Purpose: Plasma levels of pancreatic and intestinal enzymes were measured after pancreatic duct ligation (PDL) to monitor pancreatic exocrine insufficiency (PEI) in a model using young pigs.
Material/methods: Five, 6 week-old pigs (10.9±0.2kg), underwent PDL while age-matched, un-operated pigs were used as controls. Plasma levels of immunoreactive cationic trypsinogen (IRCT), amylase, lipase, and diamine oxidase (DAO) activities were analyzed for 48 days after PDL, including 1 week of oral pancreatic enzyme supplementation (PES) with Creon(®).
Results: PDL resulted in an arrested body growth and a rapid surge of pancreatic enzymes (IRCT, amylase and lipase) into the plasma. Nine days after PDL, the plasma levels of these pancreatic enzymes had decreased. IRCT then remained below the level in un-operated pigs while amylase only fell below control at 25 days. The intestinally derived marker DAO and plasma protein levels were unaffected by PDL but DAO decreased slightly with time in PEI pigs. One-week of oral PES restored body growth, but had little effect on pancreatic enzyme plasma levels, except for a tendency towards increased DAO.
Conclusions: The study showed that PEI developed within 1-2 weeks after PDL and that only IRCT is a reliable plasma enzyme marker for this. The reduced plasma DAO indicated that PEI also affected the intestines, while PES therapy restored growth of the PDL pigs and slightly increased plasma DAO, suggesting an improved intestinal function.
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http://dx.doi.org/10.1016/j.advms.2015.01.003 | DOI Listing |
Zool Res
January 2025
School of Basic Medicine, Institute of Brain Science and Disease, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Brain Diseases, Qingdao University, Qingdao, Shandong, 266071, China. E-mail:
Iron is the most abundant transition metal in the brain and is essential for brain development and neuronal function; however, its abnormal accumulation is also implicated in various neurological disorders. The olfactory bulb (OB), an early target in neurodegenerative diseases, acts as a gateway for environmental toxins and contains diverse neuronal populations with distinct roles. This study explored the cell-specific vulnerability to iron in the OB using a mouse model of intranasal administration of ferric ammonium citrate (FAC).
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, Germany.
Background: Clinical expressivity of the thrombophilic factor V Leiden (FVL) mutation is highly variable. Recently, we demonstrated an increased APC (activated protein C) response in asymptomatic FVL carriers compared with FVL carriers with a history of venous thromboembolism (VTE) after in vivo coagulation activation. Here, we further explored this association using a recently developed ex vivo model based on patient-specific endothelial colony-forming cells (ECFCs).
View Article and Find Full Text PDFFront Immunol
January 2025
Institute for Experimental Immunology and Imaging, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Post-stroke early activation of neutrophils contributes to intensive neuroinflammation and worsens disease outcomes. Other pre-existing patient conditions can modify the extent of their activation during disease, especially hypercholesterolemia. However, whether and how increased circulating cholesterol amounts can change neutrophil activation responses very early after stroke has not been studied.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Pathology, Microbiology & Immunology, New York Medical College, Valhalla, NY, United States.
Rationale: Approximately 32 million people in the United States suffer from food allergies. Some food groups, such as legumes - peanuts, tree nuts, fish, and shellfish, have a high risk of cross-reactivity. However, the murine model of multiple food group cross-reactivity is limited.
View Article and Find Full Text PDFFront Med (Lausanne)
January 2025
Department of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Congenital thrombotic thrombocytopenic purpura (cTTP) is a thrombotic microangiopathy (TMA) characterized by severe hereditary ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 motifs 13) deficiency caused by mutations. This rare autosomal recessive genetic disorder is often misdiagnosed as immune thrombocytopenia (ITP) or hemolytic uremic syndrome (HUS). Here, we report a 21-year-old male cTTP patient with a compound heterozygous mutation.
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