Delayed infarcts seen on late computed tomography but not post-procedurally were attributed to vasospasm if there was moderate or severe vasospasm in the corresponding vascular territory on angiography. Infarct volume was measured by perimeter tracing.

RESULTS: Of 276 aSAH survivors, 134 had all imaging requisite for inclusion. Fifty-four (34%) had moderate or severe vasospasm,

of whom 17 (31%) had delayed infarcts, compared with only 3 (4%) of 80 patients without vasospasm (P < .001). There were a total of 29 delayed infarcts in these 20 patients; 21 were in a territory with angiographic vasospasm, but 8 (28%) were not. Infarct volume did not differ between vasospasm-related (18 +/- 25 mL) and vasospasm-unrelated Selumetinib price (11 +/- 12 mL) infarcts (P = .54), but infarcts in the absence

of vasospasm were more likely watershed (50% vs 10%, P = .03).

CONCLUSION: Delayed infarcts following aSAH can occur in territories without angiographic vasospasm and are more likely watershed in distribution.”
“Stem pitting is a common virus-induced disease of perennial woody plants induced by a range of different viruses. The phenotype results from sporadic areas Selleckchem BTSA1 of the stem in which normal xylem and phloem development is prevented during growth of stems. These alterations interfere with carbohydrate transport, resulting in reduced plant growth and yield. Citrus tristeza virus (CTV), a phloem-limited closterovirus, induces economically important stem-pitting diseases of citrus. CTV has three nonconserved genes (p33, p18, and Dynein p13) that are not related to genes of other viruses and that are not required for systemic infection of some species of citrus, which allowed us to examine the effect of deletions of these genes

on symptom phenotypes. In the most susceptible experimental host, Citrus macrophylla, the full-length virus causes only very mild stem-pitting symptoms. Surprisingly, we found that certain deletion combinations (p33 and p18 and/or p13) induced greatly increased stem-pitting symptoms, while other combinations (p13 or p13 plus p18) resulted in reduced stem pitting. These results suggest that the stem-pitting phenotype, which is one of more economically important disease phenotypes, can result not from a specific sequence or protein but from a balance between the expression of different viral genes. Unexpectedly, using green fluorescent protein-tagged full-length virus and deletion mutants (CTV9 Delta p33 and CTV9 Delta p33 Delta p18 Delta p13), the virus was found at pitted areas in abnormal locations outside the normal ring of phloem. Thus, increased stem pitting was associated not only with a prevention of xylem production but also with a proliferation of cells that supported viral replication, suggesting that at random areas of stems the virus can elicit changes in cellular differentiation and development.