Magnesium disorders in horses with gastrointestinal disorders or systemic inflammatory response syndrome (SIRS) are scarcely characterized. The purpose of the study was to explore the association of magnesium disorders with diagnosis, SIRS and mortality in horses admitted to a referral equine hospital. In total, 75 sick horses were included in an observational prospective study and classified as: obstructive ( = 17), inflammatory ( = 10) and ischemic gastrointestinal disorders ( = 12), and other non-gastrointestinal systemic disorders ( = 36). All sick horses were also divided according to the presence ( = 26) or absence of SIRS, and survival to discharge from hospital (survivors ( = 61) and non-survivors ( = 14). In addition, 26 horses were included as controls. On admission, mean (iMg) (95% confidence interval (CI)) in the SIRS group (0.47 (0.43-0.50 mmol/L)) was within the normal range (0.4-0.6 mmol/L). The obstructive group had lower (iMg) compared to the control group (0.44 (0.38-0.51 mmol/L) vs. 0.56 (0.50-0.61 mmol/L); = 0.001). In total, 8 out of 17 (47%) horses with obstructive lesions presented with hypomagnesemia compared to controls (4% (1/26)) ( = 0.001). In conclusion, hypomagnesemia was more prevalent on admission in horses in the obstructive group, and to a lesser extent, in the inflammatory and ischemic groups. In contrast to human ICU patients, the proportion of hospitalized horses with hypomagnesemia was not associated with mortality.
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http://dx.doi.org/10.3390/ani12121479 | DOI Listing |
Arq Bras Cir Dig
January 2025
Universidade Estadual de Campinas, Faculty of Medical Sciences, Department of Surgery, Digestive Diseases Surgical Unit - Campinas (SP), Brazil.
Background: Gastric stump neoplasia is defined as a neoplasia that arises in the gastric remnant after at least 5 years of interval from the first gastric resection.
Aims: The aim of this study was to analyze 51 patients who underwent total and subtotal gastrectomy and multi-visceral resections in patients with gastric stump cancer.
Methods: The hospital records of 51 patients surgically treated for gastric stump cancer between 1989 and 2019 were reviewed.
Acta Cir Bras
January 2025
Universidade Federal de Mato Grosso do Sul - Postgraduate Program in Health and Development in the Midwest Region - Campo Grande (MS) - Brazil.
Purpose: To evaluate the molecular evolution of endoplasmic reticulum (ER) stress during colorectal cancer carcinogenesis.
Methods: Fifty-six hairless mice were divided into two groups: control (no intervention); and carcinogenesis (treated with two doses of azoxymethane at 10 mg/kg during the third and the fourth week and dextran sodium sulfate at 2.5% for seven days in the second, fifth, and eighth week).
J Bras Pneumol
January 2025
. Unidade de Fisiologia Pulmonar, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre (RS) Brasil.
Sci Transl Med
January 2025
Department of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91052 Erlangen, Germany.
Dysregulation at the intestinal epithelial barrier is a driver of inflammatory bowel disease (IBD). However, the molecular mechanisms of barrier failure are not well understood. Here, we demonstrate dysregulated mitochondrial fusion in intestinal epithelial cells (IECs) of patients with IBD and show that impaired fusion is sufficient to drive chronic intestinal inflammation.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Pediatrics, Washington University in St. Louis, School of Medicine, St. Louis, MO 63110, USA.
Children with neurodegenerative disease often have debilitating gastrointestinal symptoms. We hypothesized that this may be due at least in part to underappreciated degeneration of neurons in the enteric nervous system (ENS), the master regulator of bowel function. To test this hypothesis, we evaluated mouse models of neuronal ceroid lipofuscinosis type 1 and 2 (CLN1 and CLN2 disease, respectively), neurodegenerative lysosomal storage disorders caused by deficiencies in palmitoyl protein thioesterase-1 and tripeptidyl peptidase-1, respectively.
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