ABSTRACT
Progressive neurological signs and symptoms, in immunocompromised individuals, could be due to progressive multifocal leukoencephalopathy (PML). We report the case of a patient who present a stroke unit with symptoms that were consistent initially with a posterior circulation stroke. Prior chemotherapy with Rituximab, for a lymphoma, had predisposed the patient to infection with the JC virus. Physicians need to be aware of the condition, and patients need to aware of these risks of chemotherapy.
Subject(s)
Brain Infarction/diagnosis , Cerebellar Diseases/diagnosis , Leukoencephalopathy, Progressive Multifocal/diagnosis , Aged , Antineoplastic Agents/adverse effects , Diagnosis, Differential , Diagnostic Errors , Fatal Outcome , Humans , Immunocompromised Host , JC Virus/immunology , JC Virus/isolation & purification , Leukoencephalopathy, Progressive Multifocal/chemically induced , Leukoencephalopathy, Progressive Multifocal/immunology , Leukoencephalopathy, Progressive Multifocal/virology , Magnetic Resonance Imaging , Male , Predictive Value of Tests , Risk Factors , Rituximab/adverse effects , Tomography, X-Ray ComputedABSTRACT
Troponin (Tn) is a critical regulator of muscle contraction in cardiac muscle. Mutations in Tn subunits are associated with hypertrophic, dilated and restrictive cardiomyopathies. Improved diagnosis of cardiomyopathies as well as intensive investigation of new mouse cardiomyopathy models has significantly enhanced this field of research. Recent investigations have showed that the physiological effects of Tn mutations associated with hypertrophic, dilated and restrictive cardiomyopathies are different. Impaired relaxation is a universal finding of most transgenic models of HCM, predicted directly from the significant changes in Ca(2+) sensitivity of force production. Mutations associated with HCM and RCM show increased Ca(2+) sensitivity of force production while mutations associated with DCM demonstrate decreased Ca(2+) sensitivity of force production. This review spotlights recent advances in our understanding on the role of Tn mutations on ATPase activity, maximal force development and heart function as well as the correlation between the locations of these Tn mutations within the thin filament and myofilament function.