Abstract: The invention relates to systems and methods for determining personalized recommended daily intake, for example, the recommended daily allowance (RDA) for nutrients based on genetic information of the individual. In several embodiments, the systems and methods of the invention can be used to determine recommendations for specific nutrient supplements, foods, beverages, meals, menus, diets and recipes for an individual which are more accurately adapted to their needs based on their personal genetic risk scores.

Abstract: Provided is a measurement method whereby the amount of unbound bilirubin (UB) can be exactly reflected whether a specimen contains a large amount of conjugated bilirubin or not. The measurement method for UB according to the present invention comprises decomposition step (i), decomposition stopping step (ii), contact step (iii) and detection step (iv). In decomposition step (i), a blood sample containing unconjugated bilirubin (iD-Bil) and conjugated bilirubin (D-Bil) is subjected to an oxidative decomposition reaction of UB in iD-Bil and D-Bil. In decomposition stopping step (ii), the oxidative decomposition reaction is stopped to give a decomposition product of the sample. In contact step (iii), the decomposition product of the sample is contacted with UnaG that is capable of specifically binding to iD-Bil. Separately, an unreacted sample, which is the blood sample not subjected to decomposition step (i), is contacted with UnaG too.

Abstract: In order to provide a novel fluorescent protein and use thereof, the polypeptide according to the present invention has fluorescent properties in the presence of bilirubin and includes (1) the amino acid sequence of SEQ ID NO: 1, (2) an amino acid sequence having, for example, substitution of 1 to 21 amine acids in the amino acid sequence of SEQ ID NO: 1, (3) an amino acid sequence having 85% or more sequence identity to the amino acid sequence of SEQ ID NO: 1, or (4) the amino acid sequence encoded by a polynucleotide that hybridizes with a polynucleotide consisting of a sequence complementary to the polynucleotide encoding the polypeptide according to the amino acid sequence in (1) under a stringent condition.

Abstract: Provided is a measurement method whereby the amount of unbound bilirubin (UB) can be exactly reflected whether a specimen contains a large amount of conjugated bilirubin or not. The measurement method for UB according to the present invention comprises decomposition step (i), decomposition stopping step (ii), contact step (iii) and detection step (iv). In decomposition step (i), a blood sample containing unconjugated bilirubin (iD-Bil) and conjugated bilirubin (D-Bil) is subjected to an oxidative decomposition reaction of UB in iD-Bil and D-Bil. In decomposition stopping step (ii), the oxidative decomposition reaction is stopped to give a decomposition product of the sample. In contact step (iii), the decomposition product of the sample is contacted with UnaG that is capable of specifically binding to iD-Bil. Separately, an unreacted sample, which is the blood sample not subjected to decomposition step (i), is contacted with UnaG too.

Abstract: In order to provide a novel fluorescent protein and use thereof, the polypeptide according to the present invention has fluorescent properties in the presence of bilirubin and includes (1) the amino acid sequence of SEQ ID NO: 1, (2) an amino acid sequence having, for example, substitution of 1 to 21 amine acids in the amino acid sequence of SEQ ID NO: 1, (3) an amino acid sequence having 85% or more sequence identity to the amino acid sequence of SEQ ID NO: 1, or (4) the amino acid sequence encoded by a polynucleotide that hybridizes with a polynucleotide consisting of a sequence complementary to the polynucleotide encoding the polypeptide according to the amino acid sequence in (1) under a stringent condition.

Abstract: ATR kinase is a key regulator of checkpoint responses to incompletely replicated and damaged DNA. Without this checkpoint, cells will enter mitosis prematurely, likely resulting in cell death. The invention provides methods and reagents to either block or activate the activation of the ATR kinase checkpoint, through, for example, either blocking or activating the expression of an ATR activator TopBP1. The invention also provides screening methods to identify additional ToBP1 inhibitors or activators that may be used to modulate the activity of the ATR checkpoint.

Abstract: A light-emitting device with a protection layer for Zn inter-diffusion and a process to form the device are described. The device of the invention provides an active layer containing aluminum (Al) as a group III element, typically AlGaInAs, and protection layers containing silicon (Si) to prevent the inter-diffusion of zing (Zn) atoms contained in p-type layers surrounding the active layer. One of protection layers is put between the active layer and the p-type cladding layer, while, the other of protection layers is disposed between the active layer and the p-type burying layer.

Abstract: ATR kinase is a key regulator of checkpoint responses to incompletely replicated and damaged DNA. Without this checkpoint, cells will enter mitosis prematurely, likely resulting in cell death. The invention provides methods and reagents to either block or activate the activation of the ATR kinase checkpoint, through, for example, either blocking or activating the expression of an ATR activator TopBP1. The invention also provides screening methods to identify additional ToBP1 inhibitors or activators that may be used to modulate the activity of the ATR checkpoint.

Abstract: A light-emitting device with a protection layer for Zn inter-diffusion and a process to form the device are described. The device of the invention provides an active layer containing aluminum (Al) as a group III element, typically AlGaInAs, and protection layers containing silicon (Si) to prevent the inter-diffusion of zing (Zn) atoms contained in p-type layers surrounding the active layer. One of protection layers is put between the active layer and the p-type cladding layer, while, the other of protection layers is disposed between the active layer and the p-type burying layer.

Abstract: ATR kinase is a key regulator of checkpoint responses to incompletely replicated and damaged DNA. Without this checkpoint, cells will enter mitosis prematurely, likely resulting in cell death. The invention provides methods and reagents to either block or activate the activation of the ATR kinase checkpoint, through, for example, either blocking or activating the expression of an ATR activator TopBP1. The invention also provides screening methods to identify additional ToBP1 inhibitors or activators that may be used to modulate the activity of the ATR checkpoint.

Abstract: Claspin proteins and nucleotides encoding Claspin proteins are provided. Also provided is a method for identifying a compound that modulates cell cycle progression. A method is further provided for modulating cell cycle progression.

Abstract: The present invention provides compositions of ATR nucleic acids and proteins, as well as methods of using said compositions in screening assays. The invention further provides antibodies and transgenic animals based on the ATR compositions.

Abstract: Claspin proteins and nucleotides encoding Claspin proteins are provided. Also provided is a method for identifying a compound that modulates cell cycle progression. A method is further provided for modulating cell cycle progression.

Abstract: The present invention provides a threonine/tyrosine kinase, Myt1, that phosphorylates the cyclin-dependent kinase, Cdc2, to provide regulation of the cell cycle at the G2/M interphase. Also included are polynucleotides encoding Myt1 polypeptide and antibodies that bind to Myt1. Methods of modulating Myt1 for preventing premature entry of the cell into mitosis or to accelerate entry into mitosis are also provided, as are methods for identifying agents that modulate Myt1.

Abstract: The present invention provides a threonine/tyrosine kinase, Myt1, that phosphorylates the cyclin-dependent kinase, Cdc2, to provide regulation of the cell cycle at the G2/M interphase. Also included are polynucleotides encoding Myt1 polypeptide and antibodies that bind to Myt1. Methods of modulating Myt1 for preventing premature entry of the cell into mitosis or to accelerate entry into mitosis are also provided, as are methods for identifying agents that modulate Myt1.

Abstract: The present invention provides a threonine/tyrosine kinase, Myt1, that phosphorylates the cyclin-dependent kinase, Cdc2, to provide regulation of the cell cycle at the G2/M interphase. Also included are polynucleotides encoding Myt1 polypeptide and antibodies that bind to Myt1. Methods of modulating Myt1 for preventing premature entry of the cell into mitosis or to accelerate entry into mitosis are also provided, as are methods for identifying agents that modulate Myt1.

Abstract: The present invention provides a threonine/tyrosine kinase, Myt1, that phosphorylates the cyclin-dependent kinase, Cdc2, to provide regulation of the cell cycle at the G2/M interphase. Also included are polynucleotides encoding Myt1 polypeptide and antibodies that bind to Myt1. Methods of modulating Myt1 for preventing premature entry of the cell into mitosis or to accelerate entry into mitosis are also provided, as are methods for identifying agents that modulate Myt1.