Congenital morphological patterns of myocardial bridges.

Background: Myocardial bridging (MB) is a coronary anomaly in which a segment of the coronary artery is overlapped by a layer of myocardial tissue. Nowadays, there is no scientific agreement on if the MB are congenital or acquired or on the factors that determine their presence and/or absence.

Objective: This study is performed to analyze the anatomical characteristics of adult and children's hearts regarding the shape of the left coronary artery branching, presence of pre-bridge arterial branch, coronary dominance and its correlations to MB formation.

Effect of Photobiomodulation on Denervation-Induced Skeletal Muscle Atrophy and Autophagy: A Study in Mice.

Objective: The purpose of this study was to investigate whether photobiomodulation (PBM) can protect against and attenuate muscle atrophy owing to complete peripheral nerve lesion in mice by acting on autophagy.

Methods: C57BL/10 mice underwent right sciatic nerve transection to induce tibialis anterior muscle atrophy. After 6 hours of denervation, the mice received PBM (wavelength, 830 nm) daily, transcutaneously over the tibialis anterior muscle region for 5 or 14 days.

Checking the shape and lobation of the right atrial appendage in view of their clinical relevance.

Clinically, anatomy of the appendage of the atrium is associated with atrial fibrillation, with the shape and lobation of the appendage having been used to stratify the risk of thromboembolic events. The aim of this study was to examine the age-dependent change in the shape and lobation of the right atrial appendage. A cross-sectional evaluation of the heart of 172 adults and 61 children, fixed in 4% formalin solution was performed.

Dual Therapy Deflazacort/Doxycyclyne Is Better Than Deflazacort Monotherapy to Alleviate Cardiomyopathy in Dystrophin-Deficient mdx Mice.

Cardiomyopathy related to the absence of dystrophin is an important feature in Duchenne muscular dystrophy (DMD) and in the mdx mouse. Doxycycline (DOX) could be a potential therapy for mdx skeletal muscles dystrophy. We investigated whether the corticoid deflazacort (DFZ) plus DOX could improve cardiac mdx dystrophy better than DFZ alone, later (17 months) in dystrophy.

Suramin attenuates dystrophin-deficient cardiomyopathy in the mdx mouse model of duchenne muscular dystrophy.

Introduction: The purpose of this study was to determine the effects of suramin, an antifibrotic agent, on cardiac function and remodeling in mdx mice.

Methods: mdx mice (8 months old) received intraperitoneal injections of suramin twice a week for 3 months. Control mdx mice (8 months old) were injected with saline.

Doxycycline ameliorates the dystrophic phenotype of skeletal and cardiac muscles in mdx mice.

Introduction: We examined whether doxycycline, an antibiotic member of the tetracycline family, improves the histopathology and muscle function in mdx mice, the experimental model of DMD.

Methods: Doxycycline was administered for 36 days (starting on postnatal day 0) and for 9 months (starting at 8 months of age) in drinking water. Histopathological, biochemical (creatine kinase), and functional (forelimb muscle grip strength) parameters were evaluated in limb, diaphragm, and cardiac muscle.

N-acetylcysteine treatment reduces TNF-α levels and myonecrosis in diaphragm muscle of mdx mice.

Background & Aims: Duchenne muscular dystrophy (DMD) is a genetic muscle disease caused by the absence of dystrophin. An established animal model of DMD is the mdx mouse, which is unable to express dystrophin. Inflammation, particularly the proinflammatory cytokine tumor necrosis factor alpha (TNF-α), strongly contributes to necrosis in the dystrophin-deficient fibers of the mdx mice and in DMD.

Expression of utrophin at dystrophin-deficient neuromuscular synapses of mdx mice: a study of protected and affected muscles.

In mdx mice, intrinsic laryngeal muscles are spared and sternomastoid muscles are affected, showing cycles of muscle regeneration. We observed that utrophin and acetylcholine receptors are fragmented only in affected muscles, providing further evidence that changes in the overall distribution of molecules at dystrophic neuromuscular junctions may be correlated with muscle regeneration.

Eicosapentaenoic acid decreases TNF-α and protects dystrophic muscles of mdx mice from degeneration.

In dystrophin-deficient fibers of mdx mice and in Duchenne muscular dystrophy, inflammation and increased production of tumor necrosis factor alpha (TNF-α) contribute to myonecrosis. We examined the effects of eicosapentaenoic acid (EPA) on dystrophic muscle degeneration. Mdx mice (14 days old) received EPA for 16 days.

Fiber type composition of the sternomastoid and diaphragm muscles of dystrophin-deficient mdx mice.

The muscle fiber phenotype is mainly determined by motoneuron innervation and changes in neuromuscular interaction alter the muscle fiber type. In dystrophin-deficient mdx mice, changes in the molecular assembly of the neuromuscular junction and in nerve terminal sprouting occur in the sternomastoid (STN) muscle during early stages of the disease. In this study, we were interested to see whether early changes in neuromuscular assembly are correlated with alterations in fiber type in dystrophic STN at 2 months of age.

Calcium-binding proteins in skeletal muscles of the mdx mice: potential role in the pathogenesis of Duchenne muscular dystrophy.

Duchenne muscular dystrophy is one of the most common hereditary diseases. Abnormal ion handling renders dystrophic muscle fibers more susceptible to necrosis and a rise in intracellular calcium is an important initiating event in dystrophic muscle pathogenesis. In the mdx mice, muscles are affected with different intensities and some muscles are spared.

Treatment with an anti-inflammatory drug is detrimental for muscle regeneration at Bothrops jararacussu envenoming: an experimental study.

We evaluated the effects of deflazacort (DFZ) on muscle regeneration following Bothrops jararacussu envenoming. Tibialis anterior muscle from adult mice was injected with 80 microg of venom. Animals received DFZ during 6days.

Pharmacological and local toxicity studies of a liposomal formulation for the novel local anaesthetic ropivacaine.

This study reports an investigation of the pharmacological activity, cytotoxicity and local effects of a liposomal formulation of the novel local anaesthetic ropivacaine (RVC) compared with its plain solution. RVC was encapsulated into large unilamellar vesicles (LUVs) composed of egg phosphatidylcholine, cholesterol and alpha-tocopherol (4:3:0.07, mole %).

Nerve terminal contributes to acetylcholine receptor organization at the dystrophic neuromuscular junction of mdx mice.

Changes in the distribution of acetylcholine receptors have been reported to occur at the neuromuscular junction of mdx mice and may be a consequence of muscle fiber regeneration rather than the absence of dystrophin. In the present study, we examined whether the nerve terminal determines the fate of acetylcholine receptor distribution in the dystrophic muscle fibers of mdx mice. The left sternomastoid muscle of young (1-month-old) and adult (6-month-old) mdx mice was injected with 60 microl lidocaine hydrochloride to induce muscle degeneration-regeneration.

Intrinsic laryngeal muscles are spared from myonecrosis in the mdx mouse model of Duchenne muscular dystrophy.

Intrinsic laryngeal muscles share many anatomical and physiological properties with extraocular muscles, which are unaffected in both Duchenne muscular dystrophy and mdx mice. We hypothesized that intrinsic laryngeal muscles are spared from myonecrosis in mdx mice and may serve as an additional tool to understand the mechanisms of muscle sparing in dystrophinopathy. Intrinsic laryngeal muscles and tibialis anterior (TA) muscle of adult and aged mdx and control C57Bl/10 mice were investigated.

L-arginine enhances muscle regeneration after experimental envenomation by B. jararacussu: a future for nitric oxide-based therapy?

We investigated whether muscle fiber regeneration would be rescued by exogenous administration of l-arginine, the precursor of endogenous synthesis of nitric oxide. The right tibialis anterioris muscle of adult mice (n=20) was injected with 80 microg of venom. One group of mice (n=10) received drinking water containing l-arginine (3.

Nerve-terminal and Schwann-cell response after nerve injury in the absence of nitric oxide.

Dystrophic muscles show alterations in the dystrophin-glycoprotein complex and a lack of neuronal nitric oxide (NO) synthase. In mdx mice, presynaptic expression of neuronal NO synthase is decreased, suggesting that presynaptic signaling may be altered in dystrophic muscle. In this study, we examined the nerve-terminal and Schwann-cell responses after a crush lesion in control and NO-deficient mice.

Microvessel damage by B. jararacussu snake venom: pathogenesis and influence on muscle regeneration.

The loss of muscle mass consequent to poor muscle regeneration is a common sequela following the injection of Bothrops jararacussu snake venom. Since an intact microvasculature plays a central role in the success of muscle regeneration, the poor muscle regeneration seen after envenomation could be explained by damage to the local microvasculature. In this work, we investigated the pathogenesis of microvessel damage caused by B.

Trigeminal neuralgia is caused by maxillary and mandibular nerve entrapment: greater incidence of right-sided facial symptoms is due to the foramen rotundum and foramen ovale being narrower on the right side of the cranium.

Trigeminal neuralgia (TN) is the most important disease of the trigeminal nerve. Vascular compression of the dorsal root of the trigeminal nerve by aberrant loop of blood vessels is currently accepted as the most common cause of TN. The right side of the face is affected by TN twice as often as the left side, but there are no anatomical reasons for the blood vessels loop to be more frequent on the right side of the cranial fossa.

Muscle regeneration in dystrophic mdx mice is enhanced by isosorbide dinitrate.

Activation of muscle satellite cells, a fundamental step in the success of muscle regeneration is mediated by nitric oxide (NO). In this study, we investigated whether isosorbide dinitrate (ISD), an NO donor, could improve muscle regeneration in dystrophic mdx mice. The right tibialis anterior muscle of mdx and C57Bl/10 mice was injected with bupivacaine (0.

Cryopreserved muscle basal lamina grafts retain their grafting potential for nerve repair.

The development of alternatives to nerve autografts for nerve repair remains a goal of surgeons. Muscle basal lamina grafts have a potential use as bioprostheses, but it is not known whether such grafts retain their ability to support axonal regeneration following storage. In this study, we examined the effect of cryopreservation on the ability of muscle basal lamina grafts to repair nerve lesions.

Insights into the loss of muscle mass following B. jararacussu venom in mice.

Bothrops jararacussu snake venom produces myonecrosis and nerve degeneration. In this work, we investigated whether nerve lesions or impaired muscle regeneration contributed to the permanent loss of muscle mass, a long-term sequela of envenoming. The right soleus muscle of adult male mice was injected with B.

Distribution of calcitonin gene-related peptide at the neuromuscular junction of mdx mice.

In normal skeletal muscle, the protein dystrophin is associated with plasma membrane glycoproteins and may be involved in the stabilization of the sarcolemma. Mutant mdx mice are markedly deficient in dystrophin and show muscle fiber necrosis followed by regeneration. Changes in the distribution of acetylcholine receptors (AChRs) have been reported at the neuromuscular junction of mdx mice possibly as a result of alterations in the release or response to neural trophic factors.

Primary nerve repair by muscle autografts prepared with local anesthetic.

We evaluated the usefulness of muscle autografts obtained immediately after graft preparation with lidocaine injections for primary nerve repair. The right sciatic nerve of adult Wistar rats was sectioned, and muscle grafts obtained 15 min or 24 h after lidocaine injection were used to repair a gap 1.5 cm long.

Number and size of motor units in thenar muscles.

The number and size of motor units (MUs) in the thenar muscles of 10 fresh adult cadavers (33-74 years old) were estimated by histological methods. The average number of MUs was 161 +/- 26 and the MU size was 93 +/- 11.5.