The size of a cerebral contusion is not finite at the moment of trauma, but liable to secondary increase during the following hours and days. In the present study we investigated whether this phenomenon may be related to changes in cortical blood flow (cCBF). In rats a cortical lesion grew to 140% of its initial volume during the first 24 h after injury. During the time of most rapid lesion expansion (<6 h after the insult) marked hypoperfusion (approximately 30% of baseline) was found in the ipsilateral hemisphere by laser Doppler scanning fluxmetry. In the peri-contusional area cCBF slowly recovered to approximately 80% of baseline, while in the distant brain not affected by delayed cell death, significant hyperperfusion (approximately 160% of baseline) was observed. Thus, early hypoperfusion might be an important mechanism for secondary lesion expansion.
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http://dx.doi.org/10.1016/s0304-3940(03)00396-3 | DOI Listing |
Wounds from gunshots and other explosive devices are a source of loss of substances directly or secondary to a well- conducted debridement. In addition, these types of wounds are by definition contaminated. The major challenge in this context for any surgeon remains coverage.
View Article and Find Full Text PDFJHEP Rep
February 2025
Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
Background & Aims: Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation.
Methods: This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg).
Front Sports Act Living
January 2025
School of Human Sciences, University of Western Australia, Perth, WA, Australia.
Am J Blood Res
December 2024
Department of Pathology, University College of Medical Sciences and Guru Teg Bahadur Hospital Delhi, India.
Unlabelled: Iron deficiency anaemia (IDA) makes an individual prone to bacterial infections. The antimicrobial defence mechanism of neutrophils is orchestrated by Nicotinamide Adenine Dinucleotide Phosphate Hydrogen (NADPH) oxidative burst which is iron-dependent. The few previous studies documenting a decrease in neutrophil oxidative burst in iron-deficient children have been based mainly on the Nitro blue tetrazolium test (NBT).
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