106 research outputs found
Unveiling the orbital-selective electronic band reconstruction through the structural phase transition in TaTe
Tantalum ditelluride TaTe belongs to the family of layered transition
metal dichalcogenides but exhibits a unique structural phase transition at
around 170 K that accompanies the rearrangement of the Ta atomic network from a
"ribbon chain" to a "butterfly-like" pattern. While multiple mechanisms
including Fermi surface nesting and chemical bonding instabilities have been
intensively discussed, the origin of this transition remains elusive. Here we
investigate the electronic structure of single-crystalline TaTe with a
particular focus on its modifications through the phase transition, by
employing core-level and angle-resolved photoemission spectroscopy combined
with first-principles calculations. Temperature-dependent core-level
spectroscopy demonstrates a splitting of the Ta core-level spectra through
the phase transition indicative of the Ta-dominated electronic state
reconstruction. Low-energy electronic state measurements further reveal an
unusual kink-like band reconstruction occurring at the Brillouin zone boundary,
which cannot be explained by Fermi surface nesting or band folding effects. On
the basis of the orbital-projected band calculations, this band reconstruction
is mainly attributed to the modifications of specific Ta states, namely
the orbitals (the ones elongating along the ribbon chains) at the
center Ta sites of the ribbon chains. The present results highlight the strong
orbital-dependent electronic state reconstruction through the phase transition
in this system and provide fundamental insights towards understanding complex
electron-lattice-bond coupled phenomena.Comment: 21 pages, 5 figure
A Boy with Non-Herpes Simplex Acute Limbic Encephalitis and Antiglutamate Receptor Antibodies
This report concerns a 12-year-old male with intractable seizures over a long period. The case fulfilled the diagnostic criteria for nonherpetic acute limbic encephalitis. He had frequent convulsions starting with a partial seizure at the left angle of the mouth and progressing to secondary generalized seizures. He was treated with several anticonvulsants, combined with methylprednisolone and Ī³-globulin under mechanical ventilation. However, his convulsions reappeared after tapering of the barbiturate. His magnetic resonance imaging showed a high intensity area in the hippocampus by FLAIR and diffusion. After five months he recovered without serious sequelae. Virological studies, including for herpes simplex virus, were all negative. He was transiently positive for antiglutamate receptor antibodies in cerebrospinal fluid and serum
A Young Man with Anti-NMDAR Encephalitis following Guillain-BarrƩ Syndrome
A 19-year-old man developed rapidly progressive muscle weakness and dysesthesia in the extremities, and dyspnea after a flu-like episode. Nerve conduction studies showed reduced motor nerve conduction velocities with conduction block, and sensory nerve action potentials could not be evoked. The patient was diagnosed as having Guillain-BarrƩ syndrome (GBS), and was treated with 2 cycles of intravenous immunoglobulin (IVIg) therapy and was assisted by mechanical ventilation. During the recovery course of the illness, he experienced several attacks of psychomotor agitation from the 37th hospital day, and generalized tonic convulsive seizures suddenly developed on the 42nd hospital day. Brain MRI showed high-intensity lesions in the bilateral thalamus and medial temporal lobes. The convulsions were controlled by continuous thiopental infusion (until the 50th hospital day) and mechanical ventilation (until the 84th hospital day). Intravenous methylprednisolone pulse therapy (1,000 mg/day) for 3 days followed by dexamethasone (16 mg/day) was added. After relief of convulsive seizures, prominent orolingual dyskinesia appeared, and on MRI marked atrophy of the bilateral medial temporal lobes was seen. Anti-N-methyl-D-aspartate receptor (NMDAR) antibodies in serum and cerebrospinal fluid were positive on the 92nd hospital day. Anti-NMDAR encephalitis usually affects young females but a small number of male cases with this disease have been reported. Our male patient was unique in having GBS, a post-infectious autoimmune disease, as a preceding disease, suggesting that anti-NMDAR encephalitis itself is caused by a parainfectious autoimmune mechanism
Pc5 wave power in the quietātime plasmasphere and trough: CRRES observations
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94876/1/grl26887.pd
Combined Therapy for Anti-N-methyl D-aspartate Receptor Encephalitis
Background Anti-N-methyl- d-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune neurological disorder that usually occurs as a paraneoplastic syndrome and is particularly associated with ovarian teratoma. Standard therapy for severe cases is not established and the prognosis in patients who do not respond to first-line treatment is poor. Case Report An 11-year-old boy complained psychiatric symptoms and rapidly lost consciousness. CT scan revealed mediastinal teratoma and serum/spinal fluid was positive for anti-NMDAR antibody. He kept comatose and his brain stem function was profoundly disturbed. His symptoms were refractory to first-line therapy, which involved tumor resection, methylprednisolone (mPSL) pulse, Intravenous immunoglobulin (IVIG), and plasma exchange. We administered a combination therapy of rituximab and cyclophosphamide as second-line therapy and achieved complete recovery without adverse effects related to treatment. Conclusion Ā We consider early intensive treatment with a combination of rituximab and cyclophosphamide to be a safe and effective option for severe cases of anti-NMDAR encephalitis
A discrepancy between clinical course and magnetic resonance imaging in a case of non-herpetic acute limbic encephalitis
We report the case of a 64-year old man who presented memory disturbance, low-grade fever, weight loss, and bilateral hand tremors for three months. He was diagnosed with non-herpetic acute limbic encephalitis (NHALE). Follow-up magnetic resonance imaging (MRI) revealed new lesions after symptomatic improvement following steroid pulse therapy. This may indicate that there is a time lag between the disturbance or recovery of neurons and astrocytes. Thus, other lesions might occasionally appear during convalescence in patients with NHALE, even if only minimal lesions were found on the initial MRI
Vaccination and Infection as Causative Factors in Japanese Patients With Rasmussen Syndrome: Molecular Mimicry and HLA Class I
Rasmussen syndrome is an intractable epilepsy with a putative causal relation with cellular and humoral autoimmunity. Almost half of the patients have some preceding causative factors, with infections found in 38.2%, vaccinations in 5.9% and head trauma in 8.9% of Japanese patients. In a patient with seizure onset after influenza A infections, cross-reaction of the patient's lymphocytes with GluRĪµ2 and influenza vaccine components was demonstrated by lymphocyte stimulation test. Database analyses revealed that influenza A virus hemagglutinin and GluRĪµ2 molecules contain peptides with the patient's HLA class I binding motif (HLA ā A*0201). The relative risks of HLA class I genotypes for Rasmussen syndrome are 6.1 (A*2402), 6.4 (A*0201), 6.3 (A*2601) and 11.4 (B*4601). The relative risks of HLA class I-A and B haplotypes are infinity (A*2601+B*5401), 21.1 (A*2402+B*1501), 13.3 (A*2402+B*4801) and 5.1 (A*2402+B*5201). Some alleles and haplotypes of HLA class I may be the risk factors in Japanese patients. Cross-reactivity of cytotoxic T lymphocytes may contribute to the processes leading from infection to the involvement of CNS
Toxic Epidermal Necrolysis in a Patient with Autoimmune Limbic Encephalitis with Anti-Glutamate Receptor Antibodies
We report on a 44-year-old woman who was diagnosed with toxic epidermal necrolysis (TEN) during the recovery phase from autoimmune limbic encephalitis with anti-glutamate receptor antibodies. Both, autoimmune limbic encephalitis and TEN are very rare diseases. The co-existence of the two diseases has not yet been reported. We speculate that the total of 18 drugs needed for the treatment of encephalitis might have increased the risk of TEN. Similar reports would be required to elucidate the pathophysiology of the co-existence
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