POSSIBLE RELATIONSHIP BETWEEN TETRACYCLINE STABILITY AND EFFECT ON FOETAL SKELETON. (9/37)

A possible relationship between stability of a tetracycline and persistence in the foetal skeleton is discussed; it seems that the greater the stability of a tetracycline, the more it may interfere with bone-forming processes. Therefore, assuming that limited instability does not impair antibiotic potency in vivo, the use of a low-stability tetracycline seems to be a safer form of treatment in order to avoid undesired effects on the foetal skeleton.  (+info)

Chlortetracycline and demeclocycline inhibit calpains and protect mouse neurons against glutamate toxicity and cerebral ischemia. (10/37)

Minocycline is a potent neuroprotective tetracycline in animal models of cerebral ischemia. We examined the protective properties of chlortetracycline (CTC) and demeclocycline (DMC) and showed that these two tetracyclines were also potent neuroprotective against glutamate-induced neuronal death in vitro and cerebral ischemia in vivo. However, CTC and DMC appeared to confer neuroprotection through a unique mechanism compared with minocycline. Rather than inhibiting microglial activation and caspase, CTC and DMC suppressed calpain activities. In addition, CTC and DMC only weakly antagonized N-methyl-D-aspartate (NMDA) receptor activities causing 16 and 14%, respectively, inhibition of NMDA-induced whole cell currents and partially blocked NMDA-induced Ca2+ influx, commonly regarded as the major trigger of neuronal death. In vitro and in vivo experiments demonstrated that the two compounds selectively inhibited the activities of calpain I and II activated following glutamate treatment and cerebral ischemia. In contrast, minocycline did not significantly inhibit calpain activity. Taken together, these results suggested that CTC and DMC provide neuroprotection through suppression of a rise in intracellular Ca2+ and inhibition of calpains.  (+info)

Hyponatremia: why it matters, how it presents, how we can manage it. (11/37)

Hyponatremia is a common electrolyte disorder among hospitalized patients and has been associated with increased mortality. Most patients are asymptomatic, but many do present with symptoms, usually of a generalized neurologic nature. Based-on medical history, physical examination (including volume-status assessment), and laboratory tests, patients can be classified as having either hypervolemic, euvolemic, or hypovolemic hyponatremia. Management depends on the speed of hyponatremia onset; its degree, duration, and symptoms; and whether there are risk factors for neurologic complications. The risks of overly rapid correction must be weighed against the benefits of treating hyponatremia. Traditional therapies have significant limitations. New agents that antagonize arginine vasopressin at the V2 receptor or both the V(1A) and V2 receptors show promise for treating hypervolemic and euvolemic hyponatremia, as they induce desired free water diuresis without inducing sodium excretion.  (+info)

In vitro antimicrobial sensitivity of Mycoplasmas isolated from the bovine genital tract. (12/37)

The in vitro antimicrobial sensitivity of 14 mycoplasma and 13 ureaplasma strains isolated from the genital tracts of bulls was examined. It was found that at relatively low concentrations, tetracycline, declomycin and tylosin were lethal to both types of organisms. Lincospectin, berenil, streptomycin and erythromycin were lethal to mycoplasmas but were only inhibitory to the ureaplasma strains at the same concentrations. Polymyxin B and novobiocin were ineffective at the levels tested.  (+info)

Transepithelial water movement in response to carbamazepine, chlorpropamide and demeclocycline in toad urinary bladder. (13/37)

1. Osmotic water movement across toad isolated hemibladders was measured by a gravimetric method. 2. The influence of carbamazepine, chlorpropamide and demeclocycline on the antidiuretic hormone (ADH)-induced water flow rate was examined. 3. No antidiuretic activity due to carbamazepine alone was observed but a slight inhibition due to ADH-induced water flow was observed in the presence of carbamazepine over a selected dose-range. This was unexpected and is inconsistent with data from in vivo studies in man. 4. Chlorpropamide potentiated ADH-induced water flow, in keeping with the hypothesis that chlorpropamide sensitizes the renal tubules to ADH-induced water flow. 5. Demeclocycline inhibited ADH-induced water flow. The mechanism of action remains unclear.  (+info)

The effect of calcium hydroxide on the steroid component of Ledermix and Odontopaste. (14/37)

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A prospective clinical trial on the influence of a triamcinolone/demeclocycline and a calcium hydroxide based temporary cement on pain perception. (15/37)

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An elderly patient with chronic hyponatremia. (16/37)

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