RESUMEN
Spin current, converted from charge current via spin Hall or Rashba effects, can transfer its angular momentum to local moments in a ferromagnetic layer. In this regard, the high charge-to-spin conversion efficiency is required for magnetization manipulation for developing future memory or logic devices including magnetic random-access memory. Here, the bulk Rashba-type charge-to-spin conversion is demonstrated in an artificial superlattice without centrosymmetry. The charge-to-spin conversion in [Pt/Co/W] superlattice with sub-nm scale thickness shows strong W thickness dependence. When the W thickness becomes 0.6 nm, the observed field-like torque efficiency is about 0.6, which is an order larger than other metallic heterostructures. First-principles calculation suggests that such large field-like torque arises from bulk-type Rashba effect due to the vertically broken inversion symmetry inherent from W layers. The result implies that the spin splitting in a band of such an ABC-type artificial SL can be an additional degree of freedom for the large charge-to-spin conversion.
RESUMEN
Background: Thyroid storm (TS) is a fatal disease that leads to multiple organ failure and requires prompt diagnosis. Diabetic ketoacidosis (DKA) is a trigger for thyroid crisis. However, TS and DKA rarely occur simultaneously. Moreover, owing to the rarity of the co-occurrence, the clinical course remains unclear. In this study, we present a case of TS that developed during the follow-up for repeated DKA in a young patient. Case Presentation: A 25-year-old man with a history of recurrent DKA was brought to the emergency room frequently with similar symptoms. DKA treatment was initiated, but his tachycardia and disturbance of consciousness did not improve. Further examination of the patient revealed a Burch-Wartofsky Point Scale score of 80 points, consistent with the Japan Thyroid Association criteria. Therefore, DKA coexisting with TS was diagnosed. Antithyroid medication, inorganic iodine, and corticosteroids were then started as treatment for TS, and ß-blockers were administered to manage tachycardia. With these treatments, the patient's health improved and he recovered. Conclusions: In severe cases of recurrent DKA, the presence of TS should be considered, and early treatment should be initiated before the patient's condition worsens.
Asunto(s)
Diabetes Mellitus , Cetoacidosis Diabética , Crisis Tiroidea , Adulto , Antitiroideos/uso terapéutico , Diabetes Mellitus/tratamiento farmacológico , Cetoacidosis Diabética/complicaciones , Cetoacidosis Diabética/diagnóstico , Humanos , Japón , Masculino , Insuficiencia Multiorgánica , Crisis Tiroidea/complicaciones , Crisis Tiroidea/diagnóstico , Crisis Tiroidea/tratamiento farmacológicoRESUMEN
Sideroblastic anemia is characterized by the presence of ring sideroblasts (RSs), which are caused by iron accumulation in the mitochondria of erythroblasts and are present in both the acquired and congenital forms of the disease. However, the mechanism leading to RS formation remains elusive. Acquired sideroblastic anemia is usually observed in myelodysplastic syndrome (MDS). Because a subset of MDS harbors a somatic mutation of TET2, it may be involved in iron metabolism and/or heme biosynthesis in erythroblasts. Tet2 knockdown (Tet2trap) induced exhibited mild normocytic anemia and elevated serum ferritin levels in 4-month-old mice. Although typical RSs were not observed, increased mitochondrial ferritin (FTMT) amounts were observed in the erythroblasts of Tet2-knockdown mice. Quantitative real-time polymerase chain reaction demonstrated significant dysregulation of genes involved in iron and heme metabolism, including Hmox1, Fech, Abcb7, and Sf3b1 downregulation. After the identification of a cytosine-guanine island in the promoters of Fech, Abcb7, and Sf3b1, we evaluated DNA methylation status and found significantly higher methylation levels at the CpG sites in the erythroblasts of Tet2-knockdown mice. Furthermore, Tet2 knockdown in erythroblasts resulted in decreased heme concentration and accumulation of FTMT. Therefore, TET2 plays a role in the iron and heme metabolism in erythroblasts.