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Yuko Kozasa Hikari Takaseya Yukari Koga Teruyuki Hiraki Yasunori Mishima Shuhei Niiyama Kazuo Ushijima 《Journal of anesthesia》2013,27(5):764-767
Cerebral venous sinus thrombosis (CVST) is rare but displays various and often dramatic clinical symptoms. Few cases of CVST have been reported in the field of anesthesiology. We encountered an unexpected case of CVST that presented with delayed emergence from anesthesia after resection of a brain tumor. A 55-year-old man was scheduled for resection of an oligoastrocytoma in his right frontal lobe. After smooth induction of general anesthesia, anesthesia was maintained uneventfully for about 7 h with target-controlled infusion (TCI) of propofol and remifentanil, except for a seizure generated when the right anterior central gyrus was stimulated to allow motor evoked potential monitoring. Immediately after the cessation of TCI, spontaneous respiration was restored. However, the patient was unexpectedly comatose, and no response to painful stimuli or coughing during tracheal suctioning was observed. A computed tomogram taken 2 h after surgery showed diffuse brain edema, even though the neurosurgeons did not notice any cerebral swelling during closing of the dura mater. A magnetic resonance venogram revealed thromboses in the superior sagittal and straight sinuses. On the 9th postoperative day, the patient died without recovering consciousness or his brainstem reflexes. Anesthesiologists should be aware of CVST as a cause of delayed emergence from anesthesia after craniotomy. 相似文献
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Hidehiko Kawabata Kenta Ariga Toru Shibata Yoshito Matsui 《Journal of plastic surgery and hand surgery》2013,47(3):150-154
The aim of reconstruction of the webs for syndactyly of the foot is cosmetic improvement, so skin grafting should be avoided. We present our long-term results of 19 feet with simple cutaneous syndactyly in 15 patients who were treated by an open technique. The bottom of the web was covered with a dorsal rectangular flap and the remaining skin defect was left open to epithelialise spontaneously. This took about 4 weeks. After a mean follow-up of 5.7 years (range 3-9), no hypertrophic scar or pigmentation of the skin had developed. Creeping of the web was seen only during the first postoperative year. The final depth of the web satisfied the families of all patients. As the aim of web reconstruction for syndactyly of the foot is purely cosmetic, we conclude that this simple method is reasonable treatment. 相似文献
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Naoto Kawabata 《Contemporary psychoanalysis》2013,49(3):406-414
This article describes the foundation of a psychoanalytic institute in Japan and how its creation was based on the experience of training at the William Alanson White Institute. The process of starting a new institute is compared to the stages of growing plants, including planting seeds, sprouting, pruning, and transplanting. Creating an “ideal” institute requires a belief in education, the ability to find joy in relating to colleagues, and a capacity to deal with the evaluation process and with healthy tensions among subgroups. 相似文献
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Antibody‐mediated rejection after ABO‐incompatible pediatric living donor liver transplantation for propionic acidemia: A case report 下载免费PDF全文
Masaki Honda Seisuke Sakamoto Rieko Sakamoto Shirou Matsumoto Tomoaki Irie Koushi Uchida Keita Shimata Seiichi Kawabata Kaori Isono Shintaro Hayashida Hidekazu Yamamoto Fumio Endo Yukihiro Inomata 《Pediatric transplantation》2016,20(6):840-845
We herein present the case of a four‐yr‐old boy with PA who developed AMR after ABO‐incompatible LDLT despite undergoing B cell desensitization using rituximab. Although the CD19+ lymphocyte count decreased to 0.1% nine days after the administration of rituximab, he developed a high fever which was accompanied by arthralgia due to a streptococcal infection 13 days after rituximab prophylaxis. After the clearance of the infection, he underwent ABO‐incompatible LDLT 36 days after the administration of rituximab. The CD19+ lymphocyte count just prior to LDLT was 1.2%. He developed AMR five days after LDLT, and the antidonor‐type IgM and IgG antibody titers increased to 1:1024 and 1:1024, respectively. He was treated by plasma exchange, IVIG, steroid pulse therapy, and rituximab re‐administration; however, his liver dysfunction continued. Despite intensive treatment, he died due to complicated abdominal hernia, acute renal failure, and ARDS. This case suggests that a streptococcal infection may induce the activation of innate immune responses; thus, additional desensitization therapy should be considered prior to ABO‐incompatible LDLT if B cell reactivation is suspected. 相似文献
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Ryuichi Tsujita Maho Tsubota Yusuke Hayashi Haruka Saeki Fumiko Sekiguchi Atsufumi Kawabata 《Journal of neuroimmune pharmacology》2018,13(2):179-188
High mobility group box 1 (HMGB1), a nuclear protein, once released into the extracellular space under pathological conditions, plays a pronociceptive role in redox-dependent distinct active forms, all-thiol HMGB1 (at-HMGB1) and disulfide HMGB1 (ds-HMGB1), that accelerate nociception through the receptor for advanced glycation endproducts (RAGE) and Toll-like receptor 4 (TLR4), respectively. Thrombomodulin (TM), an endothelial membrane protein, and soluble TM, known as TMα, promote thrombin-mediated activation of protein C and also sequester HMGB1, which might facilitate thrombin degradation of HMGB1. The present study aimed at clarifying the role of thrombin in TMα-induced suppression of peripheral HMGB1-dependent allodynia in mice. Thrombin-induced degradation of at-HMGB1 and ds-HMGB1 was accelerated by TMα in vitro. Intraplantar (i.pl.) injection of bovine thymus-derived HMGB1 in an unknown redox state, at-HMGB1, ds-HMGB1 or lipopolysaccharide (LPS), known to cause HMGB1 secretion, produced long-lasting mechanical allodynia in mice, as assessed by von Frey test. TMα, when preadministered i.pl., prevented the allodynia caused by bovine thymus-derived HMGB1, at-HMGB1, ds-HMGB1 or LPS, in a dose-dependent manner. The TMα-induced suppression of the allodynia following i.pl. at-HMGB1, ds-HMGB1 or LPS was abolished by systemic preadministration of argatroban, a thrombin-inhibiting agent, and accelerated by i.pl. co-administered thrombin. Our data clearly indicate that TMα is capable of promoting the thrombin-induced degradation of both at-HMGB1 and ds-HMGB1, and suppresses the allodynia caused by either HMGB1 in a thrombin-dependent manner. Considering the emerging role of HMGB1 in distinct pathological pain models, the present study suggests the therapeutic usefulness of TMα for treatment of intractable and/or persistent pain. 相似文献