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Biomedical subjects

A Poklis

Publications and source records attributed to A Poklis.

At least 91 records · Page 5Linked to original sources
PubMed1983

Tissue mineral levels in victims of sudden infant death syndrome II. Essential minerals: copper, zinc, calcium, and magnesium.

Deficiencies of various vitamin and minerals per se have been suggested as possible causes of sudden infant death syndrome (SIDS). Further, a deficiency of essential minerals may lead to enhanced toxicity of toxic elements, in particular, lead and cadmium to explore the possibility of mineral deficiencies or interactions with the toxic metals, lead and cadmium, lung, liver, kidney, and rib specimens were obtained at autopsy from 66 SIDS infants and 23 infants who died suddenly from other cases. Tissue copper, zinc, calcium, and magnesium were measured by atomic absorption spectroscopy. No differences were found between SIDS and non-SIDS for any element in any tissue except for more magnesium in the liver (P less than 0.0001) and less copper in the lungs (P less than 0.02) in the SIDS group. Only sporadic interactions between toxic and essential elements could be found. We found no evidence of any essential mineral deficiencies per se or significant interactions of essential and toxic minerals that might potentiate the effects of toxic metals. The physiologic significance, if any, of the higher liver magnesium and lower lung copper found in SIDS is unclear.

Cadmium↗
PubMed1983

A fatal case of theophylline intoxication.

A fatal case of theophylline intoxication is presented in which a number of factors leading to a decrease in theophylline clearance and the patient's death were possibly operative. These included advanced age, chronic lung disease, liver disease, and administration of cimetidine. Since early symptoms of the toxic effects of theophylline can mimic peptic ulcer disease, cimetidine might be prescribed for the gastrointestinal symptoms with subsequent worsening of theophylline poisoning. Theophylline plasma concentration should be determined whenever drugs affecting theophylline clearance are administered simultaneously.

Aged↗
PubMed1982

Determination of pentazocine and tripelennamine in blood of T's and Blue addicts by gas-liquid chromatography with a nitrogen detector.

A procedure for the quantitative determination of pentazocine (T's) and tripelennamine (Blues) in blood obtained from T's and Blues addicts is described. The underivatized drugs were analyzed by gas-liquid chromatography with a nitrogen detector. The retention times relative to mepivicaine (internal standard) on OV-17 at 220 degrees C were: tripelennamine 0.69 and pentazocine 1.77. The linear ranges of blood standards were: tripelennamine, 0.10-1.00 microgram/ml; pentazocine, 0.50-5.0 microgram/ml. For simultaneous analysis, the within-run and between-run CVs of tripelennamine were 5.6% (n = 23) and 13% (n = 12); and for pentazocine 5.2% (n = 23) and 9.9% (n = 12). Mean recoveries over the range of standards were: tripelennamine, 103% +/- 2.5% (n = 12); pentazocine 77.8% +/- 3.6% (n = 12).

Chromatography, Gas↗
PubMed1982

The effect of inorganic lead on heptic biochemical and ultrastructural changes produced by phenobarbital.

Lead acetate (105 mumol/kg, i.p.) decreased rat hepatic cytochrome P-450 to 57% and 63% of control values when measured 24 and 48 h after lead administration, respectively. A large increase in urinary delta-aminolevulinic acid (U-ALA) was observed after lead treatment, indicating a depression of heme synthesis. In addition, lead treatment produced dilated cisternae of the smooth endoplasmic reticulum (SER). Phenobarbital (100 mg/kg, i.p.) produced an induction of cytochrome P-450, proliferation of the SER, and did not alter U-ALA content. Simultaneous lead and phenobarbital treatment produced a delayed but robust induction of cytochrome P-450, only a moderate rise in U-ALA, and a reduced proliferation of the SER of hepatocytes. Therefore, phenobarbital, an inducer of heme synthetic enzymes, is apparently capable of reversing lead-induced inhibition of heme synthesis as measured by hepatic cytochrome P-450 induction and U-ALA content.

Aminolevulinic Acid↗
PubMed1982

Evaluation of a modified alcohol dehydrogenase assay for the determination of ethanol in blood.

We evaluated a new alcohol dehydrogenase (EC 1.1.1.1) enzymic assay (ADH-glycine, Sigma Chemical Co.) for the determination of ethanol in blood. This assay differs from the manufacturer's previous assay (ADH-pyrophosphate) in that glycine replaces pyrophosphate as the buffer and hydrazine replaces semicarbazide as the trapping agent. The standard curve for the assay was linear over blood ethanol concentrations of 0.50-5.00 g/L. The reaction time of the assay was 10 min. At 1.00 g/L within-run and between-run CVs were 3.96% (n = 20) and 4.01% (n = 20), respectively. Mean analytical recovery of ethanol added to whole blood at 0.50-5.00 g/L was 99.7% (SD 2.6%). We performed 100 consecutive clinical and forensic determinations by the ADH-glycine assay, the ADH-pyrophosphate assay, and gas chromatography. Correlation coefficients of the results by least-square linear regression were 0.995 for ADH-pyrophosphate vs ADH-glycine, and 0.990 for gas chromatography vs ADH-glycine. The major advantage of the ADH-glycine assay over the ADH-pyrophosphate assay is the shorter reaction time, 10 min vs 30 min.

Alcohol Dehydrogenase↗
PubMed1982

A fatal methocarbamol intoxication.

A fatal methocarbamol intoxication is presented. Significant toxicologic findings were blood concentrations of 525 mg/L methocarbamol and 140 mg/dL ethanol. Analysis was by thin-layer, gas-liquid, and high pressure liquid chromatography. Toxicology data relevant to the interpretation of case findings are discussed.

Adult↗
PubMed1982

Evaluation of medicolegal investigators' suspicions and positive toxicology findings in 100 drug deaths.

The performance of trained medicolegal investigators was evaluated in 100 consecutive drug deaths, which occurred from January 1978 to May 1980 in St. Louis City and County. Carbon monoxide deaths were excluded from the study. The toxic agent responsible for death, as indicated by scene investigators and the decedent's drug history, was compared to the actual toxicology laboratory findings. In 84 of the cases, the toxicant was correctly indicated by the investigators. In the remaining 16 cases, 12 were suspected to be drug deaths but the major toxicant was not indicated, and in 4 cases no drugs were suspected. The manner of death had no influence on the investigators' performance. This study demonstrates the value of trained medicolegal investigators in providing helpful information to the pathologist and toxicologist before autopsy and laboratory analyses in cases of drug deaths.

Adult↗
PubMed1981

Drug deaths in St. Louis City and County: a brief survey, 1977-1979.

The vast majority of drug deaths in St. Louis City and County through 1977-1979 were of adults who ingested multiple drugs with suicidal intent. In this 3-year survey, seven deaths were due to accidental overdose of ethanol, seven to "over-the-counter" products or laboratory reagents, eight from "classic poisons," and only eight to drug abuse. The remaining 117 deaths (80%) resulted from ingestion of legally obtained prescription drugs. Sixty-two percent of all deaths were due to multiple drug administration. Only one child was fatally poisoned. Barbiturates, benzodiazepines, ethanol, propoxyphene, and tricyclic antidepressants were the most common agents encountered.

Anti-Anxiety Agents↗
PubMed1981

Treatment of massive phenobarbital overdose with dopamine diuresis.

We report a case of severe phenobarbital sodium overdose with a peak plasma concentration of 253 microgram/mL, normally considered fatal. The patient was successfully treated with forced alkaline diuresis. Treatment was unusual in that dopamine hydrochloride was used to sustain the diuresis.

Diuretics↗
PubMed1981

Estimation of the amount of drug absorbed in acetaminophen poisoning: a case report.

A case of acute acetaminophen overdose has been presented in which good agreement between the observed and the calculated urinary excretion of acetaminophen was obtained using the pharmacokinetic model of Prescott et al (1). This case exemplifies the application of pharmacokinetic principles in the determination of the actual amount of drug absorbed in instances of drug overdose.

Absorption↗
PubMed1980

Binding of gold to bovine serum albumin using flameless atomic absorption.

A graphite furnace atomic absorption spectrophotometric assay capable of accurately determining nanogram amounts of gold in biological fluids was developed. The presence of bovine serum albumin and/or phosphate in the sample reduced the method sensitivity without affecting the linear response. Binding of gold was studied by ultrafiltration using cones with a molecular weihght cutoff of 25,000. The binding of gold at various concentrations to 2 and 4% bovine serum albumin in 0.1 M phosphate buffer, pH 7.4, was independent of the gold and protein concentrations. In the 2-10 microgram/ml range, the overall binding values (mean +/- SD) of gold to 2 and 4% bovine serum albumin were 98 +/- 1.6 (n = 35) and 99 +/- 1.0% (n = 15), respectively. When ultrafiltration cones with a molecular weight cutoff of 50,000 were used, the extent of binding to 2% bovine serum albumin was 85.4 +/- 1.6% (n=11). This statistically significant difference (p less than 0.001) was due to variations in the protein retention of the two cone types. Interaction studies showed that gold was not displaced from the binding sites by salicylic acid (200 microgram/ml) or vice versa.

Animals↗
PubMed1980

Current trends in the abuse of pentazocine and tripelennamine: the metropolitan St. Louis experience.

A discussion of the intravenous use by narcotic addicts in metropolitan St. Louis of a combination of pentazocine and tripelennamine, known as "T's and blues," is presented. The folklore and ritual of "T"'s and blues" use were gleaned from interviews with addicts. The cause of, possible adverse reactions to, and medical examiners' experience with this new mode of drug abuse are discussed. Pharmacology relative to the abuse of pentazocine and tripelennamine is reviewed.

Drug Combinations↗
PubMed1979

Fatal intoxication from 3,4-methylenedioxyamphetamine.

The symptoms of MDA intoxication exhibited by the decedent prior to death closely mimic those of acute amphetamine poisoning: profuse sweating, violent and irrational behavior, and stereotypically compulsive behavior. Therefore, if amphetamines are not detected in specimens from a person displaying classic symptoms of amphetamine poisoning, hallucinogenic amphetamine derivatives may be considered. In the case described, a divided dose of 850 mg of MDA ingested within 2 h and 15 min was sufficient to cause the death of a 24-year-old male, 4 h after the final dose. While the methaqualone may have contributed to the demise of the decedent, the authors think that the MDA itself was sufficient to cause death. Results of limited recovery studies of MDA extraction from blood and elution from TLC plates supported the observations of Cimbura [13]. Approximately 85% of MDA is extracted by the method described and its elution from TLC plates is quantitative. This case points out once again the dangers of false advertising in the illicit market. The decedent, himself a dealer in the illicit drug market, and all present at the party believed the ingested white powder to be a mixture of morphine, LSD, and amphetamine, hence MDA. They were totally unfamiliar with 3,4-methylenedioxyamphetamine, MDA.

3,4-Methylenedioxyamphetamine↗