The majority of semiconductor devices are built on silicon wafers. Manufacturing of high quality silicon wafers involves several machining processes including grinding. This review paper discusses historical perspectives on grinding of silicon wafers, impacts of wafer size progression on applications of grinding in silicon wafer manufacturing, and interrelationships between grinding and two other silicon machining processes (slicing and polishing). It is intended to help * Corresponding author. Tel.: +1 785 532 3436; fax: +1 785 532 3738. E-mail address: zpei@ksu.edu (Z.J. Pei). 1 readers to gain a more comprehensive view on grinding of silicon wafers, and to be instrumental for research and development in grinding of wafers made from other materials (such as gallium arsenide, germanium, lithium niobate, sapphire, and silicon carbide).
K+ secretion in strial marginal cells (SMC) of stria vascularis (SV) is stimulated by beta1-adrenergic receptors. The aim of the present study was to determine, whether SMC from the gerbil inner ear contain muscarinic receptors that inhibit K+ secretion. Receptors were identified with pharmacological tools in functional studies where K+ secretion was monitored as transepithelial current (Isc). The cytosolic Ca2+ concentration ([Ca2+]i) was measured as fluo-4 fluorescence and cAMP production with a colorimetric immunoassay. Further, receptors were identified in SV as transcripts by cloning and sequencing of reverse-transcriptase polymerase chain reaction (RT-PCR) products. The cholinergic receptor agonist carbachol (CCh) caused a transient increase in [Ca2+]i with a half-maximal concentration value (EC50) of (5 +/- 6) x 10(-6) m (n = 29) and a decrease in basal and stimulated cAMP production. Apical CCh had no effect on Isc but basolateral CCh caused a transient increase in Isc with an EC50 of (3 +/- 1) x 10(-6) m and a sustained decrease of Isc with an EC50 of (1.2 +/- 0.2) x 10(-5) m (n = 129). The effects of CCh on Isc and [Ca2+]i were inhibited in the presence of muscarinic antagonist 10(-6) m atropine. Further, the muscarinic antagonists pirenzipine, methoctramine and para-fluoro-hexahydo-sila-defenidol (pFHHSiD) inhibited the CCh-induced transient increase of Isc with affinity constants (KDB) of 3 x 10(-8) m (pKDB = 7.54 +/- 0.19, n = 17), 2 x 10(-6) m (pKDB = 5.71 +/- 0.26, n = 19) and 2 x 10(-8) m (pKDB = 7.65 +/- 0.28, n = 19) and the sustained decrease of Isc with KDB of 7 x 10(-8) m (pKDB = 7.05 +/- 0.09, n = 33), 6 x 10(-6) m (pKDB = 5.21 +/- 0.13, n = 23), 5 x 10(-8) m (pKDB = 7.34 +/- 0.13, n = 31), respectively. RT-PCR of total RNA isolated from SV using primers specific for the M1-M5 muscarinic receptors revealed products of the predicted sizes for the M3- and M4- but not the M1-, M2- and M5-muscarinic receptor subtypes. Sequence analysis confirmed that amplified cDNA fragments encoded gene-specific nucleotide sequences. These results suggest that K+ secretion in SMC is under the control of M3- and M4-muscarinic receptors that may be located in the basolateral membrane of strial marginal cells.
Pharmacologic tools were used to identify receptors in functional studies by measuring either transepithelial current (I(sc)) in strial marginal cells (SMC) or cAMP production in stria vascularis (SV). Further, receptors were identified in SV as transcripts by cloning and sequencing of reverse-transcriptase polymerase chain reaction (RT-PCR) products. Experiments were performed using tissues isolated from gerbils unless specified otherwise. I(sc) under control conditions was 1090 +/- 21 microA/cm(2) (n = 213) in gerbil SMC and 2001 +/- 95 microA/cm(2) (n = 6) in murine SMC. Direct stimulation of adenylate cyclase with 10(-5) m forskolin but not with 10(-5) m 1,9-dideoxy-forskolin resulted in an increase in the I(sc) by a factor of 1.14 +/- 0.01 (n = 6). The vasopressin-receptor agonist 10(-8) m Arg(8)-vasopressin had no significant effect on I(sc) in gerbil and murine SMC. The beta-adrenergic agonists isoproterenol, norepinephrine and epinephrine stimulated I(sc) with an EC(50) of (6 +/- 2) x 10(-7) m (n = 28), (3 +/- 1) x 10(-6) m (n = 40) and (7 +/- 2) x 10(-6) m (n = 38), respectively. Isoproterenol stimulated cAMP production in SV with an EC(50) of (5 +/- 2) x 10(-7) m (n = 8). The beta-antagonist 10(-4) m propanolol completely inhibited 2 x 10(-5) m isoproterenol-induced stimulation of I(sc). The beta-antagonists atenolol, ICI118551 and CGP20712A inhibited isoproterenol-induced stimulation of I(sc) with a K(DB) of 1 x 10(-7) m (pK(DB) = 6.96 +/- 0.15, n = 14), 1 x 10(-7) m (pK(DB) = 7. 01 +/- 0.14, n = 15), 2 x 10(-9) m (pK(DB) = 8.73 +/- 0.13, n = 19), respectively. CGP20712A inhibited isoproterenol-induced cAMP production with a K(DB) of 1 x 10(-10) m (pK(DB) = 9.94 +/- 0.55, n = 9). RT-PCR of total RNA isolated from SV using primers specific for the beta(1)-, beta(2)- and beta(3)-adrenergic receptors revealed products of the predicted sizes for the beta(1)- and beta(2)- but not the beta(3)-adrenergic receptor. Sequence analysis confirmed that amplified cDNA fragments encoded gene-specific nucleotide sequences. These results demonstrate that K(+) secretion in SMC is under the control of beta(1)-adrenergic receptors but not beta(2)-adrenergic or vasopressin-receptors and that the beta(1)-subtype is the primary beta-adrenergic receptor in SV although SV contains transcripts for both beta(1)- and beta(2)-adrenergic receptors.
Simultaneous double side grinding (SDSG) has become an important flattening process for manufacturing of 300 mm silicon wafers. However, the literature contains only a small number of papers on SDSG. In contrast, there are a large number of patents pertinent to this process. There is no review paper summarizing all these reported experimental results. This paper reviews the literature on experimental investigations on SDSG of silicon wafers. It first describes input variables in SDSG, and then presents their effects on output variables, covering warp, flatness, surface roughness, nanotopography, wafer-thickness variation, rotational asymmetry, grinding marks, subsurface damage, wheel wear, and process cycle time. It also discusses the definition, * Corresponding author.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.