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Background/objectives: Greek Orthodox fasting (OF), which involves 180-200 days of fasting per year, is dictated by the Christian Orthodox religion. For the first time, this cross-sectional study examines the characteristics and the effects of OF on anthropometry, cardiometabolic markers and calcium homeostasis in Athonian monks (AMs).Subjects/methods: Daily intakes of energy, macro- and micronutrients of a day during a weekend of Nativity Fast, defined as non-restrictive day (NRD), and a weekday during Great Lent, labeled as restrictive day (RD) were recorded.Results: The daily energy intake of 70 AM (age=38.8±9.7 years) was low during both RD and NRD (1265.9±84.5 vs 1660±81 kcal, respectively, P<0.001). Paired samples t-test showed statistically significant difference between daily intakes in RD and NRD: carbohydrates (159.6±21.8 vs 294.3±23.4 g, P<0.0001) and saturated fat (12.7±0.0 vs 16.4±0.0 g, P<0.0001) were lower, whereas protein (89.2±1.3 vs 72.35±1.3 g, P<0.001) was higher during RD. A subsample of 50 monks (age=38.7±10.6 years) formed a study cohort for cardiometabolic and calcium homeostasis assessment. Body weight (74.3±12.9 kg) and body mass index (BMI; 23.8±4.1 kg/m2) were independent of level of physical activity. Optimal profiles for lipid and glucose parameters (total cholesterol: 183.4±41.7 mg/dl, LDL: 120.6±37.6 mg/dl, triglycerides: 72.2±31.3 mg/dl, HDL: 48.5±14.2 mg/dl and homeostasis model assessment of insulin resistance (HOMA-IR) 1.02±0.40) were found. Profound hypovitaminosis D (8.8±6.2 ng/ml), high parathyroid hormone (PTH): 115.5±48.0 pg/ml with normal serum calcium levels (8.9±3.2 mg/dl) was observed.Conclusions: Unaffected by variation in lifestyle factors, the results of this unique study offers clear evidence for the health benefits of the strict Athonian OF through optimal lipid and glucose homeostasis. [ABSTRACT FROM AUTHOR]

Background: No studies to date have assessed young adults' use of First Nations/Native tobacco, a common form of contraband tobacco in Canada. This study examined the proportion of First Nations/Native cigarette butts discarded on post-secondary campuses in the province of Ontario, and potential differences between colleges and universities and across geographical regions. Methods: In 2009, discarded cigarette butts were collected from high-traffic smoking locations at 12 universities and 13 colleges purposively selected to represent a variety of institutions from all 7 health service regions across Ontario. Cigarette butts were identified as First Nations/Native tobacco if they were: known First Nations/Native brands; had names not matching domestic and international legally-manufactured cigarettes; had no visible branding or logos. Results: Of 36,355 butts collected, 14% (95% CI = 9.75-19.04) were First Nations/Native. Use of this tobacco was apparent on all campuses, accounting for as little as 2% to as much as 39% of cigarette consumption at a particular school. Proportions of First Nations/Native butts were not significantly higher on colleges (M = 17%) than universities (M = 12%), but were significantly higher in the North region. Conclusions: The presence of cheap First Nations/Native (contraband) tobacco on post-secondary campuses suggests the need for regulation and public education strategies aimed to reduce its use. Strategies should account for regional variations, and convey messages that resonate with young adults. Care must be taken to present fair messages about First Nations/Native tobacco, and avoid positioning regulated tobacco as a healthier option than contraband. [ABSTRACT FROM AUTHOR]

Revealing of the mechanism of cascade processes has made it possible to work out an anti-emergency and self-restoration system. Its purpose would be to control automatically such a process and to attain the restoration of a power system's functioning from any stage of an emergency. The authors propose a method of preventive short-term sectioning by which a power system can be split into parts so as to unload the overloaded cross-section. This preventive short-term sectioning to the maximum extent preserves the carrying capacity of transmission lines. After the restoration of the normal operation in a separated region its reconnection proceeds by automatic synchronization, with which the emergency situation is eliminated. [ABSTRACT FROM AUTHOR]

Background: Monocyte chemotactic protein (MCP-1/CCL2), the ligand for CCR2 and CCR5, and macrophage inflammatory protein-1α (MIP-1α/CCL3), the ligand for CCR1 and CCR5, are potent chemo-attractants in vitro and produce lesions in experimental animals, which resemble immediate and delayed-type hypersensitivity (DTH) reactions. CCL3 induces mononuclear cell and granulocyte infiltration in human atopic and nonatopic skin. Whether CCL2 (MCP-1) has comparable activity in man is uncertain as is the capacity of both the chemokines to elicit immediate- and DTH-like reactions in humans. Methods: Inflammatory cells were counted by immunohistochemistry in 24 and 48-h skin biopsies from atopics and nonatopics after intradermal injection of CCL2 and CCL3. Immediate (15 min) wheals-and-flares and delayed (24 and 48 h) indurations were also recorded. Results: Both chemokines induced immediate- (15 min) and delayed (24 and 48 h) reactions, which were associated with significant infiltrations of CD68+ macrophages, CD3+, CD4+ (but not CD8+) T cells, neutrophils, and eosinophils in biopsies from injection sites. CCL2, but not CCL3, also induced infiltration of basophils. Neither chemokine produced significant changes in the numbers of tryptase+ cutaneous mast cells. There were no differences in the pattern of skin reactivity or the numbers of infiltrating leukocytes in response to CCL2 and CCL3 between atopic and nonatopic subjects. In general, maximal infiltration of inflammatory cells was observed at the 24-h, rather than the 48-h, time point. Conclusions: CCL2 and CCL3 induce both immediate and delayed skin reactions in atopics and nonatopics, and evoke a similar profile of local T cell/macrophage and granulocyte recruitment which, in general, confirm previous in vitro findings and in vivo experimental animal data. [ABSTRACT FROM AUTHOR]

Rationale: Airway hyperresponsiveness (AHR) increases up to 2 weeks after allergen inhalational challenge of subjects with asthma who show a late-phase asthmatic reaction (dual responders). Cellular inflammation and airway remodeling are increased 24 hours after allergen challenge. Objectives: To determine whether persistence of increased AHR is associated with persistent activation of remodeling and enhanced inflammation. Methods: Fiberoptic bronchoscopy was performed at baseline and at 24 hours and 7 days after allergen inhalational challenge of dual responders with mild-moderate asthma. At each time point, AHR, spirometry, and expression of tenascin (extracellular matrix protein), procollagen I, procollagen III, and heat shock protein (HSP)-47 (markers of collagen synthesis), and alpha-smooth muscle actin (myofibroblasts) were evaluated as markers of activation of airway remodeling, together with numbers of mucosal major basic protein-positive eosinophils, CD68(+) macrophages, CD3(+), CD4(+), CD8(+) T cells, elastase-positive neutrophils, and tryptase-positive mast cells. Measurements and Main Results: AHR was increased from baseline at 24 hours and 7 days after allergen challenge. Reticular basement membrane tenascin expression was elevated at 24 hours and returned to baseline levels at 7 days. Reticular basement membrane procollagen III expression was significantly elevated at 7 days. Expression of procollagen I, HSP-47, and alpha-smooth muscle actin were all higher at 7 days compared with 24 hours. At 24 hours, eosinophil, macrophage, neutrophil, and CD3(+) T cells were increased but had returned to baseline by 7 days. Conclusions: In dual responders with asthma, the 24-hour increase in airway wall cellular inflammation after allergen challenge resolves by 7 days, whereas the increases in AHR and markers of remodeling persist. [ABSTRACT FROM AUTHOR]

The pentatricopeptide repeat (PPR) is a degenerate 35-amino acid repeat motif that is widely distributed among eukaryotes. Genetic, biochemical, and bioinformatic data suggest that many PPR proteins influence specific posttranscriptional steps in mitochondrial or chloroplast gene expression and that they may typically bind RNA. However, biological functions have been determined for only a few PPR proteins, and with few exceptions, substrate RNAs are unknown. To gain insight into the functions and substrates of the PPR protein family, we characterized the maize (Zea mays) nuclear gene ppr4, which encodes a chloroplast-targeted protein harboring both a PPR tract and an RNA recognition motif. Microarray analysis of RNA that coimmunoprecipitates with PPR4 showed that PPR4 is associated in vivo with the first intron of the plastid rps12 pre-mRNA, a group II intron that is transcribed in segments and spliced in trans, ppr4 mutants were recovered through a reverse-genetic screen and shown to be defective for rps 12 trans-splicing. The observations that PPR4 is associated in vivo with rps 12-intron 1 and that it is also required for its splicing demonstrate that PPR4 is an rps 12 trans-splicing factor. These findings add trans-splicing to the list of RNA-related functions associated with PPR proteins and suggest that plastid group II trans-splicing is performed by different machineries in vascular plants and algae. [ABSTRACT FROM AUTHOR]

The general purpose of this article is to investigate the Boards of Governors of eight Ontario universities in order to determine their relationship to the Canadian power structure. More specifically, it is an attempt to determine whether or not the upper echelons of the university represent a meeting ground for what sociologist C.W. Mills terms the "power elite." To understand the members of the boards of governors as a power elite, three key factors, as outlined by Mills must be taken into account: 1) the psychological and social bases for unity; 2) the structure, mechanics and interrelatedness of the major hierarchical institutions; and 3) the explicit recognition by the power elite of the need for formal and informal coordination. Through their common educational backgrounds, similarities in career patterns, philanthropic activities, and membership in exclusive social clubs, there is formed the basis for the "social and psychological unity" among the governors. The university is not an autonomous institution separate from the social, economic and historical forces operating on the "outside" world. In fact the stratification system and power structure of the university mirrors the larger corporate society. The greatest legitimization of this occurs at the apex of the university structure where members of the "power elite" have become the "power elite of education."

Focuses on `Color Recovery' which combines dithering with a novel filtering technique to yield image quality comparable to 24-bit color. Color recovery theory; Dither process; Filtering process; Software considerations; Filter function logic; Visual results. INSET: Overview of color theory and dither..

We have used in situ hybridization (ISH) and immunohistochemistry (IHC) to investigate the kinetics of the expression for FcεRI mRNA (α-, β- and γ-chains), the α-chain protein product, as well as the phenotype of the mRNA- or protein-positive cells in allergen-induced late-phase skin reactions in atopic subjects. Compared with diluent controls, there were significant increases in the total numbers of mRNA+ cells for the α-, β-and γ-chains for FcεRI at all time-points (6, 24 and 48 hr) after allergen challenge (P<0·01). By double IHC/ISH significant increases in α-, β- and γ-chain mRNA+ macrophages, eosinophils, mast cells and CD1a+ cells were also observed after allergen challenge (P<0·05). The distribution of FcεRI subunit (α-, β-, or γ-chain) mRNA+ co-localization was CD68+ macrophages (42–47%), EG2+ eosinophils (33–39%), tryptase+ mast cells (5–11%) and CD1a+ Langerhans’ cells (2–4%). Using single IHC, significant increases in the total number of FcεRI protein+ cells (P<0·01) were observed 24 and 48 hr after allergen challenge. Double IHC showed that the distribution of FcεRI+ cells was tryptase+ mast cells (33%), CD68+ macrophages (36%), EG2+ eosinophils (20%), CD1a+ Langerhans’ cells (4%) and unidentified cells (7%), at the 24-hr allergen-challenged sites. These observations suggest that the cutaneous late-phase reaction in man is associated with up-regulation of FcεRI on eosinophils, macrophages, mast cells and Langerhans’ cells. [ABSTRACT FROM AUTHOR]

Interleukin-2 (IL-2) is an essential growth factor for T cells. Previous studies have shown that human peripheral eosinophils respond to IL-2 in chemotaxis and express the IL-2 receptor (CD25). In addition, eosinophils have been shown to transcribed messenger RNA for IL-2. The aim of the present study was to determine whether eosinophils translate mRNA for IL-2 and to determine the site of intracellular localization. By immunocytochemistry, an average of 9% of cells showed cytoplasmic staining for IL-2 in freshly isolated unstimulated blood eosinophils obtained from asthmatic subjects who were not receiving oral corticosteroid treatment (n=5). Freshly isolated, disrupted, highly purified eosinophils (> 99%, by CD16¯ immunomagnetic selection) contained an average of 6 pg/106 cells of IL-2 measured by a specific enzyme linked immunosorbent assay (ELISA) (n=7). Purified eosinophil incubated with serum-coated Sephadex beads showed an increase in the amount of intracellularly-retained IL-2 (26·2 ± 7·2 pg/106 cells) with some evidence for release of this cytokine but only in three out of six eosinophil preparations (range 1·3–5·8 pg/106 cells). [ABSTRACT FROM AUTHOR]

We have tested the hypothesis that the bronchial epithelium has the capacity to generate and release cytokines that could contribute to inflammatory events associated with inflammatory lung diseases. Messenger RNA (mRNA) for interleukin-6 (IL-6). IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) was identified in human bronchial epithelial cell primary cultures, characterized on the basis of staining for cytokeratin, using both in situ hybridization and Northern blotting. Using in situ hybridization we have shown that the majority of the cells expressed mRNA for IL-6 and IL-8, whereas fewer than 20% of cells expressed message for GM-CSF. The numbers of cells expressing message were increased by culture with tumour necrosis factor-α (TNF-α) (20 ng/ml, 24 hr). These observations were substantiated by Northern blotting, which showed that both TNF-α and IL-1β were able to induce a dose-dependent increase in IL-8-specific mRNA. Immunoreactive IL-6 and GM-CSF were detected and quantified in the culture supernatants by ELISA, and IL-8 by radioimmunoassay. The levels of immunoreactivity were increased by incubation of epithelial cells with either IL-1β or TNF-α for 24 hr. A transformed tracheal epithelial cell line (9HTEo- expressed mRNA for IL-6, IL-8 and GM-CSF but, whereas levels of immunoreactive IL-6 in culture supernatants were comparable with those in primary cell cultures, levels of IL-8 were low and GM-CSF trivial. These observations indicate that the bronchial epithelium has the potential to be a major source of IL-8 and a number of other cytokines, and that production can be amplified substantially by IL-1β and TNF-α. The bronchial epithelium is ideally situated to modulate inflammatory and immunological events in and around the airways, and these observations suggest that it could contribute to promote and sustain inflammatory and immunological processes in inflammatory lung diseases such as asthma. [ABSTRACT FROM AUTHOR]

In an attempt to identify the phenotype of the CD25+ cells previously demonstrated in late-phase allergic reactions in skin and nasal mucosa, and in the bronchial mucosa in atopic asthma we have investigated the co-expression of CD3 and CD25 using double immunofluorescent staining. Fluorescein isothiocyanate (FITC) conjugated anti-CD3 monoclonal antibody and a biotinylated anti-CD25 monoclonal antibody (which was later developed with Texas Red streptavidin) were applied simultaneously to cryostat sections or cytospins of freshly prepared samples. Skin and nasal biopsies were from antigen-induced late-phase reactions, and bronchial biopsies and cytospins of bronchoalveolar lavage cells were from subjects with moderate atopic asthma. Four to 14% ofCD3+ cells in these tissues were CD25+ and 61–100% of CD25+ cells also expressed CD3. However, CD25 was also expressed on non-CD3+ cells, assumed to be non-T cells. These results were comparable to that observed with a positive control of a tuberculin-challenged skin biopsy. Thus the majority of cells expressing CD25 in various types of atopic allergic inflammation in man were T lymphocytes. [ABSTRACT FROM AUTHOR]

Background: Bronchiectasis is a chronic suppurative lung disease characterised by irreversible dilation of the bronchi and persistent purulent sputum. The immunopathology of the disease was studied using a quantitative immunostaining technique with particular reference to T lymphocytes, macrophages, and granulocytes.Methods: Bronchial mucosal biopsy specimens were obtained by fibreoptic bronchoscopy from 12 patients with bronchiectasis (six receiving inhaled steroids) and 11 normal healthy controls. Immunostaining (APAAP method) was performed on frozen cryostat sections with a panel of monoclonal antibodies to total leucocytes (CD45), T lymphocyte phenotypic markers (CD3, CD4, CD8), macrophages (CD68), eosinophils (EG2), and neutrophils (elastase).Results: There was a mononuclear cell infiltrate in both patients with bronchiectasis and normal controls, but an overall increase in total leucocyte cell numbers (CD45+ cells) was identified in those with bronchiectasis (median values 422 cells/mm2 versus 113 cells/mm2 in control tissue, p < 0.001). Intense infiltration of CD3+ T lymphocytes was observed compared with healthy controls (292 cells/mm2 and 40 cells/mm2, respectively, p < 0.001). This comprised predominantly CD4+ T cells (118 cells/mm2) rather than CD8+ T cells (47 cells/mm2). CD3+ cells counts were reduced in those subjects on inhaled steroids compared with those not receiving inhaled steroids (197 cells/mm2 versus 369 cells/mm2, p < 0.05), as were CD4+ cell counts (82 cells/mm2 versus 190 cells/mm2, p < 0.05). Neutrophil and macrophage cell numbers were also increased in patients with bronchiectasis (114 cells/mm2 and 213 cells/mm2, respectively) compared with controls (41 neutrophils/mm2 and 40 macrophages/mm2). EG2+ (activated) eosinophil numbers were much lower than T cells, macrophages, and neutrophils in patients with bronchiectasis but were increased compared with controls (36 cells/mm2 versus 0 cells/mm2, p < 0.001). In view of the markedly increased neutrophil counts in patients with bronchiectasis, biopsy specimens were immunostained for interleukin 8 (IL-8) which was highly significantly increased compared with controls (47 cells/mm2 versus 15 cells/mm2, p < 0.01). IL-8+ cells were less prominent in steroid treated patients than in patients not receiving treatment (30 cells/mm2 versus 60 cells/mm2, p < 0.05). A further characteristic of bronchiectasis was mucous gland hypertrophy. Gland area comprised up to 40% of the tissue in some bronchiectasis sections while no hypertrophy was noted in control biopsy specimens (p < 0.05).Conclusion: Airway inflammation in bronchiectasis is characterised by tissue neutrophilia, a mononuclear cell infiltrate composed mainly of CD4+ T cells and CD68+ macrophages, and increased IL-8 expression. Inhaled corticosteroid treatment in patients with bronchiectasis is associated with a less marked infiltration by T cells and IL-8+ cells within the bronchial mucosa, although this finding requires confirmation in a prospective placebo controlled trial. [ABSTRACT FROM AUTHOR]

This study was done to examine the nature of the membrane constituents involved in the secretion of eosinophil cationic protein (ECP) from human blood eosinophils. Three mouse monoclonal antibodies were used, which showed greater binding to membrane antigens on activated, and light density eosinophils from patients with an eosinophilia, than on nonactivated or normal density eosinophils. All three antibodies (EoN4, EoN5 & EoN6) stimulated normal density human eosinophils to secrete ECP, either alone or in association with sepharose-C3b. The antibodies bound to at least two separate sites on the membrane, which were distinct from the receptors for immunoglobulins, C3b, and eosinophil activating factor. One combination of antibodies increased the amount of ECP which was secreted. The membrane antigen recognized by antibody EoN4 was a glycoprotein, molecular weight 75 kD. These findings showed that ECP secretion may be induced by a wider range of stimuli than has been previously recognized, and that the antigens recognized by these monoclonal antibodies may play an important role in the induction of eosinophil degranulation. [ABSTRACT FROM AUTHOR]

In order to study the membrane events which lead to human blood eosinophil activation and degranulation, six clone of mouse monoclonal antibodies were made to isolated blood eosinophils from a patient with the hypereosinophilic syndrome (HES). The antibodies were specific for the plasma membranes of blood eosinophils and neutrophils, eosinophil myelocytes and haemopoietic cell lines. A higher proportion of blood eosinophils from eight patients with the HES bound these antibodies compared to normal individuals. Five antibodies stained intermediate density eosinophils preferentially, and one stained the light density eosinophils most strongly. Normal blood eosinophils were induced to express more of these antigens either by culture alone (two antibodies) or culture with monocyte culture supernatant which activates eosinophils for increased cylotoxic capacity (four antibodies). It was concluded that several of the principal antigens on the eosinophil plasma membrane are also present on neutrophils and immature haemopoietic cells, and that their expression in mature blood eosinophils is related to the extent of eosinophil activation and degranulalion. It is suggested that these antigens may be useful in studying the ways in which eosinophils alter their plasma membrane during activation and degranulation in vitro, and in the blood of patients with an eosinophilia. [ABSTRACT FROM AUTHOR]

A monoclonal antibody prepared against the eosinophil major basic protein (MBP) was compared with the anti-eosinophil cationic protein (ECP) antibodies (EGl and EG2) in immunostaining of bronchial biopsies from atopic asthma and controls. Anti-MBP (designated BM K-13) did not cross-react with other eosinophii basic proteins (i.e. ECP, eosinophil peroxidase [EPO] or eosinophil-derived neurotoxin [EDN]) and stained more than 98% of peripheral blood eosinophils irrespective of their degree of activation. EG2 stained 15% of resting and 75% of activated eosinophils; EG1 recognized 74% and 78% of resting and activated cells, respectively. The numbers of BMK-13, EG1 or EG2-positive staining cells in bronchial biopsies from asthma were significantly greater than atopic non-asthmatics (P <0.02, P<0.01 and F<0.05 respectively) and normal non-atopic controls (P<0.001). For each of the various groups studied, the rank order for the number of eosinophils stained was BMK-13+EG1 >EG2. BMK-13 stained significantly more cells from bronchial biopsies of atopic asthma and atopic non asthma when compared to EG2+(P<0.001 and P < 0.05, respectively). Since only a proportion of BMK-13+ cells were EG2+, these results suggest that not all tissue eosinophils are actively secreting. Thus. BMK-13 can serve as a useful pan-eosinophil marker in tissue sections since it appears to stain most eosinophils. [ABSTRACT FROM AUTHOR]

Background: Interleukin (IL)-5 is thought to play a part in asthmatic bronchial mucosal inflammation and is a potential therapeutic target. Detectable serum IL-5 concentrations have been found previously in a proportion of patients with acute severe asthma, but not in the same patients following oral glucocorticoid therapy or in normal controls. A study was undertaken to investigate whether or not IL-5 is detectable in the serum of patients with glucocorticoid-dependent chronic severe asthma.Methods: Serum concentrations of IL-5 were measured in 29 patients with stable oral glucocorticoid-dependent chronic severe asthma (mean PEFR 59.7% predicted) and seven normal controls using a specific enzyme-linked immunoassay calibrated with recombinant human IL-5 standards (lower limit of sensitivity 40 pg/ml).Results: Interleukin 5 was detectable in the serum of 15 of the 29 patients at a median concentration of 150 pg/ml (range 40-690), but was undetectable in the serum of all the control subjects. The patients with detectable serum IL-5 concentrations did not differ from those with undetectable concentrations in terms of atopic status, disease severity (percentage predicted PEFR or FEV1), prednisolone dosage, serum IgE concentrations, or peripheral eosinophil count.Conclusions: Interleukin 5 is detectable in the serum of a proportion of both atopic and non-atopic patients with chronic severe asthma, and concentrations in these patients were higher than in normal controls. These observations are compatible with the hypothesis that IL-5 release occurs in these patients during a period of stable asthma despite systemic glucocorticoid therapy. [ABSTRACT FROM AUTHOR]

Background: No studies to date have assessed young adults' use of First Nations/Native tobacco, a common form of contraband tobacco in Canada. This study examined the proportion of First Nations/Native cigarette butts discarded on post-secondary campuses in the province of Ontario, and potential differences between colleges and universities and across geographical regions.Methods: In 2009, discarded cigarette butts were collected from high-traffic smoking locations at 12 universities and 13 colleges purposively selected to represent a variety of institutions from all 7 health service regions across Ontario. Cigarette butts were identified as First Nations/Native tobacco if they were: known First Nations/Native brands; had names not matching domestic and international legally-manufactured cigarettes; had no visible branding or logos.Results: Of 36,355 butts collected, 14% (95% CI = 9.75-19.04) were First Nations/Native. Use of this tobacco was apparent on all campuses, accounting for as little as 2% to as much as 39% of cigarette consumption at a particular school. Proportions of First Nations/Native butts were not significantly higher on colleges (M = 17%) than universities (M = 12%), but were significantly higher in the North region.Conclusions: The presence of cheap First Nations/Native (contraband) tobacco on post-secondary campuses suggests the need for regulation and public education strategies aimed to reduce its use. Strategies should account for regional variations, and convey messages that resonate with young adults. Care must be taken to present fair messages about First Nations/Native tobacco, and avoid positioning regulated tobacco as a healthier option than contraband. [ABSTRACT FROM AUTHOR]