Abstract: A system basis chip is described. The system basis chip comprises a power supply circuit configured to receive an input voltage and generate a plurality of voltages, and a control circuit. Specifically, the power supply circuit is configured to selectively switch on a first and a second voltage of the voltages as a function of a control signal. The control circuit measures a resistance value of an external resistor connected to a terminal and selects one of a plurality of configurations as a function of the measured resistance value, wherein a first configuration indicates that said first voltage should be switched on before said second voltage and a second configuration indicates that said second voltage should be switched on before said first voltage. Accordingly, the control circuit may generate the control signal in order to switch on in sequence the first and the second voltage according to the selected configuration.

Abstract: In an embodiment a timing system includes a master timing device including a master oscillator stage configured to receive a reference signal and to generate a first main clock signal frequency-locked with the reference signal, a master timing stage including a master counter configured to update value with a timing that depends on the first main clock signal, the master timing stage configured to generate a first local clock signal of a pulsed type, a timing of pulses of the first local clock signal being controllable by the master counter and a master synchronization stage configured to generate a synchronization signal synchronous with the first local clock signal, wherein the synchronization signal includes a corresponding pulse for each group of consecutive pulses of the first local clock signal formed by a number (N) of pulses, and a slave timing device including a slave oscillator stage configured to receive the reference signal and to generate a second main clock signal frequency-locked with the refer

Abstract: A method to arm an airbag, the method including determining, by a system device, that an arming condition for the airbag has been met; delivering a communication to a master device from the system device to inform the master device that the arming condition has been met; snooping the communication by an expansion device; and arming the airbag by the expansion device in response to snooping the arming condition.

Abstract: A system basis chip is described. The system basis chip comprises a power supply circuit configured to receive an input voltage and generate a plurality of voltages, and a control circuit. Specifically, the power supply circuit is configured to selectively switch on a first and a second voltage of the voltages as a function of a control signal. The control circuit measures a resistance value of an external resistor connected to a terminal and selects one of a plurality of configurations as a function of the measured resistance value, wherein a first configuration indicates that said first voltage should be switched on before said second voltage and a second configuration indicates that said second voltage should be switched on before said first voltage. Accordingly, the control circuit may generate the control signal in order to switch on in sequence the first and the second voltage according to the selected configuration.

Abstract: A circuit includes comparator circuitry to sense a current through a load and compare the intensity of the current with a comparison threshold which can be set to a first, lower threshold value and a second, higher threshold value. Logic circuitry receives from the comparator circuitry a comparison signal having a first value or a second value based on whether the intensity is lower or higher than the comparison threshold. The logic circuitry is configured to assert a first overcurrent event signal or a second overcurrent event signal based on the comparison signal having the first value or the second value and the comparison threshold set to the first or second threshold value.

Abstract: In an embodiment a timing system includes a master timing device including a master oscillator stage configured to receive a reference signal and to generate a first main clock signal frequency-locked with the reference signal, a master timing stage including a master counter configured to update value with a timing that depends on the first main clock signal, the master timing stage configured to generate a first local clock signal of a pulsed type, a timing of pulses of the first local clock signal being controllable by the master counter and a master synchronization stage configured to generate a synchronization signal synchronous with the first local clock signal, wherein the synchronization signal includes a corresponding pulse for each group of consecutive pulses of the first local clock signal formed by a number (N) of pulses, and a slave timing device including a slave oscillator stage configured to receive the reference signal and to generate a second main clock signal frequency-locked with the refer

Abstract: There is disclosed a method to predict the predisposition to an exercise performance trait in a human individual comprising: a) assaying a genetic sample obtained from the human individual for the presence of at least one genetic variation in each of the following genes: ACTN3, COL5A1, MCT1, VEGF, HFE, to obtain a polymorphism profile; b) determining a regression function associated to the polymorphism profile; c) classifying the individual's predisposition to the exercise performance trait on the basis of the value of said regression function.

Abstract: A circuit includes comparator circuitry to sense a current through a load and compare the intensity of the current with a comparison threshold which can be set to a first, lower threshold value and a second, higher threshold value. Logic circuitry receives from the comparator circuitry a comparison signal having a first value or a second value based on whether the intensity is lower or higher than the comparison threshold. The logic circuitry is configured to assert a first overcurrent event signal or a second overcurrent event signal based on the comparison signal having the first value or the second value and the comparison threshold set to the first or second threshold value.

Abstract: A mechanism for maintaining the same communication identity number when intercepted calls are forwarded is embodied in various methods, devices and media-storing software.

Abstract: A mechanism for maintaining the same communication identity number when intercepted calls are forwarded is embodied in various methods, devices and media-storing software.

Abstract: The protein pRb2/p130 represses expression of the ER-? gene. Blocking pRb2/p130 expression or altering ER-? gene methylation to alter pRb2/p130 complex binding allows transcriptional activity of the ER-? gene to be restored. Detecting and regulating the methylation state of the ER-? gene, optionally together with detecting and regulating pRb2/p130 multimolecular complexes bound to the ER-? gene promoter, allows estrogen-insensitive breast cancer cells to be identified, so that an accurate prognosis can be obtained and an appropriate course of treatment administered. Also, inhibiting pRb2/p130, or altering the methylation pattern of the ER-? gene by targeting DNMT 1 In the pRb2/p 130-E2F4/5-HDAC 1-DNMT1-SUV39H1 complex, allows estrogen-insensitive breast cancer cells to be converted to estrogen-sensitive breast cancer cells. Estrogen-sensitive breast cancer cells which are generally more susceptible to current anti-cancer treatments.

Abstract: Muscle tissue regeneration is one of the most important homeostatic processes of adult skeletal muscle, which after development retains the capacity to regenerate in response to different type of stimuli, including a direct trauma or neurological dysfunction; atrophy; and genetic defects. The present invention pertains to cdk9-55 and its ability to regenerate muscle tissue and enhance development. Cdk9-55 is specifically induced upon satellite cell differentiation and is necessary for the gene expression reprogramming required to complete the regeneration process.

Abstract: Methylation of DNA in regions involved in transcriptional regulation can induce the binding of ICBP90 and the subsequent formation of multiprotein complexes which alter gene transcription. DNA methylation in tumor suppressor genes, or in other genes which are involved in mitigating tumorigenesis, can induce binding of ICBP90 to those genes. Bound ICBP90 can interact with a pRb2/p130 regulatory complexes to remodel chromatin and inhibit transcription of the gene. DNA methyltransferases, ICBP90, and the proteins comprising the pRb2/p130 complex are therefore therapeutic targets for the treatment of cancer. Abnormalities in these proteins can also be markers of cancerous or precancerous conditions.

Abstract: Novel polypeptides or derivatives comprising cdk2 binding site are disclosed. The novel polypeptides or derivatives have growth suppressive activity. Nucleic acids encoding those polypeptides are also disclosed. The polypeptides identified herein are also useful in methods for treating or preventing cancer. The treatment methods comprise administration of the polypeptide to the patient. The methods also comprise contacting the sample with the above-described polypeptide or derivative, wherein the polypeptide or derivative also comprises a covalently attached detectable moiety, then determining whether the polypeptide or derivative is binding cdk2 from the sample.

Abstract: Novel polypeptides or derivatives comprising cdk2 binding site are disclosed. The novel polypeptides or derivatives have growth suppressive activity. Nucleic acids encoding those polypeptides are also disclosed. The polypeptides identified herein are also useful in methods for treating or preventing cancer. The treatment methods comprise administration of the polypeptide to the patient. The methods also comprise contacting the sample with the above-described polypeptide or derivative, wherein the polypeptide or derivative also comprises a covalently attached detectable moiety, then determining whether the polypeptide or derivative is binding cdk2 from the sample.

Abstract: A method for determining presence of lymphoma in a patient is disclosed. A sample of bone marrow, thymus, spleen, lymph nodes, lymph and/or lymphocytes taken from the patient t is assayed to determine expression of CDK9 and CYCLIN T1. The presence of CDK9 and/or CYCLIN T1 is indicative of a lymphoma other than a mantle cell lymphoma or marginal zone lymphoma in the patient.

Abstract: Novel polypeptides or derivatives comprising cdk2 binding site are disclosed. The novel polypeptides or derivatives have growth suppressive activity. Nucleic acids encoding those polypeptides are also disclosed. The polypeptides identified herein are also useful in methods for treating or preventing cancer. The treatment methods comprise administration of the polypeptide to the patient. The methods also comprise contacting the sample with the above-described polypeptide or derivative, wherein the polypeptide or derivative also comprises a covalently attached detectable moiety, then determining whether the polypeptide or derivative is binding cdk2 from the sample.

Abstract: The protein pRb2/p130 represses expression of the ER-? gene. Blocking pRb2/p130 expression or altering ER-? gene methylation to alter pRb2/p130 complex binding allows transcriptional activity of the ER-? gene to be restored. Detecting and regulating the methylation state of the ER-? gene, optionally together with detecting and regulating pRb2/p130 multimolecular complexes bound to the ER-? gene promoter, allows estrogen-insensitive breast cancer cells to be identified, so that an accurate prognosis can be obtained and an appropriate course of treatment administered. Also, inhibiting pRb2/p130, or altering the methylation pattern of the ER-? gene by targeting DNMT 1 In the pRb2/p 130-E2F4/5-HDAC 1-DNMT1-SUV39H1 complex, allows estrogen-insensitive breast cancer cells to be converted to estrogen-sensitive breast cancer cells. Estrogen-sensitive breast cancer cells which are generally more susceptible to current anti-cancer treatments.

Abstract: The present invention discloses a set of molecular signatures modulated by RB2/p130 for lung cancer cells and a method of determining whether to use a RB2/p130 gene expression system or a protein encoded by the system to modulate a gene or gene expression pattern in lung cancer cells of mammals.

Abstract: Substantially pure human cyclin-dependent kinase-like proteins PITALRE and PISSLRE and isolated protein complexes that comprise PITALRE or PISSLRE are disclosed. Isolated nucleic acid molecule that encode PITALRE or PISSLRE, or a fragment thereof; recombinant expression vectors that comprise nucleic acid sequence that encode PITALRE or PISSLRE; and host cells that comprise such recombinant expression vectors are disclosed. Oligonucleotide molecules that consist of a nucleotide sequence complimentary to a portion of the nucleotide sequence that encodes PITALRE or PISSLRE are disclosed. Antibodies which bind to epitopes on PITALRE or PISSLRE are disclosed. Nucleic acid molecules that comprise a nucleotide sequence that encodes phosphorylation deficient PITALRE, or a phosphorylation deficient PI SSLRE; recombinant vectors and pharmaceutical compositions that comprise such nucleotide sequences are also disclosed. Methods of identifying compounds which inhibit PITALRE activity are disclosed.