Review                   215        Biological counterpulsation with aortomyoplasty: experimental and clinical results
                                             JC Chachques, E Braunberger, P Lajos, P Argyriadis, A Shafy, C Latremouille, J-N Fabiani and  A  Carpentier    
                                             [Full text pdf 36.4Kb]

Articles                   219        Acute and chronic heart dilation model-induced in goats by carotid jugular A-V shunt
                                             G Bolotin, R Lorusso, H Kaulbach, J Schreuder, G Uretzky and FH Van Der Veen
                                             [Full text pdf 445Kb]

                                223        Imaging of skeletal muscle contraction after cardiomyoplasty
                                              M Smink, FH van der Veen, K Reesink, R Lorusso, M Barbiero, M Volterrani, T van der Nagel  and U Carraro     
                                              [Full text pdf 781Kb]

                                229        Increasing the length of the Latissimus Dorsi muscle pedicle to enhance the efficacy of cardiomyoplasty
                                              N Lila, JC Chachques, P Fornes, P Lajos, JP Carteaux, M Fardeau and A Carpentier
                                              [Full text pdf 711Kb]  

Review                    235        Environmental and genetic factors as sources of variation in skeletal muscle fibre number
                                              C Rehfeldt, NC Stickland, I Fiedler and J Wegner    [Full text pdf 307Kb]

Articles                    255        Surface integrated dynamoelectromyography for neuromuscular performance evaluation in  children
                                               C Velussi, M Zanella, G Brandi and L Chiandetti    [Full text pdf 711Kb]

                                263        Structural alterations of skeletal muscle induced by ischemia and reperfusion
                                              HJ Appell, S Glöser, JMC Soares and JA Duarte    [Full text pdf 444Kb]

Myology News       269        The Sixth Abano Terme Meeting on Rehabilitation
                                              BAM’2000 – Basics&Applications of Muscle Plasticity                                               
                                              Foundations of Muscle Plasticity                                               
                                              Dynamic Cardiomyoplasty & Cardiac-Bio-Assists
                                              Cell & Gene Muscle Therapy of Sarcomeric Muscles
                                              Abano Terme, Padova (Italy), June 11-13, 2000
 
 
 
 
 

Biological Counterpulsation with Aortomyoplasty: Experimental and Clinical Results

Juan C. Chachques, Eric Braunberger, Paul Lajos, Pantelis Argyriadis, Abdel Shafy, Christian Latremouille, Jean-Noël Fabiani and Alain Carpentier

The Department of Cardiovascular Surgery, Broussais Hospital, Paris, France

Aortomyoplasty consists of wrapping the right Latissimus Dorsi (LD) muscle around the ascending aorta or the left LD around the descending aorta for compression during diastole. The aim of aortomyoplasty is to transform the ascending or descending aorta into a new cavity, which is contractile and hemo compatible. This technique produces a biological diastolic counterpulsation effect without damaging the aortic wall. Aortomyoplasty chronically reproduces the effects of the intra-aortic ballon pump [13] by the following mechanisms: 1) decreasing left ventricular afterload; 2) increasing the coronary perfusion pressure; 3) decreasing the peripheral vascular resistance. Our animal research studies began in our laboratory in 1988 [4] and the first clinical case using the aortomyoplasty was performed at the Broussais Hospital in November 1992 [3, 7]. Since then, four operations have been performed in our department and 32 worldwide.

After a mean follow-up of 19-months, the mean NYHA Functional Class improved from 3.6 preoperatively to 2.2 postoperatively (p < 0.05), as well as the overall quality of life in most patients. Improvements were seen in their physical activity, work performance and social activities. At the same time, hemodynamic and Echo-Doppler studies showed compression of the aorta with an increase in diastolic pressure during electrostimulation of the LD wrap. Long-term clinical follow-up and a larger patient population is necessary to define the role of aortomyoplasty in the treatment of severe cardiac failure.

Key words: aortomyoplasty, biological diastolic counterpulsation, cardiac assist, Latissimus Dorsi Muscle, neoventricle.
 Basic Appl. Myol. 9 (5): 217-220, 1999

Acute and Chronic Heart Dilation Model-Induced in Goats by Carotid Jugular A-V Shunt

Gil Bolotin, Roberto Lorusso, Hans Kaulbach, Jan Schreuder, Gideon Uretzky and Frederik H. Van Der Veen

Cardiovascular Research Institute, Maastricht, The Netherlands

Congestive heart failure is characterized by impaired quality of life and markedly shortened life expectancy. There are currently many medical and surgical modalities that aim to treat patients with heart failure, which implies the need for an animal heart failure model for the development and testing of these therapeutic modalities. A variety of animal heart failure models have been developed, including those in which heart failure is induced via drugs, rapid ventricular pacing, genetic alteration, viral sources, idiopathic dilated cardiomyopathy, coronary arteries’ embolization, pressure overload, and volume overload by arterio-venous (A-V) shunt. The purpose of this study was to evaluate the acute and chronic effect of carotid-jugular A-V shunt in goat model of heart dilation. After cross clamping of the left carotid artery, an end-to-side anastomosis of 10 mm in diameter was performed between the free end of the vein and the side of the artery.

A dual-micromanometer transducer conductance catheter was used to determine the volume of the ventricle on-line, by measuring the time-varying electrical conductance of the segments of intraventricular blood. During and at the end of the eight weeks none of the animals showed signs of heart failure or distress. The acute and chronic hemodynamic changes were demonstrated by pressure-volume loops at baseline, immediately after the shunt, and after 8 weeks. There was an immediate rise in the LVEDV (104±27 ml) compared to the baseline volume (75±26 ml), and eight weeks later the LVEDV reached 111±22 ml. None of the eight goats demonstrated clinical signs of pulmonary congestion. The Swan-Ganz and the conductance catheters that were used to monitor the heart hemodynamic changes immediately after the creation of the A-V shunt revealed interesting results. Another advantage of the shunt model is that it is possible to evaluate the patency of the shunt by palpating blood thrill in the neck. The carotid jugular A-V shunt in goats causes significant left heart dilation without signs of heart failure, and is reproducible with low animal mortality. The study ended 8 weeks after the creation of the A-V shunt, leaving unanswered the question of possible heart failure development in this model after a longer follow up period.

Key words: animal heart failure model, arterio-venous (A-V) shunt, congestive heart failure, hemodynamic changes carotid-jugular A-V shunt.
 Basic Appl. Myol. 9 (5): 221-224, 1999
 Address correspondence to:
Dr Ir FH van der Veen, Cardiothoracic Surgery, PO Box 5800, 6202 AZ, Academic Hospital, Maastricht, Netherlands, Email FVV@SCPC.AZM.NL.

Imaging of Skeletal Muscle Contraction after Cardiomyoplasty

Marieke Smink, Frederik H. van der Veen, Koen Reesink, Roberto Lorusso⁽¹⁾, Mario Barbiero⁽²⁾,Mauritio Volterrani⁽³⁾,Theo van der Nagel and Ugo Carraro⁽⁴⁾

Cardiovascular Research Institute Maastricht, The Netherlands, (1) Department of Cardiothoracic Surgery, Brescia, (2) Division of Cardiology, Legnago General Hospital, Legnago, Verona, (3) Department of Cardiology , Gussago, Brescia and (4) CNR Unit for Muscle Biology and Physiopathology, University of Padua, Italy

The clinical interest in cardiac assist with a wrapped skeletal muscle has reduced in recent years, due to disappointing clinical results. Two causes might be responsible for these results. Firstly, gradual degeneration of the muscle, and secondly, transformation of the muscle into a slow and less powerful muscle. The Demand dynamic cardiomyoplasty was developed to reduce the muscle workload and so to improve muscle condition.

Two methods were developed earlier to study skeletal muscle characteristics after cardiomyoplasty. Firstly, fluoroscopic evaluation of LD muscle contraction by X-ray imaging of the stimulation electrodes within the muscle. Secondly, the mechanogram method was used which records extra-thoracic LD muscle movement. In the present study 5 patients were included, of which two patients had been stimulated according to the demand protocol, and three patients according to the daily protocol.

The mechanogram and the X-ray methods are both suitable to generate graphs which show individual contraction cycles, and can be used for further analysis. The results of these analysis showed that the two methods were comparable. The stimulator delay could be calculated (70-73 msec), and a physiological delay between the electrical pulse and muscle contraction appeared to last 31-34 msec. Also, the total contraction time was comparable as measured with both methods, respectively 381 and 386 msec.

Differences between the demand and the daily stimulated patients were not present at the clinical stimulator settings. However, at increased amplitudes the cycle length’s appeared to be shorter in the demand group, in particular when bursts of 6 pulses were applied.

In conclusion, the mechanogram offers a reliable, fast, cheap and non-invasive method to study the LD muscle in patients after cardiomyoplasty. The demand dynamic cardiomyoplasty stimulation protocol tends to keep the LD muscle as a relatively fast muscle, which might be advantageous in these patients.

Key words: cardiac assist, Latissimus dorsi, patients, X-ray imaging.
 Basic Appl. Myol. 9 (5): 225-229, 1999
 Address for correspondence:
Dr Ir FH van der Veen, Cardiothoracic Surgery, PO Box 5800, 6202 AZ, Academic Hospital, Maastricht, Netherlands, Email FVV@SCPC.AZM.NL.

Increasing the Length of the Latissimus Dorsi Muscle Pedicle to Enhance the Efficacy of Cardiomyoplasty

Nermine Lila, Juan Carlos Chachques, Paul Fornes, Paul Lajos, Jean Pierre Carteaux, Michel Fardeau and Alain Carpentier

Laboratory for the Study of Cardiac Prostheses and Grafts, Broussais Hospital, Paris, France

Objective: The efficacy of cardiomyoplasty depends upon a complete wrapping of the heart with the latissimus dorsi muscle flap (LDM). This is not possible with extremely dilated hearts. The goal of our experimental study was to increase the length of the LDM neurovascular pedicle to obtain a maximal LDM surface area and, hence, to perform a complete cardiac wrap. Three techniques were used in various combinations : a) division of the LDM tendon, b) LDM electrostimulation, c) implantation of a balloon expander behind the pedicle.

Methods: Twenty-one sheep were operated on. In group I: all animals (n = 7) had their LDM humeral tendon divided, associated in 3 of them with electrostimulation. In group II, all animals had (n = 14) a balloon tissue expander and the humeral tendon was divided. In 7 of them the LDM was electrostimulated with (n = 4) or without (n =3) fixation of the tendon on the 3rd rib. In 7 other animals of this group the LDM was not stimulated with (n = 4)or without (n = 3) fixation of the tendon to the 3rd rib.

Results: In all groups, the pedicle was elongated. Maximal elongation was observed in group II with LDM electrostimulation: average 12.3±0.61 cm versus 10.3±0.15 cm in group I. LDM force decreased in all groups, but this decrease was minimized by tendon fixation and early electrostimulation. Histology of the pedicle showed well preserved structures in group I and thickening of arterial wall and nerve injury due to compression by the expander in group II.

Conclusions: A significant elongation of the neurovascular pedicle of the latissimus dorsi up to 76.3% of its original length can be obtained by the techniques used in this study. The more efficient and less deleterious technique was the division of the tendon and early stimulation of the muscle. Preservation of the LDM force was directly related to the resting muscular tension which was improved by tendon refixation and early postoperative electrostimulation.

Key words: cardiomyoplasty, Latissimus dorsi muscle, muscle-pedicle expansion.
 Basic Appl. Myol. 9 (5): 231-236, 1999
]
 Address correspondence to:

Doctor Nermine Lila, Laboratoire d’Etude des Greffes et Prothèses Cardiaques, Hôpital Broussais, 96 rue Didot, 75014 Paris, France, phone 33 1 4395 9360, fax 33 1 4540 5049.

Environmental and Genetic Factors as Sources of Variation in Skeletal Muscle Fibre Number

Charlotte Rehfeldt⁽¹⁾, Neil C. Stickland⁽²⁾, Ilse Fiedler⁽¹⁾ and Jochen Wegner⁽¹⁾

(1) Division of Muscle Biology & Growth, Research Institute for the Biology of Farm Animals, Dummerstorf, Germany and (2) Department of Veterinary Basic Sciences, The Royal Veterinary College, University of London, London, UK

The understanding of skeletal muscle growth is an important goal in animal science and in human medicine. The purpose of this review is to demonstrate the importance of muscle fibre number for muscle growth and the influence of selected genetic and environmental factors on muscle fibre number. The total number of muscle fibres is mainly determined prenatally when multinucleated myofibres form from myoblasts. In general, muscle fibre number remains almost unchanged during postnatal growth, and it is inversely correlated to the size of the individual muscle fibre. Species-specific differences in muscle mass are primarily due to differences in the number of muscle fibres. With respect to gender, in some cases male muscles were reported to exhibit more muscle fibres than female muscles. Differences in muscle mass obtained by breeding and selection are due to changes in both muscle fibre number and muscle fibre size. Genetic variability and heritability are sufficiently high to use fibre number and fibre size in farm animal selection. Moderate postnatal feed restriction does not influence muscle fibre number, whereas strong feed restriction is able to induce fibre loss. The prenatal period of muscle development is more sensitive to nutritional deficiencies in reducing fibre number. Physical activity has been shown to influence postnatal muscle fibre number. Activity stimuli are able to induce increases, whereas disuse of muscles may be followed by decreases in muscle fibre number. The postnatal application of growth promoters induces no changes in muscle fibre number, whereas the prenatal period seems to be more sensitive to hormonal factors.

Key words: exercise, growth, muscle, muscle fibre, nutrition, review, selection.
 Basic Appl. Myol. 9 (5): 237-255, 1999
 

Address correspondence to:
Dr. Charlotte Rehfeldt, Research Institute for the Biology of Farm Animals, Wilhelm-Stahl-Allee 2, D-18196 Dummerstorf, Germany, phone +49 38208 68853, fax +49 38208 68852, Email rehfeldt@fbn-dummerstorf.de.

Surface Integrated Dynamoelectromyography for Neuromuscular Performance Evaluation in Children

Carlo Velussi, Mario Zanella, Giorgio Brandi and Lino Chiandetti⁽¹⁾

Department of Human Anatomy and Physiology, Section of Physiology and School of Sport Medicine and (1) Department of Pediatrics, The University of Padova, Padova, Italy

We developed a simple and non-invasive method for the evaluation of muscle performance in children with rheumatic muscle involvement. We tested brachial biceps force by means of a dynamometer applied to the dominant side wrist of subjects during a progressive, non-maximal, semi-isometric contraction, starting from an angle of 90° between arm and forearm. At the same time, an integrated electromyogram was recorded by bipolar transversal derivation from the muscle belly. Our study was carried out on two groups (healthy controls and subjects weakened by various generalized diseases). In pathological subjects, the neuromuscular activation index (i.e. voltage x fat-free arm area/force) proved to be significantly higher than in healthy subjects. The same was true for voltage/force and voltage/fat-free arm area values. This technique tests muscle performance in young patients, in which maximal effort requests and/or invasive needle electromyography are not suitable because of age and poor physical conditions.

Key words: muscle force, surface EMG, brachial biceps muscle, children.
 Basic Appl. Myol. 9 (5): 257-263, 1999
 

Address correspondence to:
Carlo Velussi, University of Padova, Department of Human Anatomy and Physiology, Section of Physiology, via F. Marzolo 3, 35131 Padova Italy, fax 049 827 5301.

Structural Alterations of Skeletal Muscle Induced by Ischemia and Reperfusion

Hans J. Appell^{(1, 2)}, Sabine Glöser⁽²⁾, José M.C. Soares^{(1, 3)} and José A. Duarte^{(1, 3)}

(1) The Muscle Atrophy Research Group (MARG), (2) Institute of Sport Orthopedics, German Sport University Cologne, Germany and (3) Department of Sport Biology, FCDEF, University of Porto, Portugal

The purpose of the study was to undertake a series of experiments with varying time periods of ischemia followed by reperfusion to investigate the effects on muscle morphology. Charles River mice received a tourniquet at their right limb for 60, 90, and 120 minutes, respectively, under general anesthesia which was followed by a reperfusion period of 60 minutes (n = 5 in each group). Their soleus muscles were removed, the left one serving as contralateral control, and processed for light and electron microscopic examination. Muscle fiber cross sectional areas and the thickness of the capillaries basement membranes were evaluated morphometrically. Capillary endothelial ultrastructure showed considerable pathological alterations extending to intracellular edema, and the basement membrane was thickened by about 50%. The muscle fibers were reduced in size, which depended on the period of ischemia (15-23%). Skeletal muscle morphology showed mitochondrial disturbances, condensation of contractile material, presence of lysosomes, and focal fiber necrosis, which also seemed to be aggravated the longer the ischemic period had lasted. The interstitial space was widened speaking in favor of an intramuscular edema. It is concluded that skeletal muscle morphology is severely affected under conditions of ischemia/reperfusion and that the capillary endothelium is mainly involved in the pathophysiological mechanisms.

Key words: capillary endothelium, ischemia, muscle damage, reperfusion, skeletal muscle.
 Basic Appl. Myol. 9 (5): 265-270, 1999
 

Address correspondence to:
Prof. Dr. Hans-Joachim Appell, Institute of Sport Orthopedics, German Sport University, D-50927 Cologne, Germany, phone +49 221 4982543, fax +49 221 49 12001, Email appell@hrz.dshs-koeln.de.
 

U Carraro, Padova, Italy; H Blau, Stanford, CA, USA; A Carpentier, Paris, France; D Casarotto, Padova, Italy; JC Chachques, Paris, France; J Chamberlain, Ann Arbor, MI, USA; V Chekanov, Milwaukee, WI, USA; R C-J Chiu, Montreal, Quebec, Canada; M Grounds, Perth, Australia; E Hoffman, Washington, DC, USA; G Itoh, Aichi, Japan; L Larsson, University Park, PA, USA; A Margreth, Padova, Italy; R Sabbadini, San Diego CA, USA; S Salmons, Liverpool, UK; WP Santamore, Philadelphia, PA, USA; S Schiaffino, Padova, Italy; A Wernig, Bonn, Germany; RS Williams, Dallas, TX, USA.

Aim

Reactions of normal muscles to unusual requests and of diseased muscles to normal demands

Topics

Foundations of Muscle Plasticity; Cellular Adaptation to Work Load and Exercise-induced Muscle Damage; Apoptosis in Skeletal and Cardiac Muscle; Cellular Mechanisms of DMD Progression; Dynamic Cardiomyoplasty and Cardiac-Bio-Assists; Cell & Gene Therapy in Sarcomeric Muscles

BAM’2000 Abstracts and Manuscripts Publication

Authors of Poster Presentations will be requested to submit a Manuscript in BAM COMMUNICATION style by JUNE 10, 2000. Please find Information for Authors at: http://www.bio.unipd.it/bam/bam.html

The final version of the Communications, will be printed in dedicated Issues of BAM (Ten Years of Basic and Applied Myology). The Impact factor of BAM will be known next Summer.

General Information

The official language of the Conference will be English.

Important Deadlines

Submission of Abstracts (one A4 page): April 15, 2000

Registration and Hotel Accommodation forms: April 15, 2000

Pre-registration fees: April 15, 2000

A tutorial on LD Wrap Mechanogram will be held June 12, 2000.
 
 

June 10, 2000 (Saturday)

Morning: Tour to Venice
& Late Afternoon: Opening Ceremony and BAM’2000 Gala Dinner (Locanda Cipriani) in the beautiful historical island of Torcello, Venice Laguna
BAM’2000 Keynote

"Gene Expression and Signal Transduction"
Helen Blau, Department of Molecular Pharmacology, Stanford, CA, USA

June 11, 2000 (Sunday)

9.00-13.30 Foundations of Muscle Plasticity (I) (II)

9.00 - 11.00 Foundations of Muscle Plasticity: (I) Signalling Pathways

Chairpersons: H Blau, RS Williams

11.30-13.00 Foundations of Muscle Plasticity: (II) The Muscle Transcriptome

Chairpersons: S Williams, S Schiaffino

- Lunch and Posters

14.30-19.00 Apoptosis of Sarcomeric Muscles (I) (II)

14.30 - 16.30 Apoptosis of Sarcomeric Muscles: (I) Myocardium

Chairpersons: R Sabbadini, R Gottlieb,

         - RA Gottlieb, Division of Hematology, Department of Molecular & Experimental Medicine, The Scripps Research
          Institute, La Jolla, CA, USA: Mitochondria: Ignition Chamber for Apoptosis

         - R Sabbadini, Heart Institute and Department of Biology, San Diego State University, San Diego California, USA:
         G Protein-coupled receptors, calcium deregulation and apoptosis in the heart

        - G Vescovo, Division of Internal Medicine, Adria General Hospital, Ro, Italy: Skeletal muscle apoptosys: a
          determinant of muscle atrophy in CHF?

       -  P Bernardi, Department of Biomedical Sciences, University of Padova, Italy: Mitochondria and muscle cell death

        - S Rizzuto, To be announced

Coffee Break

17.00 - 19.00 Apoptosis of Sarcomeric Muscles (II) Skeletal Muscle

Chairpersons: G Itoh and U Carraro

      -  M Sandri, Department of Biomedical Sciences and C.N.R. Unit for Muscle Biology and Physiopathology,
         University  of  Padova, Italy: Apoptosis and muscular dystrophies

      -  K Rossini, Department of Biomedical Sciences and C.N.R. Unit for Muscle Biology and Physiopathology,
         University of Padova, Italy: Activity-induced apoptosis in mdx mice

      -  C Destro, Department of Biomedical Sciences and C.N.R. Unit for Muscle Biology and Physiopathology,
         University of Padova, Italy: Fas/FasL system regulates apoptosis of macrophages and myoblasts during
         muscle regeneration

June 12, 2000 (Monday)

9.00-13.30 Dynamic Cardiomyoplasty

9.00-11.00 Dynamic Cardiomyoplasty (I)

Chairpersons: WP Santamore and V Chekanov

      - A Carpentier / J Chachques, Broussais Hospital, Paris, France: Present and future of Dynamic Cardiomyoplasty

      - JK Kirklin, Division of Cardiothoracic Surgery, University of Alabama, Birmingham, USA: One-year results of
        C-SMART

     -  RC Bourge, Division of Cardiovascular Disease, University of Alabama at Birmingham, USA: Selection of
        Patients in  Cardiomyoplasty Skeletal Muscle Assistance Randomized Trial (C-SMART)

     -  C Werling, Department of Cardiac Surgery, Herzzentrum Ludwigshafen, Germany: Dynamic Cardiomyoplasty :
         Clinical experience after seven years

     -  J Trainini, Hospital Peron, Buenos Aires, Argentina: Chronic aortic counterpulsation with latissimus dorsi:
        clinical follow-up. Cardiomyoplasty comparison

Coffee break

11.30-13.30 Dynamic Cardiomyoplasty (II)

Chairpersons: JK Kirklin, A Carpentier

     - WP Santamore, Philadelphia, PA, USA: Vascular Delay and Intermittent Stimulation: Keys to Success in
        Cardiomyoplasty

     - D Casarotto / M Barbiero: Three-year experience of Demand Dynamic Cardiomyoplasty

     - C Muneretto: To be announced

     - F Monese / F Di Gregorio, Medico spa, Padova, Italy: Implement new concepts in demand cardiomyostimulators

     - V Chekanov, Milwaukee Heart Institute, Heart Care Associates, Milwaukee, Wisconsin, USA: A new alternative
       for the use of electrical stimulation – atherosclerosis prevention

14.30-19.00 Cell and Gene Therapy in Sarcomeric Muscles (I), (II)

14.30-16.30 Cell and Gene Therapy in Sarcomeric Muscles (I) Basics

Chairpersons: A Wernig and F Rossi

     - H Blau: Lifespan and proliferation potential of satellite cells

     - Z Reuveni: A hunt for the adult myogenic stem cell: The old fashion satellite cell is still a good candidate

     - L Gorza: Cell-surface localization of the glucose-regulated protein GRP94 in skeletal myoblasts is involved
       in  myotube formation

    - GS Butler-Browne: Telomeres and Telomerases in satellite cells

    - I Dell’Aica: Telomerase activity in skeletal muscles of the mdx mouse (10 min)

Coffee break

17.00-19.00 Cell and Gene Therapy in Sarcomeric Muscles (II) Applications

    - F Rossi, Department of Molecular Pharmacology, Stanford, CA, USA : Myoblast-mediated delivery of tightly
       regulated therapeutic genes

    - JC Chachques: Cellular cardiomyoplasty in a dog model

    - A Wernig, Department of Physiology, University Bonn, Germany: Human implants into mouse muscle

    - M Cantini: Myoblast-machrophage interactions during muscle regeneration in vitro and in vivo

June 13, 2000 (Tuesday)

9.00-13.30 Cellular Mechanisms and Progression of Muscular Dystrophies

Mechanisms of Cellular Adaptation to Workload and Exercise-induced Muscle Damage (I) (II)

9.00-10.00 Cellular Mechanisms and Progression of Muscular Dystrophies

Chairpersons: L Larsson and C Reggiani

    - C Angelini, Neuromuscular Center, Department of Neurology, University of Padova, Italy: Clinico molecular
       correlations in dystrophinopathies and carriers

     - R Betto, CNR Unit for Muscle Biology and Physiopathology, University of Padova, Italy: Role of purinergic receptors
       in the pathogenesis of sarcoglycanopathies

     - M Bonifati, Neuromuscular Center, Department of Neurology, University of Padova, Italy: A multicenter double-blind
       randomized trial of deflazacort versus prednisone in duchenne muscular dystrophy: analysis after 2 years

     - R Matsuda, Department of Life Sciences, University of Tokyo, Japan: Dystrophic processes can be separated into two
       distinct stages in mdx skeletal muscle

10.00-11.10 Mechanisms of Cellular Adaptation to Workload and Exercise-induced Muscle Damage (I)
Chairpersons: C Angelini and H Kern

     - L Larsson, Physiological Research Center, The Pennsylvania State University, University Park, PA, USA:
       Regulations of human muscle contraction at the cellular and molecular level in health and disease

     - C Reggiani / Bottinelli: To be announced

     - Y Mounier: Troponine C plasticity in unloading conditions

Coffee Break

11.30-13.00 Mechanisms of Cellular Adaptation to Workload and Exercise-induced Muscle Damage (II)
Chairpersons: Y Mounier and L Larsson

    - H Kern, University of Vienna: Denervated muscles in human: First results of training with electrical stimulation

    - G Siciliano, Metabolic and muscle adaptation to aerobic training in mitochondrial myopathies

    - A Martinuzzi: Walking energy cost in children with neurogenic motor impairmen

   - C Chisari: Impaired muscle oxidative metabolism in polymyositis and dermatomyositis evaluated in vivo through
      lactic acidaemia assay

   - O Rossetto, Department of Biomedical Sciences, University of Padova: Recovery of human neuromuscular junction
      after botulinum neurotoxin therapy

   - A Jakubiec-Puka and D Biral: Sarcolemma damage in extended-stimulated muscles

   - A Megighian, Human Physiology, University of Padova: Effects of tenotomy on rat slow muscle regeneration

Lunch

14.30-19.00 Cardiac-Bio-Assists

Chairpersons: J Jarvis, NW Guldner and R Lorusso

   - U Carraro, Department of Biomedical Sciences, University of Padova, Italy: Myoblast cell therapy to augment muscle
     mass in Cardiac-Bio-Assists

   - B Voss, Department of Cardiac Surgery, Deutsches Herzzentrum München, Germany: Dynamic Cardiomyoplasty in a
     growing organism

   - V Chekanov, Milwaukee Heart Institute, Heart Care Associates, Milwaukee, Wisconsin, USA: Pharmacological
     Support of Angiogenesis Using Deferoxamine In Biological Glue For Cardiomyoplasty

   - NW Guldner, Clinic of Cardiac Surgery, Medical University of Lubeck, Germany: Biomechanical Hearts,
     Performed in a One-Step Operation and Trained Dynamically under Support of Clenbuterol

   - P Klapproth, Clinic of Cardiac Surgery, Medical University of Lubeck, Germany: Methods Evaluating the Dynamic
     Training of Skeletal Muscle Ventricles and Biomechanical Hearts

   - J Jarvis, Department of Anatomy and Cell Biology, University of Liverpool, UK: Pre-stimulation prevents
     myodystrophic lesions in Cardiac-Bio-Assists

   - R Lorusso, Cardiac Surgery, Spedali di Brescia, Italy: Muscle power after vascular delay in a sheep model
     of muscle transposition.

   - G Arpesella, Cardiac Surgery, University of Bologna, Italy: An implantable converter of muscle power
     to electrical energy

   - E Monnet, Is injury to the toracodorsal nerve present after long-term dynamic cardiomyoplasty in goats?

   - Elena Giardini, Institute of Plastic Surgery, University of Padova, Italy: Vascular delay of a LD in an experimental
     rat model for dynamic cardiomyoplasty

18.00 First Meeting of THE CARDIAC-BIO-ASSIST ASSOCIATION
 
 

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Coffee breaks and three lunches.

Conference Proceedings which will be published in Basic and Applied Myology l0 (1-3), 2000.

Dr Ir FH van der Veen, Cardiothoracic Surgery, PO Box 5800, 6202 AZ, Academic Hospital, Maastricht, Netherlands, Email FVV@SCPC.AZM.NL.

Address for correspondence:

Dr Ir FH van der Veen, Cardiothoracic Surgery, PO Box 5800, 6202 AZ, Academic Hospital, Maastricht, Netherlands, Email FVV@SCPC.AZM.NL.

Address correspondence to:

Doctor Nermine Lila, Laboratoire d’Etude des Greffes et Prothèses Cardiaques, Hôpital Broussais, 96 rue Didot, 75014 Paris, France, phone 33 1 4395 9360, fax 33 1 4540 5049.

Address correspondence to:

Dr. Charlotte Rehfeldt, Research Institute for the Biology of Farm Animals, Wilhelm-Stahl-Allee 2, D-18196 Dummerstorf, Germany, phone +49 38208 68853, fax +49 38208 68852, Email rehfeldt@fbn-dummerstorf.de.

Address correspondence to:

Carlo Velussi, University of Padova, Department of Human Anatomy and Physiology, Section of Physiology, via F. Marzolo 3, 35131 Padova Italy, fax 049 827 5301.

Address correspondence to:

Prof. Dr. Hans-Joachim Appell, Institute of Sport Orthopedics, German Sport University, D-50927 Cologne, Germany, phone +49 221 4982543, fax +49 221 49 12001, Email appell@hrz.dshs-koeln.de.