Abstract: The present invention relates to a method for dyeing hair fibres, in particular a method which involves coating hair fibres with a hair dye composition and directing radio frequency electromagnetic radiation to the coated hair fibres to cause heating within the coated hair fibres by dielectric loss. The present invention also relates to kits and appliances for use in connection with the method, as well as the use of radio frequency electromagnetic radiation in reducing the effective dye-treatment time for hair fibres. In one aspect, there is provided a method of dyeing hair fibres, said method comprising the steps of: i) coating one or more hair fibres with a hair dye composition; and ii) directing radio frequency electromagnetic radiation having one or more frequencies from 1 MHz to 300 MHz to the one or more coated hair fibres to cause heating within the one or more coated hair fibres by dielectric loss.

Abstract: The present invention relates to a method for dyeing hair fibres, in particular a method which involves coating hair fibres with a hair dye composition and directing radio frequency electromagnetic radiation to the coated hair fibres to cause heating within the coated hair fibres by dielectric loss. The present invention also relates to kits and appliances for use in connection with the method, as well as the use of radio frequency electromagnetic radiation in reducing the effective dye-treatment time for hair fibres. In one aspect, there is provided a method of dyeing hair fibres, said method comprising the steps of: i) coating one or more hair fibres with a hair dye composition; and ii) directing radio frequency electromagnetic radiation having one or more frequencies from 1 MHz to 300 MHz to the one or more coated hair fibres to cause heating within the one or more coated hair fibres by dielectric loss.

Abstract: A method is provided for repairing a defect in a noise suppression panel. The method may be used to repair defects in a panel that may occur during the manufacture of or normal use of the panel. The method includes the steps of removing the defect from the noise suppression panel to create a cavity therein, forming material comprised of a material having acoustic damping properties into an insert configured to mate with the cavity, and placing the insert into the cavity.

Abstract: A tracking system is described in which a mobile tag having an unknown position is tracked in space over time. The mobile tag transmits a signal comprising a sequence of frequency components at different frequencies. The transmitted signal is received at each of a plurality of receivers, each having a known location. Each of the receivers measures the phase of each of the tones and the phase measures are passed to a central processing unit. The central processing unit then uses the determined phase measures to determine the position of the tag at the time of the transmission. Various novel tag arrangements are described which generate new transmission signals which improve accuracy and reliability of the position measurements obtained.

Abstract: A method of and apparatus for capacity determination in a telecommunications system, in the presence of Gaussian and non-Gaussian noise. The ratio of Gaussian to non-Gaussian noise is determined utilising a statistical metric. Preferably the metric is Kurtosis or the 3rd Cumulant of the Probability Density of the signal at each frequency. The determination of the ratio of Gaussian to non-Gaussian noise enables a more accurate determination of Noise, which in turn allows greater utilisation of actual available capacity in the system.

Abstract: Disclosed within is a mouse, and cells derived therefrom, which are homozygous for a disrupted &dgr;-sarcoglycan gene, the disruption in said gene having been introduced into the mouse or an ancestor of the mouse at an embryonic stage. Said disruption prevents the synthesis of functional &dgr;-sarcoglycan in cells of the mouse and results in the mouse having a reduced amount of &bgr;- and &egr;-sarcoglycan and sarcospan, and a disruption of the sarcoglycan-sarcospan complex in smooth muscle of the mouse. Said disruption also results in a reduced amount of sarcospan, &agr;-, &bgr;-, &ggr;-, and &egr;-sarcoglycan in the sarcolemma of skeletal and cardiac muscles of the mouse, compared to the amounts of said components in a mouse lacking disrupted &dgr;-sarcoglycan genes. Preferred specific disruptions of the &dgr;-sarcoglycan gene are listed.

Abstract: Disclosed is a method for treating a patient suffering from the disease sarcoglycan-deficient limb-girdle muscular dystrophy by gene replacement therapy. Sarcoglycan gene replacement therapy produces extensive long-term expression of the sarcoglycan species which restores the entire sarcoglycan complex, results in the stable association of alph&agr;-dystroglycan with the sarcolemma, and eliminates the morphological markers of limb-girdle muscular dystrophy. In another aspect, the invention relates to a method for determining a specific defective sarcoglycan species in the tissue of a patient. The method involves culture of muscle cells obtained from the patient, and the independent introduction of expression vectors encoding each of the sarcoglycan species, &agr;, &bgr;, &ggr;, and &dgr;, into the cultured cells with subsequent assaying for restoration of the dystrophin-glycoprotein complex.

Abstract: Disclosed is a transgenic knockout mouse whose genome has a homozygous disruption in its endogenous sarcospan gene, wherein the disruption prevents the synthesis of functional sarcospan in cells of the mouse. The mouse is characterized as exhibiting from 1.4 to 6.8 fold larger epididymal fat pad deposits as compared to the epididymal fat pad deposits of a wild type mouse. Methods for production of the mouse are presented. Also disclosed are cells derived from the transgenic knockout mouse. The mouse can be used in a method for identifying therapeutic agents for the treatment of an individual diagnosed with a metabolic disorder associated with a reduction or loss of expression of wild-type sarcospan. An example of such a disorder is weight gain in the individual associated with a reduction or loss of expression of wild-type sarcospan. These specific methods are also provided.

Abstract: Disclosed is a mouse, cells derived therefrom, and methods for using the mouse, the mouse being homozygous for a disrupted &dgr;-sarcoglycan gene, the disruption in the gene having been introduced into the mouse or an ancestor of the mouse at an embryonic stage. The disruption prevents the synthesis of functional &dgr;-sarcoglycan in cells of the mouse and results in the mouse having a reduced amount of &bgr;- and &egr;-sarcoglycan and sarcospan, and a disruption of the sarcoglycan-sarcospan complex in smooth muscle of the mouse. Also disclosed is a mouse, cells derived therefrom, and methods for using the mouse, the mouse being homozygous for a disrupted &bgr;-sarcoglycan gene, the disruption in the gene having been introduced into the mouse or an ancestor of the mouse at an embryonic stage.

Abstract: A nonhuman animal having somatic and germ cells in which at least one allele of an endogenous SLP-76 gene is functionally disrupted is provided. The animal may be heterozygous or, more preferably, homozygous for the SLP-76 gene disruption and is preferably a mouse. In homozygous animals, the percentage of peripheral T cells is substantially decreased compared to wildtype animals, whereas the percentage of B cells and macrophages in the periphery is substantially normal, indicating that SLP-76 disruption causes a profound block in T cell development. The animals of the invention can be used, for example, as controls to evaluate the efficacy of SLP-76 inhibitors and to identify disease conditions that can be treated with SLP-76 inhibitors. A transgenic nonhuman animal having a functionally disrupted endogenous SLP-76 gene but which has been reconstituted with an exogenous SLP-76 transgene (e.g., a human SLP-76 gene or a SLP-76 gene whose expression in targeted to a particular cell population) is also provided.

Abstract: Disclosed is a method for inhibiting the binding of an arenavirus to a cellular receptor. The method involves providing, in soluble form, a reagent comprising .alpha.-dystroglycan or a portion thereof, the reagent being characterized by the ability to bind to the arenavirus thereby inhibiting the binding of the arenavirus to the cellular receptor. The reagent is contacted with an arenavirus particle prior to infection of a cell by the arenavirus particle. Also disclosed are methods for treating an arenavirus infection in a patient and preventing an arenavirus infection in an individual at risk. These methods involve providing a therapeutic composition comprising .alpha.-dystroglycan or a portion thereof which is characterized by the ability to bind to arenaviruses, thereby inhibiting the binding of arenaviruses to a cellular receptor; and administering the composition to the patient or individual at risk.

Abstract: A combination road and air vehicle having separate engines for each craft is disclosed. The aircraft has an air frame with wings and tail elements attached to a fuselage with a tricycle landing gear attached to the air frame. A nose platform extends forward from the bottom of the fuselage. The platform is adapted to receive and support a small land vehicle. The aircraft controls are mounted on a folding stalk attached to the top side of the platform. The land vehicle has a central opening in its body through which the control stalk may be elevated to a vertical position. The aircraft and land vehicle each have its own power plant and control system.