摘要:
A monolithic bidirectional switch formed in a semiconductor substrate of a first conductivity type having a front surface and a rear surface, including a first main vertical thyristor, the rear surface layer of which is of the second conductivity type, a second main vertical thyristor, the rear surface layer of which is of the first conductivity type. A structure for triggering each of the first and second main thyristors is arranged to face regions mutually distant from the two main thyristors, the neighboring portions of which correspond to a region for which, for the first main thyristor, a short-circuit area between cathode and cathode gate is formed.
摘要:
A zero crossing control circuit of a bidirectional switch including two transistors of complementary types connected in parallel between the gate of the bidirectional switch and the main reference terminal of the bidirectional switch, the gate of the bidirectional switch being connected to a control source via a first resistor, and each of the control terminals of the transistors being connected to the second main terminal of the bidirectional switch via a second resistor of high value, a zener diode being interposed between the second resistor and each of the control terminals according to a biasing adapted to turning on each of the transistors when the zener threshold is exceeded.
摘要:
A monolithic bidirectional switch formed in a semiconductor substrate of type N, including a first main vertical thyristor, the rear surface layer of which is of type P, a second main vertical thyristor, the rear surface layer of which is of type N, an auxiliary vertical thyristor, the rear surface layer of which is of type P and is common with that of the first main thyristor, a peripheral region of type P especially connecting the rear surface layer of the auxiliary thyristor to the layer of this thyristor located on the other side of the substrate, a first metallization on the rear surface side, a second metallization on the front surface side connecting the front surface layers of the first and second thyristors. An additional region has a function of isolating the rear surface of the auxiliary thyristor and the first metallization.
摘要:
The invention concerns a switching circuit (20) adapted to generate a pulse when there occurs a rising edge of a signal applied on an input terminal (CTRL), comprising: a first NPN type bipolar transistor (TN2) whereof the transmitter is connected to the input terminal; a second transistor (TP2) whereof a control electrode is connected, through a first resistor (Re2), to the input terminal, the base of the first transistor being connected to a supply potential (VDD) by the second transistor in series with a second resistor (Rp2); and a third transistor (TN3) connecting an output terminal (22) of the switching circuit to a reference potential (GND) and whereof a control electrode is connected to the collector of the first transistor (TN2).
摘要:
The present invention provides novel polynucleotides encoding CAN-12 polypeptides, fragments and homologues thereof. The present invention also provides polynucleotides encoding variants of CAN-12 polypeptides, CAN-12v1 and CAN-12v2. Also provided are vectors, host cells, antibodies, and recombinant and synthetic methods for producing said polypeptides. The invention further relates to diagnostic and therapeutic methods for applying these novel CAN-12, CAN-12v1, and CAN-12v2 polypeptides to the diagnosis, treatment, and/or prevention of various diseases and/or disorders related to these polypeptides, particularly neuro- and musculo-degenerative conditions. The invention further relates to screening methods for identifying agonists and antagonists of the polynucleotides and polypeptides of the present invention.
摘要:
The present invention relates to an assembly of two pairs of diodes in a single semiconductor substrate of a first type of conductivity, the first pair including a first diode in series with a second diode, the second pair including a third diode in series with a fourth diode, the two pairs of diodes being arranged in parallel. Each of the first and third diodes includes neighboring regions of distinct types of conductivity formed in a lightly-doped well of the second type of conductivity, these wells being separated; each of the second and fourth diodes includes separated regions of distinct types of conductivity; and metallizations connect the electrodes of the diodes to form the desired series-to-parallel assembly.
摘要:
The present invention provides novel polynucleotides encoding LSI-01 polypeptides, fragments and homologues thereof. Also provided are vectors, host cells, antibodies, and recombinant and synthetic methods for producing said polypeptides. The invention further relates to diagnostic and therapeutic methods for applying these novel LSI-01 polypeptides to the diagnosis, treatment, and/or prevention of various diseases and/or disorders related to these polypeptides. The invention further relates to screening methods for identifying agonists and antagonists of the polynucleotides and polypeptides of the present invention.
摘要:
Disclosed herein is a substantially pure nucleic acid sequence encoding a mammalian 35 kDa non-dystrophin component (&dgr;-sarcoglycan) of the dystrophin-glycoprotein complex. Also disclosed are the amino acid sequence and an immunogenic peptide of &dgr;-sarcoglycan. The peptide when used to immunize a mammal, stimulates the production of antibodies which bind specifically to the &dgr;-sarcoglycan. Methods to identify mutations in the &dgr;-sarcoglycan gene associated with autosomal recessive limb-girdle muscular dystrophy are also disclosed. The identification of such mutations enables the design of nucleic acid probes which hybridize specifically to a mutant form of &dgr;-sarcoglycan, or the complement thereof, but not to the DNA of the wild-type form of the gene (or the complement thereof), under stringent hybridization conditions. Such probes are useful, for example, in connection with the diagnosis of autosomal recessive limb-girdle muscular dystrophy. In addition, the identification of such mutations enables the diagnosis of autosomal recessive limb-girdle muscular dystrophy through the use of direct DNA sequencing techniques.
摘要:
The present invention provides novel polynucleotides encoding MP-1 polypeptides, fragments and homologues thereof. Also provided are vectors, host cells, antibodies, and recombinant and synthetic methods for producing said polypeptides. The invention further relates to diagnostic and therapeutic methods for applying these novel MP-1 polypeptides to the diagnosis, treatment, and/or prevention of various diseases and/or disorders related to these polypeptides. The invention further relates to screening methods for identifying agonists and antagonists of the polynucleotides and polypeptides of the present invention.
摘要:
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. In another aspect, the invention relates to a mouse, and cells derived therefrom, homozygous for a disrupted &agr;-sarcoglycan gene. The disruption prevents the synthesis of functional &agr;-sarcoglycan in cells of the mouse and results in the mutant mouse having no detectable sarcospan, &bgr;-, &ggr;-, &dgr;-sarcoglycan, and reduced &agr;-dystroglycan in the sarcolemma of skeletal and cardiac muscles, and a reduction of dystrophin in skeletal muscle, when compared to tissue of a mouse lacking a disrupted &agr;-sarcoglycan gene. In another aspect, the invention relates to methods for screening for therapeutic agents useful in the treatment of sarcoglycan-deficient limb-girdle muscular dystrophy. The methods involve administering a candidate therapeutic agent to a mouse, or cells derived therefrom, and assaying for therapeutic effects on the mouse or cells, with the determination of therapeutic effects being a reduction or reversal in disease progression, or a restoration of the dystroglycan complex.