Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Interplay”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,333 records · Page 74Linked to original sources
PubMedDate not supplied

The interplay between glottis and vocal tract during the male passaggio.

The transition between 'chest' and 'head' register is essential for male opera singers in order to reach the higher pitches. The 'passaggio', which is a scale passage where this transition takes place, but also a maneuver of register equalization, is typically difficult to learn. Studies on parameters for a definition of this transition are restricted to a small number of singers so far. Audio, electroglottographic, and equivalent subglottic pressure signals of 11 male opera singers were recorded while singing scales on open back vowels and passing the register transition. A spectrum analysis of the audio signal revealed that the second harmonic (H2) dominates in 'chest', resonated by the first formant (F1), together with the fourth harmonic (H4), supported by the second formant (F2). During the passaggio, H2 level decreases because it loses the resonance of F1, while the third harmonic (H3) gains the resonance of F2. At this point the H4 level drops because that harmonic is no longer supported by F2. The transition from 'chest' to 'head' register is marked by characteristic changes in the amplitude patterns of the partials H2, H3, and H4, and the frequency progressions of the first two formants, defining an objective distinction between the two registers.

Adult↗
PubMed2005

Inhibition of insulin receptor gene expression and insulin signaling by fatty acid: interplay of PKC isoforms therein.

Fatty acids are known to play a key role in promoting the loss of insulin sensitivity causing insulin resistance and type 2 diabetes. However, underlying mechanism involved here is still unclear. Incubation of rat skeletal muscle cells with palmitate followed by I(125)- insulin binding to the plasma membrane receptor preparation demonstrated a two-fold decrease in receptor occupation. In searching the cause for this reduction, we found that palmitate inhibition of insulin receptor (IR) gene expression effecting reduced amount of IR protein in skeletal muscle cells. This was followed by the inhibition of insulin-stimulated IRbeta tyrosine phosphorylation that consequently resulted inhibition of insulin receptor substrate 1 (IRS 1) and IRS 1 associated phosphatidylinositol-3 kinase (PI3 Kinase), phosphoinositide dependent kinase-1 (PDK 1) phosphorylation. PDK 1 dependent phosphorylation of PKCzeta and Akt/PKB were also inhibited by palmitate. Surprisingly, although PKCepsilon phosphorylation is PDK1 dependent, palmitate effected its constitutive phosphorylation independent of PDK1. Time kinetics study showed translocation of palmitate induced phosphorylated PKCepsilon from cell membrane to nuclear region and its possible association with the inhibition of IR gene transcription. Our study suggests one of the pathways through which fatty acid can induce insulin resistance in skeletal muscle cell.

Animals↗
PubMed1997

Interplay between glutathione-S-transferase and glucose-6-phosphate dehydrogenase in neonatal cord blood.

Three hundred neonatal cord blood samples were collected from two major cities in Jordan and assayed for glutathione-S-transferase (GST), glutathione, and glucose-6-phosphate dehydrogenase (G6PD). A significant positive correlation between the levels of G6PD and GST activities was detected. When the G6PD activity decreased, the GST activity declined. A similar concurrent decrease in the concentration of reduced glutathione was also observed. When the samples were divided into males and female samples, some significant variations in the levels of the two enzymes were observed. Female samples exhibited higher G6PD and GST activities as compared with male samples. Moreover, the incidence of severe and moderate G6PD deficiencies was higher in male as compared with female samples. Analyses of the samples for total bilirubin, red blood cells, hematocrit, and hemoglobin were also performed, and slight nonsignificant variations were noted.

Bilirubin↗
PubMed2003

Functional interplay between angiotensin II and nitric oxide: cyclic GMP as a key mediator.

Angiotensin II (Ang II) and nitric oxide (NO) signaling pathways mutually regulate each other by multiple mechanisms. Ang II regulates the expression of NO synthase and NO production, whereas NO downregulates the Ang II type I (AT1) receptor. In addition, downstream effectors of Ang II and NO signaling pathways also interact with each other. A feedback mechanism between Ang II and NO is critical for normal vascular structure and function. Imbalance of Ang II and NO has been implicated in the pathophysiology of many vascular diseases. In this review, we focus on the diverse ways in which Ang II and NO interact and the importance of the balance between the signaling pathways activated by these mediators.

Angiotensin II↗
PubMed2004

Functional interplay between the macrophage scavenger receptor class B type I and pitavastatin (NK-104).

BACKGROUND: Scavenger receptor class B type I (SR-BI), a receptor for high-density lipoprotein (HDL), plays an important role in the bidirectional cholesterol exchange between cells and HDL particles and the atherosclerotic lesion development. Enhancement of SR-BI expression significantly reduces, whereas lack of SR-BI expression accelerates, the atherosclerotic lesion development in proatherogenic mice. Statins, a class of inhibitors for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, significantly suppress de novo cholesterol synthesis and reduce the incidence of coronary heart disease. Statins also display multiple pleiotropic effects independently of cholesterol synthesis in the vascular cells. Here, we investigated the effects of pitavastatin (NK-104), a newly synthesized statin, on macrophage SR-BI expression. METHODS AND RESULTS: We found that pitavastatin significantly increased SR-BI mRNA and protein expression in a macrophage cell line in a concentration- and time-dependent manner. It also increased SR-BI expression in both mouse peritoneal and human monocyte-derived macrophages. Associated with increased SR-BI expression, pitavastatin enhanced macrophage HDL binding, uptake of [14C]cholesteryl oleate/HDL, and efflux of [3H]cholesterol to HDL. Pitavastatin abolished the inhibition of macrophage SR-BI expression by cholesterol biosynthetic intermediates. It also restored SR-BI expression inhibited by lipopolysaccharide and tumor necrosis factor-alpha through its inactivation of the transcription factor nuclear factor-kappaB. CONCLUSIONS: Our data demonstrate that pitavastatin can stimulate macrophage SR-BI expression by reduction of cholesterol biosynthetic intermediates and antiinflammatory action and suggest additional pleiotropic effects of statins by which they may reduce the incidence of coronary heart disease.

Animals↗
PubMed2005

Interplay between different polyunsaturated fatty acids and risk of coronary heart disease in men.

BACKGROUND: Consumption of polyunsaturated fatty acids (PUFAs) may reduce coronary heart disease (CHD) risk, but n-6 PUFAs may compete with n-3 PUFA metabolism and attenuate benefits. Additionally, seafood-based, long-chain n-3 PUFAs may modify the effects of plant-based, intermediate-chain n-3 PUFAs. However, the interactions of these PUFAs in relation to CHD risk are not well established. METHODS AND RESULTS: Among 45,722 men free of known cardiovascular disease in 1986, usual dietary intake was assessed at baseline and every 4 years by using validated food-frequency questionnaires. CHD incidence was prospectively ascertained. Over 14 years of follow-up, participants experienced 218 sudden deaths, 1521 nonfatal myocardial infarctions (MIs), and 2306 total CHD events (combined sudden death, other CHD deaths, and nonfatal MI). In multivariate-adjusted analyses, both long-chain and intermediate-chain n-3 PUFA intakes were associated with lower CHD risk, without modification by n-6 PUFA intake. For example, men with > or = median long-chain n-3 PUFA intake (> or =250 mg/d) had a reduced risk of sudden death whether n-6 PUFA intake was below (<11.2 g/d; hazard ratio [HR]=0.52; 95% confidence interval [CI]=0.34 to 0.79) or above (> or =11.2 g/d; HR=0.60; 95% CI=0.39 to 0.93) the median compared with men with a < median intake of both. In similar analyses, > or = median intake of intermediate-chain n-3 PUFAs (> or =1080 mg/d) was associated with a reduced total CHD risk whether n-6 PUFA intake was lower (HR=0.88; 95% CI=0.78 to 0.99) or higher (HR=0.89; 95% CI=0.79 to 0.99) compared with a < median intake of both. Intermediate-chain n-3 PUFAs were particularly associated with CHD risk when long-chain n-3 PUFA intake was very low (<100 mg/d); among these men, each 1 g/d of intermediate-chain n-3 PUFA intake was associated with an approximately 50% lower risk of nonfatal MI (HR=0.42; 95% CI=0.23 to 0.75) and total CHD (HR=0.53; 95% CI=0.34 to 0.83). CONCLUSIONS: n-3 PUFAs from both seafood and plant sources may reduce CHD risk, with little apparent influence from background n-6 PUFA intake. Plant-based n-3 PUFAs may particularly reduce CHD risk when seafood-based n-3 PUFA intake is low, which has implications for populations with low consumption or availability of fatty fish.

Adult↗
PubMed1997

Lead-induced hypertension: interplay of nitric oxide and reactive oxygen species.

An elevation of mean blood pressure was found in rats treated with low lead (0.01% lead acetate) for 3 months, as contrasted to paired Sprague-Dawley control rats. In these rats, measurement of plasma and urine endothelins-1 and -3 revealed that plasma concentration and urinary excretion of endothelin-3 increased significantly after 3 months (plasma: lead group, 31.8+/-2.2, versus controls, 23.0+1.7 pg/mL, P<.001; urinary excretion: lead group, 46.6+11.7, versus controls, 35.6+6.7 pg/24 h, P<.05), whereas endothelin-1 was unaffected. Plasma and urinary nitric oxide (NO) and cyclic GMP concentrations were not significantly changed. However, assay of plasma and kidney cortex malondialdehyde by high-pressure liquid chromatography, as a measure of reactive oxygen species, was elevated in lead-treated rats compared with that in control rats (plasma: lead group, 4.74+1.27, versus controls, 2.14+.49 micromol/L, P<.001; kidney cortex: lead group, 28.75+3.46, versus controls, 16.38+2.37 nmol/g wet weight, P<.001). There was increased NO synthase activity in lead-treated rat brain cortex and cerebellum. In lead-treated rat kidney cortex, the endothelial constitutive NO synthase protein mass was unaffected, whereas the inducible NO synthase protein mass was increased. These data suggest a balance between increased NO synthesis and degradation (by reactive oxygen species) in lead-treated rats, which results in normal levels of NO. Thus, the hypertension may be related to an increase in the pressure substances, endothelin-3 and reactive oxygen species, rather than to an absolute decrease in nitric NO.

Animals↗
PubMed2006

Connection and coordination: the interplay between architecture and dynamics in evolved model pattern generators.

We undertake a systematic study of the role of neural architecture in shaping the dynamics of evolved model pattern generators for a walking task. First, we consider the minimum number of connections necessary to achieve high performance on this task. Next, we identify architectural motifs associated with high fitness. We then examine how high-fitness architectures differ in their ability to evolve. Finally, we demonstrate the existence of distinct parameter subgroups in some architectures and show that these subgroups are characterized by differences in neuron excitabilities and connection signs.

Animals↗