Oxygen minimum zone: An important oceanographic habitat for deep-diving northern elephant seals, Mirounga angustirostris.

Little is known about the foraging behavior of top predators in the deep mesopelagic ocean. Elephant seals dive to the deep biota-poor oxygen minimum zone (OMZ) (>800 m depth) despite high diving costs in terms of energy and time, but how they successfully forage in the OMZ remains largely unknown. Assessment of their feeding rate is the key to understanding their foraging behavior, but this has been challenging. Here, we assessed the feeding rate of 14 female northern elephant seals determined by jaw motion events (JME) and dive cycle time to examine how feeding rates varied with dive depth, particularly in the OMZ. We also obtained video footage from seal-mounted videos to understand their feeding in the OMZ. While the diel vertical migration pattern was apparent for most depths of the JME, some very deep dives, beyond the normal diel depth ranges, occurred episodically during daylight hours. The midmesopelagic zone was the main foraging zone for all seals. Larger seals tended to show smaller numbers of JME and lower feeding rates than smaller seals during migration, suggesting that larger seals tended to feed on larger prey to satisfy their metabolic needs. Larger seals also dived frequently to the deep OMZ, possibly because of a greater diving ability than smaller seals, suggesting their dependency on food in the deeper depth zones. Video observations showed that seals encountered the rarely reported ragfish (Icosteus aenigmaticus) in the depths of the OMZ, which failed to show an escape response from the seals, suggesting that low oxygen concentrations might reduce prey mobility. Less mobile prey in OMZ would enhance the efficiency of foraging in this zone, especially for large seals that can dive deeper and longer. We suggest that the OMZ plays an important role in structuring the mesopelagic ecosystem and for the survival and evolution of elephant seals

Steady Rotation of Micropolar Fluid Sphere in Concentric Spherical Container

AbstractThe problem of slow steady rotation of a micropolar fluid sphere in concentric spherical container filled with viscous fluid is studied. The appropriate boundary conditions are taken on the surface of the sphere. The hydrodynamic couple and wall correction factor exerted on the micropolar fluid sphere is obtained. The dependence of the wall correction factor on the micropolarity parameter and spin parameter is presented graphically and discussed. The hydrodynamic couple acting on a solid sphere in a cell model and on a solid sphere in an unbounded medium are obtained from the present analysis

ドイツ民法典婚姻法批判にみるマリアンネ・ヴェーバーのフェミニズム思想

マックス・ヴェーバーの妻として彼の知的活動圏の中心部に位置し、その影響を強く受けていたマリアンネ・ヴェーバーは、ドイツ第二帝政期におけるフェミニズムの興隆のさなか、中産層女性運動に積極的に関与した人物でもあった。フェミニズムとマックス・ヴェーバーとの関連という問題領域に対する予備的考察として、本稿では、彼女のドイツ民法典婚姻法批判を題材に、そのフェミニズム思想の特質を把握することを目的とする。婚姻法に内在する家父長制支配原理を分析することによって、彼女は、一方ではそれが女性の外面的・内面的自立を妨げるよう作用していると批判するとともに、他方では、近代的な倫理的個人主義の発展にあたっての重要な基盤になったとも指摘する。彼女の家父長制の両面的理解を考察することによって、そのリベラル・フェミニズムの内実を明らかにする。Marianne Weber, influenced a great deal by Max Weber, her husband, participates in the german feminist movement under the German Empire. As preliminary consideration about the relation between Max Weber and feminism, this article is aimed at the understanding of her feminism. Throughout the analysis of the domination of patriarchy inherent in the Marriage Act in German Civil Code（1900）, she criticizes that it prevents women's internal and external independence, at the same time, indicates that it is based on the development of the modern ethical individualism. This article explores the essence of her liberal feminism, making it clear that she understands the system of patriarchy on both faces

グローバル市民社会の展望 : 人権と正戦の関係をめぐって

1990年代、「新しい戦争」といわれる武力紛争が各地に生じ、深刻な人権侵害が引き起こされた。それに対し国際社会は人権保護と正義の観点から「人道的介入」という名の武力行使を遂行した。本稿はこの問題をめぐって、カントを批判的に再構築しようとするハーバーマスの議論を取り上げる。彼はシュミットの正戦論批判に反論し、グローバルなレベルでの強制的実定法秩序の成立が、善－悪のコードに左右されずに法制度によって人権侵害に対処することを可能にすると主張する。とはいえ法権利を保障する国際法体系が不十分な現状では、民主的法治国家から成る「組織化された国際社会」が、世界市民的秩序の代行として人道的介入を行うことも止むを得ないと言う。しかし〈法の領域があるかのようにふるまうこと〉は〈法による保障そのもの〉と同じではない。このズレに善－悪のコードが忍び込みはしないのか。本稿ではこうしたハーバーマスの議論に潜む問題点を明らかにすることで、グローバル市民社会の規範的方向性を検討する。Since the 1990s, "the new war" violates human rights seriously in particular places. The international society conducts humanitarian intervention on grounds of the protection of human rights and justice. In relation to this, this article picks up Habermas's argument which reconstructs Kant critically. Habermas counters Carl Schmitt's criticism of just war and claims a vision of global legal law order which would be able to judge human-rights violationwith legal force. But now the international law system is not adequate, so he justifies that international community of democratic law-governed states conducts humanitarian intervention as surrogate of the future global civil society. However, behind the back of his argument, the good-bad code may be in hiding. This article explores the problem of Habermas's argument and then considers a normative vision of the global civil society

LATS1/2 kinases trigger self-renewal of cancer stem cells in aggressive oral cancer

Cancer stem cells (CSCs), which play important roles in tumor initiation and progression, are resistant to many types of therapies. However, the regulatory mechanisms underlying CSC-specific properties, including self-renewal, are poorly understood. Here, we found that LATS1/2, the core Hippo pathway-kinases, were highly expressed in the oral squamous cell carcinoma line SAS, which exhibits high capacity of CSCs, and that depletion of these kinases prevented SAS cells from forming spheres under serum-free conditions. Detailed examination of the expression and activation of LATS kinases and related proteins over a time course of sphere formation revealed that LATS1/2 were more highly expressed and markedly activated before initiation of self-renewal. Moreover, TAZ, SNAIL, CHK1/2, and Aurora-A were expressed in hierarchical, oscillating patterns during sphere formation, suggesting that the process consists of four sequential steps. Our results indicate that LATS1/2 trigger self-renewal of CSCs by regulating the Hippo pathway, the EMT, and cell division

Epithelial Splicing Regulatory Protein 1 is a Favorable Prognostic Factor in Pancreatic Cancer that Attenuates Pancreatic Metastases

Epithelial splicing regulatory protein 1 (ESRP1) binds the FGFR-2 auxiliary cis-element ISE/ISS-3, located in the intron between exon IIIb and IIIc, and primarily promotes FGFR-2 IIIb expression. Here we assessed the role of ESRP1 in pancreatic ductal adenocarcinoma (PDAC). Immunohistochemical analysis was performed using anti-ESRP1, FGFR-2 IIIb and FGFR-2 IIIc antibodies in 123 PDAC cases. ESRP1-expression vector and small interference RNA (siRNA) targeting ESRP1 were transfected into human PDAC cells, and cell growth, migration and invasion were analyzed. In vivo heterotopic and orthotopic implantations using ESRP1 overexpression clones were performed and effects on pancreatic tumor volumes and hepatic and pulmonary metastases determined. ESRP1 immunoreactivity was strong in the nuclei of cancer cells in well-to-moderately differentiated PDACs, but weak in poorly-differentiated cancers. Well-to-moderately differentiated cancers also exhibited high FGFR-2 IIIb and low FGFR-2 IIIc expression, whereas this ratio was reversed in the poorly-differentiated cancers. Increased ESRP1 expression was associated with longer survival by comparison with low-ESRP1 expression, and PANC-1 cells engineered to express ESRP1 exhibited increased FGFR-2 IIIb expression and decreased migration and invasion in vitro, whereas ESRP1 siRNA-transfected KLM-1 cells exhibited increased FGFR-2 IIIc expression and increased cell growth, migration and invasion. In vivo, ESRP1-overexpressing clones formed significantly fewer liver metastases as compared with control clones. ESRP1 regulates the expression pattern of FGFR-2 isoforms, attenuates cell growth, migration, invasion, and metastasis, and is a favorable prognostic factor in PDAC. Therefore, devising mechanisms to up-regulate ESRP1 may exert a beneficial therapeutic effect in PDAC

卵管における卵黄膜外層タンパク質の分泌部位の解析

To clarify the formation of the vitelline membrane outer layer we examined the proteins secreted from hen oviduct by using Western blotting analysis. Antibodies were elicited against vitelline membrane outer layer protein-I (VMO-I) and against the one of subunit (S 8) of ovomucim obtained from albumen. It was found that VMO-I was mostly secreted from the middle region of the infundibulum. On the contrary, S 8 was secreted from the lower region of the infundibulum over the lower region of the magnum. These findings indicated that 1) VMO-I is present in the infundibulum prior to the formation of the outer layer, 2) the chalaziferous layer is formed at the upper region in the magnum, 3) the albumen is formed at the middle region to the lower region in the magnum

Thioredoxin-1 maintains mechanistic target of rapamycin (mTOR) function during oxidative stress in cardiomyocytes

Thioredoxin 1 (Trx1) is a 12-kDa oxidoreductase that catalyzes thiol-disulfide exchange reactions to reduce proteins with disulfide bonds. As such, Trx1 helps protect the heart against stresses, such as ischemia and pressure overload. Mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that regulates cell growth, metabolism, and survival. We have shown previously that mTOR activity is increased in response to myocardial ischemia-reperfusion injury. However, whether Trx1 interacts with mTOR to preserve heart function remains unknown. Using a substrate-trapping mutant of Trx1 (Trx1C35S), we show here that mTOR is a direct interacting partner of Trx1 in the heart. In response to H2O2 treatment in cardiomyocytes, mTOR exhibited a high molecular weight shift in non-reducing SDS-PAGE in a 2-mercaptoethanol-sensitive manner, suggesting that mTOR is oxidized and forms disulfide bonds with itself or other proteins. The mTOR oxidation was accompanied by reduced phosphorylation of endogenous substrates, such as S6 kinase (S6K) and 4E-binding protein 1 (4E-BP1) in cardiomyocytes. Immune complex kinase assays disclosed that H2O2 treatment diminished mTOR kinase activity, indicating that mTOR is inhibited by oxidation. Of note, Trx1 overexpression attenuated both H2O2-mediated mTOR oxidation and inhibition, whereas Trx1 knockdown increased mTOR oxidation and inhibition. Moreover, Trx1 normalized H2O2-induced down-regulation of metabolic genes and stimulation of cell death, and an mTOR inhibitor abolished Trx1-mediated rescue of gene expression. H2O2-induced oxidation and inhibition of mTOR were attenuated when Cys-1483 of mTOR was mutated to phenylalanine. These results suggest that Trx1 protects cardiomyocytes against stress by reducing mTOR at Cys-1483, thereby preserving the activity of mTOR and inhibiting cell death

Neonatal Lethality in Knockout Mice Expressing the Kinase-Dead Form of the Gefitinib Target GAK Is Caused by Pulmonary Dysfunction

Gefitinib (Iressa) is an inhibitor of the epidermal growth factor receptor (EGFR) that has shown promising activity in the treatment of patients with non-small cell lung cancer (NSCLC). However, adverse side effects of gefitinib treatment, such as respiratory dysfunction, have limited the therapeutic benefit of this targeting strategy. The present results show that this adverse effect can be attributed to the inhibition of the novel gefitinib target GAK (Cyclin G-associated kinase), which is as potently inhibited by the drug as the tyrosine kinase activity of EGFR. Knockout mice expressing the kinase-dead form of GAK (GAK-kd) died within 30 min after birth primarily due to respiratory dysfunction. Immunohistochemical analysis revealed that surfactant protein A (SP-A) was abundant within alveolar spaces in GAK-kd+/+ mice but not in GAK-kd-/- pups. E-cadherin and phosphorylated EGFR signals were also abnormal, suggesting the presence of flat alveolar cells with thin junctions. These results suggest that inhibition of GAK by gefitinib may cause pulmonary alveolar dysfunction, and the present study may help prevent side effects associated with gefitinib therapy in NSCLC patients