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Satoko Kojima Kei Kawana Kensuke Tomio Aki Yamashita Ayumi Taguchi Shiho Miura Katsuyuki Adachi Takeshi Nagamatsu Kazunori Nagasaka Yoko Matsumoto Takahide Arimoto Katsutoshi Oda Osamu Wada‐Hiraike Tetsu Yano Yuji Taketani Tomoyuki Fujii Danny J. Schust Shiro Kozuma 《American journal of reproductive immunology (New York, N.Y. : 1989)》2013,69(2):134-141
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Yoshinao Asahi Ryosuke Fujii Naoko Usui Hajime Kagamiuchi Shiro Omichi Junichiro Kotani 《Anesthesia progress》2015,62(2):71-73
Noonan syndrome (NS) is an autosomal dominant disorder characterized by facial anomalies, short stature, chest deformity, congenital heart diseases, and other comorbidities. The challenges faced during anesthetic management of patients with NS could be due to congenital heart diseases, hemostatic disorders, and airway anomalies. Here we describe dental treatment under general anesthesia performed for a 28-year-old man with NS. He had characteristic features of NS along with mild pulmonary valve stenosis. Dental treatment under general anesthesia was performed successfully on 13 occasions with nasotracheal intubation under curve-tipped suction catheter guidance or insertion of a reinforced laryngeal mask airway. This case suggests that for patients with NS, who might present several challenges, dental anesthesiologists should consider the extent of the patient''s disorders to enable them to perform dental treatment safely under general anesthesia.Key Words: Repeated general anesthesia, Noonan syndromeNoonan syndrome (NS) is an autosomal dominant disorder and was first reported by Noonan and Ehmke.1 The primary features of this multisystem disorder include hypertelorism, low-set ears, down-slanting eyes, a webbed neck, congenital heart diseases, short stature, chest deformity, and intellectual impairment.2,3 NS affects males and females equally and has an estimated incidence of 1 in 1000 to 1 in 2500 live births.2,4The challenges faced during anesthetic management of patients with NS could be due to congenital heart diseases, hemostatic disorders, and airway anomalies.5–8 The present report describes repeated administration of general anesthesia performed by adopting nasotracheal intubation or reinforced laryngeal mask airway insertion for a patient with NS at the time of dental treatment in our hospital. 相似文献
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Prognostic factors of recurrent disease in upper urinary tract urothelial cancer after radical nephroureterectomy: Subanalysis of the multi‐institutional national database of the Japanese Urological Association 下载免费PDF全文
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Ishibashi M Hiasa K Zhao Q Inoue S Ohtani K Kitamoto S Tsuchihashi M Sugaya T Charo IF Kura S Tsuzuki T Ishibashi T Takeshita A Egashira K 《Circulation research》2004,94(9):1203-1210
Activated monocytes are present in the arterial walls of hypertensive patients and animals. Monocyte chemoattractant protein-1 (MCP-1), which controls monocyte function through its receptor (CCR2), is implicated in hypertensive inflammatory changes in the arterial wall. The role of CCR2 expression on monocytes in hypertension-induced vascular remodeling, however, has not been addressed. We hypothesized that CCR2 on monocytes is critical in hypertension-induced vascular inflammation and remodeling. Hypertension was induced by infusion of angiotensin II (Ang II) into wild-type mice, CCR2-deficient (CCR2-/-) mice, and bone marrow-transferred mice with a leukocyte-selective CCR2 deficiency (BMT-CCR2-/-). In wild-type mice, Ang II increased CCR2 intensity in circulating monocytes, which was prevented by an Ang II type-1 (AT1) receptor blocker or blunted in AT1 receptor-deficient mice. Enhanced CCR2 intensity on monocytes was observed in hypertensive patients and rats, and was reduced by treatment with the Ang II receptor blocker, supporting the clinical relevance of the observation in mice. In CCR2-/- and BMT-CCR2-/- mice, Ang II-induced vascular inflammation and vascular remodeling (aortic wall thickening and fibrosis) were blunted as compared with control mice. In contrast, Ang II-induced left ventricular hypertrophy developed in CCR2-/- and BMT-CCR2-/- mice. The present study suggests that CCR2 expression in monocytes has a critical role in vascular inflammation and remodeling in Ang II-induced hypertension, and possibly in other forms of hypertension. 相似文献
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Mitsumori Kawaminami Seishi Etoh Hiroko Miyaoka Mina Sakai Mayumi Nishida Shiro Kurusu Inoru Hashimoto 《Neuroendocrinology》2002,75(1):2-11
Our previous studies on annexin 5, a member of the annexin family of proteins, have shown its expression in the anterior pituitary gland, its preferential distribution in gonadotropes, and its increase after ovariectomy. In the present study, we examined (1) whether annexin 5 is synthesized in gonadotropes, (2) whether its expression is under the control of gonadotropin-releasing hormone (GnRH), and (3) the effect of annexin 5 on gonadotropin release. Large cells, also called castration cells, appeared in anterior pituitary tissue 3 weeks after ovariectomy. These cells have been confirmed to be hyperfunctioning gonadotropes and are easily discriminated from other pituitary cells without immunostaining. Using in situ hybridization with a digoxigenin-labeled ribonucleic acid probe, enhanced expression of annexin 5 messenger ribonucleic acid (mRNA) in these gonadotropes was clearly demonstrated. Northern blot analysis showed an increase in the level of annexin 5 mRNA expression 3 weeks after ovariectomy. It was lessened 3 h after the injection of Cetrorelix (GnRH antagonist, 10 microg i.v.). Administration of a GnRH analog [GnRHa; Des-Gly 10 (Pro9) GnRH ethylamide, 0.2 ml of 2.5 microg/ml saline ten times intraperitoneally at 30-min intervals] significantly increased pituitary annexin 5 mRNA. In primary cultures of anterior pituitary cells, recombinant rat annexin 5 stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release in a dose-dependent manner. Concomitant administration of annexin 5 (1 microg/ml) and GnRHa augmented the LH and FSH release induced by GnRHa. After a 1-hour incubation, cycloheximide (10 microg/ml) apparently inhibited the LH response to GnRHa, while annexin 5 (2 microg/ml) moderated this inhibition. Further, the antisense oligodeoxynucleotide to annexin 5 mRNA blunted the LH response to GnRHa. It is thus concluded that annexin 5 is synthesized in the gonadotropes under the effect of GnRH, and it is suggested that annexin 5 synthesis mediates at least partly GnRH receptor signaling to stimulate gonadotropin secretion. 相似文献