Research on User Resistance Behavior in the Post-Implementation Stage of a Hospital Information System

The development of informatization brings great opportunities for the construction of informatization in hospitals. Hospitals are increasingly dependent on information systems. However, in the process of implementing the hospital information system, user resistance has become an important factor hindering the successful implementation of the system. The existing researches on the causes of user resistance mostly stay in the pre-implementation stage before the introduction of the system. However, the pre-implementation stage does not involve the resistance caused by users\u27 real contact with the system, so the research conclusions are limited. Based on the existing three-factor resistance theory, choosing the resistance in the postimplementation stage of a hospital information system as case study object, starting from the three theoretical perspectives, this paper makes a comprehensive analysis of the reasons for the resistance behavior in the post-implementation stage of the information system, and puts forward that the reasons for the resistance behavior are caused by user motivation, system development technology, network infrastructure, organizational support, organizational management, and other comprehensive caused by multiple factors. Through this study, the conclusions of the existing information system resistance factors research field are further expanded and improved, making the conclusions more comprehensive and specific. This paper not only provides theoretical reference for researchers in related fields, but also provides substantive suggestions for the smooth implementation of information system in hospitals, promotes the transformation of hospital informatization, and improves the level of medical service and social health

Leverage Business Analytics and OWA to Recommend Appropriate Projects in Crowdfunding Platform

Nowadays, crowdfunding is becoming more and more popular. Many studies have been published on the crowdfunding platform from different perspectives. However, among all these studies, few are concerned about the recommendation methods, which, in effect, are highly beneficial to crowdfunding websites and the participants. Having considered the situation talked above, this paper works out the several features from the relative projects of user’s current browsing project. Then we give different weights to each feature based on selective attention phenomenon, and adopt the method of OWA operator to calculate the final score of each relative project and accomplish our model by picking out the four projects with different outstanding characteristics. Finally, according to the statistics on China’s famous crowdfunding website, we conducted a group of contrast experiments and eventually testified that our proposed model could, to some extent, help classify and give recommendation effectively. Furthermore, the results of this research can give guidance to the management of crowdfunding websites and they are also very significant advices for the future crowdfunding website development

PALMD regulates aortic valve calcification via altered glycolysis and NF-κB-mediated inflammation

Recent genome-wide association and transcriptome-wide association studies have identified an association between the PALMD locus, encoding palmdelphin, a protein involved in myoblast differentiation, and calcific aortic valve disease (CAVD). Nevertheless, the function and underlying mechanisms of PALMD in CAVD remain unclear. We herein investigated whether and how PALMD affects the pathogenesis of CAVD using clinical samples from CAVD patients and a human valve interstitial cell (hVIC) in vitro calcification model. We showed that PALMD was upregulated in calcified regions of human aortic valves and calcified hVICs. Furthermore, silencing of PALMD reduced hVIC in vitro calcification, osteogenic differentiation, and apoptosis, whereas overexpression of PALMD had the opposite effect. RNA-Seq of PALMD-depleted hVICs revealed that silencing of PALMD reduced glycolysis and nuclear factor-κB (NF-κB)–mediated inflammation in hVICs and attenuated tumor necrosis factor α–induced monocyte adhesion to hVICs. Having established the role of PALMD in hVIC glycolysis, we examined whether glycolysis itself could regulate hVIC osteogenic differentiation and inflammation. Intriguingly, the inhibition of PFKFB3-mediated glycolysis significantly attenuated osteogenic differentiation and inflammation of hVICs. However, silencing of PFKFB3 inhibited PALMD-induced hVIC inflammation, but not osteogenic differentiation. Finally, we showed that the overexpression of PALMD enhanced hVIC osteogenic differentiation and inflammation, as opposed to glycolysis, through the activation of NF-κB. The present study demonstrates that the genome-wide association– and transcriptome-wide association–identified CAVD risk gene PALMD may promote CAVD development through regulation of glycolysis and NF-κB–mediated inflammation. We propose that targeting PALMD-mediated glycolysis may represent a novel therapeutic strategy for treating CAVD

The genetic and epigenetic regulation of CD55 and its pathway analysis in colon cancer

BackgroundCD55 plays an important role in the development of colon cancer. This study aims to evaluate the expression of CD55 in colon cancer and discover how it is regulated by transcriptional factors and miRNA.MethodsThe expression of CD55 was explored by TIMER2.0, UALCAN, and Human Protein Atlas (HPA) databases. TRANSFAC and Contra v3 were used to predict the potential binding sites of transcription factors in the CD55 promoter. TargetScan and starBase v2.0 were used to predict the potential binding ability of miRNAs to the 3′ untranslated region (3′UTR) of CD55. SurvivalMeth was used to explore the differentially methylated sites in the CD55 promoter. Western blotting was used to detect the expression of TFCP2 and CD55. Dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay were performed to determine the targeting relationship of TFCP2, NF-κB, or miR-27a-3p with CD55. CD55-related genes were explored by constructing a protein–protein interaction (PPI) network and performing pathway analysis by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG).ResultsCD55 was highly expressed in colon cancer tissues. The mRNA and protein expression levels of TFCP2 were reduced by si-TFCP2. NF-κB mRNA was obviously reduced by NF-κB inhibitor and increased by NF-κB activator. CD55 protein was also inhibited by miR-27a-3p. Dual-luciferase reporter assays showed that after knocking down TFCP2 or inhibiting NF-κB, the promoter activity of CD55 was decreased by 21% and 70%, respectively; after activating NF-κB, the promoter activity of CD55 increased by 2.3 times. As TFCP2 or NF-κB binding site was mutated, the transcriptional activity of CD55 was significantly decreased. ChIP assay showed that TFCP2 and NF-κB combined to the promoter of CD55. The luciferase activity of CD55 3′UTR decreased after being co-transfected with miR-27a-3p mimics and increased by miR-27a-3p antagomir. As the miR-27a-3p binding site was mutated, we did not find any significant effect of miR-27a-3p on reporter activity. PPI network assay revealed a set of CD55-related genes, which included CFP, CFB, C4A, and C4B. GO and KEGG analyses revealed that the target genes occur more frequently in immune-related pathways.ConclusionOur results indicated that CD55 is regulated by TFCP2, NF-κB, miR-27a-3p, and several immune-related genes, which in turn affects colon cancer

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

[D-Ala2, D-Leu5] Enkephalin Inhibits TLR4/NF-κB Signaling Pathway and Protects Rat Brains against Focal Ischemia-Reperfusion Injury

Background. Cerebral ischemia-reperfusion (I/R) injury is the main cause of acute brain injury, which is a life-threatening disease due to the lack of effective treatments. [D-Ala2, D-Leu5] enkephalin (DADLE) is a synthetic delta-opioid receptor agonist that is reported to confer neuroprotective effect; however, the underlying mechanism is still being explored. The purpose of the present study is to determine whether DADLE administrated intracerebroventricularly could attenuate the cerebral I/R injury, to determine if this is through inhibiting the toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway and therefore inhibiting neuroinflammation in an ischemic stroke model. Methods. Rats were subjected to 120 minutes of ischemia by transient middle cerebral artery occlusion (MCAO). At 45 minutes after ischemia, DADLE or control vehicle (artificial cerebrospinal fluid, ACSF) was given to the rats intracerebroventricularly. Neurological deficit, cerebral infarct volume, and histopathological changes were assessed at 24 hours after reperfusion. Brain inflammation was assessed by measuring tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the ischemic penumbra by ELISA. The expression of TLR4 was determined by immunohistochemistry staining and western blotting. The expression of NF-κB was investigated by western blotting. Results. Compared with the vehicle-treatment (ACSF), DADEL improved neurological deficit (9.6±2.1 versus 13.8±1.9), reduced cerebral infarct volume (18.74±3.30% versus 10.57±2.50%), and increased the number of normal neurons (29.72±8.53% versus 51.37±9.18%) after cerebral I/R injury in rats (all P<0.05). Expressions of inflammatory molecules including TNF-α and IL-6 were highly expressed in the vehicle-treated rats, whereas treatment with DADLE downregulated these expressions (P<0.05). Additionally, cerebral I/R injury significantly increased the TLR4 and NF-κB expression in vehicle-control group, which was markedly inhibited by DADLE (P<0.05). Conclusions. DADLE, administrated intracerebroventricularly at 45 minutes after cerebral ischemia, significantly ameliorated I/R-induced brain damage in rats. This kind of neuroprotective effect appears to be related to the downregulation of TLR4-mediated inflammatory responses

Epistatic Association of CD14 and NOTCH2 Genetic Polymorphisms with Biliary Atresia in a Southern Chinese Population

Biliary atresia (BA) is the most common cause of endstage liver disease in infants with poor prognosis and high mortality. The etiology of BA is still unknown, but the genetic factors have been considered as an important player in BA. We investigated the association of two cis-regulated variants in CD14 (rs2569190) and NOTCH2 (rs835576) with BA susceptibility, using the largest case-control cohort, totaling 506 BA patients and 1,473 healthy controls in a Southern Chinese population. Significant epistatic interaction between the two variants in our samples was observed (p = 8.1E−03; OR = 2.78; 95% CI: 1.32–5.88). The expression of CD14 and NOTCH2 in the BA group was consistently lower than that in the control (CC) group (0.31 ± 0.02 versus 1.00 ± 0.14; p < 0.001), which might be related to the genetic susceptibility of the genes awaiting further validation. Keywords: CD14, Notch2, biliary atresia, epistasi

Additional file 1: of Metformin restores electrophysiology of small conductance calcium-activated potassium channels in the atrium of GK diabetic rats

Table S1. Raw data of blood glucose level. Table S2. Raw data of fibrotic area. Table S3. Raw data of western blotting detection of the expressions of KCa2.1, KCa2.2 and KCa2.3. Table S4. Raw data of real-time PCR detection of the expressions of KCNN1, KCNN2, and KCNN3. Table S5. Raw data of SK current intensities at − 140 mV. Table S6. Raw data of current-voltage relation of SK currents at voltages ranging from − 150 to − 20 mV. Table S7. Raw data of action potential parameters. Table S8. Raw data of action potential increase before and after exposure to apamin. (DOC 178 kb