The Experts below are selected from a list of 306 Experts worldwide ranked by ideXlab platform
Edwin L. Carstensen - One of the best experts on this subject based on the ideXlab platform.
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Ultrasonically induced Lung Hemorrhage in young swine
Ultrasound in medicine & biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, Edwin L. CarstensenAbstract:Ten-day old swine were used in the final step of a study of the age dependence of the threshold for Lung Hemorrhage resulting from exposure to diagnostically relevant levels of pulsed ultrasound. A 2.3-MHz focused transducer (pulse length of 10 microseconds, 100-Hz pulse repetition frequency) was incremented vertically at several sites for a distance of 2 or 2.5 cm over the chest of the subject for a total exposure period of 16 or 20 min. The procedure was repeated at a total of four sites per animal. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.3-MPa peak positive pressure in water and the surface of the animal or, at the surface of the Lung, 0.8-MPa peak positive pressure, 0.8-MPa fundamental pressure, 0.7-MPa maximum negative pressure and 20 Wcm-2 pulse average intensity. These values are essentially the same as those reported previously for neonatal swine, and neonatal, juvenile and adult mice.
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Age dependence of ultrasonically induced Lung Hemorrhage in mice
Ultrasound in medicine & biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, David P. Penney, Edwin L. CarstensenAbstract:Abstract Thresholds for ultrasonically induced Lung Hemorrhage were determined in neonatal mice (24–36 h old), juvenile mice (14 d old) and adult mice (8–10 weeks old) to assess whether or not the threshold for Lung Hemorrhage is dependent upon age. Ultrasonic exposures were at 1.15 MHz with a pulse length of 10 μs, pulse repetition frequency of 100 Hz and a total exposure duration of 3 min. The threshold for Lung Hemorrhage occurred at a peak positive acoustic pressure of approximately 1 MPa for mice in all three age groups. Although the thresholds were similar for neonatal, juvenile and adult mice, the sizes of the suprathreshold Hemorrhages were significantly larger in adult mice than in neonatal or juvenile mice.
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ultrasonically induced Lung Hemorrhage in young swine
Ultrasound in Medicine and Biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, Edwin L. CarstensenAbstract:Abstract Ten-day old swine were used in the final step of a study of the age dependence of the threshold for Lung Hemorrhage resulting from exposure to diagnostically relevant levels of pulsed ultrasound. A 2.3-MHz focused transducer (pulse length of 10 μs, 100-Hz pulse repetition frequency) was incremented vertically at several sites for a distance of 2 or 2.5 cm over the chest of the subject for a total exposure period of 16 or 20 min. The procedure was repeated at a total of four sites per animal. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.3-MPa peak positive pressure in water at the surface of the animal or, at the surface of the Lung, 0.8-MPa peak positive pressure, 0.8-MPa fundamental pressure, 0.7-MPa maximum negative pressure and 20 Wcm−2 pulse average intensity. These values are essentially the same as those reported previously for neonatal swine, and neonatal, juvenile and adult mice.
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Lung Hemorrhage from exposure to ultrasound.
The Journal of the Acoustical Society of America, 1996Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, David P. Penney, Edwin L. CarstensenAbstract:Thresholds for Lung Hemorrhage from exposure to pulsed ultrasound have been determined in neonatal mice (24–36 h), juvenile mice (14 days), and adult mice (8–10 weeks), and neonatal (24–36 h) and young (10 days) swine. The threshold at 2 MHz is approximately 1 MPa and the threshold increases gradually with frequency in the range from 0.1 to 4 MHz. Positive and negative pressure pulses are equally damaging. Following exposure, suprathreshold lesions are not progressive with time and are repaired by usual physiological mechanisms. Although the unique sensitivity of Lung tissue to ultrasound is associated with the presence of air in the alveolae, this does not necessarily implicate acoustic cavitation as the responsible mechanism. Thin sections of murine Lung are more sensitive than thicker regions probably because of reduced reflection at the surface of the Lung tissue.
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THRESHOLDS FOR ULTRASONICALLY INDUCED Lung Hemorrhage IN NEONATAL SWINE
Ultrasound in medicine & biology, 1996Co-Authors: Raymond B. Baggs, Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, David P. Penney, Edwin L. CarstensenAbstract:The threshold for generation of Lung Hemorrhage in adult mice by pulsed ultrasound has been shown to be approximately 1 MPa at the surface of the Lung (10-microseconds pulse and a carrier frequency of 2 MHz). This investigation used neonatal swine to determine if the findings for mice can be generalized to other species. After exploratory observations, the inverse sampling method was used in a primary study (22 animals, 88 exposure sites) to determine the threshold for Lung Hemorrhage in neonatal swine. The primary study was followed by a separate confirmation study (13 animals, 48 exposure sites), testing the conclusions of the first study and comparing damage at subthreshold levels with sham-exposed animals. A separate investigation explored the histological nature of tissue damage at suprathreshold levels. A 2.3-MHz focused transducer (10 microseconds at 100-Hz pulse-repetition frequency) was incremented vertically for a distance of 2 cm over the chest of the subject for a total exposure period of 16 min. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.5 MPa peak positive pressure in water at the surface of the animal or, at the surface of the Lung, 1.1 MPa peak positive pressure, 1 MPa fundamental pressure, 0.9 MPa maximum negative pressure, 25 W cm-2 pulse average intensity or a mechanical index of 0.6. These values are essentially the same as those reported for adult mice.
J F Zachary - One of the best experts on this subject based on the ideXlab platform.
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threshold estimation of ultrasound induced Lung Hemorrhage in adult rabbits and comparison of thresholds in mice rats rabbits and pigs
Ultrasound in Medicine and Biology, 2006Co-Authors: William D Obrien, L A Frizzell, Douglas G. Simpson, James P. Blue, Rita J. Miller, Yan Yang, J F ZacharyAbstract:Abstract The objective of this study was to assess the threshold and superthreshold behavior of ultrasound (US)-induced Lung Hemorrhage in adult rabbits to gain greater understanding about species dependency. A total of 99 76 ± 7.6-d-old 2.4 ± 0.14-kg New Zealand White rabbits were used. Exposure conditions were 5.6-MHz, 10-s exposure duration, 1-kHz PRF and 1.1-μs pulse duration. The in situ (at the pleural surface) peak rarefactional pressure, pr(in situ), ranged between 1.5 and 8.4 MPa, with nine acoustic US exposure groups plus a sham exposure group. Rabbits were assigned randomly to the 10 groups, each with 10 rabbits, except for one group that had nine rabbits. Rabbits were exposed bilaterally with the order of exposure (left then right Lung, or right then left Lung) and acoustic pressure both randomized. Individuals involved in animal handling, exposure and lesion scoring were blinded to the exposure condition. Probit regression analysis was used to examine the dependence of the lesion occurrence on in situ peak rarefactional pressure and order of exposure (first vs. second). Likewise, lesion depth and lesion root surface area were analyzed using Gaussian tobit regression analysis. Neither probability of a lesion nor lesion size measurements was found to be statistically dependent on the order of exposure after the effect of pr(in situ) was considered. Also, a significant correlation was not detected between the two exposed Lung sides on the same rabbit in either lesion occurrence or size measures. The pr(in situ) threshold estimates (in MPa) were similar to each other across occurrence (3.54 ± 0.78), depth (3.36 ± 0.73) and surface area (3.43 ± 0.77) of lesions. Using the same experimental techniques and statistical approach, great consistency of thresholds was demonstrated across three species (mouse, rat and rabbit). Further, there were no differences in the biologic mechanism of injury induced by US and US-induced lesions were similar in morphology in all species and age groups studied. The extent of US-induced Lung damage and the ability of the Lung to heal led to the conclusion that, although US can produce Lung damage at clinical levels, the degree of damage does not appear to be a significant medical problem. (E-mail: wdo@uiuc.edu )
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lesions of ultrasound induced Lung Hemorrhage are not consistent with thermal injury
Ultrasound in Medicine and Biology, 2006Co-Authors: J F Zachary, James P. Blue, Rita J. Miller, B. J. Ricconi, Gary J Eden, William D ObrienAbstract:Abstract— Thermal injury, a potential mechanism of ultrasound-induced Lung Hemorrhage, was studied by comparing lesions induced by an infrared laser (a tissue-heating source) with those induced by pulsed ultrasound. A 600-mW continuous-wave CO 2 laser (wavelength ∼10.6 μm) was focused (680-μm beamwidth) on the surface of the Lungs of rats for a duration between 10 to 40 s; ultrasound beamwidths were between 310 and 930 μm. After exposure, Lungs were examined grossly and then processed for microscopic evaluation. Grossly, lesions induced by laser were somewhat similar to those induced by ultrasound; however, microscopically, they were dissimilar. Grossly, lesions were oval, red to dark red and extended into subjacent tissue to form a cone. The surface was elevated, but the center of the laser-induced lesions was often depressed. Microscopically, the laser-induced injury consisted of coagulation of tissue, cells and fluids, whereas injury induced by ultrasound consisted solely of alveolar Hemorrhage. These results suggest that ultrasound-induced Lung injury is most likely not caused by a thermal mechanism. (E-mail: zacharyj@uiuc.edu )
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Superthreshold behavior of ultrasound-induced Lung Hemorrhage in adult rats: Role of pulse repetition frequency and pulse duration
Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine, 2006Co-Authors: W D O'brien, L A Frizzell, Douglas G. Simpson, J F ZacharyAbstract:Ultrasound-induced Lung Hemorrhage is a well-documented in vivo bioeffect in mice,1–12 rats,11–20 monkeys,21 rabbits,7,8 and pigs.7,8,22–25 Acoustic pressure Lung Hemorrhage thresholds have been estimated in mice,1,4–6,9,12 rats,11,12,14,17 rabbits, and pigs.23–25 From these threshold studies, the pressure thresholds appear to be the same for mice, rats, and rabbits; pressure thresholds do not appear different as a function of frequency or beam width for mice and rats; pressure thresholds have a significant pulse duration (PD) trend for rats; and virtually every pressure threshold (normalized to the mechanical index [MI]) is less than the US Food and Drug Administration (FDA) regulatory limit (MI < 1.926). Also, at superthreshold exposure conditions (in situ [at the pleural surface] peak rarefactional pressure, pr(in situ), = 6.1 MPa), a 3 × 3 factorial design study (pulse repetition frequency [PRF]: 17, 170, and 1700 Hz; exposure duration [ED]: 5, 31.6, and 200 s) showed that the main effects of PRF and ED were not significant for lesion occurrence and sizes, whereas the interaction term (PRF × ED; total number of pulses) was highly significant.18 These findings do not suggest, however, that PRF and ED did not have an effect. Rather, if either PRF or ED is held relatively constant, or varied over only a narrow range, then the number of pulses will appear as an effect of the nonconstant variable. These findings are consistent with those1 that showed a slightly larger proportion of mice with lesions for 100-Hz PRF compared to 10-Hz PRF. In general, however, the effect of exposure timing quantities (PD, ED, and PRF) on the threshold for ultrasound-induced Lung Hemorrhage and on the size of the lesions at superthreshold levels has been examined only to a limited extent. So far, only the interaction of PRF and ED has been examined. The interaction of PRF and PD has not been examined and thus is the purpose of this study for which the interaction term (PRF × PD) is the duty factor, the fractional amount of time the pulse is excited. Furthermore, this factorial PRF × PD study is an adjunct to the previously reported PD threshold study for which the PRF was held constant.17
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Lesions of ultrasound-induced Lung Hemorrhage are not consistent with thermal injury.
Ultrasound in medicine & biology, 2006Co-Authors: J F Zachary, James P. Blue, Rita J. Miller, B. J. Ricconi, J. Gary Eden, W D O'brienAbstract:Thermal injury, a potential mechanism of ultrasound-induced Lung Hemorrhage, was studied by comparing lesions induced by an infrared laser (a tissue-heating source) with those induced by pulsed ultrasound. A 600-mW continuous-wave CO2 laser (wavelength approximately 10.6 microm) was focused (680-microm beamwidth) on the surface of the Lungs of rats for a duration between 10 to 40 s; ultrasound beamwidths were between 310 and 930 microm. After exposure, Lungs were examined grossly and then processed for microscopic evaluation. Grossly, lesions induced by laser were somewhat similar to those induced by ultrasound; however, microscopically, they were dissimilar. Grossly, lesions were oval, red to dark red and extended into subjacent tissue to form a cone. The surface was elevated, but the center of the laser-induced lesions was often depressed. Microscopically, the laser-induced injury consisted of coagulation of tissue, cells and fluids, whereas injury induced by ultrasound consisted solely of alveolar Hemorrhage. These results suggest that ultrasound-induced Lung injury is most likely not caused by a thermal mechanism.
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Threshold estimation of ultrasound-induced Lung Hemorrhage in adult rabbits and comparison of thresholds in mice, rats, rabbits and pigs
Ultrasound in medicine & biology, 2006Co-Authors: W D O'brien, L A Frizzell, Douglas G. Simpson, James P. Blue, Rita J. Miller, Yan Yang, J F ZacharyAbstract:The objective of this study was to assess the threshold and superthreshold behavior of ultrasound (US)-induced Lung Hemorrhage in adult rabbits to gain greater understanding about species dependency. A total of 99 76 +/- 7.6-d-old 2.4 +/- 0.14-kg New Zealand White rabbits were used. Exposure conditions were 5.6-MHz, 10-s exposure duration, 1-kHz PRF and 1.1-micros pulse duration. The in situ (at the pleural surface) peak rarefactional pressure, p(r(in situ)), ranged between 1.5 and 8.4 MPa, with nine acoustic US exposure groups plus a sham exposure group. Rabbits were assigned randomly to the 10 groups, each with 10 rabbits, except for one group that had nine rabbits. Rabbits were exposed bilaterally with the order of exposure (left then right Lung, or right then left Lung) and acoustic pressure both randomized. Individuals involved in animal handling, exposure and lesion scoring were blinded to the exposure condition. Probit regression analysis was used to examine the dependence of the lesion occurrence on in situ peak rarefactional pressure and order of exposure (first vs. second). Likewise, lesion depth and lesion root surface area were analyzed using Gaussian tobit regression analysis. Neither probability of a lesion nor lesion size measurements was found to be statistically dependent on the order of exposure after the effect of p(r(in situ)) was considered. Also, a significant correlation was not detected between the two exposed Lung sides on the same rabbit in either lesion occurrence or size measures. The p(r(in situ)) threshold estimates (in MPa) were similar to each other across occurrence (3.54 +/- 0.78), depth (3.36 +/- 0.73) and surface area (3.43 +/- 0.77) of lesions. Using the same experimental techniques and statistical approach, great consistency of thresholds was demonstrated across three species (mouse, rat and rabbit). Further, there were no differences in the biologic mechanism of injury induced by US and US-induced lesions were similar in morphology in all species and age groups studied. The extent of US-induced Lung damage and the ability of the Lung to heal led to the conclusion that, although US can produce Lung damage at clinical levels, the degree of damage does not appear to be a significant medical problem.
Carol H. Raeman - One of the best experts on this subject based on the ideXlab platform.
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Thresholds for sound‐induced Lung Hemorrhage for frequencies from 100 Hz to 1 MHz
The Journal of the Acoustical Society of America, 2006Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. RaemanAbstract:Edwin L. Carstensen has made outstanding and wide‐ranging contributions to the field of biomedical ultrasound. His many achievements span the areas of bioeffects of ultrasound, acoustic cavitation, lithotripsy, thermal and mechanical mechanisms, and nonlinear acoustics. In 1990, Carstensen first reported that pulsed ultrasound at diagnostic exposure conditions could produce mammalian Lung Hemorrhage [Child et al., Ultrasound Med. and Biol. 16, 817–825 (1990)]. Recent work from our lab has quantified the thresholds for murine Lung Hemorrhage over a range of acoustic frequencies from approximately 100 Hz to 1 MHz. Various exposure systems were used to generate acoustic fields over this broad frequency range in the laboratory. Through several different investigations, we have shown that murine Lung responds to low‐frequency underwater sound as a resonant structure. The resonance frequency of adult murine Lung is approximately 325 Hz, and the pressure threshold for Lung Hemorrhage is lowest at the resonance f...
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Age dependence of ultrasonically induced Lung Hemorrhage in mice
Ultrasound in medicine & biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, David P. Penney, Edwin L. CarstensenAbstract:Abstract Thresholds for ultrasonically induced Lung Hemorrhage were determined in neonatal mice (24–36 h old), juvenile mice (14 d old) and adult mice (8–10 weeks old) to assess whether or not the threshold for Lung Hemorrhage is dependent upon age. Ultrasonic exposures were at 1.15 MHz with a pulse length of 10 μs, pulse repetition frequency of 100 Hz and a total exposure duration of 3 min. The threshold for Lung Hemorrhage occurred at a peak positive acoustic pressure of approximately 1 MPa for mice in all three age groups. Although the thresholds were similar for neonatal, juvenile and adult mice, the sizes of the suprathreshold Hemorrhages were significantly larger in adult mice than in neonatal or juvenile mice.
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Ultrasonically induced Lung Hemorrhage in young swine
Ultrasound in medicine & biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, Edwin L. CarstensenAbstract:Ten-day old swine were used in the final step of a study of the age dependence of the threshold for Lung Hemorrhage resulting from exposure to diagnostically relevant levels of pulsed ultrasound. A 2.3-MHz focused transducer (pulse length of 10 microseconds, 100-Hz pulse repetition frequency) was incremented vertically at several sites for a distance of 2 or 2.5 cm over the chest of the subject for a total exposure period of 16 or 20 min. The procedure was repeated at a total of four sites per animal. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.3-MPa peak positive pressure in water and the surface of the animal or, at the surface of the Lung, 0.8-MPa peak positive pressure, 0.8-MPa fundamental pressure, 0.7-MPa maximum negative pressure and 20 Wcm-2 pulse average intensity. These values are essentially the same as those reported previously for neonatal swine, and neonatal, juvenile and adult mice.
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ultrasonically induced Lung Hemorrhage in young swine
Ultrasound in Medicine and Biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, Edwin L. CarstensenAbstract:Abstract Ten-day old swine were used in the final step of a study of the age dependence of the threshold for Lung Hemorrhage resulting from exposure to diagnostically relevant levels of pulsed ultrasound. A 2.3-MHz focused transducer (pulse length of 10 μs, 100-Hz pulse repetition frequency) was incremented vertically at several sites for a distance of 2 or 2.5 cm over the chest of the subject for a total exposure period of 16 or 20 min. The procedure was repeated at a total of four sites per animal. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.3-MPa peak positive pressure in water at the surface of the animal or, at the surface of the Lung, 0.8-MPa peak positive pressure, 0.8-MPa fundamental pressure, 0.7-MPa maximum negative pressure and 20 Wcm−2 pulse average intensity. These values are essentially the same as those reported previously for neonatal swine, and neonatal, juvenile and adult mice.
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Lung Hemorrhage from exposure to ultrasound.
The Journal of the Acoustical Society of America, 1996Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, David P. Penney, Edwin L. CarstensenAbstract:Thresholds for Lung Hemorrhage from exposure to pulsed ultrasound have been determined in neonatal mice (24–36 h), juvenile mice (14 days), and adult mice (8–10 weeks), and neonatal (24–36 h) and young (10 days) swine. The threshold at 2 MHz is approximately 1 MPa and the threshold increases gradually with frequency in the range from 0.1 to 4 MHz. Positive and negative pressure pulses are equally damaging. Following exposure, suprathreshold lesions are not progressive with time and are repaired by usual physiological mechanisms. Although the unique sensitivity of Lung tissue to ultrasound is associated with the presence of air in the alveolae, this does not necessarily implicate acoustic cavitation as the responsible mechanism. Thin sections of murine Lung are more sensitive than thicker regions probably because of reduced reflection at the surface of the Lung tissue.
W D O'brien - One of the best experts on this subject based on the ideXlab platform.
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THRESHOLD ESTIMATION AND SUPERTHRESHOLD BEHAVIOR OF ULTRASOUND-INDUCED Lung Hemorrhage IN RATS : ROLE OF AGE DEPENDENCY
Ultrasound in medicine & biology, 2008Co-Authors: W D O'brien, Yan Yang, Douglas G. SimpsonAbstract:Age-dependent threshold and superthreshold behaviors of ultrasound-induced Lung Hemorrhage were investigated with one hundred ten 12.6 0.8-d-old rats, one hundred ten 22.9 0.8-d-old rats, and one hundred 57.7 3.9-d-old rats. Exposure conditions were: 2.8 MHz, 10-s exposure duration, 1-kHz pulse repetition frequency and 1.3-s pulse duration. The in situ (at the pleural surface) peak rarefactional pressure (pr(in situ)) ranged between 1.4 and 10.8 MPa for which there were either 9 or 10 acoustic pressure groups for each of the three rat ages (10 rats/exposure group). For each of the three rat ages there were also shams; there were no lesions in the shams. The pr(in situ) levels were randomized within each age group; rat age was not randomized. Individuals involved in animal handling, exposure and lesion scoring were blinded to the exposure condition. In addition, one hundred fifty-six 72-d-old rats were included from three completed studies (same experimental conditions) to provide a fourth age group for the analysis. Probit regression analysis was used to examine the dependence of the occurrence of lesions on pr(in situ) in the four age groups. Likewise, lesion depth and lesion root surface area were analyzed using Gaussian tobit regression analysis. Although pr(in situ) was a significant variable, no significant age dependence of the pr(in situ) effect was found. Furthermore, age had no significant effect on either the rate of occurrence or the depth of lesions. Given the occurrence of a lesion, a weak age dependence was found for the median surface area of the induced lesion (p-value 0.037). (E-mail: wdo@uiuc.edu) © 2008 World Federation for Ultrasound in Medicine & Biology.
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Evaluation of the threshold for Lung Hemorrhage by diagnostic ultrasound and a proposed new safety index.
Ultrasound in medicine & biology, 2007Co-Authors: Charles C. Church, W D O'brienAbstract:In a recent report (O’Brien et al. (2006b), it was suggested that the current expression for the mechanical index (MI) was not well suited to its function of quantifying the likelihood of an adverse biological effect after exposure of the gas-filled Lung to diagnostic ultrasound. The purpose of this study was to analyze the relatively large database of experimental thresholds for the induction of Lung Hemorrhage to: (i) determine which variable(s) best describe the data and (ii) use the resulting equation to obtain a new formulation for the MI for Lung exposures. Data from 14 studies of Lung Hemorrhage in four common laboratory animals (mouse, rat, rabbit and pig) were tabulated with regard to five common acoustic variables: center frequency (fc), pulse repetition frequency (PRF), pulse duration (PD), exposure duration (ED) and the threshold in situ peak rarefactional pressure (pr). The 34 threshold data points were fit by linear regression to: (i) a multiplicative model of the other variables, pr = AfcBPRFCPDDEDE, where A is a constant; (ii) 14 “reduced” models in which one or more variables were not included in the analysis; (iii) four models in which a multiplicative combination of variables has a common name e.g., duty factor; and (iv) the general form of the current expression for the MI. The MI was shown to provide a poor fit to the threshold data (r2 = 0.382), as were three of the four named models. The best fits were found for the complete model and for three reduced models, all of which contain the exposure duration. Because the implementation of a time-dependent safety parameter would present significant practical difficulties, a different model, pr = AfcBPRFCPDD, was chosen as the basis for the new MI. Thus, the expression for the Lung-specific mechanical index, MILung, includes several, rather than only one, of the relevant acoustic variables. This is the first potential safety index developed as a direct result of experimental measurements rather than theoretical analysis. (E-mail: cchurch@olemiss.edu)
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Superthreshold behavior of ultrasound-induced Lung Hemorrhage in adult rats: Role of pulse repetition frequency and pulse duration
Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine, 2006Co-Authors: W D O'brien, L A Frizzell, Douglas G. Simpson, J F ZacharyAbstract:Ultrasound-induced Lung Hemorrhage is a well-documented in vivo bioeffect in mice,1–12 rats,11–20 monkeys,21 rabbits,7,8 and pigs.7,8,22–25 Acoustic pressure Lung Hemorrhage thresholds have been estimated in mice,1,4–6,9,12 rats,11,12,14,17 rabbits, and pigs.23–25 From these threshold studies, the pressure thresholds appear to be the same for mice, rats, and rabbits; pressure thresholds do not appear different as a function of frequency or beam width for mice and rats; pressure thresholds have a significant pulse duration (PD) trend for rats; and virtually every pressure threshold (normalized to the mechanical index [MI]) is less than the US Food and Drug Administration (FDA) regulatory limit (MI < 1.926). Also, at superthreshold exposure conditions (in situ [at the pleural surface] peak rarefactional pressure, pr(in situ), = 6.1 MPa), a 3 × 3 factorial design study (pulse repetition frequency [PRF]: 17, 170, and 1700 Hz; exposure duration [ED]: 5, 31.6, and 200 s) showed that the main effects of PRF and ED were not significant for lesion occurrence and sizes, whereas the interaction term (PRF × ED; total number of pulses) was highly significant.18 These findings do not suggest, however, that PRF and ED did not have an effect. Rather, if either PRF or ED is held relatively constant, or varied over only a narrow range, then the number of pulses will appear as an effect of the nonconstant variable. These findings are consistent with those1 that showed a slightly larger proportion of mice with lesions for 100-Hz PRF compared to 10-Hz PRF. In general, however, the effect of exposure timing quantities (PD, ED, and PRF) on the threshold for ultrasound-induced Lung Hemorrhage and on the size of the lesions at superthreshold levels has been examined only to a limited extent. So far, only the interaction of PRF and ED has been examined. The interaction of PRF and PD has not been examined and thus is the purpose of this study for which the interaction term (PRF × PD) is the duty factor, the fractional amount of time the pulse is excited. Furthermore, this factorial PRF × PD study is an adjunct to the previously reported PD threshold study for which the PRF was held constant.17
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Lesions of ultrasound-induced Lung Hemorrhage are not consistent with thermal injury.
Ultrasound in medicine & biology, 2006Co-Authors: J F Zachary, James P. Blue, Rita J. Miller, B. J. Ricconi, J. Gary Eden, W D O'brienAbstract:Thermal injury, a potential mechanism of ultrasound-induced Lung Hemorrhage, was studied by comparing lesions induced by an infrared laser (a tissue-heating source) with those induced by pulsed ultrasound. A 600-mW continuous-wave CO2 laser (wavelength approximately 10.6 microm) was focused (680-microm beamwidth) on the surface of the Lungs of rats for a duration between 10 to 40 s; ultrasound beamwidths were between 310 and 930 microm. After exposure, Lungs were examined grossly and then processed for microscopic evaluation. Grossly, lesions induced by laser were somewhat similar to those induced by ultrasound; however, microscopically, they were dissimilar. Grossly, lesions were oval, red to dark red and extended into subjacent tissue to form a cone. The surface was elevated, but the center of the laser-induced lesions was often depressed. Microscopically, the laser-induced injury consisted of coagulation of tissue, cells and fluids, whereas injury induced by ultrasound consisted solely of alveolar Hemorrhage. These results suggest that ultrasound-induced Lung injury is most likely not caused by a thermal mechanism.
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Threshold estimation of ultrasound-induced Lung Hemorrhage in adult rabbits and comparison of thresholds in mice, rats, rabbits and pigs
Ultrasound in medicine & biology, 2006Co-Authors: W D O'brien, L A Frizzell, Douglas G. Simpson, James P. Blue, Rita J. Miller, Yan Yang, J F ZacharyAbstract:The objective of this study was to assess the threshold and superthreshold behavior of ultrasound (US)-induced Lung Hemorrhage in adult rabbits to gain greater understanding about species dependency. A total of 99 76 +/- 7.6-d-old 2.4 +/- 0.14-kg New Zealand White rabbits were used. Exposure conditions were 5.6-MHz, 10-s exposure duration, 1-kHz PRF and 1.1-micros pulse duration. The in situ (at the pleural surface) peak rarefactional pressure, p(r(in situ)), ranged between 1.5 and 8.4 MPa, with nine acoustic US exposure groups plus a sham exposure group. Rabbits were assigned randomly to the 10 groups, each with 10 rabbits, except for one group that had nine rabbits. Rabbits were exposed bilaterally with the order of exposure (left then right Lung, or right then left Lung) and acoustic pressure both randomized. Individuals involved in animal handling, exposure and lesion scoring were blinded to the exposure condition. Probit regression analysis was used to examine the dependence of the lesion occurrence on in situ peak rarefactional pressure and order of exposure (first vs. second). Likewise, lesion depth and lesion root surface area were analyzed using Gaussian tobit regression analysis. Neither probability of a lesion nor lesion size measurements was found to be statistically dependent on the order of exposure after the effect of p(r(in situ)) was considered. Also, a significant correlation was not detected between the two exposed Lung sides on the same rabbit in either lesion occurrence or size measures. The p(r(in situ)) threshold estimates (in MPa) were similar to each other across occurrence (3.54 +/- 0.78), depth (3.36 +/- 0.73) and surface area (3.43 +/- 0.77) of lesions. Using the same experimental techniques and statistical approach, great consistency of thresholds was demonstrated across three species (mouse, rat and rabbit). Further, there were no differences in the biologic mechanism of injury induced by US and US-induced lesions were similar in morphology in all species and age groups studied. The extent of US-induced Lung damage and the ability of the Lung to heal led to the conclusion that, although US can produce Lung damage at clinical levels, the degree of damage does not appear to be a significant medical problem.
Sally Z. Child - One of the best experts on this subject based on the ideXlab platform.
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Thresholds for sound‐induced Lung Hemorrhage for frequencies from 100 Hz to 1 MHz
The Journal of the Acoustical Society of America, 2006Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. RaemanAbstract:Edwin L. Carstensen has made outstanding and wide‐ranging contributions to the field of biomedical ultrasound. His many achievements span the areas of bioeffects of ultrasound, acoustic cavitation, lithotripsy, thermal and mechanical mechanisms, and nonlinear acoustics. In 1990, Carstensen first reported that pulsed ultrasound at diagnostic exposure conditions could produce mammalian Lung Hemorrhage [Child et al., Ultrasound Med. and Biol. 16, 817–825 (1990)]. Recent work from our lab has quantified the thresholds for murine Lung Hemorrhage over a range of acoustic frequencies from approximately 100 Hz to 1 MHz. Various exposure systems were used to generate acoustic fields over this broad frequency range in the laboratory. Through several different investigations, we have shown that murine Lung responds to low‐frequency underwater sound as a resonant structure. The resonance frequency of adult murine Lung is approximately 325 Hz, and the pressure threshold for Lung Hemorrhage is lowest at the resonance f...
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Age dependence of ultrasonically induced Lung Hemorrhage in mice
Ultrasound in medicine & biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, David P. Penney, Edwin L. CarstensenAbstract:Abstract Thresholds for ultrasonically induced Lung Hemorrhage were determined in neonatal mice (24–36 h old), juvenile mice (14 d old) and adult mice (8–10 weeks old) to assess whether or not the threshold for Lung Hemorrhage is dependent upon age. Ultrasonic exposures were at 1.15 MHz with a pulse length of 10 μs, pulse repetition frequency of 100 Hz and a total exposure duration of 3 min. The threshold for Lung Hemorrhage occurred at a peak positive acoustic pressure of approximately 1 MPa for mice in all three age groups. Although the thresholds were similar for neonatal, juvenile and adult mice, the sizes of the suprathreshold Hemorrhages were significantly larger in adult mice than in neonatal or juvenile mice.
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Ultrasonically induced Lung Hemorrhage in young swine
Ultrasound in medicine & biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, Edwin L. CarstensenAbstract:Ten-day old swine were used in the final step of a study of the age dependence of the threshold for Lung Hemorrhage resulting from exposure to diagnostically relevant levels of pulsed ultrasound. A 2.3-MHz focused transducer (pulse length of 10 microseconds, 100-Hz pulse repetition frequency) was incremented vertically at several sites for a distance of 2 or 2.5 cm over the chest of the subject for a total exposure period of 16 or 20 min. The procedure was repeated at a total of four sites per animal. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.3-MPa peak positive pressure in water and the surface of the animal or, at the surface of the Lung, 0.8-MPa peak positive pressure, 0.8-MPa fundamental pressure, 0.7-MPa maximum negative pressure and 20 Wcm-2 pulse average intensity. These values are essentially the same as those reported previously for neonatal swine, and neonatal, juvenile and adult mice.
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ultrasonically induced Lung Hemorrhage in young swine
Ultrasound in Medicine and Biology, 1997Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, Christopher Cox, Edwin L. CarstensenAbstract:Abstract Ten-day old swine were used in the final step of a study of the age dependence of the threshold for Lung Hemorrhage resulting from exposure to diagnostically relevant levels of pulsed ultrasound. A 2.3-MHz focused transducer (pulse length of 10 μs, 100-Hz pulse repetition frequency) was incremented vertically at several sites for a distance of 2 or 2.5 cm over the chest of the subject for a total exposure period of 16 or 20 min. The procedure was repeated at a total of four sites per animal. Animals were euthanized and Lungs were scored by visual inspection for numbers and areas of gross Hemorrhages. The threshold level for Hemorrhage was approximately 1.3-MPa peak positive pressure in water at the surface of the animal or, at the surface of the Lung, 0.8-MPa peak positive pressure, 0.8-MPa fundamental pressure, 0.7-MPa maximum negative pressure and 20 Wcm−2 pulse average intensity. These values are essentially the same as those reported previously for neonatal swine, and neonatal, juvenile and adult mice.
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Lung Hemorrhage from exposure to ultrasound.
The Journal of the Acoustical Society of America, 1996Co-Authors: Diane Dalecki, Sally Z. Child, Carol H. Raeman, David P. Penney, Edwin L. CarstensenAbstract:Thresholds for Lung Hemorrhage from exposure to pulsed ultrasound have been determined in neonatal mice (24–36 h), juvenile mice (14 days), and adult mice (8–10 weeks), and neonatal (24–36 h) and young (10 days) swine. The threshold at 2 MHz is approximately 1 MPa and the threshold increases gradually with frequency in the range from 0.1 to 4 MHz. Positive and negative pressure pulses are equally damaging. Following exposure, suprathreshold lesions are not progressive with time and are repaired by usual physiological mechanisms. Although the unique sensitivity of Lung tissue to ultrasound is associated with the presence of air in the alveolae, this does not necessarily implicate acoustic cavitation as the responsible mechanism. Thin sections of murine Lung are more sensitive than thicker regions probably because of reduced reflection at the surface of the Lung tissue.
