Students’ Views of a Learning Management System: A Longitudinal Qualitative Study

Over the past decade, Web-based learning management systems, such as Blackboard and WebCT, have been gradually integrated into college education. The strategic use and effectiveness of such systems have been investigated to a large extent. What is less covered is what students really think about such learning management systems. Understanding students’ evaluations can shed light on the development, selection, training, maintenance, use, and investment on such systems. In this paper, we report a longitudinal study that uses a bottom-up approach to gather qualitative data on student views of WebCT 6. Data were collected at three distinctive times that spanned two semesters to reflect students’ different experiences in using WebCT 6. Two different methods were used to collect qualitative data so that students could report their views in unconstrained ways. The content analyses results show that (1) students have an integrated view of their technology assisted learning environment, which can be represented by the notion of S-I-A (the system, the instructors and the administrators); (2) as students’ experience with WebCT 6 increases, their complaints and wishes for instructors and administrators increase; (3) communication-related features continuously dominate students’ views about WebCT 6; and (4) as their use of WebCT 6 increases, students grow more appreciative toward WebCT 6 features that support learning activities. The findings contribute to the literature with additional evidence on the nature and effectiveness of learning management systems. They provide a set of suggestions that should be carefully considered by all personnel involved. We identify a number of research implications. One particular research contribution is the identification of a fifth type of interaction that plays an important role in the technology-assisted learning context: the learner-administrator interaction

Assessment of serum nitrate-nitrite ratio vis-a-vis insulin sensitivity and resistance in type 2 diabetics in a tertiary hospital in Eastern India

Background: Insulin Resistance is of paramount importance in the pathophysiology of Type 2 Diabetes Mellitus along with endothelial dysfunction is mediated by Nitric Oxide (NO). Central to this endothelial dysfunction is the action of Insulin on the Nitric oxide synthase enzyme. Since NO cannot be measured because of its short half-life, metabolites of NO (namely nitrite and nitrate) are measured towards assessing their relationship along with different direct and surrogate markers of insulin resistance in patients of Diabetes Mellitus attending a tertiary care hospital in Eastern India. Aim of the study was to assess the level of Insulin resistance with the direct and surrogate markers of insulin resistance in patients of Diabetes Mellitus attending a tertiary care hospital in Eastern India.Methods: Blood samples from newly diagnosed Type 2 Diabetic patients were assayed for fasting and postprandial sugar and insulin, lipid profile and serum nitrate and nitrite and different anthropological parameters were measured. After that, HOMA-IR and QUICKI’ index were measured.Results: Values of anthropological parameters and the direct and surrogate markers of insulin resistance showed statistically significant difference between cases and controls. Bivariate analysis of post-prandial blood glucose showed strong co-relation with HOMA-IR while serum total nitrate-nitrite ratio showed a strong co-relation with QUICKI.Conclusions: Serum nitrate-nitrite ratio showed a strong co-relation with HOMA-IR and QUICKI. The significance of this study lies in the fact that measurement of the serum nitrate-nitrite may give an idea of the level of insulin resistance of a diabetic patient

ANTIPSYCHOTIC PRESCRIBING PATTERN IN A TERTIARY CARE HOSPITAL OF EASTERN INDIA

Background: Psychotropic drugs are commonly prescribed in psychiatric practice. , their utilization and consequences on real life effectiveness and safety in actual clinical practice need continuous study. Materials and Methods: A prospective cross sectional study was carried out for 3 months. All the patients using antipsychotic drugs, between 18-60 years of age, irrespective of sex, were included in the study. However, patients who were pregnant, lactating, unable to comply due to mental retardation, any systemic illness ,unconsciousness or drug addiction were excluded from the study. The prescribing pattern was analyzed by Using World Health Organization basic drug indicators. Results: Average number of drugs /prescription 1.07..atypical antipsychotics are prescribed more commonly than typical antipsychotic.among the atypical antipsychotics olanzapine is most commonly prescribed.monotherapy of antipsychotic is the commonly prescribed than trihexyphenidyl is the anticholinergic that prescribed regularly with typical antipsychotic for the prevension of extrapyramidal symptoms. Conclusion: Psychotic illness patients mainly advised monotherapy of antipsychotic drugs, mainly atypical antipsychotic drugs, and olanzapine is the most prescribed antipsychotic drugs. Trihexyphenidyl is the only antichoninergic drug co-prescribed with typical antipsychotic drugs to avoid extrapyramidal side effects. Keywords: Drug utilization study, psychotic illness, psychotropic drug

Fibrosis in systemic sclerosis: common and unique pathobiology

Fibrosis in systemic sclerosis (SSc), a complex polygenic disease associated with autoimmunity and proliferative/obliterative vasculopathy, shares pathobiologic features in common with other fibrosing illnesses, but also has distinguishing characteristics. Fibroblast activation induced by transforming growth factor-β (TGF-β), Wnts and innate immune receptors, along with oxidative stress and reactive oxygen species (ROS) are implicated in pathogenesis. On the other hand, the roles of endothelial-mesenchymal differentiation and bone marrow-derived fibrocytes remain to be established. Fibrotic responses are modulated by transcriptional activators and cofactors, epigenetic factors, and microRNAs that can amplify or inhibit ligand-induced signaling. The nuclear orphan receptor PPAR-γ appears to be important in governing the duration and intensity of fibroblast activation and mesenchymal progenitor cell differentiation, and defects in PPAR-γ expression or function in SSc may underlie the uncontrolled progression of fibrosis. Identifying the perturbations in signaling pathways and cellular differentiation programs responsible for tissue damage and fibrosis in SSc allows their selective targeting using novel compounds, or by innovative uses of already-approved drugs (drug repurposing)

Analysis of Transcripts Expressed in One-Day-Old Larvae and Fifth Instar Silk Glands of Tasar Silkworm, Antheraea mylitta

Antheraea mylitta is one of the wild nonmulberry silkworms, which produces tasar silk. An EST project has been undertaken to understand the gene expression profile of A. mylitta silk gland. Two cDNA libraries, one from the whole bodies of one-day-old larvae and the other from the silkglands of fifth instar larvae, were constructed and sequenced. A total of 2476 good-quality ESTs (1239 clones) were obtained and grouped into 648 clusters containing 390 contigs and 258 singletons to represent 467 potential unigenes. Forty-five sequences contained putative coding region, and represented potentially novel genes. Among the 648 clusters, 241 were categorized according to Gene Ontology hierarchy and showed presence of several silk and immune-related genes. The A. mylitta ESTs have been organized into a freely available online database “AmyBASE”. These data provide an initial insight into the A. mylitta transcriptome and help to understand the molecular mechanism of silk protein production in a Lepidopteran species

Pharmacological Inhibition of Toll-Like Receptor-4 Signaling by TAK242 Prevents and Induces Regression of Experimental Organ Fibrosis

Systemic sclerosis (SSc) is a poorly understood heterogeneous condition with progressive multi-organ fibrosis. Recent genetic and genomic evidence suggest a pathogenic role for dysregulated innate immunity and toll-like receptor (TLR) activity in SSc. Levels of both TLR4, as well as certain endogenous TLR ligands, are elevated in skin and lung tissues from patients with SSc and correlate with clinical disease parameters. Conversely, genetic targeting of TLR4 or its endogenous “damage-associated” ligands ameliorates progressive tissue fibrosis. Targeting TLR4 signaling therefore represents a pharmacological strategy to prevent intractable fibrosis. We examined the effect of TAK242, a small molecule TLR4 inhibitor, in preclinical fibrosis models and in SSc fibroblasts. TAK242 treatment prevented, promoted regression of, bleomycin-induced dermal and pulmonary fibrosis, and reduced the expression of several pro-fibrotic mediators. Furthermore, TAK242 ameliorated peritoneal fibrosis and reduced spontaneous hypodermal thickness in TSK/+ mice. Importantly, TAK242 abrogated collagen synthesis and myofibroblasts differentiation in explanted constitutively active SSc fibroblast. Altogether, these findings identify TAK242 as an anti-fibrotic agent in preclinical models of organ fibrosis. TAK242 might potentially represent a novel strategy for the treatment of SSc and other fibrotic diseases

Egr-1 Induces a Profibrotic Injury/Repair Gene Program Associated with Systemic Sclerosis

Transforming growth factor-ß (TGF-ß) signaling is implicated in the pathogenesis of fibrosis in scleroderma or systemic sclerosis (SSc), but the precise mechanisms are poorly understood. The immediate-early gene Egr-1 is an inducible transcription factor with key roles in mediating fibrotic TGF-ß responses. To elucidate Egr-1 function in SSc-associated fibrosis, we examined change in gene expression induced by Egr-1 in human fibroblasts at the genome-wide level. Using microarray expression analysis, we derived a fibroblast “Egr-1-responsive gene signature” comprising over 600 genes involved in cell proliferation, TGF-ß signaling, wound healing, extracellular matrix synthesis and vascular development. The experimentally derived “Egr-1-responsive gene signature” was then evaluated in an expression microarray dataset comprising skin biopsies from 27 patients with localized and systemic forms of scleroderma and six healthy controls. We found that the “Egr-1 responsive gene signature” was substantially enriched in the “diffuse-proliferation” subset comprising exclusively of patients with diffuse cutaneous SSc (dcSSc) of skin biopsies. A number of Egr-1-regulated genes was also associated with the “inflammatory” intrinsic subset. Only a minority of Egr-1-regulated genes was concordantly regulated by TGF-ß. These results indicate that Egr-1 induces a distinct profibrotic/wound healing gene expression program in fibroblasts that is associated with skin biopsies from SSc patients with diffuse cutaneous disease. These observations suggest that targeting Egr-1 expression or activity might be a novel therapeutic strategy to control fibrosis in specific SSc subsets

The Transcriptional Cofactor Nab2 Is Induced by TGF-β and Suppresses Fibroblast Activation: Physiological Roles and Impaired Expression in Scleroderma

By stimulating collagen synthesis and myofibroblasts differentiation, transforming growth factor-β (TGF- β) plays a pivotal role in tissue repair and fibrosis. The early growth response-1 (Egr-1) transcription factor mediates profibrotic TGF-β responses, and its expression is elevated in biopsies from patients with scleroderma. NGF1-A-binding protein 2 (Nab2) is a conserved transcriptional cofactor that directly binds to Egr-1 and positively or negatively modulates Egr-1 target gene transcription. Despite the recognized importance of Nab2 in governing the intensity of Egr-1-dependent responses, the regulation and function of Nab2 in the context of fibrotic TGF-β signaling is unknown. Here we show that TGF-β caused a time-dependent stimulation of Nab2 protein and mRNA in normal fibroblasts. Ectopic expression of Nab2 in these cells blocked Egr-1-dependent transcriptional responses, and abrogated TGF-β-induced stimulation of collagen synthesis and myofibroblasts differentiation. These inhibitory effects of Nab2 involved recruitment of the NuRD chromatin remodeling complex to the COL1A2 promoter and were accompanied by reduced histone H4 acetylation. Mice with targeted deletion of Nab2 displayed increased collagen accumulation in the dermis, and genetic or siRNA-mediated loss of Nab2 in fibroblasts was associated with constitutively elevated collagen synthesis and accentuation of Egr-1-dependent TGF-β responses in vitro. Expression of Nab2 was markedly up-regulated in skin biopsies from patients with scleroderma, and was localized primarily to epidermal keratinocytes. In contrast, little Nab2 could be detected in dermal fibroblasts. These results identify Nab2 as a novel endogenous negative regulator of Egr-1-dependent TGF-β signaling responsible for setting the intensity of fibrotic responses. Defective Nab2 expression or function in dermal fibroblasts might play a role in persistent fibrotic responses in scleroderma

Fibronectin signaling via toll-like receptprs: a novel paradigm for persistent fibrosis in scleroderma

Scleroderma is a systemic autoimmune disease with unknown etiology. Fibrosis, the hallmark of scleroderma, is the transformation of self-limited wound healing into a self-sustaining non-healing process. The factors responsible for maintaining persistent fibroblast activation in scleroderma and other conditions with chronic fibrosis are not well understood. We recently showed that TLR4 and fibronectin extra domain A (FnEDA), an endogenous TLR4 ligand, both are markedly elevated in the lesional skin biopsies from scleroderma patients and were shown to be involved in scleroderma disease pathogenesis. Here, we highlight the role of the FnEDA-TLR4 signaling axis in fibrosis, and the mechanisms involved in driving persistence of fibrosis in scleroderma