うっ血性心不全を合併した頻脈性上室性頻拍に対する超短時間作用型β1選択的遮断薬「ランジオロール」の効能

この博士論文は内容の要約のみの公開（または一部非公開）になっています筑波大学 (University of Tsukuba)201

Two-week administration of rivaroxaban resolved left atrial thrombus

AbstractAn 89-year-old man visited our hospital complaining of palpitation. Electrocardiography showed atrial fibrillation, and transthoracic echocardiography demonstrated a mobile thrombus of 28.6mm×20.8mm in the left atrium. Administration of a direct factor Xa inhibitor rivaroxaban (10mg/day) was started. The thrombus reduced its size and disappeared completely 2 weeks after the commencement of rivaroxaban treatment. To our knowledge, this is the first case report that rivaroxaban successfully dissolved left atrial thrombus during a short period. Rivaroxaban might have a potential, not only to prevent de novo thrombus formation, but also to dissolve established thrombi by direct inhibition of free and thrombus-associated factor Xa.<Learning objective: The incidence of nonvalvular atrial fibrillation is increasing, and left atrial thrombus is the major cause of cardiogenic thrombo-embolism that we need to prevent. Recently, novel oral anticoagulants have been developed. The effects of these agents on intracardiac thrombus resolution have not been fully elucidated. Data from a large cohort study would be required to assess efficacy of novel oral anticoagulants for thrombus resolution.

INA FOOD INDUSTRY: A COMPANY THAT MAKES EMPLOYEES HAPPY

This research illustrates how a traditional Japanese company, Ina Food Industry, focuses on talent operations, engagement, their well being and social innovation. The authors worked with key executives and talent operators from Ina Food Industry to underpin the main characteristics of their talent operations strategy and to determine how the organization draws from its corporate philosophy and core elements of traditional Japanese culture to create sustainable user engagement and to develop a unique employee value proposition. JEL Classification: M10, L6

ARE-binding protein ZFP36L1 interacts with CNOT1 to directly repress translation via a deadenylation-independent mechanism

Eukaryotic gene expression can be spatiotemporally tuned at the post-transcriptional level by cis-regulatory elements in mRNA sequences. An important example is the AU-rich element (ARE), which induces mRNA destabilization in a variety of biological contexts in mammals and can also mediate translational control. Regulation is mediated by trans-acting factors that recognize the ARE, such as Tristetraprolin (TTP) and BRF1/ZFP36L1. Although both proteins can destabilize their target mRNAs through the recruitment of the CCR4-NOT deadenylation complex, TTP also directly regulates translation. Whether ZFP36L1 can directly repress translation remains unknown. Here, we used an in vitro translation system derived from mammalian cell lines to address this key mechanistic issue in ARE regulation by ZFP36L1. Functional assays with mutant proteins reveal that ZFP36L1 can repress translation via AU-Rich elements independent of deadenylation. ZFP36L1-mediated translation repression requires interaction between ZFP36L1 and CNOT1, suggesting that it might use a repression mechanism similar to either TPP or miRISC. However, several lines of evidence suggest that the similarity ends there. Unlike, TTP, it does not efficiently interact with either 4E-HP or GIGYF2, suggesting it does not repress translation by recruiting these proteins to the mRNA cap. Moreover, ZFP36L1 could not repress ECMV-IRES driven translation and was resistant to pharmacological eIF4A inhibitor silvestrol, suggesting fundamental differences with miRISC repression via eIF4A. Collectively, our results reveal that ZFP36L1 represses translation directly and suggest that it does so via a novel mechanism distinct from other translational regulators that interact with the CCR4-NOT deadenylase complex

Acute aortic dissection with sporadic aortic calcifications during chemotherapy with sunitinib

A 66-year-old man with imatinib-resistant metastatic liver tumors of gastrointestinal stromal tumor started chemotherapy with sunitinib. Baseline computed tomography showed sporadic aortic calcifications and liver tumors (A). His systolic blood pressure increased to 160 mm Hg during chemotherapy1 and decreased to 130 mm Hg with administration of antihypertensive medication. During his sixth cycle of chemotherapy, he developed an acute aortic dissection (AAD, Stanford A) with thrombosed false lumen of the ascending aorta despite good control of blood pressure and reduction of the liver tumors (B). The entry site of the AAD was already calcified before chemotherapy as in A