Smooth muscle myosin light chain kinase is transiently expressed in skeletal muscle during embryogenesis and muscle regeneration both in vivo and in vitro

Byusing a polyclonal antibody raised against smooth muscle MyosinLight Chain Kinase of adult chicken we show that the 135 kDasmooth muscle Myosin Light Chain Kinase isoform is present inneonatal and regenerating rat skeletal muscle, as well as inadult atrial myocardium. No reaction was evident in adultskeletal muscle fibres. In neonatal and in early regeneratingmuscle smooth muscle Myosin Light Chain Kinase is associated withembryonic myosin as revealed by their co-presence in musclefibres. Experiments in vitro show the same results in myotubes.In atrial myocardium there is a patchy positivity in certaingroup of myocytes. Immunoblotting experiments show in muscle cellcultures, in neonatal and in regenerating skeletal muscle aprotein band with electrophoretic mobility corresponding to thatof smooth muscle Myosin Light Chain Kinase. These results suggestthat the expression of smooth muscle Myosin Light Chain Kinase isnot fully tissue-specific and that regulation of the contractilemachinery could be different during myogenesis and in adulthood,in relation to the peculiar dynamic characteristics of developingmuscles     

Safety of flecainide versus propafenone for the long-term management of symptomatic paroxysmal supraventricular tachyarrhythmias: Report from the Flecainide and Propafenone Italian Study (FAPIS) group

In order to compare the long-term safety of flecainide and propafenone,an open label, randomized, parallel group study was performedin 335 patients with paroxysmal atrial fibrillation (n=200)or paroxysmal supra ventricular tachycardia (n=135), and nohistory of heart disease. Patients were treated with an initialdaily dose of flecainide 100 mg (n=72) or propafenone 450 mg(n=63) for paroxysmal supraventricular tachycardia and flecainide200 mg (n=97) or propafenone 450 mg (n=103) for paroxysmal atrialfibrillation. Dose escalations were permitted after 2 attacks,up to a maximum of flecainide 300 mg or propafenone 900 mg.day^–1. Follow-up duration was 12 months, or when patientsstopped the treatment as a result of inadequate efficacy oradverse experiences. Twelve patients on flecainide reported 16 cardiac adverse experiences,of whom six discontinued the treatment. Seven propafenone patientshad eight cardiac adverse experiences, of whom five discontinuedthe treatment. Serious proarrhythmic events were infrequent:one case of ventricular tachycardia on propafenone; two casesof atrial fibrillation with rapid ventricular response on flecainide,associated in one patient with pulmonary oedema. An intention-to-treat analysis showed that the probability of12 months' safe and effective treatment of paroxysmal supraventriculartachycardia was 93% for flecainide and 86% for propafenone (P=0·24),whereas in paroxysmal atrial fibrillation it was 77% for flecainideand 75% for propafenone (P=0·72). In conclusion, flecainide and propafenone were safe in the long-termtreatment of patients with paroxysmal supraventricular tachyarrhythmiasand without evidence of clinically significant heart disease.     

Factors that predict spontaneous remission of ectopic atrial tachycardia

Ectopic atrial tachycardia (EAT) is usually considered as benignand easy to treat. The natural history of the disease, however,has not yet been clarified. The purpose of the study was toanalyse its spontaneous evolution in a cohort of EAT patientsand to define a predictive model of remission based on severalfactors. Between 1973 to 1989, 46 patients (25 male, 21 female), aged38 ± 18 years, entered the study. Clinically EAT wasparoxysmal in 23 patients, permanent in 12 and repetitive in11; six patients where asymptomatic. Thirty-five complainedof palpitations; dyspnoea, dizziness and syncope were also reportedless frequently. All patients underwent an electrophysio-logicalstudy to clarify the mechanism of the arrhythmia and to localizeits site of origin. In 15 patients no heart disease was documented,Five patients underwent surgery and were excluded from subsequentanalysis. Seven patients where discharged whithout antiarrhythmictreatment. We defined remission as the absence of recurrenceof EAT whithin 6 months from withdrawal of therapy. Logisticregression was applied to identify potential predictors of remission.Seven clinical and electrophysiological covariates were enteredin the model; univariate and multivariate tests were performed,using the GLIM3 statistical package. During a follow-up period of 5.1±4.5 years, 14 instancesof remission (34%) were observed in 5/22 patients with paroxysmalEAT, 4/8 patients with permanent EAT and 5/11 patients withrepetitive EAT. Mean age of patients with remission was 25±14years vs 45±15 years in the group without remission.No covariate had an independent predictive value. After exclusionof redundant variables, a restricted model ;was tested and ageat onset of EAT appeared to be the only predictor of recurrence. In conclusion, spontaneous remission of EAT does not seem tobe rare; the younger age of patients with remission could suggestan inflammatory pathogenesis with subsequent healing, whereasin older patients EAT may be caused by a degenerative processand thus show no spontaneous remission.     

Genetic and population structure of four Sardinian villages

1. Data on microgeographic population structure on four neighbouring villages of Sardinia island (Italy) are presented and discussed.
2. Two villages are located in the lowlands where malaria from Plasmodium falciparum was endemic until the eradication of paludism. The other two villages are located in the highlands and they were malaria-free because of the altitude.
3. Census data, inbreeding, migration matrices and surname distributions have been collected. The genetic differentiation of the four villages, tested for 31 genetic polymorphisms (106 alleles), is only in part compatible with migration rates inferred from demographic data.
4. The possible adaptive nature of some genetic markers with respect to malarial resistance is discussed. Ambiguous results from population genetics quantitative methods do not support definite answers.