Input: Gemcitabine plus vinorelbine in nonsmall cell lung carcinoma patients age 70 years or older or patients who cannot receive cisplatin. Oncopaz Cooperative Group. BACKGROUND: Although the prevalence of nonsmall cell lung carcinoma (NSCLC) is high among elderly patients, few data are available regarding the efficacy and toxicity of chemotherapy in this group of patients. Recent reports indicate that single agent therapy with vinorelbine (VNB) or gemcitabine (GEM) may obtain a response rate of 20 - 30% in elderly patients, with acceptable toxicity and improvement in symptoms and quality of life. In the current study the efficacy and toxicity of the combination of GEM and VNB in elderly patients with advanced NSCLC or those with some contraindication to receiving cisplatin were assessed. METHODS: Forty - nine patients with advanced NSCLC were included, 38 of whom were age > / = 70 years and 11 were age < 70 years but who had some contraindication to receiving cisplatin. All patients were evaluable for response and toxicity. Treatment was comprised of VNB, 25 mg / m (2), plus GEM, 1000 mg / m (2), both on Days 1, 8, and 15 every 28 days. Patients received a minimum of three courses unless progressive disease was detected. RESULTS: One hundred sixty - five courses were administered, with a median of 3. 6 courses per patient. The overall response rate was 26% (95% confidence interval, 15 - 41%). Two patients attained a complete response (4%) and 11 patients (22%) achieved a partial response. Eastern Cooperative Oncology Group performance status improved in 35% of those patients with an initial value > 0, whereas relief of at least 1 symptom without worsening of other symptoms was noted in 27 patients (55%). The median time to progression was 16 weeks and the 1 - year survival rate was 33%. Toxicity was mild. Six patients (12%) had World Health Organization Grade 3 - 4 neutropenia, 2 patients (4%) had Grade 3 - 4 thrombocytopenia, and 2 patients (4%) had Grade 3 neurotoxicity. Three patients with severe neutropenia (6%) died of sepsis. The median age of those patients developing Grade 3 - 4 neutropenia was significantly higher than that of the remaining patients (75 years vs. 72 years; P = 0. 047). CONCLUSIONS: The combination of GEM and VNB is moderately active and well tolerated except in patients age > / = 75 years. This age group had an increased risk of myelosuppression. Therefore the prophylactic use of granulocyte - colony stimulating factor should be considered with this treatment. New chemotherapy combinations with higher activity and lower toxicity are needed for elderly patients with advanced NSCLC.

Gemcitabine

vinorelbine

cisplatin

vinorelbine

VNB

gemcitabine

GEM

GEM

VNB

cisplatin

cisplatin

VNB

GEM

GEM

VNB

nonsmall cell lung carcinoma

nonsmall cell lung carcinoma

NSCLC

toxicity

toxicity

toxicity

NSCLC

NSCLC

toxicity

Toxicity

neutropenia

thrombocytopenia

neurotoxicity

neutropenia

sepsis

neutropenia

myelosuppression

toxicity

NSCLC

Gemcitabine

thrombocytopenia

gemcitabine

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

vinorelbine

thrombocytopenia

vinorelbine

thrombocytopenia

VNB

thrombocytopenia

VNB

thrombocytopenia

VNB

thrombocytopenia

VNB

thrombocytopenia

Gemcitabine

neurotoxicity

gemcitabine

neurotoxicity

GEM

neurotoxicity

GEM

neurotoxicity

GEM

neurotoxicity

GEM

neurotoxicity

vinorelbine

neutropenia

vinorelbine

neutropenia

vinorelbine

neutropenia

vinorelbine

neutropenia

vinorelbine

neutropenia

vinorelbine

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

VNB

neutropenia

Gemcitabine

neutropenia

Gemcitabine

neutropenia

Gemcitabine

neutropenia

gemcitabine

neutropenia

gemcitabine

neutropenia

gemcitabine

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

vinorelbine

neurotoxicity

vinorelbine

neurotoxicity

VNB

neurotoxicity

VNB

neurotoxicity

VNB

neurotoxicity

VNB

neurotoxicity


Input: Warfarin - induced artery calcification is accelerated by growth and vitamin D. The present studies demonstrate that growth and vitamin D treatment enhance the extent of artery calcification in rats given sufficient doses of Warfarin to inhibit gamma - carboxylation of matrix Gla protein, a calcification inhibitor known to be expressed by smooth muscle cells and macrophages in the artery wall. The first series of experiments examined the influence of age and growth status on artery calcification in Warfarin - treated rats. Treatment for 2 weeks with Warfarin caused massive focal calcification of the artery media in 20 - day - old rats and less extensive focal calcification in 42 - day - old rats. In contrast, no artery calcification could be detected in 10 - month - old adult rats even after 4 weeks of Warfarin treatment. To directly examine the importance of growth to Warfarin - induced artery calcification in animals of the same age, 20 - day - old rats were fed for 2 weeks either an ad libitum diet or a 6 - g / d restricted diet that maintains weight but prevents growth. Concurrent treatment of both dietary groups with Warfarin produced massive focal calcification of the artery media in the ad libitum - fed rats but no detectable artery calcification in the restricted - diet, growth - inhibited group. Although the explanation for the association between artery calcification and growth status cannot be determined from the present study, there was a relationship between higher serum phosphate and susceptibility to artery calcification, with 30% higher levels of serum phosphate in young, ad libitum - fed rats compared with either of the groups that was resistant to Warfarin - induced artery calcification, ie, the 10 - month - old rats and the restricted - diet, growth - inhibited young rats. This observation suggests that increased susceptibility to Warfarin - induced artery calcification could be related to higher serum phosphate levels. The second set of experiments examined the possible synergy between vitamin D and Warfarin in artery calcification. High doses of vitamin D are known to cause calcification of the artery media in as little as 3 to 4 days. High doses of the vitamin K antagonist Warfarin are also known to cause calcification of the artery media, but at treatment times of 2 weeks or longer yet not at 1 week. In the current study, we investigated the synergy between these 2 treatments and found that concurrent Warfarin administration dramatically increased the extent of calcification in the media of vitamin D - treated rats at 3 and 4 days. There was a close parallel between the effect of vitamin D dose on artery calcification and the effect of vitamin D dose on the elevation of serum calcium, which suggests that vitamin D may induce artery calcification through its effect on serum calcium. Because Warfarin treatment had no effect on the elevation in serum calcium produced by vitamin D, the synergy between Warfarin and vitamin D is probably best explained by the hypothesis that Warfarin inhibits the activity of matrix Gla protein as a calcification inhibitor. High levels of matrix Gla protein are found at sites of artery calcification in rats treated with vitamin D plus Warfarin, and chemical analysis showed that the protein that accumulated was indeed not gamma - carboxylated. These observations indicate that although the gamma - carboxyglutamate residues of matrix Gla protein are apparently required for its function as a calcification inhibitor, they are not required for its accumulation at calcification sites.

Warfarin

vitamin D

vitamin D

Warfarin

Warfarin

Warfarin

Warfarin

Warfarin

Warfarin

phosphate

phosphate

Warfarin

Warfarin

phosphate

vitamin D

Warfarin

vitamin D

vitamin K

Warfarin

Warfarin

vitamin D

vitamin D

vitamin D

calcium

vitamin D

calcium

Warfarin

calcium

vitamin D

Warfarin

vitamin D

Warfarin

vitamin D

Warfarin

gamma - carboxylated

gamma - carboxyglutamate

artery calcification

artery calcification

calcification

artery calcification

calcification of the artery

calcification

artery calcification

artery calcification

calcification of the artery

artery calcification

artery calcification

artery calcification

artery calcification

artery calcification

artery calcification

calcification of the artery

calcification of the artery

calcification

artery calcification

artery calcification

calcification

artery calcification

calcification

calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

calcification of the artery

Warfarin

calcification of the artery

Warfarin

artery calcification

Warfarin

artery calcification

Warfarin

artery calcification


Input: Antidepressant - induced mania in bipolar patients: identification of risk factors. BACKGROUND: Concerns about possible risks of switching to mania associated with antidepressants continue to interfere with the establishment of an optimal treatment paradigm for bipolar depression. METHOD: The response of 44 patients meeting DSM - IV criteria for bipolar disorder to naturalistic treatment was assessed for at least 6 weeks using the Montgomery - Asberg Depression Rating Scale and the Bech - Rafaelson Mania Rating Scale. Patients who experienced a manic or hypomanic switch were compared with those who did not on several variables including age, sex, diagnosis (DSM - IV bipolar I vs. bipolar II), number of previous manic episodes, type of antidepressant therapy used (electroconvulsive therapy vs. antidepressant drugs and, more particularly, selective serotonin reuptake inhibitors [SSRIs]), use and type of mood stabilizers (lithium vs. anticonvulsants), and temperament of the patient, assessed during a normothymic period using the hyperthymia component of the Semi - structured Affective Temperament Interview. RESULTS: Switches to hypomania or mania occurred in 27% of all patients (N = 12) (and in 24% of the subgroup of patients treated with SSRIs [8 / 33]); 16% (N = 7) experienced manic episodes, and 11% (N = 5) experienced hypomanic episodes. Sex, age, diagnosis (bipolar I vs. bipolar II), and additional treatment did not affect the risk of switching. The incidence of mood switches seemed not to differ between patients receiving an anticonvulsant and those receiving no mood stabilizer. In contrast, mood switches were less frequent in patients receiving lithium (15%, 4 / 26) than in patients not treated with lithium (44%, 8 / 18; p =. 04). The number of previous manic episodes did not affect the probability of switching, whereas a high score on the hyperthymia component of the Semistructured Affective Temperament Interview was associated with a greater risk of switching (p =. 008). CONCLUSION: The frequency of mood switching associated with acute antidepressant therapy may be reduced by lithium treatment. Particular attention should be paid to patients with a hyperthymic temperament, who have a greater risk of mood switches.

Antidepressant

antidepressants

antidepressant

antidepressant

serotonin reuptake inhibitors

SSRIs

lithium

SSRIs

lithium

lithium

antidepressant

lithium

mania

bipolar

mania

bipolar depression

bipolar disorder

manic

hypomanic

DSM - IV bipolar I

bipolar II

manic

hypomania

mania

manic

hypomanic

bipolar I

bipolar II

manic

Antidepressant

mania

Antidepressant

bipolar

Antidepressant

mania

Antidepressant

bipolar depression

Antidepressant

bipolar disorder

Antidepressant

manic

Antidepressant

hypomanic

Antidepressant

DSM - IV bipolar I

Antidepressant

bipolar II

Antidepressant

manic

Antidepressant

hypomania

Antidepressant

mania

Antidepressant

manic

Antidepressant

hypomanic

Antidepressant

bipolar I

Antidepressant

bipolar II

Antidepressant

manic

antidepressants

mania

antidepressants

bipolar

antidepressants

mania

antidepressants

bipolar depression

antidepressants

bipolar disorder

antidepressants

manic

antidepressants

hypomanic

antidepressants

DSM - IV bipolar I

antidepressants

bipolar II

antidepressants

manic

antidepressants

hypomania

antidepressants

mania

antidepressants

manic

antidepressants

hypomanic

antidepressants

bipolar I

antidepressants

bipolar II

antidepressants

manic

antidepressant

mania

antidepressant

bipolar

antidepressant

mania

antidepressant

bipolar depression

antidepressant

bipolar disorder

antidepressant

manic

antidepressant

hypomanic

antidepressant

DSM - IV bipolar I

antidepressant

bipolar II

antidepressant

manic

antidepressant

hypomania

antidepressant

mania

antidepressant

manic

antidepressant

hypomanic

antidepressant

bipolar I

antidepressant

bipolar II

antidepressant

manic

antidepressant

mania

antidepressant

bipolar

antidepressant

mania

antidepressant

bipolar depression

antidepressant

bipolar disorder

antidepressant

manic

antidepressant

hypomanic

antidepressant

DSM - IV bipolar I

antidepressant

bipolar II

antidepressant

manic

antidepressant

hypomania

antidepressant

mania

antidepressant

manic

antidepressant

hypomanic

antidepressant

bipolar I

antidepressant

bipolar II

antidepressant

manic

antidepressant

mania

antidepressant

bipolar

antidepressant

mania

antidepressant

bipolar depression

antidepressant

bipolar disorder

antidepressant

manic

antidepressant

hypomanic

antidepressant

DSM - IV bipolar I

antidepressant

bipolar II

antidepressant

manic

antidepressant

hypomania

antidepressant

mania

antidepressant

manic

antidepressant

hypomanic

antidepressant

bipolar I

antidepressant

bipolar II

antidepressant

manic

serotonin reuptake inhibitors

mania

serotonin reuptake inhibitors

bipolar

serotonin reuptake inhibitors

mania

serotonin reuptake inhibitors

bipolar depression

serotonin reuptake inhibitors

bipolar disorder

serotonin reuptake inhibitors

manic

serotonin reuptake inhibitors

hypomanic

serotonin reuptake inhibitors

DSM - IV bipolar I

serotonin reuptake inhibitors

bipolar II

serotonin reuptake inhibitors

manic

serotonin reuptake inhibitors

hypomania

serotonin reuptake inhibitors

mania

serotonin reuptake inhibitors

manic

serotonin reuptake inhibitors

hypomanic

serotonin reuptake inhibitors

bipolar I

serotonin reuptake inhibitors

bipolar II

serotonin reuptake inhibitors

manic

SSRIs

mania

SSRIs

bipolar

SSRIs

mania

SSRIs

bipolar depression

SSRIs

bipolar disorder

SSRIs

manic

SSRIs

hypomanic

SSRIs

DSM - IV bipolar I

SSRIs

bipolar II

SSRIs

manic

SSRIs

hypomania

SSRIs

mania

SSRIs

manic

SSRIs

hypomanic

SSRIs

bipolar I

SSRIs

bipolar II

SSRIs

manic

SSRIs

mania

SSRIs

bipolar

SSRIs

mania

SSRIs

bipolar depression

SSRIs

bipolar disorder

SSRIs

manic

SSRIs

hypomanic

SSRIs

DSM - IV bipolar I

SSRIs

bipolar II

SSRIs

manic

SSRIs

hypomania

SSRIs

mania

SSRIs

manic

SSRIs

hypomanic

SSRIs

bipolar I

SSRIs

bipolar II

SSRIs

manic


Input: Caffeine - induced cardiac arrhythmia: an unrecognised danger of healthfood products. We describe a 25 - year - old woman with pre - existing mitral valve prolapse who developed intractable ventricular fibrillation after consuming a " natural energy " guarana health drink containing a high concentration of caffeine. This case highlights the need for adequate labelling and regulation of such products.

Caffeine

caffeine

cardiac arrhythmia

mitral valve prolapse

ventricular fibrillation

Caffeine

ventricular fibrillation

caffeine

ventricular fibrillation


Input: Bladder retention of urine as a result of continuous intravenous infusion of fentanyl: 2 case reports. Sedation has been commonly used in the neonate to decrease the stress and pain from the noxious stimuli and invasive procedures in the neonatal intensive care unit, as well as to facilitate synchrony between ventilator and spontaneous breaths. Fentanyl, an opioid analgesic, is frequently used in the neonatal intensive care unit setting for these very purposes. Various reported side effects of fentanyl administration include chest wall rigidity, hypotension, respiratory depression, and bradycardia. Here, 2 cases of urinary bladder retention leading to renal pelvocalyceal dilatation mimicking hydronephrosis as a result of continuous infusion of fentanyl are reported.

retention of urine

pain

chest wall rigidity

hypotension

respiratory depression

bradycardia

urinary bladder retention

hydronephrosis

fentanyl

Fentanyl

fentanyl

fentanyl

fentanyl

respiratory depression

Fentanyl

respiratory depression

fentanyl

respiratory depression

fentanyl

respiratory depression

fentanyl

hypotension

Fentanyl

hypotension

fentanyl

hypotension

fentanyl

hypotension

fentanyl

urinary bladder retention

Fentanyl

urinary bladder retention

fentanyl

urinary bladder retention

fentanyl

urinary bladder retention

fentanyl

bradycardia

Fentanyl

bradycardia

fentanyl

bradycardia

fentanyl

bradycardia

fentanyl

retention of urine

Fentanyl

retention of urine

fentanyl

retention of urine

fentanyl

retention of urine


Input: Combined antiretroviral therapy causes cardiomyopathy and elevates plasma lactate in transgenic AIDS mice. Highly active antiretroviral therapy (HAART) is implicated in cardiomyopathy (CM) and in elevated plasma lactate (LA) in AIDS through mechanisms of mitochondrial dysfunction. To determine mitochondrial events from HAART in vivo, 8 - week - old hemizygous transgenic AIDS mice (NL4 - 3Delta gag / pol; TG) and wild - type FVB / n littermates were treated with the HAART combination of zidovudine, lamivudine, and indinavir or vehicle control for 10 days or 35 days. At termination of the experiments, mice underwent echocardiography, quantitation of abundance of molecular markers of CM (ventricular mRNA encoding atrial natriuretic factor [ANF] and sarcoplasmic calcium ATPase [SERCA2]), and determination of plasma LA. Myocardial histologic features were analyzed semiquantitatively and results were confirmed by transmission electron microscopy. After 35 days in the TG + HAART cohort, left ventricular mass increased 160% by echocardiography. Molecularly, ANF mRNA increased 250% and SERCA2 mRNA decreased 57%. Biochemically, LA was elevated (8. 5 + / - 2. 0 mM). Pathologically, granular cytoplasmic changes were found in cardiac myocytes, indicating enlarged, damaged mitochondria. Findings were confirmed ultrastructurally. No changes were found in other cohorts. After 10 days, only ANF was elevated, and only in the TG + HAART cohort. Results show that cumulative HAART caused mitochondrial CM with elevated LA in AIDS transgenic mice.

cardiomyopathy

AIDS

cardiomyopathy

CM

AIDS

mitochondrial dysfunction

AIDS

CM

CM

AIDS

lactate

lactate

LA

zidovudine

lamivudine

indinavir

calcium

LA

LA

LA

indinavir

cardiomyopathy

indinavir

cardiomyopathy

indinavir

CM

indinavir

CM

indinavir

CM

lamivudine

cardiomyopathy

lamivudine

cardiomyopathy

lamivudine

CM

lamivudine

CM

lamivudine

CM

zidovudine

cardiomyopathy

zidovudine

cardiomyopathy

zidovudine

CM

zidovudine

CM

zidovudine

CM


Input: Oral contraceptives and the risk of myocardial infarction. BACKGROUND: An association between the use of oral contraceptives and the risk of myocardial infarction has been found in some, but not all, studies. We investigated this association, according to the type of progestagen included in third - generation (i. e., desogestrel or gestodene) and second - generation (i. e., levonorgestrel) oral contraceptives, the dose of estrogen, and the presence or absence of prothrombotic mutations METHODS: In a nationwide, population - based, case - control study, we identified and enrolled 248 women 18 through 49 years of age who had had a first myocardial infarction between 1990 and 1995 and 925 control women who had not had a myocardial infarction and who were matched for age, calendar year of the index event, and area of residence. Subjects supplied information on oral - contraceptive use and major cardiovascular risk factors. An analysis for factor V Leiden and the G20210A mutation in the prothrombin gene was conducted in 217 patients and 763 controls RESULTS: The odds ratio for myocardial infarction among women who used any type of combined oral contraceptive, as compared with nonusers, was 2. 0 (95 percent confidence interval, 1. 5 to 2. 8). The adjusted odds ratio was 2. 5 (95 percent confidence interval, 1. 5 to 4. 1) among women who used second - generation oral contraceptives and 1. 3 (95 percent confidence interval, 0. 7 to 2. 5) among those who used third - generation oral contraceptives. Among women who used oral contraceptives, the odds ratio was 2. 1 (95 percent confidence interval, 1. 5 to 3. 0) for those without a prothrombotic mutation and 1. 9 (95 percent confidence interval, 0. 6 to 5. 5) for those with a mutation CONCLUSIONS: The risk of myocardial infarction was increased among women who used second - generation oral contraceptives. The results with respect to the use of third - generation oral contraceptives were inconclusive but suggested that the risk was lower than the risk associated with second - generation oral contraceptives. The risk of myocardial infarction was similar among women who used oral contraceptives whether or not they had a prothrombotic mutation.

Oral contraceptives

oral contraceptives

progestagen

desogestrel

gestodene

levonorgestrel

oral contraceptives

estrogen

oral - contraceptive

oral contraceptive

oral contraceptives

oral contraceptives

oral contraceptives

oral contraceptives

oral contraceptives

oral contraceptives

oral contraceptives

myocardial infarction

myocardial infarction

myocardial infarction

myocardial infarction

myocardial infarction

myocardial infarction

myocardial infarction

Oral contraceptives

myocardial infarction

Oral contraceptives

myocardial infarction

Oral contraceptives

myocardial infarction

Oral contraceptives

myocardial infarction

Oral contraceptives

myocardial infarction

Oral contraceptives

myocardial infarction

Oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral - contraceptive

myocardial infarction

oral - contraceptive

myocardial infarction

oral - contraceptive

myocardial infarction

oral - contraceptive

myocardial infarction

oral - contraceptive

myocardial infarction

oral - contraceptive

myocardial infarction

oral - contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptive

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction

oral contraceptives

myocardial infarction


Input: Effects of 5 - HT1B receptor ligands microinjected into the accumbal shell or core on the cocaine - induced locomotor hyperactivity in rats. The present study was designed to examine the effect of 5 - HT1B receptor ligands microinjected into the subregions of the nucleus accumbens (the shell and the core) on the locomotor hyperactivity induced by cocaine in rats. Male Wistar rats were implanted bilaterally with cannulae into the accumbens shell or core, and then were locally injected with GR 55562 (an antagonist of 5 - HT1B receptors) or CP 93129 (an agonist of 5 - HT1B receptors). Given alone to any accumbal subregion, GR 55562 (0. 1 - 10 microg / side) or CP 93129 (0. 1 - 10 microg / side) did not change basal locomotor activity. Systemic cocaine (10 mg / kg) significantly increased the locomotor activity of rats. GR 55562 (0. 1 - 10 microg / side), administered intra - accumbens shell prior to cocaine, dose - dependently attenuated the psychostimulant - induced locomotor hyperactivity. Such attenuation was not found in animals which had been injected with GR 55562 into the accumbens core. When injected into the accumbens shell (but not the core) before cocaine, CP 93129 (0. 1 - 10 microg / side) enhanced the locomotor response to cocaine; the maximum effect being observed after 10 microg / side of the agonist. The later enhancement was attenuated after intra - accumbens shell treatment with GR 55562 (1 microg / side). Our findings indicate that cocaine induced hyperlocomotion is modified by 5 - HT1B receptor ligands microinjected into the accumbens shell, but not core, this modification consisting in inhibitory and facilitatory effects of the 5 - HT1B receptor antagonist (GR 55562) and agonist (CP 93129), respectively. In other words, the present results suggest that the accumbal shell 5 - HT1B receptors play a permissive role in the behavioural response to the psychostimulant.

cocaine

cocaine

GR 55562

CP 93129

GR 55562

CP 93129

cocaine

GR 55562

cocaine

GR 55562

cocaine

CP 93129

cocaine

GR 55562

cocaine

GR 55562

CP 93129

locomotor hyperactivity

locomotor hyperactivity

locomotor hyperactivity

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

locomotor hyperactivity

cocaine

hyperlocomotion

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

hyperlocomotion

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

hyperlocomotion

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

hyperlocomotion

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

locomotor hyperactivity

CP 93129

hyperlocomotion


Input: Ticlopidine - induced cholestatic hepatitis. OBJECTIVE: To report 2 cases of ticlopidine - induced cholestatic hepatitis, investigate its mechanism, and compare the observed main characteristics with those of the published cases. CASE SUMMARIES: Two patients developed prolonged cholestatic hepatitis after receiving ticlopidine following percutaneous coronary angioplasty, with complete remission during the follow - up period. T - cell stimulation by therapeutic concentration of ticlopidine was demonstrated in vitro in the patients, but not in healthy controls. DISCUSSION: Cholestatic hepatitis is a rare complication of the antiplatelet agent ticlopidine; several cases have been reported but few in the English literature. Our patients developed jaundice following treatment with ticlopidine and showed the clinical and laboratory characteristics of cholestatic hepatitis, which resolved after discontinuation of the drug. Hepatitis may develop weeks after discontinuation of the drug and may run a prolonged course, but complete remission was observed in all reported cases. An objective causality assessment revealed that the adverse drug event was probably related to the use of ticlopidine. The mechanisms of this ticlopidine - induced cholestasis are unclear. Immune mechanisms may be involved in the drug' s hepatotoxicity, as suggested by the T - cell stimulation study reported here. CONCLUSIONS: Cholestatic hepatitis is a rare adverse effect of ticlopidine that may be immune mediated. Patients receiving the drug should be monitored with liver function tests along with complete blood cell counts. This complication will be observed even less often in the future as ticlopidine is being replaced by the newer antiplatelet agent clopidogrel.

Ticlopidine

ticlopidine

ticlopidine

ticlopidine

ticlopidine

ticlopidine

ticlopidine

ticlopidine

ticlopidine

ticlopidine

clopidogrel

cholestatic hepatitis

cholestatic

hepatitis

cholestatic hepatitis

cholestatic

hepatitis

cholestatic hepatitis

cholestatic

hepatitis

Cholestatic hepatitis

Cholestatic

hepatitis

jaundice

cholestatic hepatitis

cholestatic

hepatitis

Hepatitis

cholestasis

hepatotoxicity

Cholestatic hepatitis

Cholestatic

hepatitis

Ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

ticlopidine

jaundice

Ticlopidine

cholestatic hepatitis

Ticlopidine

cholestatic

Ticlopidine

cholestatic hepatitis

Ticlopidine

cholestatic

Ticlopidine

cholestatic hepatitis

Ticlopidine

cholestatic

Ticlopidine

Cholestatic hepatitis

Ticlopidine

Cholestatic

Ticlopidine

cholestatic hepatitis

Ticlopidine

cholestatic

Ticlopidine

cholestasis

Ticlopidine

Cholestatic hepatitis

Ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

ticlopidine

cholestatic hepatitis

ticlopidine

cholestatic

ticlopidine

cholestasis

ticlopidine

Cholestatic hepatitis

ticlopidine

Cholestatic

Ticlopidine

hepatitis

Ticlopidine

hepatitis

Ticlopidine

hepatitis

Ticlopidine

hepatitis

Ticlopidine

hepatitis

Ticlopidine

Hepatitis

Ticlopidine

hepatotoxicity

Ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

hepatitis

ticlopidine

Hepatitis

ticlopidine

hepatotoxicity

ticlopidine

hepatitis


Input: Epithelial sodium channel (ENaC) subunit mRNA and protein expression in rats with puromycin aminonucleoside - induced nephrotic syndrome. In experimental nephrotic syndrome, urinary sodium excretion is decreased during the early phase of the disease. The molecular mechanism (s) leading to salt retention has not been completely elucidated. The rate - limiting constituent of collecting duct sodium transport is the epithelial sodium channel (ENaC). We examined the abundance of ENaC subunit mRNAs and proteins in puromycin aminonucleoside (PAN) - induced nephrotic syndrome. The time courses of urinary sodium excretion, plasma aldosterone concentration and proteinuria were studied in male Sprague - Dawley rats treated with a single dose of either PAN or vehicle. The relative amounts of alphaENaC, betaENaC and gammaENaC mRNAs were determined in kidneys from these rats by real - time quantitative TaqMan PCR, and the amounts of proteins by Western blot. The kinetics of urinary sodium excretion and the appearance of proteinuria were comparable with those reported previously. Sodium retention occurred on days 2, 3 and 6 after PAN injection. A significant up - regulation of alphaENaC and betaENaC mRNA abundance on days 1 and 2 preceded sodium retention on days 2 and 3. Conversely, down - regulation of alphaENaC, betaENaC and gammaENaC mRNA expression on day 3 occurred in the presence of high aldosterone concentrations, and was followed by a return of sodium excretion to control values. The amounts of alphaENaC, betaENaC and gammaENaC proteins were not increased during PAN - induced sodium retention. In conclusion, ENaC mRNA expression, especially alphaENaC, is increased in the very early phase of the experimental model of PAN - induced nephrotic syndrome in rats, but appears to escape from the regulation by aldosterone after day 3.

sodium

puromycin aminonucleoside

sodium

sodium

sodium

puromycin aminonucleoside

PAN

sodium

aldosterone

PAN

sodium

Sodium

PAN

sodium

aldosterone

sodium

PAN

sodium

PAN

aldosterone

nephrotic syndrome

nephrotic syndrome

nephrotic syndrome

proteinuria

proteinuria

nephrotic syndrome

puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

PAN

proteinuria

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

nephrotic syndrome


Input: NO - induced migraine attack: strong increase in plasma calcitonin gene - related peptide (CGRP) concentration and negative correlation with platelet serotonin release. The aim of the present study was to investigate changes in the plasma calcitonin gene - related peptide (CGRP) concentration and platelet serotonin (5 - hydroxytriptamine, 5 - HT) content during the immediate headache and the delayed genuine migraine attack provoked by nitroglycerin. Fifteen female migraineurs (without aura) and eight controls participated in the study. Sublingual nitroglycerin (0. 5 mg) was administered. Blood was collected from the antecubital vein four times: 60 min before and after the nitroglycerin application, and 60 and 120 min after the beginning of the migraine attack (mean 344 and 404 min; 12 subjects). In those subjects who had no migraine attack (11 subjects) a similar time schedule was used. Plasma CGRP concentration increased significantly (P < 0. 01) during the migraine attack and returned to baseline after the cessation of the migraine. In addition, both change and peak, showed significant positive correlations with migraine headache intensity (P < 0. 001). However, plasma CGRP concentrations failed to change during immediate headache and in the subjects with no migraine attack. Basal CGRP concentration was significantly higher and platelet 5 - HT content tended to be lower in subjects who experienced a migraine attack. Platelet serotonin content decreased significantly (P < 0. 01) after nitroglycerin in subjects with no migraine attack but no consistent change was observed in patients with migraine attack. In conclusion, the fact that plasma CGRP concentration correlates with the timing and severity of a migraine headache suggests a direct relationship between CGRP and migraine. In contrast, serotonin release from platelets does not provoke migraine, it may even counteract the headache and the concomitant CGRP release in this model.

NO

calcitonin gene - related peptide

CGRP

serotonin

calcitonin gene - related peptide

CGRP

serotonin

5 - hydroxytriptamine

5 - HT

nitroglycerin

nitroglycerin

nitroglycerin

CGRP

CGRP

CGRP

5 - HT

serotonin

nitroglycerin

CGRP

CGRP

serotonin

CGRP

migraine

headache

migraine

migraineurs (without aura)

migraine

migraine

migraine

migraine

migraine

headache

headache

migraine

migraine

migraine

migraine

migraine

headache

migraine

migraine

headache

nitroglycerin

migraineurs (without aura)

nitroglycerin

migraineurs (without aura)

nitroglycerin

migraineurs (without aura)

nitroglycerin

migraineurs (without aura)

NO

migraineurs (without aura)


Input: Coronary aneurysm after implantation of a paclitaxel - eluting stent. Formation of coronary aneurysm is a rare complication of stenting with bare metal stents, but based on experimental studies drug - eluting stents may induce toxic effects on the vessel wall with incomplete stent apposition, aneurysm formation and with the potential of stent thrombosis or vessel rupture. We present a 43 - year - old man who developed a coronary aneurysm in the right coronary artery 6 months after receiving a paclitaxel - eluting stent. The patient was asymptomatic and the aneurysm was detected in a routine control. Angiography and intracoronary ultrasound demonstrated lack of contact between stent and vessel wall in a 15 - mm long segment with maximal aneurysm diameter of 6. 0 mm. The patient was successfully treated with a graft stent.

Coronary aneurysm

coronary aneurysm

aneurysm

thrombosis

vessel rupture

coronary aneurysm

aneurysm

aneurysm

paclitaxel

paclitaxel

paclitaxel

Coronary aneurysm

paclitaxel

coronary aneurysm

paclitaxel

coronary aneurysm

paclitaxel

Coronary aneurysm

paclitaxel

coronary aneurysm

paclitaxel

coronary aneurysm


Input: Behavioral effects of urotensin - II centrally administered in mice. Urotensin - II (U - II) receptors are widely distributed in the central nervous system. Intracerebroventricular (i. c. v.) injection of U - II causes hypertension and bradycardia and stimulates prolactin and thyrotropin secretion. However, the behavioral effects of centrally administered U - II have received little attention. In the present study, we tested the effects of i. c. v. injections of U - II on behavioral, metabolic, and endocrine responses in mice. Administration of graded doses of U - II (1 - 10, 000 ng / mouse) provoked: (1) a dose - dependent reduction in the number of head dips in the hole - board test; (2) a dose - dependent reduction in the number of entries in the white chamber in the black - and - white compartment test, and in the number of entries in the central platform and open arms in the plus - maze test; and (3) a dose - dependent increase in the duration of immobility in the forced - swimming test and tail suspension test. Intracerebroventricular injection of U - II also caused an increase in: food intake at doses of 100 and 1, 000 ng / mouse, water intake at doses of 100 - 10, 000 ng / mouse, and horizontal locomotion activity at a dose of 10, 000 ng / mouse. Whatever was the dose, the central administration of U - II had no effect on body temperature, nociception, apomorphine - induced penile erection and climbing behavior, and stress - induced plasma corticosterone level. Taken together, the present study demonstrates that the central injection of U - II at doses of 1 - 10, 000 ng / mouse induces anxiogenic - and depressant - like effects in mouse. These data suggest that U - II may be involved in some aspects of psychiatric disorders.

urotensin - II

Urotensin - II

U - II

U - II

U - II

U - II

U - II

U - II

U - II

apomorphine

corticosterone

U - II

U - II

hypertension

bradycardia

penile erection

psychiatric disorders

apomorphine

penile erection


Input: Recurrent dysphonia and acitretin. We report the case of a woman complaining of dysphonia while she was treated by acitretin. Her symptoms totally regressed after drug withdrawal and reappeared when acitretin was reintroduced. To our knowledge, this is the first case of acitretin - induced dysphonia. This effect may be related to the pharmacological effect of this drug on mucous membranes.

dysphonia

dysphonia

dysphonia

acitretin

acitretin

acitretin

acitretin

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia

acitretin

dysphonia


Input: Pharmacological modulation of pain - related brain activity during normal and central sensitization states in humans. Abnormal processing of somatosensory inputs in the central nervous system (central sensitization) is the mechanism accounting for the enhanced pain sensitivity in the skin surrounding tissue injury (secondary hyperalgesia). Secondary hyperalgesia shares clinical characteristics with neurogenic hyperalgesia in patients with neuropathic pain. Abnormal brain responses to somatosensory stimuli have been found in patients with hyperalgesia as well as in normal subjects during experimental central sensitization. The aim of this study was to assess the effects of gabapentin, a drug effective in neuropathic pain patients, on brain processing of nociceptive information in normal and central sensitization states. Using functional magnetic resonance imaging (fMRI) in normal volunteers, we studied the gabapentin - induced modulation of brain activity in response to nociceptive mechanical stimulation of normal skin and capsaicin - induced secondary hyperalgesia. The dose of gabapentin was 1, 800 mg per os, in a single administration. We found that (i) gabapentin reduced the activations in the bilateral operculoinsular cortex, independently of the presence of central sensitization; (ii) gabapentin reduced the activation in the brainstem, only during central sensitization; (iii) gabapentin suppressed stimulus - induced deactivations, only during central sensitization; this effect was more robust than the effect on brain activation. The observed drug - induced effects were not due to changes in the baseline fMRI signal. These findings indicate that gabapentin has a measurable antinociceptive effect and a stronger antihyperalgesic effect most evident in the brain areas undergoing deactivation, thus supporting the concept that gabapentin is more effective in modulating nociceptive transmission when central sensitization is present.

pain

pain

tissue injury

secondary hyperalgesia

Secondary hyperalgesia

neurogenic hyperalgesia

neuropathic pain

hyperalgesia

neuropathic pain

secondary hyperalgesia

gabapentin

gabapentin

capsaicin

gabapentin

gabapentin

gabapentin

gabapentin

gabapentin

gabapentin

capsaicin

secondary hyperalgesia

capsaicin

Secondary hyperalgesia

capsaicin

neurogenic hyperalgesia

capsaicin

hyperalgesia

capsaicin

secondary hyperalgesia


Input: MDMA polydrug users show process - specific central executive impairments coupled with impaired social and emotional judgement processes. In recent years working memory deficits have been reported in users of MDMA (3, 4 - methylenedioxymethamphetamine, ecstasy). The current study aimed to assess the impact of MDMA use on three separate central executive processes (set shifting, inhibition and memory updating) and also on " prefrontal " mediated social and emotional judgement processes. Fifteen polydrug ecstasy users and 15 polydrug non - ecstasy user controls completed a general drug use questionnaire, the Brixton Spatial Anticipation task (set shifting), Backward Digit Span procedure (memory updating), Inhibition of Return (inhibition), an emotional intelligence scale, the Tromso Social Intelligence Scale and the Dysexecutive Questionnaire (DEX). Compared with MDMA - free polydrug controls, MDMA polydrug users showed impairments in set shifting and memory updating, and also in social and emotional judgement processes. The latter two deficits remained significant after controlling for other drug use. These data lend further support to the proposal that cognitive processes mediated by the prefrontal cortex may be impaired by recreational ecstasy use.

MDMA

MDMA

3, 4 - methylenedioxymethamphetamine

ecstasy

MDMA

ecstasy

ecstasy

MDMA

MDMA

ecstasy

impaired social and emotional judgement processes

memory deficits

MDMA

impaired social and emotional judgement processes

MDMA

impaired social and emotional judgement processes

3, 4 - methylenedioxymethamphetamine

impaired social and emotional judgement processes

ecstasy

impaired social and emotional judgement processes

MDMA

impaired social and emotional judgement processes

ecstasy

impaired social and emotional judgement processes

ecstasy

impaired social and emotional judgement processes

MDMA

impaired social and emotional judgement processes

MDMA

impaired social and emotional judgement processes

ecstasy

impaired social and emotional judgement processes


Input: Severe citrate toxicity complicating volunteer apheresis platelet donation. We report a case of severe citrate toxicity during volunteer donor apheresis platelet collection. The donor was a 40 - year - old female, first - time apheresis platelet donor. Past medical history was remarkable for hypertension, hyperlipidemia, and depression. Reported medications included bumetanide, pravastatin, and paroxetine. Thirty minutes from the start of the procedure, the donor noted tingling around the mouth, hands, and feet. She then very rapidly developed acute onset of severe facial and extremity tetany. Empirical treatment with intravenous calcium gluconate was initiated, and muscle contractions slowly subsided over approximately 10 to 15 minutes. The events are consistent with a severe reaction to calcium chelation by sodium citrate anticoagulant resulting in symptomatic systemic hypocalcemia. Upon additional retrospective analysis, it was noted that bumetanide is a loop diuretic that may cause significant hypocalcemia. We conclude that careful screening for medications and underlying conditions predisposing to hypocalcemia is recommended to help prevent severe reactions due to citrate toxicity. Laboratory measurement of pre - procedure serum calcium levels in selected donors may identify cases requiring heightened vigilance. The case also illustrates the importance of maintaining preparedness for managing rare but serious reactions in volunteer apheresis blood donors.

citrate

citrate

bumetanide

pravastatin

paroxetine

calcium gluconate

calcium

sodium citrate

bumetanide

loop diuretic

citrate

calcium

toxicity

toxicity

hypertension

hyperlipidemia

depression

tetany

muscle contractions

hypocalcemia

hypocalcemia

hypocalcemia

toxicity

citrate

hypocalcemia

citrate

hypocalcemia

citrate

hypocalcemia

citrate

hypocalcemia

citrate

hypocalcemia

citrate

hypocalcemia

sodium citrate

hypocalcemia

sodium citrate

hypocalcemia

sodium citrate

hypocalcemia

citrate

hypocalcemia

citrate

hypocalcemia

citrate

hypocalcemia


Input: Proteinuria after conversion to sirolimus in renal transplant recipients. Sirolimus (SRL) is a new, potent immunosuppressive agent. More recently, proteinuria has been reported as a consequence of sirolimus therapy, although the mechanism has remained unclear. We retrospectively examined the records of 25 renal transplant patients, who developed or displayed increased proteinuria after SRL conversion. The patient cohort (14 men, 11 women) was treated with SRL as conversion therapy, due to chronic allograft nephropathy (CAN) (n = 15) neoplasia (n = 8); Kaposi' s sarcoma, Four skin cancers, One intestinal tumors, One renal cell carsinom) or BK virus nephropathy (n = 2). SRL was started at a mean of 78 + / - 42 (15 to 163) months after transplantation. Mean follow - up on SRL therapy was 20 + / - 12 (6 to 43) months. Proteinuria increased from 0. 445 (0 to 1. 5) g / d before conversion to 3. 2 g / dL (0. 2 to 12) after conversion (P = 0. 001). Before conversion 8 (32%) patients had no proteinuria, whereas afterwards all patients had proteinuria. In 28% of patients proteinuria remained unchanged, whereas it increased in 68% of patients. In 40% it increased by more than 100%. Twenty - eight percent of patients showed increased proteinuria to the nephrotic range. Biopsies performed in five patients revealed new pathological changes: One membranoproliferative glomerulopathy and interstitial nephritis. These patients showed persistently good graft function. Serum creatinine values did not change significantly: 1. 98 + / - 0. 8 mg / dL before SRL therapy and 2. 53 + / - 1. 9 mg / dL at last follow - up (P =. 14). Five grafts were lost and the patients returned to dialysis. Five patients displayed CAN and Kaposi' s sarcoma. Mean urinary protein of patients who returned to dialysis was 1. 26 (0. 5 to 3. 5) g / d before and 4. 7 (3 to 12) g / d after conversion (P =. 01). Mean serum creatinine level before conversion was 2. 21 mg / dL and thereafter, 4. 93 mg / dL (P =. 02). Heavy proteinuria was common after the use of SRL as rescue therapy for renal transplantation. Therefore, conversion should be considered for patients who have not developed advanced CAN and proteinuria. The possibility of de novo glomerular pathology under SRL treatment requires further investigation by renal biopsy.

Proteinuria

proteinuria

proteinuria

chronic allograft nephropathy

CAN

neoplasia

Kaposi' s sarcoma

skin cancers

intestinal tumors

renal cell carsinom

nephropathy

Proteinuria

proteinuria

proteinuria

proteinuria

proteinuria

nephrotic

membranoproliferative glomerulopathy

interstitial nephritis

CAN

Kaposi' s sarcoma

proteinuria

CAN

proteinuria

sirolimus

Sirolimus

SRL

sirolimus

SRL

SRL

SRL

SRL

creatinine

SRL

creatinine

SRL

SRL

sirolimus

Proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

Proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

Sirolimus

Proteinuria

Sirolimus

proteinuria

Sirolimus

proteinuria

Sirolimus

Proteinuria

Sirolimus

proteinuria

Sirolimus

proteinuria

Sirolimus

proteinuria

Sirolimus

proteinuria

Sirolimus

proteinuria

Sirolimus

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

sirolimus

Proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

Proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

sirolimus

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

Proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria

SRL

proteinuria


Input: In vitro characterization of parasympathetic and sympathetic responses in cyclophosphamide - induced cystitis in the rat. In cyclophosphamide - induced cystitis in the rat, detrusor function is impaired and the expression and effects of muscarinic receptors altered. Whether or not the neuronal transmission may be affected by cystitis was presently investigated. Responses of urinary strip preparations from control and cyclophosphamide - pretreated rats to electrical field stimulation and to agonists were assessed in the absence and presence of muscarinic, adrenergic and purinergic receptor antagonists. Generally, atropine reduced contractions, but in contrast to controls, it also reduced responses to low electrical field stimulation intensity (1 - 5 Hz) in inflamed preparations. In both types, purinoceptor desensitization with alpha, beta - methylene adenosine - 5' - triphosphate (alpha, beta - meATP) caused further reductions at low frequencies (< 10 Hz). The muscarinic receptor antagonists atropine, 4 - diphenylacetoxy - N - methylpiperidine (4 - DAMP) (' M (1) / M (3) / M (5) - selective'), methoctramine (' M (2) - selective') and pirenzepine (' M (1) - selective') antagonized the tonic component of the electrical field stimulation - evoked contractile response more potently than the phasic component. 4 - DAMP inhibited the tonic contractions in controls more potently than methoctramine and pirenzepine. In inflamed preparations, the muscarinic receptor antagonism on the phasic component of the electrical field stimulation - evoked contraction was decreased and the pirenzepine and 4 - DAMP antagonism on the tonic component was much less efficient than in controls. In contrast to controls, methoctramine increased - - instead of decreased - - the tonic responses at high frequencies. While contractions to carbachol and ATP were the same in inflamed and in control strips when related to a reference potassium response, isoprenaline - induced relaxations were smaller in inflamed strips. Thus, in cystitis substantial changes of the efferent functional responses occur. While postjunctional beta - adrenoceptor - mediated relaxations are reduced, effects by prejunctional inhibitory muscarinic receptors may be increased.

cyclophosphamide

cyclophosphamide

cyclophosphamide

atropine

alpha, beta - methylene adenosine - 5' - triphosphate

alpha, beta - meATP

atropine

4 - diphenylacetoxy - N - methylpiperidine

4 - DAMP

methoctramine

pirenzepine

4 - DAMP

methoctramine

pirenzepine

pirenzepine

4 - DAMP

methoctramine

carbachol

ATP

potassium

isoprenaline

cystitis

cystitis

cystitis

cystitis

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: Associations between use of benzodiazepines or related drugs and health, physical abilities and cognitive function: a non - randomised clinical study in the elderly. OBJECTIVE: To describe associations between the use of benzodiazepines or related drugs (BZDs / RDs) and health, functional abilities and cognitive function in the elderly. METHODS: A non - randomised clinical study of patients aged > or = 65 years admitted to acute hospital wards during 1 month. 164 patients (mean age + / - standard deviation [SD] 81. 6 + / - 6. 8 years) were admitted. Of these, nearly half (n = 78) had used BZDs / RDs before admission, and the remainder (n = 86) were non - users. Cognitive ability was assessed by the Mini - Mental State Examination (MMSE). Patients scoring > or = 20 MMSE sum points were interviewed (n = 79) and questioned regarding symptoms and functional abilities during the week prior to admission. Data on use of BZDs / RDs before admission, current medications and discharge diagnoses were collected from medical records. Health, physical abilities and cognitive function were compared between BZD / RD users and non - users, and adjustments were made for confounding variables. The residual serum concentrations of oxazepam, temazepam and zopiclone were analysed. RESULTS: The mean + / - SD duration of BZD / RD use was 7 + / - 7 years (range 1 - 31). Two or three BZDs / RDs were concomitantly taken by 26% of users (n = 20). Long - term use of these drugs was associated with female sex and use of a higher number of drugs with effects on the CNS, which tended to be related to diagnosed dementia. After adjustment for these variables as confounders, use of BZDs / RDs was not associated with cognitive function as measured by the MMSE. However, use of BZDs / RDs was associated with dizziness, inability to sleep after awaking at night and tiredness in the mornings during the week prior to admission and with stronger depressive symptoms measured at the beginning of the hospital stay. Use of BZDs / RDs tended to be associated with a reduced ability to walk and shorter night - time sleep during the week prior to admission. A higher residual serum concentration of temazepam correlated with a lower MMSE sum score after adjustment for confounding variables. CONCLUSIONS: Long - term use and concomitant use of more than one BZD / RD were common in elderly patients hospitalised because of acute illnesses. Long - term use was associated with daytime and night - time symptoms indicative of poorer health and potentially caused by the adverse effects of these drugs.

benzodiazepines

benzodiazepines

BZDs

BZDs

BZDs

oxazepam

temazepam

zopiclone

BZDs

BZDs

BZDs

BZDs

temazepam

dementia

dizziness

inability to sleep

tiredness

depressive symptoms

benzodiazepines

tiredness

benzodiazepines

tiredness

BZDs

tiredness

BZDs

tiredness

BZDs

tiredness

BZDs

tiredness

BZDs

tiredness

BZDs

tiredness

BZDs

tiredness

benzodiazepines

depressive symptoms

benzodiazepines

depressive symptoms

BZDs

depressive symptoms

BZDs

depressive symptoms

BZDs

depressive symptoms

BZDs

depressive symptoms

BZDs

depressive symptoms

BZDs

depressive symptoms

BZDs

depressive symptoms

benzodiazepines

inability to sleep

benzodiazepines

inability to sleep

BZDs

inability to sleep

BZDs

inability to sleep

BZDs

inability to sleep

BZDs

inability to sleep

BZDs

inability to sleep

BZDs

inability to sleep

BZDs

inability to sleep

benzodiazepines

dizziness

benzodiazepines

dizziness

BZDs

dizziness

BZDs

dizziness

BZDs

dizziness

BZDs

dizziness

BZDs

dizziness

BZDs

dizziness

BZDs

dizziness


Input: Acute vocal fold palsy after acute disulfiram intoxication. Acute peripheral neuropathy caused by a disulfiram overdose is very rare and there is no report of it leading to vocal fold palsy. A 49 - year - old woman was transferred to our department because of quadriparesis, lancinating pain, sensory loss, and paresthesia of the distal limbs. One month previously, she had taken a single high dose of disulfiram (130 tablets of ALCOHOL STOP TAB, Shin - Poong Pharm. Co., Ansan, Korea) in a suicide attempt. She was not an alcoholic. For the first few days after ingestion, she was in a confused state and had mild to moderate ataxia and giddiness. She noticed hoarseness and distally accentuated motor and sensory dysfunction after she had recovered from this state. A nerve conduction study was consistent with severe sensorimotor axonal polyneuropathy. Laryngeal electromyography (thyroarytenoid muscle) showed ample denervation potentials. Laryngoscopy revealed asymmetric vocal fold movements during phonation. Her vocal change and weakness began to improve spontaneously about 3 weeks after transfer. This was a case of acute palsy of the recurrent laryngeal nerve and superimposed severe acute sensorimotor axonal polyneuropathy caused by high - dose disulfiram intoxication.

vocal fold palsy

peripheral neuropathy

overdose

vocal fold palsy

quadriparesis

pain

sensory loss

paresthesia

ataxia

giddiness

hoarseness

polyneuropathy

palsy

polyneuropathy

disulfiram

disulfiram

disulfiram

ALCOHOL

disulfiram

disulfiram

paresthesia

disulfiram

paresthesia

disulfiram

paresthesia

disulfiram

paresthesia

disulfiram

quadriparesis

disulfiram

quadriparesis

disulfiram

quadriparesis

disulfiram

quadriparesis

disulfiram

pain

disulfiram

pain

disulfiram

pain

disulfiram

pain

disulfiram

peripheral neuropathy

disulfiram

peripheral neuropathy

disulfiram

peripheral neuropathy

disulfiram

peripheral neuropathy

disulfiram

ataxia

disulfiram

ataxia

disulfiram

ataxia

disulfiram

ataxia

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy

disulfiram

vocal fold palsy


Input: Higher optical density of an antigen assay predicts thrombosis in patients with heparin - induced thrombocytopenia. OBJECTIVES: To correlate optical density and percent inhibition of a two - step heparin - induced thrombocytopenia (HIT) antigen assay with thrombosis; the assay utilizes reaction inhibition characteristics of a high heparin concentration. PATIENTS AND METHODS: Patients with more than 50% decrease in platelet count or thrombocytopenia (< 150 x 10 (9) / L) after exposure to heparin, who had a positive two - step antigen assay [optical density (OD) > 0. 4 and > 50 inhibition with high concentration of heparin] were included in the study. RESULTS: Forty of 94 HIT patients had thrombosis at diagnosis; 54 / 94 had isolated - HIT without thrombosis. Eight of the isolated - HIT patients developed thrombosis within the next 30 d; thus, a total of 48 patients had thrombosis at day 30. At diagnosis there was no significant difference in OD between HIT patients with thrombosis and those with isolated - HIT. However, OD was significantly higher in all patients with thrombosis (n = 48, 1. 34 + / - 0. 89), including isolated - HIT patients who later developed thrombosis within 30 d (n = 8, 1. 84 + / - 0. 64) as compared to isolated - HIT patients who did not develop thrombosis (0. 96 + / - 0. 75; P = 0. 011 and P = 0. 008). The Receiver Operative Characteristic Curve showed that OD > 1. 27 in the isolated - HIT group had a significantly higher chance of developing thrombosis by day 30. None of these groups showed significant difference in percent inhibition. Multivariate analysis showed a 2. 8 - fold increased risk of thrombosis in females. Similarly, thrombotic risk increased with age and OD values. CONCLUSION: Higher OD is associated with significant risk of subsequent thrombosis in patients with isolated - HIT; percent inhibition, however, was not predictive.

thrombosis

thrombocytopenia

thrombocytopenia

HIT

thrombosis

thrombocytopenia

HIT

thrombosis

HIT

thrombosis

HIT

thrombosis

thrombosis

HIT

thrombosis

HIT

thrombosis

HIT

thrombosis

HIT

thrombosis

HIT

thrombosis

thrombosis

thrombotic

thrombosis

HIT

heparin

heparin

heparin

heparin

heparin

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

thrombotic

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

thrombotic

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

thrombotic

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

thrombotic

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

thrombotic

heparin

thrombosis

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT


Input: Central retinal vein occlusion associated with clomiphene - induced ovulation. OBJECTIVE: To report a case of central retinal vein occlusion associated with clomiphene citrate (CC). DESIGN: Case study. SETTING: Ophthalmology clinic of an academic hospital. PATIENT (S): A 36 - year - old woman referred from the infertility clinic for blurred vision. INTERVENTION (S): Ophthalmic examination after CC therapy. MAIN OUTCOME MEASURE (S): Central retinal vein occlusion after ovulation induction with CC. RESULT (S): A 36 - year - old Chinese woman developed central retinal vein occlusion after eight courses of CC. A search of the literature on the thromboembolic complications of CC does not include this severe ophthalmic complication, although mild visual disturbance after CC intake is not uncommon. CONCLUSION (S): This is the first reported case of central retinal vein occlusion after treatment with CC. Extra caution is warranted in treating infertility patients with CC, and patients should be well informed of this side effect before commencement of therapy.

retinal vein occlusion

retinal vein occlusion

infertility

blurred vision

retinal vein occlusion

retinal vein occlusion

thromboembolic

visual disturbance

retinal vein occlusion

infertility

clomiphene

clomiphene citrate

CC

CC

CC

CC

CC

CC

CC

CC

clomiphene

retinal vein occlusion

clomiphene

retinal vein occlusion

clomiphene

retinal vein occlusion

clomiphene

retinal vein occlusion

clomiphene

retinal vein occlusion

clomiphene citrate

retinal vein occlusion

clomiphene citrate

retinal vein occlusion

clomiphene citrate

retinal vein occlusion

clomiphene citrate

retinal vein occlusion

clomiphene citrate

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

CC

retinal vein occlusion

clomiphene

blurred vision

clomiphene

visual disturbance

clomiphene citrate

blurred vision

clomiphene citrate

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance

CC

blurred vision

CC

visual disturbance


Input: Nicotine - induced nystagmus correlates with midpontine activation. The pathomechanism of nicotine - induced nystagmus (NIN) is unknown. The aim of this study was to delineate brain structures that are involved in NIN generation. Eight healthy volunteers inhaled nicotine in darkness during a functional magnetic resonance imaging (fMRI) experiment; eye movements were registered using video - oculography. NIN correlated with blood oxygen level - dependent (BOLD) activity levels in a midpontine site in the posterior basis pontis. NIN - induced midpontine activation may correspond to activation of the dorsomedial pontine nuclei and the nucleus reticularis tegmenti pontis, structures known to participate in the generation of multidirectional saccades and smooth pursuit eye movements.

Nicotine

nicotine

nicotine

oxygen

nystagmus

nystagmus

NIN

NIN

NIN

NIN

Nicotine

nystagmus

Nicotine

nystagmus

Nicotine

NIN

Nicotine

NIN

Nicotine

NIN

Nicotine

NIN

nicotine

nystagmus

nicotine

nystagmus

nicotine

NIN

nicotine

NIN

nicotine

NIN

nicotine

NIN

nicotine

nystagmus

nicotine

nystagmus

nicotine

NIN

nicotine

NIN

nicotine

NIN

nicotine

NIN


Input: Protective effect of verapamil on gastric hemorrhagic ulcers in severe atherosclerotic rats. Studies concerning with pathogenesis of gastric hemorrhage and mucosal ulceration produced in atherosclerotic rats are lacking. The aim of this study is to examine the role of gastric acid back - diffusion, mast cell histamine release, lipid peroxide (LPO) generation and mucosal microvascular permeability in modulating gastric hemorrhage and ulcer in rats with atherosclerosis induced by coadministration of vitamin D2 and cholesterol. Additionally, the protective effect of verapamil on this ulcer model was evaluated. Male Wistar rats were challenged intragastrically once daily for 9 days with 1. 0 ml / kg of corn oil containing vitamin D2 and cholesterol to induce atherosclerosis. Control rats received corn oil only. After gastric surgery, rat stomachs were irrigated for 3 h with either simulated gastric juice or normal saline. Gastric acid back - diffusion, mucosal LPO generation, histamine concentration, microvascular permeability, luminal hemoglobin content and ulcer areas were determined. Elevated atherosclerotic parameters, such as serum calcium, total cholesterol and low - density lipoprotein concentration were obtained in atherosclerotic rats. Severe gastric ulcers accompanied with increased ulcerogenic factors, including gastric acid back - diffusion, histamine release, LPO generation and luminal hemoglobin content were also observed in these rats. Moreover, a positive correlation of histamine to gastric hemorrhage and to ulcer was found in those atherosclerotic rats. This hemorrhagic ulcer and various ulcerogenic parameters were dose - dependently ameliorated by daily intragastric verapamil. Atherosclerosis could produce gastric hemorrhagic ulcer via aggravation of gastric acid back - diffusion, LPO generation, histamine release and microvascular permeability that could be ameliorated by verapamil in rats.

verapamil

histamine

vitamin D2

cholesterol

verapamil

vitamin D2

cholesterol

histamine

luminal

calcium

cholesterol

histamine

luminal

histamine

verapamil

histamine

verapamil

gastric hemorrhagic

ulcers

atherosclerotic

gastric hemorrhage

atherosclerotic

gastric hemorrhage

ulcer

atherosclerosis

ulcer

atherosclerosis

ulcer

atherosclerotic

atherosclerotic

ulcers

gastric hemorrhage

ulcer

atherosclerotic

hemorrhagic

ulcer

Atherosclerosis

gastric hemorrhagic

ulcer

vitamin D2

gastric hemorrhagic

vitamin D2

gastric hemorrhage

vitamin D2

gastric hemorrhage

vitamin D2

gastric hemorrhage

vitamin D2

hemorrhagic

vitamin D2

gastric hemorrhagic

vitamin D2

gastric hemorrhagic

vitamin D2

gastric hemorrhage

vitamin D2

gastric hemorrhage

vitamin D2

gastric hemorrhage

vitamin D2

hemorrhagic

vitamin D2

gastric hemorrhagic

vitamin D2

atherosclerotic

vitamin D2

atherosclerotic

vitamin D2

atherosclerosis

vitamin D2

atherosclerosis

vitamin D2

atherosclerotic

vitamin D2

atherosclerotic

vitamin D2

atherosclerotic

vitamin D2

Atherosclerosis

vitamin D2

atherosclerotic

vitamin D2

atherosclerotic

vitamin D2

atherosclerosis

vitamin D2

atherosclerosis

vitamin D2

atherosclerotic

vitamin D2

atherosclerotic

vitamin D2

atherosclerotic

vitamin D2

Atherosclerosis

cholesterol

gastric hemorrhagic

cholesterol

gastric hemorrhage

cholesterol

gastric hemorrhage

cholesterol

gastric hemorrhage

cholesterol

hemorrhagic

cholesterol

gastric hemorrhagic

cholesterol

gastric hemorrhagic

cholesterol

gastric hemorrhage

cholesterol

gastric hemorrhage

cholesterol

gastric hemorrhage

cholesterol

hemorrhagic

cholesterol

gastric hemorrhagic

cholesterol

gastric hemorrhagic

cholesterol

gastric hemorrhage

cholesterol

gastric hemorrhage

cholesterol

gastric hemorrhage

cholesterol

hemorrhagic

cholesterol

gastric hemorrhagic

cholesterol

ulcers

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcers

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcers

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcers

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcers

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcers

cholesterol

ulcer

cholesterol

ulcer

cholesterol

ulcer

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

atherosclerosis

cholesterol

atherosclerosis

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

Atherosclerosis

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

atherosclerosis

cholesterol

atherosclerosis

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

Atherosclerosis

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

atherosclerosis

cholesterol

atherosclerosis

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

atherosclerotic

cholesterol

Atherosclerosis

vitamin D2

ulcers

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcers

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcers

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcers

vitamin D2

ulcer

vitamin D2

ulcer

vitamin D2

ulcer


Input: Adriamycin - induced autophagic cardiomyocyte death plays a pathogenic role in a rat model of heart failure. BACKGROUND: The mechanisms underlying heart failure induced by adriamycin are very complicated and still unclear. The aim of this study was to investigate whether autophagy was involved in the progression of heart failure induced by adriamycin, so that we can develop a novel treatment strategy for heart failure. METHODS: 3 - methyladenine (3MA), a specific inhibitor on autophagy was used in a heart failure model of rats induced by adriamycin. Neonatal cardiomyocytes were isolated from Sprague - Dawley rat hearts and randomly divided into controls, an adriamycin - treated group, and a 3MA plus adriamycin - treated group. We then examined the morphology, expression of beclin 1 gene, mitochondrial permeability transition (MPT), and Na + - K + ATPase activity in vivo. We also assessed cell viability, mitochondrial membrane potential changes and counted autophagic vacuoles in cultured cardiomyocytes. In addition, we analyzed the expression of autophagy associated gene, beclin 1 using RT - PCR and Western blotting in an animal model. RESULTS: 3MA significantly improved cardiac function and reduced mitochondrial injury. Furthermore, adriamycin induced the formation of autophagic vacuoles, and 3MA strongly downregulated the expression of beclin 1 in adriamycin - induced failing heart and inhibited the formation of autophagic vacuoles. CONCLUSION: Autophagic cardiomyocyte death plays an important role in the pathogenesis of heart failure in rats induced by adriamycin. Mitochondrial injury may be involved in the progression of heart failure caused by adriamycin via the autophagy pathway.

Adriamycin

adriamycin

adriamycin

3 - methyladenine

adriamycin

adriamycin

adriamycin

K

adriamycin

adriamycin

adriamycin

adriamycin

death

heart failure

heart failure

heart failure

heart failure

heart failure

death

heart failure

heart failure

Adriamycin

heart failure

Adriamycin

heart failure

Adriamycin

heart failure

Adriamycin

heart failure

Adriamycin

heart failure

Adriamycin

heart failure

Adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure

adriamycin

heart failure


Input: Confusion, a rather serious adverse drug reaction with valproic acid: a review of the French Pharmacovigilance database. INTRODUCTION: Confusion is an adverse drug reaction frequently observed with valproic acid. Some case reports are published in the literature but no systematic study from a sample of patients has been published. We performed this study in order to describe the main characteristics of this adverse drug reaction. METHODS: Using the French Pharmacovigilance database, we selected the cases of confusion reported since 1985 with valproic acid. RESULTS: 272 cases of confusion were reported with valproic acid: 153 women and 119 men. Confusion mostly occurred during the two first weeks following valproic acid exposure (39. 7%). It was " serious " for almost 2 / 3 of the patients (62. 5%) and its outcome favourable in most of the cases (82%). The occurrence of this ADR was more frequent in patients aged between 61 and 80 years. CONCLUSION: This work shows that confusion with valproic acid is a serious, rather frequent but reversible adverse drug reaction. It occurs especially in older patients and during the first two weeks of treatment.

Confusion

Confusion

confusion

confusion

Confusion

confusion

valproic acid

valproic acid

valproic acid

valproic acid

valproic acid

valproic acid

valproic acid

Confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

Confusion

valproic acid

confusion

valproic acid

confusion

valproic acid

Confusion

valproic acid

confusion