Fish collection data for surveys made at 5 localities in Flat Creek, Dawson County GA, on 6 dates that spanned a 4 to 18.5-month period following a catastrophic fish kill caused by a chemical spill near the headwater origin on Flat Creek. The data are: locality descriptions, water depth and velocity measurements made during fish sampling, and tabulated numbers and range in body length of individuals observed, by collection date and locality.

Poisoning may lead to respiratory failure, shock, cardiac arrest, or death. Extracorporeal membrane oxygenation (ECMO) may be used to provide circulatory support, termed venoarterial (VA) ECMO; or respiratory support termed venovenous (VV) ECMO. The clinical utility of ECMO in poisoned patients remains unclear and guidelines on its use in this setting are lacking. To perform a literature search and narrative review on the use of ECMO in poisonings. Additionally, to provide recommendations on the use of ECMO in poisonings from physicians with expertise in ECMO, medical toxicology, critical care, and emergency medicine. A literature search in Ovid MEDLINE from 1946 to October 14, 2020, was performed to identify relevant articles with a strategy utilizing both MeSH terms and adjacency searching that encompassed both extracorporeal life support/ECMO/Membrane Oxygenation concepts and chemically-induced disorders/toxicity/poisoning concepts, which identified 318 unique records. Twelve additional manuscripts were identified by the authors for a total of 330 articles for screening, of which 156 were included for this report. The use of ECMO in poisoned patients is significantly increasing over time. Available retrospective data suggest that patients receiving VA ECMO for refractory shock or cardiac arrest due to poisoning have lower mortality as compared to those who receive VA ECMO for non-poisoning-related indications. Poisoned patients treated with ECMO have reduced mortality as compared to those treated without ECMO with similar severity of illness and after adjusted analyses, regardless of the type of ingestion. This is especially evident for poisoned patients with refractory cardiac arrest placed on VA ECMO (termed extracorporeal cardiopulmonary resuscitation [ECPR]). We suggest VA ECMO be considered for poisoned patients with refractory cardiogenic shock (continued shock with myocardial dysfunction despite fluid resuscitation, vasoactive support, and indicated toxicologic therapies such as glucagon, intravenous lipid emulsion, hyperinsulinemia euglycemia therapy, or others), and strongly considered for patients with cardiac arrest in institutions which are structured to deliver effective ECPR. VV ECMO should be considered in poisoned patients with ARDS or severe respiratory failure according to traditional indications for ECMO in this setting. Patients with pre-existing comorbidities with low expected survival or recovery. Relative contraindications vary based on each center’s experience but often include: severe brain injury; advanced age; unrepaired aortic dissection or severe aortic regurgitation in VA ECMO; irreversible organ injury; contraindication to systemic anticoagulation, such as severe hemorrhage. ECMO may provide hemodynamic or respiratory support to poisoned patients while they recover from the toxic exposure and metabolize or eliminate the toxic agent. Available literature suggests a potential benefit for ECMO use in selected poisoned patients with refractory shock, cardiac arrest, or respiratory failure. Future studies may help to further our understanding of the use and complications of ECMO in poisoned patients.

Protein-Protein, Genetic, and Chemical Interactions for Finkelstein Y (2010):Colchicine poisoning: the dark side of an ancient drug. curated by BioGRID (https://thebiogrid.org); ABSTRACT: Colchicine is used mainly for the treatment and prevention of gout and for familial Mediterranean fever (FMF). It has a narrow therapeutic index, with no clear-cut distinction between nontoxic, toxic, and lethal doses, causing substantial confusion among clinicians. Although colchicine poisoning is sometimes intentional, unintentional toxicity is common and often associated with a poor outcome.We performed a systematic review by searching OVID MEDLINE between 1966 and January 2010. The search strategy included "colchicine" and "poisoning" or "overdose" or "toxicity" or "intoxication."Colchicine is readily absorbed after oral administration, but undergoes extensive first-pass metabolism. It is widely distributed and binds to intracellular elements. Colchicine is primarily metabolized by the liver, undergoes significant enterohepatic re-circulation, and is also excreted by the kidneys. THERAPEUTIC AND TOXIC DOSES: The usual adult oral doses for FMF is 1.2-2.4 mg/day; in acute gout 1.2 mg/day and for gout prophylaxis 0.5-0.6 mg/day three to four times a week. High fatality rate was reported after acute ingestions exceeding 0.5 mg/kg. The lowest reported lethal doses of oral colchicine are 7-26 mg.CYP 3A4 and P-glycoprotein inhibitors, such as clarithromycin, erythromycin, ketoconazole, ciclosporin, and natural grapefruit juice can increase colchicine concentrations. Co-administration with statins may increase the risk of myopathy.Colchicine's toxicity is an extension of its mechanism of action - binding to tubulin and disrupting the microtubular network. As a result, affected cells experience impaired protein assembly, decreased endocytosis and exocytosis, altered cell morphology, decreased cellular motility, arrest of mitosis, and interrupted cardiac myocyte conduction and contractility. The culmination of these mechanisms leads to multi-organ dysfunction and failure. REPRODUCTIVE TOXICOLOGY AND LACTATION: Colchicine was not shown to adversely affect reproductive potential in males or females. It crosses the placenta but there is no evidence of fetal toxicity. Colchicine is excreted into breast milk and considered compatible with lactation.Colchicine poisoning presents in three sequential and usually overlapping phases: 1) 10-24 h after ingestion - gastrointestinal phase mimicking gastroenteritis may be absent after intravenous administration; 2) 24 h to 7 days after ingestion - multi-organ dysfunction. Death results from rapidly progressive multi-organ failure and sepsis. Delayed presentation, pre-existing renal or liver impairment are associated with poor prognosis. 3) Recovery typically occurs within a few weeks of ingestion, and is generally a complete recovery barring complications of the acute illness.History of ingestion of tablets, parenteral administration, or consumption of colchicine-containing plants suggest the diagnosis. Colchicine poisoning should be suspected in patients with access to the drug and the typical toxidrome (gastroenteritis, hypotension, lactic acidosis, and prerenal azotemia).Timely gastrointestinal decontamination should be considered with activated charcoal, and very large, recent (

Protein-Protein, Genetic, and Chemical Interactions for Noguchi C (2019):The NuA4 acetyltransferase and histone H4 acetylation promote replication recovery after topoisomerase I-poisoning. curated by BioGRID (https://thebiogrid.org); ABSTRACT: Histone acetylation plays an important role in DNA replication and repair because replicating chromatin is subject to dynamic changes in its structures. However, its precise mechanism remains elusive. In this report, we describe roles of the NuA4 acetyltransferase and histone H4 acetylation in replication fork protection in the fission yeast Schizosaccharomyces pombe.Downregulation of NuA4 subunits renders cells highly sensitive to camptothecin, a compound that induces replication fork breakage. Defects in NuA4 function or mutations in histone H4 acetylation sites lead to impaired recovery of collapsed replication forks and elevated levels of Rad52 DNA repair foci, indicating the role of histone H4 acetylation in DNA replication and fork repair. We also show that Vid21 interacts with the Swi1-Swi3 replication fork protection complex and that Swi1 stabilizes Vid21 and promotes efficient histone H4 acetylation. Furthermore, our genetic analysis demonstrates that loss of Swi1 further sensitizes NuA4 and histone H4 mutant cells to replication fork breakage.Considering that Swi1 plays a critical role in replication fork protection, our results indicate that NuA4 and histone H4 acetylation promote repair of broken DNA replication forks.