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Biomedical subjects

C Cox

Publications and source records attributed to C Cox.

At least 361 records · Page 20Linked to original sources
PubMed1991

Pulsed ultrasound and the hyperbarically exposed mouse fetus.

To enhance the likelihood of cavitation, pregnant mice were subjected to hyperbaric conditions and quickly returned to atmospheric pressure. Following this treatment, they were exposed to spatial average, pulse average intensities of 100 W/cm2 (2.2-MHz, 20-microseconds pulses with a duty cycle of 1/1000 or a temporal average spatial average intensity of 0.1 W/cm2). Fetal weights, deaths and malformations were scored. No statistically significant effects were observed in the offspring.

Animals↗
PubMed1991

Effects of intoxication on the catecholamine response to multisystem injury.

In patients suffering isolated head trauma, we have previously shown that levels of circulating catecholamines obtained within 48 hours of trauma correlate with the severity of brain injury and predict outcome and that intoxication blunts this response. The effects of alcohol on the increase in catecholamines in systematically injured patients, however, have not been well defined. From 1983 to 1990, 78 patients (74% male; median age 30 years) with blunt head and multisystem injury, who also had alcohol levels measured within 5 hours of injury, were studied. Norepinephrine and epinephrine levels were assayed by a radioenzymatic technique. Injury severity was assessed by the admission Glasgow Coma Scale (GCS) score (4-15; median, 12), the Injury Severity Score (ISS) (13-50; median, 25) and the volume of blood products administered within the first 24 hours (0-14.4 L; median, 0.5 L). The impact of alcohol on the norepinephrine response to injury was analyzed using multiple linear regression models, including polynomial interaction terms. Norepinephrine levels significantly (p less than 0.0001) correlated with the GCS score and ISS. However, alcohol significantly lowered the norepinephrine response to decreasing GCS score (R = 0.49, p less than 0.002) and to increasing ISS (R = 0.51, p less than 0.0006). The blunting of the catecholamine response was most marked in those severely injured. The rise in norepinephrine concentrations seen with increasing volume of blood replacement was not affected by intoxication. An association between injury severity and epinephrine levels was also present, but not as consistently. Epinephrine concentrations rose with falling GCS score and with increasing ISS values, but unlike norepinephrine, there were no apparent effects of alcohol on changes in epinephrine levels. Thus, in patients suffering head and multisystem injury, catecholamine changes reflect the severity of injury using three different scalers. Furthermore, intoxication blunts only the norepinephrine component of this important biologic response.

Adolescent↗
PubMed1991

Effects of nitrogen dioxide exposure on pulmonary function and airway reactivity in normal humans.

Nitrogen dioxide (NO2) is a product of combustion that has become recognized as a significant component of indoor air in some homes. Despite extensive study, it remains unresolved whether exposures to low levels of NO2 affect airway function or reactivity. These studies were designed to assess effects of various levels and patterns of NO2 exposure on pulmonary function and airway reactivity in normal humans. Normal volunteers screened for the absence of airway hyperreactivity were exposed for 3 h in an environmental chamber to purified air or NO2, separated by at least 2 wk, according to three protocols: (1) continuous 0.60 ppm NO2, (2) baseline 0.05 ppm NO2 with intermittent peaks of 2.0 ppm, and (3) continuous 1.5 ppm NO2. Subjects exercised for 10 min of each 30 min at a level sufficient to result in a minute ventilation near 40 L/min. Pulmonary function was measured before, during, and after exposure. Airway reactivity to increasing doses of carbachol was assessed 30 min after exposure. NO2 did not directly alter pulmonary function in any of the exposure protocols. In addition, airway reactivity was not altered by continuous exposure to 0.60 ppm or intermittent peaks of 2.0 ppm NO2. In contrast, continuous exposure to 1.5 ppm NO2 resulted in a greater fall in FVC and FEV1 in response to carbachol than after exposure to air (percent decrease in FVC: 1.5% after air, 3.9% after NO2, p less than 0.01). We conclude that for subjects without airway hyperreactivity, exposure to 1.5 ppm NO2 for 3 h increases airway reactivity, whereas repeated 15-min exposures to 2.0 ppm NO2 do not alter airway reactivity.

Adult↗
PubMed1991

Predicting severity of depression in the elderly at six-month follow-up: a neuropsychological study.

The authors conducted psychopathological and neuropsychological assessments on a pilot sample of 15 nondemented elderly depressed patients at the outset of inpatient treatment and again after 6 months. Pretreatment performance on a test of confrontation naming was predictive of severity of depressive symptoms at follow-up. These findings tentatively suggest that the naming ability of elderly depressed subjects may have prognostic significance.

Aged↗
PubMed1991

The neuropsychology of depression in the elderly: a comparative study of normal aging and Alzheimer's disease.

The neuropsychological testing of 23 elderly depressed patients was compared to that of 23 healthy controls and 20 Alzheimer's disease (AD) patients. Depressed subjects were deficient relative to controls on most tasks, including naming and cued memory. There was a greater negative influence of age on the performance of depressed subjects (relative to controls) on some tasks. Despite their significant deficits, depressed patients were clearly distinguishable from AD patients. It is suggested that the combined effects of age and depression produce a pattern of deficits that is distinct from that of younger depressives, but less severe than that of Alzheimer's patients.

Aged↗
PubMed1991

Mechanisms of nitrogen dioxide toxicity in humans.

These studies were undertaken to evaluate short-term respiratory effects and identify markers of nitrogen dioxide toxicity during exposures designed to approximate realistic conditions. With the development of bronchoalveolar lavage as a clinical investigative technique, the evaluation focused on the assessment of effects induced at the alveolar level. The exposure protocols were designed to assess the duration of nitrogen dioxide-induced effects and determine exposure-response relationships. Groups of normal, nonsmoking volunteers of both sexes between the ages of 18 and 40 years, without airway hyperreactivity, constituted the study population. The exposure protocols required a total of three to five days for each subject, depending on the timing of bronchoalveolar lavage. Subjects were exposed to nitrogen dioxide or air for three hours in a double-blind, randomized fashion in a 45-m3 environmental chamber, with intermittent exercise sufficient to quadruple minute ventilation. Pulmonary function was measured during and after exposure, and airway reactivity to carbachol was assessed before and after exposure. Lavaged cells were examined for their capacity to inactivate influenza virus and secrete IL-1 in vitro. Cell-free lavage fluid was analyzed for total protein, albumin, alpha 2-macroglobulin, arylsulfatase, and alpha 1-protease inhibitor. The studies were undertaken in three phases, each of approximately one year's duration. In Phase 1, 15 subjects were exposed to a background concentration of 0.05 parts per million2 (ppm) nitrogen dioxide and to three 15-minute peaks of 2.0 ppm, and underwent bronchoalveolar lavage 3.5 hours after nitrogen dioxide exposure. During Phase 2, 8 subjects were exposed to continuous 0.60 ppm nitrogen dioxide and underwent bronchoalveolar lavage 18 hours later. Finally, in Phase 3, 15 subjects were exposed to continuous 1.5 ppm nitrogen dioxide and underwent bronchoalveolar lavage 3.5 hours after exposure. No significant symptomatic or pulmonary function changes could be detected in response to any of the nitrogen dioxide exposures. However, a small but significant increase in airway reactivity was observed in normal subjects after exposure to 1.5 ppm nitrogen dioxide. Following the highest dose of carbachol (10 mg/mL), the forced expiratory volume in one second decreased 7.5 +/- 1.1 percent after nitrogen dioxide exposure compared to 4.8 +/- 1.1 percent after exposure to air (p less than 0.05). No symptoms were induced in any of the groups by the carbachol exposures. Analyses of cells recovered by bronchoalveolar lavage during all three phases revealed no differences in total cell recovery, cell viability, or differential cell counts.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

Expression of autoantibodies to recombinant (U1) RNP-associated 70K antigen in systemic lupus erythematosus.

To determine the specificity of antibodies to the (U1) ribonucleoprotein antigen in systemic lupus erythematosus (SLE), patient sera were tested for binding to a recombinant human 70K antigen. By solid-phase immunoassay, we detected anti-70K reactivity in sera from 31 of 96 patients with systemic lupus erythematosus (SLE), demonstrating that anti-70K antibodies may occur in patients with SLE as well as other clinical diagnoses. In sequential sera from 2 of these patients, we found that anti-70K binding varied dramatically over the course of disease. The changes in anti-70K antibody levels did not correlate with clinical events nor evolving antibody reactivity with the Sm-specific antigens.

Autoantibodies↗
PubMed1990

Vibration sensitivity recovery after a second course of acrylamide intoxication.

Five monkeys were trained to report detection of vibration or an electrical stimulus. Three of them had been dosed previously with acrylamide administered orally until toxic signs appeared, and were then allowed to recover. Approximately 30 weeks after the end of the first dosing course, they were dosed a second time with 10 mg/kg/day of acrylamide, 5 days a week, to mimic the dosage regimen of the first dosing period. Two monkeys received vehicle, as in the first dosing period. Vibration sensitivity was reduced in the exposed monkeys to an extent comparable to the first dosing period. Analysis of covariance showed that the rate of recovery from a second exposure to acrylamide was comparable to the rate of recovery from the first exposure. Vibration sensitivity appears useful as a monitoring tool to follow the time course of acrylamide-induced peripheral nerve dysfunction.

Acrylamides↗
PubMed1990

Modification of lead distribution by diethyldithiocarbamate.

Many reports indicate that dithiocarbamates such as diethyldithiocarbamate (DDC), administered in conjunction with exposure to various metals, can elevate the brain levels of such metals at the same time that they promote excretion from other sites. To more clearly define the effects of DDC on lead (Pb) distribution after prolonged exposure to relatively low levels, male Long-Evans rats were provided with drinking water containing 0, 50, or 500 ppm Pb acetate. During the 12-week experimental period, DDC was administered by ip injection twice weekly in a dose of 100 mg/kg. Every 3-4 weeks, urine and blood samples were taken 24 hr before and after a scheduled DDC injection. DDC administration exerted no discernible effect on bone Pb levels and showed only an interaction with Pb dose, but not independent effects on kidney levels. Both liver and brain Pb levels attained much higher levels in the DDC-treated rats than in animals exposed to Pb alone. The sequential measures of Pb in blood and urine and of delta-aminolevulinic acid revealed complex patterns of change over time. One possible explanation, at least for the elevated levels of Pb in brain, is the lipophilic character of the Pb-DDC complex, which facilitates entry into the central nervous system; it may also explain the elevated levels in liver. This property, common to many chelators, suggests their use in model systems to study the neurotoxic properties of metals.

Aminolevulinic Acid↗
PubMed1990

Modification by nickel of instrumental thermoregulatory behavior in rats.

The effects of NiCl2 on the colonic temperature and thermoregulatory behavior (TRB) of rats were examined. TRB was evaluated in an instrumental (operant) setting in which rats were required to press a level to obtain convectional heat (SEEK) or to avoid heat (ESCAPE). Orthogonal polynomial regression was used to describe the response patterns in both the SEEK and ESCAPE situations. Two milligrams per kilogram of Ni (ip) caused rapid, transient hypothermia at an ambient temperature of 21 degrees C. When given access to heat reinforcement, rats responded for heat at a lower rate immediately after 2 or 5 mg/kg of Ni (up to 5-15 min) than after saline. Subsequently, response rates rose 30 min or more after Ni injection. A converse pattern was found with the heat escape situation. These observations, confirmed by two contrasting procedures, indicate that the changes were thermoregulatory in nature and cannot be explained by nonspecific suppressive or excitatory effects of Ni. They further suggest that Ni-induced hypothermia results from an altered body temperature set point. The subsequent reversal in behavior probably arises from a direct action of Ni on autonomic effector mechanisms. The origin and biological significance of these findings require further investigation. Physical requirements and response topography are discussed as critical variables in the interpretation of experiments requiring similar responses under different ambient temperatures.

Animals↗
PubMed1990

Confirmation of an ultrasound-induced mutation in two in-vitro mammalian cell lines.

In-vitro V79 and L5178Y cells were exposed in a rotating test tube to continuous-wave (CW) 1 MHz 35 W/cm2 ultrasound (0-4 or 0-3 min, respectively) and subsequently assayed for mutation as evidenced by resistance to 6-thioguanine (6-TG). There was a modest but statistically significant increase in mutation frequency in both cell types with increase in ultrasound exposure duration. X-ray exposures (3-9 Gy, a "positive control") yielded a large increase in 6-TG resistance. The data support an earlier report by Kaufman (1985) of an ultrasound-induced increase in mutation to 6-TG resistance in in-vitro mammalian cells.

Analysis of Variance↗
PubMed1990

Pressure threshold for shock wave induced renal hemorrhage.

Studies were performed with an interest in determining a pressure threshold for extracorporeal shock wave induced renal damage. Histological evidence of intraparenchymal hemorrhage was used as an indicator of tissue trauma. Depilated C3H mice were anesthetized and placed on a special frame to enhance visualization and treatment of the kidneys in situ. A Wolf electrohydraulic generator and 9 French probe designed for endoscopic use were utilized to expose the kidneys to 10 double spherically divergent shock waves. Measurements of the shock waves revealed two positive pressure peaks of similar magnitude for each spark discharge. The kidneys were exposed to different peak pressures by choice of distance from the spark source and were removed immediately after treatment for histologic processing. A dose response was noted with severe corticomedullary damage apparent following 15 to 20 MPa shocks. Hemorrhage was more apparent in the medulla where evidence of damage could be seen following pressures as low as three to five MPa. When a latex membrane was interposed to prevent possible collapse of the initial bubble from the spark source against the skin surface, histological evaluation revealed substantial reduction of severe tissue damage associated with the highest pressures tested, 20 MPa. However, the threshold level for evidence of hemorrhage remained about three to five MPa. Hydrophonic measurements indicated that the membrane allowed transmission of the acoustic shock waves and suggested that collapse of the bubble generated by electrohydraulic probes may have local effects due to a cavitation-like mechanism.

Animals↗
PubMed1990

Impairment of central auditory function in Alzheimer's disease.

Accuracy and laterality of ear preference on dichotic listening (DL) takes were compared in patients with Alzheimer's disease (AD) and a group of normal subjects, matched for age and education, using parameters (list length, stimulus matching, and order of recall), previously shown to significantly alter DL performance in normals. Alzheimer patients tended to show qualitatively similar, but significantly worse performance compared to controls as a function of increasing dichotic list length as well as stimulus set content (semantically, v. phonemically and unmatched dichotic items). Furthermore, these patients were unable to attend selectively to either the right- or left-ear and thus could not increase right- or left-ear advantages over the free recall procedure, an order of recall task easily mastered by the normal subjects. These results suggest that Alzheimer's disease is associated with a breakdown of cortical mechanisms involved in the selective allocation of attention.

Aged↗
PubMed1990

Childhood obsessive-compulsive disorder: a prospective follow-up study.

Twenty-five of 27 patients (93%) who had participated in a study of severe primary obsessive-compulsive disorder with onset in childhood or adolescence, were seen 2-7 yrs after initial examination (mean, 4.4 yrs). They were compared to a group of normal controls matched for age, sex and IQ and followed up for the same period. Continued psychopathology was striking for the patients, with only seven (28%), three males and four females, receiving no psychiatric diagnosis at follow-up. Seventeen subjects (68%) still had obsessive-compulsive disorder, 12 patients (48%) had another psychiatric disorder, most commonly anxiety and/or depression; neither initial response to clomipramine or any other baseline variable predicted outcome.

Adolescent↗
PubMed1990

Alcohol intoxication blunts sympatho-adrenal activation following brain injury.

In 46 patients experiencing traumatic brain injury, we studied the interactions of alcohol intoxication and severity of neurologic dysfunction on the resulting sympathetic nervous system activation. Sixty percent of the variation in norepinephrine (p less than 0.0001) and more than 50% of the variation in epinephrine (p less than 0.0001) were due to the initial ethanol concentrations and extent of brain injury assessed by the admission Glasgow Coma Score (GCS). As brain function deteriorated plasma cathecholamines rose (p less than 0.0001), but ethanol qualitatively and quantitatively modified this observation. The magnitude of the sympathetic response to worsening neurologic function was progressively diminished in association with increasing ethanol levels, i.e., the inverse relationship of GCS values with both norepinephrine and epinephrine was flattened. In comatose patients (GCS less than 8) increasing ethanol levels was associated with progressively decreasing norepinephrine and epinephrine responses (p less than 0.04), such that catecholamines were reduced by 80 to 90% at ethanol concentrations approaching 400 mg/dl (87.0 mmol/l). However, the impact of ethanol on the degree of sympathetic nervous system activation depended upon the degree of injury; the apparent ethanol suppression was greatest in patients with the most severe neurologic dysfunction (GCS 3 or 4), but it diminished as neurologic function improved. We conclude that the presence of alcohol appears to modify the rise in catecholamine levels following traumatic brain injury in a dose-dependent manner and alters the relationship between neurologic dysfunction and SNS activation. These alterations may have profound effects on patient morbidity in the immediate post-accident period.

Adolescent↗