Toll-like receptor gene polymorphisms are associated with allergic rhinitis: a case control study

10.1186/1471-2350-13-66BMC Medical Genetics13-BMGM

Karakteristik Dan Hasil Uji Marshall Aspal Termodifikasi Dengan Karet Alam Terdepolimerisasi Sebagai Aditif

Aspal termodifikasi polimer merupakan salah satu jenis formula aspal dengan penambahan polimer untuk mendapatkan sifat perkerasan jalan yang lebih baik, yaitu mengurangi deformasi pada perkerasan, meningkatkan ketahanan terhadap retak dan kelekatan pada agregat. Penelitian ini telah dilakukan dengan menggunakan karet alam SIR 20 terdepolimerisasi sebagai aditif pada aspal dengan konsentrasi 3%, 5%, dan 7% b/b. Dari hasil pengujian penetrasi, titik lembek, titik nyala, dan % kehilangan berat setelah pemanasan didapatkan konsentrasi terbaik, yaitu 5%. Data hasil uji Marshall yang terdiri dari stabilitas, pelelehan, stabilitas sisa setelah perendaman, dan hasil bagi Marshall berturut-turut adalah 1135,46 kg, 3,47 mm, 91,78%, dan 327,22 kg/mm. Nilai tersebut telah memenuhi persyaratan SNI untuk aspal polimer (SNI 06-2489-91) dan memiliki sifat yang lebih baik daripada aspal tanpa penambahan aditif (kontrol). Diterima : 17 November 2014; Direvisi : 29 Januari 2015; Disetujui : 7 Mei 2015 How to Cite : Prastanto, H., Cifriadi, A., & Ramadhan, A. (2015). Karakteristik dan hasil uji marshall aspal termodifikasi dengan karet alam terdepolimerisasi sebagai aditif. Jurnal Penelitian Karet, 33(1), 75-82. Retrieved from http://ejournal.puslitkaret.co.id/index.php/jpk/article/view/17

Poor Reproducibility of Allergic Rhinitis SNP Associations

10.1371/journal.pone.0053975PLoS ONE81

Databehandling i planteforedling. Samnordisk Planteforedling.

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A haplotype in the inducible T-cell tyrosine kinase is a risk factor for seasonal allergic rhinitis

Background: Identification of disease-associated single nucleotide polymorphisms (SNPs) in seasonal allergic rhinitis (SAR) may be facilitated by focusing on genes in a disease-associated pathway. Objective: To search for SNPs in genes that belong to the T-cell receptor (TCR) pathway and that change in expression in allergen-challenged CD4+ cells from patients with SAR. Methods: CD4+ cells from patients with SAR were analysed with gene expression microarrays. Allele, genotype and haplotype frequencies were compared in 251 patients and 386 healthy controls. Results: Gene expression microarray analysis of allergen-challenged CD4+ cells from patients with SAR showed that 25 of 38 TCR pathway genes were differentially expressed. A total of 62 SNPs were analysed in eight of the 25 genes; ICOS, IL4, IL5, IL13, CSF2, CTLA4, the inducible T-cell tyrosine kinase (ITK) and CD3D. Significant chi-squared values were identified for several markers in the ITK kinase gene region. A total of five SNPs were nominally significant at the 5% level. Haplotype analysis of the five significant SNPs showed increased frequency of a haplotype that covered most of the coding part of ITK. The functional relevance of ITK was supported by analysis of an independent material, which showed increased expression of ITK in allergen-challenged CD4+ cells from patients, but not from controls. Conclusion: Analysis of SNPs in TCR pathway genes revealed that a haplotype that covers a major part of the coding sequence of ITK is a risk factor for SAR

Temperature Sensing Is Distributed throughout the Regulatory Network that Controls FLC Epigenetic Silencing in Vernalization

Many organisms need to respond to complex, noisy environmental signals for developmental decision making. Here, we dissect how Arabidopsis plants integrate widely fluctuating field temperatures over month-long timescales to progressively upregulate VERNALIZATION INSENSITIVE3 (VIN3) and silence FLOWERING LOCUS C (FLC), aligning flowering with spring. We develop a mathematical model for vernalization that operates on multiple timescales-long term (month), short term (day), and current (hour)-and is constrained by experimental data. Our analysis demonstrates that temperature sensing is not localized to specific nodes within the FLC network. Instead, temperature sensing is broadly distributed, with each thermosensory process responding to specific features of the plants' history of exposure to warm and cold. The model accurately predicts FLC silencing in new field data, allowing us to forecast FLC expression in changing climates. We suggest that distributed thermosensing may be a general property of thermoresponsive regulatory networks in complex natural environments.