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M D Berger

Publications and source records attributed to M D Berger.

5 recordsLinked to original sources
PubMed2001

Design and evaluation of a tryptophanless RecA protein with wild type activity.

The C-terminal domain of the Escherichia coli RecA protein contains two tryptophan residues whose native fluorescence emission provides an interfering background signal when other fluorophores such as 1,N(6)-ethenoadenine, 2-aminopurine and other tryptophan residues are used to probe the protein's activities. Replacement of the wild type tryptophans with nonfluorescent residues is not trivial because one tryptophan is highly conserved and the C-terminal domain functions in both DNA binding as well as interfilament protein-protein contact. We undertook the task of creating a tryptophanless RecA protein with WT RecA activity by selecting suitable amino acid replacements for Trp290 and Trp308. Mutant proteins were screened in vivo using assays of SOS induction and cell survival following UV irradiation. Based on its activity in these assays, the W290H-W308F W-less RecA was purified for in vitro characterization and functioned like WT RecA in DNA-dependent ATPase and DNA strand exchange assays. Spectrofluorometry indicates that the W290H-W308F RecA protein generates no significant emission when excited with 295-nm light. Based on its ability to function as wild type protein in vivo and in vitro, this dark RecA protein will be useful for future fluorescence experiments.

2-Aminopurine↗
PubMed1988

Spontaneous compared with induced onset of sustained ventricular tachycardia.

Electrophysiological characteristics of the modes of initiation of 16 episodes of spontaneously occurring sustained ventricular tachycardia recorded in 16 patients by two-channel ambulatory electrocardiographic monitoring were compared with the characteristics of ventricular tachycardia induced by programmed electrical stimulation. Eleven episodes of spontaneous ventricular tachycardia began after a single ventricular premature depolarization (VPD), three episodes after two VPDs, and two episodes after five VPDs. By comparison, only four episodes of sustained ventricular tachycardia were induced with a single VPD. Each episode of spontaneous ventricular tachycardia was initiated by a late coupled VPD (RR':QT ratio greater than 1.0). The VPD was often morphologically similar to the ensuing ventricular tachycardia (eight of 11 episodes that began after a single VPD). No correlation was found between the modes of initiation of spontaneous and induced ventricular tachycardia. We hypothesize that concealed decremental slow conduction, reflected in the long coupling intervals of VPDs initiating ventricular tachycardia, is of critical importance in initiating ventricular tachycardia. We conclude that major differences exist in the timing and number of VPDs associated with the onsets of spontaneous and induced sustained ventricular tachycardia.

Adult↗
PubMed1983

Neurophysiological effects of -X impact acceleration.

In 19 experiments, eight unanesthetized Rhesus monkeys, with torsos restrained in a seated position, and with head and neck free to move, were subjected to peak sled accelerations in the -X direction ranging from 42 m/s2 to 963 m/s2. Recordings of cortical somatosensory evoked potentials were made using recording electrodes chronically implanted over the somatosensory cortex. Electrical pulse stimuli were delivered at a rate of 5 Hz through spinal electrodes located at L1-L2. Evoked potentials were recorded prior to impact, through the impact event, and subsequent to impact, then subjected to quantitative analysis procedures which included normalized cross-correlation and exponential regression. The results of this analysis suggest a neurophysiological effect which holds promise as an indicator of a pre-injurious central nervous system condition. This effect is a transient increase of 2% to 5% in the latency of the primary surface positive peak of the cortical evoked potential. There appears to be a threshold for these increases in latency at peak sled accelerations in the region of 600 m/s2. This is consistent with previous findings and provides the basis for applying these techniques to human volunteer experiments.

Acceleration↗
PubMed1983

Evoked potential studies of the effects of impact acceleration on the motor nervous system.

The initial results of a continuing investigation into the effects of various levels of impact acceleration on the functional integrity of the motor nervous system are summarized. The results are based on the measurement of alterations in neural transmission along the motor pathway of the Rhesus monkey as revealed by latency and amplitude changes in the motor pathway evoked potential (EP) following the delivery of various levels of impact acceleration to a test vehicle. The EPs were produced by electrical stimulation of and recording from the motor pathway of experimental animals subjected to -Y (lateral impact) acceleration and animals subjected to -X (frontal impact) acceleration. High resolution latency and amplitude measures of the EP recorded from these animals before and after impact were tracked so that the time course of recovery of nerve propagation following impact could be accurately assessed. Analysis of these EP measures revealed that the time course of recovery to preimpact values is directly related to the intensity of the acceleration impulse delivered to the test vehicle.

Acceleration↗