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Biomedical subjects

J O Harris

Publications and source records attributed to J O Harris.

At least 19 recordsLinked to original sources
PubMed2005

Cardiovascular responses of three salmonid species affected with amoebic gill disease (AGD).

The cardiovascular effects of amoebic gill disease (AGD) were investigated immediately following surgery in three salmonid species; Atlantic salmon (Salmo salar L.), brown trout (Salmo trutta L.) and rainbow trout (Oncorhynchus mykiss Walbaum). Fish, both naïve (control) and infected (AGD-affected) of each species, were fitted with dorsal aorta catheters and cardiac flow probes. Cardiac output and dorsal aortic pressures were then continuously measured over a 6-h period following surgery. Results showed that Atlantic salmon, brown trout and rainbow trout displayed similar dorsal aortic pressure, cardiac output, and systemic vascular resistance (mean dorsal aotic pressure divided by cardiac output) values. However, the only significant differences relating to disease status i.e. infected or control, were found in Atlantic salmon. Although no significant differences were seen in dorsal aortic pressure values, AGD-affected salmon displayed significantly elevated systemic vascular resistance at 4 and 6 h post surgery. Cardiac output was also approximately 35% lower in AGD-affected salmon compared to the non-affected control counterparts. These results comparatively examine cardiac function in response to AGD across three salmonid species and highlight species-specific cardiovascular responses that occur in association with disease. It is suggested that the apparent cardiac dysfunction seen in AGD-affected Atlantic salmon could, under stressful conditions, become exacerbated. Cardiac failure is therefore suggested to be a possible physiological mechanism by which AGD causes or contributes to mortality in Atlantic salmon.

Amebiasis↗
PubMed2005

Respiratory pathogenesis of amoebic gill disease (AGD) in experimentally infected Atlantic salmon Salmo salar.

The aim of this study was to investigate the respiratory responses of Atlantic salmon, Salmo salar, experimentally affected with amoebic gill disease (AGD). In Series I, arterial blood samples were taken over a 96 h period following amoebae addition to examine potential respiratory effects associated with initial exposure. No major significant treatment effects were found between fish exposed to amoebae and control (non-exposed) fish. Arterial pH (pHa) was seen to be significantly elevated at 48 h in AGD fish relative to the 0 h time point. To investigate the long-term respiratory effects associated with infection, fish were similarly exposed to amoebae and sampled over a 16 d period. As for Series I, caudal blood pH was significantly elevated by Day 2 (48 h) compared to the pre (Day 0)-time point, suggesting that initial exposure to amoebae and/or amoebae attachment may have induced an initial respiratory alkalosis via increased ventilation frequency and/or amplitude. From Day 7 onwards, and coinciding with a significant increase in the percentage of affected gill filaments, blood pH decreased significantly, possibly indicating the onset of the characteristic respiratory acidosis that has previously been described for experimentally AGD-affected Atlantic salmon. Although fish in this study showed up to 90% AGD-affected filaments, the corresponding respiratory results do not reflect a major acid-base disturbance. Therefore, the findings from the present study support the contention that, although AGD only affects the gill, AGD-associated mortality in Atlantic salmon may not be primarily associated with respiratory failure.

Acid-Base Equilibrium↗
PubMed2001

A primary care preceptorship for first-year medical students coordinated by an Area Health Education Center program: a six-year review.

In 1991, the University of Florida College of Medicine established a required primary care preceptorship coordinated by the Area Health Education Center (AHEC) Program for all students in the first semester of medical school. Six years' experience with this course, which is entirely community-based and taught by community physicians, provides evidence of the success of the preceptorship. Over the first six years, 97% of students and 92% of preceptors felt strongly that this was an appropriate and valuable experience for students in the first semester of medical school. All believed that the students were capable of interacting with patients in a meaningful fashion and that the course allowed students to gain confidence as health care providers. The course also reinforced the importance of the basic science curriculum and initiated the process of professional development by affirming students' decisions to pursue a career in medicine. The use of content analysis to further evaluate attitudes and behaviors indicated that the students were highly satisfied with their experience and were active participants in the preceptors' practices. Students' approach to patients as people, rather than cases, was positive, and increased from the first to the last day of the preceptorship. After six years, this preceptorship has been demonstrated to have a positive and meaningful impact on medical student education and development.

Area Health Education Centers↗
PubMed1994

Effect of a simple ambulatory experience on career choice and attitudes of medical students.

Students were allocated randomly to participate in a simple ambulatory experience during their third-year medicine clerkship. A convenience sample was surveyed by questionnaire in the fall of their fourth year, after decisions were made regarding future career plans. The questionnaire assessed medical student attitudes toward general internal medicine and career choice. Valuation of the effectiveness of the clerkship was associated with choosing a career in internal medicine (p = 0.007); having an ambulatory experience was not associated with subsequent career choice. Sixty-two percent of all students felt the clerkship affected their career choice a great deal or moderately; these students were likely to find a career in general internal medicine less attractive as a result of their clerkship (p = 0.008). When stratified, this association disappeared in those students who participated in the ambulatory experience (p = 0.39) but persisted in those who did not (p = 0.01). A simple experience in internal medicine clinics during a third-year clerkship was not associated with subsequent career choice, but had some positive effects on attitudes toward general internal medicine as a career.

Adult↗
PubMed1993

Systemic histiocytosis presenting as multiple sclerosis.

A patient resembling one with progressive multiple sclerosis in clinical presentation and by magnetic resonance imaging was studied in detail. Some features atypical for multiple sclerosis prompted a persistent search for an alternative cause. The diagnosis of a non-Langerhans systemic histiocytosis involving brain and bone was established and showed a partial response to radiation therapy. This patient illustrates the continued importance of a broad approach to the evaluation of possible multiple sclerosis, with particular attention to atypical features.

Biopsy↗
PubMed1992

Using gadolinium-enhanced magnetic resonance imaging lesions to monitor disease activity in multiple sclerosis.

The highly variable clinical course and the lack of a direct measurement of disease activity have made evaluation of experimental therapies in multiple sclerosis (MS) difficult. Recent studies indicate that clinically silent lesions can be demonstrated by magnetic resonance imaging (MRI) in patients with mild relapsing-remitting MS. Thus, MRI may provide a means for monitoring therapeutic trials in the early phase of MS. We studied 12 patients longitudinally for 12 to 21 months with monthly gadolinium (Gd)-enhanced MRIs. The data have been used to identify the most effective design of a clinical trial using Gd-enhanced lesions as the outcome measure. Frequent ( > 1/mo) Gd-enhancing lesions were observed in 9 of the 12 patients, indicating that the disease is active even during the early phase of the illness. The frequency of the lesions was not constant; there was marked fluctuation in lesion number from month to month. However, the magnitude of the peak number of lesions and the frequency of the peaks varied among patients. Because of this variability, the most effective use of Gd-enhancing lesions as an outcome measure in a clinical trial was a crossover design with study arms of sufficient duration to allow accurate estimation of lesion frequency. Monitoring Gd-enhancing lesions may be an effective tool to assist in the assessment of experimental therapies in early MS.

Adult↗
PubMed1991

Serial gadolinium-enhanced magnetic resonance imaging scans in patients with early, relapsing-remitting multiple sclerosis: implications for clinical trials and natural history.

Six patients with early, mild, relapsing-remitting multiple sclerosis were studied with monthly gadolinium-enhanced magnetic resonance imaging scans for 8 to 11 months. Numerous enhancing lesions were observed irrespective of clinical activity. Four of the 6 patients had one or more enhancing lesions present on each examination. The other 2 patients had enhancing lesions noted in 7 and 9 of 11 months. In contrast, only two clinical exacerbations were observed during the study period. Neither the exacerbations nor other changes in symptoms or signs correlated with occurrence of the enhancing lesions. Enhancement generally persisted for less than 1 month. The opening of the blood-brain barrier as reflected by gadolinium enhancement on magnetic resonance imaging may represent ongoing disease activity in patients with mild, relapsing-remitting multiple sclerosis who are clinically stable. The frequency of these lesions appears to be sufficient to use as an outcome measure in clinical trials testing clinical efficacy in patients with early, relapsing-remitting multiple sclerosis.

Adult↗
PubMed1990

Cerebrovascular disease in AIDS: a case-control study.

The autopsy records of adult patients dying with AIDS between 1983 and 1987 at a large, metropolitan, university-affiliated hospital were reviewed to determine the incidence and spectrum of cerebrovascular and associated cardiovascular disease. The clinical records of those patients with AIDS with cerebrovascular disease were retrospectively examined in detail. All autopsied patients between the ages of 20 and 50 years dying without AIDS in 1986 and 1987 served as the control group. At autopsy, 13 (8%) of 154 adult patients with AIDS had evidence of recent cerebrovascular disease. In comparison, 25 (23%) of the 111 control patients dying without AIDS had recent cerebrovascular disease (P less than 0.04). The spectrum of cerebrovascular diseases was similar in patients both with and without AIDS; however, cerebral vasculitis was observed only in the former. Thirty-nine (40%) of 97 patients with AIDS had significant cardiac disease, and cerebral emboli were demonstrated in four of the 13 patients with stroke. Stroke must be considered in the differential diagnosis of neurological disease in patients with AIDS, although it does not appear to be more common in this group than in a control population of young adults with other terminal illnesses. The causes of stroke occurring with AIDS are diverse and include cerebral emboli secondary to cardiac disease, cerebral hemorrhage secondary to thrombocytopenia, and cerebral vasculitis.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Cigarette smoke alters plasma membrane fluidity of rat alveolar macrophages.

This study examined the effect of cigarette smoking on the fluidity of the rat alveolar macrophage plasma membrane. Rats were subjected to 8 wk of an in vivo smoke exposure protocol, after which their alveolar macrophages were harvested. Fluidity was assessed by measuring steady-state anisotropy of isolated plasma membranes as well as of lipid vesicles made from total lipid extracts of these plasma membranes. The smoke-exposed animals showed a significant decrease in fluidity in both intact plasma membranes (p less than 0.0001) and in their lipid vesicle preparations (p less than 0.0001). To assess the time course of these changes, lipid vesicles were prepared from total cellular lipid extracts of macrophages from paired rats, control and smoke-exposed, at 1 through 4 wk after initiation of exposure. Significant decreases in fluidity were observed as early as 2 wk after smoking was begun (p less than 0.001). To assess the reversibility of these changes, paired rats were exposed for 8 wk, then withdrawn for 8, 12, and 18 wk, after which fluidity was evaluated in lipid vesicles prepared from total cellular lipids. Even after 18 wk of smoking cessation, significant decreases in fluidity persisted (p less than 0.01). We conclude that cigarette smoking causes a decrease in plasma membrane fluidity of rat alveolar macrophages. This is due at least in part to a change in the lipid portion of the membrane. These alterations occur after a very brief period of smoke exposure and persist long after cessation of smoking.

Animals↗
PubMed1986

Effects of low-yield-cigarette smoke inhalation on rat lung macrophages.

It has been suggested that low-yield cigarettes (LYC) may be less hazardous and that smokers of these cigarettes are exposed to less tar, nicotine, and carbon monoxide. Recent studies have challenged this and question the analysis techniques for measuring yields of these cigarettes. Because published LYC contents may not reflect tissue toxicity and because compensatory puffing behaviors may alter smoke delivery to end-organ tissues, we studied the effect of smoke from a typical LYC on phagolysosome fusion and phagocytosis in alveolar macrophages of rats that chronically inhaled the smoke generated by an intermittently puffing apparatus. Alveolar macrophages were obtained by lung lavage and established in monolayers. Phagolysosome fusion and phagocytosis were assessed using the acridine orange fluorochrome assay. After 8 wk of exposure, there was no difference in phagolysosome fusion between controls and smokers. Carboxyhemoglobin levels in controls versus smokers were 1.36 +/- 0.09% versus 2.13 +/- 0.32% (mean +/- SE) (p = 0.06). A group of animals was similarly exposed, but the side pores of the cigarette filters were sealed with tape to simulate the compensatory behaviors often used by LYC smokers of occluding filter pores with their lips or fingertips. This significantly increased smoke exposure, and the carboxyhemoglobin level of the smokers increased to 7.0 +/- 1.4% (versus controls, p less than or equal to 0.01). Cells from these rats showed alterations in phagocytosis and in phagolysosome fusion compared with alveolar macrophages of control rats. These data suggest that the tobacco in LYC may have toxic effects similar to those of high-yield cigarettes and that LYC are likely to be less hazardous only if smoked in a fashion similar to that of a smoke-generating apparatus.

Animals↗
PubMed1986

Pulmonary alveolar proteinosis. Further evaluation of abnormal alveolar macrophages.

To investigate the function of alveolar macrophages (AM) and the mechanisms of impairment in pulmonary alveolar proteinosis, we established in culture AM from three patients and from eight normal nonsmokers and assessed phagocytosis and phagolysosome fusion by the acridine orange assay with live yeast as the phagocytic challenge. Alveolar macrophages from the patients with pulmonary alveolar proteinosis ingested fewer yeasts per cell than did normal AM (mean +/- SE, 2.3 +/- 0.3 vs 3.3 +/- 0.2; p less than 0.05) and had decreased phagolysosome fusion (33 +/- 6 percent vs 64 +/- 1 percent; p less than 0.001). Alveolar macrophages from three normal subjects were incubated with cell-free fractions isolated by centrifugation of lavage fluid from the patients at 250 g (P1) or centrifugation of P1 supernatant at 20,000 g (P2). The P1 fraction did not decrease the number of AM ingesting yeast or the number of yeast cells ingested per cell, but the P2 fraction decreased both phagocytic indices. Conversely, phagolysosome fusion was depressed by the P1 fraction (48 +/- 3 percent vs 66 +/- 2 percent for untreated AM from the same subject; p less than 0.02) but not by the P2 fraction. Significant morphologic changes were noted in AM cocultured with both P1 and P2. Comparable concentrations of pooled P2 fractions from normal subjects did not decrease phagocytic indices in normal AM. These data confirm that AM in pulmonary alveolar proteinosis are dysfunctional, and, in particular, the finding of decreased phagolysosome fusion may be related to the high incidence of uncommon infections in these patients. We have shown that different fractions of alveolar filling material from patients with pulmonary alveolar proteinosis have unique effects on the phagocytic process in the normal AM, and the induced defects may be associated with apparent uptake of this material. These observations further support the hypothesis that in patients with pulmonary alveolar proteinosis, locally produced "toxic" substances may lead to impaired alveolar clearance and contribute to the pathogenesis of this disease.

Adult↗
PubMed1985

Rat lung macrophage tumor cytotoxin production: impairment by chronic in vivo cigarette smoke exposure.

Macrophages in the presence of bacteria-derived lipopolysaccharide (LPS) stimuli produce a soluble cytotoxin which is toxic to tumor cells. In this study, we examined various parameters of cytotoxin production from pulmonary lavage cells obtained from Fisher 344 cesarean-derived rats. Cultures of macrophages were derived from pulmonary lavage cells and stimulated in vitro with LPS. Cytotoxin production was assayed in vitro using an L-929 cell target assay. Pulmonary lavage preparations contained a relatively pure population of macrophages, and adherence studies revealed that nonadherent lavage cells contributed negligible amounts of cytotoxin, indicating that macrophages were responsible for cytotoxin production. After LPS stimulation, cytotoxin production became maximal within 10 h and thereafter plateaued. Doses of LPS above 0.1 microgram/ml were optimal for production, and in the absence of LPS, no cytotoxin was detected. Because cigarette smoke is the major etiological factor in the development of lung cancers and because smoking is known to profoundly alter the function of alveolar macrophages in humans and experimental animals, subsequent experiments examined the role of chronic cigarette smoke exposure on tumoricidal activity of lung macrophages. Rats were exposed in vivo for 8 wk to either cigarette smoke or air (sham-treated controls). When lavage cells were cultured and stimulated with LPS (1 microgram/ml), 5- to 10-fold less cytotoxin was produced by lavage cells from rats exposed to cigarette smoke. Similarly, using a direct cytotoxicity assay, lung macrophages of smoke-exposed animals also revealed marked impairment in cytotoxicity against L-929 cell targets, and this was noted over a wide range of macrophage:tumor target cell ratios. Another product of macrophages, interferon, was also decreased in rats exposed in vivo to cigarette smoke when compared to sham-treated controls. These results suggest that cigarette smoke exposure may impair pulmonary macrophage-mediated tumor defense mechanisms.

Animals↗
PubMed1984

Abnormal phagolysosome fusion in pulmonary alveolar macrophages of rats exposed chronically to cigarette smoke.

Cigarette smoking is strongly associated with functional and morphologic changes in pulmonary alveolar macrophages (PAM). Phagocytic activity is a primary function of PAM, and although the ingestion of particles appears to be normal in the PAM of cigarette smokers, published data suggest that antimicrobial activity of these cells might be diminished. Because phagolysosome fusion (PLF) is an important aspect of the phagocytic process subsequent to the ingestion phase, PLF was evaluated in PAM lavaged from the lungs of male Fisher 344 rats that had been exposed for 8 wk to whole cigarette smoke, to the gas phase of cigarette smoke, or to air as a sham control. Using the acridine orange assay with viable yeast as the phagocytic challenge, we found no difference in the numbers of PAM from each group that had phagocytic activity after a 2-h challenge. However, PLF expressed as the number of orange-fluorescing phagosomes per total number of yeast-containing phagosomes was 35 +/- 1% (X +/- SE) for the group exposed to whole smoke, 53 +/- 2% for the gas phase group, and 65 +/- 1% for the control group. These differences are highly significant, with p less than 0.001 for the whole smoke versus control and p less than 0.01 for the gas phase versus control. Tight phagosomal membranes suggest normal PLF, whereas loose membranes suggest that PLF is inhibited. When the structure of yeast-containing phagosomes was examined and PLF was calculated with the number of phagosomes with tight membranes substituted for the number of orange-fluorescing phagosomes, PLF in smoke-exposed PAM was found to be significantly (p less than 0.01) different from that in sham-exposed control PAM.(ABSTRACT TRUNCATED AT 250 WORDS)

Acridine Orange↗
PubMed1982

Strain differences in pulmonary function of laboratory rats.

The effect of strain differences on pulmonary function was studied with male Sprague-Dawley and Fischer-344 rats. The larger Sprague-Dawley rats had a larger thoracic gas volume and specific thoracic gas volume (thoracic gas volume normalized for body mass) than the Fischer-344 rats. The thoracic gas volume differences corresponded to differences in static lung compliance reported in the literature for these strains of rats. The resistance of airways was less in the Sprague-Dawley rats but the specific conductance was greater in the Fischer-344 rats. These results suggested that even though the smaller Fischer-344 rats had a smaller lung volume and smaller cross sectional area of the airways, the caliber of the airways relative to lung volume was larger than that of the Sprague-Dawley rats.

Airway Resistance↗