High-performance MIM capacitor using ALD high-k HfO/sub 2/-Al/sub 2/O/sub 3/ laminate dielectrics

For the first time, we successfully fabricated and demonstrated high performance metal-insulator-metal (MIM) capacitors with HfO/sub 2/-Al/sub 2/O/sub 3/ laminate dielectric using atomic layer deposition (ALD) technique. Our data indicates that the laminate MIM capacitor can provide high capacitance density of 12.8 fF//spl mu/m/sup 2/ from 10 kHz up to 20 GHz, very low leakage current of 3.2 /spl times/ 10/sup -8/ A/cm/sup 2/ at 3.3 V, small linear voltage coefficient of capacitance of 240 ppm/V together with quadratic one of 1830 ppm/V/sup 2/, temperature coefficient of capacitance of 182 ppm//spl deg/C, and high breakdown field of /spl sim/6 MV/cm as well as promising reliability. As a result, the HfO/sub 2/-Al/sub 2/O/sub 3/ laminate is a very promising candidate for next generation MIM capacitor for radio frequency and mixed signal integrated circuit applications.     

Pervasive 2007: It's about the User

Pervasive computing is as much about the user as it is about the technology. So, the Fifth International Conference on Pervasive Computing emphasized desirability rather than just feasibility. Featured themes included user benefits, human-computer interaction, group and social interactions, context awareness, finding and positioning people and objects, and personal privacy.     

Robust State Feedback Control Through Actuators With Generalized Sector Nonlinearities And Saturation

In control systems, actuators often have nonlinear characteristics that can not be neglected. For linear systems driven by actuators satisfying the generalized sector condition, a robust state feedback controller synthesis method is proposed to achieve the ultimate boundedness control. The method is based on the linear matrix inequality approach and is easy to apply. As an important special case of the generalized sector condition, the saturation characteristic of actuators is discussed separately, and non‐conservative results are obtained.     

Effect of race on outcome after kidney and kidney-pancreas transplantation in type 1 diabetic patients

OBJECTIVE: The racial impact on graft outcome is not well defined in diabetic recipients. The purpose of this study is to analyze our experience with kidney-alone (A) and kidney-pancreas (KP) transplantation in type 1 diabetic recipients and evaluate the impact of racial disparity on outcome. RESEARCH DESIGN AND METHODS: The records of 217 kidney transplants (118 KA, 99 KP) performed on type 1 diabetic patients between 1985 and 1995 at the Medical University of South Carolina and the University of Texas Medical Branch were reviewed. RESULTS: A total of 53 (31%) white patients and 15 (33%) black patients experienced at least one episode of biopsy-proven acute rejection of the renal graft (NS). Patient survival at 1, 2, and 5 years was similar in white (92, 87, 69%) and black (91, 91, 69%) patients (NS). Kidney graft survival at 1, 2, and 5 years in the KA group was 72, 62, and 42% in blacks, compared with 79, 76, and 53% in whites (NS). Kidney graft survival at 1, 2, and 5 years in the KP group was 92, 92, and 74% in blacks, compared with 83, 77, and 58% in whites (NS). Pancreas graft survival at 1, 2, and 5 years was 81, 81, and 81% in blacks, compared with 81, 75, and 62% in whites (NS). Cox regression analysis revealed that donor age > or = 40 years increased the risk of renal graft failure 6.2-fold (P = 0.0001), whereas the addition of a pancreas transplant to a kidney and a living-related transplant decreased the risk of failure of the kidney graft 0.2 (P = 0.005) and 0.1 times (P = 0.005). CONCLUSIONS: Our results suggest that when compared with whites, there may be a trend toward an improved kidney and pancreas graft outcome in blacks undergoing KP transplants. These findings suggest that diabetes may override the risk factors that account for the pronounced disparity in outcome observed between nondiabetic white and black recipients.     

Minimum copper loss flux-weakening control of surface mounted permanent magnet synchronous motors

This study presents a novel current loop design method capable of automatic flux-weakening control with minimum copper loss for surface mounted permanent magnet synchronous motors (SPMSM). The proposed current controller can automatically re-compute the d-axis current command to defer output voltage saturation. Consequently, the motor operations in the flux-weakening region are also contained in the stable operating region. Analysis results indicate that since the output voltage vector in the flux-weakening region produced by this controller is consistently on the boundary of the maximum output voltage vector allowed by the inverter, the corresponding flux-weakening current is the optimal value in the sense of minimum copper loss. This minimum copper loss design differs from the maximum output torque design and the constant power design of the flux-weakening control methods found in the literature. Experimental results further demonstrate the feasibility of the proposed current controller and its ability to maximize the speed range of the motor drive for a given inverter capacity.     

89-GHz fT room-temperature silicon MOSFETs

The authors report the implementation of deep-submicrometer Si MOSFETs that at room temperature have a unity-current-gain cutoff frequency (f_T) of 89 GHz, for a drain-to-source bias of 1.5 V, a gate-to-source bias of 1 V, a gate oxide thickness of 40 Å, and a channel length of 0.15 μm. The fabrication procedure is mostly conventional, except for the e-beam defined gates. The speed performance is achieved through an intrinsic transit time of only 1.8 ps across the active device region     

Cloning and expression analysis of a novel salicylate suppressible gene, Hs-CUL-3, a member of cullin/Cdc53 family

By using a mRNA differential display technique to search for salicylate suppressible genes, we identified a cDNA in human foreskin fibroblasts, which by GenBankTM DNA data base search shows sequence homology to the recently reported cullin/Cdc53 (CUL) family genes, especially CUL-3. We have cloned the full-length human CUL-3 (Hs-CUL-3) cDNA. It encodes a 768-amino acid polypeptide and has a predicted molecular weight of 88,939. The amino acid sequence of Hs-CUL-3 shows 46% homology to that of its Caenorhabditis elegans ortholog, Ce-CUL-3, and 27 and 23% to that of Hs-CUL-1 and Hs-CUL-2, respectively. Northern blot analysis showed that phorbol 12-myristate 13-acetate increased the expression of Hs-CUL-3 mRNA in a concentration- and time-dependent manner, and this increase was inhibited by sodium salicylate. Hs-CUL-3 widely expressed in human tissues and its expression in cultured COLO205 colon cancer cells was increased when compared with that in normal colon cells. It is likely that Hs-CUL-3 is involved in cell proliferation control.     

Bioavailability of phenytoin acid and phenytoin sodium with enteral feedings

In the absence of E1B, the 289-amino acid product of human adenovirus type 5 13S E1A induces p53-independent apoptosis by a mechanism that requires viral E4 gene products (Marcellus, R.C., J.C. Teodoro, T. Wu, D.E. Brough, G. Ketner, G.C. Shore, and P.E. Branton. 1996. J. Virol. 70:6207-6215) and involves a mechanism that includes activation of caspases (Boulakia, C.A., G. Chen, F.W. Ng, J. G. Teodoro, P.E. Branton, D.W. Nicholson, G.G. Poirier, and G.C. Shore. 1996. Oncogene. 12:529-535). Here, we show that one of the E4 products, E4orf4, is highly toxic upon expression in rodent cells regardless of the p53 status, and that this cytotoxicity is significantly overcome by coexpression with either Bcl-2 or Bcl-XL. Conditional expression of E4orf4 induces a cell death process that is characterized by apoptotic hallmark features, such as externalization of phosphatidylserine, loss of mitochondrial membrane potential, cytoplasmic vacuolation, condensation of chromatin, and internucleosomal DNA degradation. However, the wide-spectrum inhibitor of caspases, tetrapeptide zVAD-fmk, does not affect any of these apoptogenic manifestations, and does not alter the kinetics of E4orf4-induced cell death. Moreover, E4orf4 expression does not result in activation of the downstream effector caspase common to most apoptosis-inducing events, caspase-3 (CPP32). We conclude, therefore, that in the absence of E1A, E4orf4 is sufficient by itself to trigger a p53-independent apoptosis pathway that may operate independently of the known zVAD-inhibitable caspases, and that may involve an as yet uncharacterized mechanism.