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Background: Acute carbon monoxide poisoning (ACOP) commonly results in delayed neuropsychiatric sequelae (DNS). Currently, there are no reliable predictors. The aim of this article is to establish a practical model for predicting the development of delayed encephalopathy clinically.
Methods: Retrospective analysis of clinical data were performed at a single institution for the past 6 years. 107 patients with ACOP were recruited, of who 67 developed DNS and 40 did not. Clinical characteristics of the patients were analyzed between the two groups. The risk factors associated with DNS development were screened to identify the potential markers for predicting DNS. A predictive model was then built, and the receiver operating characteristic (ROC) curve analysis was used to assess its predictive ability.
Results: There were significant differences in 13 clinical features between the two groups. Four potential markers were identified. They were age, source of CO, Glasgow Coma Scale score and the initiation of HBOT. The potential predictive model showed an area under the curve (AUC) of 0.93 in the training set and 0.97 in the testing set.
Conclusions: Our model could calculate the probability of DNS after acute CO poisoning.
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http://dx.doi.org/10.1016/j.jocn.2021.11.022 | DOI Listing |
Genetica
September 2025
Faculty of Fisheries and Aquaculture Sciences, Universiti Malaysia Terengganu, Kuala Nerus, Terengganu, Malaysia.
Population genetics plays a critical role in creating policies for managing fisheries, conservation, and development of aquaculture. The golden snapper, Lutjanus johnii (Bloch, 1792), is a highly commercial and aquaculture important snapper species. This study used mitochondrial markers D-loop (151 specimens) and Cytochrome b (Cyt-b, 120 specimens) from 10 populations, including populations from the east South China Sea, the west South China Sea and the Strait of Malacca to investigate the genetic diversity, population connectivity, and historical demography of L.
View Article and Find Full Text PDFMetab Brain Dis
September 2025
Department of Neuroscience, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Brain ischemia is a major global cause of disability, frequently leading to psychoneurological issues. This study investigates the effects of 4-aminopyridine (4-AP) on anxiety, cognitive impairment, and potential underlying mechanisms in a mouse model of medial prefrontal cortex (mPFC) ischemia. Mice with mPFC ischemia were treated with normal saline (NS) or different doses of 4-AP (250, 500, and 1000 µg/kg) for 14 consecutive days.
View Article and Find Full Text PDFActa Diabetol
September 2025
Department of Endocrinology & Metabolism, Medical College & Hospital, Kolkata, 88, College St. College Square, Kolkata, West Bengal, 700073, India.
Background And Aims: Gestational diabetes mellitus (GDM) is defined as glucose intolerance first identified during pregnancy that does not meet the criteria for overt diabetes. Its pathophysiology shares key features with type 2 diabetes mellitus (T2D), including insulin resistance and inflammation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) are implicated in T2D.
View Article and Find Full Text PDFInflammopharmacology
September 2025
Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Background: Pentoxifylline (PTX), a methylxanthine derivative, has been recognized as a potential anti-inflammatory treatment across various conditions, yet its effects on inflammatory markers remain inconsistent. This systematic review/meta-analysis evaluated the impact of PTX on serum levels and gene expression of key inflammatory markers in randomized controlled trials (RCTs).
Methods: A systematic search was conducted in PubMed, Scopus, Embase, Web of Science, and ProQuest up to May 2025.
J Bioenerg Biomembr
September 2025
Department of Vascular, Shanghai TCM-INTEGRATED Hospital, Shanghai, 200082, China.
This study aimed to investigate the therapeutic effects of Sini Decoction on a murine model of peripheral arterial disease (PAD) and to explore its potential mechanisms of action related to mitochondrial autophagy and M1 macrophage polarization. A total of 36 specific-pathogen-free Kunming mice were used to establish a PAD model and were randomly assigned into four groups: the experimental group (EG, administered Sini Decoction via gavage), the control group (CG, administered rapamycin via gavage), the model group (MG, administered 0.9% sodium chloride solution via gavage), and the normal group (NG, administered 0.
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