Improvement in thickness uniformity of thick SOI by numerically controlled local wet etching.

Silicon-on-insulator (SOI) wafers are promising semiconductor materials for high-speed LSIs, low-power-consumption electric devices and micro electro mechanical systems (MEMS). The thickness distribution of an SOI causes the variation of threshold voltage in electronic devices manufactured on the SOI wafer. The thickness distribution of a thin SOI, which is manufactured by applying a smart cut technique, is comparatively uniform. On the other hand, a thick SOI has a large thickness distribution because a bonded wafer is thinned by conventional grinding and polishing. For a thick SOI wafer with a thickness of 1 microm, it is required that the tolerance of thickness variation is less than 50 nm. However, improving the thickness uniformity of a thick SOI layer to a tolerance of +/- 5% is difficult by conventional machining because of the fundamental limitations of these techniques. We have developed numerically controlled local wet etching (NC-LWE) technique as a novel deterministic subaperture figuring and finishing technique, which utilizes a localized chemical reaction between the etchant and the surface of the workpiece. We demonstrated an improvement in the thickness distribution of a thick SOI by NC-LWE using an HF/HNO3 mixture, and thickness variation improved from 480 nm to 200 nm within a diameter of 170 mm.

P2Y12 receptors in spinal microglia are required for neuropathic pain after peripheral nerve injury.

Extracellular nucleotides have been implicated as signaling molecules used by microglia to sense adverse physiological conditions, such as neuronal damage. They act through purinoceptors, especially the G-protein-coupled P2Y receptor P2Y(12)R. Emerging evidence has indicated that activated spinal microglia responding to nerve injury are key cellular intermediaries in the resulting highly debilitating chronic pain state, namely neuropathic pain. However, the role of microglial P2Y(12)Rs in neuropathic pain remains unknown. Here, we show that the level of P2Y(12)R mRNA expression was markedly increased in the spinal cord ipsilateral to the nerve injury and that this expression was highly restricted to ionized binding calcium adapter molecule 1-positive microglia. An increase in the immunofluorescence of P2Y(12)R protein in the ipsilateral spinal cord was also observed after nerve injury, and P2Y(12)R-positive cells were double labeled with the microglial marker OX-42. Blocking spinal P2Y(12)R by the intrathecal administration of its antagonist AR-C69931MX prevented the development of tactile allodynia (pain hypersensitivity to innocuous stimuli), a hallmark of neuropathic pain syndrome. Furthermore, mice lacking P2ry(12) (P2ry(12)(-/-)) displayed impaired tactile allodynia after nerve injury without any change in basal mechanical sensitivity. Moreover, a single intrathecal administration of AR-C69931MX or oral administration of clopidogrel (a P2Y(12)R blocker clinically in use) to nerve-injured rats produced a striking alleviation of existing tactile allodynia. Together, our findings indicate that activation of P2Y(12)Rs in spinal microglia may be a critical event in the pathogenesis of neuropathic pain and suggest that blocking microglial P2Y(12)R might be a viable therapeutic strategy for treating neuropathic pain.