PubMed · 15223467
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Daniel J DiBardino, Charles D Fraser. 2004. Persistent left fifth aortic arch.. https://doi.org/10.1016/s0003-4975(03)01049-x
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OBJECTIVE: To determine the correlation between fetoplacental blood flow and brain injury and volumes in very low birth weight (VLBW) infants. STUDY DESIGN: Antenatal blood flow from the umbilical artery (UA), middle cerebral artery (MCA), and descending aorta was determined in 70 VLBW infants. The directions of the total diastolic flow of the aortic isthmus and the end-diastolic flow of ductus venosus also were measured. Serial brain ultrasound examinations and MRI at term were performed to assess brain abnormalities. On the basis of brain imaging findings, the newborn infants were classified as normal (n = 14), intermediate brain pathology (n = 31), and major pathology (n = 25) groups. RESULTS: Abnormalities in fetoplacental blood flow were not related to anatomic brain lesions. However, an abnormal UA/MCA pulsatility index ratio was associated with reduced total brain volume (mean, 360 mL; SD, 32.5 mL) and reduced cerebral volume (344 mL; SD, 28.4 mL) compared with infants with normal UA/MCA pulsatility index ratio (mean, 405 mL; SD, 51.3 mL, P = .01, and mean, 368 mL; SD, 52.3 mL, P = .012), respectively. CONCLUSIONS: Redistribution of fetal blood flow in VLBW infants is associated with reduced brain volume at term age. Neurodevelopmental follow-up of this cohort will clarify the significance of these blood flow changes on development.
Trauma is the leading cause of death in patients younger than 40 years of age. Thoracic injuries are common and often can be managed by tube thoracostomy. In many patients, however, the thoracic injuries must be repaired surgically in one of three time periods: immediate, urgent, or delayed thoracotomy. In this article, we describe the general approach to effectively managing thoracic trauma patients. We review common injuries and scenarios that may be encountered by the surgeon and discuss the considerations and variables that enter into the decision-making process for operative intervention.
Increased oxidative stress in vascular cells is implicated in the pathogenesis of atherosclerosis. Reactive oxygen species (ROS) induce vascular inflammation via the proinflammatory cytokine/NF-kappaB pathway. Several lines of evidence suggest that peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1alpha) is an important regulator of intracellular ROS levels. However, no studies have examined the effects of PGC-1alpha on this process. We investigated the effects of PGC-1alpha on inflammatory molecule expression and activity of the redox-sensitive transcription factor, NF-kappaB, in vascular cells. PGC-1alpha expressed in human aortic smooth (HASMCs) and endothelial cells (HAECs) is upregulated by AMP-activated protein kinase activators, including metformin, rosiglitazone and alpha-lipoic acid. Tumor necrosis factor-alpha (TNF-alpha), a major proinflammatory factor in the development of vascular inflammation, stimulates intracellular ROS production through an increase in both mitochondrial ROS and NAD(P)H oxidase activity. Adenovirus-mediated overexpression of the PGC-1alpha gene in HASMCs and HAECs leads to a significant reduction in intracellular and mitochondrial ROS production as well as NAD(P)H oxidase activity. Consequently, NF-kappaB activity and MCP-1 and VCAM-1 induced by TNF-alpha are suppressed. Our data support the possibility that agents stimulating PGC-1alpha expression in the vasculature aid in preventing the development of atherosclerosis.