Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At presentation the history of an 87-year-old woman included progressive memory loss, repeated transient ischaemic attack, increasing fatigue, dizziness, palpitations and frequent falls. Investigations revealed erythrocytosis, leukocytosis, thrombocytosis, normal arterial oxygen concentration and an increased red cell volume. Polycythaemia vera was diagnosed and was successfully managed by phlebotomy with half a unit twice a week and rechecks of her haematocrit, initially; she reported marked improvement after 2 weeks of treatment. The alternative treatments for polycythaemia vera are discussed; in addition to venesection, conventional treatments include bone-marrow depressive agents such as phosphorus-32 and chemotherapy with agents such as hydroxyurea. More recent developments include isovolumic erythrocytophoresis, alpha-interferon and ticlopidine. All of the treatments are associated with complications, or other disadvantages, thrombotic complications in the case of phlebotomy, malignancies in the case of most myelosuppressive treatments, and problems of compliance in others. The optimal treatment for polycythaemia vera is a judicious combination of the alternatives, depending on the phase of the disease, the age of the patient, and other prognostic factors.
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PMID:Primary polycythaemia vera in the elderly. 802 Jun 39

Monge's disease, also known as chronic mountain sickness (CMS), is a disease that potentially threatens more than 140 million highlanders during extended time living at high altitudes (over 2500m). The prevalence of CMS in Andeans is about 15-20%, suggesting that the majority of highlanders (non-CMS) are rather healthy at high altitudes; however, CMS subjects experience severe hypoxemia, erythrocytosis and many neurologic manifestations including migraine, headache, mental fatigue, confusion, and memory loss. The underlying mechanisms of CMS neuropathology are not well understood and no ideal treatment is available to prevent or cure CMS, except for phlebotomy. In the current study, we reprogrammed fibroblast cells from both CMS and non-CMS subjects' skin biopsies into the induced pluripotent stem cells (iPSCs), then differentiated into neurons and compared their neuronal properties. We discovered that CMS neurons were much less excitable (higher rheobase) than non-CMS neurons. This decreased excitability was not caused by differences in passive neuronal properties, but instead by a significantly lowered Na(+) channel current density and by a shift of the voltage-conductance curve in the depolarization direction. Our findings provide, for the first time, evidence of a neuronal abnormality in CMS subjects as compared to non-CMS subjects, hoping that such studies can pave the way to a better understanding of the neuropathology in CMS.
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PMID:Altered iPSC-derived neurons' sodium channel properties in subjects with Monge's disease. 2555 31