Recent advances in hard-disk drive technology involve the use of a thermal fly-height control (TFC) pole tip protrusion to bring the read/write recording elements of the slider closer to the disk surface and thus achieve Terabit per square inch recording densities. A dynamic, contact mechanics-based friction model of the head-disk interface (HDI) that includes roughness and accounts for the TFC geometry and its influence on the HDI dynamics is presented. The model is based on physical parameters and does not include any empirical coefficients. Experimental flyability/touchdown measurements were performed and used to examine in detail the HDI contact criterion in the presence of surface roughness and dynamic microwaviness. Using the model, a procedure is outlined that identifies the optimal clearance and light contact conditions, i.e., the amount of thermal actuation that minimizes, both, the clearance, as well as the flying height modulation. Through calculation of the time varying interfacial forces, mean pressure and shear stress at the HDI can be predicted and used to characterize the contact regime. Based on our results, a light contact regime with reduced bouncing vibrations and low stresses (thus, low wear) that would enable surfing recording is identified.Index Terms-Dynamic model, friction, hard-disk drive (HDD), head-disk interface (HDI), thermal fly-height control (TFC).

A quasi-dynamic adhesion model is used to calculate the intermolecular adhesion forces present in ultra low flying Head Disk Interfaces (HDI’s). The model is a continuum-based micromechanics model that accounts for realistic surfaces with roughness, molecularly thin lubricants, and is valid under both static and dynamic sliding conditions. Several different levels of surface roughness are investigated ranging from extremely smooth surfaces having a standard deviation of surface heights σ=2 Å to rougher interfaces with several nanometer roughness. It is found that when the flying-height is greater than 5 nm, there are no significant adhesive forces, whereas for flying-heights less than 5 nm, adhesion forces increase sharply, which can be catastrophic to the reliability of low flying HDI’s. In addition to roughness, the apparent area of contact between the flying recording slider and the magnetic disk is also found to significantly affect the magnitude of the adhesion forces. The adhesion model is validated by direct comparisons with adhesion “pull-off” force measurements performed using an Atomic Force Microscope with controlled probe tip areas and magnetic disks having different lubricant thickness.

We have previously reported that Fas-resistant A20 cells (FasR) have phospholipase D (PLD) activity upregulated by endogenous PLD2 overexpression. In the present study, we investigated how overexpressed PLD2 in FasR could generate survival signals by regulating the protein levels of anti-apoptotic Bcl-2 and Bcl-xL. To confirm the effect of PLD2 on Bcl-2 protein levels, we transfected PLD2 into wild-type murine B lymphoma A20 cells. The transfected cells showed markedly the increases in Bcl-2 and Bcl-xL protein levels, and became resistant to Fas-induced apoptosis, similar to FasR. Treatment of wild-type A20 cells with phosphatidic acid (PA), the metabolic end product of PLD2 derived from phosphatidylcholin, markedly increased levels of anti-apoptotic Bcl-2 and Bcl-xL proteins. Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. We further confirmed the involvement of arachidonic acid (AA) in PA-induced survival signals by showing that 1,2-dipalmitoyl-sn-glycero-3-phosphate (DPPA), PA without AA, was unable to increase Bcl-2 and Bcl-xL proteins. Moreover, PA notably increased cyclooxygenase (COX)-2 protein expression, and PA-induced expression of both Bcl-2 and Bcl-xL was inhibited by NS-398, a specific inhibitor of COX-2. Taken together, these findings demonstrate that PA generated by PLD2 plays an important role in cell survival during Fas-mediated apoptosis through the increased Bcl-2 and Bcl-xL protein levels which resulted from PLA(2) and AA-COX2 pathway.

The effect of thermomechanically actuated pole tip protrusion on adhesive forces is characterized through model and experiment. The roughness of a thermomechanically actuated region is characterized by atomic force microscopy. Using the extracted roughness parameters and estimated apparent area associated with thermal actuation, the intermolecular forces at the head-disk interface (HDI) are calculated using the ISBL (improved sub-boundary lubrication) code. Both roughness and nominal area of contact are found to be significant factors determining adhesive forces. The adhesive forces for various HDI designs—including thermal actuation—are also characterized experimentally in situ using commercial hard disk drive samples. The experimental results are found to be consistent with the model calculations and imply certain advantages for thermally actuated HDI designs. However, the experiments also raise concerns regarding the field application of the technology.

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