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Articles by R. D Hansen
Total Records ( 15 ) for R. D Hansen
  V. P Suttor , C Ng , S Rutkowski , R. D Hansen , J. E Kellow and A. Malcolm
 

The role of the central nervous system in enteroenteric motor reflexes remains controversial. Our aims were as follows: 1) to evaluate colorectal, rectocolic, gastrocolonic, and gastrorectal reflex responses in patients with cervical spinal cord injury (SCI) and 2) to compare these responses with those in healthy subjects. In six patients with SCI (5 male, 42 ± 4 yr) and six healthy control subjects (5 male, 36 ± 5 yr), 2-min phasic distensions were performed randomly via dual-barostat balloons in the colon and rectum. Continuous colonic and rectal balloon volumes were recorded during distensions and after a 1,000-kcal liquid meal. Mean balloon volumes were recorded before, during, and after phasic distensions and over 60 min postprandially. The colorectal response was similar in control subjects and SCI patients (rectal volume reduction = 28 ± 11% and 15 ± 5% in SCI patients and healthy subjects, respectively); the rectocolic response was variable. The gastrocolonic response was present in all subjects (colonic volume reduction = 49 ± 4% and 44 ± 3% in SCI patients and healthy subjects, respectively), with a time effect in the first 30 min (P < 0.0001) and a group effect in the second 30 min (P < 0.004). The gastrorectal response was present in four SCI patients and five healthy subjects (rectal volume reduction = 38 ± 4% and 41 ± 3% in SCI patients and healthy subjects, respectively), with a time effect in the first 30 min (P < 0.0001) but no group effect in the second 30 min. Intact neural transmission between the spinal cord and higher centers is not essential for normal colorectal motor responses to feeding and distension; however, a degree of central nervous system and neurohormonal modulation of these responses is likely.

  B Hoeft , J Linseisen , L Beckmann , K Muller Decker , F Canzian , A Husing , R Kaaks , U Vogel , M. U Jakobsen , K Overvad , R. D Hansen , S Knuppel , H Boeing , A Trichopoulou , Y Koumantaki , D Trichopoulos , F Berrino , D Palli , S Panico , R Tumino , H.B Bueno de Mesquita , F. J.B van Duijnhoven , C. H van Gils , P. H Peeters , V Dumeaux , E Lund , J. M Huerta Castano , X Munoz , L Rodriguez , A Barricarte , J Manjer , K Jirstrom , B Van Guelpen , G Hallmans , E. A Spencer , F. L Crowe , K. T Khaw , N Wareham , S Morois , M. C Boutron Ruault , F Clavel Chapelon , V Chajes , M Jenab , P Boffetta , P Vineis , T Mouw , T Norat , E Riboli and A. Nieters
 

Colorectal cancer (CRC) is the third most common malignant tumor and the fourth leading cause of cancer death worldwide. The crucial role of fatty acids for a number of important biological processes suggests a more in-depth analysis of inter-individual differences in fatty acid metabolizing genes as contributing factor to colon carcinogenesis. We examined the association between genetic variability in 43 fatty acid metabolism-related genes and colorectal risk in 1225 CRC cases and 2032 controls participating in the European Prospective Investigation into Cancer and Nutrition study. Three hundred and ninety two single-nucleotide polymorphisms were selected using pairwise tagging with an r2 cutoff of 0.8 and a minor allele frequency of >5%. Conditional logistic regression models were used to estimate odds ratios and corresponding 95% confidence intervals. Haplotype analysis was performed using a generalized linear model framework. On the genotype level, hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD), phospholipase A2 group VI (PLA2G6) and transient receptor potential vanilloid 3 were associated with higher risk for CRC, whereas prostaglandin E receptor 2 (PTGER2) was associated with lower CRC risk. A significant inverse association (P < 0.006) was found for PTGER2 GGG haplotype, whereas HPGD AGGAG and PLA2G3 CT haplotypes were significantly (P < 0.001 and P = 0.003, respectively) associated with higher risk of CRC. Based on these data, we present for the first time the association of HPGD variants with CRC risk. Our results support the key role of prostanoid signaling in colon carcinogenesis and suggest a relevance of genetic variation in fatty acid metabolism-related genes and CRC risk.

 
 
 
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