Purpose This study aims to answer an important question of how brand-related communications, including advertising and sales promotion contents, which are disseminated on social media platforms, can enhance positive brand image and evoke favourable behavioural intention from consumers. Design/methodology/approach This study surveys 615 consumers of automotive brands across Malaysia. The data were analysed with AMOS, which was used to specify both the measurement and structural models. The mediating effect of both hedonic and functional brand images was tested using the bootstrapping approach in AMOS and Sobel test. Findings The findings reported in this research demonstrate that there are positive and significant relationships between social media advertising content, social media sales promotion content, hedonic brand image, functional brand image and behavioural intention. Both hedonic and functional brand images have significant mediating effects on social media advertising content, social media sales promotion content and behavioural intention. However, the relationship between social media advertising content and behavioural intention is insignificant. Practical implications This paper proffers insights to brand managers and marketers on how to leverage on social media contents by unearthing the roles of traditional marketing communications such as social media advertising and promotional information in enhancing brand preference and improving consumers’ purchase intention. Originality/value This research advances the discussions in the realm of social media communications and branding by examining the mediating effects of both hedonic and functional brand images of automotive brands. In addition, this study focuses on two essential marketing communications, advertising and sales promotions, which are commonly disseminated by brand managers on social media platforms.

Intra-tumor heterogeneity is one of the key confounding factors in deciphering tumor evolution. Malignant cells exhibit variations in their gene expression, copy numbers, and mutation even when originating from a single progenitor cell. Single cell sequencing of tumor cells has recently emerged as a viable option for unmasking the underlying tumor heterogeneity. However extracting features from single cell genomic data in order to infer their evolutionary trajectory remains computationally challenging due to the extremely noisy and sparse nature of the data. Here we describe 'Dhaka', a variational autoencoder method which transforms single cell genomic data to a reduced dimension feature space that is more efficient in differentiating between (hidden) tumor subpopulations. Our method is general and can be applied to several different types of genomic data including copy number variation from scDNA-Seq and gene expression from scRNA-Seq experiments. We tested the method on synthetic and 6 single cell cancer datasets where the number of cells range from 250 to 6000 for each sample. Analysis of the resulting feature space revealed subpopulations of cells and their marker genes. The features are also able to infer the lineage and/or differentiation trajectory between cells greatly improving upon prior methods suggested for feature extraction and dimensionality reduction of such data.

Over a 6-year period, we studied 791 patients with multidrug-resistant typhoid fever, of whom 6 6 s individuals (84%) developed neuropsychiatric manifestations. These were: acute confusional state (73 %); myelitis ( 6 % ) ; cerebellitis ( I'%); parkinsonism (.r%); acute psychosis (0.6%); meningo-encephalitis (0.5%); encephalitis (0.25%); sensory motor polyneuropathy, polymyositis, acute schizophrenia and bizarre neurological syndromes (O.T 2% each). Severe parkinsonian rigidity and meningo-encephalitis are associated with significant morbidity but very low mortality (0.5%").

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BACKGROUND AND PURPOSEHydrogen sulphide (H2S) is an endogenous gasotransmitter. Although it has been shown to elicit responses in vascular and other smooth muscle preparations, a role for endogenously produced H2S in mediating airway tone has yet to be demonstrated. Therefore, the aim of this study was to determine whether H2S is produced within the airways and to determine the functional effect on airway tone. EXPERIMENTAL APPROACHSmall peripheral airways (<5 mm in diameter) from porcine lungs were set up in isolated tissue baths, pre-contracted with the muscarinic agonist carbachol, and then exposed to either the H2S donor sodium hydrosulphide (NaHS), or the precursor L-cysteine. H2S production from L-cysteine or 3-mercaptopyruvate in tissue homogenates was measured by the methylene blue assay. Expression of the H2S-synthesizing enzymes cystathionine b-synthase (CBS), cystathionine g lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (3-MST) were measured by Western blotting. KEY RESULTSNaHS caused a large relaxation of the airways, which was inhibited partially by pre-contraction with KCl or exposure to tetraethylammonium, but not glibenclamide, paxilline or 4-aminopyridine. L-cysteine also caused a relaxation of the airways which was inhibited by the CBS inhibitor aminooxyacetic acid. Tissue homogenates from airways exposed to L-cysteine or 3-mercaptopyruvate in vitro showed a significant production of H2S. Western blotting demonstrated immunoreactivity to CBS, CSE and 3-MST enzymes in the airways. CONCLUSIONS AND IMPLICATIONSThese data demonstrate that H2S can be produced endogenously within porcine airways causing relaxation. The mechanism of relaxation depends, in part, on K + channel activity. Abbreviations

Supplementary data are available at Bioinformatics online.

BackgroundThe prevalence of diabetes is increasing worldwide. It has been long known that increased rates of inflammatory diseases, such as obesity (OBS), hypertension (HT) and cardiovascular diseases (CVD) are highly associated with type 2 diabetes (T2D). T2D and/or OBS can develop independently, due to genetic, behavioral or lifestyle-related variables but both lead to oxidative stress generation. The underlying mechanisms by which theses complications arise and manifest together remain poorly understood. Protein-protein interactions regulate nearly every living process. Availability of high-throughput genomic data has enabled unprecedented views of gene and protein co-expression, co-regulations and interactions in cellular systems.MethodsThe present work, applied a systems biology approach to develop gene interaction network models, comprised of high throughput genomic and PPI data for T2D. The genes differentially regulated through T2D were 'mined' and their 'wirings' were studied to get a more complete understanding of the overall gene network topology and their role in disease progression.ResultsBy analyzing the genes related to T2D, HT and OBS, a highly regulated gene-disease integrated network model has been developed that provides useful functional linkages among groups of genes and thus addressing how different inflammatory diseases are connected and propagated at genetic level. Based on the investigations around the 'hubs' that provided more meaningful insights about the cross-talk within gene-disease networks in terms of disease phenotype association with oxidative stress and inflammation, a hypothetical co-regulation disease mechanism model been proposed. The results from this study revealed that the oxidative stress mediated regulation cascade is the common mechanistic link among the pathogenesis of T2D, HT and other inflammatory diseases such as OBS.ConclusionThe findings provide a novel comprehensive approach for understanding the pathogenesis of various co-associated chronic inflammatory diseases by combining the power of pathway analysis with gene regulatory network evaluation.

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