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Albendazole is a new drug for the treatment of cerebral cysticercosis. We have recently experience a case that had shown poor therapeutic response to praziquantel. The patient have multiple parenchymal cysts. She was treated with 15㎎/㎏/day of albendazole for 1 month to confirm healing of the intracranial lesion by the follow up brain CT scan and CSF-ELISA associated with marked clinical improvement.
Primary cancers evolving from neuromuscular system are rare. However, neuromuscular system involvement is common in cancer patients. All part of neuromuscular system including motor neurons in the spinal cord, sensory dorsal root ganglia, nerve roots, plexuses, cranial nerve, peripheral nerves and neuromuscular junctions. These include metastasis, paraneoplastic syndrome, toxicity of cancer treatment, infection due to immune suppression and metabolic/nutritional issue. . In this review we discuss the diﬀerent causes and mechanisms of disorders of the neuromuscular system in patients with cancer.
An electric vehicle (EV) powertrain is comprised of a motor and reduction gear. Thus, it must be designed by considering both components to improve its dynamic and economic performances. To obtain the optimal design of powertrain components for an EV, this study employs a two-stage analysis model focusing on the motor and vehicle at each stage for accuracy and efficiency. In the first stage, a motor system model analyzes the motor characteristics, such as the maximum and minimum torque and motor losses. Using the motor design parameters, these characteristics are converted to torque curves and an efficiency map. In the second stage, a vehicle system model analyzes the target performance using converted motor data for efficient analysis of the performance. An optimization problem is formulated to minimize the maximum motor power, acceleration time, and energy consumption with dynamic constraints, including the maximum vehicle speed and ascendable gradient. To reduce the excessive computational effort when conducting the multi-objective optimization, surrogate models with respect to performance are effectively constructed by using the adaptive sampling method. From the optimization results, a Pareto front having various solutions among the objective functions is obtained.
Since Hoch et al reported the presence of antibodies to muscle specific receptor tyrosine kinase (MuSK) in seronegative myasthenia gravis (MG), MG with MuSK antibodies (MuSK-MG) has been reported to have unique clinical features, diagnostic problems and response to treatment. Patients with MuSK-MG have a tendency of early and frequent involvement of bulbar muscles, often associated with prominent facial or tongue atrophy. Diagnostic yields of edrophonium test, and electrophysiologic tests, such as repetitive nerve stimulation test (RNS) and single fiber electromyography (SFEMG) are lower than in patients with acetylcholine receptor antibodies (AChR-MG). When doing edrophonium test or treating with acetylchoinesterase inhibitors, they often show intolerance (muscarinic and nicotinic side effects) and even show worsening of muscle weakness (hypersensitivity). However, because most of studies included small numbers of MuSK-MG patients, there have been some discrepancies among reports. And there have been questions about pathogenesis of MuSK antibodies to induce muscle weakness.I would like review the pathogenesis, clinical features, diagnosis, and treatment of MuSK-MG
Compression peripheral neuropathy is relatively common but its pathophysiology in human has not been well known because of the likelihood of permanent nerve damage in vivo human experiments. Many animal models have developed to understand the pathophysiology of compression neuropathy. According to the many animal models and a few human studies, compression neuropathy involves abnormality of intraneural microcirculation, axonal transport and connective tissue (mesoneurium, epineurium, perineurium, endonurium) as well as nerve fiber itself. Low magnitude nerve compression of short duration can initiate neural structural changes which persist for at least one month. Chronic nerve compression with loose ligatures or short tubes around nerve for about weeks or months caused a break-down in blood nerve barrier and perineurial edema, followed by epineurial and perineurial fibrosis, demyelination and finally Wallerian degeneration. Recent studies tell us that compression neuropathy is likely to be a combination of Schwann cell mechanosensitivity to shear stress and acute and/or chronic ischemia. Responding to shear stress, Schwann cells decrease myelin sickness and increase in number and make phenotype switching of neurons of DRG (dorsal root ganglion) by GDNF (glial fiber neurotrophic factor) expression.