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排序方式: 共有391条查询结果,搜索用时 15 毫秒
81.
82.
Felipe A. de Oliveira Mohamed H. Shahin Yan Gong Caitrin W. McDonough Amber L. Beitelshees John G. Gums Arlene B. Chapman Eric Boerwinkle Stephen T. Turner Reginald F. Frye Oliver Fiehn Rima Kaddurah-Daouk Julie A. Johnson Rhonda M. Cooper-DeHoff 《Metabolomics : Official journal of the Metabolomic Society》2016,12(8):129
Introduction
While atenolol is an effective antihypertensive agent, its use is also associated with adverse events including hyperglycemia and incident diabetes that may offset the benefits of blood pressure lowering. By combining metabolomic and genomic data acquired from hypertensive individuals treated with atenolol, it may be possible to better understand the pathways that most impact the development of an adverse glycemic state.Objective
To identify biomarkers that can help predict susceptibility to blood glucose excursions during exposure to atenolol.Methods
Plasma samples acquired from 234 Caucasian participants treated with atenolol in the Pharmacogenomic Evaluation of Antihypertensive Responses trial were analyzed by gas chromatography Time-Of-Flight Mass Spectroscopy. Metabolomics and genomics data were integrated by first correlating participant’s metabolomic profiles to change in glucose after treatment with atenolol, and then incorporating genotype information from genes involved in metabolite pathways associated with glucose response.Results
Our findings indicate that the baseline level of β-alanine was associated with glucose change after treatment with atenolol (Q = 0.007, β = 2.97 mg/dL). Analysis of genomic data revealed that carriers of the G allele for SNP rs2669429 in gene DPYS, which codes for dihydropyrimidinase, an enzyme involved in β-alanine formation, had significantly higher glucose levels after treatment with atenolol when compared with non-carriers (Q = 0.05, β = 2.76 mg/dL). This finding was replicated in participants who received atenolol as an add-on therapy (P = 0.04, β = 1.86 mg/dL).Conclusion
These results suggest that β-alanine and rs2669429 may be predictors of atenolol-induced hyperglycemia in Caucasian individuals and further investigation is warranted.83.
Rapid Assay for In Situ Identification of Coagulase-Positive Staphylococci Recovered by Membrane Filtration from Swimming Pool Water
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A rapid, in situ thermonuclease test that identifies colonies of Staphylococcus aureus among staphylococci isolated from swimming pool water by membrane filtration recovery on various selective and differential media is described. 相似文献
84.
Summary Seven species of cestodes and two of nematodes are reported from Phoeniconaias minor from Lake Nakuru, Kenya.
Phoenicolepis nakurensis n.g., n.sp. (Hymenolepididae) is characterized by the size and shape of the hooks, scolex and strobila, structure of the terminal genital ducts, presence of an accessory sac, external seminal vesicle and stylet, and absence of an internal seminal vesicle. Gynandrotaenia stammeri. Cladogynia phoeniconaiadis, Flamingolepis tengizi, F. dolguschini and Striatofilaria phoenicopteri are redescribed; all except C. phoeniconaiadis are new for this host and for Kenya. ac]19800210Abbreviations as
accessory sac
- c
cirrus
- cs
cirrus sac
- esv
external seminal vesicle
- g
gland cells
- gs
glandular sheath
- isv
internal seminal vesicle
- md
muscular duct
- Mg
Mehlis' gland
- o
ovary
- pg
prostate gland cells
- s
stylet
- sr
seminal receptacle
- u
uterus
- v
vagina
- vd
vas deferens
- vg
vitelline gland 相似文献
85.
86.
The phase behavior of bovine rod outer segment disk lipids has been investigated using freeze-fracture and 31P nuclear magnetic resonance (NMR) techniques. 31P-NMR spectra of isolated disk membranes were taken as a function of temperature between 25°C and 45°C. The 31P-NMR spectrum characteristic of phospholipid bilayers was observed at all temperatures both in the absence of Ca2+ and in the presence of 10 mM and 50 mM Ca2+. A similar study was performed on lipids isolated from the disk membranes. In the absence of Ca2+ only lamellar phase behavior was observed. In the presence of less than 10 mM Ca2+, however, there was a change in morphology to non-lamellar structures. Removal of the Ca2+ caused the system to reassume the lamellar form. 相似文献
87.
88.
89.
New strategies for combating multidrug-resistant bacteria 总被引:2,自引:0,他引:2
Antibiotic resistance is a problem that continues to challenge the healthcare sector. In particular, multidrug resistance is now common in familiar pathogens such as Staphylococcus aureus and Mycobacterium tuberculosis, as well as emerging pathogens such as Acinetobacter baumannii. New antibiotics and new therapeutic strategies are needed to address this challenge. Advances in identifying new sources of antibiotic natural products and expanding antibiotic chemical diversity are providing chemical leads for new drugs. Inhibitors of resistance mechanisms and microbial virulence are orthogonal strategies that are also generating new chemicals that can extend the life of existing antibiotics. This new chemistry, coupled with a growing understanding of the mechanisms, origins and distribution of antibiotic resistance, position us to tackle the challenges of antibiotic resistance in the 21st century. 相似文献
90.
Tarrio ML Grabie N Bu DX Sharpe AH Lichtman AH 《Journal of immunology (Baltimore, Md. : 1950)》2012,188(10):4876-4884
PD-1, a member of the CD28 family of immune regulatory molecules, is expressed on activated T cells, interacts with its ligands, PD-L1/B7-H1 and PD-L2/B7-DC, on other cells, and delivers inhibitory signals to the T cell. We studied the role of this pathway in modulating autoreactive T cell responses in two models of myocarditis. In a CD8(+) T cell-mediated adoptive transfer model, we found that compared with Pd1(+/+) CD8(+) T cells, Pd1(-/-) CD8(+) T cells cause enhanced disease, with increased inflammatory infiltrate, particularly rich in neutrophils. Additionally, we show enhanced proliferation in vivo and enhanced cytotoxic activity of PD-1-deficient T lymphocytes against myocardial endothelial cells in vitro. In experimental autoimmune myocarditis, a disease model dependent on CD4(+) T cells, we show that mice lacking PD-1 develop enhanced disease compared with wild-type mice. PD-1-deficient mice displayed increased inflammation, enhanced serum markers of myocardial damage, and an increased infiltration of inflammatory cells, including CD8(+) T cells. Together, these studies show that PD-1 plays an important role in limiting T cell responses in the heart. 相似文献