ABSTRACT
In phosphor thermometry, the fitting of decay curves is a key task in the robust and precise determination of temperatures. These decays are generally assumed to be mono-exponential in certain temporal boundaries, where fitting is performed. The present study suggests a multi-exponential method to determine the spectral distribution in terms of decay times in order to analyze phosphorescence decays and thereby complement the mono-exponential analysis. Therefore, two methods of choice are compared and verified using simulated data in the presence of noise. Addtionally, this spectral decomposition is applied to the thermographic phosphor Mg4FGeO6 : Mn and reveals changes in the exponential distributions of decay times upon a change of the excitation laser energy.
ABSTRACT
Phosphor thermometry is a semi-invasive surface temperature measurement technique utilising the luminescence properties of doped ceramic materials. Typically, these phosphor materials are coated onto the object of interest and are excited by a short UV laser pulse. Up to now, primarily Q-switched laser systems with repetition rates of 10 Hz were employed for excitation. Accordingly, this diagnostic tool was not applicable to resolve correlated temperature transients at time scales shorter than 100 ms. This contribution reports on the first realisation of a high-speed phosphor thermometry system employing a highly repetitive laser in the kHz regime and a fast decaying phosphor. A suitable material was characterised regarding its temperature lifetime characteristic and its measurement precision. Additionally, the influence of laser power on the phosphor coating was investigated in terms of heating effects. A demonstration of this high-speed technique has been conducted inside the thermally highly transient system of an optically accessible internal combustion engine. Temperatures have been measured with a repetition rate of 6 kHz corresponding to one sample per crank angle degree at 1000 rpm.
ABSTRACT
INTRODUCTION: Autosomal dominant optic atrophy (ADOA) is considered as the most common form of hereditary optic neuropathy. Although genetic linkage studies point to the OPA1 locus on chromosome 3q28-q29 as by far the most common gene locus, previous screening studies-based on sequencing of the coding exons-detected OPA1 mutations in only 32-70% of ADOA patients. We therefore hypothesised that larger deletions or duplications that remained undetected in previous screening approaches may substantially contribute to the prevalence of OPA1 mutations in ADOA. METHODS: 42 independent ADOA patients were analysed for the presence of genomic rearrangements in OPA1 by means of multiplex ligation probe amplification (MLPA). Deletions or duplications were confirmed either by long distance polymerase chain reaction (PCR) and breakpoint sequencing or loss of heterozygosity analyses with flanking microsatellite markers. Patients underwent ophthalmological examination including visual acuity, colour vision testings, perimetry and funduscopy. RESULTS: We identified genomic rearrangements in 8 of 42 patients, including single exon deletions of exon 9 and exon 24, respectively, a deletion of exons 1-5, two different deletions of the complete OPA1 gene as well as a duplication of the exons 7-9, with the latter being present in three unrelated families. Patients' phenotypes were highly variable, similar to patients with point mutation in OPA1. DISCUSSION: Our findings show that gross genomic aberrations at the OPA1 gene locus are frequent in ADOA and substantially contribute to the spectrum and prevalence of OPA1 mutations in ADOA patients. They further strengthen the hypothesis that haploinsufficiency is a major pathomechanism in OPA1 associated ADOA.
