Input: A novel animal model to evaluate the ability of a drug delivery system to promote the passage through the BBB. The purpose of this investigation was to explore the potentiality of a novel animal model to be used for the in vivo evaluation of the ability of a drug delivery system to promote the passage through the blood - brain barrier (BBB) and / or to improve the brain localization of a bioactive compound. A Tween 80 - coated poly - L - lactid acid nanoparticles was used as a model of colloidal drug delivery system, able to trespass the BBB. Tacrine, administered in LiCl pre - treated rats, induces electrocorticographic seizures and delayed hippocampal damage. The toxic effects of tacrine - loaded poly - L - lactid acid nanoparticles (5mg / kg), a saline solution of tacrine (5mg / kg) and an empty colloidal nanoparticle suspension were compared following i. p. administration in LiCl - pre - treated Wistar rats. All the animals treated with tacrine - loaded nanoparticles showed an earlier outcome of CNS adverse symptoms, i. e. epileptic onset, with respect to those animals treated with the free compound (10 min vs. 22 min respectively). In addition, tacrine - loaded nanoparticles administration induced damage of neuronal cells in CA1 field of the hippocampus in all treated animals, while the saline solution of tacrine only in 60% of animals. Empty nanoparticles provided similar results to control (saline - treated) group of animals. In conclusion, the evaluation of time - to - onset of symptoms and the severity of neurodegenerative processes induced by the tacrine - lithium model of epilepsy in the rat, could be used to evaluate preliminarily the capability of a drug delivery system to trespass (or not) the BBB in vivo.

poly - L - lactid acid

Tacrine

LiCl

tacrine

poly - L - lactid acid

tacrine

LiCl

tacrine

tacrine

tacrine

tacrine

lithium

seizures

hippocampal damage

epileptic

damage of neuronal cells

epilepsy

LiCl

hippocampal damage

LiCl

damage of neuronal cells

LiCl

hippocampal damage

LiCl

damage of neuronal cells

Tacrine

hippocampal damage

Tacrine

damage of neuronal cells

tacrine

hippocampal damage

tacrine

damage of neuronal cells

tacrine

hippocampal damage

tacrine

damage of neuronal cells

tacrine

hippocampal damage

tacrine

damage of neuronal cells

tacrine

hippocampal damage

tacrine

damage of neuronal cells

tacrine

hippocampal damage

tacrine

damage of neuronal cells

tacrine

hippocampal damage

tacrine

damage of neuronal cells

LiCl

seizures

LiCl

seizures

Tacrine

seizures

tacrine

seizures

tacrine

seizures

tacrine

seizures

tacrine

seizures

tacrine

seizures

tacrine

seizures


Input: The antiarrhythmic effect and possible ionic mechanisms of pilocarpine on animal models. This study was designed to evaluate the effects of pilocarpine and explore the underlying ionic mechanism, using both aconitine - induced rat and ouabain - induced guinea pig arrhythmia models. Confocal microscopy was used to measure intracellular free - calcium concentrations ([Ca (2 +)] (i)) in isolated myocytes. The current data showed that pilocarpine significantly delayed onset of arrhythmias, decreased the time course of ventricular tachycardia and fibrillation, reduced arrhythmia score, and increased the survival time of arrhythmic rats and guinea pigs. [Ca (2 +)] (i) overload induced by aconitine or ouabain was reduced in isolated myocytes pretreated with pilocarpine. Moreover, M (3) - muscarinic acetylcholine receptor (mAChR) antagonist 4 - DAMP (4 - diphenylacetoxy - N - methylpiperidine - methiodide) partially abolished the beneficial effects of pilocarpine. These data suggest that pilocarpine produced antiarrhythmic actions on arrhythmic rat and guinea pig models induced by aconitine or ouabain via stimulating the cardiac M (3) - mAChR. The mechanism may be related to the improvement of Ca (2 +) handling.

pilocarpine

pilocarpine

aconitine

ouabain

calcium

Ca

pilocarpine

Ca

aconitine

ouabain

pilocarpine

acetylcholine

4 - DAMP

4 - diphenylacetoxy - N - methylpiperidine - methiodide

pilocarpine

pilocarpine

aconitine

ouabain

Ca

arrhythmia

arrhythmias

ventricular tachycardia and fibrillation

ventricular tachycardia

ventricular tachycardia and fibrillation

arrhythmia

arrhythmic

arrhythmic

ouabain

arrhythmia

ouabain

arrhythmias

ouabain

arrhythmia

ouabain

arrhythmic

ouabain

arrhythmic

ouabain

arrhythmia

ouabain

arrhythmias

ouabain

arrhythmia

ouabain

arrhythmic

ouabain

arrhythmic

ouabain

arrhythmia

ouabain

arrhythmias

ouabain

arrhythmia

ouabain

arrhythmic

ouabain

arrhythmic

aconitine

arrhythmia

aconitine

arrhythmias

aconitine

arrhythmia

aconitine

arrhythmic

aconitine

arrhythmic

aconitine

arrhythmia

aconitine

arrhythmias

aconitine

arrhythmia

aconitine

arrhythmic

aconitine

arrhythmic

aconitine

arrhythmia

aconitine

arrhythmias

aconitine

arrhythmia

aconitine

arrhythmic

aconitine

arrhythmic


Input: Disulfiram - induced transient optic and peripheral neuropathy: a case report. AIM: To report a case of optic and peripheral neuropathy after chronic use of disulfiram for alcohol dependence management. MATERIALS AND METHODS: A case report. RESULTS: A 57 - year - old male presented with gradual loss of vision in both eyes with intermittent headaches for 2 months. He also complained of paraesthesia with numbness in both feet. His vision was 6 / 15 and 2 / 60 in the right and left eyes, respectively. Fundoscopy revealed bilaterally swollen optic nerve heads. Visual field testing confirmed bilateral central - caecal scotomata. He had been taking disulfiram for alcohol dependence for the preceding 3 years. Disulfiram discontinuation lead to an immediate symptomatic improvement. CONCLUSION: Physicians initiating long - term disulfiram therapy should be aware of these adverse effects. They should recommend annual ophthalmic reviews with visual field testing. Patients should be reassured with respect to the reversibility of these adverse effects.

Disulfiram

disulfiram

disulfiram

Disulfiram

disulfiram

optic and peripheral neuropathy

optic and peripheral neuropathy

peripheral neuropathy

optic and peripheral neuropathy

optic and peripheral neuropathy

peripheral neuropathy

alcohol dependence

loss of vision

headaches

paraesthesia

numbness

scotomata

alcohol dependence

Disulfiram

paraesthesia

disulfiram

paraesthesia

disulfiram

paraesthesia

Disulfiram

paraesthesia

disulfiram

paraesthesia

Disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

Disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

disulfiram

optic and peripheral neuropathy

Disulfiram

scotomata

disulfiram

scotomata

disulfiram

scotomata

Disulfiram

scotomata

disulfiram

scotomata


Input: Sustained clinical improvement of a patient with decompensated hepatitis B virus - related cirrhosis after treatment with lamivudine monotherapy. Hepatitis B virus (HBV) infection, which causes liver cirrhosis and hepatocellular carcinoma, remains a major health problem in Asian countries. Recent development of vaccine for prevention is reported to be successful in reducing the size of chronically infected carriers, although the standard medical therapies have not been established up to now. In this report, we encountered a patient with decompensated HBV - related cirrhosis who exhibited the dramatic improvements after antiviral therapy. The patient was a 50 - year - old woman. Previous conventional medical treatments were not effective for this patient, thus this patient had been referred to our hospital. However, the administration of lamivudine, a reverse transcriptase inhibitor, for 23 months dramatically improved her liver severity. During this period, no drug resistant mutant HBV emerged, and the serum HBV - DNA level was continuously suppressed. These virological responses were also maintained even after the antiviral therapy was discontinued. Moreover, both hepatitis B surface antigen and e antigen were observed to have disappeared in this patient. The administration of lamivudine to patients with HBV - related cirrhosis, like our present case, should be considered as an initial medical therapeutic option, especially in countries where liver transplantation is not reliably available.

hepatitis B

cirrhosis

Hepatitis B virus (HBV) infection

liver cirrhosis

hepatocellular carcinoma

cirrhosis

cirrhosis

lamivudine

lamivudine

hepatitis B surface antigen and e antigen

hepatitis B surface antigen

hepatitis B surface antigen and e antigen

lamivudine

hepatitis B surface antigen and e antigen

hepatitis B

hepatitis B surface antigen and e antigen

Hepatitis B virus (HBV) infection

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

Hepatitis B virus (HBV) infection

hepatitis B surface antigen and e antigen

hepatitis B

hepatitis B surface antigen and e antigen

Hepatitis B virus (HBV) infection


Input: Dual effects of melatonin on barbiturate - induced narcosis in rats. Melatonin affects the circadian sleep / wake cycle, but it is not clear whether it may influence drug - induced narcosis. Sodium thiopenthal was administered intraperitoneally into male rats pre - treated with melatonin (0. 05, 0. 5, 5 and 50 mg / kg). Melatonin pre - treatment affected in a dual manner barbiturate narcosis, however, no dose - effect correlation was found. In particular, low doses reduced the latency to and prolonged the duration of barbiturate narcosis. In contrast, the highest dose of melatonin (50 mg / kg) caused a paradoxical increase in the latency and produced a sustained reduction of the duration of narcosis, and a reduction in mortality rate. Melatonin 0. 5 and 5 mg / kg influenced the duration but not the latency of ketamine - or diazepam - induced narcosis. Thus, the dual action of melatonin on pharmacological narcosis seems to be specific for the barbiturate mechanism of action.

melatonin

barbiturate

Melatonin

Sodium thiopenthal

melatonin

Melatonin

barbiturate

barbiturate

melatonin

Melatonin

ketamine

diazepam

melatonin

barbiturate

narcosis

narcosis

narcosis

narcosis

narcosis

narcosis

narcosis

Sodium thiopenthal

narcosis

Sodium thiopenthal

narcosis

Sodium thiopenthal

narcosis

Sodium thiopenthal

narcosis

Sodium thiopenthal

narcosis

Sodium thiopenthal

narcosis

Sodium thiopenthal

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

Melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

melatonin

narcosis

diazepam

narcosis

diazepam

narcosis

diazepam

narcosis

diazepam

narcosis

diazepam

narcosis

diazepam

narcosis

diazepam

narcosis

ketamine

narcosis

ketamine

narcosis

ketamine

narcosis

ketamine

narcosis

ketamine

narcosis

ketamine

narcosis

ketamine

narcosis


Input: Effects of NIK - 247 on cholinesterase and scopolamine - induced amnesia. The effects of NIK - 247 on cholinesterase, scopolamine - induced amnesia and spontaneous movement were examined and compared with those of the well - known cholinesterase inhibitors tacrine and E - 2020. NIK - 247, tacrine and E - 2020 all strongly inhibited acetylcholinesterase (AChE) in human red blood cells (IC50s = 1. 0 x 10 (- 6), 2. 9 x 10 (- 7) and 3. 7 x 10 (- 8) M, respectively). In addition, NIK - 247 and tacrine, but not E - 2020, strongly inhibited butyrylcholinestrase (BuChE) in human serum. All three drugs produced mixed inhibition of AChE activity. Moreover, the inhibitory effect of NIK - 247 on AChE was reversible. All compounds at 0. 1 - 1 mg / kg p. o. significantly improved the amnesia induced by scopolamine (0. 5 mg / kg s. c.) in rats performing a passive avoidance task. The three compounds at 1 and 3 mg / kg p. o. did not significantly decrease spontaneous movement by rats. These findings suggest that NIK - 247 at a low dose (0. 1 - 1 mg / kg p. o.) improves scopolamine - induced amnesia but does not affect spontaneous movement. The findings suggest that NIK - 247 may be a useful drug for the treatment of Alzheimer' s disease.

NIK - 247

scopolamine

NIK - 247

scopolamine

tacrine

E - 2020

NIK - 247

tacrine

E - 2020

NIK - 247

tacrine

E - 2020

NIK - 247

scopolamine

NIK - 247

scopolamine

NIK - 247

amnesia

amnesia

amnesia

amnesia

Alzheimer' s disease

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

E - 2020

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

NIK - 247

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

tacrine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia


Input: Nightmares and hallucinations after long - term intake of tramadol combined with antidepressants. Tramadol is a weak opioid with effects on adrenergic and serotonergic neurotransmission that is used to treat cancer pain and chronic non malignant pain. This drug was initiated in association with paroxetine and dosulepine hydrochloride in a tetraparetic patient with chronic pain. Fifty - six days after initiation of the treatment the patient presented hallucinations that only stopped after the withdrawal of psycho - active drugs and tramadol. The case report questions the long term use of pain killers combined with psycho - active drugs in chronic non malignant pain, especially if pain is under control.

hallucinations

cancer

pain

pain

tetraparetic

chronic pain

hallucinations

pain

pain

pain

tramadol

Tramadol

paroxetine

dosulepine hydrochloride

tramadol

paroxetine

hallucinations

paroxetine

hallucinations

tramadol

hallucinations

tramadol

hallucinations

Tramadol

hallucinations

Tramadol

hallucinations

tramadol

hallucinations

tramadol

hallucinations

dosulepine hydrochloride

hallucinations

dosulepine hydrochloride

hallucinations


Input: Apparent cure of rheumatoid arthritis by bone marrow transplantation. We describe the induction of sustained remissions and possible cure of severe erosive rheumatoid arthritis (RA) by bone marrow transplantation (BMT) in 2 patients. BMT was used to treat severe aplastic anemia which was caused by gold in one case and D - penicillamine in the other. In the 8 and 6 years since the transplants (representing 8 and 4 years since cessation of all immunosuppressive therapy, respectively), the RA in each case has been completely quiescent. Although short term remission of severe RA following BMT has been reported, these are the first cases for which prolonged followup has been available. This experience raises the question of the role of BMT itself as a therapeutic option for patients with uncontrolled destructive synovitis.

rheumatoid arthritis

rheumatoid arthritis

RA

aplastic anemia

RA

RA

synovitis

gold

D - penicillamine

gold

aplastic anemia

D - penicillamine

aplastic anemia


Input: Urinary enzymes and protein patterns as indicators of injury to different regions of the kidney. Acute experimental models of renal damage to the proximal tubular, glomerular, and papillary regions of the rat were produced by administration of hexachloro - 1: 3 - butadiene (HCBD), puromycin aminonucleoside (PAN), and 2 - bromoethylamine (BEA), respectively. Several routine indicators of nephrotoxicity, the enzymes alkaline phosphatase and N - acetyl - beta - glucosaminidase, and the molecular weight of protein excretion were determined on urine samples. Tubular damage produced by HCBD or BEA was discriminated both quantitatively and qualitatively from glomerular damage produced by PAN. The latter was characterized by a pronounced increase in protein excretion, especially proteins with molecular weight greater than 40, 000 Da. In contrast, protein excretion in tubular damage was raised only slightly and characterized by excretion of proteins of a wide range of molecular weights. Proximal tubular damage caused by HCBD and papillary damage caused by BEA were distinguished both by conventional urinalysis (volume and specific gravity) and by measurement of the two urinary enzymes. Alkaline phosphatase and glucose were markedly and transiently elevated in proximal tubular damage and N - acetyl - beta - glucosaminidase showed a sustained elevation in papillary damage. It is concluded that both selective urinary enzymes and the molecular weight pattern of urinary proteins can be used to provide diagnostic information about the possible site of renal damage.

injury to different regions of the kidney

Acute experimental models of renal damage

nephrotoxicity

protein excretion

glomerular damage

protein excretion

protein excretion

excretion of proteins

renal damage

hexachloro - 1: 3 - butadiene

HCBD

puromycin aminonucleoside

PAN

2 - bromoethylamine

BEA

HCBD

BEA

PAN

HCBD

BEA

glucose

puromycin aminonucleoside

Acute experimental models of renal damage

PAN

Acute experimental models of renal damage

PAN

Acute experimental models of renal damage

puromycin aminonucleoside

protein excretion

puromycin aminonucleoside

protein excretion

puromycin aminonucleoside

protein excretion

puromycin aminonucleoside

excretion of proteins

PAN

protein excretion

PAN

protein excretion

PAN

protein excretion

PAN

excretion of proteins

PAN

protein excretion

PAN

protein excretion

PAN

protein excretion

PAN

excretion of proteins

2 - bromoethylamine

Acute experimental models of renal damage

BEA

Acute experimental models of renal damage

BEA

Acute experimental models of renal damage

BEA

Acute experimental models of renal damage

hexachloro - 1: 3 - butadiene

Acute experimental models of renal damage

HCBD

Acute experimental models of renal damage

HCBD

Acute experimental models of renal damage

HCBD

Acute experimental models of renal damage


Input: Neuromuscular blockade with magnesium sulfate and nifedipine. A patient who received tocolysis with nifedipine developed neuromuscular blockade after 500 mg of magnesium sulfate was administered. This reaction demonstrates that nifedipine can seriously potentiate the toxicity of magnesium. Caution should be exercised when these two tocolytics are combined.

Neuromuscular blockade

neuromuscular blockade

toxicity

magnesium sulfate

nifedipine

nifedipine

magnesium sulfate

nifedipine

magnesium

magnesium sulfate

Neuromuscular blockade

magnesium sulfate

neuromuscular blockade

magnesium sulfate

Neuromuscular blockade

magnesium sulfate

neuromuscular blockade

nifedipine

Neuromuscular blockade

nifedipine

neuromuscular blockade

nifedipine

Neuromuscular blockade

nifedipine

neuromuscular blockade

nifedipine

Neuromuscular blockade

nifedipine

neuromuscular blockade


Input: Ifosfamide continuous infusion without mesna. A phase I trial of a 14 - day cycle. Twenty patients received 27 courses of ifosfamide administered as a 24 - hour continuous infusion for 14 days without Mesna. The goal of the study was to deliver a dose rate and total cumulative dose of ifosfamide that would be comparable to standard bolus or short - term infusions administered with Mesna. Dose escalations proceeded from 200 to 300, 400, 450, 500, and 550 mg / m2 / d. Four patients developed transient microscopic hematuria at 400, 450, and 500 mg / m2 / d. There were no instances of macroscopic hematuria. At 550 mg / m2 / d, three patients experienced nonurologic toxicity; confusion (1), nausea (1), and Grade 2 leukopenia (1). The recommended dose of 500 mg / m2 / d delivers a total dose of 7 g / m2 per cycle, which is comparable to that delivered in clinical practice for bolus or short - term infusion. Because few patients received multiple courses over time, the cumulative effects are indeterminate in the present trial. The frequency and predictability of hematuria are not precise, and at least daily monitoring by urine Hematest is essential, adding Mesna to the infusate in patients with persistent hematuria. The protracted infusion schedule for ifosfamide permits convenient outpatient administration without Mesna and reduces the drug cost of clinical usage of this agent by up to 890 per cycle. Clinical activity was demonstrated in a single patient, but a comparative trial of standard bolus schedules with the protracted infusion schedule will be necessary to determine if the clinical effectiveness of the drug is maintained.

Ifosfamide

mesna

ifosfamide

Mesna

ifosfamide

Mesna

Mesna

ifosfamide

Mesna

hematuria

hematuria

toxicity

confusion

nausea

leukopenia

hematuria

hematuria

Ifosfamide

hematuria

Ifosfamide

hematuria

Ifosfamide

hematuria

Ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

ifosfamide

hematuria

Ifosfamide

leukopenia

ifosfamide

leukopenia

ifosfamide

leukopenia

ifosfamide

leukopenia

Ifosfamide

confusion

ifosfamide

confusion

ifosfamide

confusion

ifosfamide

confusion

Ifosfamide

nausea

ifosfamide

nausea

ifosfamide

nausea

ifosfamide

nausea


Input: Myocardial infarction in pregnancy associated with clomiphene citrate for ovulation induction: a case report. BACKGROUND: Clomiphene citrate (CC) is commonly prescribed for ovulation induction. It is considered safe, with minimal side effects. Thromboembolism is a rare but life - threatening complication that has been reported after ovulation induction with CC. Spontaneous coronary thrombosis or thromboembolism with subsequent clot lysis has been suggested as one of the most common causes of myocardial infarction (MI) during pregnancy, with a subsequently normal coronary angiogram. CASE: A 33 - year - old woman with a 5 - week gestation had recently received CC for ovulation induction and presented with chest pain. An electrocardiogram showed a lateral and anterior wall myocardial infarction. Cardiac enzymes showed a peak rise in troponin I to 9. 10 ng / mL. An initial exercise stress test was normal. At the time of admission, the patient was at high risk of radiation injury to the fetus, so a coronary angiogram was postponed until the second trimester. It showed normal coronary vessels. CONCLUSION: This appears to be the first reported case documenting a possible association between CC and myocardial infarction. Thrombosis might be a rare but hazardous complication of CC. Given this life - threatening complication, appropriate prophylactic measures should be used in high - risk woman undergoing ovarian stimulation.

Myocardial infarction

Thromboembolism

coronary thrombosis

thromboembolism

myocardial infarction

MI

chest pain

myocardial infarction

radiation injury

myocardial infarction

Thrombosis

clomiphene citrate

Clomiphene citrate

CC

CC

CC

CC

CC

clomiphene citrate

Myocardial infarction

clomiphene citrate

myocardial infarction

clomiphene citrate

MI

clomiphene citrate

myocardial infarction

clomiphene citrate

myocardial infarction

Clomiphene citrate

Myocardial infarction

Clomiphene citrate

myocardial infarction

Clomiphene citrate

MI

Clomiphene citrate

myocardial infarction

Clomiphene citrate

myocardial infarction

CC

Myocardial infarction

CC

myocardial infarction

CC

MI

CC

myocardial infarction

CC

myocardial infarction

CC

Myocardial infarction

CC

myocardial infarction

CC

MI

CC

myocardial infarction

CC

myocardial infarction

CC

Myocardial infarction

CC

myocardial infarction

CC

MI

CC

myocardial infarction

CC

myocardial infarction

CC

Myocardial infarction

CC

myocardial infarction

CC

MI

CC

myocardial infarction

CC

myocardial infarction

CC

Myocardial infarction

CC

myocardial infarction

CC

MI

CC

myocardial infarction

CC

myocardial infarction

clomiphene citrate

Thromboembolism

clomiphene citrate

thromboembolism

Clomiphene citrate

Thromboembolism

Clomiphene citrate

thromboembolism

CC

Thromboembolism

CC

thromboembolism

CC

Thromboembolism

CC

thromboembolism

CC

Thromboembolism

CC

thromboembolism

CC

Thromboembolism

CC

thromboembolism

CC

Thromboembolism

CC

thromboembolism


Input: Hepatonecrosis and cholangitis related to long - term phenobarbital therapy: an autopsy report of two patients. Phenobarbital (PB) has a reputation for safety, and it is commonly believed that PB - related increases in serum aminotransferase levels do not indicate or predict the development of significant chronic liver disease. Here we report of two adult patients with a long history of epilepsy treated with PB who died suddenly: one as consequence of cardiac arrest, the other of acute bronchopneumonia. At autopsy, analysis of liver parenchyma revealed rich portal inflammatory infiltrate, which consisted of mixed eosinophil and monocyte cells, associated with several foci of necrosis surrounded by a hard ring of non - specific granulomatous tissue. Inflammatory reactions of internal and external hepatic biliary ducts were also seen. Our findings illustrate that PB may be associated with chronic liver damage, which may lead to more serious and deleterious consequences. For this reason, each clinician should recognize this entity in the differential diagnosis of PB - related asymptomatic chronic hepatic enzyme dysfunction.

Hepatonecrosis

cholangitis

liver disease

epilepsy

cardiac arrest

bronchopneumonia

necrosis

liver damage

chronic hepatic enzyme dysfunction

phenobarbital

Phenobarbital

PB

PB

PB

PB

PB

phenobarbital

cholangitis

Phenobarbital

cholangitis

PB

cholangitis

PB

cholangitis

PB

cholangitis

PB

cholangitis

PB

cholangitis

phenobarbital

liver disease

phenobarbital

liver damage

Phenobarbital

liver disease

Phenobarbital

liver damage

PB

liver disease

PB

liver damage

PB

liver disease

PB

liver damage

PB

liver disease

PB

liver damage

PB

liver disease

PB

liver damage

PB

liver disease

PB

liver damage


Input: Ethambutol - associated optic neuropathy. INTRODUCTION: Ethambutol is used in the treatment of tuberculosis, which is still prevalent in Southeast Asia, and can be associated with permanent visual loss. We report 3 cases which presented with bitemporal hemianopia. CLINICAL PICTURE: Three patients with ethambutol - associated toxic optic neuropathy are described. All 3 patients had loss of central visual acuity, colour vision (Ishihara) and visual field. The visual field loss had a bitemporal flavour, suggesting involvement of the optic chiasm. TREATMENT: Despite stopping ethambutol on diagnosis, visual function continued to deteriorate for a few months. Subsequent improvement was mild in 2 cases. In the third case, visual acuity and colour vision normalised but the optic discs were pale. OUTCOME: All 3 patients had some permanent loss of visual function. CONCLUSIONS: Ethambutol usage is associated with permanent visual loss and should be avoided if possible or used with caution and proper ophthalmological follow - up. The author postulates that in cases of ethambutol associated chiasmopathy, ethambutol may initially affect the optic nerves and subsequently progress to involve the optic chiasm.

Ethambutol

Ethambutol

ethambutol

ethambutol

Ethambutol

ethambutol

ethambutol

optic neuropathy

tuberculosis

visual loss

bitemporal hemianopia

optic neuropathy

loss of central visual acuity, colour vision (Ishihara) and visual field

visual field loss

loss of visual function

visual loss

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

Ethambutol

visual loss

Ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

Ethambutol

visual field loss

Ethambutol

loss of visual function

Ethambutol

visual loss

Ethambutol

visual loss

Ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

Ethambutol

visual field loss

Ethambutol

loss of visual function

Ethambutol

visual loss

ethambutol

visual loss

ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

ethambutol

visual field loss

ethambutol

loss of visual function

ethambutol

visual loss

ethambutol

visual loss

ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

ethambutol

visual field loss

ethambutol

loss of visual function

ethambutol

visual loss

Ethambutol

visual loss

Ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

Ethambutol

visual field loss

Ethambutol

loss of visual function

Ethambutol

visual loss

ethambutol

visual loss

ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

ethambutol

visual field loss

ethambutol

loss of visual function

ethambutol

visual loss

ethambutol

visual loss

ethambutol

loss of central visual acuity, colour vision (Ishihara) and visual field

ethambutol

visual field loss

ethambutol

loss of visual function

ethambutol

visual loss


Input: Tolerability of nimesulide and paracetamol in patients with NSAID - induced urticaria / angioedema. Previous studies evaluated the tolerance of nimesulide and paracetamol in subjects with cutaneous, respiratory and anaphylactoid reactions induced by nonsteroidal anti - inflammatory drugs (NSAIDs). In this study we investigated tolerability and reliability of nimesulide and paracetamol in a very large number of patients with an exclusive well - documented history of NSAID - induced urticaria / angioedema. Furthermore, we evaluated whether some factors have the potential to increase the risk of reaction to paracetamol and nimesulide. A single - placebo - controlled oral challenge procedure with nimesulide or paracetamol was applied to 829 patients with a history of NSAID - induced urticaria / angioedema. A total of 75 / 829 (9. 4%) patients experienced reactions to nimesulide or paracetamol. Of the 715 patients tested with nimesulide 62 (8. 6%) showed a positive test, while of 114 subjects submitted to the challenge with paracetamol, 13 (9. 6%) did not tolerate this drug. Furthermore, 18. 28% of patients with a history of chronic urticaria and 11. 8% of subjects with an history of NSAID - induced urticaria / angioedema or angioedema alone (with or without chronic urticaria) resulted to be intolerant to alternative drugs. Taken together, our results confirm the good tolerability of nimesulide and paracetamol in patients who experienced urticaria / angioedema caused by NSAIDs. However, the risk of reaction to these alternative study drugs is statistically increased by a history of chronic urticaria and, above all, by a history of NSAID - induced angioedema.

nimesulide

paracetamol

NSAID

nimesulide

paracetamol

nonsteroidal anti - inflammatory drugs

NSAIDs

nimesulide

paracetamol

NSAID

paracetamol

nimesulide

nimesulide

paracetamol

NSAID

nimesulide

paracetamol

nimesulide

paracetamol

NSAID

nimesulide

paracetamol

NSAIDs

NSAID

urticaria

angioedema

urticaria

angioedema

urticaria

angioedema

urticaria

urticaria

angioedema

angioedema

urticaria

urticaria

angioedema

urticaria

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

nimesulide

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

paracetamol

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

nonsteroidal anti - inflammatory drugs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAIDs

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema

NSAID

angioedema


Input: Effects of verapamil on atrial fibrillation and its electrophysiological determinants in dogs. BACKGROUND: Atrial tachycardia - induced remodeling promotes the occurrence and maintenance of atrial fibrillation (AF) and decreases L - type Ca (2 +) current. There is also a clinical suggestion that acute L - type Ca (2) channel blockade can promote AF, consistent with an AF promoting effect of Ca (2 +) channel inhibition. METHODS: To evaluate the potential mechanisms of AF promotion by Ca (2 +) channel blockers, we administered verapamil to morphine - chloralose anesthetized dogs. Diltiazem was used as a comparison drug and autonomic blockade with atropine and nadolol was applied in some experiments. Epicardial mapping with 240 epicardial electrodes was used to evaluate activation during AF. RESULTS: Verapamil caused AF promotion in six dogs, increasing mean duration of AF induced by burst pacing, from 8 + / - 4 s (mean + / - S. E.) to 95 + / - 39 s (P < 0. 01 vs. control) at a loading dose of 0. 1 mg / kg and 228 + / - 101 s (P < 0. 0005 vs. control) at a dose of 0. 2 mg / kg. Underlying electrophysiological mechanisms were studied in detail in five additional dogs under control conditions and in the presence of the higher dose of verapamil. In these experiments, verapamil shortened mean effective refractory period (ERP) from 122 + / - 5 to 114 + / - 4 ms (P < 0. 02) at a cycle length of 300 ms, decreased ERP heterogeneity (from 15 + / - 1 to 10 + / - 1%, P < 0. 05), heterogeneously accelerated atrial conduction and decreased the cycle length of AF (94 + / - 4 to 84 + / - 3 ms, P < 0. 005). Diltiazem did not affect ERP, AF cycle length or AF duration, but produced conduction acceleration similar to that caused by verapamil (n = 5). In the presence of autonomic blockade, verapamil failed to promote AF and increased, rather than decreasing, refractoriness. Neither verapamil nor diltiazem affected atrial conduction in the presence of autonomic blockade. Epicardial mapping suggested that verapamil promoted AF by increasing the number of simultaneous wavefronts reflected by separate zones of reactivation in each cycle. CONCLUSIONS: Verapamil promotes AF in normal dogs by promoting multiple circuit reentry, an effect dependent on intact autonomic tone and not shared by diltiazem.

verapamil

Ca

Ca

Ca

Ca

verapamil

morphine

chloralose

Diltiazem

atropine

nadolol

Verapamil

verapamil

verapamil

Diltiazem

verapamil

verapamil

verapamil

diltiazem

verapamil

Verapamil

diltiazem

atrial fibrillation

Atrial tachycardia

atrial fibrillation

AF

AF

AF

AF

AF

AF

AF

AF

AF

AF

AF

AF

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

Verapamil

atrial fibrillation

Verapamil

atrial fibrillation

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

atrial fibrillation

verapamil

atrial fibrillation

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

verapamil

AF

Verapamil

atrial fibrillation

Verapamil

atrial fibrillation

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF

Verapamil

AF


Input: Hypotension, bradycardia, and asystole after high - dose intravenous methylprednisolone in a monitored patient. We report a case of hypotension, bradycardia, and asystole after intravenous administration of high - dose methylprednisolone in a 73 - year - old patient who underwent electrocardiographic (ECG) monitoring throughout the episode. There was a history of ischemic cardiac disease 9 years earlier. The patient was admitted with a pulmonary - renal syndrome with hemoptysis, rapidly progressive renal failure, and hypoxemia that required mechanical ventilation in the intensive care unit. After receiving advanced cardiopulmonary resuscitation, the patient recovered cardiac rhythm. The ECG showed a junctional rhythm without ventricular arrhythmia. This study reviews the current proposed mechanisms of sudden death after a high dose of intravenous methylprednisolone (IVMP). These mechanisms are not well understood because, in most cases, the patients were not monitored at the moment of the event. Rapid infusion and underlying cardiac disease were important risk factors in the case reported here, and the authors discount ventricular arrhythmia as the main mechanism.

Hypotension

bradycardia

asystole

hypotension

bradycardia

asystole

ischemic

cardiac disease

pulmonary - renal syndrome

hemoptysis

renal failure

hypoxemia

ventricular arrhythmia

sudden death

cardiac disease

ventricular arrhythmia

methylprednisolone

methylprednisolone

methylprednisolone

IVMP

methylprednisolone

bradycardia

methylprednisolone

bradycardia

methylprednisolone

bradycardia

methylprednisolone

bradycardia

methylprednisolone

bradycardia

methylprednisolone

bradycardia

IVMP

bradycardia

IVMP

bradycardia

methylprednisolone

asystole

methylprednisolone

asystole

methylprednisolone

asystole

methylprednisolone

asystole

methylprednisolone

asystole

methylprednisolone

asystole

IVMP

asystole

IVMP

asystole

methylprednisolone

Hypotension

methylprednisolone

hypotension

methylprednisolone

Hypotension

methylprednisolone

hypotension

methylprednisolone

Hypotension

methylprednisolone

hypotension

IVMP

Hypotension

IVMP

hypotension


Input: Lifetime treatment of mice with azidothymidine (AZT) produces myelodysplasia. AZT has induced a macrocytic anemia in AIDS patients on long term AZT therapy. It is generally assumed that DNA elongation is stopped by the insertion of AZT into the chain in place of thymidine thus preventing the phosphate hydroxyl linkages and therefore suppresses hemopoietic progenitor cell proliferation in an early stage of differentiation. CBA / Ca male mice started on AZT 0. 75 mg / ml H2O at 84 days of age and kept on it for 687 days when dosage reduced to 0. 5 mg / ml H2O for a group, another group removed from AZT to see recovery, and third group remained on 0. 75 mg. At 687 days mice that had been on 0. 75 mg had average platelet counts of 2. 5 x 10 (6). Histological examination on 9 of 10 mice with such thrombocytopenia showed changes compatible with myelodysplastic syndrome (MDS). A variety of histological patterns was observed. There were two cases of hypocellular myelodysplasia, two cases of hypersegmented myelodysplastic granulocytosis, two cases of hypercellular marrow with abnormal megakaryocytes with bizarre nuclei, one case of megakaryocytic myelosis associated with a hyperplastic marrow, dysmyelopoiesis and a hypocellular marrow and two cases of myelodysplasia with dyserythropoiesis, hemosiderosis and a hypocellular marrow. Above mentioned AZT incorporation may have induced an ineffective hemopoiesis in the primitive hemopoietic progenitor cells, which is known to be seen commonly in the myelodysplastic syndrome.

azidothymidine

AZT

AZT

AZT

AZT

thymidine

phosphate

AZT

AZT

AZT

myelodysplasia

macrocytic anemia

AIDS

thrombocytopenia

myelodysplastic syndrome

MDS

myelodysplasia

myelodysplastic

hyperplastic marrow

dysmyelopoiesis

hypocellular marrow

myelodysplasia

dyserythropoiesis

hemosiderosis

hypocellular marrow

myelodysplastic syndrome

azidothymidine

thrombocytopenia

AZT

thrombocytopenia

AZT

thrombocytopenia

AZT

thrombocytopenia

AZT

thrombocytopenia

AZT

thrombocytopenia

AZT

thrombocytopenia

AZT

thrombocytopenia

azidothymidine

macrocytic anemia

AZT

macrocytic anemia

AZT

macrocytic anemia

AZT

macrocytic anemia

AZT

macrocytic anemia

AZT

macrocytic anemia

AZT

macrocytic anemia

AZT

macrocytic anemia

azidothymidine

myelodysplasia

azidothymidine

myelodysplastic syndrome

azidothymidine

MDS

azidothymidine

myelodysplasia

azidothymidine

myelodysplastic

azidothymidine

dysmyelopoiesis

azidothymidine

myelodysplasia

azidothymidine

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

myelodysplasia

AZT

myelodysplastic syndrome

AZT

MDS

AZT

myelodysplasia

AZT

myelodysplastic

AZT

dysmyelopoiesis

AZT

myelodysplasia

AZT

myelodysplastic syndrome


Input: Influence of diet free of NAD - precursors on acetaminophen hepatotoxicity in mice. Recently, we demonstrated the hepatoprotective effects of nicotinic acid amide, a selective inhibitor of poly (ADP - ribose) polymerase (PARP; EC 2. 4. 2. 30) on mice suffering from acetaminophen (AAP) - hepatitis, suggesting that the AAP - induced liver injury involves a step which depends on adenoribosylation. The present study investigates the effects of a diet free of precursors of NAD, the substrate on which PARP acts, in female NMRI mice with AAP hepatitis and evaluates the influence of simultaneous ethanol consumption in these animals. Liver injuries were quantified as serum activities of glutamate - oxaloacetate transaminase (GOT) and glutamate - pyruvate transaminase (GPT). While AAP caused a 117 - fold elevation of serum transaminase activities in mice kept on a standard laboratory diet, which was significantly exacerbated by ethanol and inhibited by nicotinic acid amide (NAA), adverse effects were noted in animals fed a diet free of precursors of NAD. In these animals, only minor increases of serum transaminase activities were measured in the presence of AAP, and unlike the exacerbation caused by ethanol in mice on a standard diet, the liver damage was inhibited by 50% by ethanol. A further 64% reduction of hepatitis was observed, when NAA was given to ethanol / AAP - mice. Our results provide evidence that the AAP - induced hepatitis and its exacerbation by ethanol can either be reduced by end - product inhibition of PARP by NAA or by dietary depletion of the enzyme' s substrate NAD. We see the main application of NAA as for the combinational use in pharmaceutical preparations of acetaminophen in order to avoid hepatic damage in patients treated with this widely used analgesic.

NAD

acetaminophen

nicotinic acid amide

poly (ADP - ribose)

acetaminophen

AAP

AAP

NAD

AAP

ethanol

glutamate

oxaloacetate

glutamate

pyruvate

AAP

ethanol

nicotinic acid amide

NAA

NAD

AAP

ethanol

ethanol

NAA

ethanol

AAP

AAP

ethanol

NAA

NAD

NAA

acetaminophen

hepatotoxicity

hepatitis

liver injury

hepatitis

Liver injuries

liver damage

hepatitis

hepatitis

hepatic damage

acetaminophen

hepatotoxicity

acetaminophen

hepatitis

acetaminophen

liver injury

acetaminophen

hepatitis

acetaminophen

Liver injuries

acetaminophen

liver damage

acetaminophen

hepatitis

acetaminophen

hepatitis

acetaminophen

hepatic damage

acetaminophen

hepatotoxicity

acetaminophen

hepatitis

acetaminophen

liver injury

acetaminophen

hepatitis

acetaminophen

Liver injuries

acetaminophen

liver damage

acetaminophen

hepatitis

acetaminophen

hepatitis

acetaminophen

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

AAP

hepatotoxicity

AAP

hepatitis

AAP

liver injury

AAP

hepatitis

AAP

Liver injuries

AAP

liver damage

AAP

hepatitis

AAP

hepatitis

AAP

hepatic damage

acetaminophen

hepatotoxicity

acetaminophen

hepatitis

acetaminophen

liver injury

acetaminophen

hepatitis

acetaminophen

Liver injuries

acetaminophen

liver damage

acetaminophen

hepatitis

acetaminophen

hepatitis

acetaminophen

hepatic damage

ethanol

hepatotoxicity

ethanol

hepatitis

ethanol

liver injury

ethanol

hepatitis

ethanol

Liver injuries

ethanol

liver damage

ethanol

hepatitis

ethanol

hepatitis

ethanol

hepatic damage

ethanol

hepatotoxicity

ethanol

hepatitis

ethanol

liver injury

ethanol

hepatitis

ethanol

Liver injuries

ethanol

liver damage

ethanol

hepatitis

ethanol

hepatitis

ethanol

hepatic damage

ethanol

hepatotoxicity

ethanol

hepatitis

ethanol

liver injury

ethanol

hepatitis

ethanol

Liver injuries

ethanol

liver damage

ethanol

hepatitis

ethanol

hepatitis

ethanol

hepatic damage

ethanol

hepatotoxicity

ethanol

hepatitis

ethanol

liver injury

ethanol

hepatitis

ethanol

Liver injuries

ethanol

liver damage

ethanol

hepatitis

ethanol

hepatitis

ethanol

hepatic damage

ethanol

hepatotoxicity

ethanol

hepatitis

ethanol

liver injury

ethanol

hepatitis

ethanol

Liver injuries

ethanol

liver damage

ethanol

hepatitis

ethanol

hepatitis

ethanol

hepatic damage

ethanol

hepatotoxicity

ethanol

hepatitis

ethanol

liver injury

ethanol

hepatitis

ethanol

Liver injuries

ethanol

liver damage

ethanol

hepatitis

ethanol

hepatitis

ethanol

hepatic damage


Input: Antiarrhythmic plasma concentrations of cibenzoline on canine ventricular arrhythmias. Using two - stage coronary ligation -, digitalis -, and adrenaline - induced canine ventricular arrhythmias, antiarrhythmic effects of cibenzoline were examined and the minimum effective plasma concentration for each arrhythmia model was determined. Cibenzoline suppressed all the arrhythmias, and the minimum effective plasma concentrations for arrhythmias induced by 24 - h coronary ligation, 48 - h coronary ligation, digitalis, and adrenaline were 1. 9 + / - 0. 9 (by 8 mg / kg i. v.), 1. 6 + / - 0. 5 (by 8 mg / kg i. v.), 0. 6 + / - 0. 2 (by 2 mg / kg i. v.), and 3. 5 + / - 1. 3 (by 5 mg / kg i. v.) micrograms / ml, respectively (mean + / - SDM, n = 6 - 7). The concentration for adrenaline - induced arrhythmia was significantly higher than those for the other types of arrhythmias. This pharmacological profile is similar to those of mexiletine and tocainide, and all three drugs have central nervous system (CNS) stimulant action. Because cibenzoline had only weak hypotensive and sinus node depressive effects and was found to be orally active when given to coronary ligation arrhythmia dogs, its clinical usefulness is expected.

cibenzoline

digitalis

adrenaline

cibenzoline

Cibenzoline

digitalis

adrenaline

adrenaline

mexiletine

tocainide

cibenzoline

ventricular arrhythmias

ventricular arrhythmias

arrhythmia

arrhythmias

arrhythmias

arrhythmia

arrhythmias

hypotensive

depressive

arrhythmia

adrenaline

ventricular arrhythmias

adrenaline

ventricular arrhythmias

adrenaline

arrhythmia

adrenaline

arrhythmias

adrenaline

arrhythmias

adrenaline

arrhythmia

adrenaline

arrhythmias

adrenaline

arrhythmia

adrenaline

ventricular arrhythmias

adrenaline

ventricular arrhythmias

adrenaline

arrhythmia

adrenaline

arrhythmias

adrenaline

arrhythmias

adrenaline

arrhythmia

adrenaline

arrhythmias

adrenaline

arrhythmia

adrenaline

ventricular arrhythmias

adrenaline

ventricular arrhythmias

adrenaline

arrhythmia

adrenaline

arrhythmias

adrenaline

arrhythmias

adrenaline

arrhythmia

adrenaline

arrhythmias

adrenaline

arrhythmia

digitalis

ventricular arrhythmias

digitalis

ventricular arrhythmias

digitalis

arrhythmia

digitalis

arrhythmias

digitalis

arrhythmias

digitalis

arrhythmia

digitalis

arrhythmias

digitalis

arrhythmia

digitalis

ventricular arrhythmias

digitalis

ventricular arrhythmias

digitalis

arrhythmia

digitalis

arrhythmias

digitalis

arrhythmias

digitalis

arrhythmia

digitalis

arrhythmias

digitalis

arrhythmia


Input: Immunopathology of penicillamine - induced glomerular disease. Four patients with rheumatoid arthritis developed heavy proteinuria after five to 12 months of treatment with D - penicillamine. Light microscopy of renal biopsy samples showed minimal glomerular capillary wall thickening and mesangial matrix increase, or no departure from normal. Electron microscopy, however, revealed subepithelial electron - dense deposits, fusion of epithelial cell foot processes, and evidence of mesangial cell hyperactivity. Immunofluorescence microscopy demonstrated granular capillary wall deposits of IgG and C3. The findings were similar to those in early membranous glomerulonephritis, differences being observed however in the results of staining for the early - acting complement components C1q and C4. It is tentatively concluded that complement was activated by the classical pathway.

penicillamine

D - penicillamine

glomerular disease

rheumatoid arthritis

proteinuria

membranous glomerulonephritis

penicillamine

glomerular disease

D - penicillamine

glomerular disease

penicillamine

proteinuria

D - penicillamine

proteinuria


Input: Ventricular fibrillation from diatrizoate with and without chelating agents. The toxicity of Renografin 76% was compared with that of Hypaque 76% by selective injection of each into the right coronary artery of dogs. Renografin contains the chelating agents sodium citrate and disodium edetate, while Hypaque contains calcium disodium edetate and no sodium citrate. Ventricular fibrillation occurred significantly more often with Renografin, suggesting that chelating agents contribute to toxicity in coronary angiography.

Ventricular fibrillation

toxicity

Ventricular fibrillation

toxicity

diatrizoate

Renografin 76%

Hypaque 76%

Renografin

sodium citrate

disodium edetate

Hypaque

calcium disodium edetate

sodium citrate

Renografin

Renografin 76%

Ventricular fibrillation

Renografin 76%

Ventricular fibrillation

Hypaque 76%

Ventricular fibrillation

Hypaque 76%

Ventricular fibrillation

sodium citrate

Ventricular fibrillation

sodium citrate

Ventricular fibrillation

sodium citrate

Ventricular fibrillation

sodium citrate

Ventricular fibrillation

disodium edetate

Ventricular fibrillation

disodium edetate

Ventricular fibrillation

calcium disodium edetate

Ventricular fibrillation

calcium disodium edetate

Ventricular fibrillation


Input: Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin - associated intracerebral hemorrhage. Warfarin - associated intracerebral hemorrhage (W - ICH) is a severe type of stroke. There is no consensus on the optimal treatment for W - ICH. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. Male CD - 1 mice were treated with warfarin (2 mg / kg over 24 h), resulting in a mean (+ / - s. d.) International Normalized Ratio of 3. 5 + / - 0. 9. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Forty - five minutes later, the animals were randomly treated with PCC (100 U / kg) or saline i. v. (n = 12 per group). Twenty - four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. The mean hemorrhagic blood volume was reduced in PCC - treated animals (6. 5 + / - 3. 1 microL) compared with saline controls (15. 3 + / - 11. 2 microL, P = 0. 015). In the saline group, 45% of the mice developed large hematomas (i. e., > 15 microL). In contrast, such extensive lesions were never found in the PCC group. We provide experimental data suggesting PCC to be an effective acute treatment for W - ICH in terms of reducing hemorrhagic blood volume. Future studies are needed to assess the therapeutic potential emerging from our finding for human W - ICH.

hemorrhage

intracerebral hemorrhage

intracerebral hemorrhage

ICH

stroke

ICH

hemorrhage

hemorrhage

hematomas

ICH

ICH

warfarin

Warfarin

prothrombin complex concentrate

PCC

warfarin

PCC

PCC

PCC

PCC

PCC

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

Warfarin

intracerebral hemorrhage

Warfarin

intracerebral hemorrhage

Warfarin

ICH

Warfarin

ICH

Warfarin

ICH

Warfarin

ICH

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH


Input: Impact of alcohol exposure after pregnancy recognition on ultrasonographic fetal growth measures. BACKGROUND: More than 3 decades after Jones and Smith (1973) reported on the devastation caused by alcohol exposure on fetal development, the rates of heavy drinking during pregnancy remain relatively unchanged. Early identification of fetal alcohol exposure and maternal abstinence led to better infant outcomes. This study examined the utility of biometry for detecting alcohol - related fetal growth impairment. METHODS: We obtained fetal ultrasound measures from routine ultrasound examinations for 167 pregnant hazardous drinkers who were enrolled in a brief alcohol intervention study. The fetal measures for women who quit after learning of their pregnancies were compared with measures for women who continued some drinking throughout the course of their pregnancies. Because intensity of alcohol consumption is associated with poorer fetal outcomes, separate analyses were conducted for the heavy (average of > or = 5 drinks per drinking day) alcohol consumers. Fetal measures from the heavy - exposed fetuses were also compared with measures from a nondrinking group that was representative of normal, uncomplicated pregnancies from our clinics. Analyses of covariance were used to determine whether there were differences between groups after controlling for influences of gestational age and drug abuse. RESULTS: Nearly half of the pregnant drinkers abstained after learning of their pregnancies. When women reportedly quit drinking early in their pregnancies, fetal growth measures were not significantly different from a non - alcohol - exposed group, regardless of prior drinking patterns. Any alcohol consumption postpregnancy recognition among the heavy drinkers resulted in reduced cerebellar growth as well as decreased cranial to body growth in comparison with women who either quit drinking or who were nondrinkers. Amphetamine abuse was predictive of larger cranial to body growth ratios. CONCLUSIONS: Alterations in fetal biometric measurements were observed among the heavy drinkers only when they continued drinking after becoming aware of their pregnancies. Although the reliance on self - reported drinking is a limitation in this study, these findings support the benefits of early abstinence and the potential for ultrasound examinations in the detection of fetal alcohol effects.

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

Amphetamine

alcohol

growth impairment

drug abuse

reduced cerebellar growth

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

alcohol

growth impairment

alcohol

reduced cerebellar growth

alcohol

decreased cranial to body growth

Amphetamine

growth impairment

Amphetamine

reduced cerebellar growth

Amphetamine

decreased cranial to body growth


Input: Urinary symptoms and quality of life changes in Thai women with overactive bladder after tolterodine treatment. OBJECTIVES: To study the urinary symptoms and quality of life changes in Thai women with overactive bladder (OAB) after tolterodine treatment. MATERIAL AND METHOD: Thirty women (aged 30 - 77 years) diagnosed as having OAB at the Gynecology Clinic, King Chulalongkorn Memorial Hospital from January to April 2004 were included in the present study. Tolterodine 2 mg, twice daily was given. After 8 weeks treatment, changes in micturition diary variables and tolerability were determined. Short form 36 (SF36) questionaires (Thai version) were given before and after 8 weeks of treatment. RESULTS: At 8 weeks, all micturition per day decreased from 16. 7 + / - 5. 3 to 6. 7 + / - 2. 4 times per day. The number of nocturia episodes decreased from 5. 4 + / - 4. 2 to 1. 1 + / - 1. 0 times per night. The most common side effect was dry month in 5 cases (16. 7%) with 2 cases reporting a moderate degree and 1 case with severe degree. Only one case (3. 3%) withdrew from the present study due to a severe dry mouth. The SF - 36 scores changed significantly in the domains of physical functioning, role function emotional, social function and mental heath. CONCLUSION: Tolterodine was well tolerated and its effects improved the quality of life in Thai women with OAB.

overactive bladder

overactive bladder

OAB

OAB

nocturia

dry month

dry mouth

OAB

tolterodine

tolterodine

Tolterodine

Tolterodine

tolterodine

dry month

tolterodine

dry mouth

tolterodine

dry month

tolterodine

dry mouth

Tolterodine

dry month

Tolterodine

dry mouth

Tolterodine

dry month

Tolterodine

dry mouth


Input: Absence of acute cerebral vasoconstriction after cocaine - associated subarachnoid hemorrhage. INTRODUCTION: Cocaine use has been associated with neurovascular complications, including arterial vasoconstriction and vasculitis. However, there are few studies of angiographic effects of cocaine on human cerebral arteries. Information on these effects could be obtained from angiograms of patients with cocaine - associated subarachnoid hemorrhage (SAH) who underwent angiography shortly after cocaine use. METHODS: We screened patients with SAH retrospectively and identified those with positive urine toxicology for cocaine or its metabolites. Quantitative arterial diameter measurements from angiograms of these patients were compared to measurements from control patients with SAH who were matched for factors known to influence arterial diameter. Qualitative comparisons of small artery changes also were made. RESULTS: Thirteen patients with positive cocaine toxicology were compared to 26 controls. There were no significant differences between groups in the mean diameters of the intradural internal carotid, sphenoidal segment of the middle cerebral, precommunicating segment of the anterior cerebral, or basilar arteries (p greater than 0. 05 for all comparisons, unpaired t - tests). There also were no significant differences between groups when expressing diameters as the sum of the precommunicating segment of the anterior cerebral + sphenoidal segment of the middle cerebral + supraclinoid internal carotid artery + basilar artery divided by the diameter of the petrous internal carotid artery (p greater than 0. 05, unpaired t - tests). Qualitative assessments showed two arterial irregularities in the distal vasculature in each group. CONCLUSION: No quantitative evidence for narrowing of large cerebral arteries or qualitative angiographic evidence for distal narrowing or vasculitis could be found in patients who underwent angiography after aneurysmal SAH associated with cocaine use.

cocaine

Cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

subarachnoid hemorrhage

neurovascular complications

vasculitis

subarachnoid hemorrhage

SAH

SAH

SAH

vasculitis

aneurysmal

SAH

cocaine

aneurysmal

Cocaine

aneurysmal

cocaine

aneurysmal

cocaine

aneurysmal

cocaine

aneurysmal

cocaine

aneurysmal

cocaine

aneurysmal

cocaine

aneurysmal

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH

Cocaine

subarachnoid hemorrhage

Cocaine

subarachnoid hemorrhage

Cocaine

SAH

Cocaine

SAH

Cocaine

SAH

Cocaine

SAH

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

SAH

cocaine

SAH

cocaine

SAH

cocaine

SAH


Input: Atrial fibrillation following chemotherapy for stage IIIE diffuse large B - cell gastric lymphoma in a patient with myotonic dystrophy (Steinert' s disease). The authors describe the unusual association between diffuse B - cell gastric lymphoma and myotonic dystrophy, the most common form of adult muscular dystrophy, and sudden atrial fibrillation following one cycle of doxorubicin - based chemotherapy in the same patient. Atrial fibrillation or other cardiac arrhythmias are unusual complications in patients treated with chemotherapy. The cardiac toxicity intrinsically associated with the aggressive chemotherapy employed could function as a triggering factor for the arrhythmia in the predisposed myocardium of this patient.

Atrial fibrillation

gastric lymphoma

myotonic dystrophy

Steinert' s disease

gastric lymphoma

myotonic dystrophy

muscular dystrophy

atrial fibrillation

Atrial fibrillation

cardiac arrhythmias

cardiac toxicity

arrhythmia

doxorubicin

doxorubicin

Atrial fibrillation

doxorubicin

atrial fibrillation

doxorubicin

Atrial fibrillation


Input: A phase II study of thalidomide in advanced metastatic renal cell carcinoma. OBJECTIVES: To evaluate the toxicity and activity of thalidomide in patients with advanced metastatic renal cell cancer and to measure changes of one angiogenic factor, vascular endothelial growth factor (VEGF) 165, with therapy. PATIENTS AND METHODS: 29 patients were enrolled on a study of thalidomide using an intra - patient dose escalation schedule. Patients began thalidomide at 400 mg / d and escalated as tolerated to 1200 mg / d by day 54. Fifty - nine per cent of patients had had previous therapy with IL - 2 and 52% were performance status 2 or 3. Systemic plasma VEGF165 levels were measured by dual monoclonal ELISA in 8 patients. RESULTS: 24 patients were evaluable for response with one partial response of 11 months duration of a patient with hepatic and pulmonary metastases (4%), one minor response, and 2 patients stable for over 6 months. Somnolence and constipation were prominent toxicities and most patients could not tolerate the 1200 mg / day dose level. Systemic plasma VEGF165 levels did not change with therapy. CONCLUSION: These results are consistent with a low level of activity of thalidomide in renal cell carcinoma. Administration of doses over 800 mg / day was difficult to achieve in this patient population, however lower doses were practical. The dose - response relationship, if any, of thalidomide for renal cell carcinoma is unclear.

thalidomide

thalidomide

thalidomide

thalidomide

thalidomide

thalidomide

renal cell carcinoma

toxicity

renal cell cancer

metastases

Somnolence

constipation

toxicities

renal cell carcinoma

renal cell carcinoma

thalidomide

constipation

thalidomide

constipation

thalidomide

constipation

thalidomide

constipation

thalidomide

constipation

thalidomide

constipation

thalidomide

Somnolence

thalidomide

Somnolence

thalidomide

Somnolence

thalidomide

Somnolence

thalidomide

Somnolence

thalidomide

Somnolence


Input: The striatum as a target for anti - rigor effects of an antagonist of mGluR1, but not an agonist of group II metabotropic glutamate receptors. The aim of the present study was to find out whether the metabotropic receptor 1 (mGluR1) and group II mGluRs, localized in the striatum, are involved in antiparkinsonian - like effects in rats. Haloperidol (1 mg / kg ip) induced parkinsonian - like muscle rigidity, measured as an increased resistance of a rat' s hind foot to passive flexion and extension at the ankle joint. (RS) - 1 - aminoindan - 1, 5 - dicarboxylic acid (AIDA; 0. 5 - 15 microg / 0. 5 microl), a potent and selective mGluR1 antagonist, or (2R, 4R) - 4 - aminopyrrolidine - 2, 4 - dicarboxylate (2R, 4R - APDC; 7. 5 - 15 microg / 0. 5 microl), a selective group II agonist, was injected bilaterally into the striatum of haloperidol - treated animals. AIDA in doses of 7. 5 - 15 microg / 0. 5 microl diminished the haloperidol - induced muscle rigidity. In contrast, 2R, 4R - APDC injections were ineffective. The present results may suggest that the blockade of striatal mGluR1, but not the stimulation of group II mGluRs, may ameliorate parkinsonian muscle rigidity.

glutamate

Haloperidol

(RS) - 1 - aminoindan - 1, 5 - dicarboxylic acid

AIDA

(2R, 4R) - 4 - aminopyrrolidine - 2, 4 - dicarboxylate

2R, 4R - APDC

haloperidol

AIDA

haloperidol

2R, 4R - APDC

parkinsonian

muscle rigidity

muscle rigidity

parkinsonian

muscle rigidity

Haloperidol

muscle rigidity

Haloperidol

muscle rigidity

Haloperidol

muscle rigidity

haloperidol

muscle rigidity

haloperidol

muscle rigidity

haloperidol

muscle rigidity

haloperidol

muscle rigidity

haloperidol

muscle rigidity

haloperidol

muscle rigidity


Input: Acute cholestatic hepatitis after exposure to isoflurane. OBJECTIVE: To report a case of acute cholestatic hepatitis following exposure to the inhalational anesthetic isoflurane. CASE SUMMARY: A 70 - year - old healthy woman from Iraq developed acute cholestatic hepatitis 3 weeks following repair of the right rotator cuff under general anesthesia. There was no evidence for viral, autoimmune, or metabolic causes of hepatitis. No other medications were involved except for dipyrone for analgesia. The alanine aminotransferase was elevated to a peak concentration of 1533 U / L and the serum bilirubin reached a peak of 17. 0 mg / dL. There was slow improvement over 4 months. Accidental reexposure by the patient to dipyrone was uneventful. DISCUSSION: The clinical and histologic picture of this case resembles halothane hepatitis, which has a significant mortality rate. CONCLUSIONS: Isoflurane, a common anesthetic agent, can cause severe cholestatic hepatitis.

cholestatic hepatitis

cholestatic

hepatitis

cholestatic hepatitis

cholestatic

hepatitis

cholestatic hepatitis

cholestatic

hepatitis

hepatitis

analgesia

halothane hepatitis

cholestatic hepatitis

cholestatic

hepatitis

isoflurane

isoflurane

dipyrone

alanine

bilirubin

dipyrone

Isoflurane

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

isoflurane

hepatitis

isoflurane

cholestatic hepatitis

isoflurane

hepatitis

Isoflurane

cholestatic hepatitis

Isoflurane

hepatitis

Isoflurane

cholestatic hepatitis

Isoflurane

hepatitis

Isoflurane

cholestatic hepatitis

Isoflurane

hepatitis

Isoflurane

hepatitis

Isoflurane

cholestatic hepatitis

Isoflurane

hepatitis

isoflurane

cholestatic

isoflurane

cholestatic

isoflurane

cholestatic

isoflurane

cholestatic

isoflurane

cholestatic

isoflurane

cholestatic

isoflurane

cholestatic

isoflurane

cholestatic

Isoflurane

cholestatic

Isoflurane

cholestatic

Isoflurane

cholestatic

Isoflurane

cholestatic


Input: Calcitonin gene - related peptide levels during nitric oxide - induced headache in patients with chronic tension - type headache. It has been proposed that nitric oxide (NO) induced headache in primary headaches may be associated with release of calcitonin gene - related peptide (CGRP). In the present study we aimed to investigate plasma levels of CGRP during headache induced by the NO donor glyceryl trinitrate (GTN) in 16 patients with chronic tension - type headache and 16 healthy controls. The subjects were randomly allocated to receive 0. 5 microg / kg / min GTN or placebo over 20 min on two headache - free days. Blood samples were collected at baseline, 10, 20 and 60 min after start of infusion. Both patients and controls developed significantly stronger immediate headache on the GTN day than on the placebo day and the headache was significantly more pronounced in patients than in controls. There was no difference between the area under the CGRP curve (AUCCGRP) on GTN vs. placebo day in either patients (P = 0. 65) or controls (P = 0. 48). The AUCCGRP recorded on the GTN day did not differ between patients and controls (P = 0. 36). Both in patients and controls, CGRP levels changed significantly over time, on both the GTN and placebo days (P < 0. 05). The present study indicates that NO - induced immediate headache is not associated with release of CGRP.

nitric oxide

nitric oxide

NO

NO

glyceryl trinitrate

GTN

GTN

GTN

GTN

GTN

GTN

NO

headache

tension - type headache

headache

primary headaches

headache

tension - type headache

headache

headache

headache

headache

glyceryl trinitrate

headache

glyceryl trinitrate

headache

glyceryl trinitrate

headache

glyceryl trinitrate

headache

glyceryl trinitrate

headache

glyceryl trinitrate

headache

glyceryl trinitrate

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

GTN

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

nitric oxide

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache

NO

headache


Input: Myocardial ischemia due to coronary artery spasm during dobutamine stress echocardiography. Dobutamine stress echocardiography (DSE) is a useful and safe provocation test for myocardial ischemia. Until now, the test has been focused only on the organic lesion in the coronary artery, and positive DSE has indicated the presence of significant fixed coronary artery stenosis. The aim of the present study is to examine whether myocardial ischemia due to coronary spasm is induced by dobutamine. We performed DSE on 51 patients with coronary spastic angina but without significant fixed coronary artery stenosis. All patients had anginal attacks at rest with ST elevation on the electrocardiogram (variant angina). Coronary spasm was induced by intracoronary injection of acetylcholine, and no fixed coronary artery stenosis was documented on angiograms in all patients. DSE was performed with intravenous dobutamine infusion with an incremental doses of 5, 10, 20, 30, and 40 microg / kg / min every 5 minutes. Of the 51 patients, 7 patients showed asynergy with ST elevation. All 7 patients (13. 7%) had chest pain during asynergy, and both chest pain and electrocardiographic changes were preceded by asynergy. These findings indicate that dobutamine can provoke coronary spasm in some patients with coronary spastic angina. When DSE is performed to evaluate coronary artery disease, not only fixed coronary stenosis, but also coronary spasm should be considered as a genesis of asynergy.

Myocardial ischemia

coronary artery spasm

myocardial ischemia

coronary artery stenosis

myocardial ischemia

coronary spasm

coronary spastic angina

coronary artery stenosis

anginal

variant angina

coronary artery stenosis

chest pain

chest pain

coronary spasm

coronary spastic angina

coronary artery disease

coronary stenosis

coronary spasm

dobutamine

Dobutamine

dobutamine

acetylcholine

dobutamine

dobutamine

dobutamine

coronary spastic angina

dobutamine

variant angina

dobutamine

coronary spastic angina

Dobutamine

coronary spastic angina

Dobutamine

variant angina

Dobutamine

coronary spastic angina

dobutamine

coronary spastic angina

dobutamine

variant angina

dobutamine

coronary spastic angina

dobutamine

coronary spastic angina

dobutamine

variant angina

dobutamine

coronary spastic angina

dobutamine

coronary spastic angina

dobutamine

variant angina

dobutamine

coronary spastic angina

dobutamine

coronary artery spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

Dobutamine

coronary artery spasm

Dobutamine

coronary spasm

Dobutamine

coronary spasm

Dobutamine

coronary spasm

dobutamine

coronary artery spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

dobutamine

coronary artery spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

dobutamine

coronary artery spasm

dobutamine

coronary spasm

dobutamine

coronary spasm

dobutamine

coronary spasm


Input: Nitric oxide synthase expression in the course of lead - induced hypertension. We recently showed elevated reactive oxygen species (ROS), reduced urinary excretion of NO metabolites (NOx), and increased NO sequestration as nitrotyrosine in various tissues in rats with lead - induced hypertension. This study was designed to discern whether the reduction in urinary NOx in lead - induced hypertension is, in part, due to depressed NO synthase (NOS) expression. Male Sprague - Dawley rats were randomly assigned to a lead - treated group (given lead acetate, 100 ppm, in drinking water and regular rat chow), a group given lead and vitamin E - fortified chow, or a normal control group given either regular food and water or vitamin E - fortified food for 12 weeks. Tail blood pressure, urinary NOx excretion, plasma malondialdehyde (MDA), and endothelial and inducible NOS (eNOS and iNOS) isotypes in the aorta and kidney were measured. The lead - treated group exhibited a rise in blood pressure and plasma MDA concentration, a fall in urinary NOx excretion, and a paradoxical rise in vascular and renal tissue eNOS and iNOS expression. Vitamin E supplementation ameliorated hypertension, lowered plasma MDA concentration, and raised urinary NOx excretion while significantly lowering vascular, but not renal, tissue eNOS and iNOS expression. Vitamin E supplementation had no effect on either blood pressure, plasma MDA, or NOS expression in the control group. The study also revealed significant inhibition of NOS enzymatic activity by lead in cell - free preparations. In conclusion, lead - induced hypertension in this model was associated with a compensatory upregulation of renal and vascular eNOS and iNOS expression. This is, in part, due to ROS - mediated NO inactivation, lead - associated inhibition of NOS activity, and perhaps stimulatory actions of increased shear stress associated with hypertension.

Nitric oxide

lead

oxygen

NO

NO

nitrotyrosine

lead

lead

NO

lead

lead acetate

lead

vitamin E

vitamin E

malondialdehyde

MDA

lead

MDA

Vitamin E

MDA

Vitamin E

MDA

lead

lead

NO

lead

hypertension

hypertension

hypertension

hypertension

hypertension

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension

lead

hypertension


Input: Risk for valvular heart disease among users of fenfluramine and dexfenfluramine who underwent echocardiography before use of medication. BACKGROUND: Because uncontrolled echocardiographic surveys suggested that up to 30% to 38% of users of fenfluramine and dexfenfluramine had valvular disease, these drugs were withdrawn from the market. OBJECTIVE: To determine the risk for new or worsening valvular abnormalities among users of fenfluramine or dexfenfluramine who underwent echocardiography before they began to take these medications. DESIGN: Cohort study. SETTING: Academic primary care practices. PATIENTS: 46 patients who used fenfluramine or dexfenfluramine for 14 days or more and had echocardiograms obtained before therapy. MEASUREMENTS: Follow - up echocardiography. The primary outcome was new or worsening valvulopathy, defined as progression of either aortic or mitral regurgitation by at least one degree of severity and disease that met U. S. Food and Drug Administration criteria (at least mild aortic regurgitation or moderate mitral regurgitation). RESULTS: Two patients (4. 3% [95% CI, 0. 6% to 14. 8%]) receiving fenfluramine - phentermine developed valvular heart disease. One had baseline bicuspid aortic valve and mild aortic regurgitation that progressed to moderate regurgitation. The second patient developed new moderate aortic insufficiency. CONCLUSION: Users of diet medications are at risk for valvular heart disease. However, the incidence may be lower than that reported previously.

valvular heart disease

valvular disease

valvular abnormalities

valvulopathy

aortic or mitral regurgitation

aortic or mitral regurgitation

mitral regurgitation

aortic regurgitation

mitral regurgitation

valvular heart disease

bicuspid aortic valve

aortic regurgitation

aortic insufficiency

valvular heart disease

fenfluramine

dexfenfluramine

fenfluramine

dexfenfluramine

fenfluramine

dexfenfluramine

fenfluramine

dexfenfluramine

fenfluramine

phentermine

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic insufficiency

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic insufficiency

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic insufficiency

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic insufficiency

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic or mitral regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic regurgitation

fenfluramine

aortic insufficiency

phentermine

aortic or mitral regurgitation

phentermine

aortic or mitral regurgitation

phentermine

aortic regurgitation

phentermine

aortic regurgitation

phentermine

aortic insufficiency


Input: Carboplatin toxic effects on the peripheral nervous system of the rat. BACKGROUND: The most striking of carboplatin' s advantages (CBDCA) over cisplatin (CDDP) is its markedly reduced rate of neurotoxic effects. However, the use of CBDCA higher - intensity schedules and the association with other neurotoxic drugs in polychemotherapy may cause some concern about its safety with respect to peripheral nervous system damage. MATERIALS AND METHODS: Two different schedules of CBDCA administration (10 mg / kg and 15 mg / kg i. p. twice a week for nine times) were evaluated in Wistar rats. Neurotoxicity was assessed for behavioral (tail - flick test), neurophysiological (nerve conduction velocity in the tail nerve), morphological, morphometrical and analytical effects. RESULTS: CBDCA administration induced dose - dependent peripheral neurotoxicity. Pain perception and nerve conduction velocity in the tail were significantly impaired, particularly after the high - dose treatment. The dorsal root ganglia sensory neurons and, to a lesser extent, satellite cells showed the same changes as those induced by CDDP, mainly affecting the nucleus and nucleolus of ganglionic sensory neurons. Moreover, significant amounts of platinum were detected in the dorsal root ganglia and kidney after CBDCA treatment. CONCLUSIONS: CBDCA is neurotoxic in our model, and the type of pathological changes it induces are so closely similar to those caused by CDDP that it is probable that neurotoxicity is induced in the two drugs by the same mechanism. This model can be used alone or in combination with other drugs to explore the effect of CBDCA on the peripheral nervous system.

Carboplatin

carboplatin

CBDCA

cisplatin

CDDP

CBDCA

CBDCA

CBDCA

CDDP

platinum

CBDCA

CBDCA

CDDP

CBDCA

neurotoxic

neurotoxic

peripheral nervous system damage

Neurotoxicity

peripheral neurotoxicity

Pain

neurotoxic

neurotoxicity

cisplatin

peripheral nervous system damage

cisplatin

peripheral neurotoxicity

CDDP

peripheral nervous system damage

CDDP

peripheral neurotoxicity

CDDP

peripheral nervous system damage

CDDP

peripheral neurotoxicity

CDDP

peripheral nervous system damage

CDDP

peripheral neurotoxicity

Carboplatin

peripheral nervous system damage

Carboplatin

peripheral neurotoxicity

carboplatin

peripheral nervous system damage

carboplatin

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity

CBDCA

peripheral nervous system damage

CBDCA

peripheral neurotoxicity


Input: Iatrogenic risks of endometrial carcinoma after treatment for breast cancer in a large French case - control study. F d ration Nationale des Centres de Lutte Contre le Cancer (FNCLCC). Since tamoxifen is widely used in breast cancer treatment and has been proposed for the prevention of breast cancer, its endometrial iatrogenic effects must be carefully examined. We have investigated the association between endometrial cancer and tamoxifen use or other treatments in women treated for breast cancer in a case - control study. Cases of endometrial cancer diagnosed after breast cancer (n = 135) and 467 controls matched for age, year of diagnosis of breast cancer and hospital and survival time with an intact uterus were included. Women who had received tamoxifen were significantly more likely to have endometrial cancer diagnosed than those who had not (crude relative risk = 4. 9, p = 0. 0001). Univariate and adjusted analyses showed that the risk increased with the length of treatment (p = 0. 0001) or the cumulative dose of tamoxifen received (p = 0. 0001), irrespective of the daily dose. Women who had undergone pelvic radiotherapy also had a higher risk (crude relative risk = 7. 8, p = 0. 0001). After adjusting for confounding factors, the risk was higher for tamoxifen users (p = 0. 0012), treatment for more than 3 years (all p < 0. 03) and pelvic radiotherapy (p = 0. 012). Women who had endometrial cancer and had received tamoxifen had more advanced disease and poorer prognosis than those with endometrial cancer who had not received this treatment. Our results suggest a causal role of tamoxifen in endometrial cancer, particularly when used as currently proposed for breast cancer prevention. Pelvic radiotherapy may be an additional iatrogenic factor for women with breast cancer. Endometrial cancers diagnosed in women treated with tamoxifen have poorer prognosis. Women who receive tamoxifen for breast cancer should be offered gynaecological surveillance during and after treatment. A long - term evaluation of the risk - benefit ratio of tamoxifen as a preventive treatment for breast cancer is clearly warranted.

endometrial carcinoma

breast cancer

breast cancer

breast cancer

endometrial cancer

breast cancer

endometrial cancer

breast cancer

breast cancer

endometrial cancer

endometrial cancer

advanced disease

endometrial cancer

endometrial cancer

breast cancer

breast cancer

Endometrial cancers

breast cancer

breast cancer

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers

tamoxifen

endometrial carcinoma

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

endometrial cancer

tamoxifen

Endometrial cancers