doi: 10.1016/j.mam.2005.07.006 157
Key Points The characteristic muscle weakness in myasthenia gravis (MG) is caused by antibodies directed against the neuromuscular junction MG is divided into subgroups on the basis of specific antibodies, other biomarkers, and clinical characteristics, such as age of onset, presence of thymoma, and involvement of ocular muscles The most common antibodies detected in MG are antibodies against acetylcholine receptors (AChRs), muscle-specific kinase (MuSK) and low-density lipoprotein receptor-related protein 4 (LRP4) Additional antibodies of interest in MG are directed against agrin, titin, K V 1.4, ryanodine receptors, collagen Q, and cortactin Therapy should be tailored to the individual patient and guided by MG subgroup, and can include symptomatic drug therapy, immunosuppressive drug therapy, thymectomy and/or supportive therapy The aim of treatment should be normal or near-normal function, which in most patients requires long-term immunosuppressive treatment with a drug combination that is individualized for the patient for optimal effectiveness Abstract Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies that target the neuromuscular junction, leading to muscle weakness and fatigability
Pentamidine is basically a diarylamidine antibiotic used for treating leishmaniasis, pneumonia, and trypanosomiasis (Neidle, 2001
For instance, endocrine-disrupting compounds can induce reproductive failure in aquatic vertebrates at concentrations below 1 ng L1, while persistent organic pollutants (POPs) bioaccumulate to toxic levels in higher trophic organisms.2,4,810The pseudo-persistence and bioaccumulation potential of these substances demand a paradigm shift towards advanced, robust, and highly efficient remediation technologies
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