THE EFFECTS OF A MOBILE APP-BASED SKY MAP IN TEACHING COLLEGE STUDENTS ABOUT CONSTELLATIONS

The purpose of this study was to investigate the effects of using a mobile app-based sky map to teach college students about constellations, stars, nebulae, and star clusters. The name of the app was Star Chart. The setting for the study was a community college in West Tennessee. Twenty out of 60 participants were males, with 83% of all being less than 25 years old. The first effect studied was concerning students level of attitude toward astronomy after they used the mobile app to learn about sky constellations, stars, nebulae, and star clusters. The second effect investigated in the study was regarding the ability of participating college students to identify the above astronomical objects after using the mobile app. For comparison purposes, the same measurements were taken for a control group that used a conventional print-based sky map, commonly known as a planisphere. Multivariate Analysis of Variance (MANOVA) was used to compare the experimental or app-users group (n = 30) and control group (n = 30).The results of the study showed that Star Chart app users developed significantly more positive attitude toward astronomy than the planisphere users (Hotellings Trace = 0.132, F (2, 57) = 3.751, p \u3c .05, multivariate effect size 2 = 0.12). The multivariate effect size obtained showed that the difference was substantial. On the other hand, both Star Chart and planisphere groups learned comparable skills of identifying constellations, stars, nebulae, and star clusters.Since app-based sky maps are available freely for various platforms of mobile devices, they can be added to the technology repertoire of teachers and other community members involved in astronomy education. Due to time constraints, the researcher used planetarium software to simulate the sky. Hence, future researchers are recommended to replicate this study in the context of real night sky observations

Natural killer (NK) cells from killers to regulators: Distinct features between peripheral blood and decidual NK cells

Natural killer (NK) cells are a key component of innate immunity, particularly crucial during the early phase of immune responses against certain viruses, parasites, and microbial pathogens. The role of NK cell during pregnancy has been vividly discussed over the past years and it is now becoming increasingly clear that NK cells control pregnancy maintenance at several levels. In normal pregnancy, it appears that they provide benefit by properly secreting cytokines, chemokines and angiogenic factors rather than functioning as cytotoxic effector cells. However, as they are endowed with all the cytolytic weapons, they promptly become capable of attacking fetal and maternal tissues during infection and inflammation. © 2007 The Authors Journal compilation 2007 Blackwell Munksgaard

Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD

<p>Abstract</p> <p>Background</p> <p>A suggested role for T cells in COPD pathogenesis is based on associations between increased lung cytotoxic T lymphocyte (CD8⁺) numbers and airflow limitation. CD69 is an early T cell activation marker. Natural Killer cell group 2 D (NKG2D) receptors are co-stimulatory molecules induced on CD8⁺T cells upon activation. The activating function of NKG2 D is triggered by binding to MHC class 1 chain-related (MIC) molecules A and B, expressed on surface of stressed epithelial cells. The aim of this study was to evaluate the expression of MIC A and B in the bronchial epithelium and NKG2 D and CD69 on BAL lymphocytes in subjects with COPD, compared to smokers with normal lung function and healthy never-smokers.</p> <p>Methods</p> <p>Bronchoscopy with airway lavages and endobronchial mucosal biopsy sampling was performed in 35 patients with COPD, 21 healthy never-smokers and 16 smokers with normal lung function. Biopsies were immunohistochemically stained and BAL lymphocyte subsets were determined using flow cytometry.</p> <p>Results</p> <p>Epithelial CD3⁺lymphocytes in bronchial biopsies were increased in both smokers with normal lung function and in COPD patients, compared to never-smokers. Epithelial CD8⁺lymphocyte numbers were higher in the COPD group compared to never-smoking controls. Among gated CD3⁺cells in BAL, the percentage of CD8⁺NKG2D⁺cells was enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. The percentage of CD8⁺CD69⁺cells and cell surface expression of CD69 were enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. No changes in the expression of MIC A or MIC B in the airway epithelium could be detected between the groups, whereas significantly decreased soluble MICB was detected in bronchial wash from smokers with normal lung function, compared to never-smokers.</p> <p>Conclusions</p> <p>In COPD, we found increased numbers of cytotoxic T cells in both bronchial epithelium and airway lumen. Further, the proportions of CD69- and NKG2D-expressing cytotoxic T cells in BAL fluid were enhanced in both subjects with COPD and smokers with normal lung function and increased expression of CD69 was found on CD8⁺cells, indicating the cigarette smoke exposure-induced expansion of activated cytotoxic T cells, which potentially can respond to stressed epithelial cells.</p

Cell populations in lesions of cutaneous leishmaniasis of leishmania (L.) amazonensis- infected rhesus macaques, Macaca mulatta

The cellular nature of the infiltrate in cutaneous lesion of rhesus monkeys experimentally infected with Leishmania (L.) amazonensis was characterized by immunohistochemistry. Skin biopsies from infected animals with active or healing lesions were compared to non-infected controls (three of each type) to quantitate inflammatory cell types. Inflammatory cells (composed of a mixture of T lymphocyte subpopulations, macrophages and a small number of natural killer cells and granulocytes) were more numerous in active lesions than in healing ones. T-cells accounted for 44.7 ± 13.1% of the infiltrate in active lesions (versus CD2+= 40.3 ± 5.7% in healing lesions) and T-cell ratios favor CD8+ cells in both lesion types. The percentage of cells expressing class II antigen (HLA-DR+) in active lesions (95 ± 7.1%) was significantly higher (P < 0.005) from the healing lesions (42.7 ± 12.7%). Moreover, the expression of the activation molecules CD25 (@ 16%), the receptor for interleukin-2, suggests that many T cells are primed and proliferating in active lesions. Distinct histopathological patterns were observed in lesions at biopsy, but healing lesions contained more organized epithelioid granulomas and activated macrophages, followed by fibrotic substitution. The progression and resolution of skin lesions appears to be very similar to that observed in humans, confirming the potential for this to be used as a viable model to study the immune response in human cutaneous leishmaniasis

Induction of Protective CD4+ T Cell-Mediated Immunity by a Leishmania Peptide Delivered in Recombinant Influenza Viruses

The available evidence suggests that protective immunity to Leishmania is achieved by priming the CD4+ Th1 response. Therefore, we utilised a reverse genetics strategy to generate influenza A viruses to deliver an immunogenic Leishmania peptide. The single, immunodominant Leishmania-specific LACK158–173 CD4+ peptide was engineered into the neuraminidase stalk of H1N1 and H3N2 influenza A viruses. These recombinant viruses were used to vaccinate susceptible BALB/c mice to determine whether the resultant LACK158–173-specific CD4+ T cell responses protected against live L. major infection. We show that vaccination with influenza-LACK158–173 triggers LACK158–173-specific Th1-biased CD4+ T cell responses within an appropriate cytokine milieu (IFN-γ, IL-12), essential for the magnitude and quality of the Th1 response. A single intraperitoneal exposure (non-replicative route of immunisation) to recombinant influenza delivers immunogenic peptides, leading to a marked reduction (2–4 log) in parasite burden, albeit without reduction in lesion size. This correlated with increased numbers of IFN-γ-producing CD4+ T cells in vaccinated mice compared to controls. Importantly, the subsequent prime-boost approach with a serologically distinct strain of influenza (H1N1->H3N2) expressing LACK158–173 led to a marked reduction in both lesion size and parasite burdens in vaccination trials. This protection correlated with high levels of IFN-γ producing cells in the spleen, which were maintained for 6 weeks post-challenge indicating the longevity of this protective effector response. Thus, these experiments show that Leishmania-derived peptides delivered in the context of recombinant influenza viruses are immunogenic in vivo, and warrant investigation of similar vaccine strategies to generate parasite-specific immunity

Local Increase of Arginase Activity in Lesions of Patients with Cutaneous Leishmaniasis in Ethiopia

The leishmaniases are a complex of diseases caused by Leishmania parasites. Currently, the diseases affect an estimated 12 million people in 88 countries, and approximately 350 million more people are at risk. The leishmaniases belong to the most neglected tropical diseases, affecting the poorest populations, for whom access to diagnosis and effective treatment are often not available. Leishmania parasites infect cells of the immune system called macrophages, which have the capacity to eliminate the intracellular parasites when they receive the appropriate signals from other cells of the immune system. In nonhealing persistent leishmaniasis, lymphocytes are unable to transmit the signals to macrophages required to kill the intracellular parasites. The local upregulation of the enzyme arginase has been shown to impair lymphocyte effector functions at the site of pathology. In this study, we tested the activity of this enzyme in skin lesions of patients presenting with localized cutaneous leishmaniasis. Our results show that arginase is highly upregulated in these lesions. This increase in arginase activity coincides with lower expression of a signalling molecule in lymphocytes, which is essential for efficient activation of these cells. These results suggest that increased arginase expression in the localized cutaneous lesions might contribute to persistent disease in patients presenting with cutaneous leishmaniasis

Innate and acquired immunity to Leishmania in humans : the role of the host versus the parasite

Leishmania are intracellular protozoan parasites of macrophages which induce chronic diseases in man. The study of this parasite has been instrumental in elucidating many facets of the immune system. Our study set out to understand the immune regulatory mechanisms involved in resistance and susceptibility. We have used in vitro stimulation of peripheral blood mononuclear cells and measured cell proliferation, cytokine rnRNA or protein induction and analyzed phenotype of cells by flow cytometry. Our results show that there are innate elements of immune reactivity to Leishmania antigens in unexposed donors involving cellular proliferation of NK cells and IFN[gamma] secretion. These responses are neither induced by the abundant antigens on the surface of Leishmania promastigotes nor mycobacterial antigens tested. Low molecular weight fractions of Leishmania could induce proliferative and cytokine responses in cells of both healthy and infected individuals. However, response to the high molecular weight antigens was a feature of the healthy individuals. The relevance of an NK dominated response has been tested in a Leishmaniasis endemic area where the role for NK cells in protection has unfolded. Consistent with our previous findings, NK and CD8+ cells proliferated in response to Leishmania antigen stimulation. Our results also suggested the presence of a low background level of large NK cells as an important aspect of the protective mechanisms that operate in the Leishmaniasis-resistant endemic controls which is also established following cure from the disease. Based on the results obtained we concluded that NK cells are involved in protection from and healing of Ethiopian cutaneous Leishmaniasis. As part of the quest for identifying the stimulatory molecules of Leishmania to which PBMC from non-exposed healthy individuals respond, we have tested a Leishmania homologue of receptors for activated C kinase (LACK) from L major as well as three amastigote antigens from L. pifanoi. The immuno-dominant molecule LACK induced in vitro proliferation of NK and CD8 cells coupled with high levels of IFN[gamma] and IL- 10 production. Of the amastigote antigens, P-2 and, to a lesser extent, P-8 induced proliferation in cells of healthy individuals. These responses were reduced in the presence of anti-MHC class 11 antibodies. We tested whether properties of the infecting parasite could influence induced immune response. Our results showed that regardless of whether cells were derived from healthy individuals, or from patients with localized (LCL) or diffuse (DCL) cutaneous Leishmaniasis, DCL-promastigotes preferentially induced mRNA for IL-10 while induction of IFN[gamma] was a feature of LCL-promastigotes. The importance of the properties of the infecting parasite is illustrated in a case report where a slow growing form of Leishmania showed atypical clinical symptoms in a Swedish man 15 years after infection. The focus of this thesis has been the innate and acquired immune regulatory mechanisms involved in L aethiopica infection in human. The possible cross species immune response by proteins derived from other Leishmania species are investigated in an attempt to evaluate the potential use of such proteins in a universal vaccine

Induction and abrogation of LACK reactive cells in the evolution of human leishmaniasis

Peripheral blood mononuclear cells (PBMC) from cutaneous leishmaniasis patients with ongoing Leishmania aethiopica infection and individuals cured/under treatment from L. infantum or L. donovani infection were stimulated in vitro with LACK, the Leishmania homologue of receptors for activated C kinase. The LACK protein is conserved in related leishmanial species and is expressed both in the promastigote and amastigote stages of Leishmania. Our results show that LACK induced marked NK and some CD8+ cell proliferation in PBMC from cutaneous leishmaniasis patients with active disease. These responses were coupled with high levels of IFN-γ and IL-10 production. At the concentration tested, the proliferative responses to freeze-thawed Leishmania antigen (Ft-Leish) were higher, while the levels of IFN-γ were consistently lower than that of LACK. Although cells from individuals cured of leishmaniasis could respond to whole Leishmania lysate by proliferation and IFN-γ production, there was no evident response to LACK. Ethiopian controls tested at the same time also showed LACK induced proliferation with IFN-γ and IL-10 responses. Thus LACK reactivity in terms of proliferation and cytokine induction were present in cells from some healthy donors and most of the patients with active lesions, while this response was absent in individuals cured of L. infantum or L. donovani leishmaniasis. Since cure from leishmaniasis often results in life-long protection, and active but not cured patients showed in vitro responses to LACK stimulation, questions arose as to how this highly immunodominant molecule functions during human leishmanisasis. Some possible mechanisms are discussed