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Notes: Abstract: Pharmacologic activation of endogenous protein kinase C (PKC) together with elevation of the intracellular Ca2+ level was previously shown to cause reduction of two voltage-dependent K+ currents (IA and Ica2+-K+) across the soma membrane of the type B photoreceptor within the eye of the mollusc Hermissenda crassicornis. Similar effects were also found to persist for days after acquisition of a classically conditioned response. Also, the state of phosphorylation of a low-molecular-weight protein was changed only within the eyes of conditioned Hermissenda. To examine the role of PKC in causing K+ current changes as well as changes of phosphorylation during conditioning (and possibly other physiologic contexts), we studied here the effects of endogenous PKC activation and exogenous PKC injection on phosphorylation and K+ channel function. Several phosphoproteins (20, 25, 56, and 165 kilodaltons) showed differences in phosphorylation in response to PKC activators applied to intact nervous systems or to isolated eyes. Specific differences were observed for membrane and cytosolic fractions in response to both the phorbol ester 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA) or exogenous PKC in the presence of Ca2+ and phosphatidylserine/diacylglycerol. Type B cells pretreated with DPBA responded to PKC injection with a persistent reduction of K+ currents. In the absence of DPBA, PKC injection also caused K+ current reduction only following Ca2+ loading conditions. However, the direct effect of PKC injection in the absence of DPBA was only to increase ICa2+_K+. According to a proposed model, the amplitude of the K+ currents would depend on the steady-state balance of effects mediated by PKC within the cytoplasm and membrane-associated PKC. The model further specifies that the effects on K+ currents of cytoplasmic PKC require an intervening proteolytic step. Such a model predicts that increasing the concentration of cytoplasmic protease, e.g., with trypsin, will increase K+ currents, whereas blocking endogenous protease, e.g., with leupeptin, will decrease K+ currents. These effects should be opposed by preexposure of the cells to DPBA. Furthermore, prior injection of leupeptin should block or reverse the effects of subsequent injection of PKC into the type B cell. All of these predictions were confirmed by results reported here. Taken together, the results of this and previous studies suggest that PKC regulation of membrane excitability critically depends on its cellular locus. The implications of such function for long-term physiologic transformations are discussed.

Notes: A new doping method for the vertical sidewall of a trench by electron cyclotron resonance plasma is described. The plasma was produced under a pressure of 5×10−4 Torr. A doped layer was formed uniformly along the sidewall of a trench with subhalf micron width and an aspect ratio of 6.2. By using a de-ionized water cooling system, the wafer temperature was maintained below 120 °C and the boron dopant was introduced without damage to the photoresist.

Notes: Effects of implanted hydrogen on removal of oxygen from a Si top layer on buried oxide by the post-implantation annealing were studied. The Si top layer and the buried oxide layer were analyzed by secondary ion mass spectroscopy (SIMS) and cross-sectional transmission electron microscopy (X-TEM). With implanted hydrogen, oxygen concentration in the Si top layer could be reduced below the SIMS detection limit by annealing at relatively lower temperature 1150 °C for 2 h in an ambient of N2. It is verified by X-TEM that the Si top layer is precipitate-free. An amount of hydrogen comparable to the amount of oxygen contained in the Si top layer is needed to remove the oxygen completely. This effective removal of oxygen is attributed to the suppression of oxygen precipitation and the enhanced dissolution of oxide precipitates by hydrogen.

Notes: Patients with both severe atopic dermatitis (AD) and chronic myeloid leukemia, chronic hepatitis B, or chronic hepatitis C were treated with interferon-alpha (IFN-α). IFN-α treatment improved AD. Moreover, there were also significant decreases in serum IgE and IgG4 levels and in in vitro spontaneous IgE and IgG4 production by patients' mononuclear cells.

Notes: This paper proposes a local stress concept to evaluate the fretting fatigue limit for contact edge cracks. A unique S–N curve based on the local stress could be obtained for a contact edge crack irrespective of mechanical factors such as contact pressure, relative slip, contact length, specimen size and loading type. The analytical background for the local stress concept was studied using FEM analysis. It was shown that the local stress uniquely determined the ΔK change due to crack growth as well as the stress distribution near the contact edge. The condition that determined the fretting fatigue limit was predicted by combining the ΔK change due to crack growth and the ΔKth for a short crack. The formation of a non-propagating crack at the fatigue limit was predicted by the model and it was experimentally confirmed by a long-life fretting fatigue test.

Notes: Fatigue tests on material containing small defects were performed under a wide range of mean stress for three grades of steels with different hardness. The ΔKth of small defects had a peculiar dependency on material hardness and mean stress, which was quite different from those of long cracks or plain specimens. The crack closure of short cracks was measured. It was shown that the formation of the crack closure was affected by the material hardness and mean stress. This behaviour of crack closure resulted in characteristic fatigue limit properties of materials containing small defects.

Notes: Fretting fatigue fracture of industrial machines is sometimes experienced after a long period of operation. It has been a question whether the fatigue limit which means infinite life really exists in fretting fatigue or not. Fretting fatigue tests in ultra high cycle region up to 109 cycles were performed. Test results showed that the S-N curve had a knee point around 2 × 107 cycles and a clear fatigue limit was observed in the giga-cycle regime for partial slip conditions. An electropotential drop technique was applied to detect the crack growth behaviour under the contact pad. The real-time measurement of crack depth during the fretting fatigue test at the fatigue limit showed that a crack initiated at an early stage and then ceased to grow after 2 × 107 cycles and the crack became a non-propagating crack. These results indicated that the fatigue limit exists in fretting fatigue and infinite endurance is achieved by the mechanism of forming a non-propagating crack.