Understanding Twitter’s adoption and use continuance: the Synergy between Uses and Gratifications and Diffusion of Innovations

This study explored the explanatory power of Uses and Gratifications (UG) and the Diffusion of Innovation theory (IDT) in describing Twitter phenomenon. Effects of mobile access and perceived outcomes of using Twitter were also examined and comparison of active and inactive users revealed which needs are likely to result in Twitter’s discontinuance if unmet. Online survey and data analysis with Partial Least Squares (PLS) revealed that the needs for Entertainment, Relaxation, the service’s Visibility and Compatibility were strong predictors of Twitter’s usage. ANOVA highlighted that the same dimensions were significantly lower among inactive ‘tweeters’, suggesting that the same factors may be responsible for both adoption and continuance. Mobile access of Twitter was found to be a catalyst for continued use. There is a need for the combined use of UG and IDT in describing Twitter’s adoption, with personal needs and the service’s characteristics being the use drivers by different audiences

Disentangling Twitter’s Adoption and Use (Dis)Continuance: A Theoretical and Empirical Amalgamation of Uses and Gratifications and Diffusion of Innovations

Drawing on Uses and Gratifications (UG) Theory and Diffusion of Innovation Theory (DIT), this study aimed to augment an exploration of individual user needs based on UG constructs with an analysis of the material characteristics of the innovation based on DIT constructs to provide a comprehensive explanation of people‘s motivations underlying various Twitter usage levels and frequencies. Whereas previous literature on Social Network Sites (SNS) have explored individuals‘ motivations underlying initial adoption, the equally interesting and relevant question of use (dis-) continuance has so far been largely overlooked. To fill this void in the literature, this study compares active users that have continued to use Twitter and inactive users that initially adopted, yet discontinued usage of Twitter. This study provides insights into different usage levels and frequencies through an investigation of 1) users‘ perceptions of the medium, 2) users‘ expected outcomes associated with the medium‘s use, and 3) the role and effect of mobile access. An analysis of 130 surveys with Partial Least Squares (PLS) and R2 partitioning revealed that an understanding of adoption and use (dis-) continuance of Twitter requires us to account for both user-related motivations (UG) and perceived characteristics of the medium (DIT), as combining UG and DIT increased explanatory power (R2) for the overall sample. Furthermore, our findings showed that inactive users‘ initial adoption and subsequent discontinuance was solely impacted by user-related needs, (i.e. UG constructs), whereas active users‘ continued use was largely motivated by technology characteristics, (i.e. DIT constructs). Finally, our study revealed significant differences between active and inactive users in terms of the devices and platform used for accessing Twitter, with active users reporting a significantly higher use of mobile devices. Based on these findings, we discuss contributions and implications for future research and practice

MicroRNA-29a suppresses the growth, migration, and invasion of lung adenocarcinoma cells by targeting carcinoembryonic antigen-related cell adhesion molecule 6

AbstractCarcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is an important regulator of cell adhesion, invasion, and metastasis. The aim of this study was to evaluate the functional roles of CEACAM6 in lung adenocarcinoma and to identify miRNAs that inhibit the growth, migration, and invasion of lung adenocarcinoma cells by targeting CEACAM6. CEACAM6 expression is associated with poor prognosis of patients with lung adenocarcinoma, and CEACAM6 has important functional roles in controlling the growth, migration, and invasion of lung adenocarcinoma cells in vitro and in vivo. Furthermore, miR-29a can suppress the growth, migration, and invasion of lung adenocarcinoma cells by targeting CEACAM6. Therefore, miR-29a/CEACAM6 axis represents a potential therapeutic target for treatment of lung adenocarcinoma

Raf kinase inhibitory protein suppresses a metastasis signalling cascade involving LIN28 and let-7

Raf kinase inhibitory protein (RKIP) negatively regulates the MAP kinase (MAPK), G protein-coupled receptor kinase-2, and NF-κB signalling cascades. RKIP has been implicated as a metastasis suppressor for prostate cancer, but the mechanism is not known. Here, we show that RKIP inhibits invasion by metastatic breast cancer cells and represses breast tumour cell intravasation and bone metastasis in an orthotopic murine model. The mechanism involves inhibition of MAPK, leading to decreased transcription of LIN28 by Myc. Suppression of LIN28 enables enhanced let-7 processing in breast cancer cells. Elevated let-7 expression inhibits HMGA2, a chromatin remodelling protein that activates pro-invasive and pro-metastatic genes, including Snail. LIN28 depletion and let-7 expression suppress bone metastasis, and LIN28 restores bone metastasis in mice bearing RKIP-expressing breast tumour cells. These results indicate that RKIP suppresses invasion and metastasis in part through a signalling cascade involving MAPK, Myc, LIN28, let-7, and downstream let-7 targets. RKIP regulation of two pluripotent stem cell genes, Myc and LIN28, highlights the importance of RKIP as a key metastasis suppressor and potential therapeutic agent.</p

Raf kinase inhibitory protein suppresses a metastasis signalling cascade involving LIN28 and let-7

Raf kinase inhibitory protein (RKIP) negatively regulates the MAP kinase (MAPK), G protein-coupled receptor kinase-2, and NF-κB signalling cascades. RKIP has been implicated as a metastasis suppressor for prostate cancer, but the mechanism is not known. Here, we show that RKIP inhibits invasion by metastatic breast cancer cells and represses breast tumour cell intravasation and bone metastasis in an orthotopic murine model. The mechanism involves inhibition of MAPK, leading to decreased transcription of LIN28 by Myc. Suppression of LIN28 enables enhanced let-7 processing in breast cancer cells. Elevated let-7 expression inhibits HMGA2, a chromatin remodelling protein that activates pro-invasive and pro-metastatic genes, including Snail. LIN28 depletion and let-7 expression suppress bone metastasis, and LIN28 restores bone metastasis in mice bearing RKIP-expressing breast tumour cells. These results indicate that RKIP suppresses invasion and metastasis in part through a signalling cascade involving MAPK, Myc, LIN28, let-7, and downstream let-7 targets. RKIP regulation of two pluripotent stem cell genes, Myc and LIN28, highlights the importance of RKIP as a key metastasis suppressor and potential therapeutic agent.</p

Early postnatal exposure to isoflurane causes cognitive deficits and disrupts development of newborn hippocampal neurons via activation of the mTOR pathway

Funding: Johns Hopkins ACCM Department anesthesiology.hopkinsmedicine.org (grant number StAAR) to CDM. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. NIH-NIGMS www.nih.gov (grant number 1R01GM120519-01 and 1K08GM104329-01) to CDM. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. NIH www.nih.gov (grant number NS048271 and MH105128) to GLM. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. NIH www.nih.gov (grant number NS047344) to HS. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Acknowledgments: We would like to acknowledge the helpful contributions of Sunu Kim (technical assistance) and Allan Gottschalk (critical commentary).Peer reviewedPublisher PD

Sulforaphane, a natural component of broccoli, inhibits vestibular schwannoma growth in vitro and in vivo

Vestibular schwannoma (VS) is an intracranial tumor that causes significant morbidity, including hearing loss, tinnitus, dizziness, and possibly even death from brainstem compression. However, FDA-approved pharmacologic treatments for VS do not exist. Sulforaphane (SFN) is a naturally occurring isothiocyanate found in cruciferous vegetables, such as broccoli, with potent chemoprotective effects in several cell types. Our objective was to determine whether SFN is effective against VS in vitro and in vivo. Human primary VS cells, HEI-193 schwannoma cells, and SC4 Nf2−/− Schwann cells were used to investigate the inhibitory effects of SFN in vitro. Cell proliferation was assessed by bromodeoxyuridine (BrdU) incorporation, and cell viability and metabolic activity was calculated by MTT assay. Apoptosis was measured by flow cytometry, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, and Western blot for cleaved caspases. A mouse model with a murine schwannoma allograft was also used to examine the antitumor activity of SFN. SFN exhibited significant antiproliferative activity in schwannoma cells in vitro, via the inhibition of HDAC activity and the activation of ERK. SFN treatment induced apoptosis and cell cycle arrest at the G2/M phase. SFN also significantly inhibited schwannoma growth in vivo. Our preclinical studies motivate a future prospective clinical study of SFN for the treatment of VS

A Hop Extract Lifenol® Improves Postmenopausal Overweight, Osteoporosis, and Hot Flash in Ovariectomized Rats

Objective. In order to assess the effectiveness of a hop extract (HE) for postmenopausal symptoms, the effects of Lifenol on ovariectomy-induced osteoporosis, hyperlipidemia, body weight increase, and hot flash were investigated in rats. Methods. Female Sprague-Dawley rats were ovariectomized and subjected to a daily scheduled exercise training (15 min at 15 m/min) or treated with HE (30 or 100 mg/kg, oral) or 17β-estradiol (100 μg/kg, intraperitoneal) for 12 weeks. Body and visceral fat weights, serum lipid profiles, osteoporotic parameters in serum, and femoral bones were analyzed. Separately, forced running-induced dermal and rectal temperatures and blood flow velocity were measured in ovariectomized rats. Results. Ovariectomy increased blood lipids including triglycerides, total cholesterol, and low-density lipoproteins, leading to visceral fat accumulation and overweight. Estrogen depletion caused osteoporosis, displaying decreased femoral bone weight, bone mineral density and content, and blood phosphorus level. The disturbances in lipid metabolism and bone resorption were recovered by treatment with HE in a dose-dependent manner. In addition, HE treatment shortened the duration of forced running-induced alterations in skin and rectal temperatures by reducing blood flow velocity. Conclusion. The results indicate that HE attenuated overweight, osteoporosis, and hot flash in estrogen-deficient animals by regulating blood lipid profile and fat accumulation, blood estrogen and bone resorption factors, and dermal blood flow

Notch signaling in Protein kinase C alpha overexpressing, tamoxifen-resistant breast cancer cells.

Notch signaling in Protein kinase C alpha overexpressing, tamoxifen-resistant breast cancer cells