Structural and Electronic Properties of a Triangular Lattice Magnet NaPrTe2_2 Compared with NaNdTe2_2 and NaTbTe2_2

NaPrTe2, NaNdTe2, and NaTbTe2 are found to be triangular lattice magnets with the alpha-NaFeO2 structure, where lanthanoid atoms with 4f electrons form a triangular lattice, based on the structural analysis and physical property measurements of synthesized polycrystalline samples. The alpha-NaFeO2 structure is a new polymorph of NaPrTe2, which has been reported to crystallize in the cubic LiTiO2 structure. Polytypism in NaPrTe2 was discussed based on the structural parameters determined by the Rietveld analysis. NaPrTe2 is suggested to be in the proximity of the phase boundary between the LiTiO2 and alpha-NaFeO2 types, as compared to NaNdTe2 and NaTbTe2, indicating that this compound might be interesting from the perspectives of the dimensional control of geometrically frustrated lattices. The magnetic susceptibility and heat capacity data indicated that NaPrTe2 do not show long-range magnetic order or a spin-glass transition above 2 K.Comment: 6 pages, 7 figure

A 1-bp deletion in Mc1r in a Norway rat (Rattus norvegicus) from Sado Island, Japan gives rise to a yellowish color variant: an insight into mammalian MC1R variants

The melanocortin-1 receptor gene (MC1R) controls production of the pigments eumelanin and pheomelanin. Changes in MC1R lead to variation in coat color in mammals, which can range from entirely black (melanism) to yellowish. In this study, we report a case of a wild-caught Norway rat (Rattus norvegicus) from Sado Island, Japan with a yellowish coat color. Upon sequencing the whole coding region of the Mc1r gene (954 bp), we found a 1-bp deletion at site 337 (c.337del), indicative of a frameshift mutation, which was characterized as a severe loss-of-function or null mutation. A spectrophotometer was used to measure coat color, revealing that the rat had a distinctly lighter coat, based on lightness score, than mice with homozygous similar loss-of-function mutations. This implies that loss-of-function mutations can yield different phenotypes in murine rodents. The loss-of-function-mutant rat exhibited a contrasting coat pattern consisting of darker and lighter colors along its dorsal and ventral sides, respectively. Similar patterns have been observed in homozygous MC1R-deficient mutants in other mammals, implying that the countershading pattern can still be expressed despite the absence of MC1R in the melanocyte

Superior vena cava syndrome caused by a swollen absorbable haemostat after repair of ischaemic mitral regurgitation

Surgicel, an absorbable haemostat, is widely used in cardiovascular surgery. An 81-year-old woman, who was diagnosed with ischaemic mitral regurgitation, underwent mitral valve plasty and coronary artery bypass grafting. On postoperative day two, her superior vena cava (SVC) pressure gradually rose to 38 mmHg and she developed low output syndrome. Emergent surgery revealed that the cause of SVC syndrome was external compression from a haematoma at the posterior surface of the SVC, which formed around the Surgicel

Effects of intracerebroventricular administration of 2-hydroxypropyl-β-cyclodextrin in a patient with Niemann–Pick Type C disease

Niemann–Pick Type C disease (NPC) is an autosomal recessive lysosomal storage disorder characterized by progressive neurological deterioration. Previously, we reported that intravenous administration of 2-hydroxypropyl-β-cyclodextrin (HPB-CD) in two patients with NPC had only partial and transient beneficial effects on neurological function. The most likely reason for HPB-CD not significantly improving the neurological deficits of NPC is its inability to cross the blood–brain barrier. Herein, we describe the effects of intrathecal HPB-CD in an eight-year-old patient with a perinatal onset of NPC, administered initially at a dose of 10 mg/kg every other week and increased up to 10 mg/kg twice a week. Clinically, the patient maintained residual neurological functions for two years, at which time nuclear magnetic resonance spectroscopy showed a decreased choline to creatine ratio and increased N-acetylaspartate to creatine ratio, and positron emission tomography revealed increased standardized uptake values. Total-tau in the cerebrospinal fluid (CSF) was also decreased after two years. No adverse effects were observed over the course of treatment. The CSF concentrations of HPB-CD during the distribution phase after the injections were comparable with those at which HPB-CD could normalize cellular cholesterol abnormality in vitro. Further studies are necessary to elucidate the mechanisms of action of HPB-CD in NPC, and to determine the optimal dose and intervals of HPB-CD injection