The Impact of a New App Channel on Physicians’ Performance: Evidence From Online Healthcare Natural Experiment

Besides the web browser, the introduction of the mobile app in online healthcare systems has resulted in an additional touchpoint for users. Drawing on the Media Richness theory, we aim to reveal the effect of the mobile app channel on physicians’ performance in the online health communities (OHCs). We provide direct empirical evidence on a large-scale dataset from one of the largest Chinese OHCs, Haodf, and propose a natural experiment to show the casual effect. Our results demonstrate that the introduction of the app channel to OHCs for patients has a positive impact on physicians’ responses and rating performance on the online platforms, especially for male physicians from high-ranking hospitals

Atrial-selective block of sodium channels by acehytisine in rabbit myocardium

AbstractAcehytisine, a multi-ion channel blocker, can markedly inhibit INa, ICa, IKur, If at various concentrations and effectively terminate and prevent atrial fibrillation (AF) in patients and animal models, but the molecular mechanism underlying its blockage remains elusive. In this study, we investigated the effects of acehytisine on action potentials and sodium channels of atrial and ventricular myocytes isolated from rabbit, using whole-cell recording system. We found that acehytisine exerted stronger blocking effects on sodium channels in atria than in ventricles, especially at depolarization (IC50: 48.48 ± 7.75 μmol/L in atria vs. 560.17 ± 63.98 μmol/L in ventricles). It also significantly shifted steady state inactivation curves toward negative potentials in atrial myocytes, without affecting the recovery kinetics from inactivation of sodium channels in the same cells. In addition, acehytisine inhibited INa in a use-dependent manner and regulated slow inactivation kinetics by different gating configurations. These findings indicate that acehytisine selectively blocks atrial sodium channels and possesses affinity to sodium channel in certain states, which provides additional evidence for the anti-AF of acehytisine

Esophageal cancer-related gene 4 at the interface of injury, inflammation, infection, and malignancy

In humans, esophageal cancer-related gene 4 (ECRG4) is encoded by four exons in the c2orf40 locus of chromosome 2. Translation of ECRG4 messenger ribonucleic acid produces a 148 amino acid-secreted 17 KDa protein that is then processed to 14, ten, eight, six, four, and two KDa peptides, depending on the cell in which the gene is expressed. As hypermethylation at the c2orf40 locus inhibits ECRG4 gene expression in many epithelial cancers, several investigators have speculated that ECRG4 is a candidate tumor suppressor. Indeed, overexpression of ECRG4 inhibits cell proliferation in vitro, but it also has a wide range of effects in vivo beyond its antitumor activity. ECRG4 overexpression affects apoptosis, senescence, cell migration, inflammation, injury, and infection responsiveness. ECRG4 activities also depend on its cellular localization, secretion, and post-translational processing. These cytokine/chemokine-like characteristics argue that ECRG4 is not a traditional candidate tumor suppressor gene, as originally predicted by its downregulation in cancer. We review how insights into the regulation of ECRG4 gene expression, knowledge of its primary structure, and the study of its emerging physiological functions come together to support a much more complex role for ECRG4 at the interface of inflammation, infection, and malignancy

Ecrg4 expression and its product augurin in the choroid plexus: impact on fetal brain development, cerebrospinal fluid homeostasis and neuroprogenitor cell response to CNS injury

<p>Abstract</p> <p>Background</p> <p>The content and composition of cerebrospinal fluid (CSF) is determined in large part by the choroid plexus (CP) and specifically, a specialized epithelial cell (CPe) layer that responds to, synthesizes, and transports peptide hormones into and out of CSF. Together with ventricular ependymal cells, these CPe relay homeostatic signals throughout the central nervous system (CNS) and regulate CSF hydrodynamics. One new candidate signal is augurin, a newly recognized 14 kDa protein that is encoded by <it>esophageal cancer related gene-4 </it>(<it>Ecrg4</it>), a putative tumor suppressor gene whose presence and function in normal tissues remains unexplored and enigmatic. The aim of this study was to explore whether <it>Ecrg4 </it>and its product augurin, can be implicated in CNS development and the response to CNS injury.</p> <p>Methods</p> <p><it>Ecrg4 </it>gene expression in CNS and peripheral tissues was studied by <it>in situ </it>hybridization and quantitative RT-PCR. Augurin, the protein encoded by <it>Ecrg4</it>, was detected by immunoblotting, immunohistochemistry and ELISA. The biological consequence of augurin over-expression was studied in a cortical stab model of rat CNS injury by intra-cerebro-ventricular injection of an adenovirus vector containing the <it>Ecrg4 </it>cDNA. The biological consequences of reduced augurin expression were evaluated by characterizing the CNS phenotype caused by <it>Ecrg4 </it>gene knockdown in developing zebrafish embryos.</p> <p>Results</p> <p>Gene expression and immunohistochemical analyses revealed that, the CP is a major source of <it>Ecrg4 </it>in the CNS and that <it>Ecrg4 </it>mRNA is predominantly localized to choroid plexus epithelial (CPe), ventricular and central canal cells of the spinal cord. After a stab injury into the brain however, both augurin staining and <it>Ecrg4 </it>gene expression decreased precipitously. If the loss of augurin was circumvented by over-expressing <it>Ecrg4 in vivo</it>, BrdU incorporation by cells in the subependymal zone decreased. Inversely, gene knockdown of <it>Ecrg4 </it>in developing zebrafish embryos caused increased proliferation of GFAP-positive cells and induced a dose-dependent hydrocephalus-like phenotype that could be rescued by co-injection of antisense morpholinos with <it>Ecrg4 </it>mRNA.</p> <p>Conclusion</p> <p>An unusually elevated expression of the <it>Ecrg4 </it>gene in the CP implies that its product, augurin, plays a role in CP-CSF-CNS function. The results are all consistent with a model whereby an injury-induced decrease in augurin dysinhibits target cells at the ependymal-subependymal interface. We speculate that the ability of CP and ependymal epithelium to alter the progenitor cell response to CNS injury may be mediated, in part by <it>Ecrg4</it>. If so, the canonic control of its promoter by DNA methylation may implicate epigenetic mechanisms in neuroprogenitor fate and function in the CNS.</p

Esophageal Cancer Related Gene-4 Is a Choroid Plexus-Derived Injury Response Gene: Evidence for a Biphasic Response in Early and Late Brain Injury

By virtue of its ability to regulate the composition of cerebrospinal fluid (CSF), the choroid plexus (CP) is ideally suited to instigate a rapid response to traumatic brain injury (TBI) by producing growth regulatory proteins. For example, Esophageal Cancer Related Gene-4 (Ecrg4) is a tumor suppressor gene that encodes a hormone-like peptide called augurin that is present in large concentrations in CP epithelia (CPe). Because augurin is thought to regulate senescence, neuroprogenitor cell growth and differentiation in the CNS, we evaluated the kinetics of Ecrg4 expression and augurin immunoreactivity in CPe after CNS injury. Adult rats were injured with a penetrating cortical lesion and alterations in augurin immunoreactivity were examined by immunohistochemistry. Ecrg4 gene expression was characterized by in situ hybridization. Cell surface augurin was identified histologically by confocal microscopy and biochemically by sub-cellular fractionation. Both Ecrg4 gene expression and augurin protein levels were decreased 24–72 hrs post-injury but restored to uninjured levels by day 7 post-injury. Protein staining in the supraoptic nucleus of the hypothalamus, used as a control brain region, did not show a decrease of auguin immunoreactivity. Ecrg4 gene expression localized to CPe cells, and augurin protein to the CPe ventricular face. Extracellular cell surface tethering of 14 kDa augurin was confirmed by cell surface fractionation of primary human CPe cells in vitro while a 6–8 kDa fragment of augurin was detected in conditioned media, indicating release from the cell surface by proteolytic processing. In rat CSF however, 14 kDa augurin was detected. We hypothesize the initial release and proteolytic processing of augurin participates in the activation phase of injury while sustained Ecrg4 down-regulation is dysinhibitory during the proliferative phase. Accordingly, augurin would play a constitutive inhibitory function in normal CNS while down regulation of Ecrg4 gene expression in injury, like in cancer, dysinhibits proliferation

Mobilizing Healthcare across Geography through Telemedicine Consultations

Many countries report that medical professionals such as physicians are highly concentrated in urban cities, while too few are available in rural cities. Telemedicine consultations allow patients to virtually search, receive, and pay for a physician-to-p

Empowering Patients Using Smart Mobile Health Platforms: Evidence of a Randomized Field Experiment

With today’s technological advancements, mobile phones and wearable devices have become extensions of an increasingly diffused and smart digital infrastructure. In this paper, we examine mobile health (mHealth) platforms and their health and economic impacts on the outcomes of chronic disease patients. To do so, we partnered with a major mHealth firm that provides one of the largest mobile health app platforms in Asia specializing in diabetes care. We designed and implemented a randomized field experiment based on detailed patient health activities (e.g., steps, exercises, sleep, food intake) and blood glucose values from 1,070 diabetes patients over several months. Our main findings show that the adoption of the mHealth app leads to an improvement in health behavior, which in turn leads to both short term metrics (such as reduction in patients’ blood glucose and glycated hemoglobin levels) and longer-term metrics (such as hospital visits and medical expenses). Patients who adopted the mHealth app undertook higher levels of exercise, consumed healthier food with lower calories, walked more steps and slept for longer times on a daily basis. They also were more likely to substitute offline visits with telehealth. A comparison of mobile versus PC-enabled versions of the same app demonstrates that the mobile version has a stronger effect than PC version in helping patients make these behavioral modifications with respect to diet, exercise, and lifestyle, which ultimately leads to an improvement in their healthcare outcomes. We also compared outcomes when the platform facilitates personalized health reminders to patients vis-à-vis generic (non-personalized) reminders. Surprisingly, we found that personalized mobile messages with patient-specific guidance can have an inadvertent (smaller) effect on patient app engagement and lifestyle changes, leading to a lower health improvement. However, they are more like to encourage a substitution of offline visits by telehealth. Overall, our findings indicate the massive potential of mHealth technologies and platform design in achieving better healthcare outcomes

Up-regulation of the human-specific CHRFAM7A gene in inflammatory bowel disease.

BackgroundThe α7-subunit of the α7-nicotinic acetylcholine receptor (α7-nAChR) is an obligatory intermediate for the anti-inflammatory effects of the vagus nerve. But in humans, there exists a second gene called CHRFAM7A that encodes a dominant negative α7-nAChR inhibitor. Here, we investigated whether their expression was altered in inflammatory bowel disease (IBD) and colon cancer.MethodsQuantitative RT-PCR measured gene expression of human α7-nAChR gene (CHRNA7), CHRFAM7A, TBC3D1, and actin in biopsies of normal large and small intestine, and compared to their expression in biopsies of ulcerative colitis, Crohn's disease, and colon cancer.ResultsqRT-PCR showed that CHRFAM7A and CHRNA7 gene expression was significantly (p&nbsp;&lt;&nbsp;.02) up-regulated in IBD (N&nbsp;=&nbsp;64). Gene expression was unchanged in colon cancer. Further analyses revealed that there were differences in ulcerative colitis and Crohn's Disease. Colon biopsies of ulcerative colitis (N&nbsp;=&nbsp;33) confirmed increased expression of CHRFAM7A and decreased in CHRNA7 expression (p&nbsp;&lt;&nbsp;0.001). Biopsies of Crohn's disease (N&nbsp;=&nbsp;31), however, showed only small changes in CHRFAM7A expression (p&nbsp;&lt;&nbsp;0.04) and no change in CHRNA7. When segregated by tissue source, both CHRFAM7A up-regulation (p&nbsp;&lt;&nbsp;0.02) and CHRNA7 down-regulation (p&nbsp;&lt;&nbsp;0.001) were measured in colon, but not in small intestine.ConclusionThe human-specific CHRFAM7A gene is up-regulated, and its target, CHRNA7, down-regulated, in IBD. Differences between ulcerative colitis and Crohn's disease tie to location of disease.SignificanceThe appearance of IBD in modern humans may be consequent to the emergence of CHRFAM7A, a human-specific α7-nAChR antagonist. CHRFAM7A could present a new, unrecognized target for development of IBD therapeutics