Myofibers deficient in connexins 43 and 45 expression protect mice from skeletal muscle and systemic dysfunction promoted by a dysferlin mutation.

Dysferlinopathy is a genetic human disease caused by mutations in the gene that encodes the dysferlin protein (DYSF). Dysferlin is believed to play a relevant role in cell membrane repair. However, in dysferlin-deficient (blAJ) mice (a model of dysferlinopathies) the recovery of the membrane resealing function by means of the expression of a mini-dysferlin does not arrest progressive muscular damage, suggesting the participation of other unknown pathogenic mechanisms. Here, we show that proteins called connexins 39, 43 and 45 (Cx39, Cx43 and Cx45, respectively) are expressed by blAJ myofibers and form functional hemichannels (Cx HCs) in the sarcolemma. At rest, Cx HCs increased the sarcolemma permeability to small molecules and the intracellular Ca2+ signal. In addition, skeletal muscles of blAJ mice showed lipid accumulation and lack of dysferlin immunoreactivity. As sign of extensive damage and atrophy, muscles of blAJ mice presented elevated numbers of myofibers with internal nuclei, increased number of myofibers with reduced cross-sectional area and elevated creatine kinase activity in serum. In agreement with the extense muscle damage, mice also showed significantly low motor performance. We generated blAJ mice with myofibers deficient in Cx43 and Cx45 expression and found that all above muscle and systemic alterations were absent, indicating that these two Cxs play a critical role in a novel pathogenic mechanism of dysfernolophaties, which is discussed herein. Therefore, Cx HCs could constitute an attractive target for pharmacologic treatment of dyferlinopathies.

Acetaminophen Mitigates Myocardial Injury Induced by Lower Extremity Ischemia-Reperfusion in Rat Model.

OBJECTIVE: The injury-reducing effect of acetaminophen, an effective analgesic and antipyretic on ischemia-reperfusion continues to attract great attention. This study analyzed the protective effect of acetaminophen on myocardial injury induced by ischemia-reperfusion in an experimental animal model from lower extremity ischemia-reperfusion. METHODS: Twenty-four Sprague-Dawley female rats were randomized into three groups (n=8) as (i) control group (only laparotomy), (ii) aortic ischemia-reperfusion group (60 min of ischemia and 120 min of reperfusion) and (iii) ischemia-reperfusion + acetaminophen group (15 mg/kg/h intravenous acetaminophen infusion starting 15 minutes before the end of the ischemic period and lasting till the end of the reperfusion period). Sternotomy was performed in all groups at the end of the reperfusion period and the heart was removed for histopathological examination. The removed hearts were histopathologically investigated for myocytolysis, polymorphonuclear leukocyte (PMNL) infiltration, myofibrillar edema and focal hemorrhage. RESULTS: The results of histopathological examination showed that acetaminophen was detected to particularly diminish focal hemorrhage and myofibrillar edema in the ischemia-reperfusion + acetaminophen group (P<0.001, P=0.011), while there were no effects on myocytolysis and PMNL infiltration between the groups (P=1.000, P=0.124). CONCLUSION: Acetaminophen is considered to have cardioprotective effect in rats, by reducing myocardial injury induced by abdominal aortic ischemia-reperfusion.

Síndrome do filhote nadador em gato: relato de caso / Swimmer puppy syndrome in cat: case report / Síndrome del cachorro nadador en gato: relato de caso

A síndrome do filhote nadador, também conhecida como síndrome do filhote tartaruga ou splay leg, representa um raro transtorno caracterizado pela hipoplasia miofibrilar, que afeta o desenvolvimento motor, tanto de animais de produção quanto de companhia. O presente artigo relata o caso de um filhote de gato, SRD, de 25 dias, com abdução dos quatro membros e diagnóstico clínico de síndrome do gato nadador. Foi realizado tratamento clínico com uso de bandagens, fisioterapia e termoterapia, sendo verificada recuperação completa em seis dias após o início do tratamento. A identificação precoce da desordem associado à terapia intensiva foram responsáveis pela evolução favorável deste caso, o que permite evidenciar a eficácia do tratamento clínico na resolução da síndrome do gato nadador.

Swimming cub syndrome also known as the flat turtle syndrome or splay leg, represents a rare disorder characterized by myofibrillar hypoplasia, which aftects the motor development of both production and companion animais. This article reports the case of a zs-olo-cav mongrel kitten, with abduction of the four limbs and clinical diagnosis of swimmer cat syndrome. Clinical treatment with bandages, physiotherapy and thermotherapy was performed, and complete recovery was verified six days after the start of treatment. The early identification of the disorder associated with intensive care was responsible for the favorable evolution of this case, which allows to evidence the eftectiveness of clinical treatment in the resolution of swimmer cat syndrome.

El síndrome del cría nadador, también conocido como síndrome del cachorro plano, del cachorro tortuga o splay leg, representa un raro trastorno caracterizado por la hipoplasia miofibrilar, que afecta ai desarrollo motor, tanto de animales de producción y de compaõía. El presente artículo relata el caso de un gato, SRD, de 25 días, con abducción de los cuatro miembros y el diagnóstico clínico del síndrome del gato nadador. Se realizó un tratamiento clínico con el uso de vendajes, fisioterapia y termoterapia, y se verificó una recuperación completa seis días después del inicio del tratamiento. La identificación precoz del desorden asociado a la terapia intensiva fue responsable de la evolución favorable de este caso, que permite evidenciar la eficacia del tratamiento clínico en la resolución del síndrome dei gato nadador.

Acetaminophen mitigates myocardial injury induced by lower extremity ischemia-reperfusion in rat model

Abstract Objective: The injury-reducing effect of acetaminophen, an effective analgesic and antipyretic on ischemia-reperfusion continues to attract great attention. This study analyzed the protective effect of acetaminophen on myocardial injury induced by ischemia-reperfusion in an experimental animal model from lower extremity ischemia-reperfusion. Methods: Twenty-four Sprague-Dawley female rats were randomized into three groups (n=8) as (i) control group (only laparotomy), (ii) aortic ischemia-reperfusion group (60 min of ischemia and 120 min of reperfusion) and (iii) ischemia-reperfusion + acetaminophen group (15 mg/kg/h intravenous acetaminophen infusion starting 15 minutes before the end of the ischemic period and lasting till the end of the reperfusion period). Sternotomy was performed in all groups at the end of the reperfusion period and the heart was removed for histopathological examination. The removed hearts were histopathologically investigated for myocytolysis, polymorphonuclear leukocyte (PMNL) infiltration, myofibrillar edema and focal hemorrhage. Results: The results of histopathological examination showed that acetaminophen was detected to particularly diminish focal hemorrhage and myofibrillar edema in the ischemia-reperfusion + acetaminophen group (P<0.001, P=0.011), while there were no effects on myocytolysis and PMNL infiltration between the groups (P=1.000, P=0.124). Conclusion: Acetaminophen is considered to have cardioprotective effect in rats, by reducing myocardial injury induced by abdominal aortic ischemia-reperfusion.

Síndrome do filhote nadador em gato: relato de caso / Swimmer puppy syndrome in cat: case report / Síndrome del cachorro nadador en gato: relato de caso

A síndrome do filhote nadador, também conhecida como síndrome do filhote tartaruga ou splay leg, representa um raro transtorno caracterizado pela hipoplasia miofibrilar, que afeta o desenvolvimento motor, tanto de animais de produção quanto de companhia. O presente artigo relata o caso de um filhote de gato, SRD, de 25 dias, com abdução dos quatro membros e diagnóstico clínico de síndrome do gato nadador. Foi realizado tratamento clínico com uso de bandagens, fisioterapia e termoterapia, sendo verificada recuperação completa em seis dias após o início do tratamento. A identificação precoce da desordem associado à terapia intensiva foram responsáveis pela evolução favorável deste caso, o que permite evidenciar a eficácia do tratamento clínico na resolução da síndrome do gato nadador.(AU)

Swimming cub syndrome also known as the flat turtle syndrome or splay leg, represents a rare disorder characterized by myofibrillar hypoplasia, which aftects the motor development of both production and companion animais. This article reports the case of a zs-olo-cav mongrel kitten, with abduction of the four limbs and clinical diagnosis of swimmer cat syndrome. Clinical treatment with bandages, physiotherapy and thermotherapy was performed, and complete recovery was verified six days after the start of treatment. The early identification of the disorder associated with intensive care was responsible for the favorable evolution of this case, which allows to evidence the eftectiveness of clinical treatment in the resolution of swimmer cat syndrome.(AU)

El síndrome del cría nadador, también conocido como síndrome del cachorro plano, del cachorro tortuga o splay leg, representa un raro trastorno caracterizado por la hipoplasia miofibrilar, que afecta ai desarrollo motor, tanto de animales de producción y de compaõía. El presente artículo relata el caso de un gato, SRD, de 25 días, con abducción de los cuatro miembros y el diagnóstico clínico del síndrome del gato nadador. Se realizó un tratamiento clínico con el uso de vendajes, fisioterapia y termoterapia, y se verificó una recuperación completa seis días después del inicio del tratamiento. La identificación precoz del desorden asociado a la terapia intensiva fue responsable de la evolución favorable de este caso, que permite evidenciar la eficacia del tratamiento clínico en la resolución del síndrome dei gato nadador.(AU)

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1-7) through a p38 MAPK-dependent mechanism.

Skeletal muscle atrophy induced during sepsis syndrome produced by endotoxin in the form of LPS (lipopolysaccharide), is a pathological condition characterized by the loss of strength and muscle mass, an increase in MHC (myosin heavy chain) degradation, and an increase in the expression of atrogin-1 and MuRF-1 (muscle-specific RING-finger protein 1), two ubiquitin E3 ligases belonging to the ubiquitin-proteasome system. Ang-(1-7) [Angiotensin-(1-7)], through its Mas receptor, has beneficial effects in skeletal muscle. We evaluated in vivo the role of Ang-(1-7) and Mas receptor on the muscle wasting induced by LPS injection into C57BL/10J mice. In vitro studies were performed in murine C2C12 myotubes and isolated myofibres from EDL (extensor digitorum longus) muscle. In addition, the participation of p38 MAPK (mitogen-activated protein kinase) in the Ang-(1-7) effect on the LPS-induced muscle atrophy was evaluated. Our results show that Ang-(1-7) prevents the decrease in the diameter of myofibres and myotubes, the decrease in muscle strength, the diminution in MHC levels and the induction of atrogin-1 and MuRF-1 expression, all of which are induced by LPS. These effects were reversed by using A779, a Mas antagonist. Ang-(1-7) exerts these anti-atrophic effects at least in part by inhibiting the LPS-dependent activation of p38 MAPK both in vitro and in vivo. We have demonstrated for the first time that Ang-(1-7) counteracts the skeletal muscle atrophy induced by endotoxin through a mechanism dependent on the Mas receptor that involves a decrease in p38 MAPK phosphorylation. The present study indicates that Ang-(1-7) is a novel molecule with a potential therapeutic use to improve muscle wasting during endotoxin-induced sepsis syndrome.

Base of the skull morphology and Class III malocclusion in patients with unilateral cleft lip and palate

OBJECTIVE: The aim of the present study was to determine the morphological differences in the base of the skull of individuals with cleft lip and palate and Class III malocclusion in comparison to control groups with Class I and Class III malocclusion. METHODS: A total of 89 individuals (males and females) aged between 5 and 27 years old (Class I, n = 32; Class III, n = 29; and Class III individuals with unilateral cleft lip and palate, n = 28) attending PUC-MG Dental Center and Cleft Lip/Palate Care Center of Baleia Hospital and PUC-MG (CENTRARE) were selected. Linear and angular measurements of the base of the skull, maxilla and mandible were performed and assessed by a single calibrated examiner by means of cephalometric radiographs. Statistical analysis involved ANCOVA and Bonferroni correction. RESULTS: No significant differences with regard to the base of the skull were found between the control group (Class I) and individuals with cleft lip and palate (P > 0.017). The cleft lip/palate group differed from the Class III group only with regard to CI.Sp.Ba (P = 0.015). Individuals with cleft lip and palate had a significantly shorter maxillary length (Co-A) in comparison to the control group (P < 0.001). No significant differences were found in the mandible (Co-Gn) of the control group and individuals with cleft lip and palate (P = 1.000). CONCLUSION: The present findings suggest that there are no significant differences in the base of the skull of individuals Class I or Class III and individuals with cleft lip and palate and Class III malocclusion. .

OBJETIVO: o objetivo do presente estudo foi determinar diferenças morfológicas da base do crânio de indivíduos portadores de fissura de lábio e palato e de má oclusão de Classe III, comparado-os com indivíduos controle com má oclusão de Classes I ou III. MÉTODOS: oitenta e nove indivíduos, de ambos os sexos, com idade variando entre 5 e 27 anos, Classe I (n = 32), Classe III não fissurados (n = 29) e Classe III com fissura labiopalatina unilateral (n = 28), oriundos do Centro de Odontologia e Pesquisa da PUC-MG e do Centro de Atendimento de Fissurados do Hospital da Baleia e da PUC-MG (CENTRARE), foram selecionados. Medições lineares e angulares da base do crânio, maxila e mandíbula foram realizadas e avaliadas por um único examinador calibrado, por meio de radiografias cefalométricas. Foram utilizados os testes ANCOVA e correção de Bonferroni para a análise estatística dos dados. RESULTADOS: com relação à base do crânio, os resultados não indicaram diferença estatística entre indivíduos controle (Classe I) e os indivíduos com fissuras (p > 0,017). O grupo com fissura foi diferente do grupo Classe III somente em relação à medida CI.Sp.Ba (p = 0,015). O comprimento maxilar (Co-A) apresentou diferença estatisticamente significativa na comparação entre o grupo controle (Classe I) e o grupo com fissuras (p < 0,001), sendo que os fissurados apresentaram uma maxila menor. Não foram encontradas diferenças na mandíbula (Co-Gn) entre indivíduos do grupo controle (Classe I) e indivíduos fissurados (p = 1,000). CONCLUSÃO: os resultados sugerem que não houve diferença estatisticamente significativa na base do crânio entre indivíduos Classe I e III e indivíduos com fissuras de lábio e palato com má oclusão de Classe III. .

Neuromuscular activity of Bothrops alcatraz snake venom in chick biventer cervicis preparations.

Venom (10-100 µg/ml) from Bothrops alcatraz, a pitviper from the Alcatrazes Archipelago off the coast of southeastern Brazil, caused progressive, irreversible neuromuscular blockade in chick isolated biventer cervicis preparations. The venom also inhibited contractures to exogenous ACh (110 µM) and KCl (20 mM), caused myofiber damage and increased creatine kinase release. Commercial bothropic antivenom raised against mainland Bothrops species neutralized the neuromuscular activity, depending on the venom concentration.

Trypanosoma cruzi disrupts myofibrillar organization and intracellular calcium levels in mouse neonatal cardiomyocytes.

Immunofluorescence studies of normal and Trypanosoma cruzi-infected primary cultures of heart muscle cells were performed to gather information about the arrangement of myofibrillar components during the intracellular life cycle of this parasite. By using a panel of monoclonal antibodies against various myofibrillar proteins, a progressive disruption and loss of contractile proteins (such myosin and actin) of the host cell was detected during infection. The host cell formed a loose network of myofibrillar proteins around the parasites. Breakdown of the myofibrils occurred in regions where the parasites were present, and heavily infected cells showed myofibrillar proteins at their periphery. In parallel, we investigated the effect of T. cruzi infection on intracellular calcium levels by using a Ca2+ fluorescent indicator (confocal microscopy). Infected cardiomyocytes displayed a marked impairment in contractility, and calcium influxes became irregular and less intense when compared with those of non-infected cells. Our results demonstrate that T. cruzi infection dramatically affects calcium fluxes and causes myofibrillar breakdown disturbing cardiomyocyte contractility.

Tropomodulin expression in developing hearts of normal and cardiac mutant Mexican axolotl.

In the axolotl, Ambystoma mexicanum, a simple, recessive cardiac-lethal mutation in gene "c" results in the hearts of c/c homozygous animals being deficient in sarcomeric tropomyosin (TM) and failing to form mature myofibrils. Subsequently, the mutant hearts do not beat. A three-step model of myofibril assembly recently developed in cell culture prompted a reassessment of the myofibril assembly process in mutant hearts using a relatively new late marker for thin filament assembly, tropomodulin (Tmod). This is, to the best of our knowledge, the first report of tropomodulin in an amphibian system. Tropomodulin antibodies were immunolocalized to the ends of the thin filaments. Tropomodulin was also found in discrete punctate spots in normal and mutant hearts, often in linear arrays suggestive of early myofibril formation. The tropomodulin spots assessed in stage 41/42 mutant hearts co-localized with antibodies to other myofibrillar proteins indicative of nascent myofibril formation. This suggests a failure of elongation/maturation of nascent myofibrils, which could be a consequence of decreased TM levels or increased Tmod/ TM ratio. Unlike tropomyosin, there is no apparent decrease in the level of Tmod expression in mutant hearts.

[Skeletal muscle histomorphometric study of rats in anestrus]. / Estudo histomorfométrico do músculo esquelético de ratos em anestro.

UNLABELLED: Castration, as well as the menopause, represents endocrine suppression that prevails the hypoestrogenism and their larger consequence on the skeletal muscle is to provoke sarcopenia. OBJECTIVE: To study the morphometric alteration of striated muscle of castrated female rats. METHODS: Twenty six female rats Wistar , distributed in two sub-groups, A and B, submitted initially to weigh-in place, vaginal cytology, ovariectomy, and biopsy of the muscle rectus femoris on the back paws, A group on right paw, and B on the left. Elapsed 20 days it was collected vaginal cytology to prove the anestrus status. After 70 days the animals went through weigh-in place, and new muscle biopsy, A group in left paw and B in right paw. The morphometric study was accomplished with the aids of a graduated lens, with reticules of 100 mm2, it was counted the myofibrils with six readings in the vertical and five in the horizontal in each sheet, being obtained a multiple number that applied on a specific formula to calculate the coefficient of muscular density. RESULTS: In A the muscular density varied from 60.0 to 52.33, (p<0.05%), with variation of 14.12%, and in B from 73.5 to 54.0, (p<0.05%), with variation of 26.53%. CONCLUSION: The castration provoked sarcopenia in the striated muscle and reduction of myofibrils number.

Estudo histomorfométrico do músculo esquelético de ratos em anestro / Skeletal muscle histomorphometric study of rats in anestrus

A castracão, assim como a menopausa, representa estágio de supressão endócrina em que prevalece o hipoestrogenismo e sua conseqüência maior sobre o músculo esquelético é provocar sarcopenia. OBJETIVOS: estudar as alteracões histomorfológicas do músculo esquelético de ratos fêmeas castrados. MÉTODOS: vinte e seis ratos Wistar, distribuídos em dois grupos, A e B, submetidos inicialmente à pesagem, citologia vaginal, ovariectomia e biópsia do músculo rectus femoris das patas traseiras, grupo A na direita e B na esquerda. Decorridos 20 dias foi colhido citologia vaginal para comprovar o estado de anestro. Após 70 dias os animais foram pesados e passaram por biópsia muscular, grupo A na pata E e grupo B na D. A histomorfometria foi realizada com o auxílio de uma lente gradiculada de 1cmy, com retículo de Weibel de 1mmy; contou-se as miofibrilas com seis leituras na vertical e cinco na horizontal em cada lamina, obtendo-se um número múltiplo que aplicado sobre uma formula especifica para calcular o Coeficiente de Densidade Muscular. RESULTADOS: em A a densidade muscular variou de 60.0 para 52.33 (p<0,05) com variacão de 14,12 por cento, e em B de 73.5 para 54.0 (p<0,05 por cento) com variacão de 26,53 por cento. CONCLUSAO: A castracão provocou sarcopenia no músculo esquelético e reducão do número de miofibrilas.

Centronuclear myopathy: clinical aspects of ten Brazilian patients with childhood onset.

We herein present 10 patients with the childhood onset form of centronuclear myopathy. All patients underwent a clinical and neurologic examination, and EMG/NVC. A series of ancillary examinations, consisting of muscle enzymes, EEG, EKG, echocardiogram, pulmonary function tests and head CT scan was done in most. The mean age was 16.3 years (3-25). Seven were female. There was no family history in seven and in two it was suggestive of an autosomal recessive inheritance. One patient was adopted and no history was available. Frequent gestational and neonatal abnormalities were present, namely poor fetal movements, maternal polyhydramnios, perinatal hypoxia, hypotonia at birth, and weak crying and feeding. In seven patients there was delayed motor milestones. In most patients the motor involvement was stable or slowly progressive. Upon examination the facies were myopathic and there was a global skeletal muscle involvement in all patients, with muscular hypotonia, atrophy, and areflexia. Characteristically, patients presented with ophthalmoparesis, and weakness of masticatory and facial muscles. We frequently found osteoskeletal abnormalities, namely kyphoscoliosis, tendon retractions and high-arched palate. A restrictive pulmonary function pattern was found in five patients, but only one had a cor pulmonale. CK was abnormally high in one patient, and normal in all others. EMG/NVC disclosed a myopathic pattern in nine; in three there was a mixed neurogenic picture; and in one we found myotonic discharges. A long follow-up (median 8.1 years) showed that only the patient with cor pulmonale had an unfavorable prognosis.

Ultrastructure of voluntary muscle in childhood malnutrition.

This paper is part of a study on the electron microscopy of protein-energy malnutrition, using a rapid autopsy protocol. Samples of voluntary muscle, obtained from eight children dying of severe oedematous malnutrition, were fixed in glutaraldehyde within 75 minutes of death. Atrophy of myofibres, increased prominence of satellite cells, and segmental necrobiosis were seen by light microscopy. Electron microscopy showed variable depletion of myofibrils. In the most severe case, there was focal absence of myofibrils, also disorganized Z lines, and absent M bands. Residual atrophic myofibrils measured less than 0.1 micron in width. Other specimens showed sarcomere disorganization, mitochondrial swelling, glycogen depletion, sarcoplasmic oedema, and focal contractions of sarcomeres. Though non-specific, rigor may be accelerated by free radical damage, calcium release into the cytosol, and low supplies of high-energy phosphates. These conditions may exist in severe malnutrition, complicated by terminal infection and metabolic disturbances.

Ultrastructure of voluntary muscle in childhood malnutrition

This paper is part of a study on the electron microscopy of protein-energy malnutrition, using a rapid autopsy protocol. Samples of voluntary muscle, obtained from eight children dying of severe oedematous malnutrition, were fised in glutaraldehyde within 75 minutes of death. Atrophy of myofibres, increased prominence of satellite cells, and segmental necrobiosis were seen by light microscopy. Electron microscopy showed variable depletion of myofibrils. In the most severe case, there was focal absence of myofibrils, also disorganized Z lines, and absent M bands. Residual atrophic myofibrils measured less than 0.1 æm in width. Other specimens showed sarcomere disorganization, mitochondrial swelling, glycogen depletion, sarcoplasmic oedema, and focal contractions of sarcomeres. Though non-specific, rigor may phosphates. These conditions may exist in severe malnutrition, complicated by terminal infection and metabolic disturbances (AU)

Ultrastructure of voluntary muscle in childhood malnutrition

This paper is part of a study on the electron microscopy of protein-energy malnutrition, using a rapid autopsy protocol. Samples of voluntary muscle, obtained from eight children dying of severe oedematous malnutrition, were fised in glutaraldehyde within 75 minutes of death. Atrophy of myofibres, increased prominence of satellite cells, and segmental necrobiosis were seen by light microscopy. Electron microscopy showed variable depletion of myofibrils. In the most severe case, there was focal absence of myofibrils, also disorganized Z lines, and absent M bands. Residual atrophic myofibrils measured less than 0.1 µm in width. Other specimens showed sarcomere disorganization, mitochondrial swelling, glycogen depletion, sarcoplasmic oedema, and focal contractions of sarcomeres. Though non-specific, rigor may phosphates. These conditions may exist in severe malnutrition, complicated by terminal infection and metabolic disturbances

Myofibrillar breakdown and cytoskeletal alterations in heart muscle cells during invasion by Trypanosoma cruzi: immunological and ultrastructural study.

The cytoskeletal organization of normal and Trypanosoma cruzi-infected mouse embryo heart muscle cells (HMC) in primary culture was investigated using immunofluorescence and transmission electron microscopy. Fluorescent probes revealed that in the early stages of infection, up to 24 h, the HMC cytoskeleton appeared to accommodate the intracellular parasites perinuclearly, with only a few cells displaying a slight disturbance in the distribution of filaments. However, as the infection progressed (48 to 72 h), microtubules and desmin filaments were disrupted. Breakdown of myofibrils occurred in regions where the parasites were present, followed by formation of actin polygons. Using Triton X-100 treated whole cell mount, we obtained a striking preservation of the three-dimensional architecture of the cytoskeleton. Combining electron spectroscopic imaging (ESI) with contrast tuning, we detected a highly interconnected cytoskeletal network in normal cells, and a loose network in infected cells. Bundles of filaments running under and over the parasites were also observed. Our results demonstrate that T. cruzi infection induces myofibrillar breakdown and destruction of several cytoskeleton filaments in heart muscle cells.

A congenital myopathy of unknown origin.

Parallel with the clinical and histochemical investigations, an ultrastructural examination of a muscle biopsy specimen was made, in order to detect any slight cellular alterations which cannot possibly be discovered through any other methods, and to identify a muscle disease of unknown origin.