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Biomedical subjects

G Cuda

Publications and source records attributed to G Cuda.

26 records · Page 2Linked to original sources
PubMed1993

In vitro studies of determinants of smooth muscle mechanics.

Smooth muscle contraction is dependent upon phosphorylation of the 20,000 Da light chain subunits of myosin. Whereas the kinetics of the hydrolysis of MgATP by smooth muscle myosin suggest a simple phosphorylation-dependent "on-off" mechanism, the contractile response in smooth muscle tissue is complex. Experiments to unravel this complexity have been performed in vitro using a combination of motility assays and kinetic techniques. Some insight into this complexity is obtained, but the mechanism and the regulation of smooth muscle contraction is still not completely known.

Animals↗
PubMed1993

Skeletal muscle expression and abnormal function of beta-myosin in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is an important inherited disease. The phenotype has been linked, in some kindreds, to the beta-myosin heavy chain (beta-MHC) gene. Missense and silent mutations in the beta-MHC gene were used as markers to demonstrate the expression of mutant and normal cardiac beta-MHC gene message in skeletal muscle of hypertrophic cardiomyopathy patients. Mutant beta-myosin, also shown to be present in skeletal muscle by Western blot analysis, translocated actin filaments slower than normal controls in an in vitro motility assay. Thus, single amino acid changes in beta-myosin result in abnormal actomyosin interactions, confirming the primary role of missense mutations in beta-MHC gene in the etiology of hypertrophic cardiomyopathy.

Actin Cytoskeleton↗
PubMed1991

Influence of the cardiac myosin hinge region on contractile activity.

The participation of cardiac myosin hinge in contractility was investigated by in vitro motility and ATPase assays and by measurements of sarcomere shortening. The effect on contractile activity was analyzed using an antibody directed against a 20-amino acid peptide within the hinge region of myosin. This antibody bound specifically at the hinge at a distance of 55 nm from the S1/S2 junction, was specific to human, dog, and rat cardiac myosins, did not crossreact with gizzard or skeletal myosin, and had no effect on ATPase activity of purified S1 and myofibrils. However, it completely suppressed the movement of actin filaments in in vitro motility assays and reduced active shortening of sarcomeres of skinned cardiac myocytes by half. Suppression of motion by the anti-hinge antibody may reflect a mechanical constraint imposed by the antibody upon the mobility of the S2 region of myosin. The results suggest that the steps in the mechanochemical energy transduction can be separately influenced through S2.

Amino Acid Sequence↗
PubMed1987

Malignant ventricular arrhythmia in the Wolff-Parkinson-White syndrome during amiodarone treatment.

The ventricular rate during rapid atrial rhythms is related in Wolff-Parkinson-White (WPW) syndrome to antegrade effective refractory period of the accessory pathways. Among the many antiarrhythmic drugs available, amiodarone is most commonly used for its large therapeutic window and very long half-life. We report a case of cardiac pre-excitation syndrome in a young male patient in whom amiodarone therapy (3000 mg/weekly) was instituted to modify the dangerous ventricular response during atrial fibrillation (shortest R-R interval 190 ms, ventricular rate 210 beats/min). Four months later, starting pharmacological treatment, a new electrophysiological study documented a malignant ventricular arrhythmia: during atrial fibrillation the minimum R-R interval was 160 ms and the ventricular rate 280 beats/min. Finally, the possible mechanism of paradoxical effect observed in our patient is hypothesized. Amiodarone could favor conduction over the accessory pathways by slowing or blocking conduction into the atrioventricular node and decreasing concealed retrograde conduction into the accessory bypass tract by normally conducted beats.

Adult↗
PubMed1987

[Magnesium salts in the treatment of ventricular tachycardia].

We report the results of magnesium sulphate (MgSO4) infusion in 10 patients with different ventricular arrhythmias: 6 torsade de pointes (2 with total A-V block, 1 with acute myocardial infarction and 3 with lengthening of the Q-Tc due to antiarrhythmic and/or diuretic treatment), 1 bidirectional ventricular tachycardia (on chronic treatment with digoxin (0.5 mg/day) and diuretics), and 3 polymorphic ventricular ectopic beats plus ventricular tachycardia runs (2 with hypertensive and 1 with ischemic cardiomyopathy). MgSO4 in normal saline was given at low rate (50 mg/min) and continued 2 hours after disappearance of arrhythmia, and the infusion was repeated at the same rate for 60-90 min twice daily for the next 3-4 days. In all patients the drug was effective and no side effects were observed. The heart rate and Q-Tc interval remained unchanged from baseline values. Serum creatinine concentration was normal. Serum Mg++, 60 minutes after the beginning of the infusion, was comparable to control values in all the patients, except 2 with hypomagnesemia. Finally, we can conclude that MgSO4 is an useful therapeutic tool for the treatment of various ventricular tachycardias.

Aged↗
PubMed1984

[Basal cell epithelioma of the vulva in chronic endemic regional arsenic poisoning].

A 65 years old patient with vulvar basal cell carcinoma and cutaneous manifestations of chronic arsenicism is reported; by its endemic origin is considered as hidroarsenicism ( ERCHA = endemic regional chronic hidroarsenicism ). The unusual presentation of this type of cancer is resalted , and it's attributed to its general disease . The principal characteristics of arsenical skin cancer are considered.

Aged↗
PubMedDate not supplied

Oxidative stress and lung diseases.

Several different lung diseases are characterized by an oxidant/antioxidant imbalance, which is a major cause of cell damage. Oxidative stress activates a complex network of intracellular signal transduction pathways involved in the regulation of transcription factors such as nuclear factor kappa B (NF-kappa B) and activator protein-1 (AP-1). Within this context, a key role is played by mitogen-activated protein kinases (MAPK), which are highly expressed by pulmonary endothelial and airway epithelial cells. By exposing these cell lines to oxidant agents, our group has shown that oxidative stress leads to a significant MAPK activation, which can be effectively inhibited by corticosteroids. We believe that studies such as ours may contribute to further elucidate the molecular events underlying the therapeutic action of these drugs in many respiratory disorders caused by oxidative/proinflammatory pathogenic mechanisms. In addition, our findings may help to unveil new anti-oxidant treatments based on MAPK modulation.

Humans↗