RF-SoC-expectations and required conditions Matsuzawa, A.
IEEE transactions on microwave theory and techniques,
2002-Jan., 2002-01-00, 20020101, Letnik:
50, Številka:
1
Journal Article
Recenzirano
This paper discusses the expectations for the development of radio-frequency systems-on-chip (RF-SoCs) that integrate RF, analog, and digital circuits, and the conditions under which they can be ...realized. Future RF systems will be increasingly large and complex. However, high integration technology is expected to reduce the circuit size, number of components, and total system cost. Over the past few years, rapid progress of scaled CMOS technology and the introduction of SiGe technology have improved the performance of silicon RF devices and circuits to meet the requirements for conventional RF applications. The RF-SoC, which may be said to be the ultimate goal for RF systems, is expected to improve silicon RF devices even further. However, before this is possible, strict requirements for system perfection, continuous cost reduction, ease of function and specification change, and process portability issues must be resolved. Difficulty in lowering power consumption of RF and analog circuits and of reducing the size of passive components and analog transistors diminish the appeal of the RF-SoC. The RF-SoC in deep submicrometer technology may be an unreasonable solution for some application areas. System-in-package may be one way to address this issue.
Amyloid beta (Abeta) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress ...have been implicated in Abeta-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in Abeta-induced neuronal cell death. Abeta activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly, ASK1-/- neurons were defective in Abeta-induced JNK activation and cell death. These results indicate that ROS-mediated ASK1 activation is a key mechanism for Abeta-induced neurotoxicity, which plays a central role in Alzheimer's disease.
Endochondral ossification is the result of chondrocyte differentiation, hypertrophy, death and replacement by bone. The careful timing and progression of this process is important for normal skeletal ...bone growth and development, as well as fracture repair. Apoptosis Signal-Regulating Kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK), which is activated by reactive oxygen species and other cellular stress events. Activation of ASK1 initiates a signaling cascade known to regulate diverse cellular events including cytokine and growth factor signaling, cell cycle regulation, cellular differentiation, hypertrophy, survival and apoptosis. ASK1 is highly expressed in hypertrophic chondrocytes, but the role of ASK1 in skeletal tissues has not been investigated. Herein, we report that ASK1 knockout (KO) mice display alterations in normal growth plate morphology, which include a shorter proliferative zone and a lengthened hypertrophic zone. These changes in growth plate dynamics result in accelerated long bone mineralization and an increased formation of trabecular bone, which can be attributed to an increased resistance of terminally differentiated chondrocytes to undergo cell death. Interestingly, under normal cell culture conditions, mouse embryonic fibroblasts (MEFs) derived from ASK1 KO mice show no differences in either MAPK signaling or osteogenic or chondrogenic differentiation when compared with wild-type (WT) MEFs. However, when cultured with stress activators, H2O2 or staurosporine, the KO cells show enhanced survival, an associated decrease in the activation of proteins involved in death signaling pathways and a reduction in markers of terminal differentiation. Furthermore, in both WT mice treated with the ASK1 inhibitor, NQDI-1, and ASK1 KO mice endochondral bone formation was increased in an ectopic ossification model. These findings highlight a previously unrealized role for ASK1 in regulating endochondral bone formation. Inhibition of ASK1 has clinical potential to treat fractures or to slow osteoarthritic progression by enhancing chondrocyte survival and slowing hypertrophy.
Nanoparticle monolayers at the air–water interface have received broad attention because of their potential applications owing to the tunability of their surface properties. We prepared gold ...nanoparticle monolayers by adsorption of hydrophilized nanoparticles from solution onto Langmuir monolayers of amphiphilic organic molecules (polyion complexes of deuterated stearic acid and polyallylamine) at the air–water interface, followed by adsorption of dodecyltrimethylammonium bromide onto the underside of these particles. The infrared external reflection spectra of the monolayers recorded both during and after preparation showed that the adsorption of gold nanoparticles on the Langmuir monolayers and that of dodecyltrimethylammonium bromide on the nanoparticles occurred in several tens of minutes. The infrared spectra also showed that both stearic acid and dodecyltrimethylammonium bromide molecules were highly ordered on the gold nanoparticles at the air–water interface. These results suggested that this preparation procedure is a useful fabrication method for Janus particles.
Coordination and balance between cell survival and apoptosis is crucial for normal development and homeostasis of multicellular organisms. Defects in control of this balance may contribute to a ...variety of diseases including cancer, autoimmune and neuro-degenerative conditions. Although a large number of pro- and anti-apoptotic factors acting for or against the final death event have been and are being discovered at an extraordinary pace with the recent progress in this area, the molecular mechanisms determining whether a cell lives or dies are not fully understood. Phosphorylation and dephosphorylation of intracellular effector molecules are the most common and important regulatory mechanisms in signal transduction and control a variety of cellular events from cell growth to apoptosis. Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein (MAP) kinase kinase kinase family, which activates both the SEK1-JNK and MKK3/6-p38 MAP kinase pathways and constitutes a pivotal signaling pathway in cytokine- and stress-induced apoptosis. This review provides recent findings on the molecular mechanisms which determine cell fate such as survival, proliferation, differentiation or apoptosis, with special focus on the regulatory mechanisms of ASK1-mediated apoptosis.
Chemokines have been hypothesized to contribute to the selectivity of lymphocyte trafficking not only as chemoattractants, but also by triggering integrin-dependent sticking (arrest) of circulating ...lymphocytes at venular sites of extravasation. We show that T cells roll on most Peyer's patch high endothelial venules (PP-HEVs), but preferentially arrest in segments displaying high levels of luminal secondary lymphoid tissue chemokine (SLC) (6Ckine, Exodus-2, thymus-derived chemotactic agent 4 TCA-4). This arrest is selectively inhibited by functional deletion (desensitization) of CC chemokine receptor 7 (CCR7), the receptor for SLC and for macrophage inflammatory protein (MIP)-3beta (EBV-induced molecule 1 ligand chemokine ELC), and does not occur in mutant DDD/1 mice that are deficient in these CCR7 ligands. In contrast, pertussis toxin-sensitive B cell sticking does not require SLC or MIP-3beta signaling, and occurs efficiently in SLC(low/-) HEV segments in wild-type mice, and in the SLC-negative HEVs of DDD/1 mice. Remarkably, sites of T and B cell firm adhesion are segregated in PPs, with HEVs supporting B cell accumulation concentrated in or near follicles, the target domain of most B cells entering PPs, whereas T cells preferentially accumulate in interfollicular HEVs. Our findings reveal a fundamental difference in signaling requirements for PP-HEV recognition by T and B cells, and describe an unexpected level of specialization of HEVs that may allow differential, segmental control of lymphocyte subset recruitment into functionally distinct lymphoid microenvironments in vivo.
Both extra- and intracellular stimuli elicit a wide variety of responses, such as cell survival, proliferation, differentiation, and apoptosis, through regulation of cell signaling. Recent studies ...have revealed that stress-responsive signal transduction pathways are strictly regulated by the intracellular redox state. The redox state of the cell is a consequence of the precise balance between the levels of oxidizing and reducing equivalents, such as reactive oxygen species (ROS) and endogenous antioxidants. The generation of ROS fluctuates in response to alterations of both external and internal environment and, in turn, triggers specific signaling cascades, including mitogen-activated protein kinases, which determine cell survival or cell death. This review focuses on the regulatory mechanisms of stress-responsive protein kinases and their involvement in oxidative stress-induced apoptosis. It also provides recent findings on the molecular mechanisms by which redox signaling cross-talks with stress-responsive protein kinase cascades.
We propose a feedback class-C voltage-controlled oscillator (VCO) that has robust start-up and a large oscillation amplitude. It initially starts oscillating as a conventional cross-coupled LC-VCO ...for robust start-up and subsequently transforms automatically into an amplitude-enhanced class-C VCO when it reaches steady-state to give improved noise performance. Detailed analysis of the start-up conditions, enhanced oscillation swing, and amplitude stability provides valuable insight into oscillator design considerations. The proposed VCO is implemented in a 0.18-μm CMOS process. The measured phase noise at room temperature is - 125 dBc/Hz at 1 MHz offset with a power dissipation of 3.4 mW at an oscillation frequency of 4.84 GHz. The figure-of-merit is -193 dBc/Hz.
Hepatocyte IκB kinase β (IKKβ) inhibits hepatocarcinogenesis by suppressing accumulation of reactive oxygen species (ROS) and liver damage, whereas JNK1 activation promotes ROS accumulation, liver ...damage, and carcinogenesis. We examined whether hepatocyte p38α, found to inhibit liver carcinogenesis, acts similarly to IKKβ in control of ROS metabolism and cell death. Hepatocyte-specific p38α ablation enhanced ROS accumulation and liver damage, which were prevented upon administration of an antioxidant. In addition to elevated ROS accumulation, hepatocyte death, augmented by loss of either IKKβ or p38α, was associated with release of IL-1α. Inhibition of IL-1α action or ablation of its receptor inhibited carcinogen-induced compensatory proliferation and liver tumorigenesis. IL-1α release by necrotic hepatocytes is therefore an important mediator of liver tumorigenesis.
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