Input: Tricuspid valve regurgitation and lithium carbonate toxicity in a newborn infant. A newborn with massive tricuspid regurgitation, atrial flutter, congestive heart failure, and a high serum lithium level is described. This is the first patient to initially manifest tricuspid regurgitation and atrial flutter, and the 11th described patient with cardiac disease among infants exposed to lithium compounds in the first trimester of pregnancy. Sixty - three percent of these infants had tricuspid valve involvement. Lithium carbonate may be a factor in the increasing incidence of congenital heart disease when taken during early pregnancy. It also causes neurologic depression, cyanosis, and cardiac arrhythmia when consumed prior to delivery.

Tricuspid valve regurgitation

toxicity

tricuspid regurgitation

atrial flutter

congestive heart failure

tricuspid regurgitation

atrial flutter

cardiac disease

congenital heart disease

neurologic depression

cyanosis

cardiac arrhythmia

lithium carbonate

lithium

lithium

Lithium carbonate

lithium carbonate

cyanosis

Lithium carbonate

cyanosis

lithium carbonate

cardiac arrhythmia

Lithium carbonate

cardiac arrhythmia

lithium carbonate

neurologic depression

Lithium carbonate

neurologic depression


Input: Phenobarbital - induced dyskinesia in a neurologically - impaired child. A 2 - year - old child with known neurologic impairment developed a dyskinesia soon after starting phenobarbital therapy for seizures. Known causes of movement disorders were eliminated after evaluation. On repeat challenge with phenobarbital, the dyskinesia recurred. Phenobarbital should be added to the list of anticonvulsant drugs that can cause movement disorders.

Phenobarbital

phenobarbital

phenobarbital

Phenobarbital

dyskinesia

neurologically - impaired

neurologic impairment

dyskinesia

seizures

movement disorders

dyskinesia

movement disorders

Phenobarbital

dyskinesia

Phenobarbital

dyskinesia

Phenobarbital

dyskinesia

phenobarbital

dyskinesia

phenobarbital

dyskinesia

phenobarbital

dyskinesia

phenobarbital

dyskinesia

phenobarbital

dyskinesia

phenobarbital

dyskinesia

Phenobarbital

dyskinesia

Phenobarbital

dyskinesia

Phenobarbital

dyskinesia


Input: Acute changes of blood ammonia may predict short - term adverse effects of valproic acid. Valproic acid (VPA) was given to 24 epileptic patients who were already being treated with other antiepileptic drugs. A standardized loading dose of VPA was administered, and venous blood was sampled at 0, 1, 2, 3, and 4 hours. Ammonia (NH3) was higher in patients who, during continuous therapy, complained of drowsiness (7 patients) than in those who were symptom - free (17 patients), although VPA plasma levels were similar in both groups. By measuring VPA - induced changes of blood NH3 content, it may be possible to identify patients at higher risk of obtundation when VPA is given chronically.

ammonia

valproic acid

Valproic acid

VPA

VPA

Ammonia

VPA

VPA

VPA

epileptic

drowsiness

valproic acid

drowsiness

Valproic acid

drowsiness

VPA

drowsiness

VPA

drowsiness

VPA

drowsiness

VPA

drowsiness

VPA

drowsiness

ammonia

drowsiness

Ammonia

drowsiness

drowsiness

drowsiness


Input: Effects of calcitonin on rat extrapyramidal motor system: behavioral and biochemical data. The effects of i. v. c. injection of human and salmon calcitonin on biochemical and behavioral parameters related to the extrapyramidal motor system, were investigated in male rats. Calcitonin injection resulted in a potentiation of haloperidol - induced catalepsy and a partial prevention of apomorphine - induced hyperactivity. Moreover calcitonin induced a significant decrease in nigral GAD activity but no change in striatal DA and DOPAC concentration or GAD activity. The results are discussed in view of a primary action of calcitonin on the striatonigral GABAergic pathway mediating the DA - related behavioral messages of striatal origin.

haloperidol

apomorphine

DA

DOPAC

DA

catalepsy

hyperactivity

haloperidol

catalepsy

apomorphine

hyperactivity


Input: Development of isoproterenol - induced cardiac hypertrophy. The development of cardiac hypertrophy was studied in adult female Wistar rats following daily subcutaneous injections of isoproterenol (ISO) (0. 3 mg / kg body weight). A time course was established for the change in tissue mass, RNA and DNA content, as well as hydroxyproline content. Heart weight increased 44% after 8 days of treatment with a half time of 3. 4 days. Ventricular RNA content was elevated 26% after 24 h of a single injection and reached a maximal level following 8 days of therapy. The half time for RNA accumulation was 2. 0 days. The total content of hydroxyproline remained stable during the first 2 days of treatment but increased 46% after 4 days of therapy. Ventricular DNA content was unchanged during the early stage (1 - 4 days) of hypertrophic growth but increased to a new steady - state level 19% above the controls after 8 days of treatment. Intraventricular pressures and coronary flow measures were similar for control and experimental animals following 4 days of developed hypertrophy. However, dP / dt in the ISO - treated hearts was slightly but significantly (P less than 0. 05) elevated. These data indicate that the adaptive response to ISO shows an early hypertrophic phase (1 - 4 days) characterized by a substantial increase in RNA content and cardiac mass in the absence of changes in DNA. However, prolonged stimulation (8 - 12 days) appears to represent a complex integration of both cellular hypertrophy and hyperplasia within the heart.

isoproterenol

isoproterenol

ISO

hydroxyproline

hydroxyproline

ISO

ISO

cardiac hypertrophy

cardiac hypertrophy

hypertrophic

hypertrophy

hypertrophic

hypertrophy

hyperplasia

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

ISO

cardiac hypertrophy

ISO

cardiac hypertrophy

ISO

cardiac hypertrophy

ISO

cardiac hypertrophy

ISO

cardiac hypertrophy

ISO

cardiac hypertrophy

isoproterenol

hyperplasia

isoproterenol

hyperplasia

ISO

hyperplasia

ISO

hyperplasia

ISO

hyperplasia


Input: Co - carcinogenic effect of retinyl acetate on forestomach carcinogenesis of male F344 rats induced with butylated hydroxyanisole. The potential modifying effect of retinyl acetate (RA) on butylated hydroxyanisole (BHA) - induced rat forestomach tumorigenesis was examined. Male F344 rats, 5 weeks of age, were maintained on diet containing 1% or 2% BHA by weight and simultaneously on drinking water supplemented with RA at various concentrations (w / v) for 52 weeks. In groups given 2% BHA, although marked hyperplastic changes of the forestomach epithelium were observed in all animals, co - administration of 0. 25% RA significantly (P less than 0. 05) increased the incidence of forestomach tumors (squamous cell papilloma and carcinoma) to 60% (9 / 15, 2 rats with carcinoma) from 15% (3 / 20, one rat with carcinoma) in the group given RA - free water. In rats given 1% BHA, RA co - administered at a dose of 0. 05, 0. 1, 0. 2 or 0. 25% showed a dose - dependent enhancing effect on the development of the BHA - induced epithelial hyperplasia. Tumors, all papillomas, were induced in 3 rats (17%) with 0. 25% RA and in one rat (10%) with 0. 05% RA co - administration. RA alone did not induce hyperplastic changes in the forestomach. These findings indicate that RA acted as a co - carcinogen in the BHA forestomach carcinogenesis of the rat.

carcinogenic

forestomach carcinogenesis

forestomach tumorigenesis

forestomach tumors

squamous cell papilloma

carcinoma

carcinoma

carcinoma

epithelial hyperplasia

Tumors

papillomas

forestomach carcinogenesis

retinyl acetate

butylated hydroxyanisole

retinyl acetate

RA

butylated hydroxyanisole

BHA

BHA

RA

BHA

RA

RA

BHA

RA

BHA

RA

RA

RA

RA

BHA

butylated hydroxyanisole

forestomach carcinogenesis

butylated hydroxyanisole

forestomach tumorigenesis

butylated hydroxyanisole

forestomach tumors

butylated hydroxyanisole

forestomach carcinogenesis

butylated hydroxyanisole

forestomach carcinogenesis

butylated hydroxyanisole

forestomach tumorigenesis

butylated hydroxyanisole

forestomach tumors

butylated hydroxyanisole

forestomach carcinogenesis

BHA

forestomach carcinogenesis

BHA

forestomach tumorigenesis

BHA

forestomach tumors

BHA

forestomach carcinogenesis

BHA

forestomach carcinogenesis

BHA

forestomach tumorigenesis

BHA

forestomach tumors

BHA

forestomach carcinogenesis

BHA

forestomach carcinogenesis

BHA

forestomach tumorigenesis

BHA

forestomach tumors

BHA

forestomach carcinogenesis

BHA

forestomach carcinogenesis

BHA

forestomach tumorigenesis

BHA

forestomach tumors

BHA

forestomach carcinogenesis

BHA

forestomach carcinogenesis

BHA

forestomach tumorigenesis

BHA

forestomach tumors

BHA

forestomach carcinogenesis

BHA

forestomach carcinogenesis

BHA

forestomach tumorigenesis

BHA

forestomach tumors

BHA

forestomach carcinogenesis


Input: Ketanserin pretreatment reverses alfentanil - induced muscle rigidity. Systemic pretreatment with ketanserin, a relatively specific type - 2 serotonin receptor antagonist, significantly attenuated the muscle rigidity produced in rats by the potent short - acting opiate agonist alfentanil. Following placement of subcutaneous electrodes in each animal' s left gastrocnemius muscle, rigidity was assessed by analyzing root - mean - square electromyographic activity. Intraperitoneal ketanserin administration at doses of 0. 63 and 2. 5 mg / kg prevented the alfentanil - induced increase in electromyographic activity compared with animals pretreated with saline. Chlordiazepoxide at doses up to 10 mg / kg failed to significantly influence the rigidity produced by alfentanil. Despite the absence of rigidity, animals that received ketanserin (greater than 0. 31 mg / kg i. p.) followed by alfentanil were motionless, flaccid, and less responsive to external stimuli than were animals receiving alfentanil alone. Rats that received ketanserin and alfentanil exhibited less rearing and exploratory behavior at the end of the 60 - min recording period than did animals that received ketanserin alone. These results, in combination with previous work, suggest that muscle rigidity, a clinically relevant side - effect of parenteral narcotic administration, may be partly mediated via serotonergic pathways. Pretreatment with type - 2 serotonin antagonists may be clinically useful in attenuating opiate - induced rigidity, although further studies will be necessary to assess the interaction of possibly enhanced CNS, cardiovascular, and respiratory depression.

Ketanserin

alfentanil

ketanserin

serotonin

alfentanil

ketanserin

alfentanil

Chlordiazepoxide

alfentanil

ketanserin

alfentanil

alfentanil

ketanserin

alfentanil

ketanserin

serotonin

muscle rigidity

muscle rigidity

rigidity

rigidity

rigidity

muscle rigidity

rigidity

cardiovascular, and respiratory depression

cardiovascular, and respiratory depression

respiratory depression

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

rigidity


Input: Glycopyrronium requirements for antagonism of the muscarinic side effects of edrophonium. We have compared, in 60 adult patients, the cardiovascular effects of glycopyrronium 5 micrograms kg - 1 and 10 micrograms kg - 1 given either simultaneously or 1 min before edrophonium 1 mg kg - 1. Significant differences between the four groups were detected (P less than 0. 001). Both groups receiving 10 micrograms kg - 1 showed increases in heart rate of up to 30 beat min - 1 (95% confidence limits 28 - 32 beat min - 1). Use of glycopyrronium 5 micrograms kg - 1 provided greater cardiovascular stability and, given 1 min before the edrophonium, was sufficient to minimize early, edrophonium - induced bradycardias. This low dose of glycopyrronium provided good control of oropharyngeal secretions.

Glycopyrronium

edrophonium

glycopyrronium

edrophonium

glycopyrronium

edrophonium

edrophonium

glycopyrronium

bradycardias

edrophonium

bradycardias

edrophonium

bradycardias

edrophonium

bradycardias

edrophonium

bradycardias


Input: Involvement of locus coeruleus and noradrenergic neurotransmission in fentanyl - induced muscular rigidity in the rat. Whereas muscular rigidity is a well - known side effect that is associated with high - dose fentanyl anesthesia, a paucity of information exists with regard to its underlying mechanism (s). We investigated in this study the possible engagement of locus coeruleus of the pons in this phenomenon, using male Sprague - Dawley rats anesthetized with ketamine. Under proper control of respiration, body temperature and end - tidal CO2, intravenous administration of fentanyl (50 or 100 micrograms / kg) consistently promoted an increase in electromyographic activity recorded from the gastrocnemius and abdominal rectus muscles. Such an induced muscular rigidity by the narcotic agent was significantly antagonized or even reduced by prior electrolytic lesions of the locus coeruleus or pretreatment with the alpha - adrenoceptor blocker, prazosin. Microinjection of fentanyl (2. 5 micrograms / 50 nl) directly into this pontine nucleus, on the other hand, elicited discernible electromyographic excitation. It is speculated that the induction of muscular rigidity by fentanyl may involve the coerulospinal noradrenergic fibers to the spinal motoneurons.

fentanyl

fentanyl

ketamine

fentanyl

prazosin

fentanyl

fentanyl

muscular rigidity

muscular rigidity

muscular rigidity

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity

fentanyl

muscular rigidity


Input: Cerebral sinus thrombosis as a potential hazard of antifibrinolytic treatment in menorrhagia. We describe a 42 - year - old woman who developed superior sagittal and left transverse sinus thrombosis associated with prolonged epsilon - aminocaproic acid therapy for menorrhagia. This antifibrinolytic agent has been used in women with menorrhagia to promote clotting and reduce blood loss. Although increased risk of thromboembolic disease has been reported during treatment with epsilon - aminocaproic acid, cerebral sinus thrombosis has not been previously described. Careful use of epsilon - aminocaproic acid therapy is recommended.

Cerebral sinus thrombosis

menorrhagia

sagittal and left transverse sinus thrombosis

sagittal and left transverse sinus thrombosis

left transverse sinus thrombosis

menorrhagia

menorrhagia

blood loss

thromboembolic disease

cerebral sinus thrombosis

epsilon - aminocaproic acid

epsilon - aminocaproic acid

epsilon - aminocaproic acid

epsilon - aminocaproic acid

sagittal and left transverse sinus thrombosis

epsilon - aminocaproic acid

sagittal and left transverse sinus thrombosis

epsilon - aminocaproic acid

sagittal and left transverse sinus thrombosis

epsilon - aminocaproic acid

sagittal and left transverse sinus thrombosis

epsilon - aminocaproic acid

sagittal and left transverse sinus thrombosis

epsilon - aminocaproic acid

sagittal and left transverse sinus thrombosis


Input: Hemorrhagic cystitis complicating bone marrow transplantation. Hemorrhagic cystitis is a potentially serious complication of high - dose cyclophosphamide therapy administered before bone marrow transplantation. As standard practice at our institution, patients who are scheduled to receive a bone marrow transplant are treated prophylactically with forced hydration and bladder irrigation. In an attempt to obviate the inconvenience of bladder irrigation, we conducted a feasibility trial of uroprophylaxis with mesna, which neutralizes the hepatic metabolite of cyclophosphamide that causes hemorrhagic cystitis. Of 97 patients who received standard prophylaxis, 4 had symptomatic hemorrhagic cystitis. In contrast, two of four consecutive patients who received mesna uroprophylaxis before allogeneic bone marrow transplantation had severe hemorrhagic cystitis for at least 2 weeks. Because of this suboptimal result, we resumed the use of bladder irrigation and forced hydration to minimize the risk of hemorrhagic cystitis.

Hemorrhagic cystitis

Hemorrhagic

cystitis

Hemorrhagic cystitis

Hemorrhagic

cystitis

hemorrhagic cystitis

hemorrhagic

cystitis

hemorrhagic cystitis

hemorrhagic

cystitis

hemorrhagic cystitis

hemorrhagic

cystitis

hemorrhagic cystitis

hemorrhagic

cystitis

cyclophosphamide

mesna

cyclophosphamide

mesna

cyclophosphamide

Hemorrhagic cystitis

cyclophosphamide

Hemorrhagic

cyclophosphamide

Hemorrhagic cystitis

cyclophosphamide

Hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

Hemorrhagic cystitis

cyclophosphamide

Hemorrhagic

cyclophosphamide

Hemorrhagic cystitis

cyclophosphamide

Hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis


Input: Reversal of central benzodiazepine effects by flumazenil after intravenous conscious sedation with diazepam and opioids: report of a double - blind multicenter study. The Flumazenil in Intravenous Conscious Sedation with Diazepam Multicenter Study Group II. The efficacy and safety of a new benzodiazepine antagonist, flumazenil, were assessed in a double - blind multicenter study. Flumazenil (mean dose, 0. 76 mg) or placebo (mean dose, 8. 9 ml) was administered intravenously to 130 and 67 patients, respectively, who had been given diazepam in conjunction with an opioid (fentanyl, meperidine, or morphine) for the induction and maintenance of intravenous conscious sedation for diagnostic or therapeutic surgical procedures. The group assessable for efficacy comprised 122 patients treated with flumazenil and 64 patients given placebo. After 5 minutes, 80 / 115 (70%) flumazenil - treated patients, compared with 21 / 63 (33%) placebo - treated patients, were completely awake and alert, as indicated by a score of 5 on the Observer' s Assessment of Alertness / Sedation Scale. Ninety - five percent of patients in each group who attained a score of 5 at the 5 - minute assessment showed no loss of alertness throughout the 180 - minute assessment period. Flumazenil - treated patients also performed significantly better on the Finger - to - Nose Test and the recall of pictures shown at the 5 - minute assessment. Flumazenil was well tolerated, with no serious adverse effects reported. Thirty - nine (30%) of flumazenil - treated patients, compared with 17 (25%) of placebo - treated patients had one or more drug - related adverse experiences. The most common adverse effects were nausea and vomiting in the flumazenil group and nausea and injection - site pain in the placebo group. Flumazenil was found to promptly reverse sedation induced by diazepam in the presence of opioids.

benzodiazepine

flumazenil

diazepam

Flumazenil

Diazepam

benzodiazepine

flumazenil

Flumazenil

diazepam

fentanyl

meperidine

morphine

flumazenil

flumazenil

Flumazenil

Flumazenil

flumazenil

flumazenil

Flumazenil

diazepam

nausea

vomiting

nausea

pain

flumazenil

nausea

flumazenil

nausea

Flumazenil

nausea

Flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

Flumazenil

nausea

Flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

Flumazenil

nausea

Flumazenil

nausea

Flumazenil

nausea

Flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

flumazenil

nausea

Flumazenil

nausea

Flumazenil

nausea

flumazenil

vomiting

Flumazenil

vomiting

flumazenil

vomiting

Flumazenil

vomiting

flumazenil

vomiting

flumazenil

vomiting

Flumazenil

vomiting

Flumazenil

vomiting

flumazenil

vomiting

flumazenil

vomiting

Flumazenil

vomiting


Input: Hepatic adenomas and focal nodular hyperplasia of the liver in young women on oral contraceptives: case reports. Two cases of hepatic adenoma and one of focal nodular hyperplasia presumably associated with the use of oral contraceptives, are reported. Special reference is made to their clinical presentation, which may be totally asymptomatic. Liver - function tests are of little diagnostic value, but valuable information may be obtained from both liver scanning and hepatic angiography. Histologic differences and clinical similarities between hepatic adenoma and focal nodular hyperplasia of the liver are discussed.

adenomas

focal nodular hyperplasia

adenoma

focal nodular hyperplasia

adenoma

focal nodular hyperplasia

oral contraceptives

oral contraceptives

oral contraceptives

focal nodular hyperplasia

oral contraceptives

focal nodular hyperplasia

oral contraceptives

focal nodular hyperplasia

oral contraceptives

focal nodular hyperplasia

oral contraceptives

focal nodular hyperplasia

oral contraceptives

focal nodular hyperplasia

oral contraceptives

adenomas

oral contraceptives

adenoma

oral contraceptives

adenoma

oral contraceptives

adenomas

oral contraceptives

adenoma

oral contraceptives

adenoma


Input: Arterial thromboembolism in patients receiving systemic heparin therapy: a complication associated with heparin - induced thrombocytopenia. Arterial thromboembolism is a recognized complication of systemic heparin therapy. Characteristic of the entity is arterial occlusion by platelet - fibrin thrombi with distal ischemia occurring four to twenty days after the initiation of heparin therapy, preceded by profound thrombocytopenia with platelet counts in the range of 30, 000 to 40, 000 per cubic millimeter. The clinically apparent occlusion may be preceded by gastrointestinal and musculoskeletal symptoms that appear to be ischemic in origin, and might serve to warn the clinician of these complications. Previous reports of these phenomena as well as recent studies of the effect of heparin are reviewed. The common factor relating thromboembolism and thrombocytopenia is heparin - induced platelet aggregation. Appropriate treatment consists of discontinuation of heparin, and anticoagulation with sodium warfarin if necessary. Vascular procedures are performed as indicated.

thromboembolism

thrombocytopenia

thromboembolism

arterial occlusion

thrombi

ischemia

thrombocytopenia

gastrointestinal and musculoskeletal symptoms

gastrointestinal and musculoskeletal symptoms

musculoskeletal symptoms

ischemic

thromboembolism

thrombocytopenia

platelet aggregation

heparin

heparin

heparin

heparin

heparin

heparin

heparin

sodium warfarin

heparin

arterial occlusion

heparin

arterial occlusion

heparin

arterial occlusion

heparin

arterial occlusion

heparin

arterial occlusion

heparin

arterial occlusion

heparin

arterial occlusion

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia


Input: Long - term prognosis for transplant - free survivors of paracetamol - induced acute liver failure. BACKGROUND: The prognosis for transplant - free survivors of paracetamol - induced acute liver failure remains unknown. AIM: To examine whether paracetamol - induced acute liver failure increases long - term mortality. METHODS: We followed up all transplant - free survivors of paracetamol - induced acute liver injury, hospitalized in a Danish national referral centre during 1984 - 2004. We compared age - specific mortality rates from 1 year post - discharge through 2008 between those in whom the liver injury led to an acute liver failure and those in whom it did not. RESULTS: We included 641 patients. On average, age - specific mortality rates were slightly higher for the 101 patients whose paracetamol - induced liver injury had caused an acute liver failure (adjusted mortality rate ratio = 1. 70, 95% CI 1. 02 - 2. 85), but the association was age - dependent, and no survivors of acute liver failure died of liver disease, whereas suicides were frequent in both groups. These observations speak against long - term effects of acute liver failure. More likely, the elevated mortality rate ratio resulted from incomplete adjustment for the greater prevalence of substance abuse among survivors of acute liver failure. CONCLUSIONS: Paracetamol - induced acute liver failure did not affect long - term mortality. Clinical follow - up may be justified by the cause of the liver failure, but not by the liver failure itself.

paracetamol

paracetamol

paracetamol

paracetamol

paracetamol

Paracetamol

acute liver failure

acute liver failure

acute liver failure

acute liver injury

liver injury

acute liver failure

liver injury

acute liver failure

acute liver failure

liver disease

acute liver failure

substance abuse

acute liver failure

acute liver failure

liver failure

liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure

Paracetamol

acute liver failure


Input: Serotonin 6 receptor gene is associated with methamphetamine - induced psychosis in a Japanese population. BACKGROUND: Altered serotonergic neural transmission is hypothesized to be a susceptibility factor for psychotic disorders such as schizophrenia. The serotonin 6 (5 - HT6) receptor is therapeutically targeted by several second generation antipsychotics, such as clozapine and olanzapine, and d - amphetamine - induced hyperactivity in rats is corrected with the use of a selective 5 - HT6 receptor antagonist. In addition, the disrupted prepulse inhibition induced by d - amphetamine or phencyclidine was restored by 5 - HT6 receptor antagonist in an animal study using rats. These animal models were considered to reflect the positive symptoms of schizophrenia, and the above evidence suggests that altered 5 - HT6 receptors are involved in the pathophysiology of psychotic disorders. The symptoms of methamphetamine (METH) - induced psychosis are similar to those of paranoid type schizophrenia. Therefore, we conducted an analysis of the association of the 5 - HT6 gene (HTR6) with METH - induced psychosis. METHOD: Using five tagging SNPs (rs6693503, rs1805054, rs4912138, rs3790757 and rs9659997), we conducted a genetic association analysis of case - control samples (197 METH - induced psychosis patients and 337 controls) in the Japanese population. The age and sex of the control subjects did not differ from those of the methamphetamine dependence patients. RESULTS: rs6693503 was associated with METH - induced psychosis patients in the allele / genotype - wise analysis. Moreover, this association remained significant after Bonferroni correction. In the haplotype - wise analysis, we detected an association between two markers (rs6693503 and rs1805054) and three markers (rs6693503, rs1805054 and rs4912138) in HTR6 and METH - induced psychosis patients, respectively. CONCLUSION: HTR6 may play an important role in the pathophysiology of METH - induced psychosis in the Japanese population.

Serotonin

methamphetamine

serotonin

5 - HT6

clozapine

olanzapine

d - amphetamine

5 - HT6

d - amphetamine

phencyclidine

5 - HT6

5 - HT6

methamphetamine

METH

5 - HT6

METH

METH

methamphetamine

METH

METH

METH

psychosis

psychotic disorders

schizophrenia

hyperactivity

schizophrenia

psychotic disorders

psychosis

paranoid type schizophrenia

psychosis

psychosis

psychosis

psychosis

psychosis

methamphetamine

psychosis

methamphetamine

psychotic disorders

methamphetamine

psychotic disorders

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic disorders

methamphetamine

psychotic disorders

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

METH

psychosis

METH

psychotic disorders

METH

psychotic disorders

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychotic disorders

METH

psychotic disorders

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychotic disorders

METH

psychotic disorders

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

methamphetamine

psychosis

methamphetamine

psychotic disorders

methamphetamine

psychotic disorders

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

METH

psychosis

METH

psychotic disorders

METH

psychotic disorders

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychotic disorders

METH

psychotic disorders

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychotic disorders

METH

psychotic disorders

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis

METH

psychosis


Input: Effect of increasing intraperitoneal infusion rates on bupropion hydrochloride - induced seizures in mice. BACKGROUND: It is not known if there is a relationship between input rate and incidence of bupropion - induced seizures. This is important, since different controlled release formulations of bupropion release the active drug at different rates. METHODS: We investigated the effect of varying the intraperitoneal infusion rates of bupropion HCl 120 mg / kg, a known convulsive dose 50 (CD50), on the incidence and severity of bupropion - induced convulsions in the Swiss albino mice. A total of 69 mice, approximately 7 weeks of age, and weighing 21. 0 to 29. 1 g were randomly assigned to bupropion HCl 120 mg / kg treatment by intraperitoneal (IP) administration in 7 groups (9 to 10 animals per group). Bupropion HCl was infused through a surgically implanted IP dosing catheter with infusions in each group of 0 min, 15 min, 30 min, 60 min, 90 min, 120 min, and 240 min. The number, time of onset, duration and the intensity of the convulsions or absence of convulsions were recorded. RESULTS: The results showed that IP administration of bupropion HCl 120 mg / kg by bolus injection induced convulsions in 6 out of 10 mice (60% of convulsing mice) in group 1. Logistic regression analysis revealed that infusion time was significant (p = 0. 0004; odds ratio = 0. 974) and increasing the IP infusion time of bupropion HCl 120 mg / kg was associated with a 91% reduced odds of convulsions at infusion times of 15 to 90 min compared to bolus injection. Further increase in infusion time resulted in further reduction in the odds of convulsions to 99. 8% reduction at 240 min. CONCLUSION: In conclusion, the demonstration of an inverse relationship between infusion time of a fixed and convulsive dose of bupropion and the risk of convulsions in a prospective study is novel.

bupropion hydrochloride

bupropion

bupropion

bupropion HCl

bupropion

bupropion HCl

Bupropion HCl

bupropion HCl

bupropion HCl

bupropion

seizures

seizures

convulsive

convulsions

convulsions

convulsions

convulsions

convulsions

convulsions

convulsive

convulsions

bupropion hydrochloride

seizures

bupropion hydrochloride

seizures

bupropion hydrochloride

convulsive

bupropion hydrochloride

convulsions

bupropion hydrochloride

convulsions

bupropion hydrochloride

convulsions

bupropion hydrochloride

convulsions

bupropion hydrochloride

convulsions

bupropion hydrochloride

convulsions

bupropion hydrochloride

convulsive

bupropion hydrochloride

convulsions

bupropion

seizures

bupropion

seizures

bupropion

convulsive

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsive

bupropion

convulsions

bupropion

seizures

bupropion

seizures

bupropion

convulsive

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsive

bupropion

convulsions

bupropion HCl

seizures

bupropion HCl

seizures

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion

seizures

bupropion

seizures

bupropion

convulsive

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsive

bupropion

convulsions

bupropion HCl

seizures

bupropion HCl

seizures

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsive

bupropion HCl

convulsions

Bupropion HCl

seizures

Bupropion HCl

seizures

Bupropion HCl

convulsive

Bupropion HCl

convulsions

Bupropion HCl

convulsions

Bupropion HCl

convulsions

Bupropion HCl

convulsions

Bupropion HCl

convulsions

Bupropion HCl

convulsions

Bupropion HCl

convulsive

Bupropion HCl

convulsions

bupropion HCl

seizures

bupropion HCl

seizures

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion HCl

seizures

bupropion HCl

seizures

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsions

bupropion HCl

convulsive

bupropion HCl

convulsions

bupropion

seizures

bupropion

seizures

bupropion

convulsive

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsions

bupropion

convulsive

bupropion

convulsions


Input: Detailed spectral profile analysis of penicillin - induced epileptiform activity in anesthetized rats. Penicillin model is a widely used experimental model for epilepsy research. In the present study we aimed to portray a detailed spectral analysis of penicillin - induced epileptiform activity in comparison with basal brain activity in anesthetized Wistar rats. Male Wistar rats were anesthetized with i. p. urethane and connected to an electrocorticogram setup. After a short period of basal activity recording, epileptic focus was induced by injecting 400IU / 2 microl penicillin - G potassium into the left lateral ventricle while the cortical activity was continuously recorded. Basal activity, latent period and the penicillin - induced epileptiform activity periods were then analyzed using both conventional methods and spectral analysis. Spectral analyses were conducted by dividing the whole spectrum into different frequency bands including delta, theta (slow and fast), alpha - sigma, beta (1 and 2) and gamma (1 and 2) bands. Our results show that the most affected frequency bands were delta, theta, beta - 2 and gamma - 2 bands during the epileptiform activity and there were marked differences in terms of spectral densities between three investigated episodes (basal activity, latent period and epileptiform activity). Our results may help to analyze novel data obtained using similar experimental models and the simple analysis method described here can be used in similar studies to investigate the basic neuronal mechanism of this or other types of experimental epilepsies.

penicillin

Penicillin

penicillin

urethane

penicillin - G potassium

penicillin

epileptiform activity

epilepsy

epileptiform activity

epileptic

epileptiform activity

epileptiform activity

epileptiform activity

epilepsies

penicillin - G potassium

epileptiform activity

penicillin - G potassium

epilepsy

penicillin - G potassium

epileptiform activity

penicillin - G potassium

epileptic

penicillin - G potassium

epileptiform activity

penicillin - G potassium

epileptiform activity

penicillin - G potassium

epileptiform activity

penicillin - G potassium

epilepsies


Input: High dose dexmedetomidine as the sole sedative for pediatric MRI. OBJECTIVE: This large - scale retrospective review evaluates the sedation profile of dexmedetomidine. AIM: To determine the hemodynamic responses, efficacy and adverse events associated with the use of high dose dexmedetomidine as the sole sedative for magnetic resonance imaging (MRI) studies. BACKGROUND: Dexmedetomidine has been used at our institution since 2005 to provide sedation for pediatric radiological imaging studies. Over time, an effective protocol utilizing high dose dexmedetomidine as the sole sedative agent has evolved. METHODS / MATERIALS: As part of the ongoing Quality Assurance process, data on all sedations are reviewed monthly and protocols modified as needed. Data were analyzed from all 747 consecutive patients who received dexmedetomidine for MRI sedation from April 2005 to April 2007. RESULTS: Since 2005, the 10 - min loading dose of our dexmedetomidine protocol increased from 2 to 3 microg. kg (- 1), and the infusion rate increased from 1 to 1. 5 to 2 microg. kg (- 1). h (- 1). The current sedation protocol progressively increased the rate of successful sedation (able to complete the imaging study) when using dexmedetomidine alone from 91. 8% to 97. 6% (P = 0. 009), reducing the requirement for adjuvant pentobarbital in the event of sedation failure with dexmedetomidine alone and decreased the mean recovery time by 10 min (P < 0. 001). Although dexmedetomidine sedation was associated with a 16% incidence of bradycardia, all concomitant mean arterial blood pressures were within 20% of age - adjusted normal range and oxygen saturations were 95% or higher. CONCLUSION: Dexmedetomidine in high doses provides adequate sedation for pediatric MRI studies. While use of high dose dexmedetomidine is associated with decreases in heart rate and blood pressure outside the established' awake' norms, this deviation is generally within 20% of norms, and is not associated with adverse sequelae. Dexmedetomidine is useful as the sole sedative for pediatric MRI.

dexmedetomidine

dexmedetomidine

dexmedetomidine

Dexmedetomidine

dexmedetomidine

dexmedetomidine

dexmedetomidine

dexmedetomidine

pentobarbital

dexmedetomidine

dexmedetomidine

oxygen

Dexmedetomidine

dexmedetomidine

Dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

Dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

Dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

Dexmedetomidine

bradycardia


Input: Methamphetamine causes alterations in the MAP kinase - related pathways in the brains of mice that display increased aggressiveness. Aggressive behaviors have been reported in patients who suffer from some psychiatric disorders, and are common in methamphetamine (METH) abusers. Herein, we report that multiple (but not single) injections of METH significantly increased aggressiveness in male CD - 1 mice. This increase in aggressiveness was not secondary to METH - induced hyperactivity. Analysis of protein expression using antibody microarrays and Western blotting revealed differential changes in MAP kinase - related pathways after multiple and single METH injections. There were statistically significant (p < 0. 05) decreases in MEK1, Erk2p, GSK3alpha, 14 - 3 - 3e, and MEK7 in the striata of mice after multiple injections of METH. MEK1 was significantly decreased also after a single injection of METH, but to a much lesser degree than after multiple injections of METH. In the frontal cortex, there was a statistically significant decrease in GSK3alpha after multiple (but not single) injections of METH. These findings suggest that alterations in MAP kinase - related pathways in the prefronto - striatal circuitries might be involved in the manifestation of aggressive behaviors in mice.

Methamphetamine

methamphetamine

METH

METH

METH

METH

METH

METH

METH

METH

aggressiveness

Aggressive behaviors

psychiatric disorders

aggressiveness

aggressiveness

hyperactivity

aggressive behaviors

Methamphetamine

aggressiveness

Methamphetamine

Aggressive behaviors

Methamphetamine

psychiatric disorders

Methamphetamine

aggressiveness

Methamphetamine

aggressiveness

Methamphetamine

aggressive behaviors

methamphetamine

aggressiveness

methamphetamine

Aggressive behaviors

methamphetamine

psychiatric disorders

methamphetamine

aggressiveness

methamphetamine

aggressiveness

methamphetamine

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors

METH

aggressiveness

METH

Aggressive behaviors

METH

psychiatric disorders

METH

aggressiveness

METH

aggressiveness

METH

aggressive behaviors


Input: Lamotrigine associated with exacerbation or de novo myoclonus in idiopathic generalized epilepsies. Five patients with idiopathic generalized epilepsies (IGE) treated with lamotrigine (LTG) experienced exacerbation or de novo appearance of myoclonic jerks (MJ). In three patients, LTG exacerbated MJ in a dose - dependent manner with early aggravation during titration. MJ disappeared when LTG dose was decreased by 25 to 50%. In two patients, LTG exacerbated MJ in a delayed but more severe manner, with myoclonic status that only ceased after LTG withdrawal.

Lamotrigine

lamotrigine

LTG

LTG

LTG

LTG

LTG

myoclonus

idiopathic generalized epilepsies

idiopathic generalized epilepsies

IGE

myoclonic jerks

MJ

MJ

MJ

MJ

myoclonic status

Lamotrigine

myoclonus

Lamotrigine

myoclonic jerks

Lamotrigine

MJ

Lamotrigine

MJ

Lamotrigine

MJ

Lamotrigine

MJ

Lamotrigine

myoclonic status

lamotrigine

myoclonus

lamotrigine

myoclonic jerks

lamotrigine

MJ

lamotrigine

MJ

lamotrigine

MJ

lamotrigine

MJ

lamotrigine

myoclonic status

LTG

myoclonus

LTG

myoclonic jerks

LTG

MJ

LTG

MJ

LTG

MJ

LTG

MJ

LTG

myoclonic status

LTG

myoclonus

LTG

myoclonic jerks

LTG

MJ

LTG

MJ

LTG

MJ

LTG

MJ

LTG

myoclonic status

LTG

myoclonus

LTG

myoclonic jerks

LTG

MJ

LTG

MJ

LTG

MJ

LTG

MJ

LTG

myoclonic status

LTG

myoclonus

LTG

myoclonic jerks

LTG

MJ

LTG

MJ

LTG

MJ

LTG

MJ

LTG

myoclonic status

LTG

myoclonus

LTG

myoclonic jerks

LTG

MJ

LTG

MJ

LTG

MJ

LTG

MJ

LTG

myoclonic status


Input: rTMS of supplementary motor area modulates therapy - induced dyskinesias in Parkinson disease. The neural mechanisms and circuitry involved in levodopa - induced dyskinesia are unclear. Using repetitive transcranial magnetic stimulation (rTMS) over the supplementary motor area (SMA) in a group of patients with advanced Parkinson disease, the authors investigated whether modulation of SMA excitability may result in a modification of a dyskinetic state induced by continuous apomorphine infusion. rTMS at 1 Hz was observed to markedly reduce drug - induced dyskinesias, whereas 5 - Hz rTMS induced a slight but not significant increase.

dyskinesias

Parkinson disease

dyskinesia

Parkinson disease

dyskinetic

drug - induced dyskinesias

levodopa

apomorphine

levodopa

dyskinesias

levodopa

dyskinesia

levodopa

dyskinetic

levodopa

drug - induced dyskinesias


Input: Assessment of the onset and persistence of amnesia during procedural sedation with propofol. OBJECTIVES: To assess patients' ability to repeat and recall words presented to them while undergoing procedural sedation with propofol, and correlate their recall with their level of awareness as measured by bispectral index (BIS) monitoring. METHODS: This was a prospective, single - intervention study of consenting adult patients undergoing procedural sedation with propofol between December 28, 2002, and October 31, 2003. BIS monitoring was initiated starting 3 minutes before the procedure and continuing until the patient had regained baseline mental status. At 1 - minute intervals during the procedural sedation, until the patient regained baseline mental status at the end of the procedure, a word from a standardized list was read aloud, and the patient was asked to immediately repeat the word to the investigator. The BIS score at the time the word was read and the patient' s ability to repeat the word were recorded. After the procedure, the patient was asked to state all of the words from the list that he or she could recall, and to identify the last word recalled from prior to the start of the procedure and the first word recalled from after the procedure was completed. RESULTS: Seventy - five consenting patients were enrolled; one patient was excluded from data analysis for a protocol violation. No serious adverse events were noted during the procedural sedations. The mean (+ / - standard deviation) time of data collection was 16. 4 minutes (+ / - 7. 1; range 5 to 34 minutes). The mean initial (preprocedure) BIS score was 97. 1 (+ / - 2. 3; range 92 to 99). The mean lowest BIS score occurring during these procedural sedations was 66. 9 (+ / - 14. 4; range 33 to 91). The mean lowest BIS score corresponding to the ability of the patient to immediately repeat words read from the list was 77. 1 (95% CI = 74. 3 to 80. 0). The mean highest BIS score corresponding to the inability to repeat words was 81. 5 (95% CI = 78. 1 to 84. 8). The mean BIS score corresponding to the last word recalled from prior to the initiation of the sedation was 96. 7 (+ / - 2. 4; range 84 to 98). The mean BIS score corresponding to the first word recalled after the procedure was completed was 91. 2 (95% CI = 88. 1 to 94. 3). All patients recalled at least one word that had been read to them during the protocol. The mean lowest BIS score for any recalled word was 91. 5 (+ / - 11. 1; range 79 to 98), and no words were recalled when the corresponding BIS score was less than 90. CONCLUSIONS: There is a range of BIS scores during which sedated patients are able to repeat words read to them but are not able to subsequently recall these words. Furthermore, patients had no recall of words repeated prior to procedural sedation in BIS ranges associated with recall after procedural sedation, suggestive of retrograde amnesia.

amnesia

inability to repeat words

retrograde amnesia

propofol

propofol

propofol

propofol

amnesia

propofol

inability to repeat words

propofol

amnesia

propofol

inability to repeat words

propofol

amnesia

propofol

inability to repeat words


Input: Assessment of perinatal hepatitis B and rubella prevention in New Hampshire delivery hospitals. OBJECTIVE: To evaluate current performance on recommended perinatal hepatitis B and rubella prevention practices in New Hampshire. METHODS: Data were extracted from 2021 paired mother - infant records for the year 2000 birth cohort in New Hampshire' s 25 delivery hospitals. Assessment was done on the following: prenatal screening for hepatitis B and rubella, administration of the hepatitis B vaccine birth dose to all infants, administration of hepatitis B immune globulin to infants who were born to hepatitis B surface antigen - positive mothers, rubella immunity, and administration of in - hospital postpartum rubella vaccine to rubella nonimmune women. RESULTS: Prenatal screening rates for hepatitis B (98. 8%) and rubella (99. 4%) were high. Hepatitis B vaccine birth dose was administered to 76. 2% of all infants. All infants who were born to hepatitis B surface antigen - positive mothers also received hepatitis B immune globulin. Multivariate logistic regression showed that the month of delivery and infant birth weight were independent predictors of hepatitis B vaccination. The proportion of infants who were vaccinated in January and February 2000 (48. 5% and 67. 5%, respectively) was less than any other months, whereas the proportion who were vaccinated in December 2000 (88. 2%) was the highest. Women who were born between 1971 and 1975 had the highest rate of rubella nonimmunity (9. 5%). In - hospital postpartum rubella vaccine administration was documented for 75. 6% of nonimmune women. CONCLUSION: This study documents good compliance in New Hampshire' s birthing hospitals with national guidelines for perinatal hepatitis B and rubella prevention and highlights potential areas for improvement.

hepatitis B

rubella

hepatitis B

rubella

hepatitis B

rubella

hepatitis B

hepatitis B

rubella

rubella

rubella

hepatitis B

rubella

Hepatitis B

hepatitis B

hepatitis B

rubella

rubella

hepatitis B

rubella

hepatitis B surface antigen

hepatitis B surface antigen

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

Hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

Hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B


Input: Expression of p300 protects cardiac myocytes from apoptosis in vivo. Doxorubicin is an anti - tumor agent that represses cardiac - specific gene expression and induces myocardial cell apoptosis. Doxorubicin depletes cardiac p300, a transcriptional coactivator that is required for the maintenance of the differentiated phenotype of cardiac myocytes. However, the role of p300 in protection against doxorubicin - induced apoptosis is unknown. Transgenic mice overexpressing p300 in the heart and wild - type mice were subjected to doxorubicin treatment. Compared with wild - type mice, transgenic mice exhibited higher survival rate as well as more preserved left ventricular function and cardiac expression of alpha - sarcomeric actin. Doxorubicin induced myocardial cell apoptosis in wild - type mice but not in transgenic mice. Expression of p300 increased the cardiac level of bcl - 2 and mdm - 2, but not that of p53 or other members of the bcl - 2 family. These findings demonstrate that overexpression of p300 protects cardiac myocytes from doxorubicin - induced apoptosis and reduces the extent of acute heart failure in adult mice in vivo.

Doxorubicin

Doxorubicin

doxorubicin

doxorubicin

Doxorubicin

doxorubicin

tumor

heart failure

Doxorubicin

heart failure

Doxorubicin

heart failure

doxorubicin

heart failure

doxorubicin

heart failure

Doxorubicin

heart failure

doxorubicin

heart failure


Input: Mitochondrial DNA and its respiratory chain products are defective in doxorubicin nephrosis. BACKGROUND: Doxorubicin induces a self - perpetuating nephropathy characterized by early glomerular and late - onset tubular lesions in rats. We investigated the potential role of mitochondrial injury in the onset of these lesions. METHODS: Rats were treated with intravenous doxorubicin (1 mg kg (- 1) week (- 1)) for 7 weeks and were sacrificed either 1 week (' short - term') or 30 weeks (' long - term') following the last dose. Additional rats received a single dose either 6 days or 2 h prior to euthanasia. All rats were killed at 48 weeks of age. Glomerular and tubular injury was monitored and correlated to the activity or expression of respiratory chain components. Finally, we quantified both nuclear and mitochondrial DNA (mtDNA) as well as superoxide production and the 4834 base pair' common' mtDNA deletion. RESULTS: The' long - term' group had significant glomerular and tubular lesions, depressed activities of mtDNA - encoded NADH dehydrogenase and cytochrome - c oxidase (COX) and increased citrate synthase activity. In addition, expression of the mtDNA - encoded COX subunit I was reduced and mtDNA levels were decreased. In' short - term' rats, there were fewer tubular lesions, but similar numbers of glomerular lesions activity. Among all animals, glomerular and tubular injury were inversely correlated with mtDNA levels, mtDNA - encoded respiratory chain activities and with the expression of the mtDNA - encoded respiratory chain subunit COX - I. Injury was positively correlated with superoxide production and the activities of nucleus - encoded mitochondrial or cytoplasmic enzymes. Kidneys from the' long - term' group showed more mtDNA deletions than in' short - term' animals and these were not observed in the other groups. CONCLUSIONS: These results suggest an important role for quantitative and qualitative mtDNA alterations through the reduction of mtDNA - encoded respiratory chain function and induction of superoxide in doxorubicin - induced renal lesions.

doxorubicin

Doxorubicin

doxorubicin

superoxide

citrate

superoxide

superoxide

doxorubicin

nephrosis

nephropathy

glomerular and late - onset tubular lesions

mitochondrial injury

Glomerular and tubular injury

glomerular and tubular lesions

tubular lesions

glomerular lesions

glomerular and tubular injury

renal lesions

doxorubicin

nephrosis

Doxorubicin

nephrosis

doxorubicin

nephrosis

doxorubicin

nephrosis


Input: Amphotericin B - induced seizures in a patient with AIDS. OBJECTIVE: To report a case of multiple episodes of seizure activity in an AIDS patent following amphotericin B infusion. CASE SUMMARY: A 46 - year - old African - American man experienced recurrent grand mal seizures during intravenous infusion of amphotericin B, then petit mal seizures as the infusion was stopped and the drug concentrations decreased with time. The patients concurrent medications included didanosine, hydroxyzine, promethazine, hydrocortisone, and prochlorperazine. Despite administration of phenytoin and lorazepam, the seizures persisted and occurred only during amphotercin B administration. DISCUSSION: AIDS and cryptococcal meningitis, both of which the patient had, can potentially cause seizures. The patient had a history of alcohol abuse; alcohol intake as well as withdrawal can also cause seizures. Didanosine also has a potential for inducing seizures. However, these other potential causes of seizure were ruled out. The time course of events suggested that amphotericin B was the cause of the seizures in this AIDS patient. CONCLUSIONS: Amphotericin B seems to be the probable cause of the seizures. To date, only three cases of seizures associated with amphotericin B have been reported in the literature, but healthcare providers should be aware of the potential for this rare adverse effect.

Amphotericin B

amphotericin B

amphotericin B

didanosine

hydroxyzine

promethazine

hydrocortisone

prochlorperazine

phenytoin

lorazepam

amphotercin B

alcohol

Didanosine

amphotericin B

Amphotericin B

amphotericin B

seizures

AIDS

seizure

AIDS

grand mal seizures

seizures

seizures

AIDS

cryptococcal meningitis

seizures

alcohol abuse

seizures

seizures

seizure

seizures

AIDS

seizures

seizures

Amphotericin B

seizures

Amphotericin B

seizure

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizure

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotercin B

seizures

amphotercin B

seizure

amphotercin B

seizures

amphotercin B

seizures

amphotercin B

seizures

amphotercin B

seizures

amphotercin B

seizures

amphotercin B

seizure

amphotercin B

seizures

amphotercin B

seizures

amphotercin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizure

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizure

Amphotericin B

seizures

Amphotericin B

seizures

Amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizure

amphotericin B

seizures

amphotericin B

seizures

amphotericin B

seizures


Input: Therapeutic drug monitoring of tobramycin: once - daily versus twice - daily dosage schedules. OBJECTIVE: To evaluate the effect of dosage regimen (once - daily vs. twice - daily) of tobramicyn on steady - state serum concentrations and toxicity. MATERIALS AND METHODS: Patients undergoing treatment with i. v. tobramycin (4 mg / kg / day) were randomised to two groups. Group OD (n = 22) received a once - daily dose of tobramycin and group TD (n = 21) received the same dose divided into two doses daily. Tobramycin serum concentrations (peak and trough) were measured by enzyme multiplied immunoassay. The renal and auditory functions of the patients were monitored before, during and immediately after treatment. RESULTS: The two groups were comparable with respect to sex, age, body weight and renal function. No statistically significant differences were found in mean daily dose, duration of treatment, or cumulative dose. Trough concentrations were < 2 g / ml in the two groups (100%). Peak concentrations were > 6 microg / ml in 100% of the OD group and in 67% of the TD group (P < 0. 01). Mean peak concentrations were markedly different: 11. 00 + / - 2. 89 microg / ml in OD vs. 6. 53 + / - 1. 45 microg / ml in TD (P < 0. 01). The pharmacokinetics parameters were: Ke, (0. 15 + / - 0. 03 / h in OD vs. 0. 24 + / - 0. 06 / h in TD), t1 / 2, (4. 95 + / - 1. 41 h in OD vs. 3. 07 + / - 0. 71 h in TD), Vd (0. 35 + / - 0. 11 l / kg in OD vs. 0. 33 + / - 0. 09 l / kg in TD), Cl (0. 86 + / - 0. 29 ml / min / kg in OD vs. 1. 28 + / - 0. 33 ml / min / kg in TD). Increased serum creatinine was observed in 73% of patients in OD versus 57% of patients in TD, without evidence of nephrotoxicity. In TD group, three patients developed decreased auditory function, of which one presented with an auditory loss of - 30 dB, whereas in the OD group only one patient presented decreased auditory function. CONCLUSION: This small study suggests that a once - daily dosing regimen of tobramycin is at least as effective as and is no more and possibly less toxic than the twice - daily regimen. Using a single - dose therapy, peak concentration determination is not necessary, only trough samples should be monitored to ensure levels below 2 microg / ml.

tobramycin

tobramicyn

tobramycin

tobramycin

Tobramycin

creatinine

tobramycin

toxicity

nephrotoxicity

decreased auditory function

auditory loss

decreased auditory function

tobramycin

decreased auditory function

tobramycin

auditory loss

tobramycin

decreased auditory function

tobramicyn

decreased auditory function

tobramicyn

auditory loss

tobramicyn

decreased auditory function

tobramycin

decreased auditory function

tobramycin

auditory loss

tobramycin

decreased auditory function

tobramycin

decreased auditory function

tobramycin

auditory loss

tobramycin

decreased auditory function

Tobramycin

decreased auditory function

Tobramycin

auditory loss

Tobramycin

decreased auditory function

tobramycin

decreased auditory function

tobramycin

auditory loss

tobramycin

decreased auditory function


Input: Chronic effects of a novel synthetic anthracycline derivative (SM - 5887) on normal heart and doxorubicin - induced cardiomyopathy in beagle dogs. This study was designed to investigate the chronic cardiotoxic potential of SM - 5887 and a possible deteriorating effect of SM - 5887 on low - grade cardiotoxicity pre - induced by doxorubicin in beagle dogs. In the chronic treatment, beagle dogs of each sex were given intravenously once every 3 weeks, either a sublethal dose of doxorubicin (1. 5 mg / kg) or SM - 5887 (2. 5 mg / kg). The experiment was terminated 3 weeks after the ninth dosing. Animals which received over six courses of doxorubicin demonstrated the electrocardiogram (ECG) changes, decrease of blood pressure and high - grade histopathological cardiomyopathy, while animals which were terminally sacrificed after the SM - 5887 administration did not show any changes in ECG, blood pressure and histopathological examinations. To examine a possibly deteriorating cardiotoxic effect of SM - 5887, low - grade cardiomyopathy was induced in dogs by four courses of doxorubicin (1. 5 mg / kg). Nine weeks after pre - treatment, dogs were given four courses of either doxorubicin (1. 5 mg / kg) or SM - 5887 (2. 5 mg / kg) once every 3 weeks. The low - grade cardiotoxic changes were enhanced by the additional doxorubicin treatment. On the contrary, the SM - 5887 treatment did not progress the grade of cardiomyopathy. In conclusion, SM - 5887 does not have any potential of chronic cardiotoxicity and deteriorating effect on doxorubicin - induced cardiotoxicity in dogs.

anthracycline

SM - 5887

doxorubicin

SM - 5887

SM - 5887

doxorubicin

doxorubicin

SM - 5887

doxorubicin

SM - 5887

SM - 5887

doxorubicin

doxorubicin

SM - 5887

doxorubicin

SM - 5887

SM - 5887

doxorubicin

cardiomyopathy

cardiotoxic

cardiotoxicity

cardiomyopathy

cardiotoxic

cardiomyopathy

cardiotoxic

cardiomyopathy

cardiotoxicity

cardiotoxicity

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy


Input: Posteroventral medial pallidotomy in advanced Parkinson' s disease. BACKGROUND: Posteroventral medial pallidotomy sometimes produces striking improvement in patients with advanced Parkinson' s disease, but the studies to date have involved small numbers of patients and short - term follow - up. METHODS: Forty patients with Parkinson' s disease underwent serial, detailed assessments both after drug withdrawal (" off " period) and while taking their optimal medical regimens (" on " period). All patients were examined preoperatively and 39 were examined at six months; 27 of the patients were also examined at one year, and 11 at two years. RESULTS: The percent improvements at six months were as follows: off - period score for overall motor function, 28 percent (95 percent confidence interval, 19 to 38 percent), with most of the improvement in the contralateral limbs; off - period score for activities of daily living, 29 percent (95 percent confidence interval, 19 to 39 percent); on - period score for contralateral dyskinesias, 82 percent (95 percent confidence interval, 72 to 91 percent); and on - period score for ipsilateral dyskinesias, 44 percent (95 percent confidence interval, 29 to 59 percent). The improvements in dyskinesias and the total scores for off - period parkinsonism, contralateral bradykinesia, and rigidity were sustained in the 11 patients examined at two years. The improvement in ipsilateral dyskinesias was lost after one year, and the improvements in postural stability and gait lasted only three to six months. Approximately half the patients who had been dependent on assistance in activities of daily living in the off period before surgery became independent after surgery. The complications of surgery were generally well tolerated, and there were no significant changes in the use of medication. CONCLUSIONS: In late - stage Parkinson' s disease, pallidotomy significantly reduces levodopa - induced dyskinesias and off - period disability. Much of the benefit is sustained at two years, although some improvements, such as those on the ipsilateral side and in axial symptoms, wane within the first year. The on - period symptoms that are resistant to dopaminergic therapy do not respond to pallidotomy.

Parkinson' s disease

Parkinson' s disease

Parkinson' s disease

dyskinesias

dyskinesias

dyskinesias

parkinsonism

bradykinesia

rigidity

dyskinesias

Parkinson' s disease

dyskinesias

levodopa

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinesias


Input: Neuropeptide - Y immunoreactivity in the pilocarpine model of temporal lobe epilepsy. Neuropeptide - Y (NPY) is expressed by granule cells and mossy fibres of the hippocampal dentate gyrus during experimental temporal lobe epilepsy (TLE). This expression may represent an endogenous damping mechanism since NPY has been shown to block seizure - like events following high - frequency stimulation in hippocampal slices. The pilocarpine (PILO) model of epilepsy is characterized by an acute period of status epilepticus followed by spontaneous recurrent seizures and related brain damage. We report peroxidase - antiperoxidase immunostaining for NPY in several brain regions in this model. PILO - injected animals exhibited NPY immunoreactivity in the region of the mossy fibre terminals, in the dentate gyrus inner molecular layer and, in a few cases, within presumed granule cells. NPY immunoreactivity was also dramatically changed in the entorhinal cortex, amygdala and sensorimotor areas. In addition, PILO injected animals exhibited a reduction in the number of NPY - immunoreactive interneurons compared with controls. The results demonstrate that changes in NPY expression, including expression in the granule cells and mossy fibres and the loss of vulnerable NPY neurons, are present in the PILO model of TLE. However, the significance of this changed synthesis of NPY remains to be determined.

pilocarpine

pilocarpine

PILO

PILO

PILO

PILO

temporal lobe epilepsy

temporal lobe epilepsy

TLE

seizure

epilepsy

status epilepticus

seizures

brain damage

TLE

pilocarpine

temporal lobe epilepsy

pilocarpine

temporal lobe epilepsy

pilocarpine

TLE

pilocarpine

TLE

pilocarpine

temporal lobe epilepsy

pilocarpine

temporal lobe epilepsy

pilocarpine

TLE

pilocarpine

TLE

PILO

temporal lobe epilepsy

PILO

temporal lobe epilepsy

PILO

TLE

PILO

TLE

PILO

temporal lobe epilepsy

PILO

temporal lobe epilepsy

PILO

TLE

PILO

TLE

PILO

temporal lobe epilepsy

PILO

temporal lobe epilepsy

PILO

TLE

PILO

TLE

PILO

temporal lobe epilepsy

PILO

temporal lobe epilepsy

PILO

TLE

PILO

TLE


Input: Effect of myopic excimer laser photorefractive keratectomy on the electrophysiologic function of the retina and optic nerve. PURPOSE: To assess by electrophysiologic testing the effect of photorefractive keratectomy (PRK) on the retina and optic nerve. SETTING: Eye Clinic, S. Salvatore Hospital, L' Aquila University, Italy. METHODS: Standard pattern electroretinograms (P - ERGs) and standard pattern visual evoked potentials (P - VEPs) were done in 25 eyes of 25 patients who had myopic PRK for an attempted correction between 5. 00 and 15. 00 diopters (D) (mean 8. 00 D). Testing was done preoperatively and 3, 6, 12, and 18 months postoperatively. The contralateral eyes served as controls. During the follow - up, 3 patients (12%) developed steroid - induced elevated intraocular pressure (IOP) that resolved after corticosteroid therapy was discontinued. RESULTS: No statistically significant differences were seen between treated and control eyes nor between treated eyes preoperatively and postoperatively. CONCLUSION: Myopic excimer laser PRK did not seem to affect the posterior segment. The transient steroid - induced IOP rise did not seem to cause functional impairment.

steroid

corticosteroid

steroid

elevated intraocular pressure

IOP rise

corticosteroid

elevated intraocular pressure

corticosteroid

IOP rise


Input: Liposomal daunorubicin in advanced Kaposi' s sarcoma: a phase II study. We report a non - randomized Phase II clinical trial to assess the efficacy and safety of liposomal daunorubicin (DaunoXome) in the treatment of AIDS related Kaposi' s sarcoma. Eleven homosexual men with advanced Kaposi' s sarcoma were entered in the trial. Changes in size, colour and associated oedema of selected' target' lesions were measured. Clinical, biochemical and haematological toxicities were assessed. Ten subjects were evaluated. A partial response was achieved in four, of whom two subsequently relapsed. Stabilization of Kaposi' s sarcoma occurred in the remaining six, maintained until the end of the trial period in four. The drug was generally well tolerated, with few mild symptoms of toxicity. The main problem encountered was haematological toxicity, with three subjects experiencing severe neutropenia (neutrophil count < 0. 5 x 10 (9) / l). There was no evidence of cardiotoxicity. In this small patient sample, liposomal daunorubicin was an effective and well tolerated agent in the treatment of Kaposi' s sarcoma.

daunorubicin

daunorubicin

daunorubicin

Kaposi' s sarcoma

AIDS

Kaposi' s sarcoma

Kaposi' s sarcoma

oedema

toxicities

Kaposi' s sarcoma

toxicity

toxicity

neutropenia

cardiotoxicity

Kaposi' s sarcoma

daunorubicin

neutropenia

daunorubicin

neutropenia

daunorubicin

neutropenia


Input: Failure of ancrod in the treatment of heparin - induced arterial thrombosis. The morbidity and mortality associated with heparin - induced thrombosis remain high despite numerous empirical therapies. Ancrod has been used successfully for prophylaxis against development of thrombosis in patients with heparin induced platelet aggregation who require brief reexposure to heparin, but its success in patients who have developed the thrombosis syndrome is not well defined. The authors present a case of failure of ancrod treatment in a patient with heparin - induced thrombosis.

heparin

heparin

heparin

heparin

heparin

thrombosis

thrombosis

thrombosis

platelet aggregation

thrombosis

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

thrombosis


Input: Seizure after flumazenil administration in a pediatric patient. Flumazenil is a benzodiazepine receptor antagonist used to reverse sedation and respiratory depression induced by benzodiazepines. Seizures and cardiac arrhythmias have complicated its use in adult patients. Overdose patients who have coingested tricyclic antidepressants have a higher risk of these complications. Little information exists concerning adverse effects of flumazenil in children. We report the occurrence of a generalized tonic - clonic seizure in a pediatric patient following the administration of flumazenil.

Seizure

respiratory depression

Seizures

cardiac arrhythmias

Overdose

tonic - clonic seizure

flumazenil

Flumazenil

benzodiazepine

benzodiazepines

flumazenil

flumazenil

flumazenil

Seizure

flumazenil

Seizures

flumazenil

tonic - clonic seizure

Flumazenil

Seizure

Flumazenil

Seizures

Flumazenil

tonic - clonic seizure

flumazenil

Seizure

flumazenil

Seizures

flumazenil

tonic - clonic seizure

flumazenil

Seizure

flumazenil

Seizures

flumazenil

tonic - clonic seizure


Input: Remodelling of nerve structure in experimental isoniazid neuropathy in the rat. The neuropathy caused by a single dose of isoniazid in rats was studied with a computer - assisted morphometric method. Scatter diagrams of the g ratio (quotient fibre diameter / axon diameter) define regenerating fibres as a distinct population, distinguishable from the surviving fibres by reduced sheath thickness and reduced axon calibre. There was also evidence of a subtle direct toxic effect on the entire fibre population, causing axon shrinkage masked by readjustment of the myelin sheath.

isoniazid

isoniazid

neuropathy

neuropathy

isoniazid

neuropathy

isoniazid

neuropathy

isoniazid

neuropathy

isoniazid

neuropathy


Input: Selective injection of iopentol, iohexol and metrizoate into the left coronary artery of the dog. Induction of ventricular fibrillation and decrease of aortic pressure. In twenty beagle dogs selective injections were made into the left coronary artery with iopentol, iohexol and metrizoate in doses of 4 ml, 8 ml and 16 ml. Thirty - six iopentol injections, 35 iohexol injections and 37 metrizoate injections were made. Frequencies of ventricular fibrillation were significantly lower (p less than 0. 05) after iopentol (0%) and iohexol (3%) than after metrizoate (22%). Iopentol and iohexol also produced significantly less decrease in aortic blood pressure than metrizoate at the different doses.

iopentol

iohexol

metrizoate

iopentol

iohexol

metrizoate

iopentol

iohexol

metrizoate

iopentol

iohexol

metrizoate

Iopentol

iohexol

metrizoate

ventricular fibrillation

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation

metrizoate

ventricular fibrillation


Input: Magnetic resonance imaging of cerebral venous thrombosis secondary to " low - dose " birth control pills. The clinical and radiographic features of cerebral deep venous thrombosis in a 21 - year - old white woman are presented. This nulliparous patient presented with relatively mild clinical symptoms and progressing mental status changes. The only known risk factor was " low - dose " oral contraceptive pills. The magnetic resonance image (MRI) showed increased signal intensity from the internal cerebral veins, vein of Galen, and straight sinus. The diagnosis was confirmed by arterial angiography.

venous thrombosis

deep venous thrombosis

oral contraceptive

oral contraceptive

venous thrombosis

oral contraceptive

deep venous thrombosis


Input: Relation of perfusion defects observed with myocardial contrast echocardiography to the severity of coronary stenosis: correlation with thallium - 201 single - photon emission tomography. It has been previously shown that myocardial contrast echocardiography is a valuable technique for delineating regions of myocardial underperfusion secondary to coronary occlusion and to critical coronary stenoses in the presence of hyperemic stimulation. The aim of this study was to determine whether myocardial contrast echocardiography performed with a stable solution of sonicated albumin could detect regions of myocardial underperfusion resulting from various degrees of coronary stenosis. The perfusion defect produced in 16 open chest dogs was compared with the anatomic area at risk measured by the postmortem dual - perfusion technique and with thallium - 201 single - photon emission tomography (SPECT). During a transient (20 - s) coronary occlusion, a perfusion defect was observed with contrast echocardiography in 14 of the 15 dogs in which the occlusion was produced. The perfusion defect correlated significantly with the anatomic area at risk (r = 0. 74; p less than 0. 002). During dipyridamole - induced hyperemia, 12 of the 16 dogs with a partial coronary stenosis had a visible area of hypoperfusion by contrast echocardiography. The four dogs without a perfusion defect had a stenosis that resulted in a mild (0% to 50%) reduction in dipyridamole - induced hyperemia. The size of the perfusion defect during stenosis correlated significantly with the anatomic area at risk (r = 0. 61; p = 0. 02). Thallium - 201 SPECT demonstrated a perfusion defect in all 14 dogs analyzed during dipyridamole - induced hyperemia; the size of the perfusion defect correlated with the anatomic area at risk (r = 0. 58; p less than 0. 03) and with the perfusion defect by contrast echocardiography (r = 0. 58; p less than 0. 03). Thus, myocardial contrast echocardiography can be used to visualize and quantitate the amount of jeopardized myocardium during moderate to severe degrees of coronary stenosis. The results obtained show a correlation with the anatomic area at risk similar to that obtained with thallium - 201 SPECT.

coronary stenosis

coronary occlusion

coronary stenoses

hyperemic

coronary stenosis

coronary occlusion

hyperemia

coronary stenosis

hyperemia

hyperemia

coronary stenosis

thallium

thallium

dipyridamole

dipyridamole

Thallium

dipyridamole

thallium

dipyridamole

hyperemic

dipyridamole

hyperemia

dipyridamole

hyperemia

dipyridamole

hyperemia

dipyridamole

hyperemic

dipyridamole

hyperemia

dipyridamole

hyperemia

dipyridamole

hyperemia

dipyridamole

hyperemic

dipyridamole

hyperemia

dipyridamole

hyperemia

dipyridamole

hyperemia


Input: Potential deleterious effect of furosemide in radiocontrast nephropathy. The purpose of the study was to determine the efficacy of furosemide in addition to intravenous fluids in the prevention of radiocontrast nephropathy. 18 patients, referred to a radiocontrast study, considered at risk because of preexisting renal insufficiency, were enrolled in a prospective, randomized, controlled trial, performed at the secondary care center of a 1, 100 - bed private university hospital. In addition to fluids, the treatment group received furosemide (mean dose 110 mg) intravenously 30 min prior to the injection of contrast material. The control group received fluids (mean 3 liters). Radiological studies were mostly angiographies performed with both ionic and non - ionic contrast material, at an average dose of 245 ml. Renal function significantly deteriorated in the group pretreated with furosemide (p < 0. 005 by ANOVA), with a rise in serum creatinine from 145 + / - 13 to 182 + / - 16 mumol / l at 24 h, while no change occurred in the control group (from 141 + / - 6 to 142 + / - 7 mumol / l). Renal failure was associated with weight loss in the furosemide - treated group. Furosemide may be deleterious in the prevention of radiocontrast nephropathy.

furosemide

furosemide

furosemide

furosemide

creatinine

furosemide

Furosemide

nephropathy

nephropathy

renal insufficiency

Renal function significantly deteriorated

Renal failure

weight loss

nephropathy

furosemide

Renal function significantly deteriorated

furosemide

Renal function significantly deteriorated

furosemide

Renal function significantly deteriorated

furosemide

Renal function significantly deteriorated

furosemide

Renal function significantly deteriorated

Furosemide

Renal function significantly deteriorated


Input: The renal pathology in a case of lithium - induced diabetes insipidus. A case of lithium - induced diabetes insipidus is reported. At necropsy microscopy shoed unique and extensive damage to cells lining the distal nephron. It is suggested that these changes represent a specific toxic effect of lithium, reported here for the first time in man.

lithium

lithium

lithium

diabetes insipidus

diabetes insipidus

lithium

diabetes insipidus

lithium

diabetes insipidus

lithium

diabetes insipidus

lithium

diabetes insipidus

lithium

diabetes insipidus

lithium

diabetes insipidus


Input: Etiologic factors in the pathogenesis of liver tumors associated with oral contraceptives. Within the last several years, previously rare liver tumors have been seen in young women using oral contraceptive steroids. The Registry for Liver Tumors Associated with Oral Contraceptives at the University of California, Irvine, has clearly identified 27 cases. The recent literature contains 44 case reports. Common to these 71 cases has been a histopathologic diagnosis of focal nodular hyperplasia, adenoma, hamartoma, and hepatoma. Significant statistical etiologic factors include prolonged uninterrupted usage of oral contraceptive steroids. Eight deaths and liver rupture in 18 patients attest to the seriousness of this new potentially lethal adverse phenomenon.

liver tumors

liver tumors

Liver Tumors

focal nodular hyperplasia

adenoma

hamartoma

hepatoma

rupture

oral contraceptives

oral contraceptive

steroids

Oral Contraceptives

oral contraceptive

steroids

oral contraceptives

liver tumors

oral contraceptives

liver tumors

oral contraceptives

Liver Tumors

oral contraceptive

liver tumors

oral contraceptive

liver tumors

oral contraceptive

Liver Tumors

Oral Contraceptives

liver tumors

Oral Contraceptives

liver tumors

Oral Contraceptives

Liver Tumors

oral contraceptive

liver tumors

oral contraceptive

liver tumors

oral contraceptive

Liver Tumors


Input: Graft - versus - host disease prophylaxis with everolimus and tacrolimus is associated with a high incidence of sinusoidal obstruction syndrome and microangiopathy: results of the EVTAC trial. A calcineurin inhibitor combined with methotrexate is the standard prophylaxis for graft - versus - host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (HSCT). Everolimus, a derivative of sirolimus, seems to mediate antileukemia effects. We report on a combination of everolimus and tacrolimus in 24 patients (median age, 62 years) with either myelodysplastic syndrome (MDS; n = 17) or acute myeloid leukemia (AML; n = 7) undergoing intensive conditioning followed by HSCT from related (n = 4) or unrelated (n = 20) donors. All patients engrafted, and only 1 patient experienced grade IV mucositis. Nine patients (37%) developed acute grade II - IV GVHD, and 11 of 17 evaluable patients (64%) developed chronic extensive GVHD. Transplantation - associated microangiopathy (TMA) occurred in 7 patients (29%), with 2 cases of acute renal failure. The study was terminated prematurely because an additional 6 patients (25%) developed sinusoidal obstruction syndrome (SOS), which was fatal in 2 cases. With a median follow - up of 26 months, the 2 - year overall survival rate was 47%. Although this new combination appears to be effective as a prophylactic regimen for acute GVHD, the incidence of TMA and SOS is considerably higher than seen with other regimens.

Graft - versus - host disease

sinusoidal obstruction syndrome

microangiopathy

graft - versus - host disease

GVHD

myelodysplastic syndrome

MDS

acute myeloid leukemia

AML

mucositis

GVHD

GVHD

Transplantation - associated microangiopathy

TMA

acute renal failure

sinusoidal obstruction syndrome

SOS

GVHD

TMA

SOS

everolimus

tacrolimus

methotrexate

Everolimus

sirolimus

everolimus

tacrolimus

tacrolimus

sinusoidal obstruction syndrome

tacrolimus

sinusoidal obstruction syndrome

tacrolimus

SOS

tacrolimus

SOS

tacrolimus

sinusoidal obstruction syndrome

tacrolimus

sinusoidal obstruction syndrome

tacrolimus

SOS

tacrolimus

SOS

tacrolimus

microangiopathy

tacrolimus

Transplantation - associated microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

microangiopathy

tacrolimus

Transplantation - associated microangiopathy

tacrolimus

TMA

tacrolimus

TMA

everolimus

sinusoidal obstruction syndrome

everolimus

sinusoidal obstruction syndrome

everolimus

SOS

everolimus

SOS

Everolimus

sinusoidal obstruction syndrome

Everolimus

sinusoidal obstruction syndrome

Everolimus

SOS

Everolimus

SOS

everolimus

sinusoidal obstruction syndrome

everolimus

sinusoidal obstruction syndrome

everolimus

SOS

everolimus

SOS

everolimus

acute renal failure

Everolimus

acute renal failure

everolimus

acute renal failure

tacrolimus

acute renal failure

tacrolimus

acute renal failure

everolimus

microangiopathy

everolimus

Transplantation - associated microangiopathy

everolimus

TMA

everolimus

TMA

Everolimus

microangiopathy

Everolimus

Transplantation - associated microangiopathy

Everolimus

TMA

Everolimus

TMA

everolimus

microangiopathy

everolimus

Transplantation - associated microangiopathy

everolimus

TMA

everolimus

TMA


Input: Effect of some convulsants on the protective activity of loreclezole and its combinations with valproate or clonazepam in amygdala - kindled rats. Loreclezole (5 mg / kg) exerted a significant protective action in amygdala - kindled rats, reducing both seizure and afterdischarge durations. The combinations of loreclezole (2. 5 mg / kg) with valproate, clonazepam, or carbamazepine (applied at their subprotective doses) also exhibited antiseizure effect in this test. However, only two first combinations occurred to be of pharmacodynamic nature. Among several chemoconvulsants, bicuculline, N - methyl - D - aspartic acid and BAY k - 8644 (the opener of L - type calcium channels) reversed the protective activity of loreclezole alone and its combination with valproate. On the other hand, bicuculline, aminophylline and BAY k - 8644 inhibited the anticonvulsive action of loreclezole combined with clonazepam. The results support the hypothesis that the protective activity of loreclezole and its combinations with other antiepileptics may involve potentiation of GABAergic neurotransmission and blockade of L - type of calcium channels.

loreclezole

valproate

clonazepam

Loreclezole

loreclezole

valproate

clonazepam

carbamazepine

bicuculline

N - methyl - D - aspartic acid

BAY k - 8644

calcium

loreclezole

valproate

bicuculline

aminophylline

BAY k - 8644

loreclezole

clonazepam

loreclezole

calcium

seizure

bicuculline

seizure

bicuculline

seizure

aminophylline

seizure

BAY k - 8644

seizure

BAY k - 8644

seizure


Input: Acute liver failure with concurrent bupropion and carbimazole therapy. OBJECTIVE: To report a case of fatal liver failure possibly associated with concurrent use of bupropion and carbimazole. CASE SUMMARY: A 41 - year - old Chinese man with a history of hyperthyroidism had been treated with carbimazole and propranolol for the past 5 years. He received a 10 - day course of bupropion as an aid for smoking cessation 10 weeks prior to presentation. He developed acute liver failure with rapid deterioration of renal function. Liver biopsy showed evidence of nonspecific drug - induced acute liver injury. His condition was further complicated by sepsis and coagulopathy. Death resulted 19 days after the onset of symptoms. The likelihood that bupropion induced hepatotoxicity in our patient was possible, based on the Naranjo probability scale. DISCUSSION: Although there is increasing evidence of hepatotoxicity induced by bupropion, this is the first case of fatality that could have resulted from acute liver failure in a patient receiving bupropion while on concomitant treatment with carbimazole. CONCLUSIONS: Clinicians should be aware of the possibility of acute liver insult induced by bupropion given concurrently with other hepatotoxic drugs.

Acute liver failure

liver failure

hyperthyroidism

acute liver failure

drug - induced acute liver injury

sepsis

coagulopathy

hepatotoxicity

hepatotoxicity

acute liver failure

acute liver insult

hepatotoxic

bupropion

carbimazole

bupropion

carbimazole

carbimazole

propranolol

bupropion

bupropion

bupropion

bupropion

carbimazole

bupropion

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

bupropion

drug - induced acute liver injury

bupropion

hepatotoxicity

bupropion

hepatotoxicity

bupropion

hepatotoxic

carbimazole

drug - induced acute liver injury

carbimazole

hepatotoxicity

carbimazole

hepatotoxicity

carbimazole

hepatotoxic

carbimazole

drug - induced acute liver injury

carbimazole

hepatotoxicity

carbimazole

hepatotoxicity

carbimazole

hepatotoxic

carbimazole

drug - induced acute liver injury

carbimazole

hepatotoxicity

carbimazole

hepatotoxicity

carbimazole

hepatotoxic

carbimazole

drug - induced acute liver injury

carbimazole

hepatotoxicity

carbimazole

hepatotoxicity

carbimazole

hepatotoxic

carbimazole

Acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver insult

carbimazole

Acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver insult

carbimazole

Acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver insult

carbimazole

Acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver failure

carbimazole

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult

bupropion

Acute liver failure

bupropion

acute liver failure

bupropion

acute liver failure

bupropion

acute liver insult