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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our previous studies have shown that a phagocytic challenge with IgG-coated erythrocytes (EIgG) depressed macrophage triggered H2O2 production in vitro, and in vivo there was a decrease in the survival rate following bacteremia. The phagocytosis of an equal number of IgG-coated erythrocyte ghosts had none of these effects, indicating that the contents of the erythrocytes are important for these effects. The present study evaluated the role of the scavengers of reactive oxygen intermediates within erythrocytes in the depression of H2O2 production triggered with phorbol myristate acetate following a phagocytic challenge with EIgG. Elicited rat peritoneal macrophages (PM) were challenged with EIgG prepared from normal E or E with inactivated catalase, depleted glutathione, hemoglobin converted to methemoglobin, or fixed with formaldehyde. The depression of triggered H2O2 production was similar when equal numbers of normal EIgG and EIgG with inactivated scavengers were phagocytized. When the phagocytic challenge with normal EIgG was carried out in the presence of cytochalasin B, no depression of triggered H2O2 production was observed. Cytochalasin B partially blocked the phagocytosis of EIgG, so that with larger doses of EIgG there was sufficient ingestion of EIgG to depress H2O2 production in untreated PM. These results indicate that the scavengers of reactive oxygen intermediates present in erythrocytes are neither required nor sufficient to depress H2O2 production by macrophages.
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PMID:Scavengers of reactive oxygen intermediates do not mediate the depression of macrophage hydrogen peroxide production caused by erythrocyte phagocytosis. 175 28

In a case series study we evaluated 53 composite-materials workers in an aerospace plant who filed workers' compensation claims for illness allegedly related to phenol-formaldehyde resin exposure. Symptoms ranged from mucosal and skin irritation to depression and cognitive impairment. Certain health practitioners implying they had immunologic dysfunction and organic brain injury, led workers to believe they were chemically poisoned. Industrial hygiene evaluation failed to show levels of chemicals above permissible levels. Thorough evaluation by our multidisciplinary panel failed to find significant objective abnormalities by physical exam and laboratory testing. Thirty-nine percent of the workers had sensory irritation and/or skin complaints that generally resolved rapidly with removal from exposure. Psychiatric diagnoses (including major depression and/or panic attacks) were made in 74% of the workers, but only 26% of these had antecedent disease. Fourteen (26%) had multiple somatic complaints that generally persisted despite removal from exposure, but they also had long histories of significant pre-existing psychological illness. Detailed neuropsychologic testing failed to show any definite evidence or organic brain dysfunction in any of the workers tested. We speculate that sensory irritation from low-level volatile organic compounds with autonomic arousal, reinforced by the belief they were "chemically poisoned," led to psychogenic illness.
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PMID:Depression and panic attacks related to phenol-formaldehyde composite material exposure in an aerospace manufacturing plant. 183 99

Because of its position, the sublingual gland is clinically important especially in the events of injuries and infections in the anterior part of the sublingual region. The morphology and relationships of this gland were studied by dissection methods applied on 80 fresh or formaldehyde fixed preparations of the mouth floor and of the tongue, which were partly (31 preparations) taken out together with the mandible. As for the shape of the gland, three main types were found: the cuneiform type which was the most frequent (71%), the pyramidal type which was less frequent (16%) and the fusiform type (13%) which comprised the case of a very elongated gland (up to 65 mm). The space in which the gland lied had four walls. Its internal wall consisted of the mylohyoid muscle and it comprised the hyoglossus muscle as well when the gland was very elongated. The inferior wall consisted of the mylohyoid muscle and sometimes it comprised also a narrow part of the superior surface of the geniohyoglossus muscle. An osseous depression on the internal side of the mandible represented the external wall of the sublingual gland space. The superior wall is clinically the most significant. It consists of the sublingual mucosa and a sublingual fold. This wall represents a main surgical access to the gland. In edentulous mandibles this mucous fold may be at the level of the upper mandibular border which may hinder the use of the lower dental prosthesis.
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PMID:[The surgical anatomy of the sublingual gland]. 208 85

Although formalin ingestions have previously been reported in the literature, technology has only recently been developed to measure both formaldehyde and formate levels in plasma. Methanol, formaldehyde, and formate levels were followed in the case reported here until the patient's death approximately 13 h after the ingestion. The clinical course was marked by an initial profound CNS depression followed by an apparent clinically quiescent period. Severe abdominal pain and retching preceded the development of seizures, DIC, severe hypotension, and cardiac arrest. Methanol levels rose throughout this 13-h course. Formate and formaldehyde levels increased until bicarbonate and ethanol therapy were instituted. The "fixing" of the stomach by formaldehyde may have produced delayed absorption following formalin ingestion. Therapeutic implications are discussed.
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PMID:Formate levels following a formalin ingestion. 232 60

Alternations of EEG have been investigated after single intraarterial infusion of formaldehyde, glutaric aldehyde and its mixture in 50 adult male rats. The dissolved solutions of aldehydes were shown to have complicated inhibitive activity which consists of two phases. The first phase of EEG inhibition rapidly develops and it isn't very long in its duration. The second one is much more durable. Formaldehyde causes the first phase of inhibition in general, though glutaric aldehyde promotes especially the appearance of the second phase. The mixture of two aldehydes demonstrates synergic activity which is shown as significant increase of EEG inhibition as compared to individual inhibitive activity of aldehydes. The inhibitive influence of aldehydes is fully reversible, nonspecific and doesn't cause post-experimental disorders. The highest effect of brain protection from ischaemia damages coincides with development of maximum inhibition of specific brain functions during the second phase of EEG depression.
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PMID:[Effects of weak solutions of aldehydes on EEG changes in rats]. 251 5

Formaldehyde, 0.5-4.5 mM, increased the threshold for electrical excitation of the nerve, and led to a partial and reversible inhibition of the compound action potential (cAP). The depression was not enhanced by high frequency stimulation. At 8.9 mM or higher, the depression of the nerve excitability could not be reversed. The inhibition of the nerve developed more slowly than that of the muscle, and the nerve was unaffected after 10 min exposure to 2.2 mM. Formaldehyde, 2.2 mM, caused an immediate depression of the indirectly (through the nerve) and directory (at the muscle) elicited twitch tension. After 10 min the tensions were reduced to respectively, 56% and 49% of control. However, the electromyogram was not changed, indicating that the effect was localized to the excitation-contraction coupling. Tetanic tension (100 Hz in 5 sec) was inhibited more than twitch tension during indirect stimulation, whereas the opposite was found during direct stimulation of the muscle. Thus, during high frequency stimulation, formaldehyde must have an additional effect on the neuromuscular transmission. This effect was localized presynaptically since a fall out of endplate potentials was observed in the formaldehyde-treated diaphragm. In 6.7 mM or higher concentrations the directly or indirectly induced contractions were irreversibly blocked. The resting membrane potential of the muscle cells was unchanged after exposure to formaldehyde. Formaldehyde caused myotonia-like contractions of the diaphragm, occasionally after exposure to low concentrations (2.2 mM), and always after exposure to higher concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of formaldehyde on the isolated phrenic nerve and the phrenic nerve-diaphragm preparation of the rat, in vitro. 299 83

In previous studies, diethylmaleate (DEM)- and phorone-induced hepatic glutathione (GSH) depletion in rats was accompanied by impaired evolution of 14CO2 from the N-14C-labeled methyl groups of aminopyrine, which in turn was attributed to impaired generation of formaldehyde, its subsequent oxidation to formate, or to some combination of both. In the present study, l-buthionine sulfoximine (BSO)-induced hepatic GSH depletion was also accompanied by decreased evolution of CO2 from aminopyrine, but the extent of the fall in CO2 was less than that induced by DEM or phorone, even though the decrease in hepatic GSH was comparable with all three GSH-lowering compounds. Incubation of freshly prepared normal hepatic microsomes in vitro with the GSH-lowering agents resulted in impaired aminopyrine-N-demethylase (APDM) activity with inhibition by phorone greater than DEM greater than BSO. By contrast, hepatic microsomes prepared from rats pretreated with these compounds had normal APDM activity. 14CO2 evolution from i.p. administered [14C]formaldehyde was not impaired by any of the GSH-lowering compounds. Thus, assessment of APDM activity and formaldehyde metabolism did not unequivocally establish the mechanism(s) by which CO2 evolution from aminopyrine is depressed by DEM, phorone and BSO, although low GSH is likely to impair metabolism of formaldehyde formed in liver after demethylation of aminopyrine. Quantitative differences in the degree of depression of CO2 evolution suggest that at least DEM and phorone exert an additional inhibitory effect by a GSH-independent mechanism. This may involve inhibition of aminopyrine-N-demethylase activity.
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PMID:Effect of glutathione depletion on aminopyrine and formaldehyde metabolism. 335 87

Formaldehyde is but one of many chemicals capable of causing the tight building syndrome or environmentally induced illness (EI). The spectrum of symptoms it may induce includes attacks of headache, flushing, laryngitis, dizziness, nausea, extreme weakness, arthralgia, unwarranted depression, dysphonia, exhaustion, inability to think clearly, arrhythmia or muscle spasms. The nonspecificity of such symptoms can baffle physicians from many specialties. Presented herein is a simple office method for demonstrating that formaldehyde is among the etiologic agents triggering these symptoms. The very symptoms that patients complain of can be provoked within minutes, and subsequently abolished, with an intradermal injection of the appropriate strength of formaldehyde. This injection aids in convincing the patient of the cause of the symptoms so he can initiate measures to bring his disease under control.
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PMID:Diagnosing the tight building syndrome. 344 98

This study was conducted to determine the characteristic response of Sprague-Dawley rats to formaldehyde (HCHO) challenges to the lower respiratory tract, and whether these response patterns are altered in rats that have received repeated exposures to HCHO. Male Sprague-Dawley rats were exposed to 0, 0.5, or 15 ppm HCHO for 6 hours/day, 5 days/week, for 8 or 16 weeks. Both naive rats and rats repeatedly exposed to HCHO were then administered 30 ppm HCHO test challenges by tracheal exposure, with the minute volume, respiratory rate, and tidal volume responses monitored. The pulmonary response of naive rats to HCHO tracheal challenge involved the correlation of minute volume and tidal volume depression, while respiratory rate was either unaffected or slightly increased. This was also the response pattern for rats that received 8 weeks of repeated exposure to HCHO. The only significant difference in respiratory response patterns between naive and pre-exposed animals existed in a slight increase in the respiratory rate compensatory response in the rats pre-exposed for 16 weeks to 15 ppm. There was substantial recovery of initially depressed respiratory parameters during the tracheal challenge in both naive and pre-exposed rats. The characteristic pulmonary response to HCHO in the lower respiratory tract demonstrated for Sprague-Dawley rats was thus similar to patterns of lower respiratory response to HCHO reported for other rodent species.
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PMID:Respiratory responses in the lower respiratory tract of Sprague-Dawley rats to formaldehyde inhalation. 378 32

Evoked compound-action potentials (cAP) in all three fibre types of the isolated nerve were reversibly depressed by exposure to the drugs. After 20 min exposure, lidocaine (0.5 mM) depressed the amplitude of the A and B fibre potentials significantly more than the C fibre potential. With eugenol (0.8 mM), there was no significant difference in depression of A, B and C fibre activity. With formaldehyde (4.5 mM), the latency was longer, and the C fibres were initially significantly more depressed than the A and B fibres. As dull pain from a chronically-inflamed pulp is believed to be mediated through C fibres, these results may explain the difficulties in obtaining complete local analgesia with lidocaine. They indicate that application of low concentrations of eugenol and formaldehyde to the pulp-dentine organ may have an analgesic effect on pain mediated through both A and C fibres.
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PMID:Differential inhibition of A, B and C fibres in the rat vagus nerve by lidocaine, eugenol and formaldehyde. 386 54


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