Publications by authors named "LOO P"

Alterations in several neurotransmitter systems in brain have been implicated in the pathophysiology of hepatic coma (HC). Studies on human autopsy material are few. We investigated 3H-quinuclidinylbenzilate (QNB), 3H-spiperone, 3H-imipramine, 3H-PN-200-110, 3naloxone, 3H-flunitrazepam, 3H-muscimol, 35S-t-butylbicyclophosphothionate and 3H-cyclohexyladenosine binding sites in frontal cortex from seven patients with HC and five controls.

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Solubilized microsomes from bovine liver, kidney and testis were compared with regard to their content of vitamin-K-dependent carboxylase, the presence of endogenous vitamin K as well as that of endogenous carboxylatable precursor proteins. The isolation and purification of these protein substrates was not successful. Using antibodies against various well characterized proteins containing gammacarboxyglutamic acid (Gla), we were able to identify precursors of the blood coagulation factors II, IX and X in liver microsomes.

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Several previous studies have suggested a strong GABA-mimetic action of the endogenous brain imino acid, L-pipecolic acid (L-PA). In the present study, these observations were evaluated using electrophysiological and neurochemical methods. In contrast to published data our electrophysiological studies on rat cortical neurones in situ showed only a weak, but bicuculline-sensitive depressant action of L-PA on cortical neurones.

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A single oral dose of ciprofloxacin 500 mg was used to treat five men with gonococcal urethritis and five men with gonococcal proctitis, and all were cured. In a subsequent study the dose of ciprofloxacin was reduced to 250 mg, and 54 men with 57 gonococcal infections (47 urethral, seven rectal, and three pharyngeal) were treated; of the isolates of Neisseria gonorrhoeae, four were penicillinase producing strains. All the patients were cured of gonococcal infection.

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Using an extensively washed membrane preparation and standardized incubation conditions, the actions of benzodiazepine (BZ) receptor ligands were evaluated on [3H]flunitrazepam [+/- 10 microM gamma-aminobutyric acid (GABA)], [3H]muscimol (+/- 2.5 microM etazolate) and [35S]butyl bicyclophosphorothionate (TBPS) binding. Classical BZ receptor agonists stimulated [35S]TBPS binding and [3H]muscimol binding in the presence of etazolate.

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One hundred women with uncomplicated gonorrhoea (in five cases due to penicillinase producing strains of Neisseria gonorrhoeae (PPNG)) were treated with a single oral dose of rifampicin 900 mg and erythromycin stearate 1 g. N gonorrhoeae was reisolated from the oropharynx of one patient, who was infected with a PPNG strain, but was eradicated from the genital tract in 100% of cases. The combination eradicated Chlamydia trachomatis from only 10 (28%) of the 36 patients infected.

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A group of 50 men with uncomplicated gonococcal infections were treated with single, oral doses of 2.5 g of thiamphenicol. Reexamination, which included culture for Neisseria gonorrhoeae, was performed three to four days and seven days after treatment.

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The efficacy of coupling between the benzodiazepine receptor and chloride channel as well as the coupling to the GABA receptor is differentially affected by different benzodiazepine ligands. In general, the order of efficacy with regard to allosteric effects of benzodiazepine ligands on the chloride channel ([35S]TBPS) and GABA receptor ([3H]muscimol), is: agonist greater than agonist/antagonist greater than partial agonist greater than antagonist; with inverse agonists acting in a manner opposite to the classical benzodiazepine agonists. The chloride ionophore is allosterically modulated both by benzodiazepine and GABA receptors.

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The authors analyze the personality of cranial-traumatized patients in the years that follow the accident or neuro-surgery. They point out the negative aspect of the behaviors noted: abulia, apathy, selfdenial, passiveness, and especially the failure to recognize the very special syndrome, that is no pure psychosis, nor actual neurosis, not even dementia that is well-known by the neuro-surgeons, badly-known by the experts and forgotten in the tables. The evolution of this syndrome of long duration, it lasts from two to five years, according to circumstances, and for some symptoms or occasionally chronic patients.

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