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At least 793 records · Page 44Linked to original sources
PubMed1999

Dual actions of volatile anesthetics on GABA(A) IPSCs: dissociation of blocking and prolonging effects.

BACKGROUND: Volatile agents alter inhibitory postsynaptic currents (IPSCs) at clinically relevant concentrations, an action that is thought to make an important contribution to their behavioral effects. The authors investigated the mechanisms underlying these effects by evaluating the concentration dependence of modulation by enflurane, isoflurane, and halothane of IPSCs in rat hippocampal slices. METHODS: Action potential-independent gamma-aminobutyric acid(A) IPSCs (miniature IPSCs [mIPSCs]) were recorded from CA1 pyramidal neurons. The effects on mIPSC amplitude were used to distinguish between presynaptic (altered release) and postsynaptic (altered receptor response) actions of volatile agents. The concentration dependence of blocking and prolonging actions was compared among the volatile agents to determine whether a single modulatory process could account for both effects. RESULTS: The application of volatile anesthetics prolonged the decay and reduced the amplitude of mIPSCs in a dose-dependent manner. The effects on decay time for isoflurane and enflurane could not be distinguished. However, the blocking effect of enflurane was significantly greater than that of isoflurane at all concentrations. Despite the blocking effect, the net action of these agents was enhanced inhibition, because charge transfer was always significantly greater than control. Isoflurane, and to a lesser extent enflurane and halothane, caused a picrotoxin-sensitive increase in baseline noise. Moderate increases in mIPSC frequency were also observed for all agents. CONCLUSIONS: These results show that enflurane, isoflurane, and halothane reduce IPSC amplitude through a direct postsynaptic action. Furthermore, the concentration dependence of the actions of the agents reveals a dissociation between the effects on the amplitude and the time course of IPSCs, suggesting that distinct mechanisms underlie the two actions.

Algorithms↗
PubMed1999

Effects of temperature and volatile anesthetics on GABA(A) receptors.

BACKGROUND: Potentiation of the activity of the gamma-aminobutyric acid type A (GABA(A)) receptor channel by volatile anesthetic agents is usually studied in vitro at room temperature. Systematic variation of temperature can be used to assess the relevance of this receptor to general anesthesia and to characterize the modulation of its behavior by volatile agents at normal body temperature. METHODS: Potentiation of the GABA(A) receptor by halothane, sevoflurane, isoflurane, and methoxyflurane was studied at six temperatures in the range 10-37 degrees C using the whole-cell patch-clamp technique and mouse fibroblast cells stably transfected with defined GABA(A) receptor subunits. RESULTS: Control GABA concentration-response plots showed small and physically reasonable changes in the GABA concentration required for a half-maximal effect, the Hill coefficient, and maximal response over the range 10-30 degrees C. Potentiations of GABA (1 microM) responses by aqueous minimum alveolar concentrations of the volatile anesthetic agents decreased with increasing temperature from 10-37 degrees C in an agent-specific manner (methoxyflurane > isoflurane > sevoflurane > halothane) but tended to equalize at normal body temperature (37 degrees C). These findings are in line with published results on the temperature dependence of anesthetic potencies in animals. CONCLUSIONS: These results are consistent with direct binding of volatile anesthetic agents to the GABA(A) receptor channel playing an important role in general anesthesia. The finding that the degree of anesthetic potentiation was agent-specific at low temperatures but not at 37 degrees C emphasizes the importance of doing in vitro experiments at normal body temperature.

Anesthetics, Inhalation↗
PubMed1999

GAS-1: a mitochondrial protein controls sensitivity to volatile anesthetics in the nematode Caenorhabditis elegans.

BACKGROUND: Mutations in several genes of Caenorhabditis elegans confer altered sensitivities to volatile anesthetics. A mutation in one gene, gas-1(fc21), causes animals to be immobilized at lower concentrations of all volatile anesthetics than in the wild-type, and it does not depend on mutations in other genes to control anesthetic sensitivity. gas-1 confers different sensitivities to stereoisomers of isoflurane, and thus may be a direct target for volatile anesthetics. The authors have cloned and characterized the gas-1 gene and the mutant allele fc21. METHODS: Genetic techniques for nematodes were as previously described. Polymerase chain reaction, sequencing, and other molecular biology techniques were performed by standard methods. Mutant rescue was done by injecting DNA fragments into the gonad of mutant animals and scoring the offspring for loss of the mutant phenotype. RESULTS: The gas-1 gene was cloned and identified. The protein GAS-1 is a homologue of the 49-kDa (IP) subunit of the mitochondrial NADH:ubiquinone-oxidoreductase (complex I of the respiratory chain). gas-1(fc21) is a missense mutation replacing a strictly conserved arginine with lysine. CONCLUSIONS: The function of the 49-kDa (IP) subunit of complex I is unknown. The finding that mutations in complex I increase sensitivity of C elegans to volatile anesthetics may implicate this physiologic process in the determination of anesthetic sensitivity. The hypersensitivity of animals with a mutation in the gas-1 gene may be caused by a direct anesthetic effect on a mitochondrial protein or secondary effects at other sites caused by mitochondrial dysfunction.

Amino Acid Sequence↗
PubMed2000

Volatile anesthetics activate the human tandem pore domain baseline K+ channel KCNK5.

BACKGROUND: Previous studies have identified a volatile anesthetic-induced increase in baseline potassium permeability and concomitant neuronal inhibition. The emerging family of tandem pore domain potassium channels seems to function as baseline potassium channels in vivo. Therefore, we studied the effects of clinically used volatile anesthetics on a recently described member of this family. METHODS: A cDNA clone containing the coding sequence of KCNK5 was isolated from a human brain library. Expression of KCNK5 in the central nervous system was determined by Northern blot analysis and reverse-transcription polymerase chain reaction. Functional expression of the channel was achieved by injection of cRNA into Xenopus laevis oocytes. RESULTS: Expression of KCNK5 was detected in cerebral cortex, medulla, and spinal cord. When heterologously expressed in Xenopus oocytes, KCNK5 currents exhibited delayed activation, outward rectification, proton sensitivity, and modulation by protein kinase C. Clinical concentrations of volatile general anesthetics potentiated KCNK5 currents by 8-30%. CONCLUSION: Human KCNK5 is a tandem pore domain potassium channel exhibiting delayed activation and sensitivity to volatile anesthetics and may therefore have a role in suppressing cellular excitability during general anesthesia.

Anesthetics, Inhalation↗
PubMed2000

Norepinephrine-induced apoptosis is inhibited in adult rat ventricular myocytes exposed to volatile anesthetics.

BACKGROUND: Volatile anesthetics are used to provide anesthesia to patients with heart disease under heightened adrenergic drive. The purpose of this study was to test whether volatile anesthetics can inhibit norepinephrine (NE)-induced apoptosis in cardiomyocytes. METHODS: Rat ventricular cardiomyocytes were exposed to NE (10 microm) alone or in the presence of increasing concentrations of isoflurane and halothane. RESULTS: Isoflurane at 1.6 minimum alveolar concentration (MAC) (4 +/- 2% [SD]) and halothane at 1.2 MAC (3 +/- 2%) abolished the percentage of cardiomyocytes undergoing NE-induced apoptosis (34 +/- 8%), as assessed by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) (P < 0.0001). Lower concentrations of isoflurane and halothane markedly decreased the number of TUNEL-positive cells. Similarly, isoflurane at 1.6 MAC (5 +/- 3%) and halothane at 1.2 MAC (6 +/- 3%) prevented the increase in annexinV-staining cardiomyocytes (38 +/- 7%; P < 0. 0001). These findings were corroborated with a decreased quantity of NE-induced DNA laddering by volatile anesthetics. Halothane at 1.2 MAC abolished the increase in TUNEL-positive cardiomyocytes exposed to the dihydropyridine Ca2+-channel agonist BAY K-8644 (1 microm) (BAY K-8644 + halothane: 3 +/- 2% vsBAY K-8644: 34 +/- 6%; P < 0. 0001) and the Ca2+-ionophore 4-bromo-A23187 (1 microm) (4-bromo-A23187 + halothane: 2 +/- 2% vs4-bromo-A23187: 13 +/- 4%; P = 0.03). NE treatment increased caspase-9 activity to 197 +/- 62% over control myocytes (P < 0.0001), whereas no caspase-8 activation was detectable. This increase in caspase-9 activity was blocked by isoflurane at 1.6 MAC and halothane at 1.2 MAC. CONCLUSIONS: Volatile anesthetics offer significant protection against beta-adrenergic apoptotic death signaling in ventricular cardiomyocytes. The authors present evidence that this protection is mainly mediated through modulation of cellular Ca2+ homeostasis and inhibition of the apoptosis initiator caspase-9.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2001

Interaction of volatile anesthetics with human Kv channels in relation to clinical concentrations.

BACKGROUND: Recent evidence shows that inhibition of human Kv3 channels by intravenous anesthetics occurs at clinical concentrations. The effects of volatile anesthetics on these human ion channels are unknown. This study was designed to establish whether minimum alveolar concentrations (MAC) of halothane, enflurane, isoflurane, and desflurane exhibit effects on Kv3 channeLs. To obtain an indication whether these findings may be specific to Kv3 channels, the effects of enflurane and isoflurane on human Kv1.1 channels were also investigated. METHODS: Kv3 channels natively expressed in SH-SY5Y cells and Kv1.1 channels expressed in HEK293 cells were measured with the whole cell patch clamp technique by standard protocols. Concentrations of volatile anesthetics were determined by gas chromatography. RESULTS: Halothane, enflurane, isoflurane, and desflurane reversibly inhibited Kv3 channels in a concentration-dependent manner. Concentrations at half-maximal effect (IC50 values) ranged between 1,800 and 4,600 microM. Hill coefficients were between 1.7 and 2.5. IC50 values for inhibition of Kv1.1 channels were 2,800 and 5,200 microM, and Hill coefficients were 3.9 and 5.6 for enflurane and isoflurane, respectively. CONCLUSION: Volatile anesthetics inhibit human Kv3 channels at clinical concentrations. At 1-3 MAC, inhibition would account on average for 2-12%. Inhibition would be highest with enflurane (between 3% and 22%) and lowest with isoflurane (between 0.2% and 3%). Kv1.1 channels would only be inhibited by enflurane at clinical concentrations (2% at 2 MAC and 8% at 3 MAC). Whether the degree of K channel inhibition by volatile anesthetics may contribute to their clinical action needs further study.

Anesthetics, Inhalation↗
PubMedDate not supplied

Volatile sulfur compounds produced by Helicobacter pylori.

GOALS: To assess the volatile sulfur compounds produced by three strains of Helicobacter pylori in broth cultures mixed with sulfur-containing amino acids. BACKGROUND: Halitosis has been reported in H. pylori-positive patients, and volatile sulfur compounds such as hydrogen sulfide and methyl mercaptan are known to be responsible for inducing oral malodor. Whether H. pylori produces these volatile sulfur compounds has yet to be established. STUDY: Three strains of H. pylori (ATCC 43504, SS 1, DSM 4867) were cultured with 5 mM cysteine and methionine. After 72 hours of incubation, the headspace air was aspirated and injected directly into a gas chromatograph. The concentrations of hydrogen sulfide and methyl mercaptan were analyzed and compared between experimental and control cultures RESULTS: In broth containing 5 mM cysteine, hydrogen sulfide was increased by ATCC 43504 (P < 0.01) and SS 1 (P < 0.05), while methyl mercaptan was elevated only by SS 1 (P < 0.05). In broth containing 5 mM methionine, methyl mercaptan increases were significant for SS 1 (P < 0.05) and DSM 4867 (P < 0.05). In broth containing 5 mM cysteine and 5 mM methionine, the concentration of hydrogen sulfide was higher than in controls for all three strains (P < 0.01); that of methyl mercaptan was higher only for SS 1 (P < 0.01). Cysteine addition to cultures containing methionine increased hydrogen sulfide and methyl mercaptan for ATCC 43504 (P < 0.05) and SS 1 (P < 0.05). Conversely, addition of methionine to cultures containing cysteine increased methyl mercaptan only for DSM 4867 (P < 0.01). CONCLUSIONS: The production of volatile sulfur compounds by H. pylori is not only very complicated but also strain-specific. Nevertheless, H. pylori was shown to produce hydrogen sulfide and methyl mercaptan, which suggests that this microorganism can contribute to the development of halitosis.

Chromatography, Gas↗
PubMed2006

Cardioprotection by volatile anesthetics: new applications for old drugs?

PURPOSE OF REVIEW: Pharmacological interventions may play a prominent role in reducing organ damage in response to physiologic stress. A growing body of evidence indicates that volatile anesthetics exert protective effects against ischemia-reperfusion injury in vivo. Administration of volatile anesthetics before prolonged coronary artery occlusion and reperfusion has been shown to produce cardioprotection, a phenomenon termed anesthetic-induced preconditioning. Endogenous signal transduction proteins, reactive oxygen species, mitochondria, and ion channels have been implicated in anesthetic-induced preconditioning, and new data regarding the triggering and effector roles for these various components have been discovered that advance our understanding of the mechanisms responsible for anesthetic-induced preconditioning. This review will update and integrate these recent data into the current mechanistic model of anesthetic-induced preconditioning. RECENT FINDINGS: Despite a wealth of data from animal studies, the mechanism by which preconditioning with volatile anesthetics alleviates ischemic injury remains incompletely understood. Recent data have identified important interactions between reactive oxygen species and key intracellular signal transduction enzymes and proteins implicated in anesthetic-induced preconditioning. SUMMARY: This review highlights the major recent findings examining mechanisms of volatile anesthetic cardioprotection.

Anesthetics, Inhalation↗
PubMed2005

Volatility: a new vital sign identified using a novel bedside monitoring strategy.

BACKGROUND: SIMON (Signal Interpretation and Monitoring) monitors and archives continuous physiologic data in the ICU (HR, BP, CPP, ICP, CI, EDVI, SVO2, SPO2, SVRI, PAP, and CVP). We hypothesized: heart rate (HR) volatility predicts outcome better than measures of central tendency (mean and median). METHODS: More than 600 million physiologic data points were archived from 923 patients over 2 years in a level one trauma center. Data were collected every 1 to 4 seconds, stored in a MS-SQL 7.0 relational database, linked to TRACS, and de-identified. Age, gender, race, Injury Severity Score (ISS), and HR statistics were analyzed with respect to outcome (death and ventilator days) using logistic and Poisson regression. RESULTS: We analyzed 85 million HR data points, which represent more than 71,000 hours of continuous data capture. Mean HR varied by age, gender and ISS, but did not correlate with death or ventilator days. Measures of volatility (SD, % HR >120) correlated with death and prolonged ventilation. CONCLUSIONS: 1) Volatility predicts death better than measures of central tendency. 2) Volatility is a new vital sign that we will apply to other physiologic parameters, and that can only be fully explored using techniques of dense data capture like SIMON. 3) Densely sampled aggregated physiologic data may identify sub-groups of patients requiring new treatment strategies.

Adult↗
PubMed2003

Nonlinear volatility of river flux fluctuations.

We study the spectral properties of the magnitudes of daily river flux increments, the volatility. The volatility series exhibits (i) strong seasonal periodicity and (ii) power-law correlations for time scales less than 1 yr. We test the nonlinear properties of the river flux increment series by randomizing its Fourier phases and find that the surrogate volatility series (i) has almost no seasonal periodicity and (ii) is weakly correlated for time scales less than 1 yr. We quantify the degree of nonlinearity by measuring (i) the amplitude of the power spectrum at the seasonal peak and (ii) the correlation power-law exponent of the volatility series.

Journal Article↗
PubMed1993

Prevalence of volatile solvent inhalation among junior high school students in Japan and background life style of users.

In order to estimate the prevalence of volatile solvent inhalation among junior high school students in Japan and to assess certain characteristics of the lifestyle of these users, the authors surveyed 5240 students 12-15 years of age. This was the first major survey of the prevalence of volatile solvent inhalation among junior high school students in Japan, from the point of view of the number of subjects and schools. 1.5% of subjects were students who had inhaled solvents. The regularity of life style rhythm was more significantly disturbed in Lifetime Users than in Non-Users. School life and family life were significantly less relaxed for Lifetime Users than for Non-Users. Drinking alcohol and smoking had a strong relationship with inhaling volatile solvents. The authors suggest that greatly increasing education on the harmful effects of volatile solvents inhalation and increasing the frequency with which the entire family eats dinner together will be an effective prevention strategy in Japan.

Adolescent↗
PubMed2005

Health risks and occupational exposure to volatile anaesthetics--a review with a systematic approach.

AIMS AND OBJECTIVES: To provide practicing nurse anaesthetists with evidence based knowledge as to whether they are at risk handling volatile anaesthetics by answering the question: What are the health risks threatening health care personnel occupationally exposed to volatile anaesthetics? BACKGROUND: The interpretations of results from specific scientific studies vary and preliminary research results indicate that occupational exposure to volatile anaesthetics affects the health of operating room personnel. DESIGN: Review of scientific literature with a systematic approach. METHOD: The review included a systematic search in three major databases, a screening process of abstracts/articles followed by a quality assessment of the included studies. The screening process and the quality assessment were done independently by the six reviewers and followed specific protocols. RESULTS: A systematic search of The Cochrane Library, MedLine and CINAHL resulted in a screening of 413 abstracts of which 31 articles were assessed for quality, all done independently by the reviewers. Finally, the reviewers agreed upon how to interpret the results of the assessed articles. CONCLUSIONS: The 31 articles assessed covered areas such as genotoxic effects, neurobehavioural effects, immunology, and general health effects. In the scientific literature reviewed there is no evidence of occupational exposure to volatile anaesthetics either being associated with health risks or being harmless. Studies indicating a potential health risk are all investigating circumstances ignorant of modern environmental regulations and/or with no scavenging equipment. RELEVANCE TO CLINICAL PRACTICE: Although no answer has been given, this review illuminates the methodological difficulties encountered in designing studies. The result of this review further stresses the need for scientific knowledge in this area and enhances the extensive use of scavenging equipment.

Anesthetics, Inhalation↗
PubMed2004

The tomato carotenoid cleavage dioxygenase 1 genes contribute to the formation of the flavor volatiles beta-ionone, pseudoionone, and geranylacetone.

Volatile terpenoid compounds, potentially derived from carotenoids, are important components of flavor and aroma in many fruits, vegetables and ornamentals. Despite their importance, little is known about the enzymes that generate these volatiles. The tomato genome contains two closely related genes potentially encoding carotenoid cleavage dioxygenases, LeCCD1A and LeCCD1B. A quantitative reverse transcriptase-polymerase chain reaction analysis revealed that one of these two genes, LeCCD1B, is highly expressed in ripening fruit (4 days post-breaker), where it constitutes 0.11% of total RNA. Unlike the related neoxanthin cleavage dioxygenases, import assays using pea chloroplasts showed that the LeCCD1 proteins are not plastid-localized. The biochemical functions of the LeCCD1 proteins were determined by bacterial expression and in vitro assays, where it was shown that they symmetrically cleave multiple carotenoid substrates at the 9,10 (9',10') positions to produce a C14 dialdehyde and two C13 cyclohexones that vary depending on the substrate. The potential roles of the LeCCD1 genes in vivo were assessed in transgenic tomato plants constitutively expressing the LeCCD1B gene in reverse orientation. This over-expression of the antisense transcript led to 87-93% reductions in mRNA levels of both LeCCD1A and LeCCD1B in the leaves and fruits of selected lines. Transgenic plants exhibited no obvious morphological alterations. High-performance liquid chromatography analysis showed no significant modification in the carotenoid content of fruit tissue. However, volatile analysis showed a > or =50% decrease in beta-ionone (a beta-carotene-derived C13 cyclohexone) and a > or =60% decrease in geranylacetone (a C13 acyclic product likely derived from a lycopene precursor) in selected lines, implicating the LeCCD1 genes in the formation of these important flavor volatiles in vivo.

Chloroplasts↗
PubMed1994

Forces applied during laryngoscopy in children. Are volatile anaesthetics essential for suxamethonium induced muscle rigidity?

Increased masticatory muscle tone after administration of suxamethonium has been demonstrated in children when combined with volatile anaesthetics. Whether volatiles are a prerequisite for this phenomenon is not known. In this study upper airway muscle tone, including the tone of the masticatory muscles, was determined in 54 children (age range 2-15 years), anaesthetized with propofol, fentanyl and nitrous oxide and avoiding any use of volatiles. The children were either relaxed with suxamethonium (n = 26) or vecuronium (n = 28). The forces applied during laryngoscopy were used to quantify upper airway muscle tone and were significantly greater in the suxamethonium group than in the vecuronium group: maximally applied force was 25 N versus 21 N (P = 0.008), and mean applied force was 16 N versus 13 N (P = 0.006), respectively. The results of this study indicate that upper airway muscle tone increases after administration of suxamethonium in children independent of the presence of volatile anaesthetics. Moreover, increased muscle tone had no effect on the difficulty of laryngoscopy or the intubation conditions. Increased masseter muscle rigidity after suxamethonium could be due to the very unique characteristics of this muscle.

Adolescent↗
PubMed1997

Effects of volatile anesthetics on the calcium ionophore A23187-mediated alterations in hepatic flow and metabolism in the perfused liver in fasted rats.

Alterations in intracellular calcium homeostasis have been implicated in heptic injury. Volatile anesthetics modulate the homeostasis of intracellular calcium. The effects of volatile anesthetics on the hemodynamic and metabolic alterations induced by the calcium ionophore A23187 were studied using isolated liver perfusion in fasted rats. The liver was isolated from 24 hr-fasted male Sprague-Dawley rats, and perfused through the portal vein at a constant pressure of 1.2 kPa in a recirculating perfusion-aeration system. Halothane, isoflurane and sevoflurane were administered at 2%, 3% and 4.4%, respectively. All volatile anesthetics maintained basal hepatic flow, reduced oxygen consumption, and transiently enhanced net lactate production. A23187 at initial concentrations of 0.8 to 3.2 microM decreased hepatic flow and oxygen consumption in a dose-dependent manner, and enhanced lactate production. All anesthetics significantly attenuated the decreases in hepatic flow and oxygen consumption after administration of A23187 at 1.6 microM. None of the anesthetics significantly influenced the A23187-induced enhancement of net lactate production. Volatile anesthetics may attenuate the hepatic vasoconstriction and oxygen debt induced by intracellular calcium overload.

Anesthetics, Inhalation↗
PubMed2001

Volatile anaesthetic effects on Na+-Ca2+ exchange in rat cardiac myocytes.

We examined the influence of two clinically relevant concentrations (1 and 2 MAC (minimum alveolar concentration)) of halothane and sevoflurane on both efflux and reverse modes of Na+-Ca2+ exchange (NCX) in enzymatically dissociated adult rat cardiac myocytes. We hypothesised that a volatile anaesthetic-induced decrease in myocardial contractility is mediated by a reduction in intracellular calcium concentration ([Ca2+]i) via inhibition of NCX. Cells were exposed to cyclopiazonic acid and zero extracellular Na+ and Ca2+ to block sacroplasmic reticulum (SR) re-uptake and NCX efflux, respectively. As [Ca2+]i increased under these conditions, extracellular Na+ was rapidly (< 300 ms) reintroduced in the presence or absence of a volatile anaesthetic to selectively promote Ca2+ efflux via NCX. Other cells exposed to cyclopiazonic acid and ryanodine to inhibit SR Ca2+ re-uptake and release were Na+ loaded in zero extracellular Ca2+. The reintroduction of extracellular Ca2+ was used to selectively activate Ca2+ influx via NCX. Compared to controls, both 1 and 2 MAC halothane as well as sevoflurane reduced NCX-mediated efflux. The reduction in NCX-mediated influx was concentration dependent, but comparable between the two anaesthetics. Both anaesthetics at each concentration also shifted the relationship between extracellular Na+ (or extent of Na+ loading) and NCX-mediated efflux (or influx) to the right. These data indicate that despite inhibition of NCX-mediated Ca2+ efflux, volatile anaesthetics produce myocardial depression. However, the inhibition of NCX-mediated Ca2+ influx may contribute to decreased cardiac contractility. The overall effect of volatile anaesthetics on the [Ca2+]i profile is likely to be determined by the relative contributions of influx vs. efflux via NCX during each cardiac cycle.

Anesthetics, Inhalation↗
PubMed1996

A distributed parameter physiologically-based pharmacokinetic model for dermal and inhalation exposure to volatile organic compounds.

Estimates of dermal dose from exposures to toxic chemicals are typically derived using models that assume instantaneous establishment of steady-state dermal mass flux. However, dermal absorption theory indicates that this assumption is invalid for short-term exposures to volatile organic chemicals (VOCs). A generalized distributed parameter physiologically-based pharmacokinetic model (DP-PBPK), which describes unsteady state dermal mass flux via a partial differential equation (Fickian diffusion), has been developed for inhalation and dermal absorption of VOCs. In the present study, the DP-PBPK model has been parameterized for chloroform, and compared with two simpler PBPK models of chloroform. The latter are lumped parameter models, employing ordinary differential equations, that do not account for the dermal absorption time lag associated with the accumulation of permeant chemical in tissue represented by permeability coefficients. All three models were evaluated by comparing simulated post-exposure exhaled breath concentration profiles with measured concentrations following environmental chloroform exposures. The DP-PBPK model predicted a time-lag in the exhaled breath concentration profile, consistent with the experimental data. The DP-PBPK model also predicted significant volatilization of chloroform, for a simulated dermal exposure scenario. The end-exposure dermal dose predicted by the DP-PBPK model is similar to that predicted by the EPA recommended method for short-term exposures, and is significantly greater than the end-exposure dose predicted by the lumped parameter models. However, the net dermal dose predicted by the DP-PBPK model is substantially less than that predicted by the EPA method, due to the post-exposure volatilization predicted by the DP-PBPK model. Moreover, the net dermal dose of chloroform predicted by all three models was nearly the same, even though the lumped parameter models did not predict substantial volatilization.

Absorption↗
PubMed2005

Communicating asset risk: how name recognition and the format of historic volatility information affect risk perception and investment decisions.

An experiment examined how the type and presentation format of information about investment options affected investors' expectations about asset risk, returns, and volatility and how these expectations related to asset choice. Respondents were provided with the names of 16 domestic and foreign investment options, with 10-year historical return information for these options, or with both. Historical returns were presented either as a bar graph of returns per year or as a continuous density distribution. Provision of asset names allowed for the investigation of the mechanisms underlying the home bias in investment choice and other asset familiarity effects. Respondents provided their expectations of future returns, volatility, and expected risk, and indicated the options they would choose to invest in. Expected returns closely resembled historical expected values. Risk and volatility perceptions both varied significantly as a function of the type and format of information, but in different ways. Expected returns and perceived risk, not predicted volatility, predicted portfolio decisions.

Journal Article↗