Korsakoff Patient

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Serge Nicolas - One of the best experts on this subject based on the ideXlab platform.

  • experiments on implicit memory in a Korsakoff Patient by claparede 1907
    Cognitive Neuropsychology, 1996
    Co-Authors: Serge Nicolas
    Abstract:

    A translation is given of Claparede's (1907) pioneering paper on memory and amnesia, which describes the case of a woman suffering from Korsakoff's psychosis. In order to demonstrate unconscious memory on this Patient, Claparede used Ebbinghaus's method of savings. The experimental results presented here are one of the firstdemonstrations of implicitmemory in amnesia. Adopting Janet's (1904) view, he argued that amnesia is attributable to a pathological process of dissociation that interferes with the ability to synthesise memories into the personal consciousness.

Charles K Singleton - One of the best experts on this subject based on the ideXlab platform.

  • a transketolase assembly defect in a wernicke Korsakoff syndrome Patient
    Alcoholism: Clinical and Experimental Research, 1997
    Co-Authors: James J L Wang, Peter R Martin, Charles K Singleton
    Abstract:

    Thiamine deficiency, a frequent complication of alcoholism, contributes significantly to the development of damage in various organ systems, including the brain. The molecular mechanisms that underlie the differential vulnerabilities to thiamine deficiency of tissue and cell types and among individuals are not understood. Investigations into these mechanisms have examined potential variations in thiamine utilizing enzymes. Transketolase is a homodimeric enzyme containing two molecules of noncovalently bound thiamine pyrophosphate. In the present study, we examined a his-tagged human transketolase that was produced in and purified from fscherichia coli cells. Previous findings demonstrated that purified his-transketolase had a K, app for cofactor and a thiamine pyrophosphatedependent lag period for attaining steady-state kinetics that was similar to transketolase purified from human tissues. Interestingly, the time of the lag period, which is normally independent of enzyme concentration, was found herein to be dependent on the concentration of the recombinant protein. This atypical behavior was due to production in E. coli. Generation of the normal, enzyme concentration-independent state required a cytosolic factor(s) derived from human cells. Importantly, the required factor(@ was found to be defective in a Wernicke-Korsakoff Patient whose cells in culture show

  • a transketolase assembly defect in a wernicke Korsakoff syndrome Patient
    Alcoholism: Clinical and Experimental Research, 1997
    Co-Authors: James H C Wang, Peter R Martin, Charles K Singleton
    Abstract:

    Thiamine deficiency, a frequent complication of alcoholism, contributes significantly to the development of damage in various organ systems, including the brain. The molecular mechanisms that underlie the differential vulnerabilities to thiamine deficiency of tissue and cell types and among individuals are not understood. Investigations into these mechanisms have examined potential variations in thiamine utilizing enzymes. Transketolase is a homodimeric enzyme containing two molecules of noncovalently bound thiamine pyrophosphate. In the present study, we examined a his-tagged human transketolase that was produced in and purified from Escherichia coli cells. Previous findings demonstrated that purified his-transketolase had a Km app for cofactor and a thiamine pyrophosphate-dependent lag period for attaining steady-state kinetics that was similar to transketolase purified from human tissues. Interestingly, the time of the lag period, which is normally independent of enzyme concentration, was found herein to be dependent on the concentration of the recombinant protein. This atypical behavior was due to production in E. coli. Generation of the normal, enzyme concentration-independent state required a cytosolic factor(s) derived from human cells. Importantly, the required factor(s) was found to be defective in a Wernicke-Korsakoff Patient whose cells in culture show an enhanced sensitivity to thiamine deficiency.

Peter R Martin - One of the best experts on this subject based on the ideXlab platform.

  • a transketolase assembly defect in a wernicke Korsakoff syndrome Patient
    Alcoholism: Clinical and Experimental Research, 1997
    Co-Authors: James J L Wang, Peter R Martin, Charles K Singleton
    Abstract:

    Thiamine deficiency, a frequent complication of alcoholism, contributes significantly to the development of damage in various organ systems, including the brain. The molecular mechanisms that underlie the differential vulnerabilities to thiamine deficiency of tissue and cell types and among individuals are not understood. Investigations into these mechanisms have examined potential variations in thiamine utilizing enzymes. Transketolase is a homodimeric enzyme containing two molecules of noncovalently bound thiamine pyrophosphate. In the present study, we examined a his-tagged human transketolase that was produced in and purified from fscherichia coli cells. Previous findings demonstrated that purified his-transketolase had a K, app for cofactor and a thiamine pyrophosphatedependent lag period for attaining steady-state kinetics that was similar to transketolase purified from human tissues. Interestingly, the time of the lag period, which is normally independent of enzyme concentration, was found herein to be dependent on the concentration of the recombinant protein. This atypical behavior was due to production in E. coli. Generation of the normal, enzyme concentration-independent state required a cytosolic factor(s) derived from human cells. Importantly, the required factor(@ was found to be defective in a Wernicke-Korsakoff Patient whose cells in culture show

  • a transketolase assembly defect in a wernicke Korsakoff syndrome Patient
    Alcoholism: Clinical and Experimental Research, 1997
    Co-Authors: James H C Wang, Peter R Martin, Charles K Singleton
    Abstract:

    Thiamine deficiency, a frequent complication of alcoholism, contributes significantly to the development of damage in various organ systems, including the brain. The molecular mechanisms that underlie the differential vulnerabilities to thiamine deficiency of tissue and cell types and among individuals are not understood. Investigations into these mechanisms have examined potential variations in thiamine utilizing enzymes. Transketolase is a homodimeric enzyme containing two molecules of noncovalently bound thiamine pyrophosphate. In the present study, we examined a his-tagged human transketolase that was produced in and purified from Escherichia coli cells. Previous findings demonstrated that purified his-transketolase had a Km app for cofactor and a thiamine pyrophosphate-dependent lag period for attaining steady-state kinetics that was similar to transketolase purified from human tissues. Interestingly, the time of the lag period, which is normally independent of enzyme concentration, was found herein to be dependent on the concentration of the recombinant protein. This atypical behavior was due to production in E. coli. Generation of the normal, enzyme concentration-independent state required a cytosolic factor(s) derived from human cells. Importantly, the required factor(s) was found to be defective in a Wernicke-Korsakoff Patient whose cells in culture show an enhanced sensitivity to thiamine deficiency.

James J L Wang - One of the best experts on this subject based on the ideXlab platform.

  • a transketolase assembly defect in a wernicke Korsakoff syndrome Patient
    Alcoholism: Clinical and Experimental Research, 1997
    Co-Authors: James J L Wang, Peter R Martin, Charles K Singleton
    Abstract:

    Thiamine deficiency, a frequent complication of alcoholism, contributes significantly to the development of damage in various organ systems, including the brain. The molecular mechanisms that underlie the differential vulnerabilities to thiamine deficiency of tissue and cell types and among individuals are not understood. Investigations into these mechanisms have examined potential variations in thiamine utilizing enzymes. Transketolase is a homodimeric enzyme containing two molecules of noncovalently bound thiamine pyrophosphate. In the present study, we examined a his-tagged human transketolase that was produced in and purified from fscherichia coli cells. Previous findings demonstrated that purified his-transketolase had a K, app for cofactor and a thiamine pyrophosphatedependent lag period for attaining steady-state kinetics that was similar to transketolase purified from human tissues. Interestingly, the time of the lag period, which is normally independent of enzyme concentration, was found herein to be dependent on the concentration of the recombinant protein. This atypical behavior was due to production in E. coli. Generation of the normal, enzyme concentration-independent state required a cytosolic factor(s) derived from human cells. Importantly, the required factor(@ was found to be defective in a Wernicke-Korsakoff Patient whose cells in culture show

James H C Wang - One of the best experts on this subject based on the ideXlab platform.

  • a transketolase assembly defect in a wernicke Korsakoff syndrome Patient
    Alcoholism: Clinical and Experimental Research, 1997
    Co-Authors: James H C Wang, Peter R Martin, Charles K Singleton
    Abstract:

    Thiamine deficiency, a frequent complication of alcoholism, contributes significantly to the development of damage in various organ systems, including the brain. The molecular mechanisms that underlie the differential vulnerabilities to thiamine deficiency of tissue and cell types and among individuals are not understood. Investigations into these mechanisms have examined potential variations in thiamine utilizing enzymes. Transketolase is a homodimeric enzyme containing two molecules of noncovalently bound thiamine pyrophosphate. In the present study, we examined a his-tagged human transketolase that was produced in and purified from Escherichia coli cells. Previous findings demonstrated that purified his-transketolase had a Km app for cofactor and a thiamine pyrophosphate-dependent lag period for attaining steady-state kinetics that was similar to transketolase purified from human tissues. Interestingly, the time of the lag period, which is normally independent of enzyme concentration, was found herein to be dependent on the concentration of the recombinant protein. This atypical behavior was due to production in E. coli. Generation of the normal, enzyme concentration-independent state required a cytosolic factor(s) derived from human cells. Importantly, the required factor(s) was found to be defective in a Wernicke-Korsakoff Patient whose cells in culture show an enhanced sensitivity to thiamine deficiency.