Social Media in Virtual Marketing: Antecedents to Electronic Word of Mouth Communication

Social media usage in the world and especially in Pakistan has a high growth due to which it (social media) has a potential of becoming an effective marketing tool. Despite its compar-atively low cost and significance, marketers are not effectively utilizing social media. Thus the aim of this study is to measure the influence (effect) of four social variables: social capital, trust, homophily and interpersonal influence on electronic word of mouth (eWOM) communi-cation. The sample size for the study is 300 and preselected enumerator's collected the data from the leading shopping malls of the city. Although the scales and measures adopted for this study have been earlier validated in oth-er countries, however the same were re-ascertained on the present set of data. After prelimi-nary analysis including normality and validity the overall model was tested through Structural Equation Model (SEM). This was carried out in two stages - initially CFA for all the constructs was ascertained which was followed by CFA of the overall model. Developed conceptual framework was empirically tested on the present set of data in Pa-kistan which adequately explained consumer attitudinal behavior towards electronic word of mouth (eWOM) communication. Three hypotheses failed to be rejected and one was rejected. Trust was found to be the strongest predictor of electronic word of mouth (eWOM) communi-cation, followed by homophily and social capital. Interpersonal influence has no relationship with electronic word of mouth (eWOM) communication. The results were consistent to earlier literature. Implication for markers was drawn from the results.Keywords: eWOM, social capital, trust, homophily and interpersonal influence, social medi

Lymphoblastoid Cell Lines as a Tool to Study Inter-Individual Differences in the Response to Glucose

Background: White blood cells have been shown in animal studies to play a central role in the pathogenesis of diabetic retinopathy. Lymphoblastoid cells are immortalized EBV-transformed primary B-cell leukocytes that have been extensively used as a model for conditions in which white blood cells play a primary role. The purpose of this study was to investigate whether lymphoblastoid cell lines, by retaining many of the key features of primary leukocytes, can be induced with glucose to demonstrate relevant biological responses to those found in diabetic retinopathy. Methods: Lymphoblastoid cell lines were obtained from twenty-three human subjects. Differences between high and standard glucose conditions were assessed for expression, endothelial adhesion, and reactive oxygen species. Results: Collectively, stimulation of the lymphoblastoid cell lines with high glucose demonstrated corresponding changes on molecular, cellular and functional levels. Lymphoblastoid cell lines up-regulated expression of a panel of genes associated with the leukocyte-mediated inflammation found in diabetic retinopathy that include: a cytokine (IL-1B fold change = 2.11, p-value = 0.02), an enzyme (PKCB fold change = 2.30, p-value = 0.01), transcription factors (NFKB-p50 fold change = 2.05, p-value = 0.01), (NFKB-p65 fold change = 2.82, p-value = 0.003), and an adhesion molecule (CD18 fold change = 2.59, 0.02). Protein expression of CD18 was also increased (p-value = 2.14x10-5). The lymphoblastoid cell lines demonstrated increased adhesiveness to endothelial cells (p = 1.28x10-5). Reactive oxygen species were increased (p = 2.56x10-6). Significant inter-individual variation among the lymphoblastoid cell lines in these responses was evident (F = 18.70, p Conclusions: Exposure of lymphoblastoid cell lines derived from different human subjects to high glucose demonstrated differential and heterogeneous gene expression, adhesion, and cellular effects that recapitulated features found in the diabetic state. Lymphoblastoid cells may represent a useful tool to guide an individualized understanding of the development and potential treatment of diabetic complications like retinopathy.</p

A Tie2-Notch1 signaling axis regulates regeneration of the endothelial bone marrow niche.

Loss-of-function studies have determined that Notch signaling is essential for hematopoietic and endothelial development. By deleting a single allele of the Notch1 transcriptional activation domain we generated viable, post-natal mice exhibiting hypomorphic Notch signaling. These heterozygous mice, which lack only one copy of the transcriptional activation domain, appear normal and have no endothelial or hematopoietic phenotype, apart from an inherent, cell-autonomous defect in T-cell lineage development. Following chemotherapy, these hypomorphs exhibited severe pancytopenia, weight loss and morbidity. This phenotype was confirmed in an endothelial-specific, loss-of-function Notch1 model system. Ang1, secreted by hematopoietic progenitors after damage, activated endothelial Tie2 signaling, which in turn enhanced expression of Notch ligands and potentiated Notch1 receptor activation. In our heterozygous, hypomorphic model system, the mutant protein that lacks the Notch1 transcriptional activation domain accumulated in endothelial cells and interfered with optimal activity of the wildtype Notch1 transcriptional complex. Failure of the hypomorphic mutant to efficiently drive transcription of key gene targets such as Hes1 and Myc prolonged apoptosis and limited regeneration of the bone marrow niche. Thus, basal Notch1 signaling is sufficient for niche development, but robust Notch activity is required for regeneration of the bone marrow endothelial niche and hematopoietic recovery.We thank Dr. Warren Pear for invaluable advice and for sharing the Notch1+/ΔTAD murine model system. We also thank Dr. Kishore Wary for sharing the Cdh5-CreERT2 mouse model. Drs. Jon Aster and Stephen Blacklow for advice and thoughtful discussion, Dr. Dawson Gerhardt for her help in generating the Notch1- ΔTAD plasmids and vector constructs, Dr. Jan Kitejewski for helpful advice on Notch mutant mice and Drs. Fotini Gounari and Linda Dagenstein of the University of Chicago transgenic mouse facility for help in maintaining the transgenic mouse colonies. The following cores at the University of Illinois at Chicago contributed to this study: RRC Histology Core and RRC Flow Cytometry Core. This study was funded by NIH grants 1R01HL134971 to KVP and 1R01HL136529 to DL.S

Starvation resistance of gypsy moth, Lymantria dispar (L.) (Lepidoptera: Lymantriidae): tradeoffs among growth, body size, and survival

Survival and body composition of starving gypsy moth larvae initially reared on aspen foliage or artificial diet differeing in nitrogen (N) and carbohydrate concentration were examined under laboratory conditions. Diet nitrogen concentration strongly affected starvation resistance and body composition, but diet carbohydrate content had no effects on these. Within any single diet treatment, greater body mass afforded greater resistance to starvation. However, starving larvae reared on 1.5% N diet survived nearly three days longer than larvae reared on 3.5% N diet. Larvae reared on artificial diet survived longer than larvae reared on aspen. Differences in survival of larvae reared on artificial diet with low and high nitrogen concentrations could not be attributed to variation in respiration rates, but were associated with differences in body composition. Although percentage lipid in larvae was unaffected by diet nitrogen concentration, larvae reared on 1.5% N diet had a higher percentage carbohydrate and lower percentage protein in their bodies prior to starvation than larvae reared on 3.5% N diet. Hence, larger energy reserves of larvae reared on low nitrogen diet may have contributed to their greater starvation resistance. Whereas survival under food stress was lower for larvae reared on high N diets, growth rates and pupal weights were higher, suggesting a tradeoff between rapid growth and survival. Larger body size does not necessarily reflect larger energy reserves, and, in fact, larger body size accured via greater protein accumulation may be at the expense of energy reserves. Large, fast-growing larvae may be more fit when food is abundant, but this advantage may be severely diminished under food stress. The potential ecological and evolutionary implications of a growth/survival tradeoff are discussed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47792/1/442_2004_Article_BF00317588.pd

A study of bladder dysfunction in women with type 2 diabetes mellitus

Introduction: Diabetes mellitus has been associated with an earlier onset and increased severity of urologic diseases that often result in debilitating urologic complications. Diabetic bladder dysfunction refers to a group of bladder symptoms occurring in patients with diabetes mellitus ranging from bladder over activity to impaired bladder contractility. Aim: Bladder dysfunction is an under evaluated issue in women with diabetes. Aim of our study was to investigate prevalence of bladder dysfunction and its relation with other chronic complications of diabetes in women with type 2 diabetes. Materials and Methods: In a hospital-based cross sectional study, a cohort of women with type 2 diabetes mellitus who had lower urinary tract symptoms (LUTS) were enrolled. We used the American Urological Association Symptom Index (AUA-SI) to assess the severity of LUTS and the Indevus Urgency Severity Scale (IUSS) to assess presence of overactive bladder (OAB). Age-BMI- matched controls that did not have diabetes but had lower urinary tract symptoms were also studied and compared with women with type 2 diabetes. Urodynamic evaluation was done in willing patients. Results: LUTS attributable to bladder dysfunction were reported in 67% of women with type 2 diabetes after exclusion of other causes. Out of them, 36% had moderate to severe LUTS (total AUA-SI score >7). Prevalence of OAB was 53%. Urodynamic evaluation revealed presence of stress urinary incontinence in 48% patients and changes of detrusor over activity and detrusor under activity in 23% and 11% patients, respectively. Among the chronic complications of diabetes, peripheral neuropathy, nephropathy, and presence of metabolic syndrome were significantly associated with moderate to severe LUTS and OAB. Conclusion: Bladder dysfunction is a highly prevalent complication in women with diabetes. Chronic complications of diabetes especially neuropathy, nephropathy, and presence of metabolic syndrome are important predictors of bladder dysfunction

Market Forces College of Management Sciences Antecedents to Electronic Word of Mouth Communication

Abstract Social media usage in the world and especially in Pakistan ha

Predictors and clinical complications associated with antiphospholipid antibodies in sickle cell disease

Abstract Although a higher prevalence of antiphospholipid autoantibodies (aPL) has been observed in some cohorts of sickle cell disease (SCD) patients, the clinical risk factors for the development of aPL and its associated complications remain unclear. In a retrospective study of 63 SCD patients, a lower hemoglobin concentration and higher white blood cell count were independently associated with an elevated aPL. SCD patients with elevated aPL had increased pregnancy complications (≥3 miscarriages, preterm delivery, pre‐eclampsia) and venous thrombotic events. Our findings suggest that SCD may predispose to the generation of aPL and that aPL itself may contribute to the vasculopathy of SCD. Prospective testing for aPL is warranted in patients with SCD

Embryonic Stem Cell Differentiation to Functional Arterial Endothelial Cells through Sequential Activation of ETV2 and NOTCH1 Signaling by HIF1α

The generation of functional arterial endothelial cells (aECs) from embryonic stem cells (ESCs) holds great promise for vascular tissue engineering. However, the mechanisms underlying their generation and the potential of aECs in revascularizing ischemic tissue are not fully understood. Here, we observed that hypoxia exposure of mouse ESCs induced an initial phase of HIF1α-mediated upregulation of the transcription factor Etv2, which in turn induced the commitment to the EC fate. However, sustained activation of HIF1α in these EC progenitors thereafter induced NOTCH1 signaling that promoted the transition to aEC fate. We observed that transplantation of aECs mediated arteriogenesis in the mouse hindlimb ischemia model. Furthermore, transplantation of aECs in mice showed engraftment in ischemic myocardium and restored cardiac function in contrast to ECs derived under normoxia. Thus, HIF1α activation of Etv2 in ESCs followed by NOTCH1 signaling is required for the generation aECs that are capable of arteriogenesis and revascularization of ischemic tissue