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21.
In this study, the role of the classroom instructor was redefined from a "lecturer" responsible for delivering the core curriculum to a "facilitator" at the center of an active learning environment. Web-based lectures were used to provide foundation content to students outside of the classroom, which made it possible to improve the quality of student-faculty contact time in the classroom. Students reported that this hybrid format of instruction afforded them a better understanding of the content, a higher probability of retaining the content, and the opportunity to spend more time thinking about the application of the content compared with more traditional lecture-based methods of instruction. 相似文献
22.
Kevin G. Soucy David O. Attarzadeh Raghav Ramachandran Patricia A. Soucy Lewis H. Romer Artin A. Shoukas Dan E. Berkowitz 《Radiation and environmental biophysics》2010,49(3):397-404
Radiation exposure can increase the risk for many non-malignant physiological complications, including cardiovascular disease.
We have previously demonstrated that ionizing radiation can induce endothelial dysfunction, which contributes to increased
vascular stiffness. In this study, we demonstrate that gamma radiation exposure reduced endothelial cell viability or proliferative
capacity using an in vitro aortic angiogenesis assay. Segments of mouse aorta were embedded in a Matrigel-media matrix 1 day
after mice received whole-body gamma irradiation between 0 and 20 Gy. Using three-dimensional phase contrast microscopy, we
quantified cellular outgrowth from the aorta. Through fluorescent imaging of embedded aortas from Tie2GFP transgenic mice,
we determined that the cellular outgrowth is primarily of endothelial cell origin. Significantly less endothelial cell outgrowth
was observed in aortas of mice receiving radiation of 5, 10, and 20 Gy radiation, suggesting radiation-induced endothelial
injury. Following 0.5 and 1 Gy doses of whole-body irradiation, reduced outgrowth was still detected. Furthermore, outgrowth
was not affected by the location of the aortic segments excised along the descending aorta. In conclusion, a single exposure
to gamma radiation significantly reduces endothelial cell outgrowth in a dose-dependent manner. Consequently, radiation exposure
may inhibit re-endothelialization or angiogenesis after a vascular injury, which would impede vascular recovery. 相似文献
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24.
Reyes-Alvarado Luis C. Hatzikioseyian Artin Rene Eldon R. Houbron Eric Rustrian Elena Esposito Giovanni Lens Piet N. L. 《Bioprocess and biosystems engineering》2018,41(12):1869-1882
Bioprocess and Biosystems Engineering - Biological reduction of sulphate at low hydraulic retention time (HRT) is presented in this paper. A sulphidogenic inverse fluidized-bed bioreactor (IFBB)... 相似文献
25.
Background
And Objectives: The aim of this retrospective investigation was to study the relationships among chronic kidney disease, acute kidney injury (AKI), and potential benefits by post-bypass dexmedetomidine use in patients undergoing cardiac surgery.Methods
The patient data were reviewed from the institutional Society of Thoracic Surgeons National Adult Cardiac Surgery Database after IRB approval. 1,133 patients were identified and divided into two groups: those who received dexmedetomidine or those who did not during the post-bypass period. The postoperative outcomes include the incidence of AKI, any complication and all cause of mortality.Results
Post-bypass dexmedetomidine use was associated with significantly reduced the incidence of total AKI (26.1% vs. 33.75%; adjusted OR, 0.7033; 95%CI, 0.540 to 0.916; p=0.0089). In addition, post-bypass dexmedetomidine use was more likely to reduce the incidence of AKI in these patients with preoperative normal kidney function (Stage1; 32.8% to 22.8%; p=0.0233) and mild CKD (Stage 2; 32.8% to 24.7; p=0.0003) after cardiac surgery. Post-bypass infusion of dexmedetomidine was associated with significantly reduced incidence of any complication and 30-day mortalities.Conclusions
Post-bypass dexmedetomidine use is associated with a significant reduction in the incidence of AKI, especially mild AKI in patients with preoperative normal renal function and mild CKD undergoing cardiac surgery. 相似文献26.
Lim HK Lim HK Ryoo S Benjo A Shuleri K Miriel V Baraban E Camara A Soucy K Nyhan D Shoukas A Berkowitz DE 《American journal of physiology. Heart and circulatory physiology》2007,293(6):H3317-H3324
Emerging evidence supports the idea that arginase, expressed in the vascular endothelial cells of humans and other species, modulates endothelial nitric oxide (NO) synthase-3 (NOS-3) activity by regulating intracellular L-arginine bioavailability. Arginase II is thought to be expressed in the mitochondria of a variety of nonendothelial cells, whereas arginase I is known to be confined to the cytosol of hepatic and other cells. The isoforms that regulate NOS-3 and their subcellular distribution, however, remain incompletely characterized. We therefore tested the hypothesis that arginase II is confined to the mitochondria and that mitochondrial arginase II reciprocally regulates vascular endothelial NO production. Western blot analysis, immunocytochemistry with MitoTracker, and immunoelectron microscopy confirmed that arginase II is confined predominantly but not exclusively to the mitochondria. Arginase activity was significantly decreased, whereas NO production was significantly increased in the aorta and isolated endothelial cells from arginase II knockout (ArgII(-/-)) mice compared with wild-type (WT) mice. The vasorelaxation response to acetylcholine (ACh) was markedly enhanced and the vasoconstrictor response to phenylephrine (PE) attenuated in ArgII(-/-) in pressurized mouse carotid arteries. Furthermore, inhibition of NOS-3 by N(G)-nitro-L-arginine methyl ester (L-NAME) impaired ACh response and restored the PE response to that observed in WT vessels. Vascular stiffness, as assessed by pulse wave velocity (PWV), was significantly decreased in ArgII(-/-) compared with WT mice. On the other hand, 14 days of oral L-NAME treatment significantly increased PWV in both WT and ArgII(-/-) mice, such that they were not significantly different from one another. These data suggest that arginase II is predominantly confined to the mitochondria and that this mitochondrial arginase II regulates NO production, vascular endothelial function, and vascular stiffness by modulating NOS-3 activity. 相似文献
27.
Mindy I. Davis Stefan Gross Min Shen Kimberly S. Straley Rajan Pragani Wendy A. Lea Janeta Popovici-Muller Byron DeLaBarre Erin Artin Natasha Thorne Douglas S. Auld Zhuyin Li Lenny Dang Matthew B. Boxer Anton Simeonov 《The Journal of biological chemistry》2014,289(20):13717-13725
Two mutant forms (R132H and R132C) of isocitrate dehydrogenase 1 (IDH1) have been associated with a number of cancers including glioblastoma and acute myeloid leukemia. These mutations confer a neomorphic activity of 2-hydroxyglutarate (2-HG) production, and 2-HG has previously been implicated as an oncometabolite. Inhibitors of mutant IDH1 can potentially be used to treat these diseases. In this study, we investigated the mechanism of action of a newly discovered inhibitor, ML309, using biochemical, cellular, and biophysical approaches. Substrate binding and product inhibition studies helped to further elucidate the IDH1 R132H catalytic cycle. This rapidly equilibrating inhibitor is active in both biochemical and cellular assays. The (+) isomer is active (IC50 = 68 nm), whereas the (−) isomer is over 400-fold less active (IC50 = 29 μm) for IDH1 R132H inhibition. IDH1 R132C was similarly inhibited by (+)-ML309. WT IDH1 was largely unaffected by (+)-ML309 (IC50 >36 μm). Kinetic analyses combined with microscale thermophoresis and surface plasmon resonance indicate that this reversible inhibitor binds to IDH1 R132H competitively with respect to α-ketoglutarate and uncompetitively with respect to NADPH. A reaction scheme for IDH1 R132H inhibition by ML309 is proposed in which ML309 binds to IDH1 R132H after formation of the IDH1 R132H NADPH complex. ML309 was also able to inhibit 2-HG production in a glioblastoma cell line (IC50 = 250 nm) and had minimal cytotoxicity. In the presence of racemic ML309, 2-HG levels drop rapidly. This drop was sustained until 48 h, at which point the compound was washed out and 2-HG levels recovered. 相似文献
28.
Richard B. Rothman Artin Mahboubi Victor Bykov Chong-Ho Kim Brian R. de Costa Arthur E. Jacobson Kenner C. Rice 《Peptides》1992,13(6):1137-1143
Previous studies delineated two classes of δ binding sites; a δ binding site not associated with the opioid receptor complex, termed the δncx site, and a δ site associated with the opioid receptor complex, termed the δcx site. The δncx site has high affinity for [
-Pen2,
-Pen5]enkephalin, and is synonymous with what is now identified as the δ1 binding site. Pretreatment of membranes with the δ-selective acylating agents FIT, or (+)-trans-SUPERFIT, deplete membranes of the δncx binding site, which permits the selective labeling of the δcx binding site with [3H][
-Ala2,Leu5]enkephalin. The present study compared the properties of the δcx binding site present in brain membranes pretreated with (+)-trans-SUPERFIT with the properties of the δcx site present in untreated membranes. The major findings are: 1) pretreatment of membranes with (+)-trans-SUPERFIT decreased the IC50 values of δ-preferring drugs, and increased the IC50 values of μ-preferring drugs, for the δcx binding site; 2) the degree of δ selectivity was highly correlated with the magnitude of the (+)-trans-SUPERFIT-induced shift in the IC50 values; 3) the ligand-selectivity patterns of the μ and δcx sites present in (+)-trans-SUPERFIT-pretreated membranes were poorly correlated; 4) whereas μ-preferring drugs were noncompetitive inhibitors of [3H][
-Ala2,Leu5]enkephalin binding to the δcx site, δ-preferring drugs were competitive inhibitors. Viewed collectively, these data support the hypothesis that the μ and δcx binding sites are distinct, provide additional evidence for δ receptor heterogeneity, and suggest that ( (+)-trans-SUPERFIT-pretreated membranes will provide a useful preparation for studying the δcx binding site. 相似文献