Patient self-assessment of tibial plateau fractures in 40 older adults

The prevalence of refractory partial seizure Thai patients at Prasat Neurological Institute was retrospectively from patient charts from January 1995-December 1996 and further prospectively analysed. All epileptic patients were screened by direct questions regarding the anti-epileptic drugs (AEDs) regimen, the frequency, nature of seizure attacks and risk factors of seizure. The criteria of clinical refractory partial seizure was defined as partial seizure which cannot be controlled by a combination of at least two AEDs for four weeks. The results were 3,018 cases of total epileptic patients out of 300,008 visits. These were classified as 2,802 cases of generalized seizures (92.8%), 184 cases of partial seizures (6.1%), and 32 cases of unclassified seizures (1.1%). In the partial seizures group, the number of clinical refractory partial seizures was found to be 48 cases (26.1% of partial seizure). We found that the major risk factor of refractory partial seizures was lack of therapeutic AEDs blood level monitoring (64.5% of cases) and the other risk factors were lack of compliance, loss of follow-up but continued medication, concomitant medication, and improper drug storage. AEDs dosage was adjusted until the blood levels were in the therapeutic range, and correction of other risk factors and patient counseling was given. The number of true refractory partial seizures was reduced to 10 cases (5.4% of partial seizure). This procedure revealed that AED blood level monitoring and correction of other risk factors were essential in controlling seizure frequency. Thus, the prevalence of true refractory partial seizure in our study was 3.3 cases of refractory partial seizure per 1,000 cases of the seizure population. We recommend that AEDs blood level monitoring and exclusion of other risk factors should be added to the criteria for the definition of refractory partial seizures. This criteria should be applied when considering the use of new AEDs as an add-on therapy in refractory Thai patients.     

Oral topotecan given once or twice daily for ten days: a phase I pharmacology study in adult patients with solid tumors

The development of a highly sensitive method for detection of telomerase activity, telomeric repeat amplification protocol (TRAP), has provided knowledge on telomerase activity in normal and cancer tissues. Subsequent several modifications have been achieved, including an introduction of the internal standard and hybridization protection technique that leads to simplicity and improvement of reproducibility and linearity of this method, and application of TRAP to in situ analysis to identify the cells responsible for telomerase activity. As for measurement of telomere length, fluorescence in situ hybridization technique appeared to give an information of telomere length on an individual chromosome in contrast to analysis of terminal restriction fragment, a conventional method which can express mean telomere length of all chromosomes. Further methodological improvement in this field is ongoing and showing a new sight on cell mortality and immortality.     

Hemodynamic sequelae of regression of experimental atherosclerosis

Regression of experimental atherosclerosis is characterized by decreased intimal thickness and luminal enlargement, but intimal fibrosis becomes more dense. We tested the hypothesis that fibrosis of arteries during regression might limit vasodilator capacity and restrict hemodynamic improvement despite luminal improvement. We studied limb, coronary, and cerebral hemodynamics in 11 normal cynomolgus monkeys, 10 monkeys given an atherogenic diet for 20 mo and 8 monkeys given a regression diet for an additional 18 mo. The atherogenic diet induced lesions of moderate severity (50-60% stenosis); owing to characteristic vessel growth during the atherogenic period, luminal size did not decrease correspondingly. Regression monkeys showed typical changes of regression with luminal enlargement but increased fibrosis. The iliac artery was perfused at constant blood flow and maximal vasodilatation was produced with papaverine. Blood flow was measured with microspheres during maximal vasodilatation in the coronary bed (adenosine) and cerebral bed (hypercapnia). In normal monkeys, minimal vascular resistances were 1.95 +/- 0.19 mm Hg/ml/min X 100 g (mean +/- SE) (limb), 0.13 +/- 0.01 (coronary), and 0.44 +/- 0.02 (cerebral). In atherosclerotic monkeys minimal resistance increased (P less than 0.05) 108, 62, and 166% in the limb, coronary, and cerebral beds, respectively. In regression monkeys, minimal resistance increased from values found in atherosclerotic animals in the limb (+22%), decreased inconsistently in the coronary bed (-19%), and decreased significantly in the cerebral bed (-44%, P less than 0.05). Thus morphologic regression was accompanied by significant hemodynamic improvement during maximal dilatation only in cerebral vessels. We conclude that increases in luminal size during regression of atherosclerotic lesions may not be associated with increases in vasodilator capacity, as intimal fibrosis may limit physiologically important hemodynamic improvement.     

Gas chromatographic determination of pemoline as 5-phenyl-2,4-oxazolidinedione in human urine

A simple gas chromatographic assay of the psychostimulant pemoline in human urine has been developed. Instead of extraction of the drug from urine, it is hydrolysed to 5-phenyl-2,4-oxazolidinedione with 1 N hydrochloric acid. After the extraction, this compound is methylated with diazomethane and determined by gas-liquid chromatography using a nitrogen-selective detector and a solid injection system. The method has been applied in preliminary human pharmacokinetic studies, by measuring the urinary excretion rate of pemoline following oral administration. At present, the screening procedures for doping control do not involve the detection of pemoline, but the method described can easily be incorporated in such procedures.