[Homosexuality and psychiatric disorders: correlation not found].
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Homosexuality↗
Biomedical subjects
P Schnabel
Publications and source records attributed to P Schnabel.
[Is chelation therapy in coronary heart disease useful?].
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Arteriosclerosis↗
Extended experience and subgroup analysis using cardiac troponin T for rejection monitoring after heart transplantation.
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Adolescent↗
Same-sex sexual behavior and psychiatric disorders: findings from the Netherlands Mental Health Survey and Incidence Study (NEMESIS).
BACKGROUND: It has been suggested that homosexuality is associated with psychiatric morbidity. This study examined differences between heterosexually and homosexually active subjects in 12-month and lifetime prevalence of DSM-III-R mood, anxiety, and substance use disorders in a representative sample of the Dutch population (N = 7076; aged 18-64 years). METHODS: Data were collected in face-to-face interviews, using the Composite International Diagnostic Interview. Classification as heterosexual or homosexual was based on reported sexual behavior in the preceding year. Five thousand nine hundred ninety-eight (84.8%) of the total sample could be classified: 2.8% of 2878 men and 1.4% of 3120 women had had same-sex partners. Differences in prevalence rates were tested by logistic regression analyses, controlling for demographics. RESULTS: Psychiatric disorders were more prevalent among homosexually active people compared with heterosexually active people. Homosexual men had a higher 12-month prevalence of mood disorders (odds ratio [OR] = 2.93; 95% confidence interval [CI] = 1.54-5.57) and anxiety disorders (OR = 2.61; 95% CI = 1.44-4.74) than heterosexual men. Homosexual women had a higher 12-month prevalence of substance use disorders (OR = 4.05; 95% CI = 1.56-10.47) than heterosexual women. Lifetime prevalence rates reflect identical differences, except for mood disorders, which were more frequently observed in homosexual than in heterosexual women (OR = 2.41; 95% CI = 1.26-4.63). The proportion of persons with 1 or more diagnoses differed only between homosexual and heterosexual women (lifetime OR = 2.61; 95% CI = 1. 31-5.19). More homosexual than heterosexual persons had 2 or more disorders during their lifetimes (homosexual men: OR = 2.70; 95% CI = 1.66-4.41; homosexual women: OR = 2.09; 95% CI = 1.07-4.09). CONCLUSION: The findings support the assumption that people with same-sex sexual behavior are at greater risk for psychiatric disorders.
Adolescent↗
Characterization of beta(1)-selectivity, adrenoceptor-G(s)-protein interaction and inverse agonism of nebivolol in human myocardium.
Intrinsic activity and beta(1)-selectivity are important features of beta-blockers in the treatment of patients with coronary syndromes and heart failure. In human myocardium, intrinsic activity and beta(1)-selectivity of the novel beta-adrenoceptor antagonist nebivolol have not yet been determined. The study examines intrinsic activity, beta-adrenoceptor-G-protein coupling and beta(1)-selectivity of nebivolol and bisoprolol in human ventricular myocardium. Furthermore, intrinsic activity of both compounds is compared to the one of bucindolol, carvedilol and metoprolol in human atrial myocardium. Radioligand binding studies ([(125)I]-lodocyanopindolol) were performed on membrane preparations of human failing and nonfailing myocardium and on COS-7 cells transfected with human beta(1)- and beta(2)-adrenoceptors, respectively. Functional experiments were carried out on isolated muscle preparations of human left ventricular and right atrial myocardium from failing and nonfailing hearts. Radioligand binding studies reveal 3 - 4 fold beta(1)-selectivity for nebivolol and 16 - 20 fold beta(1)-selectivity for bisoprolol in human myocardium. In COS-7-cells, beta(1)-selectivity is 3 fold for nebivolol and 15 fold for bisoprolol. Neither the binding of nebivolol nor of bisoprolol is affected by the presence of guanylylimidodiphosphate (Gpp(NH)p). Nebivolol and bisoprolol exert similar inverse agonist activity in human ventricular as well as atrial myocardium. In atrial myocardium, inverse agonism of both compounds is higher compared to bucindolol, equal to carvedilol and lower compared to metoprolol. Favourable haemodynamic effects of nebivolol in humans are not due to beta(1)-selectivity or partial agonist activity of this agent. Other mechanisms, i.e. the production of nitric oxide, may thus be responsible for its unique haemodynamic profile.
Adrenergic beta-Agonists↗
Grading of internal carotid artery stenosis: validation of Doppler/duplex ultrasound criteria and angiography against endarterectomy specimen.
OBJECTIVES: duplex ultrasound has replaced angiography prior to carotid endarterectomy (CEA) in many institutions. However, the indications for CEA are based on angiographically controlled studies and widely accepted ultrasound criteria do not exist. Consequently, the reliability of Doppler and/or duplex ultrasound to predict a high-grade ICA stenosis has to be proven. DESIGN: prospective validation study. MATERIALS: one hundred and fifty carotid bifurcations assessed by ultrasound and selective angiography and 68 acrylat outcasts of carotid specimen after eversion CEA. METHODS: ICA stenosis was measured angiographically according to the ECST criteria. Combined Doppler acoustic standard criteria (CDASC), peak systolic frequency (PSF), peak systolic velocity (PSV) and end-diastolic velocity (EDV) served as criteria for the ultrasound assessment. These criteria and the results of angiography were compared to the degree of ICA stenosis determined by specimen measurements. RESULTS: the median degree of ICA stenosis as assessed by angiography (82%, range 56-97%) and CDASC (83%, range 50-99%) corresponded well to the specimen measurements (80%, range 50-95%). The sensitivity of angiography and CDASC to predict a 70-90% ICA stenosis (ECST criteria) compared to the specimen measurements was 88% and 95%, respectively. The positive predictive value (PPV) reached 92% and 96%, respectively. CDASC were equivalent to angiography and were superior to the best single frequency or velocity parameters. If CDASC do not indicate a >/=70% ICA stenosis in spite of a PSV >/=180 cm/s and/or an EDV >/=50 cm/s, angiography may detect patients with a >70% ICA stenosis. CONCLUSIONS: CDASC are valid in the quantification of high-grade ICA stenosis. They are more reliable than single velocity and/or frequency measurements. However, if velocity criteria and CDASC do not agree, angiography should be performed.
Angiography↗
Differential regulation of phospholipase C-beta isozymes in cardiomyocyte hypertrophy.
Cardiac hypertrophy is a major predictor of heart failure and of morbidity and mortality in developed countries. Many hormones and growth factors induce cardiac hypertrophy via activation of members of the phospholipase C (PLC) family. The expression pattern of the PLCbeta isozyme subfamily was investigated in neonatal rat cardiomyocytes after stimulation with different hypertrophic stimuli. Under control conditions and after stimulation with norepinephrine, cardiomyocytes expressed similar amounts of PLCbeta3 mRNA. In the presence of fetal calf serum (FCS), additional expression of PLCbeta1 was induced. Growth hormone (GH) and insulin-like growth factor-I (IGF-I) both induced a substantial increase in PLCbeta3 mRNA expression. The response to GH could not be abolished by the IGF-I receptor blocker IGF-I analogue indicating an IGF-I-independent action of GH. The upregulation of PLCbeta3 by IGF-I was abolished by preincubation of cardiomyocytes with the IGF-I receptor antagonist IGF-I analogue, the tyrosine kinase inhibitor genistein, the extracellular signal-related kinase (ERK) inhibitor PD 98059, the phosphatidylinositol-3- (PI-3) kinase inhibitor wortmannin and the p70 S6 kinase inhibitor rapamycin. Induction of the immediate early genes c-myc, c-fos, and c-jun by IGF-I was abolished by preincubation with antisense oligos against PLCbeta3. It is concluded that the expression of PLCbeta isozymes in cardiomyocytes is differentially regulated by different hypertrophic stimuli. The upregulation of PLCbeta3 by IGF-I is dependent on the activity of tyrosine kinase, ERK, PI3 kinase, and p70 S6 kinase and PLCbeta3 expression seems to be required for the induction of immediate early genes by IGF-I. The involvement of the PLCbeta subfamily in signal transduction of receptors other than G-protein-coupled receptors is suggested.
Androstadienes↗
Usefulness of carvedilol in unstable angina pectoris.
The safety and efficacy of adding oral carvedilol (25 mg twice daily) to standardized treatment of unstable angina was assessed in a multicenter, randomized, double-blind, placebo- controlled trial on 116 patients with acute unstable angina. Patients were monitored in an intensive care unit and underwent 48-hour Holter monitoring to assess transient ischemia. Carvedilol as adjunctive therapy resulted in a significant reduction of median heart rate (65 vs 75 beats/min, p <0.05), mean systolic blood pressure (133 vs 130 mm Hg, p <0.05), and mean rate-pressure product (8,337 vs 10,042, p <0.05). Carvedilol reduced the ischemic burden during 48 hours of treatment by 75% (49 vs 204 minutes), including a 36% reduction of patients with ischemic episodes (p <0.05), a 66% reduction of the mean number of ischemic episodes (8 vs 24, p <0.05), and a 76% reduction in the mean duration of ischemic episodes (50 vs 205 minutes, p <0.05). Side effects occurred in 8 of 59 patients (13.6%) in the carvedilol group and in 5 of 54 patients (8.8%) given placebo. Although not significant, the early onset of maximal blood pressure reduction and the delayed effect on heart rate were closely correlated to drug-induced hypotension and bradycardia in the carvedilol group. Thus, carvedilol as an adjunctive to standardized treatment effectively reduces heart rate and blood pressure, and thus the ischemic burden in patients with unstable angina pectoris, but requires close monitoring of patients at risk for bradycardia or hypotension.
Acute Disease↗
Binding properties of beta-blockers at recombinant beta1-, beta2-, and beta3-adrenoceptors.
The human heart contains at least four distinct beta-adrenoceptor subtypes, three of which have been cloned. However, the binding properties of beta-blockers to the different beta-adrenoceptor subpopulations are not yet thoroughly characterized. Human beta1-, beta2- and beta3-adrenoceptors were expressed in COS-7 cells and [125I]iodocyanopindolol saturation binding, and competition experiments with commonly used beta-blockers were performed in the respective membrane preparations. Atenolol and metoprolol were about fivefold selective for beta1- versus beta2- and beta3-adrenoceptors. Bisoprolol was approximately 15-fold selective for beta1- versus beta2- and approximately 31-fold selective for beta1- versus beta3-adrenoceptors. Carvedilol was nonselective for any beta-adrenoceptor subtype. We conclude that the beta1-selectivities of atenolol, metoprolol, and bisoprolol are lower in COS cell membranes compared with previous investigations performed in native membranes. All beta-blockers investigated bind to beta3-adrenoceptors. Differential binding properties to beta3-adrenoceptors might imply different responses as to body weight, cardiac contractility, heart rate, and growth regulation. This might imply differential indications for the drugs investigated.
Adrenergic beta-Antagonists↗
Heterotrimeric G proteins in heart disease.
Guanine nucleotide binding proteins (G proteins) are largely grouped into three classes: heterotrimeric G proteins, ras-like or small molecular weight GTP binding proteins, and others like Gh. In the heart G proteins transduce signals from a variety of membrane receptors to generate diverse effects on contractility, heart rate, and myocyte growth. This central position of G proteins forming a switchboard between extracellular signals and intracellular effectors makes them candidates possibly involved in the pathogenesis of cardiac hypertrophy, heart failure, and arrhythmia. This review focuses primarily on discoveries of heterotrimeric G protein alterations in heart diseases that help us to understand the pathogenesis and pathophysiology. We also discuss the underlying molecular mechanisms of heterotrimeric G protein signalling.
Animals↗
Thrombus formation after transcatheter closure of atrial septal defect.
Thrombotic layers and/or atrial thrombi were detected by transesophageal echocardiography as a usual finding after transcatheter closure of atrial septal defects with the ASDOS device. The size of the thrombotic structures regularly decreased within 6 months without any clinical signs of embolization.
Adult↗
Expression of endothelin-1, endothelin-converting enzyme, and endothelin receptors in chronic heart failure.
BACKGROUND: Elevated plasma levels of endothelin (ET)-1 have been reported in association with heart diseases, including heart failure. Furthermore, it has been suggested that ET-1 acts as a local autocrine/paracrine factor with biological activities such as vasoconstriction, mitogenesis, and inotropic effects on the heart. This study investigated alterations of ET-1, ET receptor, and endothelin-converting enzyme (ECE) expression in left ventricular myocardium from patients with end-stage heart failure. METHODS AND RESULTS: mRNA concentrations of ETA and ETB receptors, prepro-ET-1 (ppET-1), and ECE in left ventricles from nonfailing donors hearts (NF) and from patients with end-stage chronic heart failure (NYHA functional class IV) due to dilated cardiomyopathy (DCM) were compared by use of a competitive reverse transcription-polymerase chain reaction technique. There was no significant difference in mRNA expression for ppET-1, ECE-1, and ETA receptors, whereas a significant reduction of ETB-receptor mRNA was observed in DCM hearts. 125I-labeled ET-1 radioligand binding studies demonstrated a significant downregulation of ETB receptors, whereas ETA-receptor density was increased in membranes from DCM hearts. Phosphoramidon-sensitive ECE activity and immunodetectable amounts of ECE protein in left ventricular membrane preparations did not differ between NF and DCM hearts. Finally, immunoreactive ET-1 concentrations were increased in DCM hearts. CONCLUSIONS: The present study demonstrates changes in the ET-receptor expression pattern in favor of the ETA receptor in human end-stage heart failure. Furthermore, activation of the cardiac ET system with increased tissue ET-1 concentrations in the failing myocardium is observed. This is more likely due to decreased clearance than to increased synthesis, because ppET-1 gene expression and ECE activity are unchanged.
Aspartic Acid Endopeptidases↗
Beneficial effects of amiodarone in heart failure: interaction with beta-adrenoceptors rather than G proteins.
The effect of the antiarrhythmic drug amiodarone on the human myocardial beta-adrenoceptor-G protein-adenylyl cyclase signalling cascade was investigated. Amiodarone had no effect on myocardial G proteins and maximal adenylyl cyclase activity, but acted as a beta-adrenoceptor antagonist. This mechanism might be at least partially responsible for the beneficial effects of the drug in patients with arrhythmia and heart failure.
Adenylyl Cyclases↗
[One year of Dutch Organ Donation Law)].
In the Dutch Organ Donation Law all adults are asked to register as a postmortal tissue or organ donor, or as a non-donor. Of the 12 million people sent a registration form, 4.5 million have replied, of whom 55% registered as a donor (2.5 million), 35% as a non-donor; 10% chose to leave the donation decision to their relatives. This is much better than in the former situation where only 1.3% of the decreased carried a donation codicil. The goal of the law, to obtain enough consenting donors for transplantation purposes has not yet been met, and much will depend on the response and the decision of the future eighteen-years-old, who will receive a registration form in the year they reach that age.
Adult↗
[Hormone therapy in heart failure: growth hormone and insulin-like growth factor I].
Heart disease is the major cause of mortality in the developed world. Despite recent advances in the therapy of heart failure due to ACE inhibitors and beta-blockers, the prognosis of this syndrome is still poor. In the past few years, the effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I) on heart morphology and function were extensively studied. Some studies dealing with experimental heart failure of animals and one controversial study dealing with human heart failure suggest positive hemodynamic effects of GH and/or IGF-I treatment. This review summarizes the physiological effects of GH/IGF-I on the myocardium, their signal transduction mechanisms, and the data currently available on the therapeutic use of these agents.
Animals↗
Transcatheter closure of atrial-septal defects and patent foramen ovale in adults: optimal anatomic adaptation of occlusion device.
BACKGROUND: For transcatheter closure of atrial-septal defects, different occlusion systems are available. The purpose of this study was to examine the clinical feasibility of the ASD Occlusion System (ASDOS, Dr Osypka GmbH, Grenzach-Wyhlen, Germany) and to evaluate the short- and long-term results. METHODS AND RESULTS: The study was composed of 20 consecutive patients with atrial-septal secundum defect (n = 13) or patent foramen ovale (n = 7). The device implantation was successful in all patients. For optimal closure of the defect, left atrial and right atrial umbrellas of different sizes were required in 10 of 20 patients. No major short- or long-term complications occurred. During the mean follow-up period of 13.9 +/- 5 months, 5 strut fractures without dislocation were observed, and in 8 (40%) of 20 patients transesophageal echocardiography revealed a small residual shunt. CONCLUSION: The ASDOS double umbrella system is suitable for transcatheter closure of interatrial defects in selected patients. This system showed a high procedural safety and has the unique advantage of individual adaptation of the occluding device on the defect anatomy that results in high closure effectiveness.
Adult↗
Intracardiac yolk sac tumor in an infant girl.
We report about a two and a half year old girl with a primary yolk sac tumor (YST) of the heart, located in the interventricular septum. The girl was admitted to the hospital with a systolic cardiac murmur. Echocardiography revealed a smoothly surfaced tumor which based on the interventricular septum below the aortic valve and filled out more than half of the left ventricular cavity. Diagnosis of a yolk sac tumor was established on a frozen section of a biopsy taken at surgery and confirmed by the examination of the resected material. Excessively elevated serum alpha-fetoprotein (AFP) levels contributed to this diagnosis. Follow up examinations of the patient including computed tomography (CT) of head, thorax and abdomen, did not indicate an extracardiac tumor manifestation. We found no previous report of a primary intracardial yolk sac tumor in the literature.
Child, Preschool↗
Insulin induces upregulation of vascular AT1 receptor gene expression by posttranscriptional mechanisms.
BACKGROUND: An interaction of insulin with angiotensin II effects could be pathophysiologically important for the pathogenesis of atherosclerosis and hypertension. METHODS AND RESULTS: We examined the effect of insulin on AT1 receptor gene expression in cultured vascular smooth muscle cells (VSMCs). A 24-hour incubation with insulin (100 nmol/L) produced a 2-fold increase in AT1 receptor density on VSMCs, as assessed by radioligand binding assays. This enhanced AT1 receptor expression was caused by a time- and concentration-dependent upregulation of the AT1 receptor mRNA levels, as assessed by Northern analysis. The maximal effect was detected after a 24-hour incubation of cells with 100 nmol/L insulin (270+/-20%). AT1 receptor upregulation was caused by a stabilization of the AT1 receptor mRNA, because the AT1 receptor mRNA half-life was prolonged from 5 hours under basal conditions to 10 hours after insulin stimulation. In contrast, insulin had no influence on AT1 receptor gene transcription, as assessed by nuclear run-on assays. The insulin-induced AT1 receptor upregulation was followed by an increased functional response, because angiotensin II evoked a significantly elevated intracellular release of calcium in cells that were preincubated with 100 nmol/L insulin for 24 hours. The insulin-induced AT1 receptor upregulation was dependent on tyrosine kinases, as assessed by experiments with the tyrosine kinase inhibitor genistein. Furthermore, experiments using the intracellular calcium chelator bis(2-amino-5-methylphenoxy)ethane-N, N,N',N'-tetraacetic acid tetraacetoxymethyl ester suggest that intracellular calcium release may be involved in AT1 receptor regulation. CONCLUSIONS: Insulin-induced upregulation of the AT1 receptor by posttranscriptional mechanisms may explain the association of hyperinsulinemia with hypertension and arteriosclerosis, because activation of the AT1 receptor plays a key role in the regulation of blood pressure and fluid homeostasis.
Angiotensin II↗