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The cache memory has been a predominant component in modern chips, easily taking up more than 50% of the silicon area. It is then desirable to make the cache memory flexible for different needs. Therefore, many modern processor chips allow users to configure a part of the cache memory as the scratch-pad memory (SPM), a high-speed internal memory for rapid data access. However, such approach uses only the data RAM of the cache memory while leaving the tag RAM unused and thus wasting its capacity. This paper presents a cache organization, called Tag-SPM architecture, which allows the tag RAM to be used as the SPM and thus increases its capacity. It is accomplished with small Tag/Data-SPM controllers and four additional multiplexers in the cache organization. The proposed Tag-SPM architecture has been implemented with an academic ARM-based microprocessor with 4-/4-kB four-way set-associative instruction/data caches at the register transfer level level. Experiments show that the proposed architecture boosts the SPM capacity by 12.5% and requires only 0.08% area (434 gates) overhead without impairing the cache’s circuit speed in TSMC’s 90-nm standard cell implementation. Furthermore, the power overhead is negligible. When the Tag-SPM architecture is applied to typical cache systems, such as in ARM’s Cortex-A5 and Cortex-A53 processors, additional 12.5% SPM space per way can also be gained in both cases. The analyses show that our Tag-SPM architecture is a highly cost-effective way to boost the SPM space.

This paper presents using ultrasonic spray pyrolysis deposition method to grow MgO nanorod arrays on the top surface and the sidewall of the GaN-based ultraviolet light-emitting diodes. It is found that when the thickness of the MgO film is over 60 nm, the self-assembled MgO nanorod arrays are obtained. Transmission electron microscopy, scanning electron microscopy, X-ray diffraction, X-ray photoelectron spectroscopy, refractive index, extinction coefficient, and photoluminescence spectrum are used to analyze the structural, chemical, and optical characteristics of the MgO nanorod arrays. The LED chip with the MgO nanorod arrays shows slightly degraded electrical characteristics for it requires a higher forward voltage to provide 0.35-A forward current and higher series resistance. However, the LED chip with the MgO nanorod arrays has great improvement in electroluminescence and efficiency. Compared to the LED chip with a standard SiO2 passivation layer, the LED chip with the MgO nanorod arrays shows improvement of 14.1% in light output power (LOP), 12% in external quantum efficiency and wall plug efficiency. The uniformity of the LED performance like forward voltage, LOP, and wall-plug efficiency is investigated in this paper.

This paper presents an MgO thin films deposited by an ultrasonic spray pyrolysis deposition method to serve as passivation and antireflection layers of the InGaN/GaN light-emitting diodes (LEDs). The electrical, electroluminescence (EL), and efficiency characteristics of the LEDs with 60-, 70-, and 80-nm MgO films are investigated. It is found that the LEDs with the MgO films have lower reverse currents and higher shunt resistance than that without an MgO film. However, there are no significant differences of the forward voltage at 350 mA and the series resistance between the LEDs with and without the MgO films. The significant differences between the LEDs with and without the MgO films are the light output power (LOP) and efficiency. The LED with 70-nm MgO film has the highest LOP of 556 mW (at 700 mA) and external quantum efficiency of 40.8% (at 30 mA). Further, the LED chips with the MgO films show better LOP and wall plug efficiency than those with the SiO2 and SiN x films. It is also found that the LED chips with MgO film as a passivation layer shows stable electrical and EL characteristics in the aging time test.

Since the cache system has been a predominant part in modern SoC's and its capacity is sometimes larger than necessary for specific applications, it is desirable to enhance the role of the cache system to beyond its original purpose (performance improvement). In this paper we propose a versatile data cache, called DT (data/trace) cache, by making it to function simultaneously as a regular data cache and as a trace buffer for real time software debugging and monitoring. It is accomplished by modifying the cache organization such that a portion of the cache ways can be configured as a trace buffer during the run time. The trace buffer stores the trace produced by some trace generation hardware while the rest portion of the data cache keeps its original role. The trace can be dumped out using the existing cache write back circuitry. The integration of a DT cache with an instruction cache, an academic ARM7 processor and a trace generator has been accomplished at RTL level. The hardware overhead is very minor and does not impair the global critical path delay. For a 16 KB (8 ways, 512 lines, 8 words) DT cache with only 1 way as the trace buffer, it is capable of storing 12771 cycles of the program trace at the cost of merely 553 gates and slight increase in cache miss rate on the average. The experiments show that the DT cache is a highly cost-effective approach for real time on-chip trace buffering.

The sol-gel derived technique has been proposed not only to tailor the microstructure of resistive layer but to control the amount of metal during device fabrication for resistive random access memory (ReRAM). Using the sol-gel derived technique can modulate the solution ratio to adjust the resistance and operation voltage. In addition, various metal concentrations can be doped in sol-gel derived resistive layer to significantly improve switching properties including switching speed and power consumption. Above all, forming energy and morphology of metal filament can be ordered by the sol-gel derived technique, which is desirable for practical ReRAM applications.

Background: The resuscitation guidelines indicate pre-arrival dispatcher-assisted telephone CPR (DATCPR) instructions and measurement to increase the proportion of bystander CPR (BCPR), however the impact of those guidelines on survival is not well known. Objective: To describe the impact of a comprehensive bundle of DATCPR on BCPR and survival from OHCA in a horizontal computerized-aided dispatch (CAD) system. Methods: A centralize CAD system in a metropolitan EMS is studied. Routinely in system the time from call to ambulance dispatch should be within 60 seconds. The audio recordings of confirmed OHCAs were reviewed using a standardized format linked with EMS and hospital process and outcome data. The proportions of BCPR and survival six months after implementation (P1) of a bundle that included guideline-based protocol changes, staff training, computerized audit, feedback to providers and leadership rebuilt are compared with that of the same month period in the prior year as control group (P0), using regression analysis for statistics. Results: There were 1437 OHCAs [665 P0, 772 P1; 64% male, median age 62 (IQR: 47-74)](Table 1). The rate of BCPR went from 20.6% in P0 to 35.0% in P1 (p Conclusions: The implementation of a comprehensive bundle of DATCPR in a metropolitan horizontal dispatch system was associated with significant improvements in the rates of BCPR and good neurologic outcome after OHCA.

The possible formation of a stable complex between extracellular signal-regulated kinases (ERKs) and Raf protein kinases was investigated in an attempt to understand the molecular mechanism by which Raf protein kinases were differentially regulated in response to the various stimuli, leading to the activation of ERKs in rat hippocampus. ERK3 was found to coelute with B-Raf, but not c-Raf1, after fractionation of rat hippocampal lysates by QMA anionic exchange chromatography. ERK3 was released into soluble supernatant fraction from the B-Raf, but not c-Raf1, immunoprecipitate, after incubation with ATP. These results, taken together, suggest the specific association of ERK3 with B-Raf in rat hippocampus.

Recent evidence has implicated ADP-ribosylation factor (ARF) proteins as critical regulators of the protein secretory pathway, particularly in the endoplasmic reticulum-Golgi pathway. We have examined whether Golgi membranes contain activators of ARF and the consequences of ARF activation and acylation on its membrane association. Two means were used to assess ARF activation. First, guanosine 5'-3-O-(thio)triphosphate (GTP gamma S) binding to protein was found to be greater when ARF and Golgi were incubated together than when either was incubated alone. These data suggested that ARF GTP gamma S was formed. This was confirmed by showing that the GTP gamma S-bound protein functioned as a cofactor for cholera toxin-stimulated ADP-ribosylation of Gs alpha, a reaction for which activated ARF is a necessary cofactor. Trypsin treatment of Golgi, an inhibitory ARF peptide, and brefeldin A each inhibited Golgi-mediated activation by approximately 70%, demonstrating that a specific protein interaction is required for the majority of the ARF activation. This ARF-activating protein is a strong candidate for the molecular target for brefeldin A. The ubiquitous nature of ARF proteins and their importance in both the exocytic and endocytic pathways may explain the effects of brefeldin A on both exocytic and endocytic membrane traffic in animal cells. A protease-insensitive activation of ARF by Golgi could also be demonstrated and was the dominant activity observed in submicromolar concentrations of magnesium. We believe this to be the lipid-mediated process described previously for purified ARF proteins. ARF activation resulted in tight association of ARF with phospholipid vesicles. Vesicle association required amino-terminal myristoylation of ARF whereas activation did not. These studies indicate that the brefeldin A-sensitive ARF-activating protein and other factors that determine the level of activation of ARF in animal cells are fundamental regulators of membrane traffic in animal cells.

In an attempt to identify proteins involved in the secretory response, bovine chromaffin cells were modified with N-ethylmaleimide (NEM). NEM concentrations less than 30 microM enhanced norepinephrine secretion evoked by nicotine or by K+ depolarization and increased Ca(2+)-dependent secretion from digitonin-permeabilized cells. Higher concentrations of NEM inhibited secretion. The protein modified by NEM which was responsible for the enhancement of secretory activity appeared to rapidly diffuse out of the digitonin-permeabilized cells. When proteins which diffuse from control digitonin-permeabilized cells were incubated with pertussis toxin and [32P]NAD, several proteins were ADP-ribosylated. However, when proteins from cells preincubated with 30 microM NEM were incubated with pertussis toxin and [32P]NAD, these GTP-binding proteins (G-proteins) were not ADP-ribosylated, which suggests that they were modified in the cell by NEM. Stimulation of norepinephrine secretion by NEM was not additive with that caused by pertussis toxin. Modification of chromaffin cells with pertussis toxin or with 30 microM NEM caused a 40-50% decrease in the amount of cytoskeletal F-actin. This decrease in cytoskeletal F-actin may account for the increase in secretory activity.

Hypusine formation on an 18 000-dalton cellular protein is a unique spermidine-dependent, post-translational modification that appears to be ubiquitous in mammalian cells. To determine whether this modification also exists in lower eukaryotes, we examined possible labeling in vitro and in vivo of cellular protein(s) by [3H]spermidine in a mutant strain of Neurospora crassa (arge-12 ota aga) in which ornithine and polyamine synthesis could be nutritionally manipulated. Because of poor uptake of polyamines in this organism, [3H]ornithine, the immediate precursor of polymines, was used for the in vivo labeling experiment. Both in vitro and in vivo labeling resulted in a specific labeling of a 21 000-dalton protein. Radioactive hypusine was recovered from radiolabeled 21 000-dalton protein following acid hydrolysis. The in vitro labeling of the 21 000-dalton protein was dramatically stimulated by NAD+and NADP+, but not by FMN or FAD, suggesting that an NAD+/NADP+-dependent oxidative cleavage of spermidine is involved in deoxyhypusine formation. Isoelectric focusing/sodium dodecyl sulate two-dimensional gel analysis revealed three isoforms of the in vitro labeled 21 000-dalton protein, with pI values ranging from 5.2 to 6.5. In contrast, the 21 000-dalton protein metabolically labeled in vivo gave only one spot with a pI value of approx. 3.5. © 1990.

Mitogen-activated protein kinase (MAPK) has been known to play a critical role in the regulation of the carcinogenesis in human cancers. In an effort to understand the functional role of the MAPK in the carcinogenesis of human gastric tissues, we examined the changes of MAPK levels in human gastric adenocarcinoma. We found that increased MAPK activity was accompanied by overexpression of mitogen-activated protein kinase phosphatase-1 (MKP-1), suggesting that signaling pathways leading to the activation of MAPK and the induction of MKP-1 expression are associated with carcinogenesis of human gastric adenocarcinoma.

Electroconvulsive shock (ECS) has been reported to induce the phosphorylation and activation of 42-kDa, but not 44-kDa, mitogen-activated protein kinase (MAPK) in rat hippocampus. We studied the activation and tyrosine phosphorylation of MAPKs in rat brain after ECS. We observed the increase of the activities of both 42- and 44-kDa MAPKs in rat hippocampus after ECS. The activities reached peak at 2 min and returned to basal levels by 15 min after ECS. We also observed the increased phsophorylation on the tyrosine residue of 42-kDa MAPK in rat hippocampus after ECS, but not on that of 44-kDa MAPK. However, when we examined the immunoprecipitated 44-kDa MAPK, we could demonstrate that the tyrosine phosphorylation of 44-kDa MAPK at 2 min after ECS was markedly increased, in accordance with the increase of kinase activity. These results indicate that ECS induces the transient activation and tyrosine phosphorylation of 44-kDa MAPK, as well as 42-kDa MAPK, in rat hippocampus, although the amount of tyrosine phosphorylation is far less and the kinase activity is lower in 44-kDa MAPK than in 42-kDa MAPK.