摘要:
Post-manufacture compensation for a sensing offset can be provided, at least in part, by selectively exposing one of a pair of cross-coupled transistors in a sense amplifier to a bias voltage selected to cause a compensating shift in a characteristic of the exposed transistor. In designs susceptible to post-manufacture data dependent creep in a device characteristic, such exposure may be advantageously provided in situ by causing the sense amplifier to sense values purposefully skewed toward a predominate value selected to cause the compensating shift. In some realizations, an on-chip test block is employed to identify and characterize sensing mismatch. Typically, the techniques described herein may be employed to address sensing offsets that have developed post-manufacture due to a data-dependent effect. However, in some realizations, the techniques described herein may be used to address a sensing offset arising at least in part from other or additional sources.
摘要:
According to one embodiment, a memory is disclosed. The memory includes a differential sense amplifier that receives a data input and a complementary data input; and a switching mechanism, coupled to the amplifier, that switches the data input and the complementary data input to minimize a negative bias temperature instability (NBTI) effect on the amplifier.
摘要:
Post-manufacture compensation for a sensing offset can be provided, at least in part, by selectively exposing one of a pair of cross-coupled transistors in a sense amplifier to a bias voltage selected to cause a compensating shift in a characteristic of the exposed transistor. Such exposure may be advantageously provided in situ by causing the sense amplifier to sense values purposefully skewed toward a predominate value selected to cause the compensating shift. In some realizations, purposefully skewed values (e.g., value and value_1) are introduced directly into the sense amplifier. In some realizations, an on-chip test block is employed to identify and characterize sensing mismatch.
摘要:
Post-manufacture variation of timing may be employed to address data-dependent degradation or creep in device characteristics affecting a differential circuit. One particular example of such data-dependent degradation or creep involves Negative Bias Temperature Instability (NBTI). In certain memory circuit configurations, NBTI can cause threshold voltage (Vt) of PMOS devices to increase by an amount that depends on the historical amount of voltage bias that has been applied across gate and source/drain nodes. In the case of many sense amplifier designs, a predominant value read out using the sense amp may tend to disparately affect one device (or set of devices) as compared with an opposing device (or set of devices). In other words, if the same data value is read over and over again, then one of two opposing PMOS devices of a typical sense amp will accumulate an NBTI-related Vt shift, while the opposing PMOS device will accumulate little or no shift. The accumulated mismatch tends to cause an increase in the sense amp fail-point.
摘要:
Human chemokine Alpha-3 polypeptides and DNA (RNA) encoding such chemotactic cytokines and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemotactic cytokines for the treatment of leukemia, tumors, chronic infections, auto-immune disease, fibrotic disorders, sepsis, wound healing and psoriasis and to stimulate stem cell mobilization. Antagonists against such chemotactic cytokines and their use as a therapeutic to treat rheumatoid arthritis, auto-immune and chronic and acute inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever, ARDS and bone marrow failure are also disclosed. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Also disclosed are diagnostic assays for detecting mutations in the polynucleotides encoding the chemotactic cytokines and for detecting altered levels of the polypeptide in a host.
摘要:
Human chemokine Alpha-2 polypeptides and DNA (RNA) encoding such chemotactic cytokines and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemotactic cytokines for the treatment of leukemia, tumors, chronic infections, auto-immune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemotactic cytokines and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic and acute inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Also disclosed are diagnostic assays for detecting mutations in the polynucleotides encoding the chemotactic cytokines and for detecting altered levels of the polypeptides in a host.
摘要:
The present invention relates to novel Death Domain Containing Receptor-5 (DR5) proteins which are members of the tumor necrosis factor (TNF) receptor family, and have now been shown to bind TRAIL. In particular, isolated nucleic acid molecules are provided encoding the human DR5 proteins. DR5 polypeptides are also provided as are vectors, host cells and recombinant methods for producing the same. The invention further relates to screening methods for identifying antagonists and antagonists of DR5 activity.
摘要:
Human chemotactic cytokine I polypeptides and DNA (RNA) encoding such chemotactic cytokines and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemotactic cytokines for the treatment of leukemia, tumors, chronic infections, auto-immune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemotactic cytokines and their use as a therapeutic to treat rheumatoid arthritis, auto-immune and chronic and acute inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Also disclosed are diagnostic assays for detecting mutations in the polynucleotides encoding the chemotactic cytokines and for detecting altered levels of the polypeptide in a host.
摘要:
Human chemotactic cytokine I polypeptides and DNA (RNA) encoding such chemotactic cytokines and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemotactic cytokines for the treatment of leukemia, tumors, chronic infections, auto-immune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemotactic cytokines and their use as a therapeutic to treat rheumatoid arthritis, auto-immune and chronic and acute inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Also disclosed are diagnostic assays for detecting mutations in the polynucleotides encoding the chemotactic cytokines and for detecting altered levels of the polypeptide in a host.
摘要:
The present invention relates to novel human proteins and isolated nucleic acids containing the coding regions of the genes encoding such proteins. Also provided are vectors, host cells and recombinant methods for producing the proteins of the invention. The invention further relates to diagnostic and therapeutic methods useful for diagnosing and treating disorders related to these novel human secreted proteins.