Mass Media and the Contagion of Fear: The Case of Ebola in America

Background

In the weeks following the first imported case of Ebola in the U. S. on September 29, 2014, coverage of the very limited outbreak dominated the news media, in a manner quite disproportionate to the actual threat to national public health; by the end of October, 2014, there were only four laboratory confirmed cases of Ebola in the entire nation. Public interest in these events was high, as reflected in the millions of Ebola-related Internet searches and tweets performed in the month following the first confirmed case. Use of trending Internet searches and tweets has been proposed in the past for real-time prediction of outbreaks (a field referred to as “digital epidemiology”), but accounting for the biases of public panic has been problematic. In the case of the limited U. S. Ebola outbreak, we know that the Ebola-related searches and tweets originating the U. S. during the outbreak were due only to public interest or panic, providing an unprecedented means to determine how these dynamics affect such data, and how news media may be driving these trends.

Methodology

We examine daily Ebola-related Internet search and Twitter data in the U. S. during the six week period ending Oct 31, 2014. TV news coverage data were obtained from the daily number of Ebola-related news videos appearing on two major news networks. We fit the parameters of a mathematical contagion model to the data to determine if the news coverage was a significant factor in the temporal patterns in Ebola-related Internet and Twitter data.

Conclusions

We find significant evidence of contagion, with each Ebola-related news video inspiring tens of thousands of Ebola-related tweets and Internet searches. Between 65% to 76% of the variance in all samples is described by the news media contagion model.     

SHER: A Colored Petri Net Based Random Mobility Model for Wireless Communications

In wireless network research, simulation is the most imperative technique to investigate the network’s behavior and validation. Wireless networks typically consist of mobile hosts; therefore, the degree of validation is influenced by the underlying mobility model, and synthetic models are implemented in simulators because real life traces are not widely available. In wireless communications, mobility is an integral part while the key role of a mobility model is to mimic the real life traveling patterns to study. The performance of routing protocols and mobility management strategies e.g. paging, registration and handoff is highly dependent to the selected mobility model. In this paper, we devise and evaluate the Show Home and Exclusive Regions (SHER), a novel two-dimensional (2-D) Colored Petri net (CPN) based formal random mobility model, which exhibits sociological behavior of a user. The model captures hotspots where a user frequently visits and spends time. Our solution eliminates six key issues of the random mobility models, i.e., sudden stops, memoryless movements, border effect, temporal dependency of velocity, pause time dependency, and speed decay in a single model. The proposed model is able to predict the future location of a mobile user and ultimately improves the performance of wireless communication networks. The model follows a uniform nodal distribution and is a mini simulator, which exhibits interesting mobility patterns. The model is also helpful to those who are not familiar with the formal modeling, and users can extract meaningful information with a single mouse-click. It is noteworthy that capturing dynamic mobility patterns through CPN is the most challenging and virulent activity of the presented research. Statistical and reachability analysis techniques are presented to elucidate and validate the performance of our proposed mobility model. The state space methods allow us to algorithmically derive the system behavior and rectify the errors of our proposed model.     

Imaging GFP-Based Reporters in Neurons with Multiwavelength Optogenetic Control

To study the impact of neural activity on cellular physiology, one would like to combine precise control of firing patterns with highly sensitive probes of cellular physiology. Light-gated ion channels, e.g., Channelrhodopsin-2, enable precise control of firing patterns; green fluorescent protein-based reporters, e.g., the GCaMP6f Ca²⁺ reporter, enable highly sensitive probing of cellular physiology. However, for most actuator-reporter combinations, spectral overlap prevents straightforward combination within a single cell. Here we explore multiwavelength control of channelrhodopsins to circumvent this limitation. The “stoplight” technique described in this article uses channelrhodopsin variants that are opened by blue light and closed by orange light. Cells are illuminated with constant blue light to excite fluorescence of a green fluorescent protein-based reporter. Modulated illumination with orange light negatively regulates activation of the channelrhodopsin. We performed detailed photophysical characterization and kinetic modeling of four candidate stoplight channelrhodopsins. The variant with the highest contrast, sdChR(C138S,E154A), enabled all-optical measurements of activity-induced calcium transients in cultured rat hippocampal neurons, although cell-to-cell variation in expression levels presents a challenge for quantification.     

Isolation of cold stress-responsive genes from Lepidium latifolium by suppressive subtraction hybridization

Suppression subtraction hybridization (SSH) libraries were constructed from RNA isolated from leaves of control and cold stress-induced Lepidium latifolium, a cold-tolerant plant species from high altitudes for isolation of cold-responsive genes. A total of 500 clones were obtained from the cold stress library. Dot blot expression analysis identified 157 clones that were upregulated and 75 that were downregulated during cold stress. These clones selected on the basis of their expression patterns on dot blot were sequenced. As much as 27 and 17 genes were identified from the forward and reverse libraries, respectively. The genes identified revealed homology with genes involved in diverse processes such as gene regulation/signaling, photosynthesis, DNA damage repair protein, pathogenesis-related protein, senescence-associated proteins and proteins with unknown functions.     

Acetylcholinesterase inhibitors neostigmine and physostigmine inhibit induction of alpha-amylase activity during seed germination in barley, Hordeum vulgare var. Jyoti

Acetylcholine (ACh) is an important neurotransmitter whose non-neuronal biological roles are being widely accepted. ACh and components of its metabolism are present in plants. ACh and some inhibitors of acetylcholinesterase (AChE) share structural similarity (quaternary ammonium group) with some inhibitors of biosynthesis of a plant hormone, gibberellic acid (GA); e.g., 2-Isopropyl-4-dimethylamino-5-methylphenyl-1-piperidine carboxylate methyl chloride (AMO-1618) inhibits GA biosynthesis as well as AChE. The present study explores the possibility that ACh and antiAChE may inhibit GA biosynthesis. Seeds of barley var. Jyoti were germinated in the presence of ACh, its breakdown products - choline and acetate, and two antiAChE - neostigmine and physostigmine (all 10(-5) M). Alpha amylase activity in germinating seeds was measured as a reliable indicator of the level of GA biosynthesis. Alpha amylase activity in barley seeds was significantly reduced after 72 h of treatment with antiChE but not by ACh or its breakdown products. Since germinating barley seeds contain AChE, much of the ACh may have been broken down before its uptake. Quaternary ammonium antiChE neostigmine was more effective (50% inhibition at 10(-5) M) as compared to tertiary ammonium physostigmine (15% inhibition at 10(-5) M). ACh, choline, acetate, neostigmine and physostigmine (all 10(-5) M) did not affect formation of starch-iodine complex or activity of alpha-amylase per se. Our results indicate that quaternary ammonium inhibitors of AChE may inhibit GA biosynthesis.     

Therapeutic efficacy of Kalpaamruthaa on reactive oxygen/nitrogen species levels and antioxidative system in mammary carcinoma bearing rats

Reactive oxygen species play an important role in cancer and metastasis. Kalpaamruthaa is a modified Siddha preparation, which has been formulated in our laboratory. The preparation is an amalgamation of Semecarpus anacardium (SA), Emblica officinalis (EO) and honey, which gives an extra protectiveness to mammary carcinoma bearing animals (Sprague-Dawley stains were used for this study). The aim of our research is to determine the therapeutic efficiency of the drug with respect to lipid peroxidation and antioxidant status. The levels of lipid peroxides and antioxidant levels were measured in blood, and vital organs (liver, kidney and breast tissue) of control and experimental animals. In cancer condition, the LPO was increased and antioxidant levels were decreased. On drug (SA and KA) administration, decreased LPO and increased antioxidant levels were seen in control and experimental animals. This may be due to additive property of the drugs (SA, Emblica and honey), which possesses anticancer effect. The present study shows the good therapeutic efficacy of Kalpaamruthaa against mammary carcinoma.     

Novel Robinow syndrome causing mutations in the proximal region of the frizzled-like domain of ROR2 are retained in the endoplasmic reticulum

ROR2 is a member of the cell surface receptor tyrosine kinase (RTKs) family of proteins and is involved in the developmental morphogenesis of the skeletal, cardiovascular and genital systems. Mutations in ROR2 have been shown to cause two distinct human disorders, autosomal recessive Robinow syndrome and dominantly inherited Brachydactyly type B. The recessive form of Robinow syndrome is a disorder caused by loss-of-function mutations whereas Brachydactyly type B is a dominant disease and is presumably caused by gain-of-function mutations in the same gene. We have previously established that all the missense mutations causing Robinow syndrome in ROR2 are retained in the endoplasmic reticulum and therefore concluded that their loss of function is due to a defect in their intracellular trafficking. These mutations were in the distal portion of the frizzled-like cysteine rich domain and kringle domain. Here we report the identification of two novel mutations in the frizzled-like cysteine-rich domain of ROR2 causing Robinow syndrome. We establish the retention of the mutated proteins in the endoplasmic reticulum of HeLa cells and therefore failure to reach the plasma membrane. The clustering of Robinow-causing mutations in the extracellular frizzled-like cysteine-rich domain of ROR2 suggests a stringent requirement for the correct folding of this domain prior to export of ROR2 from the endoplasmic reticulum to the plasma membrane. GenBank accession number ROR2, M97639.     

Design, synthesis, and antiproliferative and CDK2-cyclin a inhibitory activity of novel flavopiridol analogues

The design and synthesis of a small library of 8-amidoflavone, 8-sulfonamidoflavone, 8-amido-7-hydroxyflavone, and heterocyclic analogues of flavopiridol is reported. The potential activity of these compounds as kinase inhibitors was evaluated by cytotoxicity studies in MCF-7 and ID-8 cancer cell lines and inhibition of CDK2-Cyclin A enzyme activity in vitro. The antiproliferative and CDK2-Cyclin A inhibitory activity of these analogues was significantly lower than the activity of flavopiridol. Molecular docking simulations were carried out and these studies suggested a different binding orientation inside the CDK2 binding pocket for these analogues compared to flavopiridol.     

Cyclic stretch induces PlGF expression in bronchial airway epithelial cells via nitric oxide release

Mechanical strain of lung tissue is an important stimulus for the production of growth factors that are critical for lung growth and development. However, excessive mechanical strain, as may occur during mechanical ventilation, may produce an increase in growth factors that may contribute to lung injury. We hypothesized that mechanical strain of primary bronchial airway epithelial cells (BAEpCs) induced the production of placental growth factor (PlGF), a member of the VEGF family. BAEpCs were cultured on a deformable silicoelastic membrane and exposed to different magnitudes of stretch. Stretch induced PlGF and nitric oxide (NO) production that increased with increasing magnitude of stretch. Stretch also induced PlGF and inducible NO synthase (iNOS) gene expression. The stretch-induced PlGF production and NO synthesis were attenuated by PD98059, a specific mitogen-activated protein kinase kinase-1 and -2 inhibitor. Inhibition of NO generation by l-NAME or l-NMMA or scavenging NO by carboxy-PTIO prevented stretch-mediated erk1/2 activation. In addition, in unstretched BAEpCs, exogenous NO enhanced erk1/erk2 activation. Our data suggest that mechanical stretch of BAEpCs induces iNOS expression and induces PlGF release in an erk1/2 activation-dependent manner.