Instruction: Extract chemical and disease entities from the following text.

Input: Endocrine screening in 1,022 men with erectile dysfunction: clinical significance and cost-effective strategy. PURPOSE: We reviewed the results of serum testosterone and prolactin determination in 1,022 patients referred because of erectile dysfunction and compared the data with history, results of physical examination, other etiological investigations and effects of endocrine therapy to refine the rules of cost-effective endocrine screening and to pinpoint actual responsibility for hormonal abnormalities. MATERIALS AND METHODS: Testosterone and prolactin were determined by radioimmunoassay. Every patient was screened for testosterone and 451 were screened for prolactin on the basis of low sexual desire, gynecomastia or testosterone less than 4 ng./ml. Determination was repeated in case of abnormal first results. Prolactin results were compared with those of a previous personal cohort of 1,340 patients with erectile dysfunction and systematic prolactin determination. Main clinical criteria tested regarding efficiency in hormone determination were low sexual desire, small testes and gynecomastia. Endocrine therapy consisted of testosterone heptylate or human chorionic gonadotropin for hypogonadism and bromocriptine for hyperprolactinemia. RESULTS: Testosterone was less than 3 ng./ml. in 107 patients but normal in 40% at repeat determination. The prevalence of repeatedly low testosterone increased with age (4% before age 50 years and 9% 50 years or older). Two pituitary tumors were discovered after testosterone determination. Most of the other low testosterone levels seemed to result from nonorganic hypothalamic dysfunction because of normal serum luteinizing hormone and prolactin and to have only a small role in erectile dysfunction (definite improvement in only 16 of 44 [36%] after androgen therapy, normal morning or nocturnal erections in 30% and definite vasculogenic contributions in 42%). Determining testosterone only in cases of low sexual desire or abnormal physical examination would have missed 40% of the cases with low testosterone, including 37% of those subsequently improved by androgen therapy. Prolactin exceeded 20 ng./ml. in 5 men and was normal in 2 at repeat determination. Only 1 prolactinoma was discovered. These data are lower than those we found during the last 2 decades (overall prolactin greater than 20 ng./ml. in 1.86% of 1,821 patients, prolactinomas in 7, 0.38%). Bromocriptine was definitely effective in cases with prolactin greater than 35 ng./ml. (8 of 12 compared to only 9 of 22 cases with prolactin between 20 and 35 ng./ml.). Testosterone was low in less than 50% of cases with prolactin greater than 35 ng./ml. CONCLUSIONS: Low prevalences and effects of low testosterone and high prolactin in erectile dysfunction cannot justify their routine determination. However, cost-effective screening strategies recommended so far missed 40 to 50% of cases improved with endocrine therapy and the pituitary tumors. We now advocate that before age 50 years testosterone be determined only in cases of low sexual desire and abnormal physical examination but that it be measured in all men older than 50 years. Prolactin should be determined only in cases of low sexual desire, gynecomastia and/or testosterone less than 4 ng./ml.

Output: Chemical/Disease Entities: erectile dysfunction (Disease), testosterone (Chemical), erectile dysfunction (Disease), Testosterone (Chemical), testosterone (Chemical), low sexual desire (Disease), gynecomastia (Disease), testosterone (Chemical), erectile dysfunction (Disease), low sexual desire (Disease), gynecomastia (Disease), testosterone heptylate (Chemical), hypogonadism (Disease), bromocriptine (Chemical), hyperprolactinemia (Disease), Testosterone (Chemical), testosterone (Chemical), pituitary tumors (Disease), testosterone (Chemical), testosterone (Chemical), hypothalamic dysfunction (Disease), erectile dysfunction (Disease), testosterone (Chemical), low sexual desire (Disease), testosterone (Chemical), prolactinoma (Disease), prolactinomas (Disease), Bromocriptine (Chemical), Testosterone (Chemical), testosterone (Chemical), erectile dysfunction (Disease), pituitary tumors (Disease), testosterone (Chemical), low sexual desire (Disease), low sexual desire (Disease), gynecomastia (Disease), testosterone (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Thiopentone pretreatment for propofol injection pain in ambulatory patients. This study investigated propofol injection pain in patients undergoing ambulatory anaesthesia. In a randomized, double-blind trial, 90 women were allocated to receive one of three treatments prior to induction of anaesthesia with propofol. Patients in Group C received 2 ml normal saline, Group L, 2 ml, lidocaine 2% (40 mg) and Group T, 2 ml thiopentone 2.5% (50 mg). Venous discomfort was assessed with a visual analogue scale (VAS) 5-15 sec after commencing propofol administration using an infusion pump (rate 1000 micrograms.kg-1.min-1). Loss of consciousness occurred in 60-90 sec. Visual analogue scores (mean +/- SD) during induction were lower in Groups L (3.3 +/- 2.5) and T (4.1 +/- 2.7) than in Group C (5.6 +/- 2.3); P = 0.0031. The incidence of venous discomfort was lower in Group L (76.6%; P < 0.05) than in Group C (100%) but not different from Group T (90%). The VAS scores for recall of pain in the recovery room were correlated with the VAS scores during induction (r = 0.7045; P < 0.0001). Recovery room discharge times were similar: C (75.9 +/- 19.4 min); L 73.6 +/- 21.6 min); T (77.1 +/- 18.9 min). Assessing their overall satisfaction, 89.7% would choose propofol anaesthesia again. We conclude that lidocaine reduces the incidence and severity of propofol injection pain in ambulatory patients whereas thiopentone only reduces its severity.

Output: Chemical/Disease Entities: Thiopentone (Chemical), propofol (Chemical), pain (Disease), propofol (Chemical), pain (Disease), propofol (Chemical), lidocaine (Chemical), thiopentone (Chemical), propofol (Chemical), Loss of consciousness (Disease), pain (Disease), propofol (Chemical), lidocaine (Chemical), propofol (Chemical), pain (Disease), thiopentone (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Comparison of i.v. glycopyrrolate and atropine in the prevention of bradycardia and arrhythmias following repeated doses of suxamethonium in children. The effectiveness of administration of glycopyrrolate 5 and 10 micrograms kg-1 and atropine 10 and 20 micrograms kg-1 i.v. immediately before the induction of anaesthesia, to prevent arrhythmia and bradycardia following repeated doses of suxamethonium in children, was studied. A control group was included for comparison with the lower dose range of glycopyrrolate and atropine. A frequency of bradycardia of 50% was noted in the control group, but this was not significantly different from the frequency with the active drugs. Bradycardia (defined as a decrease in heart rate to less than 50 beat min-1) was prevented when the larger dose of either active drug was used. It is recommended that either glycopyrrolate 10 micrograms kg-1 or atropine 20 micrograms kg-1 i.v. should immediately precede induction of anaesthesia, in children, if the repeated administration of suxamethonium is anticipated.

Output: Chemical/Disease Entities: glycopyrrolate (Chemical), atropine (Chemical), bradycardia (Disease), arrhythmias (Disease), suxamethonium (Chemical), glycopyrrolate (Chemical), atropine (Chemical), arrhythmia (Disease), bradycardia (Disease), suxamethonium (Chemical), glycopyrrolate (Chemical), atropine (Chemical), bradycardia (Disease), Bradycardia (Disease), glycopyrrolate (Chemical), atropine (Chemical), suxamethonium (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Reduction in caffeine toxicity by acetaminophen. A patient who allegedly consumed 100 tablets of an over-the-counter analgesic containing sodium acetylsalicylate, caffeine, and acetaminophen displayed no significant CNS stimulation despite the presence of 175 micrograms of caffeine per mL of serum. Because salicylates have been reported to augment the stimulatory effects of caffeine on the CNS, attention was focused on the possibility that the presence of acetaminophen (52 micrograms/mL) reduced the CNS toxicity of caffeine. Studies in DBA/2J mice showed that: 1) pretreatment with acetaminophen (100 mg/kg) increased the interval between the administration of caffeine (300 to 450 mg/kg IP) and the onset of fatal convulsions by a factor of about two; and 2) pretreatment with acetaminophen (75 mg/kg) reduced the incidence of audiogenic seizures produced in the presence of caffeine (12.5 to 75 mg/kg IP). The frequency of sound-induced seizures after 12.5 or 25 mg/kg caffeine was reduced from 50 to 5% by acetaminophen. In the absence of caffeine, acetaminophen (up to 300 mg/kg) did not modify the seizures induced by maximal electroshock and did not alter the convulsant dose of pentylenetetrezol in mice (tests performed by the Anticonvulsant Screening Project of NINCDS). Acetaminophen (up to 150 micrograms/mL) did not retard the incorporation of radioactive adenosine into ATP in slices of rat cerebral cortex. Thus the mechanism by which acetaminophen antagonizes the actions of caffeine in the CNS remains unknown.

Output: Chemical/Disease Entities: caffeine (Chemical), toxicity (Disease), acetaminophen (Chemical), sodium acetylsalicylate (Chemical), caffeine (Chemical), acetaminophen (Chemical), caffeine (Chemical), caffeine (Chemical), acetaminophen (Chemical), toxicity (Disease), caffeine (Chemical), acetaminophen (Chemical), caffeine (Chemical), convulsions (Disease), acetaminophen (Chemical), seizures (Disease), caffeine (Chemical), seizures (Disease), caffeine (Chemical), acetaminophen (Chemical), caffeine (Chemical), acetaminophen (Chemical), seizures (Disease), pentylenetetrezol (Chemical), Acetaminophen (Chemical), adenosine (Chemical), ATP (Chemical), acetaminophen (Chemical), caffeine (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Flestolol: an ultra-short-acting beta-adrenergic blocking agent. Flestolol (ACC-9089) is a nonselective, competitive, ultra-short-acting beta-adrenergic blocking agent, without any intrinsic sympathomimetic activity. Flestolol is metabolized by plasma esterases and has an elimination half-life of approximately 6.5 minutes. This agent was well tolerated in healthy volunteers at doses up to 100 micrograms/kg/min. In long-term infusion studies, flestolol was well tolerated at the effective beta-blocking dose (5 micrograms/kg/min) for up to seven days. Flestolol blood concentrations increased linearly with increasing dose and good correlation exists between blood concentrations of flestolol and beta-adrenergic blockade. Flestolol produced a dose-dependent attenuation of isoproterenol-induced tachycardia. Electrophysiologic and hemodynamic effects of flestolol are similar to those of other beta blockers. In contrast with other beta blockers, flestolol-induced effects reverse rapidly (within 30 minutes) following discontinuation because of its short half-life. Flestolol effectively reduced heart rate in patients with supraventricular tachyarrhythmia. In patients with unstable angina, flestolol infusion was found to be safe and effective in controlling chest pain. It is concluded that flestolol is a potent, well-tolerated, ultra-short-acting beta-adrenergic blocking agent. Use of flestolol in the critical care setting is currently undergoing investigation.

Output: Chemical/Disease Entities: Flestolol (Chemical), Flestolol (Chemical), ACC-9089 (Chemical), Flestolol (Chemical), flestolol (Chemical), Flestolol (Chemical), flestolol (Chemical), Flestolol (Chemical), isoproterenol (Chemical), tachycardia (Disease), flestolol (Chemical), flestolol (Chemical), Flestolol (Chemical), supraventricular tachyarrhythmia (Disease), unstable angina (Disease), flestolol (Chemical), chest pain (Disease), flestolol (Chemical), flestolol (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Adverse effect of the calcium channel blocker nitrendipine on nephrosclerosis in rats with renovascular hypertension. The effect of a 6-week treatment with the calcium channel blocker nitrendipine or the angiotensin converting enzyme inhibitor enalapril on blood pressure, albuminuria, renal hemodynamics, and morphology of the nonclipped kidney was studied in rats with two-kidney, one clip renovascular hypertension. Six weeks after clipping of one renal artery, hypertensive rats (178 +/- 4 mm Hg) were randomly assigned to three groups: untreated hypertensive controls (n = 8), enalapril-treated (n = 8), or nitrendipine-treated (n = 10). Sham-operated rats served as normotensive controls (128 +/- 3 mm Hg, n = 8). After 6 weeks of treatment, renal hemodynamics (glomerular filtration rate and renal plasma flow) were measured in the anesthetized rats. Renal tissue was obtained for determination of glomerular size and sclerosis. Enalapril but not nitrendipine reduced blood pressure significantly. After 6 weeks of therapy, glomerular filtration rate was not different among the studied groups. Renal plasma flow increased, but albumin excretion and glomerulosclerosis did not change after enalapril treatment. In contrast, in the nitrendipine-treated group albuminuria increased from 12.8 +/- 2 progressively to 163 +/- 55 compared with 19.2 +/- 9 mg/24 hr in the hypertensive controls. Furthermore, glomerulosclerosis index was significantly increased in the nitrendipine-treated group compared with the hypertensive controls (0.38 +/- 0.1 versus 0.13 +/- 0.04). In addition, glomerular size was higher in the nitrendipine-treated group (14.9 +/- 0.17 10(-3) mm2) but lower in the enalapril-treated group (11.5 +/- 0.15 10(-3) mm2) compared with the hypertensive controls (12.1 +/- 0.17 10(-3) mm2).(ABSTRACT TRUNCATED AT 250 WORDS)

Output: Chemical/Disease Entities: calcium (Chemical), nitrendipine (Chemical), nephrosclerosis (Disease), renovascular hypertension (Disease), calcium (Chemical), nitrendipine (Chemical), angiotensin (Chemical), enalapril (Chemical), albuminuria (Disease), renovascular hypertension (Disease), hypertensive (Disease), hypertensive (Disease), enalapril (Chemical), nitrendipine (Chemical), Enalapril (Chemical), nitrendipine (Chemical), glomerulosclerosis (Disease), enalapril (Chemical), nitrendipine (Chemical), albuminuria (Disease), hypertensive (Disease), glomerulosclerosis (Disease), nitrendipine (Chemical), hypertensive (Disease), nitrendipine (Chemical), enalapril (Chemical), hypertensive (Disease)


Instruction: Extract chemical and disease entities from the following text.

Input: Treatment of tinnitus by intratympanic instillation of lignocaine (lidocaine) 2 per cent through ventilation tubes. Idiopathic subjective tinnitus (IST) is one of the most obscure otological pathologies. This paper presents the results of treating IST by intratympanic instillation of lignocaine (lidocaine) 2 per cent through a grommet, for five weekly courses. Fifty-two patients suffering from intractable tinnitus entered this therapeutic trial, but only nine finished all five courses. In one patient, the tinnitus was almost completely abolished, but in all the nine patients the decompensated tinnitus changed to a compensated one. We suggest this mode of treatment for patients that were previously treated by drugs, acupuncture and biofeedback, with disappointing results. Patients should be warned about the side effects of vertigo and vomiting, which subsides gradually with every new instillation, and that the tinnitus may not disappear but will be alleviated, enabling them to cope more easily with the disease and lead a more normal life.

Output: Chemical/Disease Entities: tinnitus (Disease), lignocaine (Chemical), lidocaine (Chemical), Idiopathic subjective tinnitus (Disease), IST (Disease), IST (Disease), lignocaine (Chemical), lidocaine (Chemical), tinnitus (Disease), tinnitus (Disease), tinnitus (Disease), vertigo (Disease), vomiting (Disease), tinnitus (Disease)


Instruction: Extract chemical and disease entities from the following text.

Input: Perhexiline maleate and peripheral neuropathy. Peripheral neuropathy has been noted as a complication of therapy with perhexiline maleate, a drug widely used in France (and in clinical trials in the United States) for the prophylactic treatment of angina pectoris. In 24 patients with this complication, the marked slowing of motor nerve conduction velocity and the electromyographic changes imply mainly a demyelinating disorder. Improvement was noted with cessation of therapy. In a few cases the presence of active denervation signified a poor prognosis, with only slight improvement. The underlying mechanism causing the neuropathy is not yet fully known, although some evidence indicates that it may be a lipid storage process.

Output: Chemical/Disease Entities: Perhexiline maleate (Chemical), peripheral neuropathy (Disease), Peripheral neuropathy (Disease), perhexiline maleate (Chemical), angina pectoris (Disease), demyelinating disorder (Disease), neuropathy (Disease)


Instruction: Extract chemical and disease entities from the following text.

Input: Effect of humoral modulators of morphine-induced increase in locomotor activity of mice. The effect of humoral modulators on the morphine-induced increase in locomotor activity of mice was studied. The subcutaneous administration of 10 mg/kg of morphine-HC1 produced a marked increase in locomotor activity in mice. The morphine-induced hyperactivity was potentiated by scopolamine and attenuated by physostigmine. In contrast, both methscopolamine and neostigmine, which do not penetrate the blood-brain barrier, had no effect on the hyperactivity produced by morphine. Pretreatment of mice with alpha-methyltyrosine (20 mg/kg i.p., one hour), an inhibitor of tyrosine hydroxylase, significantly decreased the activity-increasing effects of morphine. On the other hand, pretreatment with p-chlorophenylalamine (3 X 320 mg/kg i.p., 24 hr), a serotonin depletor, caused no significant change in the hyperactivity. The study suggests that the activity-increasing effects of morphine are mediated by the release of catecholamines from adrenergic neurons in the brain. And the results are consistent with the hypothesis that morphine acts by retarding the release of acetylcholine at some central cholinergic synapses. It is also suggested from collected evidence that the activity-increasing effects of morphine in mice are mediated by mechanisms different from those which mediate the activity-increasing effects of morphine in rats.

Output: Chemical/Disease Entities: morphine (Chemical), increase in locomotor activity (Disease), morphine (Chemical), increase in locomotor activity (Disease), morphine (Chemical), increase in locomotor activity (Disease), morphine (Chemical), hyperactivity (Disease), scopolamine (Chemical), physostigmine (Chemical), methscopolamine (Chemical), neostigmine (Chemical), hyperactivity (Disease), morphine (Chemical), alpha-methyltyrosine (Chemical), tyrosine (Chemical), morphine (Chemical), p-chlorophenylalamine (Chemical), serotonin (Chemical), hyperactivity (Disease), morphine (Chemical), catecholamines (Chemical), morphine (Chemical), acetylcholine (Chemical), morphine (Chemical), morphine (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Mechanisms of FK 506-induced hypertension in the rat. -Tacrolimus (FK 506) is a powerful, widely used immunosuppressant. The clinical utility of FK 506 is complicated by substantial hypertension and nephrotoxicity. To clarify the mechanisms of FK 506-induced hypertension, we studied the chronic effects of FK 506 on the synthesis of endothelin-1 (ET-1), the expression of mRNA of ET-1 and endothelin-converting enzyme-1 (ECE-1), the endothelial nitric oxide synthase (eNOS) activity, and the expression of mRNA of eNOS and C-type natriuretic peptide (CNP) in rat blood vessels. In addition, the effect of the specific endothelin type A receptor antagonist FR 139317 on FK 506-induced hypertension in rats was studied. FK 506, 5 mg. kg-1. d-1 given for 4 weeks, elevated blood pressure from 102+/-13 to 152+/-15 mm Hg and increased the synthesis of ET-1 and the levels of ET-1 mRNA in the mesenteric artery (240% and 230%, respectively). Little change was observed in the expression of ECE-1 mRNA and CNP mRNA. FK 506 decreased eNOS activity and the levels of eNOS mRNA in the aorta (48% and 55%, respectively). The administration of FR 139317 (10 mg. kg-1. d-1) prevented FK 506-induced hypertension in rats. These results indicate that FK 506 may increase blood pressure not only by increasing ET-1 production but also by decreasing NO synthesis in the vasculature.

Output: Chemical/Disease Entities: FK 506 (Chemical), hypertension (Disease), Tacrolimus (Chemical), FK 506 (Chemical), FK 506 (Chemical), hypertension (Disease), nephrotoxicity (Disease), FK 506 (Chemical), hypertension (Disease), FK 506 (Chemical), nitric oxide (Chemical), FR 139317 (Chemical), FK 506 (Chemical), hypertension (Disease), FK 506 (Chemical), FK 506 (Chemical), FR 139317 (Chemical), FK 506 (Chemical), hypertension (Disease), FK 506 (Chemical), NO (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Suxamethonium induced prolonged apnea in a patient receiving electroconvulsive therapy. Suxamethonium causes prolonged apnea in patients in whom pseudocholinesterase enzyme gets deactivated by organophosphorus (OP) poisons. Here, we present a similar incident in a severely depressed patient who received electroconvulsive therapy (ECT). Prolonged apnea in our case ensued because the information about suicidal attempt by OP compound was concealed from the treating team.

Output: Chemical/Disease Entities: Suxamethonium (Chemical), apnea (Disease), Suxamethonium (Chemical), apnea (Disease), organophosphorus (OP) poisons (Chemical), depressed (Disease), apnea (Disease), OP compound (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: The effects of the adjunctive bupropion on male sexual dysfunction induced by a selective serotonin reuptake inhibitor: a double-blind placebo-controlled and randomized study. OBJECTIVE: To determine the safety and efficacy of adjunctive bupropion sustained-release (SR) on male sexual dysfunction (SD) induced by a selective serotonin reuptake inhibitor (SSRI), as SD is a common side-effect of SSRIs and the most effective treatments have yet to be determined. PATIENTS AND METHODS: The randomized sample consisted of 234 euthymic men who were receiving some type of SSRI. The men were randomly assigned to bupropion SR (150 mg twice daily, 117) or placebo (twice daily, 117) for 12 weeks. Efficacy was evaluated using the Clinical Global Impression-Sexual Function (CGI-SF; the primary outcome measure), the International Index of Erectile Function (IIEF), Arizona Sexual Experience Scale (ASEX), and Erectile Dysfunction Inventory of Treatment Satisfaction (EDITS) (secondary outcome measures). Participants were followed biweekly during study period. RESULTS: After 12 weeks of treatment, the mean (sd) scores for CGI-SF were significantly lower, i.e. better, in patients on bupropion SR, at 2.4 (1.2), than in the placebo group, at 3.9 (1.1) (P= 0.01). Men who received bupropion had a significant increase in the total IIEF score (54.4% vs 1.2%; P= 0.003), and in the five different domains of the IIEF. Total ASEX scores were significantly lower, i.e. better, among men who received bupropion than placebo, at 15.5 (4.3) vs 21.5 (4.7) (P= 0.002). The EDITS scores were 67.4 (10.2) for the bupropion and 36.3 (11.7) for the placebo group (P= 0.001). The ASEX score and CGI-SF score were correlated (P= 0.003). In linear regression analyses the CGI-SF score was not affected significantly by the duration of SD, type of SSRI used and age. CONCLUSIONS: Bupropion is an effective treatment for male SD induced by SSRIs. These results provide empirical support for conducting a further study of bupropion.

Output: Chemical/Disease Entities: bupropion (Chemical), sexual dysfunction (Disease), selective serotonin reuptake inhibitor (Chemical), bupropion (Chemical), sexual dysfunction (Disease), SD (Disease), selective serotonin reuptake inhibitor (Chemical), SSRI (Chemical), SD (Disease), SSRIs (Chemical), SSRI (Chemical), bupropion (Chemical), Erectile Dysfunction (Disease), bupropion (Chemical), bupropion (Chemical), bupropion (Chemical), bupropion (Chemical), SD (Disease), SSRI (Chemical), Bupropion (Chemical), SD (Disease), SSRIs (Chemical), bupropion (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Lamivudine for the prevention of hepatitis B virus reactivation in hepatitis-B surface antigen (HBSAG) seropositive cancer patients undergoing cytotoxic chemotherapy. Hepatitis B virus (HBV) is one of the major causes of chronic liver disease worldwide. Cancer patients who are chronic carriers of HBV have a higher hepatic complication rate while receiving cytotoxic chemotherapy (CT) and this has mainly been attributed to HBV reactivation. In this study, cancer patients who have solid and hematological malignancies with chronic HBV infection received the antiviral agent lamivudine prior and during CT compared with historical control group who did not receive lamivudine. The objectives were to assess the efficacy of lamivudine in reducing the incidence of HBV reactivation, and diminishing morbidity and mortality during CT. Two groups were compared in this study. The prophylactic lamivudin group consisted of 37 patients who received prophylactic lamivudine treatment. The historical controls consisted of 50 consecutive patients who underwent CT without prophylactic lamivudine. They were followed up during and for 8 weeks after CT. The outcomes were compared for both groups. Of our control group (n= 50), 21 patients (42%) were established hepatitis. Twelve (24%) of them were evaluated as severe hepatitis. In the prophylactic lamivudine group severe hepatitis were observed only in 1 patient (2.7%) of 37 patients (p < 0.006). Comparison of the mean ALT values revealed significantly higher mean alanine aminotransferase (ALT) values in the control group than the prophylactic lamivudine group; 154:64 (p < 0.32). Our study suggests that prophylactic lamivudine significantly decreases the incidence of HBV reactivation and overall morbidity in cancer patients during and after immunosuppressive therapy. Further studies are needed to determine the most appropriate nucleoside or nucleotide analogue for antiviral prophylaxis during CT and the optimal duration of administration after completion of CT.

Output: Chemical/Disease Entities: Lamivudine (Chemical), hepatitis B (Disease), hepatitis-B surface antigen (Chemical), HBSAG (Chemical), cancer (Disease), Hepatitis B (Disease), liver disease (Disease), Cancer (Disease), hepatic complication (Disease), cancer (Disease), hematological malignancies (Disease), HBV infection (Disease), lamivudine (Chemical), lamivudine (Chemical), lamivudine (Chemical), lamivudin (Chemical), lamivudine (Chemical), lamivudine (Chemical), hepatitis (Disease), hepatitis (Disease), lamivudine (Chemical), hepatitis (Disease), alanine (Chemical), lamivudine (Chemical), lamivudine (Chemical), cancer (Disease), nucleoside (Chemical), nucleotide (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Ginsenoside Rg1 restores the impairment of learning induced by chronic morphine administration in rats. Rg1, as a ginsenoside extracted from Panax ginseng, could ameliorate spatial learning impairment. Previous studies have demonstrated that Rg1 might be a useful agent for the prevention and treatment of the adverse effects of morphine. The aim of this study was to investigate the effect of Rg1 on learning impairment by chronic morphine administration and the mechanism responsible for this effect. Male rats were subcutaneously injected with morphine (10 mg/kg) twice a day at 12 hour intervals for 10 days, and Rg1 (30 mg/kg) was intraperitoneally injected 2 hours after the second injection of morphine once a day for 10 days. Spatial learning capacity was assessed in the Morris water maze. The results showed that rats treated with Morphine/Rg1 decreased escape latency and increased the time spent in platform quadrant and entering frequency. By implantation of electrodes and electrophysiological recording in vivo, the results showed that Rg1 restored the long-term potentiation (LTP) impaired by morphine in both freely moving and anaesthetised rats. The electrophysiological recording in vitro showed that Rg1 restored the LTP in slices from the rats treated with morphine, but not changed LTP in the slices from normal saline- or morphine/Rg1-treated rats; this restoration could be inhibited by N-methyl-D-aspartate (NMDA) receptor antagonist MK801. We conclude that Rg1 may significantly improve the spatial learning capacity impaired by chonic morphine administration and restore the morphine-inhibited LTP. This effect is NMDA receptor dependent.

Output: Chemical/Disease Entities: Ginsenoside Rg1 (Chemical), impairment of learning (Disease), morphine (Chemical), Rg1 (Chemical), ginsenoside (Chemical), learning impairment (Disease), Rg1 (Chemical), morphine (Chemical), Rg1 (Chemical), learning impairment (Disease), morphine (Chemical), morphine (Chemical), Rg1 (Chemical), morphine (Chemical), Morphine (Chemical), Rg1 (Chemical), Rg1 (Chemical), morphine (Chemical), Rg1 (Chemical), morphine (Chemical), morphine (Chemical), Rg1 (Chemical), N-methyl-D-aspartate (Chemical), NMDA (Chemical), MK801 (Chemical), Rg1 (Chemical), morphine (Chemical), morphine (Chemical), NMDA (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: A study on the effect of the duration of subcutaneous heparin injection on bruising and pain. AIM: This study was carried out to determine the effect of injection duration on bruising and pain following the administration of the subcutaneous injection of heparin. BACKGROUND: Although different methods to prevent bruising and pain following the subcutaneous injection of heparin have been widely studied and described, the effect of injection duration on the occurrence of bruising and pain is little documented. DESIGN: This study was designed as within-subject, quasi-experimental research. METHOD: The sample for the study consisted of 50 patients to whom subcutaneous heparin was administered. Heparin was injected over 10 seconds on the right abdominal site and 30 seconds on the left abdominal site. Injections areas were assessed for the presence of bruising at 48 and 72 hours after each injection. Dimensions of the bruising on the heparin applied areas were measured using transparent millimetric measuring paper. The visual analog scale (VAS) was used to measure pain intensity and a stop-watch was used to time the pain period. Data were analysed using chi-square test, Mann-Whitney U, Wilcoxon signed ranks tests and correlation. RESULTS: The percentage of bruising occurrence was 64% with the injection of 10 seconds duration and 42% in the 30-second injection. It was determined that the size of the bruising was smaller in the 30-second injection. Pain intensity and pain period were statistically significantly lower for the 30-second injection than for the 10-second injection. CONCLUSIONS: It was determined that injection duration had an effect on bruising and pain following the subcutaneous administration of heparin. This study should be repeated on a larger sample. RELEVANCE TO CLINICAL PRACTICE: When administering subcutaneous heparin injections, it is important to extend the duration of the injection.

Output: Chemical/Disease Entities: heparin (Chemical), bruising (Disease), pain (Disease), bruising (Disease), pain (Disease), heparin (Chemical), bruising (Disease), pain (Disease), heparin (Chemical), bruising (Disease), pain (Disease), heparin (Chemical), Heparin (Chemical), bruising (Disease), bruising (Disease), heparin (Chemical), pain (Disease), pain (Disease), bruising (Disease), bruising (Disease), Pain (Disease), pain (Disease), bruising (Disease), pain (Disease), heparin (Chemical), heparin (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Acute reserpine and subchronic haloperidol treatments change synaptosomal brain glutamate uptake and elicit orofacial dyskinesia in rats. Reserpine- and haloperidol-induced orofacial dyskinesia are putative animal models of tardive dyskinesia (TD) whose pathophysiology has been related to free radical generation and oxidative stress. In the present study, the authors induced orofacial dyskinesia by acute reserpine and subchronic haloperidol administration to rats. Reserpine injection (one dose of 1 mg/kg s.c.) every other day for 3 days caused a significant increase in vacuous chewing, tongue protrusion and duration of facial twitching, compared to the control. Haloperidol administration (one dose of 12 mg/kg once a week s.c.) for 4 weeks caused an increase in vacuous chewing, tongue protrusion and duration of facial twitching observed in four weekly evaluations. After the treatments and behavioral observation, glutamate uptake by segments of the brain was analyzed. A decreased glutamate uptake was observed in the subcortical parts of animals treated with reserpine and haloperidol, compared to the control. Importantly, a decrease in glutamate uptake correlates negatively with an increase in the incidence of orofacial diskinesia. These results indicate that early changes in glutamate transport may be related to the development of vacuous chewing movements in rats.

Output: Chemical/Disease Entities: reserpine (Chemical), haloperidol (Chemical), glutamate (Chemical), orofacial dyskinesia (Disease), Reserpine (Chemical), haloperidol (Chemical), orofacial dyskinesia (Disease), tardive dyskinesia (Disease), TD (Disease), orofacial dyskinesia (Disease), reserpine (Chemical), haloperidol (Chemical), Reserpine (Chemical), Haloperidol (Chemical), glutamate (Chemical), glutamate (Chemical), reserpine (Chemical), haloperidol (Chemical), glutamate (Chemical), orofacial diskinesia (Disease), glutamate (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Acute psychosis due to treatment with phenytoin in a nonepileptic patient. The development of psychosis related to antiepileptic drug treatment is usually attributed to the interaction between the epileptic brain substratum and the antiepileptic drugs. The case of a nonepileptic patient who developed psychosis following phenytoin treatment for trigeminal neuralgia is described. This case suggests that the psychotic symptoms that occur following phenytoin treatment in some epileptic patients may be the direct result of medication, unrelated to seizures.

Output: Chemical/Disease Entities: Acute psychosis (Disease), phenytoin (Chemical), psychosis (Disease), epileptic (Disease), psychosis (Disease), phenytoin (Chemical), trigeminal neuralgia (Disease), psychotic symptoms (Disease), phenytoin (Chemical), epileptic (Disease), seizures (Disease)


Instruction: Extract chemical and disease entities from the following text.

Input: The effect of treatment with gum Arabic on gentamicin nephrotoxicity in rats: a preliminary study. In the present work we assessed the effect of treatment of rats with gum Arabic on acute renal failure induced by gentamicin (GM) nephrotoxicity. Rats were treated with the vehicle (2 mL/kg of distilled water and 5% w/v cellulose, 10 days), gum Arabic (2 mL/kg of a 10% w/v aqueous suspension of gum Arabic powder, orally for 10 days), or gum Arabic concomitantly with GM (80mg/kg/day intramuscularly, during the last six days of the treatment period). Nephrotoxicity was assessed by measuring the concentrations of creatinine and urea in the plasma and reduced glutathione (GSH) in the kidney cortex, and by light microscopic examination of kidney sections. The results indicated that concomitant treatment with gum Arabic and GM significantly increased creatinine and urea by about 183 and 239%, respectively (compared to 432 and 346%, respectively, in rats treated with cellulose and GM), and decreased that of cortical GSH by 21% (compared to 27% in the cellulose plus GM group) The GM-induced proximal tubular necrosis appeared to be slightly less severe in rats given GM together with gum Arabic than in those given GM and cellulose. It could be inferred that gum Arabic treatment has induced a modest amelioration of some of the histological and biochemical indices of GM nephrotoxicity. Further work is warranted on the effect of the treatments on renal functional aspects in models of chronic renal failure, and on the mechanism(s) involved.

Output: Chemical/Disease Entities: gum Arabic (Chemical), gentamicin (Chemical), nephrotoxicity (Disease), gum Arabic (Chemical), acute renal failure (Disease), gentamicin (Chemical), GM (Chemical), nephrotoxicity (Disease), gum Arabic (Chemical), gum Arabic (Chemical), gum Arabic (Chemical), GM (Chemical), Nephrotoxicity (Disease), creatinine (Chemical), urea (Chemical), glutathione (Chemical), GSH (Chemical), gum Arabic (Chemical), GM (Chemical), creatinine (Chemical), urea (Chemical), GM (Chemical), GSH (Chemical), GM (Chemical), GM (Chemical), tubular necrosis (Disease), GM (Chemical), gum Arabic (Chemical), GM (Chemical), gum Arabic (Chemical), GM (Chemical), nephrotoxicity (Disease), chronic renal failure (Disease)


Instruction: Extract chemical and disease entities from the following text.

Input: Visual hallucinations associated with zonisamide. Zonisamide is a broad-spectrum antiepileptic drug used to treat various types of seizures. Although visual hallucinations have not been reported as an adverse effect of this agent, we describe three patients who experienced complex visual hallucinations and altered mental status after zonisamide treatment was begun or its dosage increased. All three had been diagnosed earlier with epilepsy, and their electroencephalogram (EEG) findings were abnormal. During monitoring, visual hallucinations did not correlate with EEG readings, nor did video recording capture any of the described events. None of the patients had experienced visual hallucinations before this event. The only recent change in their treatment was the introduction or increased dosage of zonisamide. With either discontinuation or decreased dosage of the drug the symptoms disappeared and did not recur. Further observations and reports will help clarify this adverse effect. Until then, clinicians need to be aware of this possible complication associated with zonisamide.

Output: Chemical/Disease Entities: Visual hallucinations (Disease), zonisamide (Chemical), Zonisamide (Chemical), seizures (Disease), visual hallucinations (Disease), visual hallucinations (Disease), zonisamide (Chemical), epilepsy (Disease), visual hallucinations (Disease), visual hallucinations (Disease), zonisamide (Chemical), zonisamide (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: GLEPP1 receptor tyrosine phosphatase (Ptpro) in rat PAN nephrosis. A marker of acute podocyte injury. Glomerular epithelial protein 1 (GLEPP1) is a podocyte receptor membrane protein tyrosine phosphatase located on the apical cell membrane of visceral glomerular epithelial cell and foot processes. This receptor plays a role in regulating the structure and function of podocyte foot process. To better understand the utility of GLEPP1 as a marker of glomerular injury, the amount and distribution of GLEPP1 protein and mRNA were examined by immunohistochemistry, Western blot and RNase protection assay in a model of podocyte injury in the rat. Puromycin aminonucleoside nephrosis was induced by single intraperitoneal injection of puromycin aminonucleoside (PAN, 20 mg/100g BW). Tissues were analyzed at 0, 5, 7, 11, 21, 45, 80 and 126 days after PAN injection so as to include both the acute phase of proteinuria associated with foot process effacement (days 5-11) and the chronic phase of proteinuria associated with glomerulosclerosis (days 45-126). At day 5, GLEPP1 protein and mRNA were reduced from the normal range (265.2 +/- 79.6 x 10(6) moles/glomerulus and 100%) to 15% of normal (41.8 +/- 4.8 x 10(6) moles/glomerulus, p < 0.005). This occurred in association with an increase in urinary protein content from 1.8 +/- 1 to 99.0 +/- 61 mg/day (p < 0.001). In contrast, podocalyxin did not change significantly at this time. By day 11, GLEPP1 protein and mRNA had begun to return towards baseline. By day 45-126, at a time when glomerular scarring was present, GLEPP1 was absent from glomerulosclerotic areas although the total glomerular content of GLEPP1 was not different from normal. We conclude that GLEPP1 expression, unlike podocalyxin, reflects podocyte injury induced by PAN. GLEPP1 expression may be a useful marker of podocyte injury.

Output: Chemical/Disease Entities: tyrosine (Chemical), PAN (Chemical), nephrosis (Disease), tyrosine (Chemical), glomerular injury (Disease), Puromycin aminonucleoside (Chemical), nephrosis (Disease), puromycin aminonucleoside (Chemical), PAN (Chemical), PAN (Chemical), proteinuria (Disease), proteinuria (Disease), glomerulosclerosis (Disease), PAN (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Ticlopidine-induced aplastic anemia: report of three Chinese patients and review of the literature. In this study, three Chinese patients with ticlopidine-induced aplastic anemia were reported and another 13 patients in the English literature were reviewed. We attempted to find underlying similarities, evaluate the risk factors, and identify appropriate treatment for this complication. All but one of the patients were over 60 years old, and the 6 who died were all older than 65. Therefore, old age may be a risk factor for developing this complication. Agranulocytosis occurred 3-20 weeks after initiation of ticlopidine, so frequent examination of white cell count during treatment is recommended. There seemed to be no direct correlation between the dose or duration used and the severity of bone marrow suppression. Treatment for ticlopidine-induced aplastic anemia with colony-stimulating factors seemed to have little effect. The fact that 5 of the 6 patients who received concurrent calcium channel blockers died, should alert clinicians to be more cautious when using these two drugs simultaneously.

Output: Chemical/Disease Entities: Ticlopidine (Chemical), aplastic anemia (Disease), ticlopidine (Chemical), aplastic anemia (Disease), Agranulocytosis (Disease), ticlopidine (Chemical), bone marrow suppression (Disease), ticlopidine (Chemical), aplastic anemia (Disease), calcium (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Facilitation of memory retrieval by pre-test morphine and its state dependency in the step-through type passive avoidance learning test in mice. Amnesia produced by scopolamine and cycloheximide were reversed by morphine given 30 min before the test trial (pre-test), and pre-test morphine also facilitated the memory retrieval in the animals administered naloxone during the training trial. Similarly, pre-test scopolamine partially reversed the scopolamine-induced amnesia, but not significantly; and pre-test cycloheximide failed to reverse the cycloheximide-induced amnesia. These results suggest that the facilitation of memory retrieval by pre-test morphine might be the direct action of morphine rather than a state dependent effect.

Output: Chemical/Disease Entities: morphine (Chemical), Amnesia (Disease), scopolamine (Chemical), cycloheximide (Chemical), morphine (Chemical), morphine (Chemical), naloxone (Chemical), scopolamine (Chemical), scopolamine (Chemical), amnesia (Disease), cycloheximide (Chemical), cycloheximide (Chemical), amnesia (Disease), morphine (Chemical), morphine (Chemical)


Instruction: Extract chemical and disease entities from the following text.

Input: Test conditions influence the response to a drug challenge in rodents. These studies were conducted to examine the differential response to a drug challenge under varied experimental test conditions routinely employed to study drug-induced behavioral and neurophysiological responses in rodents. Apomorphine, a nonselective dopamine agonist, was selected due to its biphasic behavioral effects, its ability to induce hypothermia, and to produce distinct changes to dopamine turnover in the rodent brain. From such experiments there is evidence that characterization and detection of apomorphine-induced activity in rodents critically depends upon the test conditions employed. In rats, detection of apomorphine-induced hyperactivity was facilitated by a period of acclimatization to the test conditions. Moreover, test conditions can impact upon other physiological responses to apomorphine such as drug-induced hypothermia. In mice, apomorphine produced qualitatively different responses under novel conditions when compared to those behaviors elicited in the home test cage. Drug-induced gross activity counts were increased in the novel exploratory box only, while measures of stereotypic behavior were similar in both. By contrast, apomorphine-induced locomotion was more prominent in the novel exploratory box. Dopamine turnover ratios (DOPAC:DA and HVA:DA) were found to be lower in those animals exposed to the exploratory box when compared to their home cage counterparts. However, apomorphine-induced reductions in striatal dopamine turnover were detected in both novel and home cage environments. The implications of these findings are discussed with particular emphasis upon conducting psychopharmacological challenge tests in rodents.

Output: Chemical/Disease Entities: Apomorphine (Chemical), dopamine agonist (Chemical), hypothermia (Disease), dopamine (Chemical), apomorphine (Chemical), apomorphine (Chemical), hyperactivity (Disease), apomorphine (Chemical), hypothermia (Disease), apomorphine (Chemical), apomorphine (Chemical), Dopamine (Chemical), DOPAC (Chemical), DA (Chemical), HVA (Chemical), DA (Chemical), apomorphine (Chemical), dopamine (Chemical)