Digital Advertising and News: Who Advertises on News Sites and How Much Those Ads Are Targeted

Analyzes trends in advertising in twenty-two news operations, including shifts to digital advertising, use of consumer data to target ads, types of ads, and industries represented among advertisers by media type

Resting-State Functional Connectivity in Late-Life Depression: Higher Global Connectivity and More Long Distance Connections

Functional magnetic resonance imaging recordings in the resting-state (RS) from the human brain are characterized by spontaneous low-frequency fluctuations in the blood oxygenation level dependent signal that reveal functional connectivity (FC) via their spatial synchronicity. This RS study applied network analysis to compare FC between late-life depression (LLD) patients and control subjects. Raw cross-correlation matrices (CM) for LLD were characterized by higher FC. We analyzed the small-world (SW) and modular organization of these networks consisting of 110 nodes each as well as the connectivity patterns of individual nodes of the basal ganglia. Topological network measures showed no significant differences between groups. The composition of top hubs was similar between LLD and control subjects, however in the LLD group posterior medial-parietal regions were more highly connected compared to controls. In LLD, a number of brain regions showed connections with more distant neighbors leading to an increase of the average Euclidean distance between connected regions compared to controls. In addition, right caudate nucleus connectivity was more diffuse in LLD. In summary, LLD was associated with overall increased FC strength and changes in the average distance between connected nodes, but did not lead to global changes in SW or modular organization

Resting-state functional magnetic resonance imaging in late-life depression and dementia

The aim of this research was to use novel functional imaging approaches to investigate connectivity between key brain regions affected in late-life depression (LLD), Alzheimer‟s disease (AD) and dementia with Lewy bodies (DLB). Using functional magnetic resonance imaging (fMRI), spontaneous low-frequency fluctuations (SLFs) in the blood oxygenation level dependent (BOLD) signal were measured at rest. SLFs represent synchronisation of neuronal activity; therefore differences between subjects reflect differences in underlying networks. Methods The first resting-state study investigated connectivity in LLD and involved 33 subjects aged 65 years and over; 17 control and 16 LLD subjects. It was planned to apply this methodology in the dementia study also. However, a global synchronicity pattern was evident in some subjects, which had not previously been seen in the LLD study. Methods were investigated to correct for these spurious fluctuations, thought to be unrelated to neuronal activity (e.g. physiological artefacts), meaning connectivity of neuronal origin only was investigated. The second study investigated connectivity in 47 subjects aged 60 years and over; 16 control, 16 AD and 15 DLB subjects. Additional pre-processing steps were used to remove non-neuronal fluctuations, informed by the previous study. All subjects were scanned using a 3 Tesla MRI System. Functional connectivity was measured by extracting the mean BOLD signal time-series from seed regions in the brain and cross-correlating with all other brain voxels using the FMRIB Software Library (FSL) tools. Results In the LLD study, control subjects showed frontal connectivity with the head of caudate nucleus, whereas the LLD group showed a more widespread pattern of connectivity. LLD subjects showed significantly greater connectivity than controls between the bilateral caudate and a number of brain regions, whereas controls showed no brain regions of greater connectivity than LLD subjects. Pre-processing methods, to correct for non-neuronal fluctuations, were found to remove global synchronicity and improve data accuracy. In the second study, AD and DLB subjects showed significantly greater functional connectivity with a number of seed regions compared to the control group. No brain regions showed significantly greater connectivity in control compared to AD or DLB subjects. Additionally, specific seed regions showed greater connectivity in AD compared to DLB, and vice versa. Conclusions This study reported abnormalities in connectivity in LLD, AD and DLB. The potential outcome of these findings is that they will inform greater understanding of the neurobiology of these disorders and in turn aid in early diagnosis and in the development of specific treatments to target the abnormally functioning brain regions.EThOS - Electronic Theses Online ServiceMedical Research Council : Alzheimer's Research Trust : North East DeNDRoN Network : Biomedical Research CentreGBUnited Kingdo

Rekonstruksi Fungsi Ruang pada Bangunan Kantor Pos Sebagai Langkah Optimalisasi Aset

Aset merupakan sumber daya yang dapat dikendalikan oleh perusahaan, negara, maupun individu dengan nilai ekonomi yang dapat menunjung berjalannya aktivitas sebuah perusahaan hingga mampu memberikan manfaat dan keuntungan di masa yang akan datang. Salah satu jenis aset yang dimiliki perusahaan adalah aset berwujud seperti gedung, tanah, barang dagang, mesin, dan surat berharga. PT Pos Indonesia (Persero) sebagai salah satu perusahaan BUMN yang bergerak di bidang pelayanan pos dan jasa keuangan, memiliki banyak sekali aset yang tersebar di seluruh Indonesia. Namun, akibat perkembangan teknologi seperti email dan pesan singkat, serta penghapusan sistem monopoli pelayanan pos di Indonesia, jumlah pengguna pos semakin mengalami penurunan, sehingga kebutuhan ruang di kantor pos pun menjadi semakin berkurang. Oleh karena itu, untuk memaksimalkan potensi ruang yang ada di kantor pos, perlu dilakukan optimalisasi supaya aset-aset tersebut tetap optimal. Optimalisasi ini akan berdampak kepada perubahan ataupun penambahan fungsi aset itu sendiri. Untuk melakukan perubahan/penambahan fungsi ruang tersebut perlu dibuatkan skema/model perubahan fungsi ruang sebagai acuan bagi para pengambil keputusan atas aset-aset yang akan diubah/ditambah fungsinya. Metode yang digunakan dalam penelitian ini adalah metode kualitatif deskriptif dengan teknik pengumpulan data berupa survey dan wawancara dengan pejabat terkait, kajian pustaka, dan hasil analisis data yang sudah pernah ada. Dari hasil penelitian ini, dibuatlah “Skema Optimalisasi Aset dan Perubahan Fungsi Ruang di PT Pos Indonesia (Persero)”, dimana skema ini berpengaruh besar terhadap perubahan aksesibilitas, perubahan tata ruang, perubahan tampak, perubahan peralatan kerja, perubahan signage, serta perubahan fasilitas dan sarananya. Kata kunci : aset, fungsi, gedung, optimalisasi, perubahan, ruang./ Assets are resources that can be controlled by companies, countries, or individuals with economic value and that can support the activities of a company so that it is able to provide benefits and profits in the future. One type of asset owned by the company is tangible, such as buildings, land, merchandise, machinery, and securities. PT Pos Indonesia (Persero), as a state-owned company engaged in postal services and financial services, has a lot of assets spread throughout Indonesia. However, due to technological developments such as e-mail and short messages, as well as the abolition of the monopoly system for postal services in Indonesia, the number of postal users has decreased, so that the need for space in the post office has also decreased. Therefore, in order to maximize the potential of the space in the post office, it is necessary to optimize it so that these assets remain optimal. This optimization will have an impact on changes or additions to the function of the asset itself. In order to change or add to the function of the space, it is necessary to make a scheme or model for changing the function of the space as a reference for decision-makers on the assets whose functions will be changed or added. The method used in this research is a descriptive qualitative method with data collection techniques in the form of surveys and interviews with relevant officials, a literature review, and the results of data analysis that has already existed. From the results of this study, a "Scheme for Optimization of Assets and Changes in Spatial Functions at PT Pos Indonesia (Persero)" was created, where this scheme has a major influence on changes in accessibility, changes in spatial planning, changes in appearance, changes in work equipment, changes in signage, and changes in facilities and amenities. Keywords: asset, function, building, optimization, change, and space

Pengaruh Ruang Terbuka Hijau Terhadap Psikologis Masyarakat di Kota Bekasi Khususnya Kecamatan Jatiasih

In the 21 st century, mental health disorders such as depression is the most important challenges in urban area. Many residents in urban areas are more at risk of developing depression due to various factors such as lifestyle and unfavorable urban conditions, so we need a space that able to prevent and reduce mental health disorders for urban residents. The aims of this study to examine how the effect of the availability of green open spaces in helping to reduce the level of depression in urban areas. Research methodology that used in this study is descriptive qualitative method, that collects primary by online survey via google docs regarding the Geriatric Depression Scale (GDS), and then continued with an online survey in “The Effect of Green Open Space for Society’s Psychology Communities in Urban”, as well as conducting a survey of several open space in Jatiasih District, and conducting a review of existing literature studies. The result of the analysis that has been carried out, that Green Open Space has influence on psychology, especially to help reduce depression in urban areas. Keywords: green open space; psychology; depression; healing architecture; healing garde

Allergic airway inflammation induces upregulation of the expression of IL-23R by macrophages and not in CD3 + T cells and CD11c+F4/80- dendritic cells of the lung

Interleukin 23 and the interleukin 23 receptor (IL-23-IL23R) are described as the major enhancing factors for Interleukin 17 (IL-17) in allergic airway infammation. IL-17 is considered to induce neutrophilic infammation in the lung, which is often observed in severe, steroid-resistant asthma-phenotypes. For that reason, understanding of IL-23 and IL-17 axis is very important for future therapy strategies, targeting neutrophil pathway of bronchial asthma. This study aimed to investigate the distribution and expression of IL-23R under physiological and infammatory conditions. Therefore, a house dust mite (HDM) model of allergic airway infammation was performed by treating mice with HDM intranasally. Immunofuorescence staining with panel of antibodies was performed in lung tissues to examine the macrophage, dendritic cell, and T cell subpopulations. The allergic airway infammation was quantifed by histopathological analysis, ELISA measurements, and airway function. HDM-treated mice exhibited a signifcant allergic airway infammation including higher amounts of NE+ cells in lung parenchyma. We found only a small amount of IL-23R positives, out of total CD3+T cells, and no upregulation in HDMtreated animals. In contrast, the populations of F4/80+ macrophages and CD11c+F4/80− dendritic cells (DCs) with IL-23R expression were found to be higher. But HDM treatment leads to a signifcant increase of IL-23R+ macrophages, only. IL23R was expressed by every examined macrophage subpopulation, whereas only Mϕ1 and hybrids between Mϕ1 and Mϕ2 phenotype and not Mϕ2 were found to upregulate IL-23R. Co-localization of IL-23R and IL-17 was only observed in F4/80+ macrophages, suggesting F4/80+ macrophages express IL-23R along with IL-17 in lung tissue. The study revealed that macrophages involving the IL-23 and IL-17 pathway may provide a potential interesting therapeutic target in neutrophilic bronchial asthma

3D culture models of normal and malignant breast epithelial cells

This report describes a robust and generalized method for the clustering of various human breast cell lines in 3D and describes the preparation of cellular extracts from these cultures for molecular analysis

P2X7 Receptor-Dependent microRNA Expression Profile in the Brain Following Status Epilepticus in Mice

The ionotropic ATP-gated P2X7 receptor is an important contributor to inflammatory signaling cascadesviathe release of Interleukin-1 beta, as well as having roles in cell death, neuronal plasticity and the release of neurotransmitters. Accordingly, there is interest in targeting the P2X7 receptor for the treatment of epilepsy. However, the signaling pathways downstream of P2X7 receptor activation remain incompletely understood. Notably, recent studies showed that P2X7 receptor expression is controlled, in part, by microRNAs (miRNAs). Here, we explored P2X7 receptor-dependent microRNA expression by comparing microRNA expression profiles of wild-type (wt) and P2X7 receptor knockout mice before and after status epilepticus. Genome-wide microRNA profiling was performed using hippocampi from wt and P2X7 receptor knockout mice following status epilepticus induced by intra-amygdala kainic acid. This revealed that the genetic deletion of the P2X7 receptor results in distinct patterns of microRNA expression. Specifically, we found that in vehicle-injected control mice, the lack of the P2X7 receptor resulted in the up-regulation of 50 microRNAs and down-regulation of 35 microRNAs. Post-status epilepticus, P2X7 receptor deficiency led to the up-regulation of 44 microRNAs while 13 microRNAs were down-regulated. Moreover, there was only limited overlap among identified P2X7 receptor-dependent microRNAs between control conditions and post-status epilepticus, suggesting that the P2X7 receptor regulates the expression of different microRNAs during normal physiology and pathology. Bioinformatic analysis revealed that genes targeted by P2X7 receptor-dependent microRNAs were particularly overrepresented in pathways involved in intracellular signaling, inflammation, and cell death;processes that have been repeatedly associated with P2X7 receptor activation. Moreover, whereas genes involved in signaling pathways and inflammation were common among up- and down-regulated P2X7 receptor-dependent microRNAs during physiological and pathological conditions, genes associated with cell death seemed to be restricted to up-regulated microRNAs during both physiological conditions and post-status epilepticus. Taken together, our results demonstrate that the P2X7 receptor impacts on the expression profile of microRNAs in the brain, thereby possibly contributing to both the maintenance of normal cellular homeostasis and pathological processes

Dampak Ekologis Akibat Peningkatan Urbanisasi di Sepanjang Daerah Aliran Sungai Cikapundung Kota Bandung

Melonjaknya angka urbanisasi ke wilayah perkotaan mengakibatkan semakin tingginya permintaan akan kebutuhan tempat tinggal di wilayah perkotaan. Hal itu menyebabkan semakin tingginya harga lahan maupun harga rumah di wilayah perkotaan. Akhirnya, banyak pendatang yang membangun rumah petak di sepanjang Daerah Aliran Sungai dan akhirnya berubah menjadi Kawasan Permukiman Kumuh. Hal ini terjadi di sepanjang Daerah Aliran Sungai Cikapundung, di Kelurahan Tamansari Kecamatan Bandung Wetan, Jawa Barat. Tujuan penelitian ini adalah untuk mengetahui dampak ekologis apa saja yang timbul akibat meningkatnya urbanisasi di sepanjang Daerah Aliran Sungai Cikapundung. Penelitian ini menggunakan pendekatan kualitatif dengan metode induktif. Dari hasil analisis yang telah dilakukan, penulis dapat menyimpulkan bahwa dampak ekologis yang timbul akibat meningkatnya urbanisasi di sepanjang Daerah Aliran Sungai Cikapundung adalah kondisi drainase yang sangat terbatas, fasilitas MCK seadanya, kesulitan mendapatkan air bersih, pencemaran sungai akibat pembuangan air limbah, pencahayaan dan sirkulasi yang buruk akibat tidak adanya jarak antar bangunan membuat rumah menjadi tidak sehat. Kata-kunci : Cikapundung, dampak ekologis, permukiman kumuh, urbanisas

Spatiotemporal progression of ubiquitin-proteasome system inhibition after status epilepticus suggests protective adaptation against hippocampal injury.

BACKGROUND: The ubiquitin-proteasome-system (UPS) is the major intracellular pathway leading to the degradation of unwanted and/or misfolded soluble proteins. This includes proteins regulating cellular survival, synaptic plasticity and neurotransmitter signaling; processes controlling excitability thresholds that are altered by epileptogenic insults. Dysfunction of the UPS has been reported to occur in a brain region- and cell-specific manner and contribute to disease progression in acute and chronic brain diseases. Prolonged seizures, status epilepticus, may alter UPS function but there has been no systematic attempt to map when and where this occurs in vivo or to determine the consequences of proteasome inhibition on seizure-induced brain injury. METHOD: To determine whether seizures lead to an impairment of the UPS, we used a mouse model of status epilepticus whereby seizures are triggered by an intra-amygdala injection of kainic acid. Status epilepticus in this model causes cell death in selected brain areas, in particular the ipsilateral CA3 subfield of the hippocampus, and the development of epilepsy after a short latent period. To monitor seizure-induced dysfunction of the UPS we used a UPS inhibition reporter mouse expressing the ubiquitin fusion degradation substrate ubiquitin(G76V)-green fluorescent protein. Treatment with the specific proteasome inhibitor epoxomicin was used to establish the impact of proteasome inhibition on seizure-induced pathology. RESULTS AND CONCLUSIONS: Our studies show that status epilepticus induced by intra-amygdala kainic acid causes select spatio-temporal UPS inhibition which is most evident in damage-resistant regions of the hippocampus, including CA1 pyramidal and dentate granule neurons then appears later in astrocytes. In support of this exerting a beneficial effect, injection of mice with the proteasome inhibitor epoxomicin protected the normally vulnerable hippocampal CA3 subfield from seizure-induced neuronal death in the model. These studies reveal brain region- and cell-specific UPS impairment occurs after seizures and suggest UPS inhibition can protect against seizure-induced brain damage. Identifying networks or pathways regulated through the proteasome after seizures may yield novel target genes for the treatment of seizure-induced cell death and possibly epilepsy