Copper Iodide on Spacer Fabrics as Textile Thermoelectric Device for Energy Generation.

The integration of electronic functionalities into textiles for use as wearable sensors, energy harvesters, or coolers has become increasingly important in recent years. A special focus is on efficient thermoelectric materials. Copper iodide as a p-type thermoelectrically active, nontoxic material is attractive for energy harvesting and energy generation because of its transparency and possible high-power factor. The deposition of CuI on polyester spacer fabrics by wet chemical processes represents a great potential for use in textile industry for example as flexible thermoelectric energy generators in the leisure or industrial sector as well as in medical technologies. The deposited material on polyester yarn is investigated by electron microscopy, x-ray diffraction and by thermoelectric measurements. The Seebeck coefficient was observed between 112 and 153 µV/K in a temperature range between 30 °C and 90 °C. It is demonstrated that the maximum output power reached 99 nW at temperature difference of 65.5 K with respect to room temperature for a single textile element. However, several elements can be connected in series and the output power can be linear upscaled. Thus, CuI coated on 3D spacer fabrics can be attractive to fabricate thermoelectric devices especially in the lower temperature range for textile medical or leisure applications.

Actual Five-year Survival After Upfront Resection for Pancreatic Ductal Adenocarcinoma: Who Beats the Odds?

OBJECTIVE: To determine actual five-year survival (5YS) rates associated with a strategy of upfront surgery and adjuvant therapy in pancreatic ductal adenocarcinoma (PDAC). BACKGROUND: The rate of actual 5YS in PDAC remains controversial. Available data is restricted to cohorts acquired over several decades and series of resection after patient selection by neoadjuvant therapy. METHODS: All patients undergoing upfront resection for resectable and borderline-resectable PDAC from 10/2001 to 12/2011 were identified from a prospective database. Actual overall survival was assessed after a follow-up of at least 5 years. Uni- and multivariable logistic regression analyses were performed. RESULTS: Median survival of 937 patients was 22.1 months. The actual 5YS rate was 17.0% (n = 159) including 89 (9.5%) patients without evidence of disease >5 years after resection. 5YS rates in patients with or without adjuvanttherapy were 18.8% vs. 12.2%, respectively. Tumorgrading, number of positive lymph nodes, a context of intraductal papillary mucinous neoplasia, and vascular resections were independently associated with 5YS. Patient-related parameters and CA 19-9 levels were associated with observed survival up to 3 years, but lost relevance thereafter. The extent of lymph node involvement was the strongest predictor of 5YS. Patients with pN0R0 had a 5YS rate of 38.2%. in patients with exclusively favorable factors the observed 5YS rate was above 50%. CONCLUSIONS: This is the largest series of long-term survivors with histologically confirmed PDAC. With upfront resection and adjuvant therapy an actual overall 5YS rate of 18.8% can be expected. in favorable subgroups actual 5YS is above 50%.

Antisense transcription-dependent chromatin signature modulates sense transcript dynamics.

Antisense transcription is widespread in genomes. Despite large differences in gene size and architecture, we find that yeast and human genes share a unique, antisense transcription-associated chromatin signature. We asked whether this signature is related to a biological function for antisense transcription. Using quantitative RNA-FISH, we observed changes in sense transcript distributions in nuclei and cytoplasm as antisense transcript levels were altered. To determine the mechanistic differences underlying these distributions, we developed a mathematical framework describing transcription from initiation to transcript degradation. At GAL1, high levels of antisense transcription alter sense transcription dynamics, reducing rates of transcript production and processing, while increasing transcript stability. This relationship with transcript stability is also observed as a genome-wide association. Establishing the antisense transcription-associated chromatin signature through disruption of the Set3C histone deacetylase activity is sufficient to similarly change these rates even in the absence of antisense transcription. Thus, antisense transcription alters sense transcription dynamics in a chromatin-dependent manner.

New insights in endogenous modulation of ligand-gated ion channels: histamine is an inverse agonist at strychnine sensitive glycine receptors.

Histamine is involved in many physiological functions in the periphery and is an important neurotransmitter in the brain. It acts on metabotropic H1-H4 receptors mediating vasodilatation, bronchoconstriction and stimulation of gastric acid secretion. In the brain histamine is produced by neurons in the tuberomamillary nucleus (TMN), which controls arousal. Histamine is also a positive modulator of the inhibitory Cys-loop ligand-gated ion channel GABAA. We investigated now its effect on the second member of inhibitory Cys-loop ligand-gated ion channels, the strychnine sensitive glycine receptor. We expressed different human and rat glycine receptor subunits in Xenopus laevis oocytes and characterized the effect of histamine using the two electrode voltage clamp technique. Furthermore we investigated native glycine receptors in hypothalamic neurons using the patch-clamp technique. Histamine inhibited α1ß glycine receptors with an IC50 of 5.2±0.3 mM. In presence of 10 mM histamine the glycine dose-response curve was shifted, increasing the EC50 for glycine from 25.5±1.4 µM to 42.4±2.3 µM. In addition, histamine blocked the spontaneous activity of RNA-edited α3ß glycine receptors. Histamine inhibited glycine receptors expressed in hypothalamic TMN neurons with an IC50 of 4.6±0.3 mM. Our results give strong evidence that histamine is acting on the same binding site as glycine, being an inverse agonist that competitively antagonizes glycine receptors. Thus, we revealed histamine as an endogenous modulator of glycine receptors.