When evaluating the effects of schistosomes/schistosome components on snail defence cell gene expression, it is valuable to consider also how such effects might initially be mediated. It has been shown that the activity of the ERK pathway is suppressed by ESPs in haemocytes from schistosome susceptible snails but not in those from the resistant strain. One transcription factor that is likely activated by ERK in B. glabrata is Elk-1 and in humans this transcription factor appears to target genes that are involved in expression control, including basal transcriptional machinery components and the spliceosome and ribosome. Thus the reduced expression of certain susceptible-specific genes both here and in other studies may be due to the attenuation of ERK GDC-0449 signalling in susceptible snail haemocytes. Despite multiple gene expression studies there is still much to learn concerning the schistosome-snail host-parasite relationship and the nature of resistance to the parasite. It is clear, however, that schistosome ESPs produced during early parasite development do affect host snail haemocytes. Investigations into the effects of the ciliary epidermal plates that are shed rapidly upon snail invasion on haemocyte physiology and gene expression patterns are also needed. Through integration of gene expression studies and functional biology it is hoped that we will arrive at a more complete understanding of B. glabrata-S. mansoni molecular interactions, a necessary prerequisite to the design of schistosomiasis control strategies, which challenge successful infections in natural populations. Tako-Tsubo Cardiomyopathy is an acute reversible condition characterized by left ventricular apical ‘ballooning’ and mimics acute myocardial infarction. It was first described in Japan in 1990 by Sato et al. and the Japanese name ‘tako-tsubo’ describes the visual appearance of left ventricle on ventriculography resembling a fishing jar used to trap octopus. Since then, several cases have been described all over the world and TTC has been recognized as a primary acquired cardiomyopathy in the American Heart Association classification of cardiomyopathies. Several studies have estimated that approximately 1% to 2% of all patients presenting with an initial primary diagnosis of acute coronary syndrome have TTC. TTC typically affects aged postmenopausal women, with less than 3% of patients being younger than 50 years. While TTC is usually triggered by a profound emotional or physical stress, in around 30% of cases no preceding stressful event could be identified. The clinical presentation of TTC mimics ACS with ischemia-like chest pain and ischemia-like electrocardiographic changes contrasting with minimal elevation of cardiac enzymes despite the presence of large regions of focal myocardial akinesia involved. At coronary angiography there is a lack of identifiable obstructive coronary artery disease. Transient left apical and middle ventricular walls dysfunction with akinesia or dyskinesia is detectable.