System for surface roughness: control of plane and spherical very smooth surfaces

1994 ◽  
Author(s):  
Oleg V. Angelsky ◽  
Ivan A. Buchkovsky ◽  
Peter P. Maksimyak
Keyword(s):  
Surface Roughness ◽  
Smooth Surfaces ◽  
Title System ◽  
Roughness Control

Adhesion and Pull-Off Forces for Polysilicon MEMS Surfaces Using the Sub-Boundary Lubrication Model

2002 ◽  
Vol 125 (1) ◽  
pp. 193-199 ◽  
Author(s):  
Allison Y. Suh ◽  
Andreas A. Polycarpou
Keyword(s):  
Surface Roughness ◽  
Boundary Lubrication ◽  
Intermolecular Forces ◽  
Contact Forces ◽  
Root Mean Square Roughness ◽  
Magnetic Storage ◽  
Smooth Surfaces ◽  
Adhesion Forces ◽  
Disk Interface ◽  
Adhesion Model

Miniature devices including MEMS and the head disk interface in magnetic storage often include very smooth surfaces, typically having root-mean-square roughness, σ of the order of 10 nm or less. When such smooth surfaces contact, or come into proximity of each other, either in dry or wet environments, then strong intermolecular (adhesive) forces may arise. Such strong intermolecular forces may result in unacceptable and possibly catastrophic adhesion, stiction, friction and wear. In the present paper, a model termed sub-boundary lubrication (SBL) adhesion model is used to calculate the adhesion forces, and an elastic-plastic model is used to calculate the contact forces at typical MEMS interfaces. Several levels of surface roughness are investigated representing polished and as-deposited polysilicon films that are typically found in MEMS. The SBL adhesion model reveals the significance of the surface roughness on the adhesion and pull-off forces as the surfaces become smoother. The validity of using the SBL adhesion model to estimate the pull-off forces in miniature systems is further supported by direct comparison with experimental pull-off force measurements performed on silicon and gold interfaces. Finally, the significance of the interfacial forces as relate to the reliability of MEMS interfaces is discussed.

Epitaxial Growth and Surface Roughness Control of Ferromagnetic Thin Films on Si by Sputter Deposition

2007 ◽  
Vol 37 (3) ◽  
pp. 355-360 ◽  
Author(s):  
Jianhua Joshua Yang ◽  
C.-X. Ji ◽  
Ying Yang ◽  
Hua Xiang ◽  
Y. A. Chang
Keyword(s):  
Thin Films ◽  
Surface Roughness ◽  
Epitaxial Growth ◽  
Sputter Deposition ◽  
Ferromagnetic Thin Films ◽  
Roughness Control

Optimization of the Properties of Macroporous Chromatography Silica Supports through Surface Roughness Control

2009 ◽  
Vol 21 (9) ◽  
pp. 1884-1892 ◽  
Author(s):  
Anne Galarneau ◽  
Nathalie Calin ◽  
Julien Iapichella ◽  
Maud Barrande ◽  
Renaud Denoyel ◽  
...  
Keyword(s):  
Surface Roughness ◽  
Silica Supports ◽  
Roughness Control

Arachidonic Acid and Prostaglandin E2 Influence Human Osteoblast (MG63) Response to Titanium Surface Roughness

2008 ◽  
Vol 34 (6) ◽  
pp. 303-312 ◽  
Author(s):  
David D. Dean ◽  
Casey M. Campbell ◽  
Scott F. Gruwell ◽  
John W. M. Tindall ◽  
Hui-Hsiu Chuang ◽  
...  
Keyword(s):  
Surface Roughness ◽  
Arachidonic Acid ◽  
Thymidine Incorporation ◽  
Specific Activity ◽  
Rough Surfaces ◽  
Cell Number ◽  
Smooth Surfaces ◽  
Implant Surface ◽  
Implant Placement ◽  
Effect Of Treatment

Abstract Prior studies have shown that implant surface roughness affects osteoblast proliferation, differentiation, matrix synthesis, and local factor production. Further, cell response is modulated by systemic factors, such as 1,25(OH)2D3 and estrogen as well as mechanical forces. Based on the fact that peri-implant bone healing occurs in a site containing elevated amounts of prostaglandin E2 (PGE2), the hypothesis of the current study is that PGE2 and arachidonic acid (AA), the substrate used by cyclooxygenase to form PGE2, influence osteoblast response to implant surface roughness. To test this hypothesis, 4 different types of commercially pure titanium (cpTi) disks with surfaces of varying roughness (smooth Ti, Ra 0.30 μm; smooth and acid etched Ti [SAE Ti], Ra 0.40 μm; rough Ti, Ra 4.3 μm; rough and acid etched Ti [RAE Ti], Ra 4.15μm) were prepared. MG63 osteoblasts were seeded onto the surfaces, cultured to confluence, and then treated for the last 24 hours of culture with AA (0, 0.1, 1, and 10 nM), PGE2 (0, 1, 10, 25, and 100 nM), or the general cyclooxygenase inhibitor indomethacin (0 or 100 nM). At harvest, the effect of treatment on cell proliferation was assessed by measuring cell number and [3H]-thymidine incorporation, and the effect on cell differentiation was determined by measuring alkaline phosphatase (ALP) specific activity. The effect of AA and PGE2 on cell number was somewhat variable but showed a general decrease on plastic and smooth surfaces and an increase on rough surfaces. In contrast, [3H]-thymidine incorporation was uniformly decreased with treatment on all surfaces. ALP demonstrated the most prominent effect of treatment. On smooth surfaces, AA and PGE2 dose-dependently increased ALP, while on rough surfaces, treatment dose-dependently decreased enzyme specific activity. Indomethacin treatment had either no effect or a slightly inhibitory effect on [3H]-thymidine incorporation on all surfaces. In contrast, indomethacin inhibited ALP on smooth surfaces and stimulated ALP on rough. Taken together, the results indicate that both AA and PGE2 influence osteoblast response by promoting osteoblast differentiation on smooth surfaces, while inhibiting it on rough surfaces. Because implants with rough surfaces are acknowledged to be superior to those with smooth surfaces, these results suggest that use of nonsterioidal anti-inflammatory drugs to block PGE2 production and reduce inflammation may be beneficial in the postoperative period after implant placement. They also indicate that manipulation of the AA metabolic pathway may offer a new therapeutic approach for modulating bone healing after implant placement. Because peri-implant healing takes place in a complex cellular environment quite different from the one used in the present study, additional work will be necessary to substantiate these possibilities.

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