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Characterization of Pressure Transients Generated by Nanosecond Electrical Pulse (nsEP) Exposure.

ABSTRACT: The mechanism(s) responsible for the breakdown (nanoporation) of cell plasma membranes after nanosecond pulse (nsEP) exposure remains poorly understood. Current theories focus exclusively on the electrical field, citing electrostriction, water dipole alignment and/or electrodeformation as the primary mechanisms for pore formation. However, the delivery of a high-voltage nsEP to cells by tungsten electrodes creates a multitude of biophysical phenomena, including electrohydraulic cavitation, electrochemical interactions, thermoelastic expansion, and others. To date, very limited research has investigated non-electric phenomena occurring during nsEP exposures and their potential effect on cell nanoporation. Of primary interest is the production of acoustic shock waves during nsEP exposure, as it is known that acoustic shock waves can cause membrane poration (sonoporation). Based on these observations, our group characterized the acoustic pressure transients generated by nsEP and determined if such transients played any role in nanoporation. In this paper, we show that nsEP exposures, equivalent to those used in cellular studies, are capable of generating high-frequency (2.5?MHz), high-intensity (>13?kPa) pressure transients. Using confocal microscopy to measure cell uptake of YO-PRO®-1 (indicator of nanoporation of the plasma membrane) and changing the electrode geometry, we determined that acoustic waves alone are not responsible for poration of the membrane.

SUBMITTER: Roth CC

PROVIDER: S-EPMC4598730 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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Characterization of Pressure Transients Generated by Nanosecond Electrical Pulse (nsEP) Exposure.

Roth Caleb C CC Barnes Ronald A RA Ibey Bennett L BL Beier Hope T HT Christopher Mimun L L Maswadi Saher M SM Shadaram Mehdi M Glickman Randolph D RD

Scientific reports 20151009

The mechanism(s) responsible for the breakdown (nanoporation) of cell plasma membranes after nanosecond pulse (nsEP) exposure remains poorly understood. Current theories focus exclusively on the electrical field, citing electrostriction, water dipole alignment and/or electrodeformation as the primary mechanisms for pore formation. However, the delivery of a high-voltage nsEP to cells by tungsten electrodes creates a multitude of biophysical phenomena, including electrohydraulic cavitation, elect ...[more]

PMID: 26450165

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Project description:BackgroundTraffic exposure may increase cardiovascular disease (CVD) risk via systemic inflammation and elevated blood pressure, two important clinical markers for managing disease progression.ObjectivesWe assessed degree and consistency of association between traffic exposure indicators as predictors of C-reactive protein (CRP) and pulse pressure (PP) in an adult U.S. Puerto Rican population (n = 1,017).MethodsCross-sectional information on health and demographics and blood data was collected. Using multiple linear regression, we tested for associations between CRP, PP, and six traffic exposure indicators including residential proximity to roads with > 20,000 vehicles/day and traffic density [vehicle miles traveled per square mile (VMT/mi2)]. Diabetes and obesity [body mass index (BMI) >or= 30 kg/m2] were tested as effect modifiers.ResultsCRP was positively associated with traffic density in the total population [36% CRP difference with 95% confidence interval (CI) 2.5-81%] for residence within the highest versus lowest VMT/mi2 level. With BMI >or= 30, CRP showed significant positive associations with five of six traffic indices including residence <or= 200 m versus > 200 m of a roadway [22.7% CRP difference (95% CI, 3.15-46.1)] and traffic density in the third highest versus lowest VMT/mi2 level [28.1% difference (95% CI, 1.0-62.6)]. PP was positively associated with residence within <or= 100 m of a roadway for the total population [2.2 mmHg (95% CI, 0.13-4.3 mmHg)] and persons with BMI >or= 30 [3.8 mmHg (95% CI, 0.88-6.8)]. Effect estimates approximately doubled for residence within <or= 200 m of two or more roadways, particularly in persons with diabetes [8.1 mmHg (95% CI, 2.2-14.1)].ConclusionsTraffic exposure at roadway volumes as low as 20,000-40,000 vehicles/day may increase CVD risk through adverse effects on blood pressure and inflammation. Individuals with elevated inflammation profiles, that is, BMI >or= 30, may be more susceptible to the effects of traffic exposure.

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Characterization of Pressure Transients Generated by Nanosecond Electrical Pulse (nsEP) Exposure.

Publications

Characterization of Pressure Transients Generated by Nanosecond Electrical Pulse (nsEP) Exposure.

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