A parametric study of the acoustic properties of thermal cladding systems

Thermal cladding systems have developed and modernised since the first systems were implemented, and predictions of single figure sound insulation improvement, ΔRW, based on the natural frequency, f0, of the spring-mass covering may no longer be reliable. To identify aspects of the compound acoustic behaviour due to multiple power flow paths of the thermal insulating system, a statistical energy analysis (SEA) based prediction model was developed. A simplified calculation of sound insulation improvement, ΔR, is described, allowing the high frequency (f > f0) behaviour of thermal cladding systems to be predicted. A parametric study in which the impact of different construction materials in the model is discussed; the damping constants, elastic properties of the interlayer and fixings, number of fixings, thickness and material properties (including bending stiffness) of the weatherproof outer layer and the heavyweight wall are assessed. While agreement within 4.0 dB (mean absolute differences) between calculated and measured results for thick render (≥8.0 mm) and curtain wall systems can be obtained at high frequencies (f > f0) using the simplified methodology, this approach was not successful at predicting single figure values. This is because single figure values are weighted towards the low frequencies. Correlation of calculated f0 with measured ΔRW is slightly improved (r.m.s. differences of 2.62 compared with 3.21 using the f0 calculation methodology in EN ISO12354 Annex D) when a modified method to calculate the combined stiffness is used. To improve predictions further, a methodology must be developed to obtain the transfer function, Ytr, used to calculate non-resonant coupling loss factor due to the spring-mass resonance of thermal cladding on the heavyweight wall. The mobility of the connections, Yc, should also be accurately characterised to ensure accurate predictions at high frequencies

Renovation and innovation using thermal insulation lining systems - Acoustic performance

Retrofit and design of thermal cladding systems provide an opportunity to improve the acoustic properties of a building. However, the complexity of the calculation process to predict sound insulation improvement may inhibit rather than encourage novelty and innovation. This paper investigates whether it is realistic to calculate the frequency dependant sound insulation improvement due to modern thermal insulation wall lining systems with just a few input parameters. The calculation procedure is tested using measured results for one external thermal insulation composite system (ETICS) and three curtain wall systems. The accuracy of the procedure is examined using three factors: (1) precision of the measurement, (2) variation of some of the basic parameters of the calculation procedure, and (3) an estimation of the standard error of the calculation. For the ETICS, agreement within <6.0 dB is achieved across much of the frequency range and the trend of the extended dip due to the spring-mass action of the panel is corroborated. The case for using this methodology on curtain wall systems is adequate, however, the trend of calculated results is mostly outside of the 95% confidence limits of the measured results. Possible reasons for this include lack of airtightness of all curtain wall systems and additional transmission due to radiation into and out of the cavity, neither of which are included in the model. The assumption of radiating points or lines, rather than a radiating surface involving the whole panel, gave better agreement at high frequencies for three of the four measured systems (f ≥ 2500 Hz)

Epidermal-specific deletion of CD44 reveals a function in keratinocytes in response to mechanical stress

CD44, a large family of transmembrane glycoproteins, plays decisive roles in physiological and pathological conditions. CD44 isoforms are involved in several signaling pathways essential for life such as growth factor-induced signaling by EGF, HGF or VEGF. CD44 is also the main hyaluronan (HA) receptor and as such is involved in HA-dependent processes. To allow a genetic dissection of CD44 functions in homeostasis and disease, we generated a Cd44 floxed allele allowing tissue- and time-specific inactivation of all CD44 isoforms in vivo. As a proof of principle, we inactivated Cd44 in the skin epidermis using the K14Cre allele. Although the skin of such Cd44Δker mutants appeared morphologically normal, epidermal stiffness was reduced, wound healing delayed and TPA induced epidermal thickening decreased. These phenotypes might be caused by cell autonomous defects in differentiation and HA production as well as impaired adhesion and migration on HA by Cd44Δker keratinocytes. These findings support the usefulness of the conditional Cd44 allele in unraveling essential physiological and pathological functions of CD44 isoforms.We are grateful to Professor Ben Wielockx (DIPP,Dresden, Germany) for help with the in vivo wound healing assay, to Professors Pierre Chambon and Daniel Metzger (IGBMC, Strasbourg, France) for the kind gift of the K14 Cre mice. We thank Karin Müller-Decker (DKFZ, Heidelberg, Germany) and Peter Angel (DKFZ) for their help with the TPA induction experiments. We are extremely grateful to the animal facility of our institute (ITG, KIT) and especially to Selma Huber for their help with animal experiments. We also want to thank R. Saffrich. (Department of Medicine V (Hematology, Oncology & Rheumatology, University of Heidelberg, Heidelberg) for technical assistance in time-lapse imaging. We are grateful to Julia Gutjahr (Laboratory for Immunological and Molecular Cancer Research, Salzburg, Austria) for her help with the immunohistological pictures. We also thank Ana Guío-Carrión (Spanish National Cancer Centre, Genes Development and Disease Group, Cancer Cell Biology Programme, Madrid, Spain) for technical assistance. MT and ASB thank the German Research Foundation (Collaborative Research Center, CRC 873 B07) for support. ASB thank C. Monzel (Laboratoire Physico-Chimie, Institut Curie, Paris, France) for assistance in data analysis. iCeMS is supported by World Premier International Research Center Initiative (WPI), MEXT (Japan). EFW and LB are supported by grants from the Spanish Ministry of Economy (BFU2012 – 40230, and SAF2015 – 70857, co-funded by the ERDF-EU)S

Common variants in myocardial ion channel genes modify the QT interval in the general population: Results from the KORA study.

Altered myocardial repolarization is one of the important substrates of ventricular tachycardia and fibrillation. The influence of rare gene variants on repolarization is evident in familial long QT syndrome. To investigate the influence of common gene variants on the QT interval we performed a linkage disequilibrium based SNP association study of four candidate genes. Using a two-step design we analyzed 174 SNPs from the KCNQ1, KCNH2, KCNE1, and KCNE2 genes in 689 individuals from the population-based KORA study and 14 SNPs with results suggestive of association in a confirmatory sample of 3277 individuals from the same survey. We detected association to a gene variant in intron 1 of the KCNQ1 gene (rs757092, +1.7 ms/allele, P=0.0002) and observed weaker association to a variant upstream of the KCNE1 gene (rs727957, +1.2 ms/allele, P=0.0051). In addition we detected association to two SNPs in the KCNH2 gene, the previously described K897T variant (rs1805123, &minus;1.9 ms/allele, P=0.0006) and a gene variant that tags a different haplotype in the same block (rs3815459, +1.7 ms/allele, P=0.0004). The analysis of additive effects by an allelic score explained a 10.5 ms difference in corrected QT interval length between extreme score groups and 0.95% of trait variance (P&lt;0.00005). These results confirm previous heritability studies indicating that repolarization is a complex trait with a significant heritable component and demonstrate that high-resolution SNP-mapping in large population samples can detect and fine map quantitative trait loci even if locus specific heritabilities are small

The non-synonymous coding IKr-channel variant KCNH2-K897T is associated with atrial fibrillation: Results from a systematic candidate gene-based analysis of KCNH2 (HERG).

AIMS: Atrial fibrillation (AF) is the most frequent arrhythmia in humans. Rare familial forms exist. Recent evidence indicates a genetic susceptibility to common forms of AF. The alpha-subunit of the myocardial I(Kr)-channel, encoded by the KCNH2 gene, is crucial to ventricular and atrial repolarization. Patients with mutations in KCNH2 present with higher incidence of AF. Common variants in KCNH2 have been shown to modify ventricular repolarization. We intended to investigate, whether such variants may also modulate atrial repolarization and predispose to AF. METHODS AND RESULTS: In a two-stage association study we analysed 1207 AF-cases and 2475 controls. In stage I 40 tagSNPs (single nucleotide polymorphisms) from the KCNH2 genomic region were genotyped in 671 AF-cases and 694 controls. Of five associated variants, the common K897-allele of the KCNH2-K897T variant was replicated in n = 536 independent AF cases and n = 1781 controls in stage II [overall odds ratio 1.25, 95% confidence interval 1.11-1.41, P = 0.00033]. This association remained significant after adjustment for gender and age. CONCLUSION: We report a genetic association finding including positive replication between the K897-allele and higher incidence of AF. This provides a molecular correlate for complex genetic predispositions to AF. The consequences of the K897T variant at the atrial level will require further functional investigations

Epidermal-specific deletion of CD44 reveals a function in keratinocytes in response to mechanical stress

CD44, a large family of transmembrane glycoproteins, plays decisive roles in physiological and pathological conditions. CD44 isoforms are involved in several signaling pathways essential for life such as growth factor-induced signaling by EGF, HGF or VEGF. CD44 is also the main hyaluronan (HA) receptor and as such is involved in HA-dependent processes. To allow a genetic dissection of CD44 functions in homeostasis and disease, we generated a Cd44 floxed allele allowing tissue- and time-specific inactivation of all CD44 isoforms in vivo. As a proof of principle, we inactivated Cd44 in the skin epidermis using the K14Cre allele. Although the skin of such Cd44Δker mutants appeared morphologically normal, epidermal stiffness was reduced, wound healing delayed and TPA induced epidermal thickening decreased. These phenotypes might be caused by cell autonomous defects in differentiation and HA production as well as impaired adhesion and migration on HA by Cd44Δker keratinocytes. These findings support the usefulness of the conditional Cd44 allele in unraveling essential physiological and pathological functions of CD44 isoforms