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Pieter Scheerlinck

Pieter Scheerlinck

· M.D., Associate Professor

University of California, Davis · Emergency Medicine

Active 2006–2023

h-index10
Citations409
Papers113 last 5y
Funding
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About

Pieter H. Scheerlinck, M.D., is an Assistant Clinical Professor in the Department of Emergency Medicine at UC Davis Health. His specialties include Emergency Medicine and Toxicology. He is board certified by the American Board of Emergency Medicine since 2017 and in Medical Toxicology since 2018. Dr. Scheerlinck completed his undergraduate studies with a B.S. in Neuroscience from Bowdoin College in 2005. He earned his medical degree (M.B.B.S.) from the University of Queensland Mayne Medical School in Brisbane, Queensland, Australia, in 2012. His residency in Emergency Medicine was completed at UC Davis Medical Center from 2009 to 2012, and he also completed a fellowship in Medical Toxicology at the same institution from 2016 to 2018. His research and publication record include work on various topics related to toxicology, including carbon monoxide toxicity, hydrocarbon exposure, and mushroom poisoning, among others.

Research topics

  • Medicine
  • Environmental health
  • Neuroscience
  • Toxicology
  • Psychology

Selected publications

  • Bodybuilding supplements leading to copper toxicity, encephalopathy, fulminant hepatic failure and rhabdomyolysis

    The American Journal of Emergency Medicine · 2020 · 15 citations

    • Medicine
    • Intensive care medicine
    • Physical therapy
  • Acute and Chronic Carbon Monoxide Toxicity from Tobacco Smoking

    Military Medicine · 2019-10-31 · 45 citations

    article

    INTRODUCTION: Carbon monoxide (CO) is produced from incomplete combustion of hydrocarbons and is a by-product of tobacco smoking. Chronic cigarette smokers often have carboxyhemoglobin (COHb) concentrations as high as 10%. We report a case of severely elevated COHb and polycythemia because of tobacco smoking and provide a review of the literature regarding elevated COHb in smokers. MATERIALS AND METHODS: A comprehensive search of PubMed and Google Scholar was performed looking for articles on tobacco smoking and CO, COHb, CO poisoning, cigarettes, pipes, cigars and water pipes/hookah smokers. RESULT: COHb levels in frequent cigarette smokers generally range from 4.2% presmoking to 8.6% postsmoking. A heavy cigarette smoker presented twice with symptoms of CO toxicity and was found to have levels 21.8 to 24.2%. Cigar smokers have been found to have COHb ranging as high as 13.0 to 38.6% in case reports. Waterpipe or "hookah" smokers generally have COHb levels 10.1% +/-2.5% and case reports, and series of even higher levels associated with CO toxicity symptoms are common. Waterpipe smokers have been found to have COHb levels as high as 39.2% after smoking. CONCLUSIONS: Many active duty military and military veterans are tobacco smokers and these patients and their health care providers should be aware of the adverse effects of CO toxicity from tobacco smoking. Patients may have symptoms such as headaches, syncope, and ataxia in the setting of acute CO toxicity; however, the chronic effects of CO may not be completely understood. Future work could explore chronic CO toxicity and its effects on strength and exercise tolerance in military personnel and provide education to service members, veterans, and health care providers.

  • <i>Amanita phalloides</i>Mushroom Poisonings — Northern California, December 2016

    MMWR Morbidity and Mortality Weekly Report · 2017-06-01 · 35 citations

    articleOpen access

    Amanita phalloides, colloquially known as the "death cap," belongs to the Phalloideae section of the Amanita family of mushrooms and is responsible for most deaths following ingestion of foraged mushrooms worldwide (1). On November 28, 2016, members of the Bay Area Mycological Society notified personnel at the California Poison Control System (CPCS) of an unusually large A. phalloides bloom in the greater San Francisco Bay Area, coincident with the abundant rainfall and recent warm weather. Five days later, CPCS received notification of the first human A. phalloides poisoning of the season. Over the following 2 weeks, CPCS was notified of an additional 13 cases of hepatotoxicity resulting from A. phalloides ingestion. In the past few years before this outbreak, CPCS received reports of only a few mushroom poisoning cases per year. A summary of 14 reported cases is presented here. Data extracted from patient medical charts revealed a pattern of delayed gastrointestinal manifestations of intoxication leading to dehydration and hepatotoxicity. Three patients received liver transplants and all but one recovered completely. The morbidity and potential lethality associated with A. phalloides ingestion are serious public health concerns and warrant medical provider education and dissemination of information cautioning against consuming foraged wild mushrooms.

  • Lithium pilocarpine-induced status epilepticus in postnatal day 20 rats results in greater neuronal injury in ventral versus dorsal hippocampus

    Neuroscience · 2011-06-19 · 36 citations

    article
  • A Simple Quantitative Method for Analyzing Electrographic Status Epilepticus in Rats

    Journal of Neurophysiology · 2009-01-08 · 64 citations

    articleOpen access

    Electrographic status epilepticus (ESE) is a medical emergency consisting of repetitive seizures and may result in death or severe brain damage. Epilepsy can develop following ESE. The properties of ESE (e.g., duration and intensity) are variable, as are the effects of putative therapeutic treatments. Therefore a straightforward method to quantify different components of ESE would be beneficial for both researchers and clinicians. A frequency range close to the gamma band was selected for extraction of seizure-related activity from the EEG. This filtering strategy reduced motion artifacts and other noise sources in the electrophysiological recordings, thus increasing the signal-to-noise ratio of the EEG spike activity. EEG spiking was quantified using an energy operator and modeled by an eighth-order polynomial. In a benzodiazepine-resistant rat model of pilocarpine-induced ESE, the efficacy of various pharmaceutical agents at suppressing ESE was analyzed with this and other methods on data collected for < or =24 h after ESE induction. This approach allows for the objective, quantitative, and rapid assessment of the effects of both short- and long-lasting pharmacological manipulations on ESE and other forms of prolonged repetitive electrical activity.

  • A potential model of pediatric posttraumatic epilepsy

    Epilepsy Research · 2009-06-12 · 80 citations

    article
  • Identification, physiological actions, and distribution of VYRKPPFNGSIFamide (Val<sup>1</sup>‐SIFamide) in the stomatogastric nervous system of the American lobster <i>Homarus americanus</i>

    The Journal of Comparative Neurology · 2006-03-24 · 61 citations

    article

    In this study, the peptide VYRKPPFNGSIFamide (Val(1)-SIFamide) was identified in the stomatogastric nervous system (STNS) of the American lobster, Homarus americanus, using matrix-assisted laser desorption/ionization-Fourier transform mass spectrometry (MALDI-FTMS). When bath-applied to the stomatogastric ganglion (STG), synthetic Val(1)-SIFamide activated the pyloric motor pattern, increasing both burst amplitude and duration in the pyloric dilator (PD) neurons. To determine the distribution of this novel SIFamide isoform within the lobster STNS and neuroendocrine organs, a rabbit polyclonal antibody was generated against synthetic Val(1)-SIFamide. Whole-mount immunolabeling with this antibody showed that this peptide is widely distributed within the STNS, including extensive neuropil staining in the STG and commissural ganglia (CoGs) as well as immunopositive somata in the CoGs and the oesophageal ganglion. Labeling was also occasionally seen in the pericardial organ (PO), but not in the sinus gland. When present in the PO, labeling was restricted to fibers-of-passage and was never seen in release terminals. Adsorption of the antibody by either Val(1)-SIFamide or Gly(1)-SIFamide abolished all Val(1)-SIFamide staining within the STNS, including the STG neuropil, whereas adsorption by other lobster neuropeptides had no effect on immunolabeling. These data strongly suggest that the staining we report is a true reflection of the distribution of this peptide in the STNS. Collectively, our mass spectrometric, physiological, and anatomical data are consistent with Val(1)-SIFamide serving as a locally released neuromodulator in the lobster STG. Thus, our study provides the first direct demonstration of function for an SIFamide isoform in any species.

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