Publications by authors named "Romany Stansborough"
Purpose: Radiotherapy-induced gut toxicity (RIGT) is a debilitating effect of radiotherapy for cancer, often resulting in significant diarrhea and pain. Previous studies have highlighted roles of the intestinal microvasculature and matrix metalloproteinases (MMPs) in the development of RIGT. We hypothesized vascular mediators would be significantly altered in a dark agouti (DA) rat model of RIGT.
View Article and Find Full Text PDFPurpose: Radiotherapy-induced gut toxicity (RIGT) is associated with significant diarrhoea, pain and rectal bleeding. Matrix metalloproteinases (MMPs) have been reported to be involved in chemotherapy-induced gut toxicity and RIGT following single-dose irradiation in vivo. We therefore proposed MMPs would be involved in the pathobiology of RIGT following fractionated irradiation.
View Article and Find Full Text PDFArticle Synopsis
- Gastrointestinal toxicities, such as nausea and diarrhea, are common side effects of proteasome inhibitors like bortezomib, affecting up to 84% of patients.
- Newer inhibitors like carfilzomib show less neurotoxicity but similar gastrointestinal issues compared to bortezomib, while orally bioavailable options like ixazomib are being studied for their safety.
- Despite ongoing reports of gastrointestinal side effects, the underlying mechanisms of these toxicities remain largely unclear, highlighting the need for further research to enhance treatment safety.
Article Synopsis
- The study investigates radiotherapy-induced gut toxicity (RIGT), characterized by symptoms like diarrhea and rectal bleeding, focusing on alterations in the microvasculature of the gastrointestinal tract after radiation exposure.
- Female Dark Agouti rats were subjected to a specific 6-week radiation treatment, with assessments conducted at 3, 6, and 15 weeks for signs of injury, including cell death and structural changes.
- Results showed significant apoptosis of microvascular cells in the jejunum and colon at later time points, along with histopathological changes like thickened blood vessels, indicating that the intestinal microvasculature undergoes both acute and chronic alterations due to fractionated radiotherapy.
Objective: To investigate the effect of caffeic acid phenethyl ester (CAPE) on local and systemic inflammation and bone loss in collagen antibody-induced arthritis (CAIA) mice.
Methods: Four groups of mice (n = 8 per group) were allocated; control, CAPE (1 mg/kg), CAIA and CAIA + CAPE (1 mg/kg). Local inflammation and bone loss were evaluated using clinical paw scores, in vivo micro-computed tomography (micro-CT), histological assessment and tartrate-resistant acid phosphatase (TRAP) staining.
Article Synopsis
- The study aimed to assess whether blocking TLR4 signaling with (-)-naloxone would reduce gut toxicity caused by irinotecan and affect tumor growth in rats.
- Female Dark Agouti rats were treated with irinotecan alone, (-)-naloxone alone, or a combination of both, with daily monitoring of weight loss, diarrhea, and tumor growth.
- Results showed that (-)-naloxone did not mitigate irinotecan-induced gut toxicity and actually increased tumor growth, suggesting potential safety concerns for patients using both medications simultaneously.
Purpose To review the literature surrounding the involvement of the endothelium and matrix metalloproteinases (MMP) in radiotherapy-induced gut toxicity (RIGT) and further elucidate its complex pathobiology. Results RIGT involves damage to the gastrointestinal mucosa and is associated with diarrhoea, pain, and rectal bleeding depending on the area of exposure. The mechanisms underpinning RIGT are complex and have not yet been elucidated.
View Article and Find Full Text PDFChemotherapy-induced mucositis is a common condition caused by the breakdown of the mucosal barrier. Symptoms can include pain, vomiting and diarrhoea, which can often necessitate chemotherapy treatment breaks or dose reductions, thus compromising survival outcomes. Despite the significant impact of mucositis, there are currently limited clinically effective pharmacological therapies for the pathology.
View Article and Find Full Text PDFChemotherapy for cancer causes significant gut toxicity, leading to severe clinical manifestations and an increased economic burden. Despite much research, many of the underlying mechanisms remain poorly understood hindering effective treatment options. Recently there has been renewed interest in the role tight junctions play in the pathogenesis of chemotherapy-induced gut toxicity.
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