Ppm Carbon Monoxide Research Articles

Hydrogen separation through the use of mixed oxygen ion and electron conducting membranes (I): theoretical analysis

Membrane-based processes are becoming increasingly important in the field of industrial gas separation. Such processes are attractive from the standpoint of high separation selectivity and high conversion ratios in cases involving gas phase and gas–solid reactions. In particular, the application of dense ceramic mixed ionic and electronic conducting membranes to separate gases such as oxygen through ambipolar transport of oxygen ions and electrons and hydrogen through ambipolar transport of protons and electrons from gas mixtures at elevated temperatures (>500°C) is gaining increasing importance. As a specific example, the requirement of high-purity tonnage hydrogen with less than 10 ppm carbon monoxide impurity levels would be absolutely essential for low-temperature proton exchange membrane fuel cells to gain wide market acceptance. We analyze herein a novel membrane-based hydrogen separation process which has heretofore not been widely reported in the literature.

A Smart Single-Chip Micro-Hotplate-Based Gas Sensor System in CMOS-Technology

This paper presents a monolithic chemical gas sensor system fabricated in industrial CMOS-technology combined with post-CMOS micromachining. The system comprises metal-oxide-covered (SnO2) micro-hotplates and the necessary driving and signal-conditioning circuitry. The SnO2 sensitive layer is operated at temperatures between 200 and 350°C. The on-chip temperature controller regulates the temperature of the membrane up to 350°C with a resolution of 0.5°C. A special heater-design was developed in order to achieve membrane temperatures up to 350°C with 5 V supply voltage. The heater design also ensures a homogeneous temperature distribution over the heated area of the hotplate (1–2% maximum temperature fluctuation). Temperature sensors, on- and off-membrane (near the circuitry), show an excellent thermal isolation between the heated membrane area and the circuitry-area on the bulk chip (chip temperature rises by max 6°C at 350°C membrane temperature). A logarithmic converter was included to measuring the SnO2 resistance variation upon gas exposure over a range of four orders of magnitude. An Analog Hardware Description Language (AHDL) model of the membrane was developed to enable the simulations of the complete microsystem. Gas tests evidenced a detection limit below 1 ppm for carbon monoxide and below 100 ppm for methane.

Room temperature carbon monoxide sensor using ITO/ n-GaAs Schottky contact

In this paper we report the potential of ITO/ n-GaAs Schottky diode sensor for carbon monoxide detection at room temperature. The ITO/ n-GaAs Schottky contacts were developed using an evaporation system in our laboratory. Due to the very low operating temperature of the diode which shows rapid response to carbon monoxide (CO) it can be applied to micro-sized devices for IC technology. It has been found that the diode exhibited a saturation current of 1×10 −10 A at room temperature in the absence of CO gas, whereas a value of 1.1×10 −9 A was obtained for saturation current at room temperature in the presence of 1000 ppm CO gas. This excellent responsivity of ITO/ n-GaAs diode sensor at room temperature can be due to penetration of CO molecules into the thin ITO layer (150 nm) and changing its work function to a lower value to form a lower Schottky barrier. A comparative study showed that Schottky gas sensor fabricated with gold metal contact presented different sensitivities to CO gas. The relation between different Schottky contacts subjected to carbon monoxide is discussed.

CMOS Monolithic Metal–Oxide Sensor System Comprising a Microhotplate and Associated Circuitry

A gas sensor system fabricated in industrial CMOS technology is presented, which includes, for the first time, a microhotplate and the necessary driving and control circuitry on a single chip. Post-complementary-metal-oxide-semiconductor (CMOS) fabrication steps, such as micromachining of the membrane structure, the deposition of noble metal on the electrodes, and the processing of the sensitive metal-oxide layer, have been developed to be fully compatible with the industrial CMOS process. Temperatures up to 350/spl deg/C were reached on the hotplates using a low-voltage power supply (5 V). A symmetric hotplate design with a temperature homogeneity of better than 2% in the heated area was realized. The integrated temperature controller regulates the membrane temperature with a resolution of /spl plusmn/0.3/spl deg/C in the tracking mode. The temperature increase on the bulk chip owing to heat transfer through the membrane is less than 2% of the respective membrane operation temperature (6/spl deg/C at 350/spl deg/C membrane temperature). The gas sensing performance of the sensor was assessed by test measurements with carbon monoxide (CO). The gas tests evidenced a limit of detection of less than 5 ppm CO.

Prenatal exposure to carbon monoxide affects postnatal cellular electrophysiological maturation of the rat heart: a potential substrate for arrhythmogenesis in infancy.

Maternal smoking is an independent risk factor for sudden infant death syndrome (SIDS). Carbon monoxide (CO) is a major component of smoke. No information is available about the effect of CO and/or smoking on postnatal maturation of the heart. The aim of this study was to investigate the effect of prenatal exposure to CO on cellular electrophysiological maturation in male Wistar rats. The patch-clamp technique was used to measure action potential (AP) and ionic currents (I(to) and I(Ca,L)) from rat ventricular myocytes. During growth, AP duration measured at -20 and -50 mV (APD(-)(20) and APD(-)(50)) decreased progressively in both groups; the process was significantly delayed in rats exposed prenatally to 150 ppm CO: At 4 weeks, APD(-)(20) and APD(-)(50) were 89.5+/-18.2 and 147.7+/-24.5 ms in CO (n=13) and 35.6+/-4.5 and 77.8+/-8.3 ms in control rats (Ctr; n=14; P<0.01 and P<0.05, respectively) and normalized at 8 weeks. At 4 weeks, the density of I(Ca,L) was significantly higher (21.3+/-1.6 pA/pF, n=17, versus 15.9+/-1.6 pA/pF, n=22; P<0.05) and the density of I(to) significantly lower (9.6+/-1.5, n=22, versus 15.2+/-2.2 pA/pF, n=19; P<0.01) in CO than in Ctr and normalized thereafter. Prenatal CO exposure affects the physiological shortening of APD in neonatal rats. We speculate that a prolonged myocyte repolarization induced by prenatal exposure to smoke may establish a period of vulnerability for life-threatening arrhythmias in infancy.

Effect of dietary protein, zinc, and carbon monoxide on fetal zinc concentration in mice.

Dietary protein and zinc deficiencies known to be detrimental to the developing fetus are common in pregnant women in developing countries. Everyone in modern society is at risk of exposure to carbon monoxide (CO). This study was conducted to observe the effect of dietary protein, zinc, and exposure to CO on the fetal zinc concentrations by factorial experimentation. Pregnant mice of CD-1 strain were maintained on 17% (control) or 9% (deficient) protein diets mixed with deficient, normal (control), or supplemental zinc throughout gestation. The dams in each dietary group were exposed to air (control) or 500 ppm CO in air in environmental chambers from gestation day 8 to gestational day 18. The dams were sacrificed on d 18 and fetal zinc levels were measured by atomic absorption spectrophotometry. Carbon monoxide levels used in this study had no significant effect on fetal zinc concentration in any treatment group. When both dietary protein and zinc levels were normal, the mean fetal zinc concentrations were higher than all other dietary protein/zinc combinations (15.2 +/-6.0 and 14.2 +/- 4.1 microg Zn/g of tissue for 0 and 500 ppm CO levels). However, when dietary protein levels were deficient, supplemental zinc increased the fetal zinc concentrations significantly (12.7+/-3.8 and 13.1+/-0.3.6 microg Zn/g of tissue, in 0 and 500 ppm CO groups) as compared to zinc-deficient groups (8.7 +/- 3.0 and 10.0 +/- 3.3 microg Zn/g of tissue in 0 and 500 ppm CO groups). The results of this study may be relevant to populations that experience both marginal zinc and protein diets during gestation.

METHODOLOGY FOR DEVELOPING AN AIR POLLUTION INDEX (API) FOR SOUTH AFRICA

The Dynamic Air Pollution Prediction System (DAPPS) involves the development and integration of the following elements: Downscaling the current numerical urban-scale weather prediction to a finer spatial and temporal resolution, and establishing a comprehensive air pollutant emission inventory that will include industrial, motor vehicle and domestic emissions, and temporal variations in these emissions. The enhanced meteorological data and the emission inventory data will be used as inputs into a photochemical dispersion model, the Comprehensive Air Quality Model with Extensions (CAMx), to produce air pollution fields for the forecast meteorology. Local air quality affects how we live and what we breathe. Like the weather, it can change from day to day - sometimes from hour to hour. The known and recognized health effects of air pollution include the increased risk of the exacerbation of respiratory symptoms such as increased asthma attacks and reduced lung function, increased hospital admissions for respiratory and cardio-vascular diseases, and increased mortality. An Air Quality or Air Pollution Index (API) is a quantitative tool through which air pollution data can be reported, providing information on how clean or polluted the air is, and the associated health concerns the public should be aware of. These indices usually focus on short-term health effects - those that can happen within a few hours or days of exposure to polluted air. A key feature of the DAPPS is that the final model output is a set of Air Pollution Indices. Several countries employ some type of air pollution index to communicate the quality of their air. Some of these systems rely on relating measured (monitored) or predicted concentrations of air pollutants to a numerical scale, for example ranging from 0 and 100. This scale may be enhanced by verbal descriptors such as high or moderate. The advantage of such a system is that the public does not have to interpret a number of different concentrations - one for each pollutant. They also do not need to recall that, the health effects of, for example 1 ppm of ozone is very different from those of 1 ppm of carbon monoxide. The simplistic use of a single index to reflect air pollution levels creates several difficulties. Different pollutants may have different health endpoints, information that may be lost through the use of a single index. Members of the public may also find it difficult to obtain details of how to translate a unified pollution index back into the disaggregated 'real' pollutant levels. In addition, it can be difficult to use an index to compare pollutant levels with national or international standards or guidelines, or with indices used in other countries. The use of a single standardized or unified scale doesn't solve the problems of how to report raised concentrations of a number of pollutants. The DAPPS proposes the development of a health-based Air Pollution Index as opposed to an Air Quality Index. The basic concept of this index is that of using a combination of modelled pollutant concentrations and exposure-response functions. The initial modelling output would be pollutant-specific numerical values indicating the degree of pollution in an area of the modelled domain. Normalising these values with exposure-response functions will result in normalised bands corresponding to a scale (for example, a scale of 1 to 10) and colour coding system that reflects the possible health impacts. Advice and information on possible health effects associated with each value on the scale would reflect information applicable to both the 'normal healthy' population and 'sensitive' groups within the exposed population (such as asthmatics, the aged or the very young). The index will be modified where possible to account for known additive and/or synergistic effects.

MKK3 Mitogen-Activated Protein Kinase Pathway Mediates Carbon Monoxide-Induced Protection Against Oxidant-Induced Lung Injury

The stress-inducible gene heme oxygenase (HO-1) has previously been shown to provide cytoprotection against oxidative stress. The mechanism(s) by which HO-1 provides this cytoprotection is poorly understood. We demonstrate here that carbon monoxide (CO), a byproduct released during the degradation of heme by HO, plays a major role in mediating the cytoprotection against oxidant-induced lung injury. We show in vitro that CO protects cultured epithelial cells from hyperoxic damage. By using dominant negative mutants and mice deficient in the genes for the various MAP kinases, we demonstrate that the cytoprotective effects of CO are mediated by selective activation of the MKK3/p38 beta protein MAP kinase pathway. In vivo, our experiments demonstrate that CO at a low concentration protects the lungs, extends the survival of the animals, and exerts potent anti-inflammatory effects with reduced inflammatory cell influx into the lungs and marked attenuation in the expression of pro-inflammatory cytokines.

Mild carbon monoxide exposure and auditory function in the developing rat

We have examined the influence of chronic mild exposure to carbon monoxide (CO) on cognitive (learning) and auditory function in the developing rat. We have demonstrated that the auditory pathway is compromised at exposures less than 50 ppm, whereas learning was not influenced at 100 ppm. Artificially reared rat pups were exposed to CO during the brain growth spurt and onset of myelination. Spatial learning was assessed using the Morris Water Maze and three tests of auditory function: (1) auditory brainstem conduction times; (2) the amplitude of the eighth nerve's action potential; and (3) otoacoustic emissions carried out on rat pups (age 22- 24 days). The pups were gastrostomy-reared on a rat milk substitute and chronically exposed to CO at discrete concentrations in the range of 12-100 ppm from 6 days of age to post-weaning at 21-23 days of age. We found no difference in auditory brainstem conduction times at all CO concentrations in comparison to non-exposed controls. There was a difference in otoacoustic emissions for test and controls at CO concentrations of 50 ppm but not at lower concentrations. There was a consistent attenuation of the amplitude of the eighth nerve's action potential, even at the lowest CO exposure examined. The attenuation of the amplitude of the action potential of the eighth nerve at 50 ppm carbon monoxide exposure did not completely recover by 73 days of age. We conclude that prolonged mild exposure to carbon monoxide during development causes measurable functional changes at the level of the eighth cranial nerve.

Hypothermia attenuates delayed cortical cell death and ROS generation following CO inhalation

Carbon monoxide (CO) is the most popular cause of poisoning. The bilateral basal ganglia lesion characterizes the delayed neuronal cell death (DCD). We demonstrated there were both apoptosis and necrosis in the cortex, basal ganglia and hippocampus in a case of human CO accident. To elucidate the mechanism of DCD after CO inhalation, histological studies on the rat brain were conducted. Rats were ventilated with nitrous oxide (sham group), 10% O 2 (hypoxia group) or 1005 ppm CO (CO group) for 90 min, while the pericranial temperature was controlled at either 32, 37, or 39 °C during CO inhalation. After reoxygenation for 30 min, the rats were allowed to recover for 48 h. The ratio of eosinophilic and HNE-positive neurons in the cortex were higher in the CO group than in the hypoxia group at 37 °C, while the PaO 2 was much lower in the hypoxia than in the CO group. The damage was alleviated in the hypothermia (32 °C) as compared with normothermia, while the hyperthermia (39 °C) did not significantly increased it. CO inhalation injures neuron by reactive oxygen species (ROS), independent of hypoxia, as can be concluded from the histological comparison of DCD with HNE immunoreactivity.

Low-dose carbon monoxide reduces airway hyperresponsiveness in mice.

Carbon monoxide (CO) in expired gas has been shown to be elevated with asthma; however, its function is not known, and there is some potential that it may serve a bronchoprotective role to decrease airway hyperresponsiveness (AHR). Thus the ability of CO to reverse methacholine (MCh)-induced bronchoconstriction was evaluated in C57BL/6 (C57) and A/J mice with and without airway inflammation produced by ovalbumin (OVA). Acutely administered CO (1% in air, 10 min) reduced MCh-driven increases in lung resistance in OVA-challenged C57 mice by an average of 50% (from 14.5 to 7.1 cmH2O.ml-1.s-1), whereas no effect was observed in naïve C57 mice or OVA-challenged C57 mice inhaling air alone. Acutely inhaled CO (500 ppm = 0.05%, for 10 min) reduced MCh-induced airway reactivity (AR) by 20-60% in airway hyperresponsive naïve A/J mice, whereas repeated 10-min administrations of 500 ppm CO over a 5-day period decreased AR by 50%. Repeated administration of low-dose CO [250 (0.025%) and (0.05%) 500 ppm, 1 h/day, 5 days] to A/J mice with airway inflammation likewise resulted in a drop of AR by 50%, compared with those not receiving CO. Inhibition of guanylyl cyclase/guanosine 3',5'-cyclic monophosphothioate (cGMP) using 1H-[1,2,4] oxydiazolo[4,3-a]quinoxalin-1-one or a competitive inhibitor, Rp diastereomers of 8-bromo-cGMP, resulted in inhibition of the effect of CO on AHR, suggesting that the effects of CO were mediated through this mechanism. These results indicate that low-dose CO can effectively reverse AHR in the presence and absence of airway inflammation in mice and suggest a potential role for CO in the modulation of AHR.

A highly sensitive self heated SnO 2 carbon monoxide sensor

SnO 2 thin films were deposited on Pyrex substrates by chemical vapor deposition (CVD) using diluted SnCl 4 solution as precursor. The application of sensing film itself as heater by passing ac voltage through it is proposed to enhance the sensitivity of the SnO 2 gas sensor. Such a self heated sensor has a heating efficiency of about 87 °C/W. A comparative study showed that SnO 2 gas sensors operated with different techniques present different sensitivities to carbon monoxide. The self heated SnO 2 gas sensor exhibits an excellent characteristic change with a sensitivity value as high as 37% in response to 1000 ppm carbon monoxide, which is one order of magnitude higher than that of the SnO 2 sensor operated by an external heater formed underneath the substrate. We explain the excellent sensitivity of the SnO 2 gas sensor operated by ac voltage in terms of a simple grain dispersion model taking into account the highly porous architecture of the sensing film, which increases adsorption centers. Scanning electron microscopy (SEM) shows a highly porous structure of the SnO 2 gas sensor operated by ac voltage. Further, X-ray diffraction (XRD) was used to investigate the changes in crytallographic structures of the sensing films. It was observed that structure of the sensing film changes dramaticaly as we used ac voltage to heat the sample.

Characterization of suppression of nitric oxide production by carbon monoxide poisoning in the striatum of free-moving rats, as determined by in vivo brain microdialysis

We examined the effect of carbon monoxide (CO) poisoning on the nitric oxide (NO) system in the striatum of free-moving rats by means of in vivo brain microdialysis. The extracellular levels of the oxidative NO products, nitrite (NO 2 −) and nitrate (NO 3 −), decreased during exposure to CO at 3000 ppm for 40 min, a condition which causes CO poisoning. The extracellular levels of citrulline (Cit; a by-product of NO production) and arginine (Arg; an NO precursor) also decreased during CO exposure. Following reoxygenation by withdrawal of CO, the NO 2 − and NO 3 − levels gradually recovered to the control values, though Arg and Cit remained at lower levels, except for a rapid, but transient, recovery shortly before and after reoxygenation, respectively. Simultaneous application of exogenous l-Arg (50 and 100 mM) with CO exposure attenuated the decreases in NO 2 − and NO 3 − during the CO exposure and accelerated their recovery following reoxygenation. However, d-Arg (100 mM) had no effect on the decrease in NO 2 − and NO 3 −, except for slight and transient attenuation shortly after reoxygenation. Exogenous l-Cit (10 and 100 mM) failed to attenuate the CO-induced decrease in NO 2 − and NO 3 − levels. The decrease in the NO 2 − and NO 3 − levels during 8% O 2 exposure for 40 min, which was comparable with that in response to 3000 ppm CO, was resistant to exogenous 100 mM l-Arg, but the recovery of the NO 2 − and NO 3 − levels following reoxygenation was strongly accelerated. These findings suggest that CO poisoning suppresses NO production in rat striatum in vivo though a mechanism which may not be common with that in hypoxic hypoxia.

Gas-sensing properties of indium-doped SnO 2 thin films with variations in indium concentration

The dependence of sensitivity of SnO 2 gas sensors on indium concentration has been studied. Undoped and indium-doped SnO 2 gas sensors have been prepared by chemical vapor deposition (CVD) using SnCl 4 as precursor solution without or with InCl 3 as doping solution, respectively. The response of the sensors is observed to increase significantly with 20 wt.% InCl 3 content towards 1000 ppm hydrogen, methanol, and carbon monoxide. Indium-doped SnO 2 gas sensors with sensitivity as high as 17%, four times higher than that of undoped sensor, are obtained for 1000 ppm methanol. Above an amount of 20 wt.% InCl 3, the sensitivity of the sensors decreases drastically. A concentration of 40 wt.% InCl 3 decreases the response of the sensors down to the sensitivity value of the undoped sensor. Scanning electron microscopy (SEM) was used to investigate the morphology and pore structure of the undoped and indium-doped sensing films with variations in indium concentration. Further, the sensing films were characterized by X-ray diffraction (XRD) to identify the changes in their crystallographic structures. The relation between structure of the films and gas sensitivity is discussed. It is observed that structure of the sensors changes as the doping concentration increases.

Making sense out of sulfated tin dioxide mesostructures

An in-depth investigation into the synthesis, characterization and sensor response of mesoporous SnO2 materials formed utilizing tin(IV) chloride, sodium dodecylsulfonate, and urea is described. The structures have been stabilized towards calcination by increasing the condensation of the tin oxide network utilizing urea as a slow-release base. PXRD, FT-Raman, N2 gas adsorption, thermal gravimetric analysis, and pyrolysis mass spectroscopy were used to monitor the two-step surfactant decomposition in which a sulfated tin oxide surface is formed followed by removal of the sulfate groups at elevated calcination temperatures. In situ a.c. impedance measurements of the materials in dry air and 2000 ppm carbon monoxide showed that the sensitivity of these materials towards carbon monoxide was inhibited by the presence of sulfate groups on the surface, whereas after the sulfate groups were removed the materials became much more sensitive towards carbon monoxide. These materials could find promising applications as gas-selective chemical sensors, super-acid catalysts, and anode materials for lithium battery applications.

CARDIAC MORPHOLOGY AND FUNCTION FOLLOWING LONG-TERM EXPOSURE TO CARBON MONOXIDE AT HIGH ALTITUDE IN RATS

Although chronic exposure to high altitude or carbon monoxide (CO) induces several cardiovascular adaptations in mammals, very little information is available on the cardiovascular effects due to exposure to these concomitant stresses. In particular, cardiac functional responses to chronic CO inhalation at high altitude has never been investigated. Thirty-two male Dark Agouti rats were exposed for 10 wk in steel chambers to (1) normoxic conditions (N rats), (2) 4000 m simulated high altitude (chronic hypobaric hypoxia, CH rats), (3) 50 ppm CO (CO rats), or (4) 50 ppm CO at 4000 m simulated high altitude (CH + CO rats). Left ventricular (LV) morphology and function were evaluated in normoxic conditions (1) using transthoracic Doppler echocardiography, just before as well as after exposure to environments, and (2) using transparietal intraventricular catheterisms following a short ventilatory-controlled thoracotomy (10 ml/kg volume inflow, pO2 ~159 torr) after exposure. Right ventricular (RV) function was evaluated using the same catheterism process after exposure. Body weight increased in all groups during exposure, but to a lesser extent in CH and CH + CO than in N and CO rats. At the end of exposure, hematocrit ratio was higher in CH than in CO rats, and in CH + CO than in CH rats. Carboxyhemoglobin levels were higher in CH + CO than in CO, CH, or N rats. Although neither a simulated high altitude nor CO alone had an effect on LV morphology and function, combined environments increased LV + septum weight, interventricular and posterior wall thicknesses, relative wall thickness, and LV systolic function. LV diastolic function was not altered by environmental conditions in the four groups. CO intensified the altitude-induced RV hypertrophy as well as the altitude-induced decrease in RV diastolic function. RV systolic function increased in CH rats, but adding CO did not amplify this adaptation process. Moreover, significant polynomial relationships were obtained between hematocrit ratio and LV + septum weight or left ventricular systolic pressure. Our results indicate that CO at high altitude induced severe hematological responses that could be involved in morphological and functional cardiac adaptations of both ventricles. Data indicate that CO at high altitude may be more detrimental to cardiac function than CO inhaled at sea level.

Determination of carbon monoxide in ambient air using piezoelectric crystal sorption detection

A new piezoelectric quartz crystal (PQC) sorption detector was developed to monitor carbon monoxide (CO) at sub-ppm level in ambient air. Out of the 28 coating materials studied, the palladium(II) acetamide complex with a 1:10 mole ratio of Pd(II) to acetamide was found to be the best. The detection is based on a non-reversible gas/coating interaction with sensitivity depending on gas flowrate. For 5–15 min exposure at a flowrate of 50 ml/min, the working ranges were found to vary from 0.7 to 40 ppm (total exposure from 8 to 160 μg CO) and detection limits (S/N=2) from 0.7 to 2 ppm CO (total exposure to 8 μg CO). The repeatability at 10 ppm CO was 11.8% (R.S.D. for n=3). The sensor lifetime was found dependent on exposure up to 160 μg CO or not exceeding 1000 Hz accumulative shift of frequency to avoid saturation of active sites at the crystal surface. No interference to CO detection was found for H 2, H 2S, SO 2, NO 2, CO 2, HCHO, gasoline and water vapors at concentrations much higher than ambient air. Compared to existing CO monitor, the PQC detector developed has advantages of adequate selectivity, high sensitivity, fast response and a much lower detection limit for detecting CO at sub-ppm levels. However, it is limited by the total exposure to a maximum of 160 μg CO that restricts its application to intermittent monitoring of low CO concentration. The present work has demonstrated the advantages of using strong non-reversible interaction to enhance PQC sensitivity, as the total exposure can be adjusted easily by a suitable control of the gas flowrate.

Concomitant clozapine reduces smoking in patients treated with risperidone

This pilot study examines the smoking behaviors of patients treated with either risperidone alone or in combination with clozapine. Smoking behavior was evaluated using expired carbon monoxide (CO) measurements, the Fagerstrom Test for Nicotine Dependence (FTND), and a semi-structured interview. Our results indicate that patients co-prescribed clozapine with risperidone smoke significantly less than patients treated with risperidone alone (19.1±9.3 vs. 37.8±19.1 ppm CO, respectively, P=0.03). These data are consistent with previous studies showing that clozapine treatment is associated with significantly reduced smoking behavior relative to other antipsychotic agents.

An integrated gas sensor technology using surface micro-machining

We report the first silicon based integrated gas sensor technology using surface micro-machined micro-hotplate (MHP). In this work, the thermally isolated hotplate was fabricated using surface silicon micro-machining technique. Various etching window designs for the polysilicon sacrificial etch were also explored to optimize the surface micro-machining process yield. The front-side surface micro-machined MHP provide excellent manufacturing yield compared to the bulk micro-machined counterpart and at the same time retains all the desirable thermal characteristics that are essential to the integrated gas sensor application. Integrated gas sensors with sensitivity down to 1 ppm of carbon monoxide were demonstrated using this technology. This approach has been extended to integrated gas sensor array.

MECHANISMS UNDERLYING THE CORONARY VASODILATION IN THE ISOLATED PERFUSED HEARTS OF RATS SUBMITTED TO ONE WEEK OF HIGH CARBON MONOXIDE EXPOSURE IN VIVO

We examined the possible mechanisms for carbon monoxide (CO)-induced effects in hearts isolated from Wistar rats exposed for 1 wk to 530 ppm CO. They were treated by daily intraperitoneal injections of either methylene blue (10 mg/kg), glibenclamide (3 mg/kg), or apamin (125 nmol/kg), known to inhibit vasodilatory mechanisms. Hearts were excised, cannulated, and retrogradely perfused through the coronary artery, using the Langendorff method with a constant perfusion pressure. After stabilization, we investigated the degree of resistance to an in vitro transient global low-flow ischemia. Oneweek CO exposure induced a significant increase in hematocrit and a cardiomegaly, which were not affected by any of these drugs. An enhancement of coronary flow was observed concomitantly with a decrease in ischemic contracture after CO exposure. However, no improvement of contractile recovery was noted. Since methylene blue did not interact with the CO effects, a cGMP signaling pathway can be excluded. On the contrary, as glibenclamide and to a greater extend apamin blocked the vasodilatory effects of CO, we conclude that K + channels may be involved in these CO effects.