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[en] For the assessment of antithyroid effect of lithium carbonate, it was administered to the 17 hyperthyroid and 5 euthyroid patients, who visited the Seoul National University Hospital from Jan. to Aug., 1977. Thyroid function tests were performed just before the administration of Lithium carbonate, 2 weeks and 2 months after lithium treatment. The results were as follows; 1) In the 5 euthyroid patients, no significant changes in thyroid function tests were obtained before and after lithium treatment. 2) In the 17 hyperthyroid patients, the values of the T3RIA were 370±121 ng/dl 2 weeks after lithium treatment as compared with 506±121 ng/dl before the administration, of which the mean percentage fall was 26.9%. T3RU was varied from 56.8±8.0% to 47.3±8.1% (16.7% in mean percentage fall), T4 was changed from 24.2±2.4 ug/dl to 22.0±4.2 ug/dl (9.1% in meanfall), and T7, from 13.82±2.25 to 10.55±3.12 (23.7% in mean fall). 3) In the 5 hyperthyroid patients, serial thyroid function tests were performed 2 weeks and 2 months later. The mean percentage falls of T3RIA were 36.6 and 61.3%, 2 weeks and 2 months after lithium treatment respectively. Those of T3RU were 17.5 and 35.1%, those of T4 were 20.4 and 44.0%, T7, 35.0 and 60.7%. 4) Approximately 45-60% of mean fall in thyroid function tests were obtained within the second week. Normal thyroid function tests were observed in 2 among 17 patients within the second week, and 2 among 5 patients within the second month. 18 patients, however, became clinically euthyroid within the 4th week. 5) Single case of hypothyroidism was experienced, and 5 patients (29.4%) complained mild side effect. Lithium salts could be safely administered to hyperthyroid patients who are allergic to thioamides or iodine. Its use is indicated in cases of acute thyrotoxicosis in which it's necessary to reduce hormone levels very rapidly, and lithium-thioamides drug combination is a highly effective and safe means of initial routine control of hyperthyroidism.
[en] The Seebeck coefficient is reported for thermoelectric cells with gas electrodes and a molten electrolyte of one salt, lithium carbonate, at an average temperature of 750 °C. We show that the coefficient, which is 0.88 mV K−1, can be further increased by adding an inorganic oxide powder to the electrolyte. We interpret the measurements using the theory of irreversible thermodynamics and find that the increase in the Seebeck coefficient is due to a reduction in the transported entropy of the carbonate ion when adding solid particles to the alkali carbonate. Oxides of magnesium, cerium and lithium aluminate lead to a reduction in the transported entropy from 232 ± 12 to around 200 ± 4 J K−1 mol−1. This is of importance for design of thermoelectric converters.
[en] Highlights: • Lithium suppresses Akt activity by reducing PI3K-mediated Akt phosphorylation. • Lithium enhances GSK-3β activity by reducing Akt-mediated GSK-3β phosphorylation. • Lithium suppresses GSK-3β activity through its direct inhibition. - Abstract: Accumulating evidence has pointed to the direct inhibitory action of lithium, an anti-depressant, on GSK-3β. The present study investigated further insight into lithium signaling pathways. In the cell-free assay Li2CO3 significantly inhibited phosphoinositide 3-kinase (PI3K)-mediated phosphorylation of Akt1 at Ser473, but Li2CO3 did not affect PI3K-mediated PI(3,4,5)P3 production and 3-phosphoinositide-dependent protein kinase 1 (PDK1)-mediated phosphorylation of Akt1 at Thr308. This indicates that lithium could enhance GSK-3β activity by suppressing Akt-mediated Ser9 phosphorylation of GSK-3β in association with inhibition of PI3K-mediated Akt activation. There was no direct effect of Li2CO3 on Akt1-induced phosphorylation of GSK-3β at Ser9, but otherwise Li2CO3 significantly reduced GSK-3β-mediated phosphorylation of β-catenin at Ser33/37 and Thr41. This indicates that lithium directly inhibits GSK-3β in an Akt-independent manner. In rat hippocampal slices Li2CO3 significantly inhibited phosphorylation of Akt1/2 at Ser473/474, GSK-3β at Ser9, and β-catenin at Ser33/37 and Thr41. Taken together, these results indicate that lithium exerts its potentiating and inhibiting bidirectional actions on GSK-3β activity
[en] The compressive strength and the volume porosity of calcium aluminate cement pastes have been studied in order to connect their relationship. The influence of mass fraction of lithium carbonate on compressive strength and porosity of calcium aluminate cement (CAC) has been investigated at different water-cement (w/c) ratios. The functions proposed in the literature for different technical materials were tested on obtained strength and porosity data. Those functions have been a base for further development of more general functional dependence of strength and porosity for cement materials. Thus, we propose the following equation to relate the strength and porosity for CAC pastes:σ=σP01-PP02
[en] Lithium has been suggested for mood disorders and neurodegenerative diseases. Its ability to increase the gray matter and provision of protection against neuronal death makes it tempting to be marketed as brain food. Moreover it also ameliorates the effects of stress on brain dendrites; however lithium has a narrow therapeutic range. Brain serotonin (5-HT) neurotransmission may mediate the actions of lithium. Preclinical studies have shown that single restraint stress produces behavioral and neurochemical deficits. The present study was designed to investigate a potential role of Lithium in attenuation of stress induced behavioral and neurochemical deficits in rats. Moreover the study also monitored the esponsiveness of pre and post synaptic serotonin 1 A receptor following restraint and administration of lithium carbonate. Pre stress behavioral activities were monitored after 15 and 30 days of consumption of 0.1% lithium carbonate in drinking water while post stress were monitored on day 31. Pre and post synaptic 5-HT -1 A responsiveness was monitored by injecting 0.25mg/ml/kg of 8-OH-DPAT. Although lithium produced hypo activity but attenuated stress induced behavioral deficits. Whole brain neurochemical analysis revealed that its administration increased tryptophan, 5-HT and 5-Hydroindoleacetic acid (5-HIAA). 8-OH-DPAT elicited hyperactivity and fore paw treading were enhanced in lithium treated rats. Lithium induced pre synaptic changes together with the super sensitivity of post synaptic receptors may be able to produce antidepressant effect. (author)
[en] Several classes of drugs can promote renal retention of lithium and, occasionally, can induce lithium intoxication. The antimicrobial agent metronidazole hydrochloride (Flagyl I.V.) was also implicated in producing such a reaction in one woman. The authors describe two patients who experienced toxic reactions to lithium following brief use of metronidazole. However, in these two patients, in contrast to the previous case, the degree of acute intoxication was less severe and treatment with metronidazole was completed without apparent suspicion, but persistent signs of renal damage later emerged