Objective: To investigate the changes in the myocardial expression of aquaporin-1 (AQP1) protein and its association with myocardial edema in rats with severe burns.
Methods: Forty-eight healthy adult Wistar rats were randomly divided into normal control group (n=6) and burn injury group with third degree burn of 30% total body surface area, and the latter group was further divided into 2, 4, 8, 12, 24, 48 and 72 h groups. The changes of myocardial water content were investigated by dry-wet weight methods. Enzyme-linked immunosorbent assay was used to detect the changes in AQP1 expression at different time points after sever burns.
Results: The myocardial water content and AQP1 expression increased significantly 2 h after the burn injury, reaching the peak levels at 12 h and remaining higher than the normal level at 48 h. A significant positive correlation was found between myocardial water content and AQP1 expression in the rats (r=0.868, P<0.01).
Conclusion: The severity of myocardial edema after severe burn is correlated to the expression level of AQPl protein, suggesting the important role of AQPl protein in pathological progression of myocardial edema.
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Dis Aquat Organ
January 2025
Mississippi Aquarium, Department of Veterinary Services, Gulfport, Mississippi 39502, USA.
This report documents complications in false pilchard Harengula clupeola and scad Decapterus macarellus associated with a salinomycin (60 mg kg-1) and amprolium (100 mg kg-1) gel feed treatment, along with prolonged temperature increase, for an Enteromyxum leei outbreak in a salt water, mixed species, public aquarium exhibit. Shortly after administration, a mass mortality event ensued where hundreds of false pilchards and a few scad died. Medicated gel feed was noted within the gastrointestinal tracts of all affected fish.
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Department of Public Health, Yekatit 12 Hospital Medical College, Addis Ababa, Ethiopia.
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Department of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing 400014, China.
Sci Rep
January 2025
Department of Pharmacology, "Grigore T. Popa" University of Medicine and Pharmacy, 16 University St., Iași, Romania.
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Department of Occupational and Radiological Diseases, Changzhou Center for Disease Prevention and Control, Changzhou 213022, China.
This paper reports two cases of occupational severe toxic encephalopathy caused by inhaling excessive nitrogen in an accident. The main reasons are failure to performing field-work standards of limited space operation and emergency rescue. Hypoxia asphyxia is the main pathogenic link of nitrogen toxicity, which can cause brain edema.
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