Multi-Touch Books in Higher Education: A Study of Educational Leadership and Policy for Schools of Education

Technology points to gaps in higher education adoption of learning technologies where decisions are based on a digital tool’s efficacy and unique capabilities, rather than the role they play in effective teaching and learning (Grush, 2019). Higher Education institutions and their faculty postpone technical decision-making. This results in an educational system ill-equipped to meet the needs of students, faculty, and sufficient digital fluency of graduates and the workforce. By integrating current, interactive tools into teaching materials, such as multi-touch books, or iBooks, faculty can meet their students’ learning needs, thereby improving competencies and ability to track their assessment and engagement throughout a program. This Dissertation-in-practice (DiP) appraises an interactive multi-touch book, Educational Leadership and Policy, as an effective delivery tool for faculty in Schools of education in order to improve student engagement and success. The study examines the adoption of iBook by faculty and their students at a higher education institution in the Southeastern United States to understand what relationship exist with multi-touch books and student success. Given that new technologies within higher education are relatively recent, this study is relevant and may add to the evidence available on this emerging topic

The multifaced role of stat3 in cancer and its implication for anticancer therapy

Signal transducer and activator of transcription (STAT) 3 is one of the most complex regulators of transcription. Constitutive activation of STAT3 has been reported in many types of tumors and depends on mechanisms such as hyperactivation of receptors for pro-oncogenic cytokines and growth factors, loss of negative regulation, and excessive cytokine stimulation. In contrast, somatic STAT3 mutations are less frequent in cancer. Several oncogenic targets of STAT3 have been recently identified such as c-myc, c-Jun, PLK-1, Pim1/2, Bcl-2, VEGF, bFGF, and Cten, and inhibitors of STAT3 have been developed for cancer prevention and treatment. However, despite the oncogenic role of STAT3 having been widely demonstrated, an increasing amount of data indicate that STAT3 functions are multifaced and not easy to classify. In fact, the specific cellular role of STAT3 seems to be determined by the integration of multiple signals, by the oncogenic environment, and by the alternative splicing into two distinct isoforms, STAT3α and STAT3β. On the basis of these different conditions, STAT3 can act both as a potent tumor promoter or tumor suppressor factor. This implies that the therapies based on STAT3 modulators should be performed considering the pleiotropic functions of this transcription factor and tailored to the specific tumor type

Direct-acting antivirals and visceral leishmaniasis: A case report

Background: Visceral leishmaniasis is a vector-borne parasitic disease caused by protozoa belonging to the genus Leishmania. The clinical presentation of visceral leishmaniasis strictly depends on the host immunocompetency, whereas depressive conditions of the immune system impair the capability to resolve the infection and allow reactivation from sites of latency of the parasite. Case presentation: We describe a case of visceral leishmaniasis (VL) that occurred in a patient with chronic hepatitis C treated with direct-acting antiviral drugs (DAA). The hypothesized mechanism is the alteration of protective inflammation mechanisms secondary to DAA therapy. Downregulation of type II and III IFNs, their receptors, which accompany HCV clearance achieved during treatment with sofosbuvir and ribavirin might have a negative impact on a risk for reactivation of a previous Leishmania infection. We know indeed that IFN-\u3b3 is important to enhance killing mechanisms in macrophages, which are the primary target cells of Leishmania. Conclusion: Since VL is endemic in Sicily as well as in other countries of the Mediterranean basin, physicians should be aware of the possible unmasking of cryptic Leishmania infection by DAAs

Mycobacterium tuberculosis Drives Expansion of Low-Density Neutrophils Equipped With Regulatory Activities

In human tuberculosis (TB) neutrophils represent the most commonly infected phagocyte but their role in protection and pathology is highly contradictory. Moreover, a subset of low-density neutrophils (LDNs) has been identified in TB, but their functions remain unclear. Here, we have analyzed total neutrophils and their low-density and normal-density (NDNs) subsets in patients with active TB disease, in terms of frequency, phenotype, functional features, and gene expression signature. Full-blood counts from Healthy Donors (H.D.), Latent TB infected, active TB, and cured TB patients were performed. Frequency, phenotype, burst activity, and suppressor T cell activity of the two different subsets were assessed by flow cytometry while NETosis and phagocytosis were evaluated by confocal microscopy. Expression analysis was performed by using the semi-quantitative RT-PCR array technology. Elevated numbers of total neutrophils and a high neutrophil/lymphocyte ratio distinguished patients with active TB from all the other groups. PBMCs of patients with active TB disease contained elevated percentages of LDNs compared with those of H.D., with an increased expression of CD66b, CD33, CD15, and CD16 compared to NDNs. Transcriptomic analysis of LDNs and NDNs purified from the peripheral blood of TB patients identified 12 genes differentially expressed: CCL5, CCR5, CD4, IL10, LYZ, and STAT4 were upregulated, while CXCL8, IFNAR1, NFKB1A, STAT1, TICAM1, and TNF were downregulated in LDNs, as compared to NDNs. Differently than NDNs, LDNs failed to phagocyte live Mycobacterium tuberculosis (M. tuberculosis) bacilli, to make oxidative burst and NETosis, but caused significant suppression of antigen-specific and polyclonal T cell proliferation which was partially mediated by IL-10. These insights add a little dowel of knowledge in understanding the pathogenesis of human TB

The Role of Emotional Intelligence in Health Care Professionals Burnout

The purpose of this study is to explore the relationship between Emotional Intelligence (EI) and burnout in health care professionals. More specifically, this survey has the purpose of demonstrating the role of EI as a protective factor against the risk of burnout. Health professionals (doctors, nurses, and other caregivers) composed the sample. Data, collected during professional training, provided 148 employees. Major results of this survey underline the relationship between EI and burnout. As we expected, there is a negative and significant correlation between burnout and Emotional Intelligence. Moreover, burnout varies depending on length of service: burnout increases between 5 and 10 years of experience and decreases over 10 years. Indeed, burnout is differently expressed amongst healthcare professionals: more specifically, Psycho-physical exhaustion, Detriment of the relationships and Burnout (total score) has an impact on physician (doctors) more than other investigated health professionals. These findings seem to suggest the opportunity to improve Emotional Intelligence abilities through specific training programs, useful to promote the ability to cope with stress and to enrich the relationships in the workplace

Humoral immunological parameters in Italian patients with oral lichen planus

Serum humoral immunological parameters were determined in 25 patients with atrophic-erosive forms of oral lichen planus (OLP) (Group 1), in 28 patients with reticular-plaque-like lesions of OLP (Group 2) and in 21 healthy patients without oral lesions (Group 3). Comparing patients affected by atrophic-erosive forms of OLP (Group 1) with normal Controls (Group 3), increased levels of serum IgG approaching the statistical significance were found (Kruskal-Wallis test p = 0.0572). It was also found a significantly higher value of kappa (Kruskal-Wallis test p = 0.0017; Mann-Whitney test with Bonferroni’s correction p < 0.001) and lambda (Kruskal-Wallis test p = 0.0346; Mann-Whitney test with Bonferroni’s correction p = 0.013) light chains in patients with atrophic-erosive OLP (Group 1) as compared with normal controls (Group 3). However these higher levels were probably caused by strong prevalence of chronic liver diseases (40%), in patients with atrophic-erosive variety of OLP. No one of these patients was affected by autoimmune liver disease. No differences were noted between atrophic-erosive OLP (Group 1) and hyperkeratosic OLP (Group 2). This study does not confirm the suggestion that patients with OLP may have a generalized immunologic disorder and it also add some evidences that the role of humoral immunity in the pathogenesis of OLP is probably secondary to the cell-mediated reaction against basal keratinocytes.Les principaux aspects de l’immunologie humorale ont été évalués dans deux groupes de malades porteur d’un lichen plan de la muqueuse buccale, 25 à formes atrophiques-érosives (Groupe 1), 28 à formes en réseaux ou en plaques blanches (Groupe 2), et chez 21 sujets sains. Au terme de cette étude les différences les plus remarquables sont les suivantes: le taux des IgG sériques est nettement plus élevé chez les sujets du Groupe 1 ce qui est presque significatif par rapport au Groupe 3 (p = 0.0577). L’analyse statistique a surtout révélé des différences significatives entre le Groupe 1 et le Groupe 3 (contrôle) en ce qui concerne les taux sériques des chaînes Kappa (Kruskal-Wallis test p = 0.0017; Mann-Whitney test corrigé par Bonferroni p < 0.001 ) et des chaînes Lambda (Kruskal-Wallis test p = 0.0346; Mann-Whitney test corrigé par Bonferroni p = 0.013). Aucune autre différence significative entre les trois groupes n’a été observee. Nous pensons que ces résultats sont probablement dus à la présence d’une hépatopathie chronique non auto-immune qui a été diagnostiquée dans 40% des cas du Groupe 1. Cette étude ne confirme donc pas la thèse selon laquelle les sujets atteints de lichen plan buccal pourraient avoir une défaillance de l’immunité humorale. Elle nous permet de penser que le rôle de cette dernière dans la pathogénèse de la maladie est probablement secondaire à la réaction cellulaire dirigée contre les kératinocytes

Crosslinking constraints and computational models as complementary tools in modeling the extracellular domain of the glycine receptor

The glycine receptor (GlyR), a member of the pentameric ligand-gated ion channel superfamily, is the major inhibitory neurotransmitter-gated receptor in the spinal cord and brainstem. In these receptors, the extracellular domain binds agonists, antagonists and various other modulatory ligands that act allosterically to modulate receptor function. The structures of homologous receptors and binding proteins provide templates for modeling of the ligand-binding domain of GlyR, but limitations in sequence homology and structure resolution impact on modeling studies. The determination of distance constraints via chemical crosslinking studies coupled with mass spectrometry can provide additional structural information to aid in model refinement, however it is critical to be able to distinguish between intra- and inter-subunit constraints. In this report we model the structure of GlyBP, a structural and functional homolog of the extracellular domain of human homomeric α1 GlyR. We then show that intra- and intersubunit Lys-Lys crosslinks in trypsinized samples of purified monomeric and oligomeric protein bands from SDS-polyacrylamide gels may be identified and differentiated by MALDI-TOF MS studies of limited resolution. Thus, broadly available MS platforms are capable of providing distance constraints that may be utilized in characterizing large complexes that may be less amenable to NMR and crystallographic studies. Systematic studies of state-dependent chemical crosslinking and mass spectrometric identification of crosslinked sites has the potential to complement computational modeling efforts by providing constraints that can validate and refine allosteric models. © 2014 Liu et al

The socio-ecology of zoonotic infections

AbstractThe resurgence of infectious diseases of zoonotic origin observed in recent years imposes a major morbidity/mortality burden worldwide, and also a major economic burden that extends beyond pure medical costs. The resurgence and epidemiology of zoonoses are complex and dynamic, being influenced by varying parameters that can roughly be categorized as human-related, pathogen-related, and climate/environment-related; however, there is significant interplay between these factors. Human-related factors include modern life trends such as ecotourism, increased exposure through hunting or pet owning, and culinary habits, industrialization sequelae such as farming/food chain intensification, globalization of trade, human intrusion into ecosystems and urbanization, significant alterations in political regimes, conflict with accompanying breakdown of public health and surveillance infrastructure, voluntary or involuntary immigration, loosening of border controls, and hierarchy issues in related decision-making, and scientific advances that allow easier detection of zoonotic infections and evolution of novel susceptible immunocompromised populations. Pathogen-related factors include alterations in ecosystems and biodiversity that influence local fauna synthesis, favouring expansion of disease hosts or vectors, pressure for virulence/resistance selection, and genomic variability. Climate/environment-related factors, either localized or extended, such as El Niño southern oscillation or global warming, may affect host–vector life cycles through varying mechanisms. Emerging issues needing clarification include the development of predictive models for the infectious disease impact of environmental projects, awareness of the risk imposed on immunocompromised populations, recognition of the chronicity burden for certain zoonoses, and the development of different evaluations of the overall stress imposed by a zoonotic infection on a household, and not strictly a person