記述言語：英語   掲載種別：研究論文（学術雑誌）  

Objective The admission glucose level is a predictor of mortality even in patients with acute pulmonary embolism (APE). However, whether or not the admission glucose level is associated with the severity of APE itself or the underlying disease of APE is unclear. Methods This study was a retrospective observational study. A pulmonary artery (PA) catheter was used to accurately evaluate the severity of APE. The percentage changes in the mean PA pressure (PAPm) upon placement and removal of the inferior vena cava filter (IVCF) were evaluated. We hypothesized that the admission glucose level was associated with the improvement in the PA pressure in patients with APE. Patients A total of consecutive 22 patients with submassive APE who underwent temporary or retrievable IVCF insertion on admission and repetitive PA catheter measurements upon placement and removal of IVCFs were enrolled. Results There was a significant positive correlation between the admission glucose levels and the percentage changes in the PAPm (r=0.543, p=0.009). A univariate linear regression analysis showed that the admission glucose level was the predictor of the percentage change in PAPm (β coefficient=0.169 per 1 mg/dL; 95% confidence interval, 0.047-0.291; p=0.009). A multivariate linear regression analysis with the forced inclusion model showed that the admission glucose level was the predictor of the percentage change in PAPm independent of diabetes mellitus, PAPm on admission, troponin positivity, and brain natriuretic peptide level (all p<0.05). Conclusion The admission glucose level was associated with the improvement in the PAPm in patients with submassive-type APE.

DOI： 10.2169/internalmedicine.9473-17

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Contrast-induced nephropathy (CIN) is associated with poor outcomes in patients with acute myocardial infarction. However, the predictors of CIN have yet to be fully elucidated. METHODS AND RESULTS: The study included 273 consecutive patients with a first-time ST-segment elevation myocardial infarction who underwent reperfusion within 12 hours of symptom onset. The exclusion criteria were hemodialysis, mechanical ventilation, or previous coronary artery bypass grafting. All patients underwent arterial blood gas analysis soon after reperfusion. CIN was defined as an increase of 0.5 mg/dL in serum creatinine or a 25% increase from baseline between 48 and 72 hours after contrast medium exposure. Acidosis was defined as an arterial blood pH <7.35. CIN was observed in 35 patients (12.8%). Multivariable logistic regression analysis with forward stepwise algorithm revealed a significant association between CIN and the following: reperfusion time, the prevalence of hypertension, peak creatine kinase-MB, high-sensitivity C-reactive protein on admission, and the incidence of acidosis (P<0.05). Multivariable logistic regression analysis revealed that the incidence of acidosis was associated with CIN when adjusted for age, male sex, body mass index, amount of contrast medium used, estimated glomerular filtration rate on admission, glucose level on admission, high-sensitivity C-reactive protein on admission, and left ventricular ejection fraction (P<0.05). Moreover, the incidence of acidosis was associated with CIN when adjusted for the Mehran CIN risk score (odds ratio: 2.229, P=0.049). CONCLUSIONS: The incidence of acidosis soon after reperfusion was associated with CIN in patients with a first-time ST-segment elevation myocardial infarction.

DOI： 10.1161/JAHA.117.006380

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-LISS  

Human magphinin proteins are translation products of differentially spliced transcripts from the 5' region of the human trophinin gene (TRO), whose 3' region encodes trophinin, a unique cell adhesion molecule involved in human embryo implantation. Magphinins belong to the MACE (melanoma-associated antigen) family, and a previous study of mouse magphinins showed their expression in male and female germ cells, suggesting a role in germ cell development. Here, we characterized the structure and subcellular localization of human magphinins. Confocal microscopy analysis of ectopically expressed magphinins revealed that magphinin-alpha and -beta localize in the cytoplasm, whereas magphinin-gamma lacking the peptide encoded by exon-3 is nuclear. Following Triton X-100 extraction, DNA digestion, and high salt extraction magphinin-gamma remained nuclear, suggesting strong association with the nuclear matrix. A series of magphinin-gamma deletion mutants were generated and assayed for localization, which showed that the N-terminal region of the MACE homology domain is necessary for nuclear localization. When magphinin-gamma was expressed in NIH3T3 cells, cells underwent G1 arrest. These results suggest that human magphinin-gamma inhibits cell cycle progression through nuclear activity.

DOI： 10.1002/jcb.21446

Web of Science

PubMed

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

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記述言語：英語   出版者・発行元：日本成人先天性心疾患学会  

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記述言語：英語   出版者・発行元：日本成人先天性心疾患学会  

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記述言語：英語   出版者・発行元：日本成人先天性心疾患学会  

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