In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[EX Q]: Context: Progress in the management of patients with medically intractable epilepsy is impeded because we do not fully understand why pharmacoresistance happens and how it can be predicted. The presence of multiple seizures prior to medical treatment has been suggested as a potential predictor of poor outcome. In the present study, we used an animal model of temporal lobe epilepsy to investigate whether pharmacoresistant rats differ in seizure frequency from pharmacoresponsive animals.', 'Epilepsy with spontaneous recurrent seizures (SRS) was induced by status epilepticus. Frequency of SRS was determined by video/EEG (electroencephalography) monitoring in a total of 33 epileptic rats before onset of treatment with phenobarbital (PB).', 'Thirteen (39%) rats did not respond to treatment with PB. Before treatment with PB, average seizure frequency in PB nonresponders was significantly higher than seizure frequency in responders, which, however, was due to six nonresponders that exhibited > 3 seizures per day. Such high seizure frequency was not observed in responders, demonstrating that high seizure frequency predicts pharmacoresistance in this model, but does not occur in all nonresponders.\Question: Is high seizure frequency prior to antiepileptic treatment a predictor of pharmacoresistant epilepsy in a rat model of temporal lobe epilepsy?
[EX A]: The data from this study are in line with clinical experience that the frequency of seizures in the early phase of epilepsy is a dominant risk factor that predicts refractoriness. However, resistance to treatment also occurred in rats that did not differ in seizure frequency from responders, indicating that disease severity alone is not sufficient to explain antiepileptic drug (AED) resistance. These data provide further evidence that epilepsy models are useful in the search for predictors and mechanisms of pharmacoresistance.

[EX Q]: Context: Extended-release niacin effectively lowers plasma TG levels and raises plasma high-density lipoprotein (HDL) cholesterol levels, but the mechanisms responsible for these effects are unclear.', 'We examined the effects of extended-release niacin (2 g/d) and extended-release niacin (2 g/d) plus lovastatin (40 mg/d), relative to placebo, on the kinetics of apolipoprotein (apo) A-I and apoA-II in HDL, apoB-100 in TG-rich lipoproteins (TRL), intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), and apoB-48 in TRL in 5 men with combined hyperlipidemia. Niacin significantly increased HDL cholesterol and apoA-I concentrations, associated with a significant increase in apoA-I production rate (PR) and no change in fractional catabolic rate (FCR). Plasma TRL apoB-100 levels were significantly lowered by niacin, accompanied by a trend toward an increase in FCR and no change in PR. Niacin treatment significantly increased TRL apoB-48 FCR but had no effect on apoB-48 PR. No effects of niacin on concentrations or kinetic parameters of IDL and LDL apoB-100 and HDL apoA-II were noted. The addition of lovastatin to niacin promoted a lowering in LDL apoB-100 attributable to increased LDL apoB-100 FCR.\Question: Does extended-release niacin alter the metabolism of plasma apolipoprotein ( Apo ) A-I and ApoB-containing lipoproteins?
[EX A]: Niacin treatment was associated with significant increases in HDL apoA-I concentrations and production, as well as enhanced clearance of TRL apoB-100 and apoB-48.

[EX Q]: Context: The incidence of ureteral stenosis in kidney transplant recipients is 3%-8%. The treatment of ureteral stenosis has been traditionally operative reconstruction, although such intervention is associated with high rates of serious complications, including graft loss and even perioperative mortality. More recently, endourological treatment has been proposed due to its low morbidity.', 'The objective of this study was to assess the usefulness of balloon percutaneous dilatation as a treatment technique for ureteral stenosis in kidney transplant recipients.', 'Among 1000 kidney transplantations performed between 1980 and 2004, the coexistence of high creatinine values and urinary tract dilatation in the postoperative period, after discarding concomitant causes, was managed with a percutaneous nephrostomy. Once renal function recovered, antegrade pyelography was performed to confirm the presence and determine the location of ureteral stenosis. Ureteral dilatation was performed using a 5-French balloon-fitted angioplasty catheter.', 'Fifty-six patients were diagnosed with ureteral stenosis during follow-up, an incidence of 5.6%. Transluminal balloon dilatation was the first therapeutic option in 45 cases, whereas surgery was performed directly on 11 patients. Disappearance of the stenosis as well as maintenance of an improved creatinine level was verified in 45% of cases (20 patients). Two patients experienced graft loss. Both a short time to diagnosis after transplantation (P = .06) and the presence of a previous acute rejection episode (P < .05) were good prognosis factors for the endourologic solution of a ureteral stricture.\Question: Is endourological management better in early-onset ureteral stenosis in kidney transplantation?
[EX A]:
Balloon dilatation may be considered the definitive procedure for treatment of ureteral stenosis in selected cases. Percutaneous nephrostomy should be used for initial diagnosis and improvement in the renal function before attempting an open procedure.