. Distinct deficiencies arise either from genetic mutation of carnitine transporters or in association with other disorders such as liver or kidney disease. Carnitine deficiency occurs in aberrations of carnitine regulation in disorders such as diabetes, sepsis, cardiomyopathy, malnutrition, cirrhosis, endocrine disorders and with aging. Nutritional supplementation of L-carnitine, the biologically active form of carnitine, is ameliorative for uremic patients, and can improve nerve conduction, neuropathic pain and immune function in diabetes patients while it is life-saving for patients suffering primary carnitine deficiency. Clinical application of carnitine holds much promise in a range of neural disorders such as Alzheimer's disease, hepatic encephalopathy and other painful neuropathies. Topical application in dry eye offers osmoprotection and modulates immune and inflammatory responses. Carnitine has been recognized as a nutritional supplement in cardiovascular disease and there is increasing evidence that carnitine supplementation may be beneficial in treating obesity, improving glucose intolerance and total energy expenditure.

Verified
Journal Article
Open access
PDF file
Katrina BrowneKatrina Browne
Katrina Browne
SCSudip Chakraborty
Sudip Chakraborty
RCRenxun Chen
Renxun Chen
Mark WillcoxMark Willcox
Mark Willcox
David BlackDavid Black
David Black
Naresh KumarNaresh Kumar
Naresh Kumar
Antimicrobial resistance is a multifaceted crisis, imposing a serious threat to global health. The traditional antibiotic pipeline has been exhausted, prompting research into alternate antimicrobial strategies. Inspired by nature, antimicrobial peptides are rapidly gaining attention for their clinical potential as they present distinct advantages over traditional antibiotics. Antimicrobial peptides are found in all forms of life and demonstrate a pivotal role in the innate immune system. Many antimicrobial peptides are evolutionarily conserved, with limited propensity for resistance. Additionally, chemical modifications to the peptide backbone can be used to improve biological activity and stability and reduce toxicity. This review details the therapeutic potential of peptide-based antimicrobials, as well as the challenges needed to overcome in order for clinical translation. We explore the proposed mechanisms of activity, design of synthetic biomimics, and how this novel class of antimicrobial compound may address the need for effective antibiotics. Finally, we discuss commercially available peptide-based antimicrobials and antimicrobial peptides in clinical trials.

1 July 2017 in The Ocular Surface
Verified
Journal Article
Closed access
DSDavid A. Sullivan
David A. Sullivan
Eduardo RochaEduardo Rocha
Eduardo Rocha
PAPasquale Aragona
Pasquale Aragona
JCJanine Clayton
Janine Clayton
JDJuan Ding
Juan Ding
Mark WillcoxMark Willcox
Mark Willcox

5 December 2018 in Materials
Verified
Journal Article
Open access
PDF file
MUHAMMAD YASIRMUHAMMAD YASIR
MUHAMMAD YASIR
Mark WillcoxMark Willcox
Mark Willcox
DDDebarun Dutta
Debarun Dutta
Microbes are known to colonize surfaces and form biofilms. These biofilms are communities of microbes encased in a self-produced matrix that often contains polysaccharides, DNA and proteins. Antimicrobial peptides (AMPs) have been used to control the formation and to eradicate mature biofilms. Naturally occurring or synthetic antimicrobial peptides have been shown to prevent microbial colonization of surfaces, to kill bacteria in biofilms and to disrupt the biofilm structure. This review systemically analyzed published data since 1970 to summarize the possible anti-biofilm mechanisms of AMPs. One hundred and sixty-two published reports were initially selected for this review following searches using the criteria ‘antimicrobial peptide’ OR ‘peptide’ AND ‘mechanism of action’ AND ‘biofilm’ OR ‘antibiofilm’ in the databases PubMed; Scopus; Web of Science; MEDLINE; and Cochrane Library. Studies that investigated anti-biofilm activities without describing the possible mechanisms were removed from the analysis. A total of 17 original reports were included which have articulated the mechanism of antimicrobial action of AMPs against biofilms. The major anti-biofilm mechanisms of antimicrobial peptides are: (1) disruption or degradation of the membrane potential of biofilm embedded cells; (2) interruption of bacterial cell signaling systems; (3) degradation of the polysaccharide and biofilm matrix; (4) inhibition of the alarmone system to avoid the bacterial stringent response; (5) downregulation of genes responsible for biofilm formation and transportation of binding proteins.