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J W Johnson

Publications and source records attributed to J W Johnson.

At least 19 recordsLinked to original sources
PubMed2001

Free intracellular Mg(2+) concentration and inhibition of NMDA responses in cultured rat neurons.

1. Intracellular Mg(2+) (Mg(2+)(i)) blocks single-channel currents and modulates the gating kinetics of NMDA receptors. However, previous data suggested that Mg(2+)(i) inhibits whole-cell current less effectively than predicted from excised-patch measurements. We examined the basis of this discrepancy by testing three hypothetical explanations. 2. To test the first hypothesis, that control of free Mg(2+)(i) concentration ([Mg(2+)](i)) during whole-cell recording was inadequate, we measured [Mg(2+)](i) using mag-indo-1 microfluorometry. The [Mg(2+)](i) measured in cultured neurons during whole-cell recording was similar to the pipette [Mg(2+)] measured in vitro, suggesting that [Mg(2+)](i) was adequately controlled. 3. To test the second hypothesis, that open-channel block by Mg(2+)(i) was modified by patch excision, we characterised the effects of Mg(2+)(i) using cell-attached recordings. We found the affinity and voltage dependence of open-channel block by Mg(2+)(i) similar in cell-attached and outside-out patches. Thus, the difference between Mg(2+)(i) inhibition of whole-cell and of patch currents cannot be attributed to a difference in Mg(2+)(i) block of single-channel current. 4. The third hypothesis tested was that the effect of Mg(2+)(i) on channel gating was modified by patch excision. Results of cell-attached recording and modelling of whole-cell data suggest that the Mg(2+)(i)-induced stabilisation of the channel open state is four times weaker after patch excision than in intact cells. This differential effect of Mg(2+)(i) on channel gating explains why Mg(2+)(i) inhibits whole-cell NMDA responses less effectively than patch responses.

Animals↗
PubMed2001

A synthetic validity approach to testing differential prediction hypotheses.

A new method is presented for conducting differential prediction analyses that makes it possible to test differential prediction hypotheses with adequate statistical power even when the sample size within a job or a job family is very small. This method, called synthetic differential prediction analysis, represents an application of the logic of synthetic validation to differential prediction analyses. The authors explain this new method and describe its application in a selection-system validation study conducted in a large organization.

Decision Making↗
PubMed2001

The relative importance of task and contextual performance dimensions to supervisor judgments of overall performance.

Although evidence supports the unique contribution of task performance and contextual performance to overall evaluations, little is known about the relative contribution that specific dimensions of contextual performance make to overall performance judgments. This study evaluated the extent to which supervisors consider task and contextual performance by using relative weights (J. W. Johnson, 2000) to statistically describe the relative importance of specific dimensions of each type of performance to overall performance ratings. Within each of 8 job families in a large organization, each of 4 dimensions of contextual performance made not only a unique contribution but a relatively important contribution to the overall evaluation. Evidence also supports the adaptive performance dimension of handling work stress as an aspect of contextual performance and job-task conscientiousness as an aspect of both task and contextual performance.

Adult↗
PubMed2001

Correlation of head-to-body delivery intervals in shoulder dystocia and umbilical artery acidosis.

OBJECTIVE: Our goal was to determine the effect of shoulder dystocia on umbilical artery acidosis. STUDY DESIGN: We performed a retrospective analysis of 134 mother-infant pairs of shoulder dystocia cases at our institution from January 1, 1994, through December 31, 1997. Cases were identified from the obstetric database, and charts were abstracted for demographics, head-to-body delivery interval, umbilical blood gas parameters, and neonatal outcome. Pooled student t tests were used to compare mean blood gas values with data previously reported from our patient population. Regression analysis was performed regarding head-to-body delivery interval and blood gas parameters. RESULTS: The mean umbilical artery pH of shoulder dystocia cases (7.23 +/-.082) was less than the mean arterial pH of all vaginal deliveries in our institution (7.27 +/-.069), P <.001. Head-to-body delivery intervals (available for 44 cases) were not associated with statistically significant alterations in umbilical artery pH (r(2) =.0004), PCO(2) (r(2) =.011), or base deficit (r(2) =.006). Increasing head-to-body delivery interval was also not significantly correlated with decreasing 5-minute Apgar score (r =.0278). CONCLUSION: In our study population, shoulder dystocia resulted in statistically significant but clinically insignificant reductions in mean umbilical artery blood gas parameters. No statistically significant linear relationship was identified between the head-to-body delivery interval and fetal acid-base status.

Apgar Score↗
PubMed2001

Evolution in damage control for exsanguinating penetrating abdominal injury.

OBJECTIVE: Damage control (DC) has proven valuable in exsanguinated patients. The purpose of this study was to quantify and qualify the impact of current damage control principles applied in a penetrating abdominal injury (PAI) population. METHODS: Over a 3-year period (June 1997-May 2000), of 271 laparotomies for PAI, 24 patients underwent DC (8.9%). Demographics, injury grade, resuscitative and operative parameters, acid-base status, coagulation profiles, fluid/transfusion requirements, definitive repairs, abdominal closure, complications, and outcomes were reviewed. Data were compared with our DC experience a decade earlier. Fisher's exact test was used for comparisons. RESULTS: Overall survival improved for equivalent Injury Severity Score, Revised Trauma Score, TRISS, admission systolic blood pressure, operating room systolic blood pressure, and Penetrating Abdominal Trauma Index score. Solids (1.2 vs. 1.3), hollow organ (1.5 vs. 1.7), and major vascular injuries (0.5 vs. 0.8) per patient remain unchanged. Currently, there was less hypothermia with equivalent operating room times. In intensive care unit survivors, acid-base status was similar but coagulopathy and hypothermia were less severe. Definitive colon management has shifted from ostomies to anastomoses. Eventual fascial closure occurred in 14 of 19 (74%) compared with 12 of 14 (86%) in the historical group. There were three gastrointestinal fistulae (one pancreatic), one anastomotic leak, and three intra-abdominal abscesses. CONCLUSION: Continued application of DC principles has led to improved survival with PAI. Better control of temperature, experience with the open abdomen, and intensive care unit care may be causative.

Abdominal Injuries↗
PubMed2000

Persistent activation of ERK contributes to glutamate-induced oxidative toxicity in a neuronal cell line and primary cortical neuron cultures.

Oxidative stress can trigger neuronal cell death and has been implicated in several chronic neurological diseases and in acute neurological injury. Oxidative toxicity can be induced by glutamate treatment in cells that lack ionotrophic glutamate receptors, such as the immortalized HT22 hippocampal cell line and immature primary cortical neurons. Previously, we found that neuroprotective effects of geldanamycin, a benzoquinone ansamycin, in HT22 cells were associated with a down-regulation of c-Raf-1, an upstream activator of the extracellular signal-regulated protein kinases (ERKs). ERK activation, although often attributed strictly to neuronal cell survival and proliferation, can also be associated with neuronal cell death that occurs in response to specific insults. In this report we show that delayed and persistent activation of ERKs is associated with glutamate-induced oxidative toxicity in HT22 cells and immature primary cortical neuron cultures. Furthermore, we find that U0126, a specific inhibitor of the ERK-activating kinase, MEK-1/2, protects both HT22 cells and immature primary cortical neuron cultures from glutamate toxicity. Glutamate-induced ERK activation requires the production of specific arachidonic acid metabolites and appears to be downstream of a burst of reactive oxygen species (ROS) accumulation characteristic of oxidative stress in HT22 cells. However, inhibition of ERK activation reduces glutamate-induced intracellular Ca(2+) accumulation. We hypothesize that the precise kinetics and duration of ERK activation may determine whether downstream targets are mobilized to enhance neuronal cell survival or ensure cellular demise.

Animals↗
PubMed2000

Inhibition by intracellular Mg(2+) of recombinant N-methyl-D-aspartate receptors expressed in Chinese hamster ovary cells.

Intracellular Mg(2+) (Mg(i)(2+)) inhibits the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors in cultured cortical neurons. To examine the effects of Mg(i)(2+) on recombinant NMDA receptors composed of subunit combinations found in cortical neurons, we expressed heteromeric receptors composed of NR1/NR2A and of NR1/NR2B subunits in Chinese hamster ovary (CHO) cells. We recorded whole-cell currents from the recombinant receptors in the absence and presence of Mg(i)(2+). The voltage dependence of control (0 Mg(i)(2+)) NMDA-activated currents obtained from CHO cells transfected with NR1/NR2A and with NR1/NR2B receptors showed outward rectification, a property that has been observed previously in native cortical NMDA receptors. The magnitude and voltage dependence of inhibition by Mg(i)(2+) of NMDA-activated currents were similar in CHO cells transfected with NR1/NR2A receptors, CHO cells transfected with NR1/NR2B receptors, and in cultured neurons expressing native NMDA receptors. These observations suggest that Mg(i)(2+) has uniform effects on the native NMDA receptors expressed in cortical neurons. Furthermore, inhibition by Mg(i)(2+) must not depend on intracellular factors or post-translational receptor modifications that are specific to neurons. Finally, the results indicate that the previously observed differences between whole-cell and outside-out patch measurements of Mg(i)(2+) inhibition could not result from poor control of voltage or Mg(i)(2+) concentration in the dendrites of neurons. The most likely alternative explanation is that patch excision causes an alteration in NMDA receptors that results in more effective inhibition by Mg(i)(2+).

Animals↗
PubMed1999

Permeant ion regulation of N-methyl-D-aspartate receptor channel block by Mg(2+).

Block of the channel of N-methyl-D-aspartate (NMDA) receptors by external Mg(2+) (Mg(o)(2+)) has broad implications for the many physiological and pathological processes that depend on NMDA receptor activation. An essential property of channel block by Mg(o)(2+) is its powerful voltage dependence. A widely cited explanation for the strength of the voltage dependence of block is that the Mg(o)(2+)-binding site is located deep in the channel of NMDA receptors; Mg(o)(2+) then would sense most of the membrane potential field during block. However, recent electrophysiological and mutagenesis studies suggest that the blocking site cannot be deep enough to account for the voltage dependence of Mg(o)(2+) block. Here we describe the basis for this discrepancy: the magnitude and voltage dependence of channel block by Mg(o)(2+) are strongly regulated by external and internal permeant monovalent cations. Our data support a model in which access to the channel by Mg(o)(2+) is prevented when permeant ion-binding sites at the external entrance to the channel are occupied. Mg(o)(2+) can block the channel only when the permeant ion-binding sites are unoccupied and then can either unblock back to the external solution or permeate the channel. Unblock to the external solution is prevented if external permeant ions bind while Mg(2+) blocks the channel, although permeation is still permitted. The model provides an explanation for the strength of the voltage dependence of Mg(o)(2+) block and quantifies the interdependence of permanent and blocking ion binding to NMDA receptors.

Animals↗
PubMed1999

Corrosion of stainless steel, nickel-titanium, coated nickel-titanium, and titanium orthodontic wires.

Orthodontic wires containing nickel have been implicated in allergic reactions. The potential for orthodontic wires to cause allergic reactions is related to the pattern and mode of corrosion with subsequent release of metal ions, such as nickel, into the oral cavity. The purpose of this study was to determine if there is a significant difference in the corrosive potential of stainless steel, nickel titanium, nitride-coated nickel titanium, epoxy-coated nickel titanium, and titanium orthodontic wires. At least two specimens of each wire were subjected to potentiostatic anodic dissolution in 0.9% NaCl solution with neutral pH at room temperature. Using a Wenking MP 95 potentiostat and an electrochemical corrosion cell, the breakdown potential of each wire was determined. Photographs were taken of the wire speci mens using a scanning electron microscope, and surface changes were qualitatively evaluated. The breakdown potentials of stainless steel, two nickel titanium wires, nitride-coated nickel titanium, epoxy-coated nickel titanium, and titanium were 400 mV, 300 mV, 750 mV, 300 mV, 1800 mV, and >2000 mV, respectively. SEM photographs revealed that some nickel titanium and stainless steel wires were susceptible to pitting and localized corrosion. The results indicate that corrosion occurred readily in stainless steel. Variability in breakdown potential of nickel titanium alloy wires differed across vendors' wires. The nitride coating did not affect the corrosion of the alloy, but epoxy coating decreased corrosion. Titanium wires and epoxy-coated nickel titanium wires exhibited the least corrosive potential. For patients allergic to nickel, the use of titanium or epoxy-coated wires during orthodontic treatment is recommended.

Coated Materials, Biocompatible↗
PubMed1998

Comparison of results in two implantable defibrillators. Jewel 7219D Investigators.

The Jewel 7219D was the first non-thoracotomy implantable cardioverter-defibrillator (ICD) with biphasic shock capability small enough to be placed in the prepectoral subcutaneous position. Size reduction of ICDs is desirable, but safety and efficacy of smaller devices must be demonstrated. Outcomes of patients treated with the Jewel 7219D defibrillator (n = 1,781) and with its precursor model PCD 7217B (n = 2,637) were compared. To use PCD patients (n = 2,637) as historical (n = 2,574) and concurrent controls (n = 63), statistical adjustments using the Cox proportional-hazards regression model were made. Jewel recipients (n = 1,781) treated in 106 US and 32 non-US centers exhibited similar characteristics including a mean age of 59 years, 78% men, ejection fraction of 34%, history of aborted sudden cardiac death in 41%, and coronary artery disease in 70%. Implantation was completed in 1,777 of 1,781 (99.9%) attempts and success with the first electrode configuration and polarity was 89.5%. Kaplan-Meier cumulative first-year survivals for cardiac and all-cause mortality were 98.5% and 93.3%. Complication-free first-year survival for Jewel implants in prepectoral subcutaneous (n = 582), subpectoral submuscular (n = 366), and abdominal (n = 449) positions did not differ (p > 0.05). First-year survival free of pocket-related complications exceeded 98% in all locations. Adjusted cardiac and all-cause first-year mortality, and efficacy in terminating spontaneous tachyarrhythmias did not differ between the 2 device groups. In conclusion, the safety and efficacy of Jewel model 7219D in the prepectoral subcutaneous position are at least equal to either those of Jewel models implanted in different positions or to those of the previously extensively characterized PCD 7217B.

Cardiac Surgical Procedures↗
PubMed1998

Open channel block and alteration of N-methyl-D-aspartic acid receptor gating by an analog of phencyclidine.

We investigated inhibition of the N-methyl-D-aspartic acid (NMDA) receptor-channel complex by N-ethyl-1,4,9, 9alpha-tetrahydro-4alphaR-cis-4alphaH-fluoren-++ +4alpha-amine (NEFA), a structural analog of phencyclidine (PCP). Using the whole-cell recording technique, we demonstrated that NEFA inhibits NMDA responses with an IC50 of 0.51 microM at -66 mV. We determined that NEFA binds to the open channel, and subsequently the channel can close and trap the blocker. Once the channel has closed, NEFA is unable to dissociate until the channel reopens. Single-channel recordings revealed that NEFA reduces the mean open time of single NMDA-activated channels in a concentration-dependent manner with a forward blocking rate (k+) of 39.9 microM-1 s-1. A computational model of antagonism by NEFA was developed and constrained using kinetic measurements of single-channel data. By multiple criteria, only models in which blocker binding in the channel causes a change in receptor operation adequately fit or predicted whole-cell data. By comparing model predictions and experimental measurements of NEFA action at a high NMDA concentration, we determined that NEFA affects receptor operation through an influence on channel gating. We conclude that inhibition of NMDA receptors by PCP-like blockers involves a modification of channel gating as well as block of current flow through the open channel.

Animals↗
PubMed1998

Immunolymphoscintigraphy in breast cancer: evaluation using 131I-labeled monoclonal antibody B72.3.

Noninvasive axillary lymph node staging was investigated using [131I]murine monoclonal antibody B72.3 in 16 patients with breast cancer scheduled for axillary dissection. [131I]B72.3 was injected into ipsilateral finger webs or around the breast biopsy. Scintigraphy to 72 h and gamma-counting/immunohistochemistry of nodes were performed. Specific antibody uptake (%ID/g) and the ratio of specific:nonspecific antibody uptake were not significantly different in tumor-positive versus tumor-negative nodes, suggesting that [131I]B72.3 is unsuitable to discriminate axillary node tumor involvement.

Antibodies, Monoclonal↗
PubMed1998

Binding sites for permeant ions in the channel of NMDA receptors and their effects on channel block.

We report the presence of binding sites for permeant monovalent cations at the internal and external entrances to the channel of NMDA receptors. We measured the effects of changing internal cesium (Cs+) and external sodium (Na+) concentrations on the channel-blocking kinetics of the adamantane derivatives IEM-1754 and IEM-1857. Binding of Na+, or of Cs+ after it permeates the channel, to sites at the external channel entrance prevents blockers from entering the channel. Binding of Na+ to a blocked channel prevents blocker unbinding. Cs+ binding to a site at the internal channel entrance prevents IEM-1754 from occupying the deeper of its two sites of block. The results show the critical effects of permeant ions on the kinetics, affinity and voltage-dependence of channel blockers.

Adamantane↗
PubMed1997

The etiology of fetal acidosis as determined by umbilical cord acid-base studies.

OBJECTIVE: Our purpose was to determine whether umbilical cord acid-base values might be used to differentiate abruptio placentae from cord prolapse. STUDY DESIGN: By use of a retrospective study design, umbilical cord blood acid-base values of 32 cases of severely acidotic acute abruptio placentae were statistically compared with those of 19 cases of severely acidotic acute cord prolapse with Fisher's exact test, Mann-Whitney U tests, and receiver-operator curve characteristic analyses. RESULTS: No significant differences in electronic fetal heart rate record interpretations were detected. Highly significant differences in umbilical arterial and umbilical venous blood gas values were noted between the two groups. Most notable were the differences between umbilical venous and arterial blood gas values in the cord prolapse group. Receiver-operator characteristic curve analysis demonstrated that an umbilical venous-arterial pH difference of 0.15 was an effective cutoff value in differentiating cord prolapse from abruptio placentae (accuracy 92%). CONCLUSION: Umbilical arterial blood gas values combined with umbilical venous blood gas values can assist in determining the pathogenesis of marked fetal acidosis.

Abruptio Placentae↗
PubMed1997

Complications associated with pectoral implantation of cardioverter defibrillators. World-Wide Jewel Investigators.

Pectoral placement of ICD pulse generators is now routine after downsizing of these devices. However, the safety of this approach is not well documented. The aim of this study was to evaluate complications in a large cohort of patients undergoing initial pectoral ICD implantation. The subjects for this study were 1,000 consecutive patients receiving a Medtronic Jewel ICD at 93 centers worldwide. Cumulative follow-up for all patients was 634 patient-years, with 64.9% of patients followed for 6 months or longer. The complications evaluated were erosion, pocket hematoma, seroma, wound infection, dehiscence, device migration, lead fracture, and dislodgment. In this series, 1.8% of patients experienced a pocket complication with only 3 (0.3%) erosions and 2 (0.2%) infections. Lead complications were observed in 2.1% of subjects, most commonly early dislodgment of the RV lead. We conclude that pectoral implantation of a downsized ICD system can be performed with a low rate of complications. However, careful attention to anchoring techniques and close early monitoring is important given the 1.7% rate of lead dislodgment that occurred primarily during the first month following implantation.

Cohort Studies↗
PubMed1997

Trapping channel block of NMDA-activated responses by amantadine and memantine.

We investigated the mechanisms by which the antiparkinsonian and neuroprotective agents amantadine and memantine inhibit responses to N-methyl-D-aspartic acid (NMDA). Whole cell recordings were performed using cultured rat cortical neurons or Chinese hamster ovary (CHO) cells expressing NMDA receptors. Both amantadine and memantine blocked NMDA-activated channels by binding to a site at which they could be trapped after channel closure and agonist unbinding. For neuronal receptors, the IC50s of amantadine and memantine at -67 mV were 39 and 1.4 microM, respectively. When memantine and agonists were washed off after steady-state block, one-sixth of the blocked channels released rather than trapped the blocker; memantine exhibited "partial trapping." Thus memantine appears to have a lesser tendency to be trapped than do phencyclidine or (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[1,d]cyclihepten-5,1 0-imine (MK-801). We next investigated mechanisms that might underlie partial trapping. Memantine blocked and could be trapped by recombinant NMDA receptors composed of NR1 and either NR2A or NR2B subunits. In these receptors, as in the native receptors, the drug was released from one-sixth of blocked channels rather than being trapped in all of them. The partial trapping we observed therefore was not due to variability in the action of memantine on a heterogeneous population of NMDA receptors in cultured cortical neurons. Amantadine and memantine each noncompetitively inhibited NMDA-activated responses by binding at a second site with roughly 100-fold lower affinity, but this form of inhibition had little effect on the extent to which memantine was trapped. A simple kinetic model of blocker action was used to demonstrate that partial trapping can result if the presence of memantine in the channel affects the gating transitions or agonist affinity of the NMDA receptor. Partial trapping guarantees that during synaptic communication in the presence of blocker, some channels will release the blocker between synaptic responses. The extent to which amantadine and memantine become trapped after channel block thus may influence their therapeutic effects and their modulation of NMDA-receptor-mediated excitatory postsynaptic potentials.

Amantadine↗