Helen Barrie

Dr. Helen Barrie

orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

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

Representative Publications

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4 March 2011 in Hepatology
Verified
Journal Article
Open access
PDF file
AMAlexander R Moschen
Alexander R Moschen
TFTeresa Fritz
Teresa Fritz
ACAndrew D. Clouston
Andrew D. Clouston
IRIlka Rebhan
Ilka Rebhan
OBOliver Bauhofer
Oliver Bauhofer
HTHerbert Tilg
Herbert Tilg
Interleukin 32 (IL-32) is a recently described proinflammatory cytokine that activates p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB), thereby inducing proinflammatory cytokines such as IL-1β and tumor necrosis factor alpha (TNF-α). We investigated the role of IL-32 in patients with chronic hepatitis C virus (HCV) infection. Steady-state hepatic messenger RNA (mRNA) levels of IL-32 were determined in a cohort of 90 subjects; anti-IL-32 staining was used in a second cohort of 132 consecutive untreated chronic HCV patients. Correlations with histological features of steatosis, inflammation, and fibrosis were made. In vitro, endogenous IL-32 in monocytes and in the human hepatoma cell line Huh-7.5 were examined. The effects of IL-32-overexpression and IL-32-silencing on HCV replication were studied using HCV luciferase reporter viruses. There were highly significant positive associations between hepatic IL-32 mRNA expression and liver steatosis, inflammation, fibrosis, smooth muscle actin (SMA) area, and serum alanine aminotransferase (ALT) levels. IL-32 protein expression was positively associated with portal inflammation, SMA area, and ALT. In vitro, IL-1β and TNF-α significantly induced IL-32 expression in human Huh-7.5 cells. Alone, stimulation with interferon alpha (IFN-α) did not induce IL-32 expression in Huh-7.5. However, IFN-α exerted a significant additive effect on TNF-α-induced but not IL-1β-induced IL-32 expression, particularly in CD14+ monocytes. This effect was dependent both on NF-κB and Jak/STAT signaling. Viral infection of Huh-7.5 cells resulted in a significant (11-fold) induction of IL-32 mRNA expression. However, modulation of IL-32 in Huh-7.5 cells by overexpression or silencing did not influence HCV virus replication as determined by luciferase assays. Conclusion: IL-32 is a novel proinflammatory cytokine involved in HCV-associated liver inflammation/fibrosis. IL-32 is expressed by human hepatocytes and hepatoma cells and its expression is regulated by proinflammatory stimuli. (HEPATOLOGY 2011;)

20 June 2008 in Hepatology
Verified
Journal Article
Open access
PDF file
JJJulie R. Jonsson
Julie R. Jonsson
HBHelen Barrie
Helen Barrie
POPeter O'ROurke
Peter O'ROurke
ACAndrew D. Clouston
Andrew D. Clouston
EPElizabeth E. Powell
Elizabeth E. Powell
Obesity and fatty liver are commonly observed among patients with chronic hepatitis C virus (HCV) and are risk factors for increased hepatic fibrosis. Obesity is accompanied by a low‐grade, chronic inflammatory response that may contribute to pathogenesis of obesity‐related comorbidities. To assess whether obesity and steatosis potentiate expression of inflammatory markers in chronic HCV, serum protein and hepatic messenger RNA (mRNA) levels of c‐reactive protein (CRP), interleukin‐6 (IL‐6), and tumor necrosis factor‐alpha (TNF‐α) were measured in 171 patients with chronic HCV. The relationships of body mass index, steatosis, histological features of inflammation and fibrosis with serum and hepatic levels of these factors were determined. In comparison with lean patients, overweight and obese subjects had increased circulating (P < 0.001) and hepatic (P = 0.003) CRP, and there was a significant correlation between serum protein and hepatic CRP mRNA levels (rs= 0.51, P < 0.001). Obesity (P = 0.001) and steatosis (P < 0.001) were associated with increased circulating but not hepatic IL‐6, and a weak correlation was seen between serum protein and hepatic IL‐6 mRNA levels (rs= 0.29, P = 0.003). An independent relationship was seen between hepatic TNF‐α mRNA levels and higher total inflammatory score (P < 0.001) and stage of fibrosis (P = 0.037). Subjects with HCV genotype 3 had lower hepatic TNF‐α mRNA levels compared with subjects with genotype 1 (P = 0.017), but there was no relationship between serum TNF‐α protein and hepatic TNF‐α mRNA levels. Conclusion: In patients with chronic HCV, obesity and steatosis are associated with increased expression of selected inflammatory markers; however, circulating levels of IL‐6 and TNF‐α do not reflect hepatic expression. Hepatic TNF‐α was associated with both increased inflammatory activity and hepatic fibrosis, providing support for the key role of this pro‐inflammatory cytokine in liver injury in chronic HCV. (HEPATOLOGY 2008;48:80–87.)

JSJackie Mary Street
Jackie Mary Street
HBHelen Barrie
Helen Barrie
JEJaklin Ardath Eliott
Jaklin Ardath Eliott
LCLucy Carolan
Lucy Carolan
FMFidelma McCorry
Fidelma McCorry
OGon behalf of the Smart Ageing Research Group
on behalf of the Smart Ageing Research Group
Globally, there is an urgent need for solutions that can support our aging populations to live well and reduce the associated economic, social and health burdens. Implementing smart technologies within homes and communities may assist people to live well and ‘age in place’. To date, there has been little consultation with older Australians addressing either the perceived benefits, or the potential social and ethical challenges associated with smart technology use. To address this, we conducted five World Cafés in two Australian states, aiming to capture citizen knowledge about the possibilities and challenges of smart technologies. The participants (n = 84) were aged 55 years and over, English-speaking, and living independently. Grounding our analysis in values-based social science and biomedical ethical principles, we identified the themes reflecting the participants’ understanding, resistance, and acceptance of smart technologies, and the ethical principles, including beneficence, non-maleficence, autonomy, privacy, confidentiality, and justice. Similar to other studies, many of the participants demonstrated cautious and conditional acceptance of smart technologies, while identifying concerns about social isolation, breaches of privacy and confidentiality, surveillance, and stigmatization. Attention to understanding and incorporating the values of older citizens will be important for the acceptance and effectiveness of smart technologies for supporting independent and full lives for older citizens.

1 August 2019 in Experimental Gerontology
Verified
Journal Article
Closed access
DTD. Taylor
D. Taylor
HBHelen Barrie
Helen Barrie
JLJ. Lange
J. Lange
MTM.Q. Thompson
M.Q. Thompson
OTOlga Theou
Olga Theou
RVRenuka Visvanathan
Renuka Visvanathan

1 September 2019 in Archives of Gerontology and Geriatrics
Verified
Journal Article
Closed access
BMBeatriz Arakawa Martins
Beatriz Arakawa Martins
RVRenuka Visvanathan
Renuka Visvanathan
HBHelen Barrie
Helen Barrie
CHChi Hsien Huang
Chi Hsien Huang
EMEiji Matsushita
Eiji Matsushita
MKMasafumi Kuzuya
Masafumi Kuzuya

1 December 2008 in Journal of Hepatology
Verified
Journal Article
Closed access
SMStuart McPherson
Stuart McPherson
JJJulie R. Jonsson
Julie R. Jonsson
HBHelen Barrie
Helen Barrie
POPeter O’rourke
Peter O’rourke
ACAndrew D. Clouston
Andrew D. Clouston
EPElizabeth E. Powell
Elizabeth E. Powell