Jeremy S. Wilson

ORCID: 0000-0003-2355-8632
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About
Contact & Profiles
Research Areas
  • Pancreatitis Pathology and Treatment
  • Pancreatic and Hepatic Oncology Research
  • Liver Disease Diagnosis and Treatment
  • Pancreatic function and diabetes
  • Phagocytosis and Immune Regulation
  • Cancer Cells and Metastasis
  • Alcohol Consumption and Health Effects
  • Liver physiology and pathology
  • Forest Management and Policy
  • Diet, Metabolism, and Disease
  • Forest Ecology and Biodiversity Studies
  • Forest ecology and management
  • Forest Biomass Utilization and Management
  • Endoplasmic Reticulum Stress and Disease
  • Fire effects on ecosystems
  • Gastrointestinal disorders and treatments
  • Ecology and Vegetation Dynamics Studies
  • Cancer Genomics and Diagnostics
  • Diet and metabolism studies
  • Metabolism and Genetic Disorders
  • Forest Insect Ecology and Management
  • Neuroendocrine Tumor Research Advances
  • Adipose Tissue and Metabolism
  • Tree Root and Stability Studies
  • Helicobacter pylori-related gastroenterology studies

UNSW Sydney
2014-2024

South Western Sydney Local Health District
2008-2024

Ingham Institute
2014-2024

Sydney Children's Hospital
2024

Liverpool Hospital
2006-2018

St Vincent's Clinic
2016

The King's College
1935-2013

Institute of Forest Science
2013

Sydney South West Area Health Service
2011

University of Maine System
2011

The pathogenesis of pancreatic fibrosis is unknown. In the liver, stellate cells (vitamin A storing cells) play a significant role in development fibrosis.To determine whether resembling hepatic are present rat pancreas, and if so, to compare their number with isolate culture these from pancreas.Liver sections chow fed rats were immunostained for desmin, glial fibrillary acidic protein (GFAP), alpha smooth muscle actin (alpha-SMA). Pancreatic shaped isolated using Nycodenz gradient, cultured...

10.1136/gut.43.1.128 article EN Gut 1998-07-01

Objectives: Pancreatic cancer has a very poor prognosis, largely due to its propensity for early local and distant spread. Histopathologically, most pancreatic cancers are characterized by prominent stromal/fibrous reaction in around tumor tissue. The aims of this study were determine whether (1) the cells responsible formation stromal human activated stellate (PSCs) (2) an interaction exists between PSCs that may facilitate invasion tumor. Methods: Serial sections tissue stained desmin...

10.1097/00006676-200410000-00002 article EN Pancreas 2004-09-14

The pathogenesis of pancreatic fibrosis is unknown. In the liver, stellate cells play a major role in fibrogenesis by synthesising increased amounts collagen and other extracellular matrix (ECM) proteins when activated profibrogenic mediators such as cytokines oxidant stress.To determine whether cultured rat produce ECM proteins, exhibit signs activation exposed to platelet derived growth factor (PDGF) or transforming beta (TGF-beta).Cultured were immunostained for procollagen III, I,...

10.1136/gut.44.4.534 article EN Gut 1999-04-01

Abstract Pancreatic stellate cells (PSC) produce the stromal reaction in pancreatic cancer, but their role cancer progression is not fully elucidated. We examined influence of PSCs on growth using (a) an orthotopic model and (b) cultured human (hPSC) cell lines MiaPaCa-2 Panc-1. Athymic mice received intrapancreatic injection saline, hPSCs, cells, or hPSCs + MiaPaCa-2. After 7 weeks, tumor size, metastases, histology were assessed. In vitro studies assessed effect secretions PSC migration...

10.1158/0008-5472.can-07-2477 article EN Cancer Research 2008-04-01

The field of pancreatic stellate cell (PSC) biology is very young, as the essential in-vitro tools to study these cells (ie, methods isolate and culture PSC) were only developed recently in 1998. Nonetheless, there has been an exponential increase research output this over past decade, with numerous groups around world focusing their energies into elucidating function cells. It now well established that PSC are responsible for producing stromal reaction (fibrosis) two major diseases...

10.1136/gutjnl-2011-301220 article EN cc-by-nc Gut 2011-11-24

REVIEW article Front. Physiol., 28 August 2012Sec. Gastrointestinal Sciences https://doi.org/10.3389/fphys.2012.00344

10.3389/fphys.2012.00344 article FR cc-by Frontiers in Physiology 2012-01-01

Abstract Cancer‐associated fibroblasts (CAF) are orchestrators of the pancreatic ductal adenocarcinoma (PDAC) microenvironment. Stromal heterogeneity may explain differential pathophysiological roles stroma (pro‐ versus anti‐tumoural) in PDAC. We hypothesised that multiple CAF functional subtypes exist PDAC, contribute to stromal through interactions with cancer cells. Using molecular and analysis patient‐derived primary cultures, we demonstrated human PDAC‐derived CAFs display a high level...

10.1002/path.5224 article EN cc-by The Journal of Pathology 2018-12-21

Pancreatic stellate cells (PSCs, which produce the stroma of pancreatic cancer (PC)) interact with to facilitate PC growth. A candidate growth factor pathway that may mediate this interaction is HGF–c-MET pathway. Effects HGF inhibition (using a neutralising antibody AMG102) alone or in combination gemcitabine were assessed (i) vivo using an orthotopic model PC, and (ii) vitro cultured (AsPC-1) human PSCs. We have shown PSCs (hPSCs) secrete but do not express receptor c-MET, present...

10.1038/bjc.2015.478 article EN cc-by-nc-sa British Journal of Cancer 2016-01-14

Pancreatic exocrine insufficiency (PEI) occurs when the amounts of enzymes secreted into duodenum in response to a meal are insufficient maintain normal digestive processes. The main clinical consequence PEI is fat maldigestion and malabsorption, resulting steatorrhoea. function commonly assessed by conducting 3-day faecal test measuring levels elastase-1 serum trypsinogen. enzyme replacement therapy mainstay treatment for PEI. In adults, initial recommended dose pancreatic 25 000 units...

10.5694/j.1326-5377.2010.tb04000.x article EN The Medical Journal of Australia 2010-10-01
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