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.

morphine

morphine

morphine

morphine

scopolamine

physostigmine

methscopolamine

neostigmine

morphine

alpha - methyltyrosine

tyrosine

morphine

p - chlorophenylalamine

serotonin

morphine

catecholamines

morphine

acetylcholine

morphine

morphine

increase in locomotor activity

increase in locomotor activity

increase in locomotor activity

hyperactivity

hyperactivity

hyperactivity

scopolamine

increase in locomotor activity

scopolamine

increase in locomotor activity

scopolamine

increase in locomotor activity

scopolamine

hyperactivity

scopolamine

hyperactivity

scopolamine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

increase in locomotor activity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity


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.

FK 506

Tacrolimus

FK 506

FK 506

FK 506

FK 506

nitric oxide

FR 139317

FK 506

FK 506

FK 506

FR 139317

FK 506

FK 506

NO

hypertension

hypertension

nephrotoxicity

hypertension

hypertension

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

Tacrolimus

hypertension

Tacrolimus

hypertension

Tacrolimus

hypertension

Tacrolimus

hypertension

Tacrolimus

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension

FK 506

hypertension


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.

Suxamethonium

Suxamethonium

organophosphorus (OP) poisons

OP compound

apnea

apnea

depressed

apnea

organophosphorus (OP) poisons

apnea

organophosphorus (OP) poisons

apnea

organophosphorus (OP) poisons

apnea

OP compound

apnea

OP compound

apnea

OP compound

apnea

Suxamethonium

apnea

Suxamethonium

apnea

Suxamethonium

apnea

Suxamethonium

apnea

Suxamethonium

apnea

Suxamethonium

apnea


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.

bupropion

selective serotonin reuptake inhibitor

bupropion

selective serotonin reuptake inhibitor

SSRI

SSRIs

SSRI

bupropion

bupropion

bupropion

bupropion

bupropion

SSRI

Bupropion

SSRIs

bupropion

sexual dysfunction

sexual dysfunction

SD

SD

Erectile Dysfunction

SD

SD

selective serotonin reuptake inhibitor

Erectile Dysfunction

selective serotonin reuptake inhibitor

Erectile Dysfunction

SSRI

Erectile Dysfunction

SSRIs

Erectile Dysfunction

SSRI

Erectile Dysfunction

SSRI

Erectile Dysfunction

SSRIs

Erectile Dysfunction


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.

Lamivudine

hepatitis - B surface antigen

HBSAG

lamivudine

lamivudine

lamivudine

lamivudin

lamivudine

lamivudine

lamivudine

alanine

lamivudine

lamivudine

nucleoside

nucleotide

hepatitis B

cancer

Hepatitis B

liver disease

Cancer

hepatic complication

cancer

hematological malignancies

HBV infection

hepatitis

hepatitis

hepatitis

cancer

hepatitis - B surface antigen

hepatitis B

hepatitis - B surface antigen

Hepatitis B

hepatitis - B surface antigen

HBV infection

HBSAG

hepatitis B

HBSAG

Hepatitis B

HBSAG

HBV infection


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.

Ginsenoside Rg1

morphine

ginsenoside

morphine

morphine

morphine

morphine

Morphine

morphine

morphine

morphine

N - methyl - D - aspartate

NMDA

morphine

morphine

NMDA

impairment of learning

learning impairment

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

Morphine

impairment of learning

Morphine

learning impairment

Morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment

morphine

impairment of learning

morphine

learning impairment

morphine

learning impairment


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.

heparin

heparin

heparin

heparin

Heparin

heparin

heparin

heparin

bruising

pain

bruising

pain

bruising

pain

bruising

pain

bruising

bruising

pain

pain

bruising

bruising

Pain

pain

bruising

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

Heparin

pain

Heparin

pain

Heparin

pain

Heparin

pain

Heparin

pain

Heparin

pain

Heparin

Pain

Heparin

pain

Heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

pain

heparin

Pain

heparin

pain

heparin

pain

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

Heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising

heparin

bruising


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.

reserpine

haloperidol

glutamate

Reserpine

haloperidol

reserpine

haloperidol

Reserpine

Haloperidol

glutamate

glutamate

reserpine

haloperidol

glutamate

glutamate

orofacial dyskinesia

orofacial dyskinesia

tardive dyskinesia

TD

orofacial dyskinesia

orofacial diskinesia

haloperidol

orofacial dyskinesia

haloperidol

orofacial dyskinesia

haloperidol

tardive dyskinesia

haloperidol

TD

haloperidol

orofacial dyskinesia

haloperidol

orofacial diskinesia

haloperidol

orofacial dyskinesia

haloperidol

orofacial dyskinesia

haloperidol

tardive dyskinesia

haloperidol

TD

haloperidol

orofacial dyskinesia

haloperidol

orofacial diskinesia

haloperidol

orofacial dyskinesia

haloperidol

orofacial dyskinesia

haloperidol

tardive dyskinesia

haloperidol

TD

haloperidol

orofacial dyskinesia

haloperidol

orofacial diskinesia

Haloperidol

orofacial dyskinesia

Haloperidol

orofacial dyskinesia

Haloperidol

tardive dyskinesia

Haloperidol

TD

Haloperidol

orofacial dyskinesia

Haloperidol

orofacial diskinesia

haloperidol

orofacial dyskinesia

haloperidol

orofacial dyskinesia

haloperidol

tardive dyskinesia

haloperidol

TD

haloperidol

orofacial dyskinesia

haloperidol

orofacial diskinesia

reserpine

orofacial dyskinesia

reserpine

orofacial dyskinesia

reserpine

tardive dyskinesia

reserpine

TD

reserpine

orofacial dyskinesia

reserpine

orofacial diskinesia

Reserpine

orofacial dyskinesia

Reserpine

orofacial dyskinesia

Reserpine

tardive dyskinesia

Reserpine

TD

Reserpine

orofacial dyskinesia

Reserpine

orofacial diskinesia

reserpine

orofacial dyskinesia

reserpine

orofacial dyskinesia

reserpine

tardive dyskinesia

reserpine

TD

reserpine

orofacial dyskinesia

reserpine

orofacial diskinesia

Reserpine

orofacial dyskinesia

Reserpine

orofacial dyskinesia

Reserpine

tardive dyskinesia

Reserpine

TD

Reserpine

orofacial dyskinesia

Reserpine

orofacial diskinesia

reserpine

orofacial dyskinesia

reserpine

orofacial dyskinesia

reserpine

tardive dyskinesia

reserpine

TD

reserpine

orofacial dyskinesia

reserpine

orofacial diskinesia


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.

Acute psychosis

psychosis

epileptic

psychosis

trigeminal neuralgia

psychotic symptoms

epileptic

seizures

phenytoin

phenytoin

phenytoin

phenytoin

Acute psychosis

phenytoin

psychosis

phenytoin

psychosis

phenytoin

psychotic symptoms

phenytoin

Acute psychosis

phenytoin

psychosis

phenytoin

psychosis

phenytoin

psychotic symptoms

phenytoin

Acute psychosis

phenytoin

psychosis

phenytoin

psychosis

phenytoin

psychotic symptoms


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.

gum Arabic

gentamicin

gum Arabic

gentamicin

GM

gum Arabic

gum Arabic

gum Arabic

GM

creatinine

urea

glutathione

GSH

gum Arabic

GM

creatinine

urea

GM

GSH

GM

GM

GM

gum Arabic

GM

gum Arabic

GM

nephrotoxicity

acute renal failure

nephrotoxicity

Nephrotoxicity

tubular necrosis

nephrotoxicity

chronic renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

GM

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure

gum Arabic

acute renal failure


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.

Visual hallucinations

seizures

visual hallucinations

visual hallucinations

epilepsy

visual hallucinations

visual hallucinations

zonisamide

Zonisamide

zonisamide

zonisamide

zonisamide

zonisamide

Visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

Zonisamide

Visual hallucinations

Zonisamide

visual hallucinations

Zonisamide

visual hallucinations

Zonisamide

visual hallucinations

Zonisamide

visual hallucinations

zonisamide

Visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

Visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

Visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations

zonisamide

visual hallucinations


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.

tyrosine

PAN

tyrosine

Puromycin aminonucleoside

puromycin aminonucleoside

PAN

PAN

PAN

nephrosis

glomerular injury

nephrosis

proteinuria

proteinuria

glomerulosclerosis

PAN

proteinuria

PAN

proteinuria

Puromycin aminonucleoside

proteinuria

Puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

nephrosis

PAN

nephrosis

Puromycin aminonucleoside

nephrosis

Puromycin aminonucleoside

nephrosis

puromycin aminonucleoside

nephrosis

puromycin aminonucleoside

nephrosis

PAN

nephrosis

PAN

nephrosis

PAN

nephrosis

PAN

nephrosis

PAN

nephrosis

PAN

nephrosis


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.

Ticlopidine

ticlopidine

ticlopidine

ticlopidine

calcium

aplastic anemia

aplastic anemia

Agranulocytosis

bone marrow suppression

aplastic anemia

Ticlopidine

aplastic anemia

Ticlopidine

aplastic anemia

Ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

ticlopidine

aplastic anemia

Ticlopidine

Agranulocytosis

ticlopidine

Agranulocytosis

ticlopidine

Agranulocytosis

ticlopidine

Agranulocytosis


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.

morphine

scopolamine

cycloheximide

morphine

morphine

naloxone

scopolamine

scopolamine

cycloheximide

cycloheximide

morphine

morphine

Amnesia

amnesia

amnesia

scopolamine

Amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

Amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

Amnesia

scopolamine

amnesia

scopolamine

amnesia

cycloheximide

Amnesia

cycloheximide

amnesia

cycloheximide

amnesia

cycloheximide

Amnesia

cycloheximide

amnesia

cycloheximide

amnesia

cycloheximide

Amnesia

cycloheximide

amnesia

cycloheximide

amnesia


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.

Apomorphine

dopamine agonist

dopamine

apomorphine

apomorphine

apomorphine

apomorphine

apomorphine

Dopamine

DOPAC

DA

HVA

DA

apomorphine

dopamine

hypothermia

hyperactivity

hypothermia

Apomorphine

hypothermia

Apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

apomorphine

hypothermia

Apomorphine

hyperactivity

apomorphine

hyperactivity

apomorphine

hyperactivity

apomorphine

hyperactivity

apomorphine

hyperactivity

apomorphine

hyperactivity

apomorphine

hyperactivity