The disposition of deuterium-labelled cannabidiol, 2H2-CBD, was studied in five young men who were marihuana smokers. The pattern of use ranged from infrequent to frequent use of the drug. Plasma concentrations, determined by mass fragmentography, were followed for 72 h after both intravenous administration of 20 mg 2H2-CBD and smoking of an estimated amount of 18.8-19.4 mg 2H2-CBD. Systemic availability after smoking was determined by comparing the areas under the plasma concentration versus time curves for the two treatments and was found to be 31 +/- 13%. A four-fold difference in the availability of the compound was noted for the five subjects. Based on the area under the curve and the dose after intravenous administration, a plasma clearance of 960-1560 ml min-1 was calculated. A terminal elimination phase was not reached at 72 h, but the kinetic parameters were estimated from the 72 h beta-elimination. A half-life of 31 +/- 4 h after smoking and 24 +/- 6 h after injection was estimated as well as a distribution volume of 2520 +/- 470 l (32.7 +/- 8.61 kg-1).
Five male endurance-trained subjects performed exhaustive exercise on a cycle ergometer at a work rate corresponding to 75% of their VO2max after reduction of their muscle glycogen stores. During exercise the subjects were given in random order a 6% carbohydrate solution continuing 7 g L-1 of branched-chain amino acids (BCAA), a 6% CHO solution and flavoured water. The physical performance was lowered in four of the five subjects when they were given flavoured water during exercise as compared with the two conditions when CHO was supplied. No difference in performance was found when the subjects were given CHO + BCAA or only CHO during exercise. When CHO + BCAA was supplied the plasma and muscle (vastus lateralis) concentrations of BCAA increased during exercise by 120 and 35%, respectively. In the other conditions there was no change or a slight decrease in the plasma concentrations of BCAA, but the muscle concentrations of BCAA were decreased after exercise. The plasma concentration of glutamine over the whole exercise period and 5 min after exercise was higher when CHO + BCAA were supplied during exercise compared with a supply of CHO alone or water. However, exercise caused no change in the muscle concentration of glutamine, whereas that of glutamate decreased in all three conditions. A supply of CHO + BCAA or CHO alone did not affect the exercise-induced increase in the plasma and muscle concentration of aromatic amino acids, indicating that neither BCAA nor CHO influenced the net protein degradation during exercise.
Background. Theoretical considerations have raised the suspicion that transurethral resection of the prostate (TURP) may increase the risk of developing prostate cancer in clinically benign prostate glands. Previous studies have not shown an increased risk among men who had undergone TURP for benign prostatic hyperplasia compared with the risk in age‐matched control subjects. However, in all of these studies, all men with stage T1 prostate cancer in the TURP‐group were excluded, possibly creating a bias, because no similar exclusion could be made for the controls.
Methods. The incidence and mortality of clinical prostate cancer were studied in 198 patients who had TURP and in 203 age‐matched male control subjects. In both groups, all patients with known prostate cancer and patients with suspected cancer by digital rectal examination were excluded from the study. However, patients with stage T1 cancer found by the TURP were included in the comparison between the groups.
Results. The mean age in the two groups was 67 ± 6 years. The patients were followed for an average of 10.2 ± 1.2 years and 10.4 ± 1.8 years in the TURP group and the control group, respectively. Clinical prostate cancer developed in six patients who had TURP and subsequently in five control (odds ratio, 0.8 [0.2‐3.11; P < 0.97]. Before follow‐up, three men in each group died because of prostate cancer (odds ratio, 1.3 (0.24‐7.45); P < 0.97).
Conclusions. The results of this study suggest that neither benign prostatic hyperplasia nor TURP increased the risk of developing clinical prostate cancer over the next 10 years in patients with a benign prostate gland determined by rectal examination before TURP.
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