bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma Hydrazine Concentrations in Man after Isoniazid and Hydralazine Administration
Authors: Blair I.A. , Mansilla Tinoco R. , Brodie M.J. , Clare R.A. , Dollery C.T. , Timbrell J.A. , Beever I.A. 
Published: December 2008

1 By using a specific sensitive stable-isotope dilution gas chromatography-mass spectrometry (GC-MS) assay, hydrazine was detected in the plasma of eight healthy male volunteer subjects taking isoniazid (300 mg daily) for 2 weeks.2 Accumulation of hydrazine occurred in slow-acetylator phenotypes.3 Hydrazine was also detected in the plasma of eight out of 14 hypertensive patients treated chronically with hydralazine (200 mg daily).4 However, the concentrations of hydrazine observed were much lower than in the isoniazid study and were close to the limit of detection.5 As hydrazine is hepatotoxic, mutagenic and carcinogenic in animals, its presence in human plasma has important toxicological implications.
Meprobamate Overdosage
Authors: Dennison J. , Edwards J.N. , Volans G.N. 
Published: December 2008

Meprobamate is a non-barbiturate hypnotic/tranquillizer, first used clinically in 1955. One preparation (Tenavoid; Edwin Burgess) contains meprobamate and bendrofluazide and is prescribed for pre-menstrual tension. In adults therapeutic plasma meprobamate concentrations range up to 10 mg/l and unwanted side-effects occur at greater than 40 mg/l. Light coma occurs at 60-120 mg/l and deep coma at 100-240 mg/l (Baselt, 1982). There are no data on toxic plasma concentrations in children. We report two cases of overdosage in children who regained consciousness at times when plasma meprobamate concentrations were greater than 100 mg/l.
Studies on the Possible Central and Peripheral Effects in Man of a Cholinesterase Inhibitor (Pyridostigmine)
Authors: Borland R.G. , Brennan D.H. , Nicholson A.N. , Smith P.A. 
Published: December 2008

1 The effect of a reversible cholinesterase inhibitor (pyridostigmine: 30 mg, 8-hourly for 3 days) on psychomotor performance and visual function and on the electrical activity of the brain was studied in healthy man. 2 It was not possible to detect any change during the six individual experimental sessions over the 3 days, but with pooling of the data there was a drug effect. The threshold for detection of a flickering light was increased and less responses were missed on a dynamic visual-acuity task. Visuo-motor coordination was impaired. 3 The observations were consistent with the known activity of the drug and suggest an increase in central arousal and minimal alteration in motor coordination.
Screening the in vitro Sperm-immobilizing Effect of some Anticancer Drugs
Authors: Hong C.Y. , Chiang B.N. , Ku J. , Wu P. 
Published: December 2008

1 The in vitro sperm-immobilizing effect of seven anticancer agents, namely cyclophosphamide, 5-fluorouracil, cytarabine, mitomycin-C, 6-mercaptopurine, doxorubicin and vinblastine were screened with a transmembrane migration method. 2 Only doxorubicin and vinblastine inhibited human sperm motility. 3 Because colchicine, a microtubular inhibitor, had no sperm-immobilizing effect, we suggest that the sperm membrane is the site of action of these two anticancer drugs to inhibit human sperm motility.
Use of DTPA for Increasing the Rate of Elimination of Plutonium-238 and Americium-241 from Rodents after their Inhalation as the Nitrates
Authors: Stather J.W. , Stradling G.N. , Gray S.A. , Moody J. , Hodgson A. 
Published: December 2008

This study has shown that: 1 both inhaled (2 μmol/kg) and injected (30 μmol/kg) diethylenetriaminepentaacetic acid (DTPA) can reduce the lung deposit of 238Pu and 241 Am inhaled as nitrate to about 1% of that in untreated controls; 2 injection of DTPA is more effective than aerosolized DTPA for reducing deposits of 238 Pu and 241Am in the liver and skelton; 3 combined treatment involving early inhalation of DTPA followed by repeated intravenous injections is likely to be the most effective treatment for workers who have accidentally inhaled plutonium and americium nitrates.
4-Dimethylaminophenol and Dicobalt Edetate (Kelocyanor) in the Treatment of Experimental Cyanide Poisoning
Authors: Marrs T.C. , Swanston D.W. , Bright J.E. 
Published: December 2008

1 The efficacy of dicobalt edetate (Kelocyanor) was compared against that of 4-dimethylaminophenol (DMAP) in experimental cyanide poisoning. 2 DMAP gave better survival. 3 The efficacy has been related to the toxicity of the two compounds.
HPLC Method for Determination of Ergot Alkaloids and Some Derivatives in Human Plasma
Authors: Žorž M. , Culig J. , Kopitar Z. , Milivojevic D. , Marušič A. , Bano M. 
Published: December 2008

1 Ergot alkaloids and their dihydrogenated methanesulphonate (ms) salts were determined and measured in human plasma. 2 High-performance liquid chromatography (HPLC) with fluorometric detection was used for separation of ergot alkaloids in plasma. 3 Several ergot alkaloids and their derivatives, including lysergide (LSD), can be identified in cases of poisoning.
Seasonal Variation and Recurring Peaks of Reported Poisonings During a 3-year Period
Authors: Eskola J. , Poikolainen K. 
Published: December 2008

1 Seasonality of poisonings was studied among 28 692 cases reported during the years 1980-1982 in Finland with special reference to recurring peak months over years. Poisonings predominated in the summer. For all age-groups peaks of envenomations, plant poisonings and pesticide poisonings recurred between June and September. 2 Among children aged 0-6 years, there were in addition recurrent peaks in poisonings by tobacco between June and August, by corrosive agents in September and by vitamins, trace elements and external medicines in October. Among children aged 7-15 years, fertilizer poisonings peaked recurrently in August. Among adults, poisonings by petroleum products peaked recurrently in July and December, psychopharmacologic drugs in July and October, paints, glues and plastics in November, alcohols in December and antimicrobial drugs in August and October. 3 Of all poisonings, 33% occurred in July, August or September in contrast to the expected 25%. Preventive efforts should thus be intensified during the summer.
Survival after Massive Ingestion of Carbon Tetrachloride Treated by Intravenous Infusion of Acetyleysteine
Authors: Mathieson P.W. , Williams G. , MacSweeney J.E. 
Published: December 2008

1 A 61-year-old man ingested a large amount of carbon tetrachloride, well in excess of the adult lethal dose.2 The level of the compound was assayed in his blood and the levels were the highest ever recorded by the Guy's Hospital Poisons Unit.3 He was treated by intravenous infusion of acetylcysteine and survived with relatively mild clinical and biochemical evidence of toxicity.4 Possible reasons for his survival are discussed, as are the implications for the management of future cases.
A Study on the Neurotoxicity of Broxyquinoline and Brobenzoxaldine Combination in Therapeutic Doses
Authors: Swain R. , Bapna J.S. , Das A.K. , Chandrasekar S. , Swaminathan R.P. , Bosco B. , Veliath S. , Thombre D.P. 
Published: December 2008

1 The neurotoxicity of a combination of broxyquinoline and brobenzoxaldine (Intestopan Forte, containing 500 mg and 100 mg of the drugs respectively per capsule) was investigated by prospective clinical and electrophysiological studies in patients and volunteer subjects given the drugs in therapeutic doses (two capsules three times a day for 5 days). 2 Of 16 patients with intestinal amoebiasis given the drugs (study A), 13 (81.25%) were cured. Adverse effects were mild and did not affect treatment. No neurological adverse effect was reported. Neurological examinations revealed no abnormality in any patient after treatment. 3 Seven volunteer subjects underwent medical, neurological and ophthalmological examinations, and electrophysiological studies of ulnar and peroneal nerve conduction before and after treatment with the drugs in therapeutic doses (study B). Transient parasthesiae were reported by one subject on the fourth day of treatment. No medical, neurological or ophthalmological abnormality was detected in any subject after treatment. There was no significant change in motor nerve conduction velocities. There was a significant (P<0.001) increase in the stimulus strength for distal ulnar stimulation and a significant (P<0.01) decrease in stimulus duration for proximal and distal ulnar stimulation. No significant changes were seen in the peroneal nerves in these parameters. No qualitative abnormality was seen in the oscilloscopic patterns of nerve conduction after treatment. 4 Literature on the neurotoxicity of the halogenated hydroxyquinolines is reviewed. 5 It is concluded that broxyquinoline and brobenzoxaldine (and probably other halogenated hydroxyquinolines as well) are safe and effective in therapeutic doses; neurotoxicity is unlikely to occur when these drugs are used according to therapeutic recommendations.
Impairment of Exercise Tolerance due to Broxyquinoline-Brobenzoxaldine Combination
Authors: Swain R. , Bapna J.S. 
Published: December 2008

1 A case report of impaired exercise tolerance during administration of broxyquinoline-brobenzoxaldine combination in therapeutic doses is presented. 2 The first author of this paper, a 28-year-old healthy male, volunteered as a subject for a prospective study on the neurotoxicity of halogenated hydroxyquinolines and took a course of broxyquinoline-brobenzoxaldine combination. 3 The author, who is a karate enthusiast, observed impairment of exercise tolerance during the course of treatment with the drugs. 4 A challenge course of treatment with the same drugs in the same doses produced similar effects. 5 Since halogenated hydroxyquinolines are still used widely in many countries, such an adverse effect would be of practical relevance, particularly in asymptomatic cyst-passers of Entamoeba histolytica whose occupations involve physical labour.
Choice Reaction Time in Workers Exposed to Styrene Vapour
Authors: Mackay C.J. , Kelman G.R. 
Published: December 2008

1 Behavioural effects of occupational exposure to vapour from styrene-based resin were investigated in 10 female workers with a portable test of choice reaction time. Testing was carried out both at the beginning and end of the day's shift. 2 Uptake and metabolism of styrene were assessed by monitoring post-shift urinary mandelic acid excretion rates. By using these data workers were allocated to three groups reflecting zero, low )r high exposure. 3 After exposure slowing of reaction times was found in those with the highest mandelic acid excretion rates, whereas a slight improvement or no change was found in those with low or zero exposure. 4 Subsequent improvements in extraction and ventilation in the workroom were shown to be associated with both decreased mandelic acid excretion and absence of long reaction times in those previously most heavily exposed.
Asthma and Rhinitis after Exposure to Glutaraldehyde in Endoscopy Units
Authors: Corrado O.J. , Osman J. , Davies R.J. 
Published: December 2008

1 Four nurses working in endoscopy units complained of respiratory symptoms on exposure to alkaline glutaraldehyde used as a disinfectant for fibre-optic endoscopes. 2 A provocation test was positive in two of these patients. 3 This is the first report to use provocation testing to confirm a relation between exposure to alkaline glutaraldehyde and respiratory disease.
Uses and Usefulness of Paraquat
Authors: Sagar G.R. 
Published: December 2008

1 Paraquat was discovered in 1955 and introduced to the market place in 1962. During the 23 years between introduction and the present day numerous successful practical uses of the herbicide have been developed. In addition the characteristics of the chemical have allowed significant changes to be made in the ways that some crops are grown. 2 Paraquat is a relatively non-selective foliage-applied contact herbicide. It is inactivated on contact with almost all naturally occurring soils and it was this property, perhaps above all others, that provided the greatest breakthrough in chemical weed control at the time of its discovery. 3 Inactivation on contact with soil means that no biologically active residues remain in the soil, thus allowing planting or sowing to be carried out almost immediately after spraying. Although the non-systemic (contact) property of paraquat makes it less than ideal for the long-term control of perennial weeds, the same property is of real advantage when parts of crop plants are sprayed accidentally, for usually only the part receiving the spray is affected. 4 Total annual usage of all herbicides in agriculture and horticulture in England and Wales, UK, over the period of 1980-1983 has been estimated at 26 360 tonnes used on 12 402 x 103 ha (1 hectare = 1 x 104 m2). For paraquat (not including its mixtures with diquat and monolinuron) 270 tonnes were sprayed over 392 218 ha/year. It is estimated from sales records that in Europe 5 x 106 ha are sprayed annually with paraquat. 5 The paper reviews the need for the use of herbicides and the properties that are important for particular crop-weed situations, but concentrates on the properties of paraquat that make it an essential agent of weed control in many areas of agriculture, horticulture and forestry.
Mechanism of Paraquat Toxicity in Lung and its Relevance to Treatment
Authors: Smith L.L. 
Published: December 2008

1 The symptoms of paraquat poisoning depend largely on the amount of compound consumed, although in many cases the most characteristic feature of poisoning is lung damage, causing severe anoxia which leads to death. 2 Studies in experimental animals have demonstrated that paraquat produces an acute damaging phase in the lung, followed by a reparative phase dominated by an extensive fibrosis. The latter is a major contributor to the lung lesion that causes anoxia. The specific toxicity in the lung can be explained in part by the selective accumulation of paraquat into this organ in comparison with other tissues. The accumulation is energy-dependent and probably specific to certain lung cells. 3 It is now known that paraquat is accumulated into the lung by a recently described diamine transport process located in the alveolar epithelial cells and the Clara cells of the airways. When accumulated, paraquat undergoes a NADPH-dependent one-electron reduction to form its free radical which almost instantly reacts with molecular oxygen to reform the cation and concomitantly produce superoxide anion. This species of oxygen radical can contribute to the formation of more toxic species of radical which may directly damage vital cellular constituents. 4 Paraquat has been shown to stimulate rapidly the pentose phosphate pathway and inhibit the synthesis of fatty acids in the lung in a dose-dependent manner. In addition there is a rapid increase in the pulmonary levels of mixed disulphides and the eventual reduction of NADPH levels in the lung. 5 These results are consistent with the suggestion that paraquat causes a rapid and pronounced oxidation of NADPH which initiates compensatory biochemical responses in the lung. 6 With toxic levels of paraquat the compensatory biochemical processes are insufficient to maintain levels of NADPH consistent with cell viability. Thus, cell death may result from NADPH depletion, or the loss of this vital co-factor may render the lung more susceptible to free-radical attack and thereby peroxidation of vital cellular constituents.
Paraquat Poisoning: The Rationale for Current Treatment Regimes
Authors: Davies D.S. 
Published: December 2008

1 The critical events leading to death from the ingestion of paraquat are absorption from the gastrointestinal tract, active accumulation in the lung almost certainly preceded by acute renal failure and redox cycling in the lung which initiates certain, as yet unidentified, biochemical events leading to cell death with subsequent destruction of the lung and death from anoxia. 2 Present evidence suggests that absorption of paraquat is rapid and the use of adsorbents more than 6 hours after ingestion is likely to be ineffective. Further work is needed to characterize the mechanism of absorption and to identify an innocuous chemical which could be added to formulations of paraquat to inhibit absorption; this approach may be the best solution to the problem of paraquat poisoning. 3 Steps to actively remove paraquat from the systemic circulation will probably only succeed in a small number of patients taking moderate doses and developing early renal failure. The 'window' for such treatment may be as narrow as 6-18 h after ingestion. This 'window' would also operate for chemicals designed to inhibit the pulmonary uptake of paraquat. 4 The biochemical events leading to paraquat-induced cell death are not sufficiently defined to permit the design of treatments to prevent or reverse these processes.
Paraquat poisoning: clinical features and immediate general management
Authors: Vale J.A. , Meredith T.J. , Buckley B.M. 
Published: December 2008

1 In contrast to 10-15 years ago most cases of paraquat poisoning are now due to deliberate self-poisoning with parasuicidal or suicidal intent rather than to accidental ingestion. Less commonly, poisoning may follow careless handling of paraquat during occupational use. Although paraquat can be absorbed through the skin if improperly handled, poisoning usually follows ingestion and has rarely been reported after subcutaneous, intravenous or intraperitoneal injection. 2 Clinically, three degrees of intoxication may be distinguished. (a) Mild poisoning occurs after the ingestion or injection of less than 20 mg of paraquat ion/kg body weight. In these cases patients are either asymptomatic or symptoms are confined to the gastrointestinal system. All patients recover fully. (b) Moderate to severe poisoning usually follows the ingestion (rarely injection) of 20-40 mg of paraquat ion/kg body weight. Non-specific symptoms of ill health together with local gastrointestinal symptoms precede the development of renal failure (which may recover spontaneously) and pulmonary fibrosis which may not be manifest for days or weeks. Death occurs in the majority of cases but is usually delayed for 2-3 weeks. (c) Acute fulminant poisoning follows the ingestion of substantial quantities of paraquat (> 40 mg of paraquat ion/kg body weight). In addition to local symptoms, multiple organ (cardiac, respiratory, hepatic, renal, adrenal, pancreatic, neurological) failure occurs. Death may supervene within hours and is never delayed for more than a few days. 3 Initial general management has four priorities. Firstly, fluid loss should be replaced; secondly, the prognosis should be determined by measurement of the plasma paraquat concentration; thirdly, symptoms due to ulceration of the oropharynx must be relieved; fourthly, supportive care for patients and relatives must be provided. 4 Experience suggests that management of the terminally ill patient with acute fulminant poisoning is a far greater clinical challenge to medical and nursing expertise than simply the employment of methods to prevent absorption or increase elimination of paraquat.
Treatment of Paraquat Poisoning in Man: Methods to Prevent Absorption
Authors: Meredith T.J. , Vale J.A. 
Published: December 2008

Theoretically, absorption of an ingested dose of paraquat may be reduced by (1) gastric lavage, (2) induced emesis, (3) whole-gut lavage or (4) by the oral administration of adsorbent substances. 1 Animal experiments suggest that paraquat is absorbed poorly from the stomach and absorbed incompletely (< 5%) from the small intestine over a 1-6-h period. Although gastric lavage would therefore seem a logical way to ameliorate the toxicity of an ingested dose of paraquat, peak plasma concentrations are attained rapidly and evidence for the efficacy of gastric lavage in man is poor. 2 In 1977, a potent emetic (PP796) was added to liquid and solid formulations of paraquat because experiments in primates had demonstrated a fivefold reduction in toxicity. In man, ingestion of formulations containing an emetic is more likely to cause spontaneous vomiting within 30 min than non-emetic preparations. However, definite evidence of benefit, as judged by improved patient prognosis, has yet to be established. 3 Gut lavage has been shown to remove only a small proportion of an ingested dose of paraquat. At the flow rates employed in man (75 ml/min), approximately 0.5-1.0 litres of lavage fluid/h may be absorbed across the intestinal wall. Since there is a theoretical risk of increasing paraquat absorption, the use of whole-gut lavage cannot be recommended. 4 Bipyridilium herbicides are adsorbed by soil and clay minerals, and montmorillonite in particular has been shown to be a strong binding agent in vitro. Accordingly, the use of Fuller's Earth (calcium montmorillonite) and Bentonite (sodium montmorillonite) for the treatment of poisoning has been investigated in animal models. Both agents reduce plasma paraquat concentrations and mortality in animals when administered after an oral dose of paraquat. Recently, other adsorbent materials have been found to have high maximum adsorption capacities for paraquat. In particular, activated charcoals and cation-exchange resins have attracted interest. Unfortunately, as yet, there is no evidence that the use of adsorbents in man is of therapeutic value.
Prognostic Value of Plasma and Urine Paraquat Concentration
Authors: Scherrmann J.M. , Houze P. , Bismuth C. , Bourdon R. 
Published: December 2008

1 A non-exponential mathematical equation was used to extrapolate the 'predictive line' for plasma paraquat concentrations beyond 24 h. Plasma paraquat concentrations were measured in 30 patients who were admitted more than 24 h after overdose. The extrapolated line accurately predicted the outcome in 27 of these 30 patients. 2 Urine paraquat concentrations were measured in 53 patients. All patients with urine paraquat concentrations of less than 1 mg/l (colourless or light blue test result using the colorimetric test) within 24 h of overdose survived. In contrast, patients with urine paraquat concentrations of more than 1 mg/l had a high probability of death. 3 Even if plasma paraquat concentrations have a higher predictive value, urine data may contribute to a more rapid evaluation of prognosis.
Poisoning with Dextropropoxyphene in Denmark
Authors: Segest E. 
Published: December 2008

The sale of dextropropoxyphene is rising in Denmark, and the number of both fatal and non-fatal cases of poisoning with dextropropoxyphene is similarly rising. A total of 124 fatal and 297 non-fatal hospitalized cases of poisoning caused by dextropropoxyphene were reported to the National Board of Health in 1984. These figures are judged to be minimum figures. There is an accumulation of cases in the municipality of Copenhagen as compared to the remainder of the country. Cases of poisoning with dextropropoxyphene occur more frequently in socially and mentally encumbered groups. It is often difficult to determine with certainty the method of poisoning, but it is considered that the distribution is roughly one-third suicide or attempted suicide, about the same from accidental or simple over-dosage, while the remainder are uncertain. It is judged that the number of suicides or attempted suicides in normal persons is small, while the numbers in persons not entirely normal or carried out as an impulsive act are considerably higher. Other intoxicants, most frequently alcohol, have in more than one half of the cases been consumed together with dextropropoxyphene. The mortality rate for those cases reaching medical aid has been found to be 3.6% which is lower than the figure reported in other investigations. Very many of the cases of poisoning, however, are fatal at the time of discovery. Serious sequelae after non-fatal cases of poisoning are extremely rare. The steps being taken by the National Board of Health to reduce the number of cases of poisoning are mentioned, and the possibilities of reducing the number of cases are also discussed.