TUDIES SHOW THAT TISSUE LEVels of arachadonic acid-and eicosopentaenoic acid (EPA)derived eicosanoids influence many physiological processes, including calcium transport across cell membranes, angiogenesis, apoptosis, cell proliferation, and immune cell function. [1][2][3][4] These processes are integral to the immune system and hence the pathogenesis of autoimmune diseases such as arthritis, systemic lupus erythematosus, and asthma, as well as cancer. Epidemiological studies have suggested that groups of people who consume diets high in omega-3 fatty acids may experience a lower prevalence of some types of cancer, 5-8 and many small trials have attempted to assess the effects of omega-3 fatty acids on cancer treatment by adding omega-3 fatty acid to the diet either as omega-3 fatty acid-rich foods or as dietary supplements. [9][10][11][12][13][14][15][16][17][18][19][20][21][22] In addition, dietary omega-3 fatty acids have been found to modulate mammary tumor formation and proliferation in rodents. 23 In response to this evidence, a number of omega-3 fatty acid-containing dietary supplements have appeared on the market claiming to protect against the development of a variety of conditions including cancer. To assess the va-Author Affiliations are listed at the end of this article.
Abstract:The characteristic pathological features of the postmortem brain of Alzheimer's disease (AD) patients include, among other features, the presence of neuritic plaques composed of amyloid /3-peptide (A~3)and the loss of basal forebrain cholinergic neurons, which innervate the hippocampus and the cortex. Studies of the pathological changes that characterize AD and several other lines of evidence indicate that A/3 accumulation in vivo may initiate and/or contribute to the process of neurodegeneration and thereby the development of AD. However, the mechanisms by which Aj3 peptide influences/causes degeneration of the basal forebrain cholinergic neurons and/or the cognitive impairment characteristic of AD remain obscure. Using in vitro slice preparations, we have recently reported that A/3-related peptides, under acute conditions, potently inhibit K~-evokedendogenous acetyicholine (ACh) release from hippocampus and cortex but not from striatum. In the present study, we have further characterized A/3-mediated inhibition of ACh release and also measured the effects of these peptides on choline acetyltransferase (ChAT) activity and high-affinity choline uptake (HACU) in hippocampal, cortical, and striatal regions of the rat brain. A/3 1_40(10 8M) potently inhibited veratridine-evoked endogenous ACh release from rat hippocampal slices and also decreased the K~-evokedrelease potentiated by the nitric oxidegenerating agent, sodium nitroprusside (SNP). It is interesting that the endogenous cyclic GMP level induced by SNP was found to be unaltered in the presence of 1AT
The decrease in the rate at which novel medical products are reaching the market, despite major scientific achievements and investment that might have predicted otherwise, is causing much concern. Although this 'pipeline problem' has often been discussed in the context of drug development, it is also crucial to examine the unique characteristics of the pipeline for biomarkers and diagnostics. Here, we characterize the pipeline problem for biomarkers and diagnostics, and consider what steps could be taken to solve it.
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