We present a Raman study on the phase transitions of organic/inorganic hybrid perovskite materials, CH3NH3PbX3 (X = I, Br), which are used as solar cells with high power conversion efficiency. The temperature dependence of the Raman bands of CH3NH3PbX3 (X = I, Br) was measured in the temperature ranges of 290 to 100 K for CH3NH3PbBr3 and 340 to 110 K for CH3NH3PbI3. Broad ν1 bands at ~326 cm−1 for MAPbBr3 and at ~240 cm−1 for MAPbI3 were assigned to the MA–PbX3 cage vibrations. These bands exhibited anomalous temperature dependence, which was attributable to motional narrowing originating from fast changes between the orientational states of CH3NH3+ in the cage. Phase transitions were characterized by changes in the bandwidths and peak positions of the MA–cage vibration and some bands associated with the NH3+ group.

Aquaporin 4 (AQP4)-IgG-positive neuromyelitis optica spectrum disorder (AQP4-IgG+NMOSD) is an autoimmune astrocytopathic disease pathologically characterized by the massive destruction and regeneration of astrocytes with diverse types of tissue injury with or without complement deposition. However, it is unknown whether this diversity is derived from differences in pathological processes or temporal changes. Furthermore, unlike for the demyelinating lesions in multiple sclerosis, there has been no staging of astrocytopathy in AQP4-IgG+NMOSD based on astrocyte morphology. Therefore, we classified astrocytopathy of the disease by comparing the characteristic features, such as AQP4 loss, inflammatory cell infiltration, complement deposition and demyelination activity, with the clinical phase. We performed histopathological analyses in eight autopsied cases of AQP4-IgG+NMOSD. There were six women and two men, with a median age of 56.5 years (range, 46–71 years) and a median disease duration of 62.5 months (range, 0.6–252 months). Astrocytopathy in AQP4-IgG+NMOSD was classified into the following four stages defined by the astrocyte morphology and immunoreactivity for glial fibrillary acidic protein (GFAP): (a) astrocyte lysis: Extensive loss of astrocytes with fragmented and/or dust-like particles; (b) progenitor recruitment: Loss of astrocytes except small nucleated cells with GFAP-positive fibre-forming foot processes; (c) protoplasmic gliosis: Presence of star-shaped astrocytes with abundant GFAP-reactive cytoplasm; and (d) fibrous gliosis: Lesions composed of densely packed mature astrocytes. The astrocyte lysis and progenitor recruitment stages dominated in clinically acute cases (within 2 months after the last recurrence). Findings common to both stages were the loss of AQP4, a decreased number of oligodendrocytes, the selective loss of myelin-associated glycoprotein and active demyelination with phagocytic macrophages. The infiltration of polymorphonuclear cells and T cells (CD4-dominant) and the deposition of activated complement (C9neo), which reflects the membrane attack complex, a hallmark of acute NMOSD lesions, were selectively observed in the astrocyte lysis stage (98.4% in astrocyte lysis, 1.6% in progenitor recruitment, and 0% in protoplasmic gliosis and fibrous gliosis). Although most of the protoplasmic gliosis and fibrous gliosis lesions were accompanied by inactive demyelinated lesions with a low amount of inflammatory cell infiltration, the deposition of complement degradation product (C3d) was observed in all four stages, even in fibrous gliosis lesions, suggesting the past or chronic occurrence of complement activation, which is a useful finding to distinguish chronic lesions in NMOSD from those in multiple sclerosis. Our staging of astrocytopathy is expected to be useful for understanding the unique temporal pathology of AQP4-IgG+NMOSD.

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A series of halogenated compounds, (E,E,E)-1,6-di(4-X-phenyl)hexa-1,3,5-trienes (1: X = F, 2: X = Cl, 3: X = Br, 4: X = I), were synthesized and their crystal structures and fluorescence emission properties were systematically investigated. Single-crystal X-ray analysis reveals that molecules are arranged via X/X halogen bonds and/or CH/X-type hydrogen bonds to form a herringbone structure in 1 and π-stacked structures in 2−4. In the structures of 2 and 3, which are almost isomorphous, the distance and displacement for the nearest stacking molecules are smaller than those in 4. Although the structures of 2−4 are basically not greatly different from each other, the nearest-neighbor arrangements are π-stacked in 2 and 3, but herringbone in 4. Steady-state and time-resolved measurements show that the solid-state fluorescence properties also strongly depend on the halogen size. The fluorescence spectra are red-shifted and the Stokes shifts are large in 2 and 3 relative to those in 1 and 4, resulting from the difference in molecular arrangement in the crystal structure. The experimentally observed clear correlation between crystal structure and optical transition energy is reproduced fairly well by quantum chemical calculations for the excited states of molecular pairs in the X-ray determined structures of 1−4. ■ INTRODUCTIONα,ω-Diphenylpolyenes have long received considerable attention due to their interesting spectroscopic properties 1,2 and are expected to be potential optical 3 and photofunctional 4−6 materials. Due to the highly emissive properties, they can be new fluorescent probes and imaging agents in medicinal chemistry. 7−10 The electronic excited states of these polyenes have also been the subjects of many theoretical studies. 11−14 Among diphenylpolyenes, (E,E,E)-1,6-diphenylhexa-1,3,5-triene (DPH) is the shortest chromophore in which the 2A g state is clearly lower in energy than the 1B u state. It is wellknown that DPH exhibits dual fluorescence from the first (S 1 ) (2A g ) and the second (S 2 ) (1B u ) singlet excited states to the ground state (S 0 ) (1A g ) in solution. 2 As for the emission properties of DPHs in the solid state, we first showed that the unsubstituted parent compound exhibited measurable fluorescence in the microcrystalline state. 15 The solid-state fluorescence from DPH 16,17 and related linear polyenes 18 has attracted much attention recently due to their efficient singlet fission processes. 19 Our recent studies further revealed the strong correlation between crystal structure and fluorescence properties for a number of symmetrically 20−23 and asymmetrically 24 substituted DPHs. For a series of ringfluorinated DPHs having different substitution patterns, the increase in the number of fluorine atom leads to the decrease in distance and displacement between the nearest stacking molecules in the crystal structures. 20 The solid-state fluorescence spectra shift to longer wavelengths as the number of fluorine atom increases, while the spectra in solution (i.e., the properties of isola...

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disorder (MOGAD) is a newly identified autoimmune demyelinating disorder that is often associated with acute disseminated encephalomyelitis and usually occurs postinfection or postvaccination. Here we report a case of MOGAD after mRNA severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. A previously healthy 68-year-old woman presented to our department with gradually worsening numbness on the right side of her face, which began 14 days after her second dose of an mRNA-1273 vaccination. The patient's brain MRI revealed a right cerebellar peduncle lesion with gadolinium enhancement, a typical finding of MOGAD. A neurological examination revealed paresthesia on her right V2 and V3 areas. Other neurological examinations were unremarkable. Laboratory workups were positive for serum MOG-IgG as assessed by live cell-based assays and the presence of oligoclonal bands in the cerebrospinal fluid (CSF). The patient's serum test results for cytoplasmic-antineutrophil cytoplasmic antibodies, perinuclear-cytoplasmic-antineutrophil cytoplasmic antibodies, GQ1b-antibodies, and aquaporin-4 antibodies (AQP4-IgG) were all negative. Tests for soluble interleukin (IL)-2 receptors in the serum, IL-6 in the CSF and skin pricks, and angiotensin converting enzyme tests were all unremarkable. The patient was diagnosed with MOGAD after receiving an mRNA SARS-CoV-2 vaccination. After two courses of intravenous methylprednisolone treatment, the patient's symptoms improved and her cerebellar peduncle lesion shrunk slightly without gadolinium enhancement. To date, there have only been two cases of monophasic MOGAD following SARS-CoV-2 vaccination, including both the ChAdOx1 nCOV-19 and mRNA-1273 vaccines, and the prognosis is generally similar to other typical MOGAD cases. Although the appearance of MOG antibodies is relatively rare in post-COVID-19–vaccine demyelinating diseases, MOGAD should be considered in patients with central nervous system (CNS) demyelinating diseases after receiving a SARS-CoV-2 vaccine.