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1.  T-ray Imaging and Tomography 
Journal of Biological Physics  2003;29(2-3):247-256.
We demonstrate two algorithms used forreconstructing the target's structure basedon the diffracted pulses and additionallyshow that a three-dimensional target can bereconstructed using the broadband pulsesand a Fresnel lens by virtue of itsfrequency dependent focal length. Oneadvantage of T-ray imaging is the abilityto measure the far-infrared spectralresponse of the target. To highlight theimportance of this spectral information, wedemonstrate T-ray classification imagingwith different biological samples using asimple classification algorithm and twodimensional T-ray spectroscopic images.
doi:10.1023/A:1024457212578
PMCID: PMC3456432  PMID: 23345841
Imaging; tomography; T-rays
2.  Modulation of meningeal nociceptors mechanosensitivity by peripheral proteinase-activated receptor-2: the role of mast cells 
Inflammatory-related activation and sensitization of meningeal nociceptors is believed to play a key role in promoting the intracranial throbbing pain of migraine. We have shown recently that mast cell activation and various mast cell-derived inflammatory mediators can promote activation and sensitization of meningeal nociceptors. Mast cell tryptase has also been proposed to promote pain hypersensitivity by activating the proteinase-activated receptor 2 (PAR2) that is expressed on nociceptive neurons. In this study using in vivo single-unit recording in the trigeminal ganglion of anaesthetized rats, we found that local meningeal activation of PAR2 using the specific agonist SLIGRL-NH2 promoted sensitization of the threshold response while provoking desensitization of the suprathreshold responses. SLIGRL-NH2 also excited a subpopulation of meningeal nociceptors. Chronic mast cell depletion enhanced the sensitizing effects of PAR2 activation while curbing its desensitizing effects. Mast cell depletion did not change the PAR2-mediated excitatory effect. We propose that by enhancing the mechanical sensitivity of meningeal nociceptors local PAR2 activation could play a role in promoting the throbbing pain of migraine and that local mast cell degranulation may modulate such an effect.
doi:10.1111/j.1468-2982.2007.01523.x
PMCID: PMC2504502  PMID: 18254896
Headache; mast cells; meningeal nociceptor; migraine; PAR2
3.  Quantification of glyceryl trinitrate effect through analysis of the synthesised ascending aortic pressure waveform 
Heart  2002;88(2):143-148.
Objective: To establish through analysis of the radial pressure pulse waveform the dose dependent effects of glyceryl trinitrate (GTN) on properties of different blood vessels.
Design: Radial pulse waveform was measured in randomised order before, during a five hour application of a GTN patch delivering 0.104–0.625 mg/h, and for two hours after patch removal. The radial pressure waveform (Millar applanation tonometer) was convolved into an ascending aortic wave using a generalised transfer function (SphygmoCor process) enabling measurement of aortic systolic, diastolic, pulse, mean, and augmented pressure and left ventricular ejection duration in addition to standard brachial cuff pressures.
Setting: Fu Wai and Ren Ming hospitals in Beijing, China.
Patients: 46 recumbent hospitalised patients aged 56 (9) years, awaiting electrophysiological or other diagnostic studies, fasting, and with other treatments suspended.
Major outcome measures: Conventional brachial pressure measures and data from the synthesised aortic pulse.
Results: There was no consistent change in heart rate or brachial pressures except for a decrease in systolic and pulse pressures (p < 0.01) at dose > 0.416 mg/h. In contrast, there were substantial and significant (p < 0.0001) decreases in aortic systolic, pulse, and augmented pressures at all doses, mean pressure (p < 0.001) at doses > 0.416 mg/h, and ejection duration (p < 0.001) at doses > 0.208 mg/h.
Conclusions: Pulse waveform analysis exposes dose dependent effects of GTN on the aortic waveform, suggesting muscular conduit arterial dilatation with reduced wave reflection at the lowest dose, arteriolar dilatation and decreased peripheral resistance at the highest dose, and venous dilatation at the intermediate dose.
PMCID: PMC1767201  PMID: 12117838
glyercyl trinitrate; pulsed waveform analysis; aortic pressure waveform
4.  Indirect validation of benzene exposure assessment by association with benzene poisoning. 
Environmental Health Perspectives  1996;104(Suppl 6):1343-1347.
We present a validation study of a quantitative retrospective exposure assessment method used in a follow-up study of workers exposed to benzene. Assessment of exposure to benzene was carried out in 672 factories in 12 cities in China. Historical exposure data were collected for 3179 unique job titles. The basic unit for exposure assessment was a factory/work unit/job title combination over seven periods between 1949 and 1987. A total of 18,435 exposure estimates was developed, using all available historical information, including 8477 monitoring data. Overall, 38% of the estimates were based on benzene monitoring data. The highest time-weighted average exposures were observed for the rubber industry (30.7 ppm) and for rubber glue applicators (52.6 ppm). Because of its recognized link with benzene exposure, the association between a clinical diagnosis of benzene poisoning and benzene exposure was evaluated to validate the assessment method that we used in the cohort study. Our confidence in the assessment method is supported by the observation of a strong positive trend between benzene poisoning and various measures, especially recent intensity of exposure to benzene.
PMCID: PMC1469750  PMID: 9118918
5.  A retrospective cohort study of leukemia and other cancers in benzene workers 
A retrospective cohort study was carried out in 1982–1983 among 28,460 benzene-exposed workers (15,643 males, 12,817 females) from 233 factories and 28,257 control workers (16,621 males, 12,366 females) from 83 factories in 12 large cities in China. All-cause mortality was significantly higher among the exposed (265.46/100,000 person-years) than among the unexposed (139.06/100,000 person-years), as was mortality from all malignant neoplasms (123.21/100,000 versus 54.7/100,000, respectively). For certain cancers, increased mortality was noted among benzene-exposed males in comparison with that among unexposed males; the standardized mortality ratios (SMR) were elevated for leukemia (SMR = 5.74), lung cancer (SMR = 2.31), primary hepatocarcinoma (SMR = 1.12), and stomach cancer (SMR = 1.22). For females only leukemia occurred in excess among the exposed. Risk of leukemia rose as duration to exposure to benzene increased up to 15 years, and then declined with additional years of exposure. Leukemia occurred among some workers with as little as 6 to 10 ppm average exposure and 50 ppm-years (or possibly less) cumulative lifetime exposure (based on all available measurements for the exposed work units). Among the 30 leukemia cases identified in the exposed cohort, the proportion of subjects with acute lymphocytic leukemia was substantially lower and the proportion with acute nonlymphocytic leukemias was higher than in the general population. During 1972 to 1981, the annual incidence of leukemia ranged from 5.83 to 28.33 per 100,000 with higher rates occurring in the interval 1977 to 1981 than in the earlier years of the study period. Future studies should evaluate more precisely the relationship between exposure levels, job title, and development of leukemia among cases and noncases within the exposed cohort.
PMCID: PMC1568128  PMID: 2792042

Results 1-5 (5)