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1.
Ann Pharm Fr ; 64(3): 161-72, 2006 May.
Artigo em Francês | MEDLINE | ID: mdl-16710114

RESUMO

Two retrospective epidemiologic studies have shown that cannabis is the main psychoactive substance detected in the blood of drivers suspected of driving under the influence of psychotropic drugs. An oral administration double-blind crossover study was carried out with eight healthy male subjects, aged 22 to 30 years, all occasional cannabis smokers. Three treatments and one placebo were administered to all participants at a two week interval: 20 mg dronabinol, 16.5 mg D9-tétrahydrocannabinol (THC) and 45.7 mg THC as a cannabis milk decoction. Participants were asked to report the subjective drug effects and their willingness to drive under various circumstances on a visual analog scale. Clinical observations, a psychomotor test and a tracking test on a driving simulator were also carried out. Compared to cannabis smoking, THC, 11-OH-THC and THC-COOH blood concentrations remained low through the whole study (<13.1 ng THC/mL,<24.7 ng 11-OH-THC/mL and<99.9 ng THC-COOH/mL). Two subjects experienced deep anxiety symptoms suggesting that this unwanted side-effect may occur when driving under the influence of cannabis or when driving and smoking a joint. No clear association could be found between these adverse reactions and a susceptibility gene to propensity to anxiety and psychotic symptoms (genetic polymorphism of the catechol-O-methyltransferase). The questionnaires have shown that the willingness to drive was lower when the drivers were assigned an insignificant task and was higher when the mission was of crucial importance. The subjects were aware of the effects of cannabis and their performances on the road sign and tracking test were greatly impaired, especially after ingestion of the strongest dose. The Cannabis Influence Factor (CIF) which relies on the molar ratio of active and inactive cannabinoids in blood provided a good estimate of the fitness to drive.


Assuntos
Condução de Veículo , Cannabis/efeitos adversos , Dronabinol/efeitos adversos , Alucinógenos/efeitos adversos , Adulto , Método Duplo-Cego , Humanos , Masculino , Desempenho Psicomotor/efeitos dos fármacos
2.
Osteoporos Int ; 12(6): 493-9, 2001.
Artigo em Inglês | MEDLINE | ID: mdl-11446566

RESUMO

The urine-acidifying properties of food constituents depend on their content of non-oxidizable acids or precursors. Acidifying constituents such as animal proteins may negatively affect calcium metabolism and accelerate bone resorption, thus representing an aggravating factor for osteoporosis. This four-period, double-crossover study investigated whether a diet intervention specifically focused on acid load could modify calcium metabolism in humans. Eight healthy volunteers underwent a four-day metabolic preparation with two types of diets, one rich in acid ash-forming nutrients, and one providing base-forming nutrients (including bicarbonate-rich mineral water), both having similar contents of calcium, phosphate, sodium, proteins and calories. On the fourth day, a single oral dose of 1 g calcium was given, either as carbonate or as gluconolactate. Serial blood and urine samples revealed that the diet affected blood pH (average difference 0.014, p=0.002) and urine pH (average difference 1.02, p<0.0001) in the expected direction, but had no influence on the absorption of the calcium supplement. The acid-forming diet increased urinary calcium excretion by 74% when compared with the base-forming diet (p<0.0001), both at baseline and after the oral calcium load, and C-telopeptide excretion by 19% (p=0.01), suggesting a skeletal origin for the excess calcium output. This observation confirms that renally excreted acids derived from food influence calcium metabolism, and that alkalizing nutrients inhibit bone resorption. Further studies are needed to determine the clinical impact of dietary counseling for avoiding diet acids as a preventive measure against osteoporosis.


Assuntos
Ácidos/farmacologia , Álcalis/farmacologia , Osso e Ossos/metabolismo , Cálcio/metabolismo , Osteoporose/dietoterapia , Ácidos/administração & dosagem , Adulto , Álcalis/administração & dosagem , Bicarbonatos/uso terapêutico , Colágeno/urina , Colágeno Tipo I , Dieta , Humanos , Concentração de Íons de Hidrogênio , Masculino , Osteoporose/metabolismo , Osteoporose/prevenção & controle , Peptídeos/urina
3.
Acta Cytol ; 44(2): 218-22, 2000.
Artigo em Inglês | MEDLINE | ID: mdl-10740609

RESUMO

OBJECTIVE: To determine the patterns of CD34 reactivity in hepatocellular adenoma and focal nodular hyperplasia and to evaluate the utility of CD34 reactivity in the diagnosis of hepatocellular carcinoma. STUDY DESIGN: Seventeen cases of well-differentiated hepatocellular carcinoma, 14 cases of cirrhosis, 9 cases of focal nodular hyperplasia and 7 cases of hepatocellular adenoma were stained with immunoperoxidase antibodies to CD34. The slides were scored according to the degree of lesional reactivity. RESULTS: Fourteen of 17 cell blocks with hepatocellular carcinoma showed unequivocal sinusoidal or peripheral reactivity for CD34. Five of seven cases of hepatocellular adenoma and four of nine cases of focal nodular hyperplasia showed > 50% sinusoidal reactivity for CD34. All 14 cases of cirrhosis showed peripheral to no sinusoidal reactivity. CONCLUSION: CD34 reactivity in a diffuse sinusoidal pattern can be helpful in the diagnosis of hepatocellular carcinoma. However, consideration should be given to the possibility of hepatocellular adenoma and focal nodular hyperplasia, which can also exhibit significant diffuse CD34 reactivity. In these cases, a reticulin stain may be helpful with the differential diagnosis.


Assuntos
Adenoma de Células Hepáticas/metabolismo , Antígenos CD34/metabolismo , Hiperplasia Nodular Focal do Fígado/metabolismo , Cirrose Hepática/metabolismo , Neoplasias Hepáticas/metabolismo , Adenoma de Células Hepáticas/patologia , Biópsia por Agulha , Diagnóstico Diferencial , Hiperplasia Nodular Focal do Fígado/patologia , Humanos , Técnicas Imunoenzimáticas , Cirrose Hepática/patologia , Neoplasias Hepáticas/patologia
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