Alkaline fuel cells: contemporary advancement and limitations

ZeTek Power recently introduced mass manufacturable and cost effective alkaline fuel cells on the market. Today's research is focused on further improvement both in terms of performance increase and cost reduction. This research is classically performed using small (4 cm²) experimental electrodes in the half-cell configuration. This allows the primary electrochemical losses in an anode or cathode to be determined independently. Additional performance losses occur when one integrates large electrodes into a module of 24 cells and in a stack comprised of many modules. By comparing the performance of half-cell experiments to that of modules, these losses can be distinguished and addressed. The information thus obtained, both for the small electrodes and in up-scaling is vital if one is to identify the key areas in which improvement is possible and where to focus future research. Furthermore, the identification of the losses in a module and system allows us to predict the final performance from half-cell measurements of a new laboratory scale experimental electrode.     

Kommentar II

Ohne Zusammenfassung     

集成产品开发

本文描述了集成产品开发（ＩＰＤ）,它是一种优化开发过程的集成的、整体的并以人为中心的方法。ＩＰＤ是一个框架、它必须根据具体企业的环境和战略定位来确定。ＩＰＤ描述了综合的各处观点,它们之间应是怎样的关系和应如何付之实施以最大减少开发费用。     

模块化机器的安全白皮书

SmartFactory~(KL)工作组1 "智能基础设施"专门处理模块化工业4.0生产设施的安全问题。其旨在提供一种工厂结构,通过模块化等手段确保其灵活性和可变性。本安型模块具有常规的功能安全性。但是,模块间依然存在依赖关系。在支持未知模块的模块化系统中,还需要一个新的安全体系结构。去年,该概念被整合到了工业4.0生产设施中,以实例证明该概念可在当今技术的基础上得以实施。在安全和机器通信的实施中,仅采用了一条单线共存。机器和机器模块可以在运行期间插入生产线或从生产线移除,而不会影响工厂的其它部分。必要的安全相关参数将根据此处导入的安全配置文件自动进行协商、配置和发布。要求如下文所述。     

Acute poisoning with L-triiodothyroinine, L-thyroxine and phendimetrazine bitartrate with suicidal intention]

It is reported on an acute intoxication after application of 8 mg L-thyroxin, 2 mg L-triiodotyronine (200 tablets Thyreotom) and 4.5 g hendimetrazine bitartrate (100 tablets Sedafamem). The clinical picture is described. An endangering of the vital function of the organism was not observed. The symptoms disappeared after 4 days. The pharmacological aspects of the intoxication after application of the hormone of the thyroid gland, its significance for the pathogenesis of the thyreotoxic crisis and its therapy are discussed     

A new deal for translation quality

Universal Access in the Information Society - Given the rich body of technical developments and a relatively long history of industrial use of Machine Translation (MT), it is astonishing of how...     

马来西亚电厂可靠性管理

YTL发电厂是马来西亚最大的独立电力生产厂家之一，拥有Paka和Pasir Gudang两个电站。电厂的运行和维护由YTL电力服务公司(YTLPS)来完成，它是西门子（占51%的股份）和YTL发电厂（占49%的股份）的合营公司。 YTLPS有大约180名雇员，其中20名在位于Kuala Lumpur的总部工作，主要负责处理商务、财经和管理方面的事务，在Pasir Gudang电站有65名，而在Paka电站有95名。他们中的大部分是马来西亚人，个别人员是来自西门子的管理人员。 两个电站的运行维护协议规定了，自最后一个联合循环机组移交后6年内，YTLPS将对电站的运…     

In Vitro Characterization of Renal Drug Transporter Activity in Kidney Cancer

The activity of drug transporters is central to the secretory function of the kidneys and a defining feature of renal proximal tubule epithelial cells (RPTECs). The expression, regulation, and function of these membrane-bound proteins is well understood under normal renal physiological conditions. However, the impact of drug transporters on the pathophysiology of kidney cancer is still elusive. In the present study, we employed different renal cell carcinoma (RCC) cell lines and a prototypical non-malignant RPTEC cell line to characterize the activity, expression, and potential regulatory mechanisms of relevant renal drug transporters in RCC in vitro. An analysis of the uptake and efflux activity, the expression of drug transporters, and the evaluation of cisplatin cytotoxicity under the effects of methylation or epidermal growth factor receptor (EGFR) inhibition showed that the RCC cells retained substantial drug transport activity. In RCC cells, P-glycoprotein was localized in the nucleus and its pharmacological inhibition enhanced cisplatin toxicity in non-malignant RPTECs. On the other hand, methylation inhibition enhanced cisplatin toxicity by upregulating the organic cation uptake activity in RCC cells. Differential effects of methylation and EGFR were observed in transporter expression, showing regulatory heterogeneity in these cells. Interestingly, the non-malignant RPTEC cell line that was used lacked the machinery responsible for organic cation transport, which reiterates the functional losses that renal cells undergo in vitro.     

Identification of the Regulatory Targets of miR-3687 and miR-4417 in Prostate Cancer Cells Using a Proteomics Approach

MicroRNAs (miRNA) are ubiquitous non-coding RNAs that have a prominent role in cellular regulation. The expression of many miRNAs is often found deregulated in prostate cancer (PCa) and castration-resistant prostate cancer (CRPC). Although their expression can be associated with PCa and CRPC, their functions and regulatory activity in cancer development are poorly understood. In this study, we used different proteomics tools to analyze the activity of hsa-miR-3687-3p (miR-3687) and hsa-miR-4417-3p (miR-4417), two miRNAs upregulated in CRPC. PCa and CRPC cell lines were transfected with miR-3687 or miR-4417 to overexpress the miRNAs. Cell lysates were analyzed using 2D gel electrophoresis and proteins were subsequently identified using mass spectrometry (Maldi-MS/MS). A whole cell lysate, without 2D-gel separation, was analyzed by ESI-MS/MS. The expression of deregulated proteins found across both methods was further investigated using Western blotting. Gene ontology and cellular process network analysis determined that miR-3687 and miR-4417 are involved in diverse regulatory mechanisms that support the CRPC phenotype, including metabolism and inflammation. Moreover, both miRNAs are associated with extracellular vesicles, which point toward a secretory mechanism. The tumor protein D52 isoform 1 (TD52-IF1), which regulates neuroendocrine trans-differentiation, was found to be substantially deregulated in androgen-insensitive cells by both miR-3687 and miR-4417. These findings show that these miRNAs potentially support the CRPC by truncating the TD52-IF1 expression after the onset of androgen resistance.