Undamaged Regions Research Articles

Role of damage on the flow and fracture of particulate reinforced alloys and metal matrix composites

A large number of models exist to predict the tensile behaviour of two-phase materials. They fail, however, to predict the behaviour at high strain because they do not properly account for the role which damage accumulation plays during plastic flow. A new model is proposed here which incorporates damage. It uses an incremental self-consistent method developed previously. In the new application, the model treats damaged and undamaged regions as distinct continuous “phases” and allows the relative volume fraction of each phase to vary during deformation. The stress redistribution due to damage during the evolution is carefully analysed. The model considers the influence of particle size via a Weibull analysis and incorporates the results of existing FEM calculations. The model agrees well with existing experimental data and provides a new method to evaluate the role of microstructural parameters.

Lateral damage extension during masked ion implantation into GaAs

We have studied both experimentally and theoretically the generation of damage in GaAs due to ion implantation through mask openings of small dimensions. We show that it is possible to master the generation of damage, i.e., the amorphization phenomenon in the direction perpendicular to the ion beam and close to the mask edges. A theoretical model is used to simulate the ion implantation process and damage accumulation through Ti–Au masks. After comparing the shape of the crystalline/amorphous interfaces as revealed by cross-sectional electron microscopy with our simulations, this model is used to predict the evolution of the two-dimensional damage distributions beneath the mask edges as functions of ion beam and implantation mask parameters. Undamaged regions of nanometer dimensions can be preserved even when using masks of reasonable dimensions (100–200 nm). This can be done only by adjusting the ion beam parameters through the accurate simulation of the two-dimensional damage generation.

Ballistic electron emission microscopy studies of electron scattering in Au/GaAs Schottky diodes damaged by focused ion beam implantation

Ballistic electron emission microscopy is used to investigate the electron scattering properties of undamaged and focused ion beam implanted Au/GaAs diodes. Implanted regions show decreased ballistic electron transmission attributed to increased scattering. A quantitative model of electron transport is developed that includes quantum mechanical transmission at the interface, scattering effects from optical phonons and implantation induced defects in the semiconductor, and scattering in the metal layer. Model predictions of scattering in undamaged regions show good agreement with the data. However, we conclude additional scattering effects must be included to describe the implanted structures.

Quantifying Local Microcrack Density in Ceramics: A Comparison of Instrumented Indentation and Thermal Wave Techniques

Instrumented indentation and thermal wave techniques are used as local, quantitative probes of microcrack density in a silicon nitride that has been subjected to severe Hertzian contact stress. The techniques act as local probes, sampling volumes of material <10−3 mm3. Microcracked regions are created using a tungsten carbide spherical indenter, as a result of high shear stress in the compressive zone beneath the indenter. The microcracked zones, studied in cross section using a “bonded interface” technique, increased both in size and in degree of damage with increasing Hertzian load. Within the zones, Young's modulus is measured using instrumented indentation, and the thermal diffusivity using a thermal wave technique; both quantities are lower in the damaged regions than in the undamaged regions. The shifts in modulus and diffusivity are used independently to calculate microcrack densities using related models of the effect of microcracks on each property. The two techniques show the same functional relationship between Hertzian contact load and microcrack density, and yield densities that agree to within a factor of approximately 2.

Neuroprotective Effect of Ketamine Administered After Status Epilepticus Onset

We investigated the neuroprotective effect of the noncompetitive N-methyl-D-asparatate (NMDA) antagonist ketamine when administered after onset of lithium-pilocarpine-induced status epilepticus (SE). Seizures were induced in Wistar rats with lithium chloride (3 mEq/kg) and pilocarpine (PC) (30-60 mg/kg intraperitoneally, i.p.). Fifteen minutes after SE onset, either ketamine 100 mg/kg or normal saline was injected i.p., and 3 h after SE onset atropine, diazepam (DZP), and phenobarbital (PB) were administered i.p. to terminate the seizures. Twenty-four hours later, rats underwent brain perfusion-fixation, with subsequent brain processing for light-microscopic examination. Rats adminstered saline (n = 5) had neuronal damage in 24 of 25 brain regions examined. Rats administered ketamine (n = 7) had significant neuroprotection in 22 of 24 damaged regions. Ketamine reduced the amplitude of seizure discharges, and in 3 rats EEG seizure activity ceased in 30 min; none of these rats had neuronal damage. In the other 4 rats, EEG seizure discharges persisted > 90 min; in these animals, 21 of 24 damaged regions were protected. In contrast, rats with 1-h high-dose PC-induced SE (400 mg/kg i.p. without lithium chloride preadministration) had 14 damaged regions, of which 7 were significantly different from the undamaged regions of the ketamine subgroup with persistent electrographic seizures. Thus, ketamine is remarkably neuroprotective when administered after onset of SE, whether or not seizure discharges are eliminated.

Extracellular glutamate is increased in thalamus during thiamine deficiency-induced lesions and is blocked by MK-801.

The current study measured extracellular fluid (ECF) levels of excitatory amino acids before and during the onset of thiamine deficiency-induced pathologic lesions. Male Sprague-Dawley rats were treated with daily pyrithiamine (0.25 mg/kg i.p.) and a thiamine-deficient diet (PTD). Microdialysates were simultaneously collected from probes inserted acutely via guide cannulae into right paracentral and ventrolateral nuclei of thalamus and left hippocampus of PTD and pair-fed controls. Hourly samples were collected from unanesthetized and freely moving animals. Basal levels obtained at a prelesion stage (day 12 of PTD treatment) were unchanged from levels in pair-fed controls. In samples collected 4-5 h after onset of seizures (day 14 of PTD), the levels of glutamate were elevated an average 640% of basal levels in medial thalamus and 200% in hippocampus. Glutamine levels declined, taurine and glycine were elevated, and aspartate, GABA, and alanine were unchanged during this period. Within 7 h after seizure onset glutamine was undetectable in both areas, whereas glutamate had declined to approximately 200% in thalamus and 70% in hippocampus. No significant change in glutamate, aspartate, or other amino acids was observed in dialysates collected from probes located in undamaged dorsal-lateral regions of thalamus. Number of neurons within ventrolateral nucleus of thalamus was significantly greater in PTD animals in which the probe was dialyzed compared with nondialyzed, suggesting that removal of excitatory amino acids was protective. No significant pathologic damage was evident in hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effect of Fluid Diversion on the Acid Stimulation of a Perforation

Summary A previously developed model that considers the effect of acidizing on the productivity of a single perforation penetrating a sandstone reservoir was extended to account for the effect of particulate diverting agents on acid distribution inside the perforation. Cases were run that simulate various types of formation damage, including damage from drilling-mud infiltration and damage caused by perforating itself. The model predicts the evolution of the perforation skin factor as acid dissolves formation minerals in the surrounding region. The primary result of this work is that, for the types of damage simulated, fluid diversion within a perforation has little effect on stimulation performance. Although the diverting agent significantly changes the acid distribution at the perforation surface, the acid tends to migrate rapidly to undamaged regions in the formation. This paper presents results from a series of case studies that emphasized the effect of fluid diversion inside a perforation.

Resident macrophages (ED2- and ED3-positive) do not phagocytose degenerating rat skeletal muscle fibres

Two soleus muscles with degenerating muscle fibres were serially sectioned and adjacent sections from various levels of the skeletal muscles were stained with antibodies that react with either monocytes and inflammatory macrophages (ED1) or with the major subpopulations of resident macrophages (ED2 and ED3). ED2+ and ED3+ resident macrophages were abundant throughout the muscles but were not present within the degenerating fibres. ED1+ cells, in contrast, were rarely observed within the undamaged regions of the muscles but were abundant within the degenerating fibres and in the perimysium between arterioles and degenerating fibres. It is concluded that the phagocytosis of damaged muscle fibres is not carried out by the major subpopulations of resident macrophages.

LETTUCE SEEDLING RESPONSE TO DETERGENTS RECOMMENDED FOR SPACE TRAVEL

Water contributes approximately 90% of the life support consumables in a closed space environment, therefore, regeneration of pure water from waste streams is important for long term space travel. Controlled Ecological Life Support Systems (CELSS) will rely on plants to produce food, oxygen, consume CO2 and purify water. Igepon TC42, Amide coco N-methyl N-2-sulphoethyl sodium salt, is the main ingredient of the soap recommended for showering and hand washing aboard Space Station Freedom. To determine the soap concentration which causes plant toxicity, lettuce seeds were germinated in 0.1 strength modified Hoagland's nutrient solution and a series of increasing concentrations of Igepon. After 5 days, the seedlings were examined and primary root length measured. The dose response curve indicates an Igepon acute toxicity threshold of 0.2 g l-1 Below the threshold concentration the curve is similar to that of the control, but drops linearly upon reaching the toxic threshold. Seedlings exposed to concentrations of soap greater than the toxic threshold exhibited root damage characterized by the browning of cells in bands above the root cap resulting in reduced growth rates. The damaged cells enlarged becoming round in appearance prior to departing from adjacent cells. The underlying cells appeared clear and uniform making up a thinner, more fragile root mass when compared to undamaged root regions.

Video-enhanced DIC images of the noise-damaged and regenerated chick tectorial membrane

Exposure of the chick cochlea to acoustic overstimulation results in a loss of hair cells and a disruption of the tectorial membrane. With time, new hair cells are produced to replace those that are lost and, concurrently, a new tectorial membrane is regenerated. Previous studies of tectorial membrane regeneration examined tissues that were fixed and processed for scanning and transmission electron microscopy. This processing results in a considerable shrinkage of the membrane, and, therefore, it was unclear how the noise damage and subsequent regeneration affected the unfixed, in situ structure of the tectorial membrane. We have recently developed techniques for studying the unfixed tectorial membrane with video-enhanced differential-interference-contrast (DIC) light microscopy. Exposure to a 1500-Hz pure tone at 120 dB SPL for 24 h causes localized damage to the hair cells and tectorial membrane in the mid-proximal region of the basilar papilla. Examination of the unfixed membrane immediately after noise exposure shows that the damage to the tectorial membrane is actually caused by the acoustic trauma and is not an artifact of fixation. After 14 days of recovery, a thick, honeycomb of new matrix has grown from the supporting cells in the basilar papilla and has formed new connections with the stereocilia of surviving and regenerating hair cells. Moreover, this new honeycomb has fused with the remainder of the surrounding, undamaged tectorial membrane, thus reestablishing a continuity in the structure of the membrane across both the damaged and undamaged regions of the basilar papilla.

Hole Diffusion Length Measurement for n‐type Semiconductors by Using Photoelectrochemical Etching Technique

This paper theoretically and experimentally demonstrates a new technique for hole diffusion length measurement in n‐type semiconductors. The technique utilizes the photoelectrochemical etching process of n‐type semiconductors, because a very low interface recombination velocity at the electrolyte/semiconductor interface is expected, and furthermore a photoelectrochemical etching profile of n‐type semiconductors with a relatively large bandgap such as is precisely reflected by photogenerated hole concentration profile at the sample surface. For a sample surface with a selectively damaged region where hole lifetime is markedly reduced, an etching profile is theoretically calculated from a photogenerated hole concentration profile at the surface. The theoretical analysis shows that hole diffusion length in the undamaged region can be estimated from the etching profile near the boundary between damaged and undamaged regions. It is also shown that a bulk hole diffusion length can be measured without influences of the interface recombination velocity when the interface recombination velocity at the electrolyte/semiconductor interface is less than about 105 cm/s. This technique is successfully applied to the hole diffusion length measurement in n‐type and bulk crystals. Hole diffusion length data larger than those previously reported are obtained for these samples. This indicates a low interface recombination velocity at the electrolyte/semiconductor interface.

Effects of low-dose Si implantation damage on diffusion of phosphorus and arsenic in Si

The effects of low-dose Si implantation damage on diffusion of low-concentration P and As in Si wafers are investigated. Dopants are implanted at a low dose and subsequently preannealed to remove any self-damage. An enhanced diffusion of P is observed by directly comparing dopant profiles in damaged and undamaged regions. Monitoring effective diffusivity of P at various annealing temperatures and times reveals that the enhanced diffusion is a transient process with a time constant which is larger at lower temperature. This enhancement is larger and of longer duration the lower the annealing temperature is. In contrast to P, As diffusion in the damaged region does not show any enhancement. This implies that the defects induced by the Si implants have separate mechanisms for interaction with each type of dopant.

Collisional Energy Deposition Threshold for Extended Damage Depths in Ion-Implanted Silicates

ABSTRACTMany properties of implanted fused silica (e.g., surface stress, hardness) exhibit maximum implantation-induced changes for collisional energy deposition values of ∼1020 keV/cm3. We have observed a second critical energy deposition threshold value of about 1022 keV/cm3 in stress and hardness measurements as well as in many other experiments on silicate glasses (leaching, alkali depletion, etching rate, gaseous implant redistribution). The latter show evidence for damage depths exceeding TRIM ranges by about a factor of 2. For crystalline quartz, a similar threshold value value has been found for extended damage depths (greater than TRIM) for 250 kev ions (H-Au) as measured by RBS and interference fringes. This phenomenon at high damage deposition energy may involve the large stress gradients between damaged and undamaged regions and the much increased diffusion coefficient for defect transport.

The UvrABC endonuclease system of Escherichia coli — A view from Baltimore

Nucleotide excision is initiated by the UvrABC endonuclease system in which the initial DNA interaction is with UvrA which was dimerized in the presence of ATP. Nucleoprotein formation most likely takes place on undamaged regions of DNA by (UvrA)2 which has been dimerized in the presence of ATP. Topological unwinding of DNA, driven by ATP binding, is increased by the presence of UvrB to approximately a single helical turn. The Uvr(A)2B complex translocates to a damaged site by the combined Uvr(A)2B helicase in which the driving force is provided by the UvrB-associated ATPase. The dual incision reaction is initiated by the binding of the UvrC protein to the Uvr(A)2B-nucleoprotein complex. The proteins in this post-incision nucleoprotein complex do not turn over and require the presence of the UvrD protein and DNA polymerase I under polymerizing conditions. The final integrity of the DNA strands is restored with polynucleotide ligase.

Glutamate decarboxylase-immunoreactive neurons are preserved in human epileptic hippocampus

The present study was designed to determine whether inhibitory neurons in human epileptic hippocampus are reduced in number, which could reduce inhibition on principal cells and thereby be a basis for seizure susceptibility. We studied the distribution of GABA neurons and puncta by using glutamate decarboxylase (GAD) immunocytochemistry (ICC) together with Nissl stains. Using quantitative comparisons of GAD-immunoreactive (GAD-IR) neurons and puncta in human epileptic hippocampus and in the normal monkey hippocampus, we found that GAD-IR neurons and puncta are relatively unaffected by the hippocampal sclerosis typical of hippocampal epilepsy where 50-90% of principal (non-GAD-IR) cells are lost. GAD-IR neurons and puncta were not significantly decreased compared with normal monkey. In 6 patients, prior in vivo electrophysiology demonstrated that the anterior hippocampus generated all seizures. The anterior and posterior hippocampus were processed simultaneously, and the counts of hippocampal GAD-IR neurons were numerically greater in anterior than in the posterior hippocampus, where no seizures were initiated. These results indicate that GABA neurons are intact in sclerotic and epileptogenic hippocampus. Computerized image analysis of puncta densities in fascia dentata, Ammon's horn, and subicular complex in epileptic hippocampi (n = 7) were not different from puncta densities in the same regions in normal monkey (n = 2). Hence, despite the significant loss of principal cells (50-90% loss) GABA terminals (GAD-IR puncta) were normal, which suggests GABA hyperinnervation of the remnant pyramidal cells and/or dendrites in human epileptic hippocampus. The apparent increase in puncta ranged from 2 (fascia dentata) to 3.3 (CA1) times normal puncta densities. These findings would suggest increased inhibition and less excitability; however, those regions were epileptogenic. We suggest that GABA terminal sprouting or hyperinnervation of the few remnant projection cells may serve to synchronize their membrane potentials so that subsequent excitatory inputs will trigger a larger population of neurons for seizure onset in the hippocampus and propagation out to undamaged regions of subiculum and neocortex.

Selective Ion Bombardment for the Control of Laser‐Induced Photochemical Dry Etching of Semiconductors

The etch rate of a solid‐excitation‐based photochemical etching process for semiconductor materials is determined by the balance between recombination of photogenerated carriers and carrier participation in the surface etching reaction. Ion implantation‐induced damage of the semiconductor can shift the balance between recombination and reaction, permitting selective etching of undamaged regions of a semiconductor surface relative to ion‐implanted, damaged regions. Spatially selective photochemical dry etching of has been achieved by this approach.

Capillary density and fine structure in rabbit papillary muscles after a high dose of norepinephrine

Two days after an iv infusion of norepinephrine (NE) (4 μg · kg −1 · min −1 × 60 min) in rabbits, patchy myocardial damage in frozen cross sections of right and left papillary muscles was associated with loss of staining for alkaline phosphatase (ALP), an enzyme present in normal capillary endothelium, whereas a regular pattern of staining was observed in control normal muscles. Semithin cross sections of the same muscles after resin embedment gave comparable estimates of capillary density in control muscles and undamaged regions of norepinephrine-treated muscles. In damaged regions the complete absence of ALP staining corresponded with an apparent reduction in number, but not absence, of capillaries identifiable in semithin sections with light microscopy. Electron microscopy, however, revealed capillaries present in these regions in numbers similar to control undamaged tissue. Around 90% of these capillaries exhibited marked morphological abnormalities, with an 18% increase in endothelial cell volume density and a corresponding reduction in luminal volume density. These changes are similar to those reported after ischemia in cardiac and skeletal muscle. Myocardial damage induced by a high dose of NE is therefore associated 48 hr later with loss of ALP staining and endothelial cell disruption and edema, which may impair capillary perfusion and contribute to limited working cardiac performance observed previously.

Axotomy-induced alterations in the synthesis and transport of neurofilaments and microtubules in dorsal root ganglion cells

Changes in the synthesis and axonal transport of neurofilament (NF) proteins and tubulin were examined after various selective axotomies of adult rat DRG cells. For axonal transport studies, DRGs were labeled by microinjection of 35S-methionine 14 d after axonal injuries, and nerves were retrieved 7 or 14 d after labeling. Slowly transported proteins were examined by quantitative PAGE/fluorography. After distal peripheral nerve crush (50-55 mm from the DRG), the cytoskeleton that entered undamaged regions of peripheral branch DRG axons by slow axonal transport differed from normal, while the cytoskeleton that entered dorsal root axons did not. Specifically, smaller-than-normal ratios of labeled NF protein/tubulin were transported in peripheral DRG axons after distal peripheral nerve crush. This change was almost entirely due to a selective decrease in the output of labeled NF proteins rather than to an increase in the amount of tubulin transported with NF proteins. Since the efficiency of axonal regeneration is known to be lower after cut injury than after nerve crush, we compared the effect of cut versus crush axotomy of peripheral DRG axons on cytoskeletal protein output. A more substantial reduction in the labeled NF/tubulin transport resulted in peripheral DRG axons if the distal sciatic nerve was cut rather than crushed but, even under these axotomy conditions, the labeled NF/tubulin ratios in dorsal root axons were not reduced. Peripheral cut axotomy did result in a lag in the advance of the labeling peak of the NF/microtubule protein wave in dorsal root axons, suggesting either that these proteins were delayed in exiting the cell body or that a slowing of the rate of their transport occurred. Pulse-labeling DRGs in vitro using 35S-methionine, and analysis of labeled proteins by 2-dimensional PAGE-fluorography demonstrated that the incorporation of radioactivity into NF proteins was significantly reduced, while the labeling of tubulins was unchanged 14 d after distal peripheral axotomy. In contrast to the results of peripheral axotomy, dorsal root crushes made close to the DRG (2-3 mm) or considerably distal (at the CNS entry zone 28-30 mm from the DRG) did not produce detectable changes in the amount of labeled NF or tubulin transport in central or peripheral branch axons. These findings indicate that the down-regulation of NF production/output that is exhibited at 14 d after peripheral branch axotomy is not present after central branch injury.(ABSTRACT TRUNCATED AT 400 WORDS)

Measuring creep damage using microradiography

Microradiographic techniques employing synchrotron radiation were used to investigate creep damage in several ferrous alloys. Creep damage, in the form of voids and microcracks, was imaged through differential absorption of the transmitted X-ray beam in the damaged and undamaged regions. The images were recorded on high resolution plates which were placed directly behind the samples. Slow strain rate tensile tests were performed at temperatures between 500 °C and 700 °C. The tests were interrupted after various test times, and 1.0 to 2.0 mm thick slices were cut from each sample. The creep damage in these sections was then examined using microradiography and the amount and distribution of damage was observed.

Left hemisphere contribution to motor programming of aphasic speech: A reaction time experiment in aphasic patients

Simple reaction time to lateralized visual dot stimuli was studied in 10 fluent and 10 non-fluent right-handed chronic aphasics with left hemisphere lesions. As well as the standard simple reaction time condition, the patients were given a concomitant verbal task, requiring overt articulation while reacting to the visual stimuli. Compared with the control condition, in both aphasic groups the verbal task produced an overall lengthening of latencies, with a significant slowing down of responses to the stimuli located in the right visual half-field. According to these results the verbal concurrent activity appears to involve the left hemisphere as in normal subjects, suggesting that the undamaged regions of the left hemisphere have a role to play in the motor programming of aphasic speech. As a collateral finding, the difference between latencies to stimuli ipsilateral and contralateral to the responding hand—a measure of interhemispheric transmission time—is greatly increased in patients with motor deficits. This is consistent with the view that, in simple visuo-motor reaction time, interhemispheric transfer takes place between anterior regions of the brain.