The influence of caffeine on energy content of sugar-sweetened beverages : the caffeine–calorie effect

Background/Objectives: Caffeine is a mildly addictive psychoactive chemical and controversial additive to sugar-sweetened beverages (SSBs). The objective of this study is to assess if removal of caffeine from SSBs allows co-removal of sucrose (energy) without affecting flavour of SSBs, and if removal of caffeine could potentially affect population weight gain. Subjects/Methods: The research comprised of three studies; study 1 used three-alternate forced choice and paired comparison tests to establish detection thresholds for caffeine in water and sucrose solution (subjects, n ¼ 63), and to determine if caffeine suppressed sweetness. Study 2 (subjects, n ¼ 30) examined the proportion of sucrose that could be co-removed with caffeine from SSBs without affecting the flavour of the SSBs. Study 3 applied validated coefficients to estimate the impact on the weight of the United States population if there was no caffeine in SSBs. Results: Detection threshold for caffeine in water was higher (1.09±0.08 mM) than the detection threshold for caffeine in sucrose solution (0.49 ± 0.04 mM), and a paired comparison test revealed caffeine significantly reduced the sweetness of sucrose (Po0.001). Removing caffeine from SSBs allowed co-removal of 10.3% sucrose without affecting flavour of the SSBs, equating to 116 kJ per 500 ml serving. The effect of this on body weight in adults and children would be 0.600 and 0.142 kg, which are equivalent to 2.08 and 1.10 years of observed existing trends in weight gain, respectively. Conclusion: These data suggest the extra energy in SSBs as a result of caffeine's effect on sweetness may be associated with adult and child weight gain

Up-regulation of brain-derived neurotrophic factor in primary afferent pathway regulates colon-to-bladder cross-sensitization in rat

Background In humans, inflammation of either the urinary bladder or the distal colon often results in sensory cross-sensitization between these organs. Limited information is known about the mechanisms underlying this clinical syndrome. Studies with animal models have demonstrated that activation of primary afferent pathways may have a role in mediating viscero-visceral cross-organ sensitization. Methods Colonic inflammation was induced by a single dose of tri-nitrobenzene sulfonic acid (TNBS) instilled intracolonically. The histology of the colon and the urinary bladder was examined by hematoxylin and eosin (H&E) stain. The protein expression of transient receptor potential (TRP) ion channel of the vanilloid type 1 (TRPV1) and brain-derived neurotrophic factor (BDNF) were examined by immunohistochemistry and/or western blot. The inter-micturition intervals and the quantity of urine voided were obtained from analysis of cystometrograms. Results At 3 days post TNBS treatment, the protein level of TRPV1 was increased by 2-fold (p \u3c 0.05) in the inflamed distal colon when examined with western blot. TRPV1 was mainly expressed in the axonal terminals in submucosal area of the distal colon, and was co-localized with the neural marker PGP9.5. In sensory neurons in the dorsal root ganglia (DRG), BDNF expression was augmented by colonic inflammation examined in the L1 DRG, and was expressed in TRPV1 positive neurons. The elevated level of BDNF in L1 DRG by colonic inflammation was blunted by prolonged pre-treatment of the animals with the neurotoxin resiniferatoxin (RTX). Colonic inflammation did not alter either the morphology of the urinary bladder or the expression level of TRPV1 in this viscus. However, colonic inflammation decreased the inter-micturition intervals and decreased the quantities of urine voided. The increased bladder activity by colonic inflammation was attenuated by prolonged intraluminal treatment with RTX or treatment with intrathecal BDNF neutralizing antibody. Conclusion Acute colonic inflammation increases bladder activity without affecting bladder morphology. Primary afferent-mediated BDNF up-regulation in the sensory neurons regulates, at least in part, the bladder activity during colonic inflammation

Custom Integrated Circuits

Contains reports on nine research projects.Analog Devices, Inc.International Business Machines CorporationJoint Services Electronics Program Contract DAAL03-89-C-0001U.S. Air Force - Office of Scientific Research Contract AFOSR 86-0164BDuPont CorporationNational Science Foundation Grant MIP 88-14612U.S. Navy - Office of Naval Research Contract N00014-87-K-0825American Telephone and TelegraphDigital Equipment CorporationNational Science Foundation Grant MIP 88-5876

Custom Integrated Circuits

Contains reports on twelve research projects.Analog Devices, Inc.International Business Machines, Inc.Joint Services Electronics Program (Contract DAAL03-86-K-0002)Joint Services Electronics Program (Contract DAAL03-89-C-0001)U.S. Air Force - Office of Scientific Research (Grant AFOSR 86-0164)Rockwell International CorporationOKI Semiconductor, Inc.U.S. Navy - Office of Naval Research (Contract N00014-81-K-0742)Charles Stark Draper LaboratoryNational Science Foundation (Grant MIP 84-07285)National Science Foundation (Grant MIP 87-14969)Battelle LaboratoriesNational Science Foundation (Grant MIP 88-14612)DuPont CorporationDefense Advanced Research Projects Agency/U.S. Navy - Office of Naval Research (Contract N00014-87-K-0825)American Telephone and TelegraphDigital Equipment CorporationNational Science Foundation (Grant MIP-88-58764

Custom Integrated Circuits

Contains reports on ten research projects.Analog Devices, Inc.IBM CorporationNational Science Foundation/Defense Advanced Research Projects Agency Grant MIP 88-14612Analog Devices Career Development Assistant ProfessorshipU.S. Navy - Office of Naval Research Contract N0014-87-K-0825AT&TDigital Equipment CorporationNational Science Foundation Grant MIP 88-5876

P2Y receptors and pain transmission

It is widely accepted that the most important ATP receptors involved in pain transmission belong to the P2X3 and P2X2/3 subtypes, selectively expressed in small diameter dorsal root ganglion (DRG) neurons. However, several types of the metabotropic ATP (P2Y) receptors have also been found in primary afferent neurons; P2Y1 and P2Y2 receptors are typically expressed in small, nociceptive cells. Here we review the results available on the involvement of P2Y receptors in the modulation of pain transmission