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  • Arousal  (1)
  • Gulf of Maine USA  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Craniofacial Electromyogram Activation Response: Another Indicator of Anesthetic Depth (1998)
    Springer
    Journal of clinical monitoring and computing 14 (1998), S. 5-17 
    Details
    ISSN: 1573-2614
    Keywords: Anesthesia: general, depth, isoflurane, computer simulation ; Arousal ; Monitoring: anesthetic depth, electromyogram, EMG ; Memory: awareness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Computer Science , Medicine
    Notes: Abstract Objective. After finding that craniofacial EMG preceding a stimulus was a poor predictor of movement response to that stimulus, we evaluated an alternative relation between EMG and movement: the difference in anesthetic depth between the endpoint of EMG responsiveness to a stimulus and endpoint of movement responsiveness to that stimulus. We expressed this relation as the increment of isoflurane between the two endpoints. Methods. We measured EMG over the frontalis muscle, over the corrugator muscle, and between the Fp2 and the mastoid process as patients emerged from general anesthesia during suture closing of the surgical incision. Anesthesia was decreased by controlled washout of isoflurane while maintaining 70% N2O, and brain isoflurane concentrations (CisoBrain) were calculated. We studied a control group of 10 patients who received only surgical stimulation, and 30 experimental patients who intermittently received test stimuli in addition to the surgical stimulation. Patients were observed for movement responses and EMG records were evaluated for EMG activation responses. We defined an EMG activation response to be a rapid voltage increase of at least 1.0 µV RMS above baseline, with a duration of at least 30 s, in at least one of the three EMG channels. Patient responses to stimuli were classified as either an EMG activation response without a move response (EMG+, a move response without an EMG activation response (MV+), both an EMG activation response and a move response (EMG+MV+), or no response. We defined the EMG+ endpoint to be the threshold between EMG+ response and nonresponse to a stimulus, and estimatedC isoBrain at this endpoint. We similarly defined the move endpoint and estimated the move endpointC isoBrain. We then calculated the increment ofC isoBrain at the EMG+ endpoint relative to the move endpoint. Main results. For the 30 experimental patients, the initial response to a test stimulus was an EMG+ in 14 patients (47%), an EMG+MV+ in 12 patients (40%), and a MV+ in 1 patient (3%); no response occurred by the time surgery was completed in 3 patients (10%). No response occurred in 7 of the control patients (70%). Of the 14 patients with an initial EMG+ response to a test stimulus, 9 patients later had a move response. For these 9 patients, the increment of CisoBrain between the EMG+ endpoint and move endpoint was 0.11 ± 0.04 vol% (mean ± SD). Conclusions. Our results suggest that, given the circumstances of our study, an EMG activation response by a nonmoving patient indicates that the patient is at an anesthetic level close to that at which movement could occur. However, because the first EMG activation response may occur simultaneously with movement, the EMG activation response cannot be relied upon to always herald a move response before it occurs. Our results also suggest that EMG responsiveness to a test stimulus may be used to estimate the anesthetic depth of an individual patient.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007489321321
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    Paper (German National Licenses)
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  • 2
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    Dihydrodinophysistoxin-1 produced by Dinophysis norvegica in the Gulf of Maine, USA and its accumulation in shellfish (2020)
    Toxins
    Details
    Publication Date: 2022-05-26
    Description: © The Author(s), 2020. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Deeds, J. R., Stutts, W. L., Celiz, M. D., MacLeod, J., Hamilton, A. E., Lewis, B. J., Miller, D. W., Kanwit, K., Smith, J. L., Kulis, D. M., McCarron, P., Rauschenberg, C. D., Burnell, C. A., Archer, S. D., Borchert, J., & Lankford, S. K. Dihydrodinophysistoxin-1 produced by Dinophysis norvegica in the Gulf of Maine, USA and its accumulation in shellfish. Toxins, 12(9), (2020): E533, doi:10.3390/toxins12090533.
    Description: Dihydrodinophysistoxin-1 (dihydro-DTX1, (M-H)−m/z 819.5), described previously from a marine sponge but never identified as to its biological source or described in shellfish, was detected in multiple species of commercial shellfish collected from the central coast of the Gulf of Maine, USA in 2016 and in 2018 during blooms of the dinoflagellate Dinophysis norvegica. Toxin screening by protein phosphatase inhibition (PPIA) first detected the presence of diarrhetic shellfish poisoning-like bioactivity; however, confirmatory analysis using liquid chromatography-tandem mass spectrometry (LC-MS/MS) failed to detect okadaic acid (OA, (M-H)−m/z 803.5), dinophysistoxin-1 (DTX1, (M-H)−m/z 817.5), or dinophysistoxin-2 (DTX2, (M-H)−m/z 803.5) in samples collected during the bloom. Bioactivity-guided fractionation followed by liquid chromatography-high resolution mass spectrometry (LC-HRMS) tentatively identified dihydro-DTX1 in the PPIA active fraction. LC-MS/MS measurements showed an absence of OA, DTX1, and DTX2, but confirmed the presence of dihydro-DTX1 in shellfish during blooms of D. norvegica in both years, with results correlating well with PPIA testing. Two laboratory cultures of D. norvegica isolated from the 2018 bloom were found to produce dihydro-DTX1 as the sole DSP toxin, confirming the source of this compound in shellfish. Estimated concentrations of dihydro-DTX1 were 〉0.16 ppm in multiple shellfish species (max. 1.1 ppm) during the blooms in 2016 and 2018. Assuming an equivalent potency and molar response to DTX1, the authority initiated precautionary shellfish harvesting closures in both years. To date, no illnesses have been associated with the presence of dihydro-DTX1 in shellfish in the Gulf of Maine region and studies are underway to determine the potency of this new toxin relative to the currently regulated DSP toxins in order to develop appropriate management guidance.
    Description: Partial support for this research was received from the National Oceanic and Atmospheric Administration, National Centers for Coastal Ocean Science Competitive Research, Ecology and Oceanography of Harmful Algal Blooms Program under awards NA17NOS4780184 and NA19NOS4780182 to Juliette Smith (VIMS) and Jonathan Deeds (US FDA), and Prevention, Control, and Mitigation of Harmful Algal Blooms program award NA17NOS4780179 to Stephen Archer. This paper is ECOHAB publication number EC0956.
    Keywords: diarrhetic shellfish poisoning ; dihydro-DTX1 ; Dinophysis norvegica ; Gulf of Maine USA
    Repository Name: Woods Hole Open Access Server
    Type: Article
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