By Talat Kiris
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01) (Fig. 2b). 001), but the increase of intrathecal sFas levels during the same period is not significant. This finding verifies the exponential increase of FasL after SAH, whereas sFas Table 2. 004 ‘‘p’’ values First 3 days Day 5 Day 7 shows a linear increase. Table 2 summarizes the statistical results related to sFas and FasL in SAH patients and control. Table 3. 00001 ‘‘p’’ values First 3 days Day 5 Day 7 20 IL-1, IL-6 and TNF- levels in CSF and serum The levels of IL-1, IL-6 and TNF- were measured on days 1 to 3, 5 and 7 after SAH, and were detected in all collected CSF and serum samples.
A. A. 2 Summary Aneurismal subarachnoid haemorrhage (SAH) is a devastating disease that is associated with significant morbidity and mortality. The mortality is approximately 50%, with 30% of survivors having significant morbidity. There is substantial evidence to suggest that oxidative stress is significant in the development of acute brain injury and cerebral vasospasm following SAH. There are several sources for the excessive generation of free radicals following SAH, including disrupted mitochondrial respiration and extracellular hemoglobin.
SAH). The pathogenesis of cerebral vasospasm is unclear but many studies indicate that apoptosis plays a putative role [1, 8, 9]. C-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase group, has been shown to be involved in the response of a variety of extracellular stresses and has been implicated in numerous physiological processes, such as cell proliferation, cell survival, apoptosis, inflammation, and embryonic development. Therefore, we hypothesised that the JNK signaling pathway might be a therapeutic target for cerebral vasospasm from the point of view of apoptosis.