Clusters of health behaviours in Queensland adults are associated with different socio-demographic characteristics.

BACKGROUND: The co-occurrence of unhealthy lifestyles, calls for interventions that target multiple health behaviours. This study investigates the clustering of health behaviours and examines demographic differences between each cluster. METHODS: In total, 934 adults from Queensland, Australia completed a cross-sectional survey assessing multiple health behaviours. A two-step hierarchical cluster analysis using multiple iterations identified the optimal number of clusters and the subset of distinguishing health behaviour variables. Univariate analyses of variance and chi-squared tests assessed difference in health behaviours by socio-demographic factors and clusters. RESULTS: Three clusters were identified: the 'lower risk' cluster (n = 436) reported the healthiest profile and met all public health guidelines. The 'elevated risk' cluster (n = 105) reported a range of unhealthy behaviours such as excessive alcohol consumption, sitting time, fast-food consumption, smoking, inactivity and a lack of fruit and vegetables. The 'moderate risk behaviour' cluster (n = 393) demonstrated some unhealthy behaviours with low physical activity levels and poor dietary outcomes. The 'elevated risk' cluster were significantly younger and more socio-economically disadvantaged than both the 'lower and moderate risk' clusters. DISCUSSION: Younger people who live in more deprived areas were largely within the 'elevated risk' cluster and represent an important population for MHBC interventions given their wide range of unhealthy behaviours.

Can you elaborate on that? Addressing participants' need for cognition in computer-tailored health behavior interventions.

Computer-tailored interventions, which deliver health messages adjusted based on characteristics of the message recipient, can effectively improve a range of health behaviours. Typically, the content of the message is tailored to user demographics, health behaviours and social cognitive factors (e.g., intentions, attitudes, self-efficacy, perceived social support) to increase message relevance, and thus the extent to which the message is read, considered and translated into attitude and behaviour change. Some researchers have suggested that the efficacy of computer-tailored interventions may be further enhanced by adapting messages to suit recipients' need for cognition (NFC) - a personality trait describing how individuals tend to process information. However, the likely impact of doing so, especially when tailored in conjunction with other variables, requires further consideration. It is possible that intervention effects may be reduced in some circumstances due to interactions with other variables (e.g., perceived relevance) that also influence information processing. From a practical point of view, it is also necessary to consider how to optimally operationalise and measure NFC if it is to be a useful tailoring variable. This paper aims to facilitate further research in this area by critically examining these issues based on relevant theories and existing evidence.

Designing more engaging computer-tailored physical activity behaviour change interventions for breast cancer survivors: lessons from the iMove More for Life study.

BACKGROUND: Participating in regular physical activity is a recommended cancer recovery strategy for breast cancer survivors. However, tailored support services are not widely available and most survivors are insufficiently active to obtain health benefits. Delivering tailored programs via the Internet offers one promising approach. However, recent evaluations of such programs suggest that major improvements are needed to ensure programs meet the needs of users and are delivered in an engaging way. Understanding participants' experiences with current programs can help to inform the next generation of systems. PURPOSE: The purposes of this study are to explore breast cancer survivor's perspectives of and experiences using a novel computer-tailored intervention and to describe recommendations for future iterations. METHODS: Qualitative data from a sub-sample of iMove More for Life study participants were analysed thematically to identify key themes. Participants long-term goals for participating in the program were explored by analysing open-ended data extracted from action plans completed during the intervention (n = 370). Participants negative and positive perceptions of the website and recommendations for improvement were explored using data extracted from open-ended survey items collected at the immediate intervention follow-up (n = 156). RESULTS: The majority of participants reported multi-faceted goals, consisting of two or more outcomes they hoped to achieve within a year. While clear themes were identified (e.g. 'being satisfied with body weight'), there was considerable variability in the scope of the goal (e.g. desired weight loss ranged from 2 to 30 kg). Participants' perceptions of the website were mixed, but clear indications were provided of how intervention content and structure could be improved. CONCLUSIONS: This study provides insight into how to better accommodate breast cancer survivors in the future and ultimately design more engaging computer-tailored interventions.

How do different delivery schedules of tailored web-based physical activity advice for breast cancer survivors influence intervention use and efficacy?

PURPOSE: The purpose of the study is to investigate the impact of differing delivery schedules of computer-tailored physical activity modules on engagement and physical activity behaviour change in a web-based intervention targeting breast cancer survivors. METHODS: Insufficiently active breast cancer survivors (n = 492) were randomly assigned to receive one of the following intervention schedules over 12 weeks: a three-module intervention delivered monthly, a three-module intervention delivered weekly or a single module intervention. Engagement with the website (number of logins, time on site, modules viewed, action plans completed) was measured using tracking software. Other outcomes (website acceptability, physical activity behaviour) were assessed using online surveys. Physical activity outcomes were analysed using regression models for both study completers and when applying intention-to-treat (using multiple imputation). RESULTS: Completers allocated to the monthly module group rated the intervention higher (b = 2.2 95 % CI = 0.02-4.53) on acceptability and had higher levels of resistance-training (IRR = 1.88, 95 % CI = 1.16-3.04) than those in the single module group. When accounting for missing data, these differences were no longer significant. The completion of at least two action plans was higher among those allocated to the monthly module group compared to those in the weekly module group (53 vs 40 %, p = 0.02); though the completion of at least two modules was higher in the weekly module group compared to the monthly module group (60 vs 46 %; p = 0.01). There were no other significant between group differences observed. CONCLUSION: This study provides preliminary evidence that web-based computer-tailored interventions can be used to increase physical activity among breast cancer survivors. Further, there were some outcome differences based on how the tailored modules were delivered, with the most favourable outcomes observed in the monthly delivery group. IMPLICATIONS FOR CANCER SURVIVORS: This study will be useful for informing the design of future web-based interventions targeting breast cancer survivors.

TaylorActive--Examining the effectiveness of web-based personally-tailored videos to increase physical activity: a randomised controlled trial protocol.

BACKGROUND: Physical inactivity levels are unacceptably high and effective interventions that can increase physical activity in large populations at low cost are urgently needed. Web-based interventions that use computer-tailoring have shown to be effective, though people tend to 'skim' and 'scan' text on the Internet rather than thoroughly read it. The use of online videos is, however, popular and engaging. Therefore, the aim of this 3-group randomised controlled trial is to examine whether a web-based physical activity intervention that provides personally-tailored videos is more effective when compared with traditional personally-tailored text-based intervention and a control group. METHODS/DESIGN: In total 510 Australians will be recruited through social media advertisements, e-mail and third party databases. Participants will be randomised to one of three groups: text-tailored, video-tailored, or control. All groups will gain access to the same web-based platform and a library containing brief physical activity articles. The text-tailored group will additionally have access to 8 sessions of personalised physical activity advice that is instantaneously generated based on responses to brief online surveys. The theory-based advice will be provided over a period of 3 months and address constructs such as self-efficacy, motivation, goal setting, intentions, social support, attitudes, barriers, outcome expectancies, relapse prevention and feedback on performance. Text-tailored participants will also be able to complete 7 action plans to help them plan what, when, where, who with, and how they will become more active. Participants in the video-tailored group will gain access to the same intervention content as those in the text-tailored group, however all sessions will be provided as personalised videos rather than text on a webpage. The control group will only gain access to the library with generic physical activity articles. The primary outcome is objectively measured physical activity. Secondary outcomes include website engagement and retention, quality of life, depression, anxiety, stress, sitting time, sleep and psychosocial correlates of physical activity. Outcomes will be measured at baseline, 3, and 9 months. DISCUSSION: This study presents an ideal opportunity to study the effectiveness of an isolated feature within a web-based physical activity intervention and the knowledge generated from this study will help to increase intervention effectiveness. TRIAL REGISTRATION: Australian New-Zealand Clinical Trial Registry: ACTRN12615000057583 . Registered 22 January 2015. CQUniversity Ethics Project Number: H14/07-163.

Methodologic considerations for the use of canine in vivo aged biotinylated erythrocytes to study RBC senescence.

Biotinylation of erythrocytes has been developed in rabbits as a tool to retrieve labeled cells following various periods in circulation. This retrieval capability allows biochemical studies to be conducted on red blood cells (RBC) that have aged for desired times in vivo. However, because erythrocyte life span is much shorter in rabbits than in humans, and because cell removal is measurably age-independent in rabbits, we have sought to validate the same protocol in dogs, whose cell life span and age-dependent removal characteristics are similar to humans'. Canine RBC were biotinylated in vivo by infusion of N-hydroxysuccinimidyl biotin dissolved in dimethylacetamide or dimethylsulfoxide. Cell life spans were evaluated using 14C-cyanate labeling followed by scintillation counting or avidin-FITC labeling followed by flow cytometry. Both methods gave identical results. The life span of the biotin-conjugated cells was found to be normal (approximately 110 days), and the stability of the biotin ligand was adequate for efficient retrieval of cells using avidin-coated magnetic beads (magnetic cell sorting [MACS]). From each isolation, approximately 20 microL of packed biotinylated cells of approximately 90% purity (i.e., 10% contamination by unlabeled cells) could be harvested. On average, approximately 60% of the biotinylated cells in any sample could be retrieved. Either multiple isolations or use of larger collection columns will facilitate collection of cell numbers sufficient for biochemical tests. After incorporating several modifications in the previous biotinylation protocol that were required for adaptation to the dog, the methodology can be used to study red cell senescence in an animal that has several pertinent similarities to humans.

Clinical and clinical laboratory correlates in sea otters dying unexpectedly in rehabilitation centers following the Exxon Valdez oil spill.

Following the Exxon Valdez oil spill, 347 oiled sea otters (Enhydra lutris) were treated in rehabilitation centers. Of these, 116 died, 94 within 10 days of presentation. Clinical records of 21 otters dying during the first 10 days of rehabilitation were reviewed to define the laboratory abnormalities and clinical syndromes associated with these unexpected deaths. The most common terminal syndrome was shock characterized by hypothermia, lethargy, and often hemorrhagic diarrhea. In heavily and moderately oiled otters, shock developed within 48 hours of initial presentation, whereas in lightly oiled otters shock generally occurred during the second week of captivity. Accompanying laboratory abnormalities included leukopenia with increased numbers of immature neutrophils (degenerative left shift), lymphopenia, anemia, azotemia (primarily prerenal), hyperkalemia, hypoproteinemia/hypoalbuminemia, elevations of serum transaminases, and hypoglycemia. Shock associated with hemorrhagic diarrhea probably occurred either as a direct primary effect of oiling or as an indirect effect secondary to confinement and handling in the rehabilitation centers. Lightly oiled otters were less likely to die from shock than were heavily oiled otters (22% vs. 72%, respectively). Heavily oiled otters developed shock more rapidly and had greater numbers of laboratory abnormalities, suggesting that exposure to oil was an important contributing factor.

Clinical pathology and hemostatic abnormalities in experimental African horsesickness.

Infection of naive North American horses with 10(4) cell culture infectious doses (CCID50) of virulence variants of African horsesickness virus (AHSV), designated AHSV/4SP, AHSV/9PI, and AHSV/4PI, reproduced three classical forms of African horsesickness: acute (pulmonary), subacute (cardiac), and febrile, respectively. Distinct clinicopathologic and hemostatic abnormalities were associated with each form of disease. Hemostatic abnormalities included increased concentration of fibrin degradation products and prolongation of prothrombin, activated partial thromboplastin, and thrombin clotting times. Hemostatic findings indicated activation of the coagulation and fibrinolytic systems with clotting factor consumption in acute and subacute cases of African horsesickness. Hematologic abnormalities in acute and subacute cases of African horsesickness included leukopenia, decreased platelet counts, elevated hematocrit, and increased erythrocyte counts and hemoglobin concentration. Leukopenia was characterized by lymphopenia, neutropenia, and a left shift. Increased levels of serum creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase, hypocalcemia, hypoalbuminemia, hypoproteinemia, and elevated creatinine, phosphorus, and total bilirubin levels were present in some but not all horses. Metabolic acidosis, indicated by decreased total bicarbonate and increased lactate and anion gap, was present in horses with the acute form of disease. Mild thrombocytopenia and leukopenia were occasionally associated with the febrile form of disease. These results suggest a role for intravascular coagulation in the pathogenesis of African horsesickness.

Specific biological effects of an anti-rat PMN antiserum intraperitoneally infected into f344/n rats.

Neutropenia can be produced with antimitotic chemicals, but this method lacks specificity. An alternative is to use antibody-dependent cytotoxicity to produce neutropenia; however, this method has not been completely evaluated with respect to efficacy, specificity, and potential collateral damage, especially to constituents of bone marrow. This study used in vitro and in vivo methods to evaluate specific biological effects of a commercially available rabbit anti-rat neutrophil (PMN) antiserum in F344/N rats. The viability of rat pulmonary alveolar macrophages (PAMs), PMNs, and lymphocytes in vitro was quantified using a trypan blue dye exclusion test. Amounts of antiserum in vitro that rendered PMNs 100% nonviable did not decrease the viability or phagocytic ability of the PAMs and did not decrease the viability of the lymphocytes. Intraperitoneal (IP) injection of the antiserum into rats resulted in complete depletion of the PMNs and about a 50% depletion of the lymphocytes in circulating blood within 24 hours. The numbers of both cell types remained lowered for 5 days, but returned to control values by Day 6 after the IP injection. The antiserum had no effect on the numbers of PAMs or lymphocytes in the pulmonary alveolar airspaces, as determined by quantifying the numbers of these cell types in bronchoalveolar lavage fluid (BALF). The numbers of PMNs in BALF, however, decreased on Days 3 and 4 after IP injection of antiserum, but were not different from control values by Day 5. The viability of the PAMs in BALF of treated rats was not different from control values at any time point. There were no morphological indications that the injected antiserum damaged lung tissue or stem cells in bone marrow. Results demonstrate that the anti-rat PMN antiserum administered IP to F344/N rats depletes circulating PMNs and partially depletes lymphocytes for a period of about 6 days without adversely affecting the precursors of red or white blood cells in bone marrow. We concluded that the antiserum is a relatively specific way to temporarily render rats neutropenic without damaging precursor cells in bone marrow.

Expression of transforming growth factor alpha and epidermal growth factor receptor in rat lung neoplasms induced by plutonium-239.

Ninety-two rat lung proliferative lesions and neoplasms induced by inhaled 239PuO2 were evaluated for aberrant expression of transforming growth factor alpha (TGF-alpha) and epidermal growth factor receptor (EGFR). Expression of TGF-alpha protein, measured by immunohistochemistry, was higher in 94% of the squamous cell carcinomas and 87% of the foci of alveolar epithelial squamous metaplasia than that exhibited by the normal-appearing, adjacent lung parenchyma. In contrast, only 20% of adenocarcinomas and foci of epithelial hyperplasia expressed elevated levels of TGF-alpha. Many neoplasms expressing TGF-alpha also expressed excessive levels of EGFR mRNA. Southern and DNA slot blot analyses showed that the elevated EGFR expression was not due to amplification of the EGFR gene. These data suggest that increased amounts of TGF-alpha were early alterations in the progression of plutonium-induced squamous cell carcinoma, and these increases may occur in parallel with overexpression of the receptor for this growth factor. Together, these alterations create a potential autocrine loop for sustaining clonal expansion of cells initiated by high-LET radiation.

Plutonium-induced proliferative lesions and pulmonary epithelial neoplasms in the rat: immunohistochemical and ultrastructural evidence for their origin from type II pneumocytes.

Immunohistochemistry and transmission electron microscopy were used to clarify the cellular origin for plutonium-239-induced pulmonary proliferative (preneoplastic) epithelial lesions and epithelial neoplasms in F344 rats. Examples of each histologic type of proliferative lesion and neoplasm were stained by the avidin-biotin complex immunoperoxidase method using antibodies to rat surfactant apoprotein and Clara cell antigen. Rat surfactant apoprotein immunostaining was detected in type II pneumocytes in sections of normal lung, in the cells of the proliferative lesions classified histologically as alveolar epithelial hyperplasia (51) and mixed foci (alveolar epithelial hyperplasia with fibrosis) (30), and in adenomas (2), adenocarcinomas (3), and adenosquamous carcinomas (2). With the exception of one adenosquamous carcinoma, Clara cell antigen immunostaining was not detected in any of the pulmonary lesions but was detected in nonciliated cuboidal epithelial (Clara) cells in normal bronchioles. The epithelial cells of the proliferative lesions and neoplasms had ultrastructural features consistent with type II pneumocytes, i.e., the presence of cytoplasmic lamellar and multivesicular bodies. The results of these studies indicate that the majority of plutonium-induced proliferative epithelial lesions and neoplasms in the rat originate from alveolar type II pneumocytes.

Senescence of canine biotinylated erythrocytes: increased autologous immunoglobulin binding occurs on erythrocytes aged in vivo for 104 to 110 days.

We have evaluated senescence related changes in canine red blood cells (RBCs) using the biotinylation system, where RBCs are labeled in vivo with biotin at the beginning of their life span, and retrieved from circulation on immobilized avidin at the end of their life span. This approach avoids the controversial use of density gradient centrifugation to collect presumably old RBCs. Furthermore, the dog is an appropriate model for human RBC senescence because it has a low degree of random RBC loss and a similarly long RBC life span (approximately 110 days). Two dogs had 97% to 100% of their circulating RBCs biotinylated by infusion of N-hydroxysuccinimido biotin (Clontech, Palo Alto, CA; Calbiochem, La Jolla, CA) dissolved in dimethyl sulfoxide. At postbiotinylation days 104 and 107 for one dog and day 110 for the other dog, biotinylated RBCs were isolated by magnetic cell sorting and analyzed for the presence of autologous IgG using 125I-labeled sheep-antidog IgG (SAD IgG). On all 3 days, there were at least three times more SAD IgG molecules per RBC on senescent biotinylated RBCs than on control (unfractionated) RBCs (day 104: 11,677 v 3,399; day 107: 6,710 v 2,115; day 110: 6,042 v 1,838 molecules of SAD IgG per senescent v control RBC). Furthermore, it is unlikely that an immune response to the conjugated biotin had been elicited, because fresh in vitro biotinylated RBCs that were incubated in autologous plasma (taken after exposure to circulating biotinylated RBCs for 113 days) and then exposed to the SAD IgG showed no increase in antibody binding over control (non-biotinylated) RBCs (1,431 v 1,378 cpm/10(8) biotinylated v control RBCs; P > .20). These results suggest that senescence of canine biotinylated RBCs is characterized by binding of autologous IgG and that antibiotin antibodies do not contribute to this process.

Ultracentrifugal and electrophoretic characteristics of the plasma lipoproteins of miniature schnauzer dogs with idiopathic hyperlipoproteinemia.

To better characterize the idiopathic hyperlipoproteinemia of Miniature Schnauzer dogs, the plasma lipoproteins of 20 Miniature Schnauzers (MS) and 11 dogs of other breeds (DOB) were evaluated by ultracentrifugation, electrophoresis, and biochemical tests. Seventeen MS were healthy; 3 had diabetes mellitus. Plasma from 6 of 17 healthy and all 3 diabetic MS was visibly lipemic. Lipemia was slight to marked in healthy lipemic MS, and marked in diabetic ones. All DOB had clear plasma; 8 were healthy and 3 had diabetes. All healthy lipemic MS and diabetic lipemic MS had hypertriglyceridemia associated with excess very low density lipoproteins. Chylomicronemia was present in 4 of 6 healthy lipemic MS and all 3 diabetic lipemic MS. Lipoproteins with ultracentrifugal and electrophoretic characteristics of normal low density lipoprotein were lacking in 4 of 6 healthy lipemic MS. The lipoprotein patterns of 4 of 11 healthy nonlipemic MS were characterized by mild hypertriglyceridemia associated with increased very low density lipoproteins and a lack of lipoproteins with characteristics of normal low density lipoproteins. Lipoprotein patterns of diabetic DOB closely resembled those of healthy DOB; those of diabetic lipemic MS resembled those of markedly lipemic healthy lipemic MS. In conclusion, the hyperlipoproteinemia of Miniature Schnauzers is characterized by increased very low density lipoproteins with or without accompanying chylomicronemia; some affected dogs may have decreased low density lipoproteins.

Sequential analysis of the pathogenesis of plutonium-induced pulmonary neoplasms in the rat: morphology, morphometry, and cytokinetics.

Light microscopy, morphometry, and cytokinetic techniques were used to examine the dynamics of plutonium-induced pulmonary proliferative lesions and neoplasms in rats at several intervals to 450 days after inhalation exposure to aerosols of 239PuO2. Maximal increases in alveolar and bronchiolar epithelial cell labeling were seen at 30 days; decreasing subsequently, the levels remained elevated above control indices. Focal proliferative epithelial lesions developed in the lung by 180 days and before the onset of pulmonary neoplasms. Pulmonary neoplasms, predominantly adenocarcinomas and squamous cell carcinomas, were initially observed at 308 days. The proliferative lesions progressed through a succession of morphological changes leading to the development of neoplasms. The volume density (fraction) and epithelial surface area of foci of alveolar epithelial hyperplasia increased progressively between 180 and 450 days after exposure, in contrast to the other proliferative lesions. We conclude that plutonium-induced pulmonary neoplasms develop through a succession of focal proliferative lesions that represent developmental preneoplastic lesions. Progressive increases in volume and epithelial surface area of the alveolar epithelial hyperplasias suggest that they may be more at risk for neoplastic transformation than the other histological types of proliferative foci.

General responses of the bone marrow to injury.

Hematologic responses in a toxicologic setting may be quite complex and may involve both local as well as systemic manifestations of toxicity and/or pharmacologic responses. Direct toxicity to bone marrow can lead to changes such as marrow necrosis, marrow dysplasia, and macrophage hyperplasia. Some toxic compounds can directly stimulate or suppress the development of 1 or more marrow cell lines. The marrow may also respond to injury at distant sites with increased production of various blood cell elements. Accurate interpretation of hematologic responses generally involves integration of peripheral blood data with bone marrow findings as well as toxicologic findings in other organ systems. This manuscript overviews the various marrow changes encountered in toxicologic studies and provides a perspective of how these changes are best approached from an interpretive viewpoint.

Cytologic evaluation of the respiratory tract.

Evaluation of respiratory tract disease is a challenge for several reasons: no serum biochemical or hematologic tests that localize injury to the respiratory system are available, imaging techniques do not usually lead to etiologic diagnoses, and excisional biopsies are often very difficult to obtain from respiratory lesions. For these reasons, specific diagnosis of respiratory tract disease often resides in cytologic evaluation. This article reviews the various cytologic collection techniques that yield high-quality specimens from the upper and lower respiratory tract. Cytologic features of the normal respiratory tract as well as common respiratory disorders are described and illustrated.

Clinical pathology testing recommendations for nonclinical toxicity and safety studies. AACC-DACC/ASVCP Joint Task Force.

Clinical pathology testing in nonclinical toxicity and safety studies is an important part of safety assessment. In recent years, clinical laboratory testing has rapidly expanded and improved. Some government regulatory agencies provide guidelines for clinical pathology testing in nonclinical toxicity and safety studies. To improve these testing guidelines and the resultant safety assessments, the American Association for Clinical Chemistry's Division of Animal Clinical Chemistry and the American Society for Veterinary Clinical Pathology formed a joint committee to provide expert recommendations for clinical pathology testing of laboratory species involved in subchronic and chronic nonclinical toxicity and safety studies. These recommendations include technical recommendations on blood collection techniques and hematology, serum chemistry, and urinalysis tests.

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

The effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Modifying effects of preexisting pulmonary fibrosis on biological responses of rats to inhaled 239PuO2.

We investigated the modifying effects of preexisting, bleomycin-induced pulmonary fibrosis on the deposition, retention, and biological effects of inhaled 239PuO2 in the rat. Among rats exposed to similar airborne concentrations of 239PuO2, initial lung burdens of 239Pu per kilogram body mass were similar whether or not pulmonary fibrosis was present. However, clearance of 239Pu from the lungs was significantly decreased in the rats with preexisting pulmonary fibrosis. The incidence of lung lesions (epithelial hyperplasia, diffuse macrophage increases and aggregation, and loose and dense connective tissue) was significantly greater among rats with preexisting pulmonary fibrosis than among the exposed controls. Rats with preexisting fibrosis had shorter life spans than 239PuO2-exposed control rats. When groups of rats with similar alpha doses to the lungs were compared, the incidences of neoplastic lesions in the lung, the times to death of rats with lung neoplasms, and the risk of lung tumors per unit of alpha dose to the lungs in rats with or without pulmonary fibrosis were similar. The results of this study suggest that humans with uncomplicated pulmonary fibrosis may not be more sensitive to the carcinogenic effects of inhaled 239PuO2 than are individuals with normal lungs, assuming that the total alpha doses to the lungs are similar.