Evaluation of the association between the optic nerve sheath diameter and extracorporeal life support time during cardiac surgery in newborns.

OBJECTIVE: Congenital heart disease (CHD), a birth defect, is a major cause of neonatal mortality; however, improvements in surgical procedures and medical treatments have resulted in decreased mortality rates. Nonetheless, postoperative morbidity, particularly cerebral dysfunction, remains an issue in patients receiving extracorporeal life support (ECLS) for cardiac surgeries. Herein, we aimed to assess the association between optic nerve sheath diameter (ONSD) and ECLS time in newborns receiving ECLS for cardiac surgery. PATIENTS AND METHODS: We enrolled 25 newborn patients who received ECLS for cardiac surgery at our hospital. ONSD was measured at four different time points during the surgery: baseline (T1), 15 min after cross-clamping (T2), after displacement of cross-clamping (T3) and at the end of the surgery (T4). Furthermore, the ECLS time, aortic cross-clamp time, and surgery time were recorded. RESULTS: The regression analysis revealed a significant association between ONSD and ECLS time, cross-clamp time and surgery time. The correlation analysis showed strong associations between baseline ONSD and ONSD at T2, T3, and T4. Moreover, ONSDs significantly increased at T2 compared with those at baseline during cardiac surgery. CONCLUSIONS: Our findings suggest an association between ONSD and ECLS time in newborns receiving ECLS for cardiac surgery. Monitoring ONSD may provide valuable information about intracranial pressure changes in these patients.

NF-kappaB, macrophage migration inhibitory factor and cyclooxygenase-inhibitions as likely mechanisms behind the acetaminophen- and NSAID-prevention of the ovarian cancer.

Recent epidemiological studies indicated risk reductions in ovarian cancer with consumption of acetaminophen or non-steroid anti-inflammatory drugs. Until now, there is not a systematic analysis, why these agents may reduce risk of ovarian cancer, as it has been performed to explain aspirin-reduction of colon cancer risk. This review tries to explain molecular mechanisms pertinent to acetaminophen- and NSAID-reduction of ovarian cancer. It is proposed that the major mechanism by these anti-inflammatory agents is a shared pathway dependent on the suppression of NF-kappaB activity, which may subsequently decrease transcription of growth factors, chemokines and proteases such as COX-2, VEGF, IL-8/CXCL8, MCP-1/CCL-2, MIP1alpha/CCL-3, tPA and uPA, which are shown to be elevated in ovarian carcinoma, and which play diverse roles such as inducing angiogenesis, invasion, autocrine growth loops and resistance to apoptosis. Besides these, specific mechanisms of action can be attributed to acetaminophen-reduction of ovarian cancer risk via I. Induction of specific reproductive atrophy due its sex-steroid resembling phenolic ring; II. Reduction of glutathione pools due to its NAPQI metabolite, which may play an important role for sterilizing pre-malignant ovarian lesions, since they are shown to lack proper levels of glutathione; III. Inhibition of tautomerization activity of MIF (macrophage migration inhibitory factor), which is shown to be released from ovarian cancer, and which is necessary for proper ovulation; IV. Inhibition of cytokine-induced and endothelia-origined cyclooxygenases. Except the chemosensitization studies, acetaminophen and NSAIDs should be investigated in animal models to test likely benefits in ovarian cancer, since most of their activity may origin from intervening with the cancer growth-stimulating inflammatory stimuli, rather than with the direct cellular toxicity.