Search

The purpose of this study was to investigate the influence of sensitivity to sensory input, including pain, on the conditioned pain modulation (CPM) effect of oxious Electrical Stimulation (NxES). Seventeen healthy participants (24.8 (+/- 2) years) were enrolled in this study that was approved by the IRB. Each person participated in a familiarization session, and 2 testing sessions 24 hours apart. Sensory sensitivity was assessed with the Sensory Hypersensitivity Scale, touch and heat/cold detection thresholds. Pain sensitivity was assessed with the Pain Sensitivity Questionnaire, heat/cold pain thresholds, and pressure pain threshold (PPT). Pain modulation was assessed with temporal summation (TS) and CPM involved a test stimulus of PPT and conditioning stimulus was immersion in a cold water bath for 2 min. The NxES: 20 min of electrical stimulation (400 μs pulse duration, 50 pulses/s; 10s on:10s off; intensity was maximum tolerated). The difference between PPT before and after the NxES comprised the treatment effect. Neither Sensitivity to touch or temperature sensations nor pain sensitivity related to the treatment effect of the NxES. A higher the amplitude of pain perception of NxES was associated with greater treatment effect. The NxES was effective in inhibiting pain and reduced the extent of pain facilitation 24 hours after the treatment. CPM was no different after the NxES. The finding suggests that people who are more sensitive to sensations also experience pain inhibition from NxES. The nervous system is not as “reactive” to pain after a treatment of NxES and the lack of change in the CPM after the treatment of NXES suggests that artificially inducing pain inhibition with NXES does not interfere with the normal pain inhibitory function of the nervous system. Thus, any inhibition due to NXES treatment could augment that which is produced by a patient's own nervous system.

Abstract Evidence can be obtained from clinical trials and bacteriological studies. The latter consist mainly of measuring reductions in colonization, or reductions in bacterial counts on naturally or artificially contaminated surfaces, following the introduction of the measure to be tested. Controlled clinical trials usually provide the best evidence, but are infrequently carried out due to the large number of subjects required, low initial infection rates and a multiplicity of associated factors. Bacteriological studies can be carried out more easily and can often provide statistically significant results not readily available in clinical studies, but they require care in interpretation. Studies involving bacterial counts in the inanimate environment are particularly likely to give misleading results, but have often provided useful confirmatory evidence in eliminating rituals.

The title compound (1) has been synthesized in seven steps and in 42% overall yield from the nucleophilic diene (2). The relative configuration of (1) has been confirmed by a single-crystal X-ray study.

The isolation and structural characterization of 1 : 1 adducts of copper(1) chloride (1) and bromide (2) with pyridine-4-carbonitrile (L) is described; crystals of the two complexes are isomorphous (monoclinic, P21/c, a ≈ 3.9, b ≈ 14.7, c ≈ 13.0 , β ≈ 96°, Z 4; R0.047, 0.063 for No 630, 707 'observed' reflections respectively). Unlike the 1 : 1 adducts with the parent pyridine and benzonitrile ligands which are 'stair' polymers, these complexes comprise 'split-stair' strands woven into a two-dimensional sheet by crosslinking ambidentate ligands. Cu-N ( nitrile ) (1.942(9), 1.96(1) ) are appreciably shorter than Cu-N (pyridine) (2.066(8), 2.04(1) ), as in the parent base complexes. The two Cu-X are similar in each case: 2.336(6), 2.366(3) (CI); 2.460(3), 2.486(3) (Br). The iodide adduct (3) isolated is of novel stoichiometry (Cul : L, 4 : 5) (monoclinic, P21/c; a 10.140(5), b 12.214(6), c 15.157(8) , β 99.99(4)° Z 2; R 0.048, No 2416). It is a linear polymer, comprising tetranuclear Cu414L4 'step' units, crosslinked across inversion centres by disordered ambidentate ligands.