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TRAIL agonists rescue mice from radiation-induced lung, skin or esophageal injury.
J Clin Invest
January 2025
Laboratory of Translational Oncology and Translational Cancer Therapeutics, Warren Alpert Medical School of Brown University, Providence, United States of America.
Radiotherapy can be limited by pneumonitis which is impacted by innate immunity, including pathways regulated by TRAIL death receptor DR5. We investigated whether DR5 agonists could rescue mice from toxic effects of radiation and found two different agonists, parenteral PEGylated trimeric-TRAIL (TLY012) and oral TRAIL-Inducing Compound (TIC10/ONC201) could reduce pneumonitis, alveolar-wall thickness, and oxygen desaturation. Lung protection extended to late effects of radiation including less fibrosis at 22-weeks in TLY012-rescued survivors versus un-rescued surviving irradiated-mice.
View Article and Find Full Text PDFSynthesis and Structure-Activity Relationships of Novel Benzofuran Derivatives with Osteoblast Differentiation-Promoting Activity.
Chem Pharm Bull (Tokyo)
January 2025
Drug Discovery Research Department, Kyoto Pharmaceutical Industries, Ltd.
Osteoporosis is caused by an imbalance between bone resorption and formation, which decreases bone mass and strength and increases the risk of fracture. Therefore, osteoporosis is treated with oral resorption inhibitors, such as bisphosphonates, and parenteral osteogenic drugs, including parathyroid hormone and antisclerostin antibodies. However, orally active osteogenic drugs have not yet been developed.
View Article and Find Full Text PDFNose to brain strategy coupled to nano vesicular system for natural products delivery: Focus on synaptic plasticity in Alzheimer's disease.
J Pharm Anal
December 2024
Laboratory of Neuropharmacology, EBRI Rita Levi-Montalcini Foundation, Rome, 00161, Italy.
A wide number of natural molecules demonstrated neuroprotective effects on synaptic plasticity defects induced by amyloid-β (Aβ) in and Alzheimer's disease (AD) models, suggesting a possible use in the treatment of this neurodegenerative disorder. However, several compounds, administered parenterally and orally, are unable to reach the brain due to the presence of the blood-brain barrier (BBB) which prevents the passage of external substances, such as proteins, peptides, or phytocompounds, representing a limit to the development of treatment for neurodegenerative diseases, such as AD. The combination of nano vesicular systems, as colloidal systems, and nose to brain (NtB) delivery depicts a new nanotechnological strategy to overtake this limit and to develop new treatment approaches for brain diseases, including the use of natural molecules in combination therapy for AD.
View Article and Find Full Text PDFExploring the Efficacy and Safety of Ketamine for Managing Acute Renal Colic in Emergency Departments: A Systematic Review of Recent Clinical Trials.
Int J Mol Sci
January 2025
Nursing Department, College of Staten Island, City University of New York, Staten Island, NY 10314, USA.
Kidney stones typically present as renal colic in emergency departments (EDs), where patients experience severe pain and often require parenteral therapy for symptom management. The economic burden associated with managing kidney stones exceeds USD 5 billion annually in the US and accounts for more than a million visits to EDs each year. There is clear evidence emphasizing the need for innovative and alternative pain control options for patients with renal colic.
View Article and Find Full Text PDFThe Gut in Critical Illness.
Curr Gastroenterol Rep
December 2025
Division of Pulmonary, Critical Care, and Sleep Medicine, Medical College of Wisconsin, 8701 West Watertown Plank Road, 8th Floor: HUB for Collaborative Medicine, Milwaukee, WI, 53226, USA.
Purpose Of Review: The purpose of this narrative review is to describe the mechanisms for gut dysfunction during critical illness, outline hypotheses of gut-derived inflammation, and identify nutrition and non-nutritional therapies that have direct and indirect effects on preserving both epithelial barrier function and gut microbiota during critical illness.
Recent Findings: Clinical and animal model studies have demonstrated that critical illness pathophysiology and interventions breach epithelial barrier function and convert a normally commensal gut microbiome into a pathobiome. As a result, the gut has been postulated to be the "motor" of critical illness and numerous hypotheses have been put forward to explain how it contributes to systemic inflammation and drives multiple organ failure.
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