Changing styles of informal academic communication in the age of the web:Orthodox, moderate and heterodox responses

Purpose- The purpose of this paper is to report the findings of a study to investigate changes in scholarly communication practices among a group of scholars in the UK and build upon the results that were published in a previous paper. Design/methodology/approach- The study deployed a naturalistic inquiry approach using semi-structured interviews as a qualitative research tool. A sample of 40 participants from four UK universities were interviewed to explore the changes in informal scholarly communication behaviour. Findings- The analysis of the interviews revealed that there are three ideal types of behaviour: the ?Orthodox? uses formal and traditional scholarly communication approaches; the ?Moderate? prioritises formal communication approaches, but at the same time is trying to get benefits from informal channels; and, the ?Heterodox? uses all channels available in scholarly communication. Originality and value - The value of the current study lies in using a naturalistic inquiry approach to investigate the changes in scholarly communication practices, and to explore different scholarly communication styles. In the context of this study, the use of a naturalistic approach and grounded theory principles in connection with coding provided a stance that allows for the gathering of rich information to enable understanding and explanation of scholarly communication activities in addition to uncovering themes that related to scholarly behaviour.authorsversionPeer reviewe

Factors affecting undergraduate students’ information sharing behaviour when dealing with COVID-19 misinformation: theory of reasoned action

Sharing misinformation has become a widespread phenomenon. Social media networks have significantly contributed to spreading and sharing misinformation, especially during crises and pandemics. However, little is known about why people share misinformation. The study aims to identify the factors affecting undergraduate students’ information sharing behaviour when dealing with unverified information. The study also seeks to discover any statistically significant differences (α=0.05) in students’ behaviour of sharing information related to COVID-19 without verification attributed to demographic variables, self-efficiency, attitude towards verifying information, individual’s beliefs, and subjective norms. The study adopted the theory of reasoned action. A quantitative research approach was adopted via the use of questionnaires. An e-mail was sent to all undergraduate students enrolled at Sultan Qaboos University during 2020-2021, yielding 407 valid answers from various colleges. The reliability of the survey is 0.916 as a whole, 0.741 for the individual’s self-efficacy scale, 0.312 for the attitude towards verifying information scale, 0.809 for the individual’s beliefs scale, 0.916 for the subjective norms scale, and 0.846 for the behaviour of using and sharing information related to COVID-19 without verification scale. The effect of self-efficacy, Attitude Towards Verifying Information, beliefs, and Subjective norms on the behaviour of sharing information related to COVID-19 without verification were tested. Quantitative data retrieved from the questionnaire were analysed using SPSS 24. Several analysis tests such as frequencies, T-test, and multiple regression tests were conducted.Results. The findings support that there’s a significant effect of demographic variables, self-efficacy, attitude towards verifying information, individual’s beliefs, and subjective norms on students’ behaviour of sharing information related to COVID-19 without verification. This research showed that many factors affect information sharing behaviour. The research concluded that the students’ information behaviour could be enhanced by focusing on information literacy skills.Peer Reviewe

Scholarly communication trends in the digital age: Informal scholarly publishing and dissemination, a grounded theory approach

Purpose – The purpose of this paper is to investigate scholars’ attitudes toward informal publishing and dissemination to provide a view of the challenges and advantages of using such channels. Although considerable research has been carried out in relation to peer-reviewed scholarly publishing, relatively few studies have investigated the adoption of informal scholarly communication platforms in the scholarly publishing process. Design/methodology/approach – The paper deployed a grounded theory approach using semi-structured interviews as a qualitative research tool. A theoretical sample of 40 researchers in 4 universities were interviewed to gather data regarding informal publishing, platforms, factors that affect the researchers’ decision and the use of informal channels in dissemination. Findings – Results of the interviews suggest that there is an increasing trend among researchers toward informal publishing and dissemination throughout the scholarly communication cycle. The paper shows that there are three types of scholars who are involved in the scholarly communication process: conventional, modern and liberal scholars. Each of these scholars carries different beliefs regarding the scholarly communication process. Research limitations/implications – This paper was conducted on a relatively small sample of academic researchers, and therefore, the results cannot be easily generalized into a wider community of scholars. Originality/value – The paper provides insight into informal scholarly publishing practices using a grounded theory approach. This approach helped to capture the changes in both scholarly publishing practices and the adoption of informal techniques among the scholarly community. </jats:sec

BM-MSCs alleviate diabetic nephropathy in male rats by regulating ER stress, oxidative stress, inflammation, and apoptotic pathways

Introduction: Diabetic nephropathy (DN), a chronic kidney disease, is a major cause of end-stage kidney disease worldwide. Mesenchymal stem cells (MSCs) have become a promising option to mitigate several diabetic complications.Methods: In this study, we evaluated the therapeutic potential of bone marrow-derived mesenchymal stem cells (BM-MSCs) in a rat model of STZ-induced DN. After the confirmation of diabetes, rats were treated with BM-MSCs and sacrificed at week 12 after treatment.Results: Our results showed that STZ-induced DN rats had extensive histopathological changes, significant upregulation in mRNA expression of renal apoptotic markers, ER stress markers, inflammatory markers, fibronectin, and intermediate filament proteins, and reduction of positive immunostaining of PCNA and elevated P53 in kidney tissue compared to the control group. BM-MSC therapy significantly improved renal histopathological changes, reduced renal apoptosis, ER stress, inflammation, and intermediate filament proteins, as well as increased positive immunostaining of PCNA and reduced P53 in renal tissue compared to the STZ-induced DN group.Conclusion: In conclusion, our study indicates that BM-MSCs may have therapeutic potential for the treatment of DN and provide important insights into their potential use as a novel therapeutic approach for DN

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease