Modified Imidazoles: Degradation Inhibitors and Adhesion Promoters for Polyimide Films on Copper Substrates

Polyimide films on copper substrates that are exposed to elevated temperatures and an oxidizing environment will be subject to degradation. In order to halt this degradation without changing the properties of the system, a polymeric agent could be placed between the polyimide and the copper. This paper will investigate three such materials that will not only slow down the degradation of the polyimide and the oxidation of the copper, but will also improve adhesion within the system. Fourier transform infrared reflection-absorption spectroscopy (FTIR-RAS) will be used to investigate the polyimide/polymeric agent/copper system.     

Quasi-bound states determination using a perturbed wavenumbersmethod in a large quantum box

A perturbed wavenumbers method (PWM) is presented that is capable of determining the quasi-bound-state eigenenergies and their lifetimes for quantum heterostructures having arbitrary potential profiles. The numerical method presented solves the single-band effective-mass Schrodinger equation without using complex energies. It is applicable to quantum structures that are symmetric, asymmetric, unbiased, or biased. For multiple quantum heterostructures, extensive comparisons of this numerical method with other currently used techniques are included. In addition, a modified density of states formulation is presented and applied to these example cases     

A novel on-chip electrostatic discharge (ESD) protection withcommon discharge line for high-speed CMOS LSIs

A novel on-chip electrostatic discharge (ESD) protection for high-speed CMOS LSI's that operate at higher than 500 MHz has been developed. Introduction of a newly developed common discharge line (CDL) can completely eliminate the protection device influence on the inner circuit operation. This enables minimization of the I/O capacitance by shrinking the dimension of the output transistor, which also serves as a protection device in conventional devices. This new protection (CDL protection) was applied to a high-speed DRAM of which I/O pin capacitance specification is 2 pF. As a result, the ESD tolerance of 4 kV for the charged device model test, 4 kV for the human body model test, and 700 V for the machine model test were obtained. In addition, the DRAM data rate higher than 660 MHz at room temperature was achieved. The results show significant improvement for both ESD and the I/O capacitance, compared with the conventional structure     

'Sheltered disruption' of Neurospora crassa MOM22, an essential component of the mitochondrial protein import complex

MOM22 is a component of the protein import complex of the mitochondrial outer membrane of Neurospora crassa. Using the newly developed procedure of 'sheltered disruption', we created a heterokaryotic strain harboring two nuclei, one with a null allele of the mom-22 gene and the other with a wild-type allele. Homokaryons bearing the mom-22 disruption could not be isolated, suggesting that mom-22 is an essential gene. The mutant nucleus can be forced to predominate in the heterokaryon through the use of specific nutritional and inhibitor resistance markers. Cultivation of the heterokaryon under conditions favoring the mutant nucleus resulted in selective depletion of MOM22. MOM22-depleted cells did not grow and contained mitochondria with an altered morphology and protein composition. Protein import into isolated, MOM22-depleted mitochondria was abolished for most precursor proteins destined for all subcompartments. In contrast, precursors of MOM19, MOM22 and MOM72 became inserted normally into the outer membrane, defining a novel MOM22-independent import pathway which remained intact in mutant mitochondria. Furthermore, the specific binding of the ADP/ATP carrier to the outer membrane was unaffected, but subsequent transport across the outer membrane did not occur. Our data show that MOM22 is an essential component of Neurospora cells specifically required for the biogenesis of mitochondria.     

The cranial MRI in severe cerebral palsy: a comparative study with clinical data

The magnetic resonance examination was performed in 38 patients with severe cerebral palsy (CP; 15 males and 23 females) who had both motor delay (unable to move anywhere) and mental retardation (I. Q or D. Q below 30). Neuroimaging findings were compared with the CP type, etiology, and grade of understanding of language. Cranial magnetic resonance imagings (MRI) in CP were divided into five types. Type 1 : nine predominantly showed cyst-liked ventricles and periventricular hyperintensity on T2-weighted imaging (PVH) and only scarred basal ganglia and thalamus were visible. All suffered from neonatal asphyxia and the clinical type was rigospastic tetraplegia (RST). Type 2: eleven predominantly showed PVH and hyperintensity on T2-weighted (HT2) in basal ganglia and thalamus. All suffered from neonatal asphyxia and the clinical type was RST or rigospastic diplegia. Type 3: five showed PVH and three had cortical atrophy. All suffered from neonatal asphyxia and the clinical type was spastic diplegia. Type 4: four predominantly showed HT 2 in putamen and thalamus. Three had cortical atrophy. All suffered from neonatal asphyxia. The clinical type was athetotic CP (ATH). Type 5: nine predominantly showed HT 2 in globus pallidus. Four had cortical atrophy and two had hippocampal atrophy. All suffered from neonatal jaundice and the clinical type was ATH. All patients who suffered from neonatal asphyxia and spastic CP had MRI in PVH. All patients who suffered from neonatal asphyxia and ATH showed HT 2 in putamen and thalamus. Almost patients who suffered neonatal jaundice and ATH showed HT 2 in globus pallidus. With athetotic CP, cases with atrophy of the cerebral cortex or/and hippocampus were lower grade of understanding of language than no atrophy of both. The result of studies of MRI are in agreement with neuropathological findings.     

The Cdc7 protein kinase is required for origin firing during S phase

The Cdc7p protein kinase plays an essential, but undefined, role promoting S phase in the budding yeast, Saccharomyces cerevisiae. Previous experiments have shown that the essential function of Cdc7 is executed near the G1-S boundary; after Start but before the elongation phase of DNA replication. Origins of DNA replication fire throughout S phase in budding yeast. Therefore, the G1-S transition is a cell-cycle event that precedes, and is distinct from, the activation of individual origins. Consequently, we have asked whether Cdc7 is only required for S-phase entry or if it plays a role during S phase in origin firing. In this article, we show that partial loss of Cdc7 function results in slow progression through S phase rather than slow entry into S phase and that Cdc7 is still required for the timely completion of S phase after a block to elongation with hydroxyurea. This is because Cdc7 is still required for the activation of late-firing origins after the hydroxyurea block. These experiments show that, rather than acting as a global regulator of the G1-S transition, Cdc7 appears to play a more direct role in the firing of replication origins during S phase.