18,927 research outputs found
Erratum: Noninvasive Measurements and FEM Analyses for Estimating the Rotor Bar-Lamination Contact Resistance (IEEE Trans. Ind. Appl. (2021) 57: 1 (208-217) DOI: 10.1109/tia.2020.3028347)
No full textIn [1], the correct author affiliations should read: Z. Gmyrek is with the Institute of Mechatronics and Information Systems, Lodz University of Technology, Lodz 90-924, Poland (e-mail: [email protected]). S. Vaschetto, M. Ahmadi Darmani, and A. Cavagnino are with the Politecnico di Torino, Dipartimento Energia, Turin 10129, Italy (e-mail: [email protected]; [email protected]; andrea. [email protected])
Lyman break galaxies and the star formation rate of the Universe at z ~ 6
No full textWe determine the space density of UV-luminous starburst galaxies at z≈ 6 using deep HST ACS SDSS-i′ (F775W) and SDSS-z′ (F850LP) and VLT ISAAC J and Ks band imaging of the Chandra Deep Field South. We find eight galaxies and one star with (i′−z′) > 1.5 to a depth of z′AB= 25.6 (an 8σ detection in each of the 3 available ACS epochs). This corresponds to an unobscured star formation rate of ≈15 h−270 M⊙ yr−1 at z= 5.9, equivalent to L* for the Lyman-break population at z= 3–4 (ΩΛ= 0.7, ΩM= 0.3). We are sensitive to star-forming galaxies at 5.6 ≲z≲ 7.0 with an effective comoving volume of ≈1.8 × 105h−370 Mpc3 after accounting for incompleteness at the higher redshifts due to luminosity bias. This volume should encompass the primeval subgalactic-scale fragments of the progenitors of about a thousand L* galaxies at the current epoch. We determine a volume-averaged global star formation rate of (6.7 ± 2.7) × 10−4h70 M⊙ yr−1 Mpc−3 at z∼ 6 from rest-frame UV selected starbursts at the bright end of the luminosity function: this is a lower limit because of dust obscuration and galaxies below our sensitivity limit. This measurement shows that at z∼ 6 the star formation density at the bright end is a factor of ∼6 times less than that determined by Steidel et al. for a comparable sample of UV-selected galaxies at z= 3–4, and so extends our knowledge of the star formation history of the Universe to earlier times than previous work and into the epoch where reionization may have occurred
Transition to turbulence in a qblique shock-wave/boundary-layer interaction at M=15
No full textDirect numerical simulations are carried out for different forcing techniques to trigger transition during the interaction between an oblique shock-wave and a laminar boundary-layer at M = 1.5. Three forcing methods are used: a) forcing of oblique unstable modes, whose shape and behaviour are determined by the local linear stability theory, b) broadband free-stream acoustic disturbances, and c) a cold plasma flow control device. While the oblique-mode breakdown is dominant for low-amplitude forcing, long streaky structures drive the transition process in a high-amplitude disturbance environment. LES are also performed on the experimental setup by the Institute of Theoretical and Applied Mechanics (ITAM) from Novosibirsk State University with cold plasma actuation. As well as the disturbance type, the effect of Reynolds number and forcing amplitude will be investigated
Dynamical simulation of heavy-ion collisions in the energy range from a few tens MeV/A to a few hundreds MeV/A
No full textThe overlapping stage of heavy-ion reactions can be simulated by dynamical microscopical models, such as those built on the basis of the Molecular Dynamics (MD) approaches, allowing to study the fragment formation process. The present performances of the Quantum MD (QMD) code developed at the University of Milano are discussed, showing results concerning fragment and particle production at bombarding energies up to \lsim 700 MeV/A, as well as a preliminary analysis on the isoscaling behaviour of isotopic yield ratios for reactions with isospin composition N/Z in the (1 - 1.2) range, at a 45 MeV/A bombarding energy
Assessment of Planetary Boundary-Layer Schemes in the Weather Research and Forecasting Mesoscale Model Using MATERHORN Field Data
No full textThe study was aimed at understanding the deficiencies of numerical mesoscale models by comparing predictions with a new high-resolution meteorological dataset collected during the Mountain Terrain Atmospheric Modelling and Observations (MATERHORN) Program. The simulations focussed on the stable boundary layer (SBL), the predictions of which continue to be challenging. High resolution numerical simulations (0.5-km horizontal grid size) were conducted to investigate the efficacy of six planetary boundary-layer (PBL) parametrizations available in the advanced research version of the Weather Research and Forecasting model. One of the commonly used PBL schemes was modified to include eddy diffusivities that account for enhanced momentum transport compared to heat transport in the SBL, representing internal wave dynamics. All of the tested PBL schemes, including the modified scheme, showed a positive surface temperature bias. None of the PBL schemes was found to be superior in predicting the vertical wind and temperature profiles over the lowest 500 m, however two of the schemes appeared superior in capturing the lower PBL structure. The lowest model layers appear to have a significant impact on the predictions aloft. Regions of sporadic flow interactions delineated by the MATERHORN observations were poorly predicted, given such interactions are not represented in typical PBL schemes
The Benefits of Being Economics Professor A (and not Z)
No full textAlphabetic name ordering on multi-authored academic papers, which is the convention in the economics discipline and various other disciplines, is to the advantage of people whose last name initials are placed early in the alphabet. As it turns out, Professor A, who has been a first author more often than Professor Z, will have published more articles and experienced afaster growth rate over the course of her career as a result of reputation and visibility. Moreover, authors know that name ordering matters and indeed take ordering seriously: Several characteristics of an author group composition determine the decision to deviate from the default alphabetic name order to a significant extent.performance measurement, incentives, economists, name ordering
dimitrova
No full textK e y w o r d s : grehlin signaling, hormone, orexigenic, prostaglaudin, smooth muscle, tromboxane Furthermore, hormones and local mediators often change the conductivity of ion channels in the cell membrane, which can be used as sensors for proper signaling. Our pilot study showed that ghrelin reduces the iberiotoxin-sensitive Ca 2+ -activated potassium current (I K(Ca) ) elicited in freshly isolated smooth muscle cells of human mesenteric arteries via PLD-and PKCdependent mechanism (15). The sarcoplasmic reticulum is also necessary for this signaling as the blockade of sarco-endoplasmic reticulum Ca 2+ ATPase or IP 3 -activated Ca 2+ channels of internal Ca 2+ stores inhibit the effect of ghrelin on I K(Ca) In the present study, we used pharmacological tools to identify the participants of ghrelin signaling and found a second mediator involved. MATERIALS AND METHODS The investigation conformed to the 'Declaration of Helsinki' 1975Helsinki' (revised 1983. Mesenteric arteries were isolated from extracted specimens of human mesentery taken during abdominal surgery on patients -63 men aged 64.6±1.5 years and 43 women aged 59.3±1.9 -and transported to the laboratory in ice-cold saline. Half of the patients were operated for malignant growths (carcinoma sigma) and the rest -for nonmalignant conditions. Contraction studies Segments of mesenteric arteries were dissected, carefully cleaned of adipose and connective tissues and kept in ice-cold low Ca 2+ solution containing (mmol): 118 NaCl, 5 KCl, 1.2 MgCl 2 , 0.16 CaCl 2 , 10 glucose, 1.2 Na 2 HPO 4 and 24 HEPES. Arterial rings (2 mm long) were mounted on a wire-myograph for isometric tension recording DMT, model 410A (Danish Myo Technology, Aarhus, Denmark) whose chamber was filled with the same ice-cold low Ca 2+ solution. After the mounting of the vessel rings, the organ bath solution was replaced with the same solution containing 2.5 mmol CaCl 2 . The bath was heated up to 37°C and continually bubbled with carbogen (95% O 2 and 5% CO 2 ). The isometric force of contraction was recorded using the program Myodaq (DMT, Aarhus, Denmark). The arterial segments were equilibrated for 1 hour at 37°C in a buffer, which was changed at least 3 times during this equilibration period. In most experiments, the endothelium was removed by careful rubbing with a rat whisker. Then vessels were stretched to their optimal lumen diameter, corresponding to 90% of the passive diameter of the vessel at 100 mm Hg. The viability of the preparations was tested twice by application of 10 µmol noradrenaline. The integrity of the endothelium was tested with 10 µmol acetylcholine added to 10 µmol noradrenaline contracted rings. After the viability tests, the strips were contracted with 1 nmol ET-1, which produced relatively stable isometric contractions allowing the study of the effect of the increasing concentrations of ghrelin. The tension reached a steady state in about 40 minutes after the application of ET-1. Then ghrelin was applied to the bath in increasing concentrations of 10, 30, 100, 300 and 1000 nmol, i.e. starting from a value that is about 10 times higher than its plasma level. It led to a significant effect on native artery preparations (with endothelium and in the absence of TTX) at a 30-100 times higher concentration than in human circulation (11). A possible explanation of this result is that ghrelin has a low diffusion rate through the adventitia, which decreases its interaction with receptors of smooth muscle cells when applied to the bath solution. Other researchers have also used higher ghrelin concentrations while studying the effect of ghrelin on vascular preparations (12), probably due to the same reason. It is also possible that ghrelin reaches such values in the smooth muscle layer of the arterial wall due to its paracrine release from human vascular endothelium (16). Additionally, guinea pigs may have a higher plasma level of ghrelin if compared to humans or rats. The ghrelin-induced changes in tension were expressed as a percentage of the maximum tension elicited by 1 nmol ET-1. The influence of different pharmacological agents (inhibitors) on ghrelin effect was studied by means of their addition to the bath about 40 min after ET-1 application and incubated for about 30 min before the application of ghrelin. The effects of inhibitors were studied using several types in vitro preparations: i) native (untreated) preparations of small human mesenteric arteries; ii) endothelium-denuded preparations; iii) native preparations with tetrodotoxin (TTX, 300 nmol) and mainly iv) endotheliumdenuded and TTX-treated preparations. The time control preparations were equally treated, but instead of ghrelin, an equal volume of solvent (deionised water) was added at the same time intervals. The inhibitors and antagonist were applied to block (to switch off) the studied enzyme or receptor activity and not to induce a partial inhibition only. This forced us to use a higher concentration of these substances. On the other hand, the possibility of a non-specific effect of the pharmacological tools restricted us to using them in lower concentrations. Thus, the aim to choose the optimal concentration of each substance for our experiments was not easy. For almost all of the blockers, however, there are at least several studies on arterial preparations in vitro, in some cases with dose-response curves and/or tests for cross-reaction. Besides, the choice of each concentration was based on our earlier experience with a significant part of the substances used either in electrophysiological or functional studies of different vascular beds. Whole-cell patch-clamp experiments This method has been described in detail elsewhere (17). In brief, whole-cell voltage-clamp experiments were performed on single smooth muscle cells, freshly isolated from human mesenteric arteries. The arteries were cut into 3 mm long pieces and placed in 0.1 mmol Ca 2+ -containing physiological salt solution (PSS, for composition see below) warmed to 37°C and containing 1.5 mg ml -1 collagenase II, 1 mg ml -1 papain, 15 µl ml -1 elastase and 1 mg ml -1 albumin. After 30 to 35 min incubation at 37°C with continuous O 2 bubbling, the enzymes were washed away and the tissue pieces triturated 5 times in Ca 2+ -free PSS using a pipette with a small tip opening. The remainder of the tissue was put back into the enzyme-containing solution for another 5 min and then carefully washed with Ca 2+ -free PSS. Single smooth muscle cells were obtained by gentle trituration in 2 ml of the same Ca 2+ -free solution. Cells could be stored for up to 8 hours in this solution at 4-6°C. The external solution (PSS) for single-cell voltage experiments contained (in mmol): 126 NaCl, 5.6 KCl, 10 HEPES, 20 taurine, 20 glucose, 1.1 MgCl 2 , 0.8 CaCl 2 , 5 Napyruvate and pH was adjusted to 7.4 with NaOH. The same solution was used for the isolation of cells. The solutions in the recording pipette contained (in mmol): 125 KCl, 6 NaCl, 10 HEPES, 1 MgCl 2 , 3 EGTA, 0.1 ATP, 5 Na-pyruvate, 5 succinate, 5 oxalacetate, 5 glucose and 2.15 CaCl 2 to give a calculated free Ca 2+ of 200 nmol and pH was adjusted to 7.4 with KOH. Chemicals Most of the substances used for solution preparation were obtained from ICN (Irvine, CA, USA). NaOH, BSA, 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC), pertussis toxin, indomethacin, O-(octahydro-4,7-methano-1H-inden-5-yl) carbonopotassium dithioate (D-609), collagenase type II, prostaglandine F 2α (PGF 2α ), (5Z,13E) -(9S,11S,15R)-384 9,15,dihydroxy-11-fluoro-15-(2-indanyl)- Data analysis Current densities were expressed in pA/pF and plotted as functions of the potential applied to obtain data suitable for statistical analysis. The significance of differences between means was assessed using Tukey-Kramer multiple comparison test with p<0.05 regarded significant. The force of contraction was evaluated as a difference in tension (N/m) measured before ET-1 application and the plateau reached afterwards. The contractile effect of ghrelin was expressed as a percentage of the maximal ET-1 induced contraction, taken as 100%. Values were expressed as means±S.E.M. From five to ten human mesenteric arterial preparations (n) were included in the construction of each concentration-response curve of ghrelin. Data were subjected to a comparative statistical analysis one-way ANOVA with Bonferroni correction (p<0.05). RESULTS Octanoyl ghrelin, herein referred to as ghrelin, dosedependently increased the force of contraction of isometric human mesenteric artery preparations constricted with ET-1 The application of increasing doses of ghrelin to external solution containing either NCDC (50 mol) ( The application of increasing concentrations of ghrelin to TTX-and ET-1-containing bath solution failed to influence significantly the force of contraction of endothelium-denuded human mesenteric arteries in the presence of PP2 (10 µmol) -a selective Src family kinase inhibitor The addition of ghrelin (100 nmol) almost entirely inhibited the iberiotoxin-sensitive I K(Ca) recorded during a 500 ms depolarizing pulse to +40 mV from a holding potential of -50 mV (12). Rp-cAMPS (200 µmol), a specific membranepermeable inhibitor of PKA, was without effect on the total outward potassium current (I K ) (n=5), while the subsequent addition of ghrelin (100 nmol) decreased I K to the same degree as in the absence of this PKA inhibitor in single smooth muscle cells from human mesenteric arteries (n=5; p<0.01) DISCUSSION Ghrelin and des-octanoyl ghrelin are equipotent antagonists of ET-1 induced vasoconstriction of human mammary artery (13) while in single smooth muscle cells isolated from human mesenteric arteries des-octanoyl ghrelin blocks the ghrelininduced inhibition of I K(Ca) . This difference supposes the operation of more than one ghrelin receptors in human vascular beds -the des-octanoyl ghrelin-blockable GHS-R1a in human mesenteric arteries and another type in human mammary artery (for a review of ghrelin receptors see 19). Kleinz et al. (13) routinely applied indomethacin to exclude the possibility of endothelium dependent vasodilatation. This treatment however blocks not only endothelial COX1/2 but also those in the tunica media of the artery and thus eliminates the influence of COX1/2 downstream products generated in smooth muscle cells, as suggested by our study. Indeed, such a mechanism is unexpected in blood vessels but is reported in non-vascular smooth muscle (lower esophageal sphincter) that maintains mainly tonic type of contraction similarly to arteries (20). Therefore, it is still difficult to summarize the mechanisms of ghrelin effects on human arteries due to their opposite influences -relaxation and contraction, the different experimental conditions applied and the need for more detailed studies of the intracellular participants. Most often GHS-R1a interacts with heterotrimeric G q/11 proteins and stimulates the G q/11 /PI-PLC/IP 3 +Ca 2+ +DAG/PKC signaling (2). It was reported that the application of a specific PKC inhibitor entirely abolished the effect of ghrelin on I K(Ca) , recorded in single smooth muscle cells of human mesenteric arteries (15). In our study the force of contraction of human mesenteric arteries did not respond to ghrelin application if iberiotoxin or GF109203x were present in the bath solution. Thus, ghrelin requires activation of PKC and suppresses K Ca channels with a large conductance (BK Ca channels) to increase the force of contraction. Ghrelin regulates cAMP/PKA (3-5) and cGMP/PKG signaling (6), which can further influence ion channels. Han et al. (6) reported a ghrelin-induced reduction of voltage-gated I K of rat anterior pituitary tumor (GH3) cells by a PKG-dependent mechanism and Kohno et al. (21) -a ghrelin-induced activation of N-type Ca 2+ channels that required PKA. BK Ca channels are involved in the formation of the spontaneous artery tone, counteract the elevation of the agonist-induced cytosolic free Ca 2+ and participate in the relaxation induced by cAMP/PKAand cGMP/PKG-coupled agonists (22). Therefore, we investigated the participation of both cyclic nucleotides using specific inhibitors Rp-cAMPS for PKA and ODQ for soluble guanylate cyclase. The presence of inhibitors of PKA or soluble guanylate cyclase in the bath solution did not prevent the effect of ghrelin on I K(Ca) . We concluded that the second messengers cAMP and cGMP are not involved in the observed ghrelininduced inhibition of I K(Ca) . On the other hand, in human mesenteric arteries the effect of ghrelin on the force of contraction is blocked by pertussis toxin, which suggests the participation of G i -proteins. In rat islet β-cells ghrelin decreases the insulin secretion by a G αi2 -protein sensitive activation of voltage-gated K + channels and this effect is blocked by D-Lys 3 -GHRP-6, a specific GHS-R1a inhibitor (23). Ghrelin inhibits BK Ca channels in the guinea pig femoral artery via a pertussis toxin and GHS-R1a sensitive pathway (17). Ghrelin also activates G i -protein in cell cultures Ca 2+ released from sarcoplasmic reticulum activates BK Ca channels of smooth muscles cells (24). In human mesenteric arteries IP 3 -sensitive Ca 2+ release is essential for the ghrelininduced decrease of I K(Ca) (15) and for the increase of the force of contraction. Additionally, IP 3 -induced Ca 2+ release from sarcoplasmic reticulum participates in the ET-1 evoked contraction of this vascular bed. Our pharmacological studies suggest that several DAG-producing phospholipases (PI-PLC and PC-PLC) are important in establishing the effect of ghrelin in human mesenteric arteries. We presume that PI-PLC is essential mainly for triggering the contraction (25) and for the IP 3 -induced Ca 2+ release-dependent translocation of PKC to the plasma membrane, while the sustained DAG producer PC-PLC (25) is responsible for the long lasting PKC activation. This suggestion is indirectly supported by the slowly developing inhibition (in 10-14 min) of I K(Ca) by ghrelin in this tissue (15). Using different inhibitors we reveal several new enzymes participating in the ghrelin effect in human mesenteric arteries. Thus, the selective inhibition of MEK or Src kinase entirely blocks the ghrelin-induced contractions in endothelium-denuded human mesenteric arteries with suppressed neurotransmission. The nonselective COX1/2 inhibitor indomethacin eliminates either the ghrelin-induced constriction of human mesenteric arteries or the ghrelin-induced decrease of I K in single smooth muscle cells isolated from the same tissue. All these data suggest the existence of a ghrelin-induced and pertussis toxin-sensitive mechanism, which increases the force of contraction by a consequent activation of Src kinase, MEK and ERK. Similar G iprotein initiated signaling was reported for non-vascular tissues (for review see 26). Next, the stimulated ERK may activate the cytosolic PLA 2 (27), which increases vascular arachidonic acid production -the rate-limiting step for prostaglandin synthesis (28). COX1/2 transform this arachidonic acid into PGE 2 , and then PGE 2 into PGH 2 , which may further yield contracting prostaglandin or thromboxane, as reported for non-vascular smooth muscle It was reported that ghrelin receptor type GHR-R1a has the ability to oligomerize with prostanoid receptors, when they are transiently over-expressed in human embryonic kidney 293 cells (32). The same authors stated that this co-transfection significantly influenced GHR-R1a activity without changes in its affinity for ghrelin. Similarly, as an alternative explanation of our data, it is suggested that ghrelin first binds to GHS-R1a and then activates prostanoid receptor via a direct interaction in the existing GHS-R1a/prostanoid receptor heteromeric complex. If this is the case, the enzymes necessary to demonstrate the effect of ghrelin on the contractile activity (Src kinase, MEK, COX-1 and thromboxane synthase) only support the steady-state thromboxane A 2 production and are not additionally activated by ghrelin. The second explanation of our data, however, seems to be less probable as several new articles report a direct activation of ERK1/2 (3, 7, 33) and Src kinase (34) by ghrelin signaling. Ghrelin decreases the mean arterial pressure of the rat by a COX-insensitive and NOS-sensitive mechanism (35). In rat mesenteric arteries both ghrelin and desacyl ghrelin evoke endothelium-dependent dilation by NOS-and COX-insensitive mechanism (36). Ghrelin inhibits the contraction of human aortic smooth muscle cells by cAMP/PKA pathway activation (4). Ghrelin and desacyl ghrelin antagonize the ET-1-induced contraction of human internal mammary artery (13). Ghrelin decreases the mean arterial pressure in humans as well (11). On the other hand, contractile effects of ghrelin were reported in guinea pig femoral (37) and renal (17) arteries and in rat coronary artery (38). Ghrelin increases the force of contraction of human mesenteric arteries partially constricted with ET-1. The effect is stronger in endothelium-denuded preparations and most pronounced in endothelium-denuded artery segments with blocked action potential propagation of perivascular neurons. These data point to a relaxing effect of ghrelin via endothelium and axonal projections in adventitia, which antagonize the direct and stronger contractile action of ghrelin on the smooth muscle layer of the vascular wall. Additionally, if compared to native preparations during the first half of the experiments, the higher force of contractions of endothelium-denuded human mesenteric arteries suggest that endothelium, as well as perivascular neurotransmission are functional, i.e. they are not badly damaged by the therapy before the surgical intervention or during the transportation. It can be concluded that ghrelin either increases or decreases the force of contraction of arteries depending on their type and the species. Thus, ghrelin and desacyl ghrelin may influence the artery resistance similarly to other regulators of the circulation with opposite effects on different vascular beds. For example, catecholamines redistribute the blood flow throughout the body, depending on the physiological needs, via different adrenergic receptors and intracellular mechanisms. In summary, ghrelin has been shown to increase the force of contraction of human mesenteric arteries by a novel mechanism that requires active Src kinase, MEK, COX-1 and thromboxane synthase and that depends on the release of a local mediator -a T prostanoid receptor agonist. Additionally, our data suggest a novel physiological regulation, in which an empty stomachinitiated increase of ghrelin secretion reduces the abdominal circulation in adult humans until next meal. Acknowledgement
Color Stability Determination of CAD/CAM Milled and 3D Printed Acrylic Resins for Denture Bases: A Narrative Review
No full textThe aim of this paper is to review the available literature on the different methods for color stability determination of CAD/CAM milled and 3D printed resins for denture bases. The methodology included applying a search strategy, defining inclusion and exclusion criteria and selecting studies to summarize the results. Searches of PubMed, Scopus, and Embase databases were performed independently by three reviewers to gather the literature published between 1998 and 2022. A total of 186 titles were obtained from the electronic database, and the application of exclusion criteria resulted in the identification of 66 articles pertaining to the different methods for color stability determination of CAD/CAM acrylic resins for denture bases. Color change in dental materials is clinically very important for the dental operator, as it determines the clinical serviceability of the material. Discoloration of the denture bases can be evaluated with various instruments and methods. Dental resins may undergo color changes over time due to intrinsic and/or extrinsic factors. The extrinsic factors are considered the more frequent causes of color changes. According to a number of studies, CAD/CAM fabricated acrylics have achieved better color stability than the conventional PMMA (polymethyl methacrylate) resins
GUIDELINES FOR ENVIRONMENTAL PUBLIC MANAGEMENT IN BULGARIA- PERCEPTIVITY OF THE CITIZENS
No full textThe public sector has realized the importance of successful internal changes in the means of environmental management of public administrations for improving its specific policies, targets, products and services. To embed in the public sector environmental indicators can help to provide, as for the private sector, useful information concerning Earth modifications by human actions for the top decision-makers.
The aim of this study is to examine the citizen concerns and expectations by implementation of environmental public management (EPM) carried out by local authorities in Bulgaria. Based on the perceptivity of the Bulgarian citizens, also illustrated by relevant questionnaire, the authors of the present paper give some proposals about the creation of appropriate communication channels for environmental public management between institutions and citizens
Logarithmic variance profiles and the corresponding f-1 spectra of temperature fluctuations in turbulent Rayleigh-Bénard convection
No full textWe report experimental results for the temperature variance 2(z) and the corresponding frequency spectra P(f) in turbulent Rayleigh-Bénard convection (RBC) in a cylindrical sample of aspect ratioT= D/L = 1:00 (D = 1:12 m is the diameter and L = 1:12 m the height). The measurements were conducted in the Rayleigh-number range 1011 < Ra < 1:35 1014 and Pr ' 0:8. For Ra = 1:35x1014, 2(z) could be described well by a logarithmic dependence on the vertical position z in a range of z 1 < z < z 2 with z 1 ' 70 and z 2 = 0:1L. Here L=(2Nu) is the thickness of a thin thermal sublayer adjacent to the horizontal plate where the heat flux (denoted by the Nusselt number Nu) is carried mostly by thermal diffusion. In the log layer, we found that the temperature spectra had a significant frequency range over which P(f) f with close to 1. As Ra decreased, increased so that the log layer became thinner. At Ra = 2:05 1011, z 2 < z 1 and therefore there was no range for a log layer. Correspondingly, the temperature spectrum near the horizontal plate did not have the f1 scaling form either
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