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1.
Kensuke Kudou Hiroshi Saeki Yuichiro Nakashima Shun Sasaki Tomoko Jogo Kosuke Hirose Qingjiang Hu Yasuo Tsuda Koichi Kimura Ryota Nakanishi Nobuhide Kubo Koji Ando Eiji Oki Tetsuo Ikeda Yoshihiko Maehara 《American journal of surgery》2019,217(4):757-763
Background
There were few studies assessed the postoperative sarcopenia in patients with cancers. The objective of present study was to assess whether postoperative development of sarcopenia could predict a poor prognosis in patients with adenocarcinoma of esophagogastric junction, (AEG) and upper gastric cancer (UGC).Methods
Patients with AEG and UGC who were judged as non-sarcopenic before surgery were reassessed the presence of postoperative development of sarcopenia 6 months after surgery. Patients were divided into the development group or non-development group, and clinicopathological factors and prognosis between these two groups were analyzed.Results
The 5-year overall survival rates were significantly poorer in the development group than non-development group (68.0% vs. 92.6%, P?=?0.0118). Multivariate analyses showed that postoperative development of sarcopenia was an independent prognostic factor for poor overall survival (P?=?0.0237).Conclusions
Postoperative development of sarcopenia was associated with a poor prognosis in patients with AEG and UGC. 相似文献2.
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Takako Fujita Yukiko Ihara Hitomi Hayashi Atsushi Ishii Hiroshi Ideguchi Takahito Inoue Taichi Imaizumi Toshiyuki Yamamoto Shinichi Hirose 《Congenital anomalies》2020,60(6):189-193
Coffin-Siris syndrome (CSS) is a congenital anomaly syndrome characterized by developmental delay, coarse facial features, and hypoplasia of the fifth digit's nail or phalanges. Herein, we report a case of the 8-year-old female patient who showed developmental delay associated with dysplasia in the macular and large toe area. Comprehensive genomic analysis showed no possible candidate variants, but the subsequent genomic copy number analysis revealed a novel exonic deletion in the coding region of AT-rich interactive domain-containing protein 1B (ARID1B), a gene responsible for CSS. Genomic copy number analysis can aid in diagnosing CSS by confirming undiagnosed exonic deletions in ARID1B. Furthermore, this is the first report of CSS associated with bilateral macular dysplasia. 相似文献
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Katja Kobow Christopher A. Reid Erwin A. van Vliet Albert J. Becker Gemma L. Carvill Alica M. Goldman Shinichi Hirose Iscia Lopes-Cendes Hela Mrabet Khiari Annapurna Poduri Michael R. Johnson David C. Henshall 《Epileptic Disord》2020,22(2):127-141
Epigenetics refers broadly to processes that influence medium to long‐term gene expression by changing the readability and accessibility of the genetic code. The Neurobiology Commission of the International League Against Epilepsy (ILAE) recently convened a Task Force to explore and disseminate advances in epigenetics to better understand their role and intersection with genetics and the neurobiology of epilepsies and their co‐morbidities, and to accelerate translation of these findings into the development of better therapies. Here, we provide a topic primer on epigenetics, explaining the key processes and findings to date in experimental and human epilepsy. We review the growing list of genes with epigenetic functions that have been linked with epilepsy in humans. We consider potential practical applications, including using epigenetic signals as biomarkers for tissue‐ and biofluid‐based diagnostics and the prospects for developing epigenetic‐based treatments for epilepsy. We include a glossary of terms, FAQs and other supports to facilitate a broad understanding of the topic for the non‐expert. Last, we review the limitations, research gaps and the next challenges. In summary, epigenetic processes represent important mechanisms controlling the activity of genes, providing opportunities for insight into disease mechanisms, biomarkers and novel therapies for epilepsy. 相似文献
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Nariai Maika Abe Hiroko Hoshioka Yumi Makino Yohsuke Iwase Hirotaro 《International journal of legal medicine》2022,136(4):1075-1090
International Journal of Legal Medicine - Acute metabolic disorders of diabetes mellitus (DM), such as diabetic ketoacidosis, hyperosmolar hyperglycemic state, and hypoglycemia, are... 相似文献
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Kazuhiko Sawada Shigeyoshi Saito Miwa Horiuchi‐Hirose Kenya Murase 《Congenital anomalies》2014,54(2):87-93
Alterations in histoarchitecture of the brainstem were examined immunohistochemically in 4‐week‐old rats with a single whole body X‐irradiation at a dose of 0.5, 1.0, or 1.5 Gy on embryonic day (ED) 15 using anti‐heat shock protein 25 (HSP25). HSP25 immunostaining was seen in the neuronal perikarya of cranial nerve motoneurons, that is, the motor and mesencephalic nuclei of the trigeminal nerve, facial nucleus, abducens nucleus and accessory facial nucleus in the pons, and the ambiguous nucleus, dorsal nucleus of vagus nerve and hypoglossus nucleus in the medulla oblongata of intact controls. In 0.5 to 1.5 Gy‐irradiated rats, HSP25 immunostaining in those neurons was more intense than in controls, while the most intense immunostaining was marked in 1.5 Gy‐irradiated rats. HSP25 immunostaining was also apparent in the spinal tract of the trigeminal nerve and facial nerve tracts in 0.5 to 1.5 Gy‐irradiated rats, but was faint in controls. Interestingly, HSP25 immunostaining was aberrantly enhanced in dendritic arbors in the magnocellular region of medial vestibular nucleus of 0.5–1.5 Gy‐irradiated rats. Those arbors were identified as excitatory secondary vestibulo‐ocular neurons by double immunofluorescence for HSP25 and SMI‐32. The results suggest an increase of HSP25 expression in cranial nerve motoneurons and their related fiber tracts from prenatal exposure to ionizing irradiation. This may be an adaptive response to chronic hypoxia due to malformed brain arteries caused by prenatal ionizing irradiation. 相似文献
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