Biomedical subjects

M R McLaughlin

Publications and source records attributed to M R McLaughlin.

41 records · Page 3Linked to original sources

PubMed1995

Hyperventilation therapy for severe traumatic brain injury.

The management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. That hyperventilation therapy might exacerbate secondary brain injury seems likely based on abnormalities in cerebral blood flow (CBF) and metabolism which result from TBI, and the potential for hyperventilation to worsen those abnormalities. Both global and regional CBF are critically reduced, and metabolism increased, during the first several hours and days after injury. As a result, focal ischemia is common following severe TBI. Hyperventilation causes a further decrease in CBF, often without a concomitant reduction in ICP. In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.

Brain↗

PubMed1993

The use of antibodies targeted against the neurofilament subunits for the detection of diffuse axonal injury in humans.

Axonal injury is a common feature of human traumatic brain injury. Typically, damaged axons cannot be recognized unless a patient survives the injury by at least 10-12 hours (h). Limitations associated with the use of the traditional silver methods have been linked with this inability to recognize early posttraumatic reactive axonal change. Recently, we reported that antibodies targeting the neurofilament subunits proved useful in recognizing early traumatically induced axonal change in traumatically brain-injured animals. Accordingly, in the present communication, we employed antibodies to detect at the light microscopic level the 68 kD Nf-L and 170-200 kD Nf-H neurofilament subunits in head-injured patients who survived the traumatic event for periods ranging from 6 h to 59 days. Antibodies targeting all of the above-described subunits revealed a progression of reactive axonal change. Antibodies to the 68 kD subunit proved most useful, as they were not complicated by concomitant immunoreactivity in surrounding nuclei and/or dendritic and somatic elements. These immunocytochemical strategies revealed, at 6 h postinjury, focally swollen axons which appeared intact. By 12 h, this focal swelling had progressed to disconnection, with the immunoreactive swelling undergoing further expansion over 1 week postinjury. These findings demonstrate the utility of the previously described immunocytochemical strategies for detecting reactive axonal change in brain-injured humans, particularly in the early posttraumatic course. More importantly, these methods also demonstrate in humans that reactive axonal change is not necessarily caused by traumatically induced tearing.

Accidental Falls↗

PubMed1989

Monoclonal antibodies produced to bean yellow mosaic virus, clover yellow vein virus, and pea mosaic virus which cross-react among the three viruses.

Monoclonal antibodies prepared against individual potyviruses that infect forage legumes cross-reacted among the viruses. The reaction occurs between capsid subunits and presumably involves epitopes located in the trypsin-resistant core of the coat protein.

Animals↗

PubMed1984

Use of experimental designs with quantitative ELISA.

Precise use of enzyme-linked immunosorbent assay (ELISA) as a quantitative technique depends on repeatability of color development and its measurement. Variation in measured response among wells, within and among microtiter plates, often precludes such precision. For example, plates with all wells treated uniformly exhibited unacceptable optical density differences in excess of 0.35 and 0.25 O.D. U among row and column averages, respectively. Arrangement of samples on plates according to classical experimental designs, with compact blocking features and two-dimensional control over spatial patterns, provides a possible remedy. Analysis of variations over uniformly treated plates demonstrated the potential for increased precision when such designs are used instead of random arrangements. Retrospective analysis of more than 100 tests performed with various experimental designs confirmed that this potential was realized when using Youden square and lattice square designs. Several designs appropriate for microtiter plates are presented and their conduct described.

Analysis of Variance↗

PubMed1981

Improved ELISA conditions for detection of plant viruses.

Clover yellow vein virus (CYVV) and homologous antisera were used to test effects of time and temperature on enzyme-linked immunosorbent assay (ELISA) in polystyrene substrate plates. Replicated lattice square and Youden square experimental designs were used to measure and account for variation in absorption values associated with sample position within polystyrene plates. Adsorption of coating antibody to polystyrene was relatively rapid, reaching optimum assay efficiency in 1 h at 5 degrees C when applied at 2.5 microgram/ml. Binding of antigen and enzyme-linked antibody (conjugate) in their respective steps during ELISA was also rapid. Incubation of antigen and conjugate for 2 h each was adequate to enable detection of 20 ng CYVV in a 100 microliter sample, but longer incubation of either reactant improved results. At this virus concentration, reduction in antigen incubation time by one-half could be compensated by doubling the conjugate incubation time and vice versa. Incubation of conjugates at 5 degrees C rather than 30 degrees C increased final ELISA readings (A400nm) more than two-fold. Substrate hydrolysis followed classic first order kinetics at room temperature. Greater efficiency of late antisera in ELISA was demonstrated by comparison of antisera produced relatively early and late during a rabbit's immune response. Alfalfa mosaic virus and peanut stunt virus with their homologous antisera were used to test the effects of antigen and conjugate incubation times for optimum assay efficiency. The results of these time course experiments with both viruses were similar to those obtained with CYVV. These time and temperature effects on ELISA should be applicable to most rabbit serum-virus combinations.

Antibodies, Viral↗