A5046958371- Pancreatitis Pathology and Treatment
- Pancreatic and Hepatic Oncology Research
- Liver Disease Diagnosis and Treatment
- Neonatal Health and Biochemistry
- Lipid metabolism and disorders
- Pancreatic function and diabetes
- Diabetes and associated disorders
- Signaling Pathways in Disease
- Neuropeptides and Animal Physiology
- Cardiac, Anesthesia and Surgical Outcomes
- Retinal Diseases and Treatments
- Pediatric Hepatobiliary Diseases and Treatments
- Retinal Imaging and Analysis
- Mitochondrial Function and Pathology
- Gallbladder and Bile Duct Disorders
- Appendicitis Diagnosis and Management
- Peroxisome Proliferator-Activated Receptors
- Cancer, Lipids, and Metabolism
- Abdominal Surgery and Complications
- Genetic Neurodegenerative Diseases
- Vector-borne infectious diseases
- Social Media in Health Education
- Inflammasome and immune disorders
- Sepsis Diagnosis and Treatment
- COVID-19 and Mental Health
University of Liverpool
2016-2025
Adamas University
2024
Aintree University Hospitals NHS Foundation Trust
2020-2024
Leeds Teaching Hospitals NHS Trust
2020-2023
St James's University Hospital
2020-2023
Musgrove Park Hospital
2023
R. G. Kar Medical College and Hospital
2022
Medical College and Hospital, Kolkata
2015-2022
Bankura Sammilani Medical College
2022
Royal Liverpool University Hospital
2009-2021
<h3>Objective</h3> Acute pancreatitis is caused by toxins that induce acinar cell calcium overload, zymogen activation, cytokine release and death, yet without specific drug therapy. Mitochondrial dysfunction has been implicated but the mechanism not established. <h3>Design</h3> We investigated of induction consequences mitochondrial permeability transition pore (MPTP) in pancreas using biological methods including confocal microscopy, patch clamp technology multiple clinically...
<h3>Objective</h3> Non-oxidative metabolism of ethanol (NOME) produces fatty acid ethyl esters (FAEEs) via carboxylester lipase (CEL) and other enzyme action implicated in mitochondrial injury acute pancreatitis (AP). This study investigated the relative importance oxidative non-oxidative pathways dysfunction, pancreatic damage development alcoholic AP, whether deleterious effects NOME are preventable. <h3>Design</h3> Intracellular calcium ([Ca<sup>2+</sup>]<sub>C</sub>), NAD(P)H, membrane...
Caffeine reduces toxic Ca2+ signals in pancreatic acinar cells via inhibition of inositol 1,4,5-trisphosphate receptor (IP3R)-mediated signalling, but effects other xanthines have not been evaluated, nor on experimental acute pancreatitis (AP). We determined caffeine and its xanthine metabolites IP3R-mediated signalling AP.Isolated were exposed to secretagogues, uncaged IP3 or toxins that induce AP xanthines, non-xanthine phosphodiesterase (PDE) inhibitors cyclic adenosine monophosphate...
Pyroptosis is a lytic form of pro-inflammatory cell death characterised as caspase 1 dependent with canonical NLRP3 inflammasome-induced gasdermin D (GSDMD) activation. We aimed to investigate the role acinar pyroptotic in pancreatic injury and systemic inflammation AP.Pancreatic pathway activation upon toxin stimulation vitro vivo was investigated. Effects pharmacological (NLRP3 caspase-1 inhibitors), constitutive (Nlrp3-/- , Casp1-/- Gsdmd-/- ) conditional (Pdx1Cre Nlrp3Δ/Δ Pdx1Cre...
BackgroundThe level of hypertriglyceridaemia (HTG) at which the risk acute pancreatitis (AP) increases and impact HTG on AP attributable to other aetiologies remains unclear.MethodsWe compared clinical outcomes patients admitted within 48 h onset abdominal pain from a first episode admission serum triglyceride levels either <5.65 mmol/l (<500 mg/dl) or ≥5.65 <11.3 (moderate HTG) ≥11.3 (≥1000 mg/dl, severe HTG).ResultsAmong cohort 1,233 with there were significant progressive in all major...
Acute pancreatitis (AP) is a common digestive disease without specific treatment, and its pathogenesis features multiple deleterious amplification loops dependent on translation, triggered by cytosolic Ca
Stress hyperglycemia is common in critical illness but it has not been clearly studied patients with acute pancreatitis (AP). This study aimed to investigate the specific blood glucose (BG) level that defines stress and determine impact of on clinical outcomes AP patients. admitted ≤ 48 h after abdominal pain onset were retrospectively analyzed. Patients stratified by pre-existing diabetes was defined using BG levels for non-diabetes compared. There 967 non-diabetic 114 diabetic (10.5%) met...
Huntington's disease (HD) is an inherited neurodegenerative disorder caused by abnormal expansion of glutamine repeats in the protein huntingtin. In HD brain, mutant huntingtin undergoes proteolytic processing, and its N-terminal fragment containing poly-glutamine accumulate as insoluble aggregates leading to defect cellular quality control system heat shock response (HSR). Here we demonstrate that defective HSR brain due down-regulation factor 1 (HSF1) both mice fly models HD....
Hereditary pancreatitis (HP) is an autosomal dominant disease that displays the features of both acute and chronic pancreatitis. Mutations in human cationic trypsinogen (PRSS1) are associated with HP have provided some insight into pathogenesis pancreatitis, but mechanisms responsible for initiation not been elucidated role apoptosis necrosis has much debated. However, it generally accepted trypsinogen, prematurely activated within pancreatic acinar cell, a major process. Functional studies...
Although oxidative stress has been strongly implicated in the development of acute pancreatitis (AP), antioxidant therapy patients so far discouraging. The aim this study was to assess potential protective effects a mitochondria-targeted antioxidant, MitoQ, experimental AP using vitro and vivo approaches. MitoQ blocked H 2 O -induced intracellular ROS responses murine pancreatic acinar cells, an action not shared by control analogue dTPP. did reduce mitochondrial depolarisation induced...
Pancreatic acinar cells require high rates of amino acid uptake for digestive enzyme synthesis, but excessive concentrations can trigger acute pancreatitis (AP) by mechanisms that are not well understood. We have used three basic natural acids L-arginine, L-ornithine and L-histidine to determine acid-induced pancreatic injury whether these common all acids. Caffeine markedly inhibited necrotic cell death pathway activation in isolated induced L-ornithine, whereas caffeine accelerated...