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Biomedical subjects

C E Becker

Publications and source records attributed to C E Becker.

At least 55 records · Page 3Linked to original sources
PubMed1986

Computer searching for occupational medicine.

Occupational and environmental medical literature that confronts a physician is difficult to grasp. The development of the microcomputer makes it easier for the occupational medicine physician to perform computer literature searches. Occupational medical residents and physicians both familiar and unfamiliar with computers submitted identical searches to identify strengths and weaknesses of combinations of computer databases and assisting software. The combination of DIALOG databases and In-Search software were judged to be the most useful for the occupational medicine physician.

Occupational Medicine↗
PubMed1985

Neurotoxic esterase in rooster testis.

Neurotoxic esterase (NTE) is the putative target protein in the nervous system for the initiation of organophosphorus-induced delayed neuropathy. Here it is reported that NTE activity is present in rooster testis. Complete titration of rooster testis phenyl valerate esterases with paraoxon shows that about 15% of the enzymic activity is resistant to paraoxon. NTE activity after complete mipafox titration accounts for 30% of paraoxon-resistant phenyl valerate esterases and corresponds to 7.93 +/- 0.39 nmol/min/mg of protein (mean +/- SD, n = 7). Testis NTE is inhibited in vitro similarly to brain NTE by several organophosphorus compounds. Subcellular fractionation studies of the testis indicate that most NTE activity is particle bound. Testis NTE is also inhibited in vivo by several organophosphorus esters but to a lesser extent than brain NTE. Birds doses with organophosphorus compounds, causing delayed neuropathy, became grossly ataxic, but no testicular pathology was noted by light microscopy in roosters killed 15 days after administration. Serum testosterone levels also measured 15 days after dosing were not different from those of a control group. Recovery of NTE activity was faster in testis than in brain (4 days vs 6 days to recover to 50% of initial activity) in animals that received a high dose of an organophosphorus ester which cause delayed neuropathy.

Animals↗
PubMed1985

The role of cyanide in fires.

Cyanide is a potent and rapidly lethal poison whose clinical and laboratory diagnosis is difficult. Cyanide is released in fire settings involving wool, silk and many synthetic polymers posing a definite risk. Interactions of carbon monoxide released in a fire and cyanide have important physiological consequences. Although the classic mechanisms for the toxicology and antagonism of cyanide have been studied for many years, recent studies have cast doubt as to the mechanism of some of these antagonists. In the fire setting it is not clinically acceptable to administer nitrites to create methemoglobinemia. Cobalt salts are currently too toxic. Oxygen should be administered but there is no proven benefit of hyperbaric oxygen. Oxygen, thiosulfate and hydroxycobalamin are probably the best and safest currently available antidotes to manage this difficult setting. In the future, encapsulated rhodanese enzyme may provide additional rapid therapeutic intervention. It is anticipated that oxygen, thiosulfate and hydroxycobalamin are a safer and more clinically acceptable antidotal combination in the management of cyanide exposure in the fire setting. Our current understanding of combustion toxicology should provide an opportunity to remove building materials and furnishings which pose a cyanide hazard in a fire setting.

Animals↗
PubMed1984

Two fatalities after acute occupational exposure to ethylene dibromide.

A worker collapsed while working inside a tank that was later found to contain residues of ethylene dibromide. He died 12 hours later with metabolic acidosis, depression of the CNS, and laboratory evidence of liver damage. A supervisor attempting to rescue the first victim also collapsed inside the tank and died 64 hours later with intractable metabolic acidosis and hepatic and renal failure. The clinical, pathological, and toxicological findings, as well as results of industrial hygiene sampling, are reported. Pathophysiological mechanisms and possible therapeutic interventions are discussed. The cases demonstrate the extreme hazards of exposure to the highly toxic chemical. The importance of protective work practices wherever there is potential exposure to ethylene dibromide is emphasized.

Adult↗
PubMed1984

Organophosphate polyneuropathy: pathogenesis and prevention.

Organophosphorus-induced delayed polyneuropathy (OPIDP) is initiated by the phosphorylation of a protein neurotoxic esterase (NTE) in the nervous system. A second step, the "aging" of the phosphoryl-enzyme complex, is required to produce the toxic effect. The experimental evidence for this molecular target and the importance of the aging process are reviewed. The catalytic activity of NTE has been used to develop an in vitro screening test that may distinguish the organophosphorus compounds (OPs) that cause neuropathy from those that do not, thereby providing a means for prevention of OPIDP. Moreover, a biochemical screening test, the determination of NTE activity in blood lymphocytes, may predict the development of OPIDP after acute or chronic exposure to OPs, and requires evaluation by carefully designed studies of occupational exposure to OPs.

Animals↗
PubMed1984

Recent advances in occupational cancer.

The contribution of occupational and environmental exposures to the etiology of cancer is a topic of considerable scientific and public interest. If an occupational environmental exposure is associated with cancer in man, then both the exposure and the disease are preventable by appropriate protection. In order to enhance the awareness and timeliness of new information concerning occupational cancer, the University of California, San Francisco, School of Medicine in conjunction with the Northern California Occupational Health Center and the National Institutes of Occupational Safety and Health, the American Cancer Society sponsored a two day meeting in San Francisco at the end of 1983. Five of the presentations are highlighted in this review. In addition, twenty special questions of clinical relevance concerning occupational and environmental cancers are reviewed with the consensus answers given.

Acquired Immunodeficiency Syndrome↗
PubMed1984

The alcoholic patient as a toxic emergency.

The author reviews key physical findings in an alcoholic patient with a toxic emergency, important laboratory tests for alcoholic patients, and management of the intoxicated patient. Also considered are special alcohol toxidromes and other alcohol-related toxic emergencies.

1-Propanol↗
PubMed1984

Alcohol and drug use--is there a 'safe' amount?

All human endeavors are associated with quantifiable risks. Knowledge of the risk is essential for personal health maintenance. Nontherapeutic use of psychoactive drugs poses an important danger to individual persons and society. What are the quantitative estimates of these risks? Are they acceptable?Because the basic mechanism of the toxic effect of alcohol or other drugs is unknown, deciding on acceptable risks is difficult. Based on current information, the recreational abuse of inhalants, hallucinogens, stimulants, narcotics and sedative-hypnotic drugs poses unacceptable individual and societal risks. Groups at special risk should not consume alcohol or any drug unless they are under medical supervision. The threshold for increased morbidity from the regular use of alcohol in adults is in the range of three to five drinks per day; this rises sharply after six drinks per day. The apparent "safe" level of alcohol consumption appears to be one to two drinks per day. Further basic studies are required to refine these risk estimates.

Adult↗
PubMed1983

Methanol poisoning.

Methanol poisoning is an uncommon but an extremely hazardous intoxication. Since methanol is a versatile fuel and is having increasing usage in an energy-conscious society, a high index of suspicion and swift laboratory confirmation is essential in managing this poisoning. Methanol poisoning may occur in sporadic or epidemic circumstances. Chronic exposure may occur in the occupational setting. Man is uniquely susceptible to methanol toxicity, perhaps dependent upon folate metabolism. Classic symptoms of methanol toxicity can only occur in laboratory animals who are rendered folate deficient. Folate may be useful in humans enhancing removal of the toxic products of methanol poisoning. The enzyme responsible for metabolism of methanol is alcohol dehydrogenase. Ethanol has a higher affinity for this enzyme and is preferentially metabolized. Simultaneous ethanol and methanol administration may confuse the onset of the intoxication. Pyrazoles may also be used to inhibit alcohol dehydrogenase thus preventing the intoxication. The most important initial symptom of methanol poisoning is visual disturbance. The symptoms may be delayed up to 24 hours after ingestion due to simultaneous alcohol administration and metabolic processes. Laboratory evidence of severe metabolic acidosis with increased anion and osmolar gaps strongly suggest the clinical diagnosis. There may be an important association between mean corpuscular volume which is significantly higher in cases of severe methanol poisoning than in mild cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Treatment of acute organophosphate poisoning: evidence of a direct effect on central nervous system by 2-PAM (pyridine-2-aldoxime methyl chloride).

Management of acute organophosphate poisoning in man includes rapid treatment with atropine and oximes. Oximes are thought to be unable to enter the central nervous system. We describe a case of parathion poisoning in a 3-1/2 year-old child and the effect of treatment with oxime 2-PAM (34 mg/kg) on EEG activity and clinical symptoms. The prompt improvement of cortical electrical activity documented by EEG could not be explained by any improvement of circulatory or respiratory function and has to be considered a direct effect of oximes on the central nervous system.

Brain↗