Undersea optical stationkeeping: Improved methods

Submersibles require the capability to accurately maintain their position when they are observing, photographing, or working at a site. The most direct way for an ROV or AUV to maintain position in the near bottom environment is to track or lock onto stationary objects on the ocean floor. A particular advantage of an optical stationkeeping system is its ability to use natural rather than manmade beacons. Several improvements to our previously reported optical flow methods for the detection of vehicle motion have been investigated. Experimental results indicate that an adaptation of Newton-Raphson search combined with the use of a low-noise, high accuracy camera can drastically reduce the number of image points at which computations need be made. Other experiments with an algorithm, which accounts for illumination variations that one may encounter in undersea environments, show significant improvement in the estimation of optical flow and vehicle motion.     

Case Study of an Aerosol Explosion and a Method to Determine Explosion Temperatures

A failure analysis case study is presented for a two-piece aerosol containing tetrafluoroethane, commonly referred to as Refrigerant 134a. A gentleman was preparing to recharge the air conditioning system of an automobile when the bottom exploded off the aerosol container, propelling the body of the aerosol container like a rocket, which hit the man in the eye and blinded him in that eye. The aerosol was never connected to the air conditioner, therefore backpressure from the air conditioner (AC) compressor was ruled out as a cause for the explosion. The objective of the study was to determine why the aerosol exploded. Several recently developed test methods were used, including two types of heat-to-burst tests and a puncture chamber to measure the pressure-versus-temperature behavior of aerosols. More common test methods were also used, such as water bath pressure tests, hydro pressure burst tests, pneumatic pressure burst tests, hardness measurements, weight measurements, metallography, scanning electron microscopy (SEM), energy-dispersive spectroscopy (EDS), and an accident scenario recreation. A semi-empirical correlation between the hardness and weights of the container bottoms was used to determine the explosion temperature and/or pressure. This semi-empirical correlation agrees in principle with an analysis of the explosion pressures using finite-element analysis (FEA). The root cause for the explosion was determined to be a lack of strength of the bottom of the two-piece aerosol coupled with heating the aerosol to temperatures significantly above room temperature.     

Deletions in one domain of the Friend virus-encoded membrane glycoprotein overcome host range restrictions for erythroleukemia

Although the Friend virus-encoded membrane glycoprotein (gp55) activates erythropoietin receptors (EpoR) to cause erythroblastosis only in certain inbred strains of mice but not in other species, mutant viruses can overcome aspects of mouse resistance. Thus, mice homozygous for the resistance allele of the Fv-2 gene are unaffected by gp55 but are susceptible to mutant glycoproteins that have partial deletions in their ecotropic domains. These and other results have suggested that proteins coded for by polymorphic Fv-2 alleles might directly or indirectly interact with EpoR and that changes in gp55 can overcome this defense. A new viral mutant with an exceptionally large deletion in its ecotropic domain is now also shown to overcome Fv-2rr resistance. In all cases, the glycoproteins that activate EpoR are processed to cell surfaces as disulfide-bonded dimers. To initiate analysis of nonmurine resistances, we expressed human EpoR and mouse EpoR in the interleukin 3-dependent mouse cell line BaF3 and compared the abilities of Friend virus-encoded glycoproteins to convert these cells to growth factor independence. Human EpoR was activated in these cells by erythropoietin but was resistant to gp55. However, human EpoR was efficiently activated in these cells by the same viral mutants that overcome Fv-2rr resistance in mice. By construction and analysis of human-mouse EpoR chimeras, we obtained evidence that the cytosolic domain of human EpoR contributes to its resistance to gp55 and that this resistance is mediated by accessory cellular factors. Aspects of host resistance in both murine and nonmurine species are targeted specifically against the ecotropic domain of gp55.     

Vector quantization by deterministic annealing

A deterministic annealing approach is suggested to search for the optimal vector quantizer given a set of training data. The problem is reformulated within a probabilistic framework. No prior knowledge is assumed on the source density, and the principle of maximum entropy is used to obtain the association probabilities at a given average distortion. The corresponding Lagrange multiplier is inversely related to the `temperature' and is used to control the annealing process. In this process, as the temperature is lowered, the system undergoes a sequence of phase transitions when existing clusters split naturally, without use of heuristics. The resulting codebook is independent of the codebook used to initialize the iterations     

The effects of carrier-velocity saturation on high-current BJToutput resistance

Modern bipolar junction transistors (BJTs) tend to operate with saturated carrier velocity in the collector space-charge region. A physical analysis of the effects of velocity saturation on the output resistance of BJTs, especially for high current levels is presented. Physical analyses show that when the collector current density approaches a critical value, the Early voltage can increase significantly due to carrier-velocity saturation as the resulting base push-out partially offsets base-width modulation. This effect is also demonstrated in simulations with PISCES and MMSPICE     

Electroencephalogram asymmetry in response to the approach of a stranger and maternal separation in 10-month-old infants.

We recently reported the presence of reliable asymmetries in frontal-brain electrical activity in infants that distinguished between certain positive- and negative-affect elicitors. In order to explore the degree to which these asymmetries in brain activity are associated with individual differences in affective response, 35 ten-month-old female infants were presented with a stranger-approach, mother-approach, and maternal-separation experience while an electroencephalogram (EEG) from the left- and right-frontal and left- and right-parietal scalp regions was recorded and facial and other behavioral responses were videotaped. Changes in frontal-EEG asymmetry reflected behavioral changes between conditions. In addition, individual differences in affective response to separation were related to differences in frontal-brain asymmetries. These findings indicate that lawful changes exist in asymmetries of frontal-brain activation during the expression of certain emotions in the first year of life and that individual differences in emotional responsivity are related to these measures of brain activity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A PET study of the neural systems of stuttering

The cause of stuttering is unknown. Failure to develop left-hemispheric dominance for speech is a long-standing theory although others implicated the motor system more broadly, often postulating hyperactivity of the right (language nondominant) cerebral hemisphere. As knowledge of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postulating hyperactivity of premotor cortex, either directly or through connectivity with the thalamus and basal ganglia. Alternative theories target the auditory and speech production systems. By contrasting stuttering with fluent speech using positron emission tomography combined with chorus reading to induce fluency, we found support for each of these hypotheses. Stuttering induced widespread overactivations of the motor system in both cerebrum and cerebellum, with right cerebral dominance. Stuttered reading lacked left-lateralized activations of the auditory system, which are thought to support the self-monitoring of speech, and selectively deactivated a frontal-temporal system implicated in speech production. Induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed the auditory-system underactivations and the deactivation of the speech production system. Thus stuttering is a disorder affecting the multiple neural systems used for speaking.     

Reduced dosage of genes encoding ribosomal protein S18 suppresses a mitochondrial initiation codon mutation in Saccharomyces cerevisiae

A yeast mitochondrial translation initiation codon mutation affecting the gene for cytochrome oxidase subunit III (COX3) was partially suppressed by a spontaneous nuclear mutation. The suppressor mutation also caused cold-sensitive fermentative growth on glucose medium. Suppression and cold sensitivity resulted from inactivation of the gene product of RPS18A, one of two unlinked genes that code the essential cytoplasmic small subunit ribosomal protein termed S18 in yeast. The two S18 genes differ only by 21 silent substitutions in their exons; both are interrupted by a single intron after the 15th codon. Yeast S18 is homologous to the human S11 (70% identical) and the Escherichia coli S17 (35% identical) ribosomal proteins. This highly conserved family of ribosomal proteins has been implicated in maintenance of translational accuracy and is essential for assembly of the small ribosomal subunit. Characterization of the original rps18a-1 missense mutant and rps18a delta and rps18b delta null mutants revealed that levels of suppression, cold sensitivity and paromomycin sensitivity all varied directly with a limitation of small ribosomal subunits. The rps18a-1 mutant was most affected, followed by rps18a delta then rps18b delta. Mitochondrial mutations that decreased COX3 expression without altering the initiation codon were not suppressed. This allele specificity implicates mitochondrial translation in the mechanism of suppression. We could not detect an epitope-tagged variant of S18 in mitochondria. Thus, it appears that suppression of the mitochondrial translation initiation defect is caused indirectly by reduced levels of cytoplasmic small ribosomal subunits, leading to changes in either cytoplasmic translational accuracy or the relative levels of cytoplasmic translation products.