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Objective/Background To investigate the prevalence of bovine arch (BA) among patients with type A and B aortic dissection, and to provide insight into the implication of this variation on the outcome of patients with acute or subacute type B aortic dissection (a/sTBAD). Methods This retrospective cohort analysis includes patients with a/sTBAD admitted between January 2006 and December 2016. Computed tomographic angiograms (CTAs) of patients referred because of type A aortic dissection were also re-evaluated with regard to the presence of BA. As a control group, 110 oncological patients who had undergone a chest CTA for disease staging during the study period were enrolled. A total of 154 patients with a/sTBAD and 168 with type A aortic dissection were identified during the study period. Results An overall prevalence of 17.6% for BA variants was revealed. The comparison between patients with aortic dissection and the control group showed no statistically significant difference in BA prevalence (17.7% vs. 17.3%; p = 1.0). No statistically significant difference in BA prevalence was observed when comparing patients with type A aortic dissection with those with type B aortic dissection (16.6% vs. 18.8%; p = .66). During a median follow-up period of 27.8 months, 30 patients died. The mortality rate among patients presenting a BA variant was 34.5%, whereas among patients without, it was 16.0% (p = .04). Multivariate analysis revealed the presence of a BA as an independent predictor of mortality (adjusted odds ratio 3.4, 95% confidence interval 1.2–9.8). Conclusion The BA should be considered as a predictor of the outcome for patients with type B aortic dissection.

Summary: Background: The aim of this study is to evaluate perioperative as well as long-term outcomes in patients operated with carotid endarterectomy (CEA) or stenting (CAS) due to symptomatic or asymptomatic high-grade restenosis of the internal carotid artery (ICA). Patients and methods: In a retrospective analysis of our electronic database including 2980 patients who underwent carotid endarterectomy or stenting due to a symptomatic or asymptomatic high-grade stenosis of the ICA, between 2000 and 2016, we enrolled 111 patients with recurrent ICA stenosis. Results: An ipsilateral 2nd time restenosis (> 80 % in the asymptomatic and > 50 % in the symptomatic patients according to NASCET criteria) of ICA was detected in 13 patients (12 %); 3 of them were symptomatic. These patients were managed with either CEA (n = 5/38 %) or CAS (n = 8/62 %) with no perioperative stroke or death. The stroke-free survival rates at 2 and 8 years for CEA were 98 % and 98 % versus 100 % and 100 % for CAS respectively (P = .271). The type of the initial procedure (patch, CAS or interposition) did not play any significant role for the development of a 2nd time restenosis (P = .841). Conclusions: Redo-CEA/CAS seem to have similar results as primary procedures (as reported in the literature) with favorable periprocedural and long-term outcomes.

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).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.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, P0.001). 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, P0.0001) and saturated fat (12.7±0.0 vs 16.4±0.0 g, P0.0001) were lower, whereas protein (89.2±1.3 vs 72.35±1.3 g, P0.001) 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/mUnaffected 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.

Background Both transforming growth factor (TGF)-β 1 and activin-A have been implicated in airway remodeling in asthma, but the modulation of their specific signaling pathways after disease activation remains undefined. Objective To define the expression kinetics of TGF-β 1 , activin-A ligands, and follistatin (a natural activin inhibitor), their type I and type II receptors (activin-like kinase[ALK]–1, ALK-5, ALK-4, TβRII, and ActRIIA/RIIB) and activation of signaling (via phosphorylated (p) Smad2), in the asthmatic airway after allergen challenge. Methods Immunohistochemistry was performed on bronchial biopsies from 15 mild atopic patients with asthma (median age, 25 years; median FEV 1 % predicted, 97%) at baseline and 24 hours after allergen inhalation. Functional effects of activin-A were evaluated by using cultured normal human bronchial epithelial (NHBE) cells. Results pSmad2 + epithelial cells increased at 24 hours ( P = .03), and pSmad2 was detected in submucosal cells. No modulation of activin-A, follistatin, or TGF-β 1 expression was demonstrated. Activin receptor + cells increased after allergen challenge: ALK-4 in epithelium ( P = .04) and submucosa ( P = .04), and ActRIIA in epithelium ( P = .01). The TGF-β receptor ALK-5 expression was minimal in the submucosa at baseline and after challenge and was downregulated in the epithelium after challenge ( P = .02), whereas ALK-1 and TβRII expression in the submucosa increased after allergen challenge ( P = .03 and P = .004, respectively). ALK-1 and ALK-4 expression by T cells was increased after allergen challenge. Activin-A induced NHBE cell proliferation, was produced by NHBE cells in response to TNF-α, and downregulated TNF-α and IL-13–induced chemokine production by NHBE cells. Conclusion Both TGF-β and activin signaling pathways are activated on allergen provocation in asthma. Activin-A may contribute to resolution of inflammation.

Background Anti-IgE (omalizumab) inhibited early and late asthmatic reactions and infiltration of inflammatory cells in asthmatic bronchial biopsies at baseline. The effect of chronic allergen exposure on these outcomes is unknown. Repeat allergen challenge in human skin represents a suitable model to address this question. Objective To study the effect of anti-IgE (omalizumab) on early-phase (EPR) and late-phase (LPR) skin reactions and cellular infiltration by using a repeat skin allergen challenge designed to imitate chronic allergen exposure. Methods Twenty-four atopic allergic volunteers received omalizumab or placebo for 12 weeks. Paired intradermal challenges of allergen (30 biological units) and diluent control were administered on 9 occasions at 2-week intervals. Early-phase and late-phase skin reactions and cellular infiltration in skin biopsies (using immunohistochemistry and in situ hybridization) were measured at intervals. Results Compared with placebo, omalizumab-treated patients had a progressive reduction in the LPR that was significantly greater than its effect on the EPR (median, −63% vs −24% respectively; P =.009). In addition, significant reduction of the LPR was reached within 2 weeks of commencing treatment, compared with 8 weeks for the EPR. There was a priming effect of repeated allergen challenge on infiltration of eosinophil, neutrophil, T H 2 (CD3 + /IL-4 + ), and total FcɛRI + cells in patients on placebo that was abrogated in those receiving omalizumab. Conclusion The more marked effect of omalizumab on the LPR and prevention of the repeat-dose priming effect on several inflammatory cell types support a role for anti-IgE treatment in conditions associated with chronic allergic inflammation.

CD4+ T-cells are likely to be involved as a source of pro-inflammatory cytokines in asthma. This study assessed the effects of an infusion of keliximab (IDEC CE9.1), an anti-CD4+ monoclonal antibody, on peripheral blood CD4+ T-cells in corticosteroid-dependent asthmatics.Three cohorts of patients (termed C0.5: n=6, C1.5: n=5, and C3.0: n=5) received a single infusion of 0.5, 1.5 or 3.0 mg·kg−1, respectively, with a fourth receiving placebo (Cpl: n=6), and were followed-up for 4 weeks. By flow cytometry in peripheral blood, pre- and postinfusion assessment was made of: a) CD4 and CD8 counts and mean fluorescence; b) CD25, human leukocyte antigen-DR (HLA-DR), CD45RO and CD45RA expression on CD4+ T-cells; and c) interferon (IFN)-γ, interleukin (IL)-4 and IL-5 expression in CD4+ T-cells. Keliximab'sin vitroeffects on allergen-specific peripheral blood mononuclear cells (PBMC) proliferation in atopic asthmatics were also evaluated.There was a significant increase in lung function (peak expiratory flow rate) in the C3.0group. Following infusion in C0.5, C1.5and C3.0but not Cpl: 1) the CD4, but not CD8 count was significantly decreased; 2) there was total loss of Leu3a staining; 3) there were significant reductions in the mean fluorescence of OKT4 binding; and 4) there were significant reductions in the numbers of CD25, HLA-DR, CD45RO and CD45RA/CD4+ cells. There were no changes in CD4+ cell expression of IFN-γ, IL-4 or IL-5. Keliximab caused a significant reduction in T-cell proliferation as compared to a control monoclonal antibody.Keliximab, as an anti-CD4 monoclonal antibody, leads to a transient reduction in the number of CD4+ T-cells and modulation of CD4+ receptor expression in severe asthmatics. The effects of keliximab may be mediated through a decrease in CD4+ surface expression and T-lymphocyte numbers, in addition to a reduction in allergen-induced proliferation.

For many years, the only practical way to display high-quality true-color images was on a computer having a graphics subsystem with at least 24 color planes. The high cost of color graphics devices with 24 planes led many users to choose 8-, 12-, or 16-plane systems. Unfortunately, using a system with fewer color planes sacrifices some color capabilities to save money. The paper discusses an innovation called color recovery that provides a method for displaying millions of colors within the cost constraints of an eight-plane system. One of the primary design goals for color recovery was to supply the additional color capabilities without giving up interactive performance. Another goal was to be able to work with all types of applications running in a windowed environment. An implementation of color recovery described in this article meets these goals.

Recent blackouts of major power systems in North America, Europe, Russia and in other parts of the world clearly show the topicality of the blackout problem and the necessity to call attention to this phenomenon once more. Based on thorough analysis, the authors hold that the overloads on transmission lines are the primary cause of cascade-like processes followed by blackout development. The solutions proposed in the paper allow perfecting the anti-emergency protection system, which now is broken in sets. At the same time, the effect of automatic restoration of normal operating conditions is taken on special significance, thus transforming severe emergency into short transient process, which is almost unnoticed to consumers.

Background: We investigated the association among tissue eosinophilia, cellular infiltration, and cytokine mRNA expression in chronic hyperplastic sinusitis (CHS). Methods: Percutaneous biopsies of the maxillary sinuses and nasal polyps were performed in 12 adult patients (six men and six women) of whom seven were nonallergic and 11 were asthmatic. Tissues were compared with biopsy specimens from the inferior and middle turbinates of normal control subjects. Results: Histologically, an eosinophil-predominant inflammatory infiltrate was seen in 10 of 12 patients, whereas a mild to moderate neutrophilic infiltrate was seen in 4 of 12 patients. As determined by immunocytochemistry, diseased tissues and normal control tissues differed significantly in terms of the number of activated (EG2 + ) eosinophils ( p = 0.005) but not in terms of CD3 + or CD4 + T lymphocytes, elastase-positive neutrophils or CD68 + macrophages. The number of eosinophils did not correlate with that of any other cell type. By in situ hybridization, CHS tissues showed significantly higher numbers of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-3 mRNA-positive cells than normal control tissues ( p = 0.002 and 0.0005, respectively) per high-powered field. There was a significant correlation between the number of infiltrating EG2 + eosinophils and cells that expressed mRNA for GM-CSF ( r = 0.60, p=0.041) or IL-3 ( r = 0.69, p=0.013). Furthermore, epithelial cells did not show detectable mRNA expression for GM-CSF or IL-3. No significant correlation was found between IL-5 mRNA expression and infiltrating EG2 + eosinophils in diseased tissues. However, the IL-5 density was significantly higher in the five patients with CHS who had positive allergy skin test results than in the seven patients with negative skin test results ( p = 0.017) or in normal control subjects. Conclusions: Our data support a role for GM-CSF and IL-3 in the eosinophilia characteristic of CHS and show that IL-5 mRNA expression is not a prominent feature of nonallergic inflammation. The cellular sources of GM-CSF and IL-3 in CHS remain to be definitely determined.

The power systems blackouts regularly occur around the world evidencing that the structure of protection of power system need to be improved. The already available protections in the case of disturbance, does not always allow localize emergency with following self-restoration of the normal operation conditions without personal participation. Taking into account the above considerations the research direction was chosen, proposing new concept and solutions for prevention of the system blackouts and the resumption of normal operating conditions without staff participation. The centralized component inclusion in this structure will ensure the hierarchical operating principles at a higher level. (5 pages)

In the work, new protection principles are proposed to form a basis for anti-collapse complexes of power systems. The principles are founded on the detailed analysis of blackouts, the response of generating sources to the deviations in emergency parameters, the analysis of existing technical solutions, and on the long-term experience in liquidation of blackouts. As a result, a conception has been created for the anti-collapse preventive complex, according to which the emergency events are returned to their optimal course, the blackouts are eliminated within some tens of seconds without personnel participation, using feasible technical solutions that are verified in practice.

The use of two sampling methods, the precise point-sampling algorithm and the extended Bresenham algorithm (EBA), for rendering hardware is discussed, showing where the two methods converge and diverge. Two antialiasing techniques are then presented: an oversampling method and a stochastic method. Practical application of both is described. The use of filtering and sophisticated features with these methods is considered. Hardware support for antialiasing of polygons is discussed. >

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.

A vector generation method is described in which a high quality image rendering scheme is coupled with a high speed scan-conversion algorithm.The rendering scheme consists of two parts. First a prefiltering method is used to antialias the vectors. Second a compositing technique is used to compose the vectors into the frame-buffer.The scan-conversion algorithm presented allows a single vector to be scan-converted by a either by a single processor or a set of processors running in parallel. When using parallel processors, antialiased vectors may be scan-converted and written to a frame store at the same high speed as aliased vectors. The VLSI technology used to implement this algorithm is capable of drawing over two million high quality antialiased vectors per second.

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 -smooth muscle actin (myofibroblasts) were evaluated as markers of activation of airway remodeling,togetherwithnumbersofmucosalmajorbasicprotein– 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 -smooth muscle actin were all higherat7dayscompared with24hours.At 24hours, 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 inairwaywallcellularinflammationafterallergenchallengeresolves by 7 days, whereas the increases in AHR and markers of remodeling persist.

Blackouts of power systems occur in transmission networks (TNs) as the result of dangerous emergency overloading. These are followed by cascade tripping of transmission lines and power plants and, finally, by collapse of a power system. Since the known automatic emergency protection means are insufficiently universal, the authors propose an additional simple and reliable tool that would allow for turning off such a collapse, with fast self-restoration of normal operating condition within only ~100 seconds.

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.

A method to produce true color images from a typical low cost 8-bit frame buffer is discussed. This method, called Color Recovery, is a two part process. The first part of the process is to sample true color data generated by an application in order to reduce 24-bit color to 8 bits for storage in the frame buffer. The second part of the process is to use specialized digital signal processing logic to reconstruct the true color image from the 8-bit frame buffer. This part of the process is preformed as the data is being scanned from the frame buffer to the display.

Human allergen-induced rhinitis is associated with recruitment and activation of CD4+ T lymphocytes and eosinophils. RANTES is a novel CC chemokine that is a potent chemoattractant for both memory T cells and eosinophils. We therefore investigated RANTES in the nasal mucosa after local allergen provocation. Nasal lavage was performed, and biopsies from the inferior nasal turbinate were taken from 14 atopic, seasonal rhinitic patients and seven normal subjects for as long as 6 h after challenge with a grass pollen extract and after a control (allergen diluent) challenge. In five of seven rhinitics tested, radioimmunoassay of nasal fluid demonstrated increases in RANTES at 2 to 4 h (p0.05). Nasal allergen challenge provoked significant increases in RANTES mRNA (p = 0.0015) and protein (p = 0.01) containing cells in the nasal submucosa at 6 h. No changes were observed in normal subjects. Increases in RANTES mRNA+ cells correlated with the associated increases in eosinophils (r = 0.78, p = 0.001). Colocalization studies revealed that the majority of RANTES mRNA+ cells were macrophages (51%) followed by eosinophils (15%), T lymphocytes (11%), and mast cells (3%). Our results demonstrate that allergen-induced rhinitis is associated with release of RANTES and upregulation of RANTES mRNA and protein+ cells, predominantly macrophages, in the nasal mucosa. RANTES synthesis, release, or receptor antagonism may represent a potential target for antiallergy treatment.

Currently graphics devices that offer both high performance and high quality interactive rendering have been priced at a level that places them out of the reach of the broad number of users that constitutes the massmarket. Because of the cost constraints placed on graphics devices designed for the massmarket, they often trade off image quality in order to get reasonable rendering rates with minimum use of hardware. This approach is not leading to a rapid adoption of true 3D graphics technology for the broadest number of users. The goal of the Talisman initiative is to make 3D graphics truly ubiquitous. This requires that both high performance and high quality interactive rendering be made available at mass-market price points. This means that trading off image quality, as a means to obtain high performance rendering is unacceptable. In this paper it will be shown that high quality rendering is a natural extension of the highperformance rendering architecture embodied in Talisman.

Intrinsic (nonatopic) asthma is considered to be a distinct pathogenetic variant of asthma since, unlike extrinsic (atopic) asthma, patients with the disease are skin test-negative to common aeroallergens, and have total serum IgE concentrations within the normal range. Nevertheless, the recent demonstration of increased numbers of cells expressing the high-affinity IgE receptor in bronchial biopsies from atopic and nonatopic asthmatic subjects, together with epidemiologic evidence indicating that serum IgE concentrations relate closely to asthma prevalence regardless of atopic status, suggests that IgE-mediated mechanisms may participate in the pathogenesis of both atopic and nonatopic asthma. Furthermore both variants of the disease are associated with bronchial mucosal eosinophilic inflammation. Interleukin-4 (IL-4) is an essential cofactor for IgE synthesis, and there is strong evidence that IL-5 plays a major role in eosinophil accumulation in asthmatic inflammation. For these reasons we compared the expression of IL-4 and IL-5 mRNA and protein product using a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) amplification, in situ hybridization, and immunohistochemistry in bronchial biopsies from symptomatic atopic and nonatopic asthmatic subjects and atopic and nonatopic controls. The results showed that as compared with controls, biopsies from both groups of asthmatic subjects had increased numbers of IL-4 and IL-5 mRNA copies relative to beta-actin mRNA as detected by RT-PCR. Similarly, in situ hybridization and immunohistochemistry demonstrated increased numbers of cells expressing IL-4 and IL-5 mRNA and protein in asthmatic subjects, irrespective of their atopic status. We conclude that individuals with either atopic or nonatopic asthma show infiltration of the bronchial mucosa with cells expressing Th2-type cytokines, providing further evidence for similarities in the immunopathogenesis of these clinically distinct forms of asthma.

A monoclonal antibody prepared against the eosinophil major basis protein (MBP) was compared with the anti-eosinophil cationic protein (ECP) antibodies (EG1 and EG2) in immunostaining of bronchial biopsies from atopic asthma and controls. Anti-MBP (designated BMK-13) did not cross-react with other eosinophil 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 less than 0.02, P less than 0.01 and P less than 0.05, respectively) and normal non-atopic controls (P less than 0.001). For each of the various groups studied, the rank order for the number of eosinophils stained was BMK-13 greater than EG1 greater than EG2. BMK-13 stained significantly more cells from bronchial biopsies of atopic asthma and atopic non asthma when compared to EG2 (P less than 0.001 and P less than 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.

In atopic asthma, activated T helper lymphocytes are present in bronchial-biopsy specimens and bronchoalveolar-lavage (BAL) fluid, and their production of cytokines may be important in the pathogenesis of this disorder. Different patterns of cytokine release are characteristic of certain subgroups of T helper cells, termed TH1 and TH2, the former mediating delayed-type hypersensitivity and the latter mediating IgE synthesis and eosinophilia. The pattern of cytokine production in atopic asthma is unknown.We assessed cells obtained by BAL in subjects with mild atopic asthma and in normal control subjects for the expression of messenger RNA (mRNA) for interleukin-2, 3, 4, and 5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon gamma by in situ hybridization with 32P-labeled complementary RNA. Localization of mRNA to BAL T cells was assessed by simultaneous in situ hybridization and immunofluorescence and by in situ hybridization after immunomagnetic enrichment or depletion of T cells.As compared with the control subjects, the subjects with asthma had more BAL cells per 1000 cell that were positive for mRNA for interleukin-2 (P less than 0.05), 3 (P less than 0.01), 4 (P less than 0.001), and 5 (P less than 0.001) and GM-CSF (P less than 0.001). There was no significant difference between the two groups in the number of cells expressing mRNA for interferon gamma. In the subjects with asthma, mRNA for interleukin-4 and 5 was expressed predominantly by T lymphocytes.Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.

The kinetics and phenotype of T lymphocytes infiltrating the airways of guinea pigs undergoing late-phase asthmatic reactions (LAR) were studied with monoclonal antibodies, cytofluorimetry, and immunocytochemistry. Challenge of sensitized animals with aerosolized ovalbumin was followed by early (2 h) and late-phase (17 h) bronchoconstriction. The induction of hypersensitivity, by aerosolized antigen, was associated with an increase in mucosal T cell numbers, which consisted almost entirely of CD8+ T cells. Following allergen challenge of fully sensitized animals, a biphasic rise in total T cell (CD3+) numbers was observed in the bronchial mucosa, peaking at 17 and 48 h. A similar pattern of T cell accumulation was observed in the bronchial adventitia but with an extra early peak at 2 h. In contrast to the T cell influx of the sensitization phase, the postchallenge infiltrate consisted largely of CD3+, CD8- cells. Eosinophil numbers were elevated in both submucosa and adventitia, with a single broad peak between 17 and 48 h. T cell infiltration was compared with eosinophil accumulation; while correlations between T cell and eosinophil numbers varied over the 96 h of the experiment, strong associations were observed between CD8+ numbers and eosinophils in the adventitia at 6 h (r = 0.733, p less than 0.01) and between CD3+ numbers and eosinophils in the submucosa at 72 h (r = 0.88, p less than 0.001). No significant changes were detected in T cell or eosinophil numbers in the lung parenchyma. There was a postchallenge increase in eosinophils (but not T cells) in bronchoalveolar lavage (BAL).(ABSTRACT TRUNCATED AT 250 WORDS)

Mouse monoclonal antibodies were raised to the storage and secreted forms of eosinophil cationic protein (ECP), and were used to study the presence of activated eosinophils and secreted ECP in the tissues of patients with a variety of allergic diseases. Immunocytochemical localization was shown with alkaline phosphatase-linked second antibodies, and fast-red substrate. Deposition of a red reaction product indicated sites in tissues where eosinophils had become activated, and where secreted ECP was present. Activated eosinophils and secreted ECP were found together in (1) skin lesions of patients with chronic urticaria, (2) gut lesions of patients with eosinophilic gastroenteritis and ulcerative colitis, and (3) tissues containing granulomas in patients with allergic granulomatosis and vasculitis – the Churg and Strauss syndrome. These results show the value of these techniques for determining the sites of eosinophil activation and secretion in allergic diseases. They support the suggestion that ECP may be involved in the development of these tissue lesions.

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.