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The wavelength-independent, non-reciprocal splitting properties of the asymmetric, multimode Y-junction make it an ideal device for use as a low-loss, low-power tap in a concatenated linear bus. The properties of a two-dimensional slab model of the junction are investigated and the results of ray-tracing, modal and numerical beam propagation method (BPM) techniques are compared. Minimization of splicing loss between the ports of a square-core, three-dimensional buried channel waveguide version of the device and a multimode fibre is also addressed.

In this paper we report two novel evanescent-field devices based on tapered singlemode optical fibres. In both devices single-mode optical fibre is tapered to waist diameters of around 2 μm such that transmission remains close to 100%. In the first device successive coating layers of sol-gel containing fluorescent material are baked on. The major application is in the field of sensing through changes in the absorption and fluorescence characteristics. In the second device, the taper is immersed in a solution of poly(vinyl acetate), also containing fluorescent material. This solidifies, creating a solid-state device. Applications are miniaturized amplifiers and lasers.

The transverse shift in the field distribution and the correction to the propagation constant of the fundamental and symmetric cladding modes on bent finite-clad single-mode fibres and slab waveguides are evaluated from perturbation theory for effective index values extending below the cladding index. Analytical results are derived in both geometries for the step-profile that are valid within the overall limitations of the theory. However, it is found that, for the fibre geometry only, the method breaks down at certain discrete wavelengths because of degeneracies that occur between the HE12 (LP02) and TE01 (LP11) mode propagation constants.

This paper examines the operation of tapered optical fibres and polished or D-fibres as evanescent field devices. Both devices operate through the evanescent field outside the fibre interacting with chemicals in the surrounding external medium. The incoming field is absorbed and may be reradiated through fluorescence. The absorption and fluorescence recapture characteristics of both configurations are compared, showing that the tapered fibre device permits a stronger interaction and is therefore more efficient. Furthermore, it is shown that the characteristics of both configurations are sensitive to the refractive index of the external medium.

Anomolous spikes in the loss spectrum of practical depressed-cladding fibres with a finite cladding and absorbing jacket can be explained in terms of a combination of three effects — the excitation conditions, the absorption behaviour of core and cladding modes, and the slight variation in the fibre diameter along its length.

The 5×5 coupler is of interest because of its application to coherent detection. The supermodes of the entire structure are determined by analysing the coupling of the component fibre modes through coupled-mode theory. The beating of the supermodes along the coupler determines the output power in each of the cores. Equal power splitting is a requirement for coherent detection. We show that this condition is not easily satisfied.

The paper reviews the area of tapered optical fibers which have significant potential as evanescent field sensing devices. They minimize some of the problems associated with any such device and can be much more sensitive to changes in fluorescence and absorption characteristics. This paper firstly discusses two evanescent field devices which are currently used and then describes the prototype tapered optical fiber device which has been fabricated to demonstrate the principal of operation. Results are presented using the dye Rhodamine 6G as the 'sensing' chemical. Problems associated with the device are considered. Two alternative tapered fiber arrangements are also presented.© (1994) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

Mucolipidosis II (ML II, I-cell disease) and mucolipidosis III (ML III, pseudo-Hurler polydystrophy) are human autosomal recessive genetic disorders resulting from deficient UDP-N-acetylglucosamine:lysosomal enzyme precursor N-acetylglucosamine-1-phosphotransferase (GNPT) activity. Normally, this enzyme is involved in the processing of most lysosomal enzymes. Cultured fibroblasts from individuals with either disorder are deficient in a broad array of lysosomal enzymes as a result of the diminished GNPT activity. We report the correction of this phenotype by fusing transformed ML III cells generated for this study to lethally irradiated rodent cells. This method of gene transfer does not require selection for the gene of interest, animal models, nor any knowledge of the gene product except a screening method for its presence. It has generated corrected cell hybrids that contain approximately 1% hamster-derived sequences. These cell lines, which contain the hamster analogue to the human phosphotransferase gene, are useful for the molecular cloning of the gene defective in ML II and ML III.

The polyamines are known to be essential for cellular proliferation. Ornithine decarboxylase (ODC) is a rate-limiting enzyme in the synthesis of these amines, and activity is elevated in colorectal tumors and polyps. Two ODC genes (designated ODC1 and ODC2) were localized by somatic cell hybridization and in situ techniques to 2p25 and 7q31-qter, respectively. Investigation of the expression of ODC in colorectal neoplasia reveals a consistent increase in mRNA expression compared with normal adjacent mucosa and control mucosa, ranging from 1.3- to 12.2-fold. No amplification of the loci was seen. Comparison of ODC mRNA expression with ODC activity from the same samples revealed no direct correlation, suggesting that regulation of ODC in this system occurs at the posttranscriptional level.

Arylsulfatase C is a microsomal membrane-bound enzyme previously thought to be the same as steroid sulfatase, the only X-linked enzyme known to escape from X inactivation in man. We had shown that arylsulfatase C actually consists of two biochemically distinct isozymes, s and f. Only the s form has steroid sulfatase activity. The f and s forms were thought to be related through posttranslational or posttranscriptional modification of the same gene product. In part consistent with this hypothesis, we now report that in a panel of 28 rodent-human somatic cell hybrids, expression of both s and f was concordant only with the human X chromosome, thus showing that the f form is also X linked. In three separate somatic hybrids containing human X chromosomes in an inactive state, the f form was still expressed. Thus, similar to the s form, the f form also escapes from X inactivation. However, contrary to expectations, the s and f forms were not related by posttranslational modification of the same gene product. A full-length cDNA for the s form failed to hybridize to transcripts produced from an f-expressing cell line, showing that there is little sequence identity between the two. They are also not related by differential splicing of a common primary transcript, since fibroblasts from some patients with steroid sulfatase deficiency due to gene deletion of the s form continue to express the f form. Therefore, although the f and s isozymes of arylsulfatase C are X linked and escape from X inactivation, they are products from separate genes, thus providing a unique isoenzyme system to study possible gene duplication and regulation in the part of the human X chromosome that escapes inactivation.

An anomalous loss spike observed in the absorption spectrum beyond the cutoff wavelength of the fundamental mode of a straight depressed-cladding fibre can be attributed to supermode coupling caused by slight variations in fibre diameter occurring during the fabrication process. Bending of the fibre shifts this coupling to a higher wavelength. >

A simple variational method is used to determine the modal properties of single-mode couplers and Y junctions when the cores are close together or coalesce. The results complement the well-known perturbation expressions for large core separation. Together the two approximation methods provide accurate approximations over the complete range of separation from infinite separation to complete coalescence.

A lithium-drifted germanium p-i-n diode was used as detector to measure the prompt radiation emitted by the reaction 12 C (d,p) 13 C during the irradiation of steels with low-energy deuterons. Typical spectra obtained using a diode and a thalliumactivated sodium iodide crystal are compared, and results given for a number of standard steel samples.

Tissue factor (tissue thromboplastin, coagulation factor III), a protein component of cell membranes, is an essential cofactor for factor VII-dependent initiation of blood coagulation. Since no tissue factor-deficient condition has been described, it is one of only a few proteins of the coagulation system for which the pattern of inheritance has not been ascertained. Because of the species-specificity of tissue factor activity and the availability of a very sensitive chromogenic assay, it was possible in the present study to use somatic cell hybrids to assign the chromosomal location of the tissue factor structural gene (F3) to human chromosome 1 (1pter----1p21).

Fifteen malignant melanomas were subjected to chromosomal analysis, in order to determine whether the number of chromosomes in a tumor cell could be correlated to a clinical prognosis. The protocol involved a direct technique which utilized a Colcemid blockade of spindle formation in mitosis to allow study of metaphase chromosomes. The direct method was chosen to reveal chromosome changes in the tumor cell in situ rather than changes in the cultured cell. Two tumors yielded chromosome spreads which could be counted and correlated with a clinical prognosis. Failure to obtain other adequate chromosome spreads were accounted for by the presence of tissue necrosis and the absence of viable tumor cells.

A complementary DNA (cDNA) probe for the predominant (pI 7) form of human monocyte-derived interleukin-1 (IL1) and a collection of 30 human-mouse somatic cell hybrids were used to assign the IL1 gene to human chromosome 2 by Southern blot analysis of hybrid cell DNA digested with the restriction endonuclease BglII. In situ hybridization to human metaphase chromosomes localized the IL1 gene to the long arm of chromosome 2 at position 2q13-2q21 between two fragile sites.

The inherited human disorders sialidosis and galactosialidosis are the result of deficiencies of glycoprotein-specific alpha-neuraminidase (acylneuraminyl hydrolase, EC 3.2.1.18; sialidase) activity. Two genes were determined to be necessary for expression of neuraminidase by using human-mouse somatic cell hybrids segregating human chromosomes. A panel of mouse RAG-human hybrid cells demonstrated a single-gene requirement for human neuraminidase and allowed assignment of this gene to the (pter----q23) region of chromosome 10. A second panel of mouse thymidine kinase (TK)-deficient LM/TK- -human hybrid cells demonstrated that human neuraminidase activity required both chromosomes 10 and 20 to be present. Analysis of human neuraminidase expression in interspecific hybrid cells or polykaryocytes formed from fusion of mouse RAG (hypoxanthine/guanine phosphoribosyltransferase deficient) or LM/TK- cell lines with human sialidosis or galactosialidosis fibroblasts indicated that the RAG cell line complemented the galactosialidosis defect, but the LM/TK- cell line did not. This eliminates the requirement for this gene in RAG-human hybrid cells and explains the different chromosome requirements of these two hybrid panels. Fusion of LM/TK- cell hybrids lacking chromosome 10 or 20 (phenotype 10+,20- and 10-,20+) and neuraminidase-deficient fibroblasts confirmed by complementation analysis that the sialidosis disorder results from a mutation on chromosome 10, presumably encoding the neuraminidase structural gene. Galactosialidosis is caused by a mutation in a second gene required for neuraminidase expression located on chromosome 20.

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A combination chemical-spectrographic method for determining metallic impurities in high-purity chromium is described. Chromium is removed from the metallic impurities by volatilization as chromyl chloride. The remaining solution is examined spectrographically for elements such as iron, nickel, aluminum, manganese, titanium, vanadium, magnesium, and copper in the 0.1- to 30-ppm range. Direct arcing of chromic sulfate is used for the determination of silicon.

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A methodology has been developed and demonstrated which is capable of determining total amounts of asbestos fibers and fibrils in air ranging from as low as fractional nanograms per cubic meter (ng/m3) of air to several micrograms/m3. The method involves the collection of samples on an absolute filter and provides an unequivocal identification and quantification of the total asbestos contents including fibrils in the collected samples.The developed method depends on the trituration under controlled conditions to reduce the fibers to fibrils, separation of the asbestos fibrils from other collected air particulates (beneficiation), and the use of transmission microscopy for identification and quantification. Its validity has been tested by comparative analyses by neutron activation techniques. It can supply the data needed to set emissions criteria and to serve as a basis for assessing the potential hazard for asbestos pollution to the populace.

CONVENTIONAL techniques of activation analysis usually require the measurement, some time after the completion of the irradiation, of the radiation emitted by a radioactive nuclide manufactured during the irradiation, with or without prior separation of the radionuclide to be determined, and sensitive analytical methods have been devised for most elements using thermal neutrons as bombarding particles1,2. However, for the light elements, low cross-sections and inconvenient half-lives of the product nuclides often preclude the use of thermal neutron irradiation as the basis of an analytical method, and charged particles, γ-protons2,3, and neutrons of non-thermal energies4 have been used instead.

In an adiabatic taper, spot size is determined by the fundamental local mode alone. In non-adiabatic tapers, some of the power in the fundamental mode is coupled into cladding local modes, so that spot size is determined by a superposition of all these modes and can depart significantly from the adiabatic result. Both analytical and numerical solutions are presented.

The reduction of excess loss in practical single-mode fibre tapers requires the local taper angle to be smaller than an intuitive value. This qualitative criterion is quantified for various taper shapes. For a given taper length, loss is minimal for shapes which are similar to the shape obtained by assuming the intuitive value of angle everywhere along the taper.