著者

Hiroyuki Ishiyama Junko Ishii Hajime Yoshimura Marie Tsunogae. Satoru Fujiwara Satomi Hiya Ryoma Inui Yuma Shiomi Shinsaku Nakazawa Masamune Kimura Takehito Kuroda Yasutaka Murakami Kota Maekawa Nobuyuki Ohara Nobuo Kohara Michi Kawamoto

出版者

The Japanese Society of Internal Medicine

雑誌

Internal Medicine (ISSN:09182918)

巻号頁・発行日

pp.7802-21, (Released:2021-09-11)

参考文献数

40

被引用文献数

4

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Objective Various neurological manifestations have been increasingly reported in coronavirus disease 2019 (COVID-19). We determined the neurological features and long-term sequelae in hospitalized COVID-19 patients. Methods We retrospectively studied 95 consecutive hospitalized patients with COVID-19 between March 1 and May 13, 2020. Acute neurological presentations (within two weeks of the symptom onset of COVID-19) were compared between 60 non-severe and 35 severely infected patients who required high-flow oxygen. In the 12 ventilated patients (the most severe group), we evaluated neurological complications during admission, subacute neurological presentations, and neurological sequelae (51 and 137 days from the onset [median], respectively). Results Of the 95 patients (mean age 53 years old; 40% women), 63% had acute neurological presentations, with an increased prevalence in cases of severe infections (83% vs. 52%, p<0.001). Impaired consciousness and limb weakness were more frequent in severe patients than in non-severe ones (0% vs. 49%; p<0.001, and 0% vs. 54%; p<0.001, respectively). In the most severe group (mean age 72 years old; 42% women), 83% of patients had neurological complications (cerebrovascular disease [17%], encephalopathy [82%], and neuropathy [55%]), and 92% had subacute neurological presentations (impaired consciousness [17%], higher brain dysfunction [82%], limb weakness [75%], and tremor [58%]). Neurological sequelae were found in 83% of cases, including higher brain dysfunction (73%), limb weakness (50%), and tremor (58%). Conclusions Neurological manifestations are common in COVID-19, with the possibility of long-lasting sequelae.

著者

Junko Ishii Yukiko Shishido-Hara Michi Kawamoto Satoru Fujiwara Yukihiro Imai Kazuo Nakamichi Nobuo Kohara

出版者

The Japanese Society of Internal Medicine

雑誌

Internal Medicine (ISSN:09182918)

巻号頁・発行日

pp.0696-17, (Released:2018-04-27)

参考文献数

22

被引用文献数

11

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A 37-year-old woman with systemic lupus erythematosus (SLE) presented with gait disturbance and cognitive dysfunction. Brain magnetic resonance imaging (MRI) revealed small, punctate, T2-/fluid-attenuated inversion recovery-hyperintense and T1-hypointense lesions without gadolinium enhancement, which is atypical for progressive multifocal leukoencephalopathy (PML). On a pathological examination of biopsied brain tissues, JC virus-infected cells were hardly detected via immunohistochemistry but were certainly detected via in situ hybridization, conclusively verifying the PML diagnosis. After tapering off the immunosuppressant and mefloquine administration, the MRI findings revealed gradual improvement, and she has been stable for over 18 months. A punctate MRI pattern is not specific to natalizumab-associated PML but may be a ubiquitous early sign useful for the early diagnosis of PML.

著者

Tatsuhito Matsuo Soichi Takeda Toshiro Oda Satoru Fujiwara

出版者

一般社団法人 日本生物物理学会

雑誌

Biophysics and Physicobiology (ISSN:21894779)

巻号頁・発行日

vol.12, pp.145-158, 2015 (Released:2015-12-22)

参考文献数

59

被引用文献数

10

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Troponin (Tn), consisting of three subunits, TnC, TnI, and TnT, is a protein in the thin filaments in muscle, and, together with another thin-filament protein tropomyosin (Tm), plays a major role in regulation of muscle contraction. Various mutations of Tn cause familial hypertrophic cardiomyopathy. These mutations are directly related to aberrations in this regulatory mechanism. Here we focus on the mutations E244D and K247R of TnT, which reside in the middle of the pathway of the Ca2+-binding signal from TnC to Tm. These mutations induce an increase in the maximum tension of cardiac muscle without changes in Ca2+-sensitivity. As a first step toward elucidating the molecular mechanism underlying this functional aberration, we carried out small-angle X-ray scattering experiments on the Tn core domain containing the wild type subunits and those containing the mutant TnT in the absence and presence of Ca2+. Changes in the overall shape induced by the mutations were detected for the first time by the changes in the radius of gyration and the maximum dimension between the wild type and the mutants. Analysis of the scattering curves by model calculations shows that TnC adopts a dumbbell structure regardless of the mutations, and that the mutations change the distributions of the conformational ensembles so that the flexible N- and C-terminal regions of TnT become close to the center of the whole moelcule. This suggests, since these regions are related to the Tn-Tm interactions, that alteration of the Tn-Tm interactions induced by the mutations causes the functional aberration.