China
Africa
Explore chapters and articles related to this topic
Garcinia xanthochymus Hook. f. ex T. Anderson: An Ethnobotanically Important Tree Species of the Similipal Biosphere Reserve, India
Published in Jayanta Kumar Patra, Gitishree Das, Sanjeet Kumar, Hrudayanath Thatoi, Ethnopharmacology and Biodiversity of Medicinal Plants, 2019
Rajkumari Supriya Devi, Subhendu Chakroborty, Sanjeet Kumar, Nabin Kumar Dhal
Test for Tannin: 0.7 ml of the extract was taken in test tube with dissolution in 50ml of DI water and was heated for 10 minutes. After cooling few drops of 1%, ferric chloride was added. Color of sample changed from light to dark creamy precipitate.
Models of Focal Epilepsy in Rodents
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
The usual amount of ferric chloride to produce epileptic discharges appears to be in the order of 5 μl of a 100 mM solution of FeCl3.27 The solution is applied to a small area of the cerebral cortex exposed following surgery, as described above for cobalt. The dura and pia mater are punctured to allow the direct instillation to the cerebral cortex. The solution is administered slowly (0.5 μl/min) via a syringe. Rats prepared similarly, but that, instead of receiving the iron salt, have received a solution of physiological saline, also slowly administered, serve as controls.
Glycerine Analysis
Published in Eric Jungermann, Norman O.V. Sonntag, Glycerine, 2018
FCC and USP standards call for comparison of glycerine colors with aqueous ferric chloride solution. Typically, a concentrated solution of ferric chloride is made by dissolving excess ferric chloride hexahydrate in 25 volumes of hydrochloric acid and 975 volumes of water. The ferric chloride concentration is calculated iodometrically after appropriate dilution, addition of iodide, and titration of the iodide with thiosulfate. The solution is then diluted with 25 volumes of hydrochloric acid and 975 volumes of water to correspond exactly to 45.0 g/L of ferric chloride.
Ferric chloride ingestion with corrosive gastritis
Published in Clinical Toxicology, 2022
Mark Pucci, Pavlos Theodorou, Neel Patel
Ferric chloride, or iron (III) chloride (FeCl3), is a compound with industrial uses including copper etching and water treatment. It forms a strongly acidic solution with high iron content, and therefore has the potential for severe toxicity to humans, although oral ingestions are rare. A retrospective study which included 13 cases of accidental or intentional oral ingestion of ferric chloride found major symptoms and signs were: nausea and vomiting, sore throat, abdominal pain, oral ulceration, metabolic acidosis, aspiration pneumonia, respiratory failure, diarrhea, and hypotension [1]. Common laboratory findings include leucocytosis, metabolic acidosis, coagulopathy, and elevated serum iron concentration [1,2]. Direct corrosive effects can lead to gastrointestinal tract ulceration and inflammation, with perforation and necrosis in severe cases [1–3]. Desferrioxamine as an iron chelating agent may be indicated if there are features of severe iron toxicity, but supportive care and management of complications remain the mainstay of treatment [1].
How useful are ferric chloride models of arterial thrombosis?
Published in Platelets, 2020
Steven P. Grover, Nigel Mackman
Additional studies have demonstrated that ferric chloride exposure can lead to aggregation of erythrocytes and platelets independently of the endothelial surface [9]. In an in vitro microfluidic system exposure of washed erythrocyte or platelets to ferric chloride under flow was sufficient to induce aggregation and accumulation on a non-endothelialized chamber surface [9]. Moreover, in this microfluidic system ferric chloride exposure induced plasma protein agglutination [9]. The ability of ferric chloride to rapidly induce aggregation of cells and proteins suggests that a physiochemical mechanism is likely involved. Indeed, ferric chloride is a flocculant, a chemical species that facilitates binding of molecules, that is used in chemical processes to remove suspended impurities [10].
Salicylate toxicity after undetectable serum salicylate concentration: a retrospective cohort study
Published in Clinical Toxicology, 2019
Michael J Moss, J Ashton Fisher, Tara A Kenny, Allison C Palmer, John A Thompson, Hannah Wolfer, Robert G Hendrickson
Several cases of salicylate toxicity with initially undetectable [ASA] have been reported. Kaufman reported an 18-month female who ingested 10 to 15 tablets of a delayed release aspirin, paramethasone, and propoxyphene product. Serum [ASA] was undetectable at 4 h but at 16 h a repeat urine ferric chloride test was positive and [ASA] was 33 mg/dL [8]. Wortzman described a 22-year-old male who ingested 88 tabs of 325 mg delayed release aspirin. [ASA] at 1 and 3 h were undetectable [11]. At 7 h [ASA] was 13.3 mg/dL and peaked at 35.8 mg/dL at 24 h after ingestion. Elko reported a 12-year-old female who ingested an unknown quantity of enteric coated aspirin 325 mg [6]. [ASA] was <2.8 mg/dL at 2 h and peaked at 34 mg/dL 20 h after ingestion. Herres reported a 53-year-old male who ingested 200 tablets of 325 mg aspirin [7]. Approximately 45 min after ingestion [ASA] was undetectable but was elevated to 33 mg/dL at 3 h. He was transferred to a psychiatric ward and ultimately died 20 h after ingestion with a peak [ASA] of 128 mg/dL. Grandey reported 13 cases of initial [ASA] that were <10 mg/dL but not necessarily undetectable [12]. They do specifically report one patient with an undetectable [ASA] that later peaked at 54.8 mg/dL though further detail is not available beyond an abstract. These authors hypothesized several factors that could contribute to delayed detection and absorption of salicylates such as enteric coated or delayed release preparations, ingestion of agents delaying gastric emptying, pylorospasm, pharmacobezoar formation, or repeated ingestions while under medical care and after initial blood draws.