Magnetization models for particle-based simulations of magnetorheological fluids

In this study, three-dimensional particle-based simulations are used to model magnetorheological fluids. The numerical model of the MRF is implemented in the framework of the Discrete Element Method (DEM) and takes into account the coupling of the magnetic dipoles, the hydrodynamic drag forces and steric forces between particles. To accurately treat the magnetic interaction between particles, the magnetic field at the particles’ position is computed and an appropriate magnetization model is implemented. DEM simulations with different volume fractions of the MRF are carried out and the resulting magnetization curves are put in comparison with experimental data

Magnetization models for particle-based simulations of magnetorheological fluids

In this study, three-dimensional particle-based simulations are used to model magnetorheological fluids. The numerical model of the MRF is implemented in the framework of the Discrete Element Method (DEM) and takes into account the coupling of the magnetic dipoles, the hydrodynamic drag forces and steric forces between particles. To accurately treat the magnetic interaction between particles, the magnetic field at the particles’ position is computed and an appropriate magnetization model is implemented. DEM simulations with different volume fractions of the MRF are carried out and the resulting magnetization curves are put in comparison with experimental data

Traumatic rupture of a solitary splenic hydatid cyst: A case report

SummaryThe rupture of an Echinococcus granulosus hydatid cyst in the spleen due to trauma is a rare event. In this case report we describe the case of a 39-year-old Lebanese male victim of a motor vehicle accident with a ruptured solitary splenic hydatid cyst discovered by CT scan and excised during exploratory laparotomy.Echinococcosis or hydatid disease is a parasitic infestation by the Echinococcus genus of tapeworm. The eggs of E. granulosus, a species of Echinococcus, are fecal-orally transmitted to human hosts, most often from dog feces, and manifest as cystic lesions termed hydatid. E. granulosus most commonly affects the liver (75%), lungs (15%), and rarely the spleen (2–5%) [1,2]. E. granulosus is particularly endemic to cattle rearing areas of the Middle East. Infected patients most commonly present with vague abdominal pain, as a result of mass effect or spontaneous rupture of the cyst. Nevertheless, patient presentation may be due to traumatic rupture of a hydatid cyst; however, this is very rare. Herein we report a case of traumatic rupture of a solitary splenic hydatid cyst in a 39-year-old male following a motor vehicle crash, managed following the Advanced Trauma Life Support (ATLS) protocol

Dysfunction of the CaV2.1 calcium channel in cerebellar ataxias

Mutations in the CACNA1A gene are associated with episodic ataxia type 2 (EA2) and spinocerebellar ataxia type 6 (SCA6). CACNA1A encodes the α-subunit of the P/Q-type calcium channel or CaV2.1, which is highly enriched in the cerebellum. It is one of the main channels linked to synaptic transmission throughout the human central nervous system. Here, we compare recent advances in the understanding of the genetic changes that underlie EA2 and SCA6 and what these new findings suggest about the mechanism of the disease

Episodic ataxia type 1

Clinical characteristics: Episodic ataxia type 1 (EA1) is a potassium channelopathy characterized by constant myokymia and dramatic episodes of spastic contractions of the skeletal muscles of the head, arms, and legs with loss of both motor coordination and balance. During attacks individuals may experience a number of variable symptoms including vertigo, blurred vision, diplopia, nausea, headache, diaphoresis, clumsiness, stiffening of the body, dysarthric speech, and difficulty in breathing, among others. EA1 may be associated with epilepsy. Other findings can include delayed motor development, cognitive disability, choreoathetosis, and carpal spasm. Usually, onset is in childhood or early adolescence. Diagnosis/testing: Diagnosis is based on clinical findings, an electrophysiologic test of axonal superexcitability and threshold electrotonus, and/or molecular genetic testing of KCNA1, the only gene in which pathogenic variants are known to cause EA1. Management: Treatment of manifestations: Acetazolamide (ACTZ), a carbonic-anhydrase (CA) inhibitor, may reduce the frequency and severity of the attacks in some but not all affected individuals. Antiepileptic drugs (AEDs) may significantly reduce the frequency of the attacks in some individuals.peer-reviewe

Diagnostic and prognostic value of anti-cN1A antibodies in inclusion body myositis

Inclusion body myositis (IBM) is an acquired idiopathic inflammatory myopathy more commonly seen in individuals aged above 50. Unlike other idiopathic inflammatory myopathies, there is no response to immunosuppression/immunomodulation. The lack of response to such therapies led the focus away from considering IBM as a purely immune-mediated condition. However, the discovery of antibodies against cytosolic 5'-nucleotidase 1A (cN1A) in patients with IBM has reinvig-orated interest in autoimmunity as a key role in its pathogenesis. Over the last decade different methods have been developed to detect anti-cN1A antibodies. There has been an interest in whether these assays can be utilised in the diagnosis of IBM. Furthermore, there has been focus on whether anti-cN1A antibodies can be used to prognosticate and predict the clinical phenotype in IBM. Anti-cN1A antibodies appear to have a high specificity and moderate sensitivity for IBM. There have been some exploratory clinicopathological associations described in seropositive IBM patients, but sample sizes in most studies have been small so far. Antibody testing is yet to be standardised; which somewhat limits our ability to draw robust conclusions from current investi-gations. In this article we review the literature on anti-cN1A antibodies and discuss whether they have a role in clinical practice

Rebranding a South Los Angeles Corner Store: The Unique Logic of Retail Brands

Retail brands are important mediators of culture and value that help us understand contemporary consumption. Drawing on a collaborative ethnographic approach to a corner store-rebranding project in South Los Angeles, we demonstrate the ways in which physical retail spaces and their curated product mix can shape specific types of shopping experiences and behaviors. Building on recent studies of brand, we argue that retail curation is another important consideration for understanding how brand communications are formed, filtered and expressed. Expanding on theorizations of brand we demonstrate how retail brands, as physical sites of experience, can attempt to influence relationships between consumption, identity and behavior

Predominantly myalgic phenotype caused by the c.3466G > A p.A1156T mutation in SCN4A gene

Objective: To characterize the clinical phenotype in patients with p.A1156T sodium channel mutation. Methods: Twenty-nine Finnish patients identified with the c.3466G>A p.A1156T mutation in the SCN4A gene were extensively examined. In a subsequent study, 63 patients with similar myalgic phenotype and with negative results in myotonic dystrophy type 2 genetic screening (DM2-neg group) and 93 patients diagnosed with fibromyalgia were screened for the mutation. Functional consequences of the p.A1156T mutation were studied in HEK293 cells with whole-cell patch clamp. Results: The main clinical manifestation in p.A1156T patients was not myotonia or periodic paralysis but exercise-and cold-induced muscle cramps, muscle stiffness, and myalgia. EMG myotonic discharges were detected in most but not all. Electrophysiologic compound muscle action potentials exercise test showed variable results. The p.A1156T mutation was identified in one patient in the DM2-neg group but not in the fibromyalgia group, making a total of 30 patients so far identified. Functional studies of the p.A1156T mutation showed mild attenuation of channel fast inactivation. Conclusions: The unspecific symptoms of myalgia stiffness and exercise intolerance without clinical myotonia or periodic paralysis in p.A1156T patients make the diagnosis challenging. The symptoms of milder SCN4A mutations may be confused with other similar myalgic syndromes, including fibromyalgia and myotonic dystrophy type 2.Peer reviewe