Cold isostatic compaction of nano-size powders: Surface densification and dimensional asymmetry

2002 ◽  
Vol 17 (11) ◽  
pp. 2794-2801 ◽  
Author(s):  
Wenxia Li ◽  
John J. Lannutti

Cold isostatic pressing (CIP) is often used in the compaction of nano-sized powders. For technological reasons, however, uniaxial pressing prior to CIP takes place. This paper reveals the first quantitative measurements of density gradients within and the asymmetric sintering response of nanoscale zirconia compacts formed by (i) simple uniaxial compaction and (ii) specific ratios of uniaxial and CIP pressure. We find that CIP forms an exterior “skin” of higher but variable surface density and decreases the width of the density distribution. It does not eliminate density gradients; nonuniform shrinkage still occurs during sintering. The high- and low-density zones (the moving and fixed ram ends, respectively) that form during uniaxial compaction are reversed during CIP. Considering both density distribution width and spring-back cracking, the “best” uniaxial-CIP pressure combination is 1–20 ksi for this particular powder and an L/D of 1.0. The greater final compaction of the low-density zone during CIP causes relatively large variations in final dimensions (nearly 400 microns) in spite of the smaller density distribution width. The usually neglected uniaxial pressing step has definite technological impacts on the production of nanostructured components via compaction.

Blood ◽  
1984 ◽  
Vol 63 (2) ◽  
pp. 482-485 ◽  
Author(s):  
BA van Oost ◽  
AP Timmermans ◽  
JJ Sixma

Abstract The relation between platelet buoyant density and beta-thromboglobulin (beta-TG), a marker for platelet alpha-granule content, was assessed by three independent approaches. (1) Platelets were separated on iso- osmolar discontinuous Stractan density gradients into five fractions, ranging in density from 1.061 g/ml to 1.091 g/ml (20 degrees C). The beta-TG content (mean +/- SD, n = 17) increased with the platelet density from 27.8 +/- 8.6 micrograms beta-TG/10(9) cells (20% less- dense platelets) up to 65.6 +/- 15.5 micrograms beta-TG/10(9) cells (15% most-dense platelets). (2) Activation of platelets in platelet- rich plasma with thrombin, adenosine diphosphate, collagen, or epinephrine resulted in a decreased density of the platelets. This was only seen when there was simultaneous secretion of beta-TG. (3) The less-dense and the more-dense platelet fractions, after isolation by density gradient centrifugation, were separately treated with thrombin. After complete degranulation, the density distribution of the originally less-dense and more-dense platelets were identical and were much narrower than the density distribution of resting platelets.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1244-1244
Author(s):  
Mary E. Fabry ◽  
Anne C. Rybicki ◽  
Sandra M. Suzuka ◽  
M. Cherif Rahimy ◽  
Rajagopal Krishnamoorthy ◽  
...  

Abstract Red cell density distribution affects both hemolysis and vaso-occlusion; however, currently recognized factors cannot account for all of the variation seen. We hypothesized that a range of genetically controlled factors contributes to red cell density distribution and hemolysis, which has recently received a great deal of attention from Gladwin et al for its role in sickle cell anemia (SCA) and its impact on NO metabolism. Our previous studies have demonstrated that although RBC density distribution varies significantly from patient to patient, the pattern for individual patients is stable in the absence of disease. Some genetically determined factors that affect red cell density distribution have been defined, such as alpha-thalassemia and % HbF (Fabry et al, Blood, 1982); however, neither of these factors completely predicts density distribution. The study of identical twins offers the unique opportunity to minimize some of the genetic variability between individuals that may not be relevant to RBC density while allowing the remaining differences to be detected. Because SCA patients from the US have a complex mixture of Caucasian, other ethnicities, and genes from all parts of Africa including all of the sickle haplotypes, we have chosen to recruit our population from Benin that has a single beta-globin haplotype, thus further minimizing differences arising from admixture from inside and outside of Africa. We have collected samples from six sets of monozygous twins from Benin and validated their monozygosity by DNA analysis. Of the 6 twin sets analyzed to date, 4 have alpha-thalassemia. We compared density gradients on two separate occasions, approximately one year apart, for these twins and found that density gradients for both members of all twin sets without medical complications (malaria, painful crisis) were indistinguishable. This is not true for pairs of randomly chosen individuals even after their % HbF and alpha-thalassemia status has been determined and matched. After elimination of WBCs, we were able to isolate sufficient RNA to obtain microarray data without amplification. We compared subjects with a low % dense cells vs a high % dense cells. In the combinations that were analyzed, we found a consistent pattern of up- and down-regulated genes. Down-regulated genes included the Gardos channel (KCNN4), K-Cl cotransporter (KCC1), NOS3, CAIV, and PKC. Up-regulated genes included ferritin heavy chain (probably in mitochondria that are present in reticulocytes) and 2,3-bisphosphomutase that was elevated in twins with higher MCHC (density). The latter is consistent with our previous observations and those of Poillon et al that DPG can affect polymer formation and RBC density. We conclude that the study of twins demonstrates that there is a strong genetic component in the control of sickle cell density distribution and that a better understanding of factors controlling density distribution may lead to new forms of treatment.


FEBS Letters ◽  
1999 ◽  
Vol 456 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Sandrine Wouters ◽  
Etienne Decroly ◽  
Michel Vandenbranden ◽  
Daniela Shober ◽  
Renate Fuchs ◽  
...  

1997 ◽  
Vol 139 (1) ◽  
pp. 245-256 ◽  
Author(s):  
J.J. Emeis ◽  
Y. van den Eijnden-Schrauwen ◽  
C.M. van den Hoogen ◽  
W. de Priester ◽  
A. Westmuckett ◽  
...  

In previous studies we have shown that, after stimulation by a receptor ligand such as thrombin, tissue-type plasminogen activator (tPA) and von Willebrand factor (vWf) will be acutely released from human umbilical vein endothelial cells (HUVEC). However, the mechanisms involved in the secretion of these two proteins differ in some respects, suggesting that the two proteins may be stored in different secretory granules. By density gradient centrifugation of rat lung homogenates, a particle was identified that contained nearly all tPA activity and antigen. This particle had an average density of 1.11–1.12 g/ml, both in Nycodenz density gradients and in sucrose density gradients. A similar density distribution of tPA was found for a rat endothelial cell line and for HUVEC. After thrombin stimulation of HUVEC to induce tPA secretion, the amount of tPA present in high-density fractions decreased, concomitant with the release of tPA into the culture medium and a shift in the density distribution of P-selectin. vWf, known to be stored in Weibel-Palade bodies, showed an identical distribution to tPA in Nycodenz gradients. In contrast, the distribution in sucrose gradients of vWf from both rat and human lung was very different from that of tPA, suggesting that tPA and vWf were not present in the same particle. Using double-immunofluorescence staining of HUVEC, tPA- and vWf-containing particles showed a different distribution by confocal microscopy. The distribution of tPA also differed from the distribution of tissue factor pathway inhibitor, endothelin-1, and caveolin. By immunoelectronmicroscopy, immunoreactive tPA could be demonstrated in small vesicles morphologically different from the larger Weibel-Palade bodies. It is concluded that tPA in endothelial cells is stored in a not-previously-described, small and dense (d = 1.11– 1.12 g/ml) vesicle, which is different from a Weibel-Palade body.


1982 ◽  
Vol 58 (1) ◽  
pp. 44-46 ◽  
Author(s):  
S. L. Scott ◽  
J. E. Barker ◽  
I. K. Morrison ◽  
N. W. Foster

Basic wood density was measured at eight bole positions within and below the green crown in a jack pine (Pinus banksiana, Lamb.) fertilization and thinning trial near Chapleau, Ontario. Analysis showed a 6% reduction of average density in wood laid down during the first 5 years following treatment. A significant height × fertilizer interaction was noted during the same period indicating that bole density gradients specific to fertilized trees should be used to calculate biomass gains from fertilization if substantial underestimates of response are to be avoided. The portion of the bole where the wood changed most rapidly from low density, juvenile-type to higher density mature-type wood appeared to be just beneath the base of the green crown.


Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 386-393
Author(s):  
B Savage ◽  
PR McFadden ◽  
SR Hanson ◽  
LA Harker

The relationship between platelet density and platelet age has been studied using continuous linear Percoll density gradients and 111In- labeling of autologous platelets in baboons. To investigate changes in platelet density during senescence in the circulation, baboons were infused with 111In-labeled autologous platelets, and blood was collected at one hour postinfusion and twice daily thereafter for six days. Platelets were isolated from these samples in high yield (greater than 95%) and separated in continuous linear Percoll density gradients following density equilibrium centrifugation. Although at one hour postinfusion the density distribution of radiolabeled platelets coincided closely with the distribution of the total platelet population, a detectable symmetrical shift toward higher densities was observed after five days. The relative specific radioactivity (RSR) of high-density platelets (1.064 to 1.067 g/mL) decreased at a slower rate than that of the total platelet population (platelets of all densities), whereas the RSR of low-density platelets (1.053 to 1.056 g/mL) showed a more immediate and rapid decrease. These results give rise to one of two interpretations: (1) low-density platelets have a shorter survival time than more dense platelets and are therefore cleared from the circulation at a faster rate, or (2) platelets of all densities increase in density upon aging in the circulation. To determine the explanation for changing RSR of different density fractions we studied the in vivo disappearance characteristics of low- and high-density 111In-labeled platelets. There were no significant differences between the mean survival times of low-density platelets (5.0 +/- 0.49 days, +/- 1 SD, n = 6), high-density platelets (4.9 +/- 0.56 days, n = 6), or control platelets representing platelets of all densities (4.9 +/- 0.38 days, n = 6). Although a slight increase in the density of all platelets during platelet senescence is indicated by these studies, we conclude that platelet density heterogeneity is not primarily a consequence of age-related changes in platelet density.


Blood ◽  
1984 ◽  
Vol 63 (2) ◽  
pp. 482-485
Author(s):  
BA van Oost ◽  
AP Timmermans ◽  
JJ Sixma

The relation between platelet buoyant density and beta-thromboglobulin (beta-TG), a marker for platelet alpha-granule content, was assessed by three independent approaches. (1) Platelets were separated on iso- osmolar discontinuous Stractan density gradients into five fractions, ranging in density from 1.061 g/ml to 1.091 g/ml (20 degrees C). The beta-TG content (mean +/- SD, n = 17) increased with the platelet density from 27.8 +/- 8.6 micrograms beta-TG/10(9) cells (20% less- dense platelets) up to 65.6 +/- 15.5 micrograms beta-TG/10(9) cells (15% most-dense platelets). (2) Activation of platelets in platelet- rich plasma with thrombin, adenosine diphosphate, collagen, or epinephrine resulted in a decreased density of the platelets. This was only seen when there was simultaneous secretion of beta-TG. (3) The less-dense and the more-dense platelet fractions, after isolation by density gradient centrifugation, were separately treated with thrombin. After complete degranulation, the density distribution of the originally less-dense and more-dense platelets were identical and were much narrower than the density distribution of resting platelets.


2020 ◽  
Author(s):  
Fayez Harash

<p><strong>3-D density structure of the upper-mantle from gravity inversion constrained by seismic velocity model: A case study of the Mediterranean Sea and surrounding region </strong></p><p><strong> </strong></p><p>Harash Fayez<sup>1</sup>, Chao Chen<sup>1,</sup><sup>2</sup>, Qing Liang<sup>1</sup><sup>,2</sup>, Chenming Tu<sup>1</sup></p><p><sup>1</sup>Institute of Geophysics & Geomatics, China University of Geosciences, Wuhan 430074, P.R. China (Corresponding  author:  Harash Fayez).</p><p><sup>2</sup>Subsurface Multi-Scale Imaging Lab, Institute of Geophysics & Geomatics, China University of Geosciences,</p><p> Wuhan 430074, P.R. China.</p><p> </p><p><strong>Summary </strong></p><p>A 3-D density structure of the lithosphere and upper-mantle beneath the Mediterranean Sea and adjacent region was constructed based on inversion of gravity anomaly constrained by seismic tomography model. In this study, we have removed the terrain and crustal effects from the observed gravity field (EIGEN-6C4), in order to obtain the mantle gravity anomaly which was used to investigate the lithospheric and the upper-mantle density distribution. The 3-D inversion process is constrained by a reference density model estimated from shear-wave velocity model (SL2013sv). Our result shows some characteristics of density distribution in the lithosphere and upper-mantle that might be related to the tectonic signification beneath the Mediterranean Sea and adjacent region. A low-density zone dominates the lithosphere beneath the Mediterranean Sea except the area around Arabia shield and North Anatolian fault belt. A thinner high-density layer appears beneath the southwest of Mediterranean Sea, and it may be related to the older oceanic lithosphere fragments. The high-density anomalies appear below depth of 280 km beneath the Mediterranean Sea and the Turkish Aegean Sea Plate. However, the low-density anomalies appears at the top of the upper-mantle beneath trenches of the southwestern of Mediterranean Sea, the eastern of Aegean Sea, the Red Sea, the Black Sea and the middle of Arabia shield. It may indicate the intensity and origination of tectonic movement referring the deep structure below the Eratosthenes seamount in the Mediterranean Sea. Furthermore, the convergence region of two low-density anomaly zones may be interpreted as a significant tectonic unit.</p><p> </p>


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