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Papers by Robert Simpson
InflammoPharmacology, 2003
The pathogenesis of non-steroidal anti-in ammatory drug (NSAID)-induced gastroenteropathy may inv... more The pathogenesis of non-steroidal anti-in ammatory drug (NSAID)-induced gastroenteropathy may involve a number of key events leading to increased intestinal permeability and in ammation (topical effect) and the development of ulcers (micro-vascular effects of COX-1 inhibition and prostaglandin de ciency). Many strategies have been employed in an attempt to reduce the toxic effects of NSAIDs and these have been targeted at the different pathogenic stages of lesion development. One of the latest in this long chain of damage limitation has been the development of nitric oxide (NO) sequestering NSAIDs (NO-NSAIDs). It is suggested that the NO, which is released as the compounds are broken down, may counteract the consequences of the NSAID-induced decrease in mucosal prostaglandins. Here we examine the proposed mechanisms for NSAID-induced gastrointestinal damage together with some of the methods employed to address these mechanisms. We also consider the physiologic roles of NO in the gut together with how it may be potentially employed as an agent for limiting the side effects of NSAIDs in the gastrointestinal tract.
Gastroenterology, 2003
Bacteroides (BA) 1. There were 6 times of rotavirus infection in 8 CMT patients. Conclusion : Dia... more Bacteroides (BA) 1. There were 6 times of rotavirus infection in 8 CMT patients. Conclusion : Diarrhea in BMT recipients happened with complicated infection of various pathogens in many cases 473%) 9 They were CMV, RV, and some bacteria (CD, MRS& KOX, BA). We proposed that complicated infection would introduce or deteriorate the diarrhea symptom in considerable cases although GVHD might cause diarrhea by itself. CMV is a well established etiological agent of disease in the gastrointestinal tract in this group, but RV should be noticed as the second wrus.
InflammoPharmacology, 2003
The pathogenesis of non-steroidal anti-in ammatory drug (NSAID)-induced gastroenteropathy may inv... more The pathogenesis of non-steroidal anti-in ammatory drug (NSAID)-induced gastroenteropathy may involve a number of key events leading to increased intestinal permeability and in ammation (topical effect) and the development of ulcers (micro-vascular effects of COX-1 inhibition and prostaglandin de ciency). Many strategies have been employed in an attempt to reduce the toxic effects of NSAIDs and these have been targeted at the different pathogenic stages of lesion development. One of the latest in this long chain of damage limitation has been the development of nitric oxide (NO) sequestering NSAIDs (NO-NSAIDs). It is suggested that the NO, which is released as the compounds are broken down, may counteract the consequences of the NSAID-induced decrease in mucosal prostaglandins. Here we examine the proposed mechanisms for NSAID-induced gastrointestinal damage together with some of the methods employed to address these mechanisms. We also consider the physiologic roles of NO in the gut together with how it may be potentially employed as an agent for limiting the side effects of NSAIDs in the gastrointestinal tract.
Gastroenterology, 2003
Bacteroides (BA) 1. There were 6 times of rotavirus infection in 8 CMT patients. Conclusion : Dia... more Bacteroides (BA) 1. There were 6 times of rotavirus infection in 8 CMT patients. Conclusion : Diarrhea in BMT recipients happened with complicated infection of various pathogens in many cases 473%) 9 They were CMV, RV, and some bacteria (CD, MRS& KOX, BA). We proposed that complicated infection would introduce or deteriorate the diarrhea symptom in considerable cases although GVHD might cause diarrhea by itself. CMV is a well established etiological agent of disease in the gastrointestinal tract in this group, but RV should be noticed as the second wrus.