Real-time ultra-wideband video streaming in long-reach passive optical networks with wireless radiation in the 10 and 60 GHz Bands

This paper was published in Chinese Optics Letters and is made available as an electronic reprint with the permission of OSA. The paper can be found at the following URL on the OSA website: http://www.opticsinfobase.org/col/abstract.cfm?URI=col-11-10-100605 . Systematic or multiple reproduction or distribution to multiple locations via electronic or other means is prohibited and is subject to penalties under law.[EN] Real-time video streaming using ultra-wideband (UWB) technology is experimentally demonstrated along long-reach passive optical networks (LR-PONs) with different wired and wireless reaches. Experimental tests using external and direct modulation with UWB wireless radiation in the 10- and 60-GHz bands are performed. An ultra-bendable fiber is also considered for a last-mile distribution. The video quality at the output of the optical fiber infrastructure of the LR-PON is assessed using the error vector magnitude (EVM), and the link quality indicator (LQI) is used as a figure of merit after wireless radiation. An EVM below -17 dB is achieved for both externally and directly modulated LR-PONs comprising up to 125 km of optical fiber. EVM improvement is observed for longer LR-PONs when directly modulated lasers (DMLs) are used because of the amplitude gain provided by the combined effect of dispersion and DML's chirp. Compared with optical back-to-back operation, the LQI level degrades to the maximum around 20% for LR-PONs ranging between 75 and 125 km of fiber reach and with a wireless coverage of 2 m in the 10-GHz UWB band. The same level of LQI degradation is observed using the 60-GHz UWB band with a LR-PON integrating 101 km of access network, a last-mile distribution using ultra-bendable fiber, and a 5.2-m wireless link.This work was supported by the Fundação para a Ciˆencia e a Tecnologia from Portugal under projects PEst-OE/EEI/LA0008/2013 and TURBO-PTDC/EEATEL/ 104358/2008 and also by the European FIVER-FP7-ICT-2009-4-249142 project.Alves, TMF.; Morant Perez, M.; Cartaxo, AVT.; Llorente Sáez, R.; Cluzeaud, P.; Sambaraju, R. (2013). Real-time ultra-wideband video streaming in long-reach passive optical networks with wireless radiation in the 10 and 60 GHz Bands. Chinese Optics Letters. 11(10):1006051-1006056. https://doi.org/10.3788/col201311.100605S10060511006056111

Localization and induction by dehydration of ClC-K chloride channels in the rat kidney

We investigate the intrarenal expression of two recently cloned chloride channels, rClC-K1 and rClC-K2, by reverse transcriptase-polymerase chain reaction on single microdissected tubules from the rat kidney and by immunohistochemistry using a polyclonal antibody that recognizes both highly homologous channels. Both rClC-K1 and rClC-K2 mRNAs were detected in outer medullary late proximal tubules (S3), papillary ascending thin limbs (ATL), and outer medullary (MTAL) and cortical (CTAL) thick ascending limbs, distal tubules (DCT), and cortical, outer medullary, and inner medullary collecting ducts. Indirect immunofluorescence studies demonstrated that the rClC-K proteins were restricted to the basolateral membranes from ATL, DCT, and collecting ducts cells, whereas CTAL and MTAL exhibited a more diffuse basal staining. When rats were dehydrated, a condition which increased the expression of rClC-K1 in cortex and medulla, a weak cytoplasmic staining was found in late proximal tubule cells. Thus these results demonstrate that rat kidney ClC-K channels are predominantly located in the basolateral membranes from cells of the late segments of the renal tubule where most of chloride reabsorption takes place

Tissue distribution and subcellular localization of the ClC-5 chloride channel in rat intestinal cells

ClC-5 is the Cl- channel that is mutated in Dent's disease, an X-chromosome-linked disease characterized by low molecular weight proteinuria, hypercalciuria, and kidney stones. It is predominantly expressed in endocytically active renal proximal cells. We investigated whether this Cl- channel could also be expressed in intestinal tissues that have endocytotic machinery. ClC-5 mRNA was detected in the rat duodenum, jejunum, ileum, and colon. Western blot analyses revealed the presence of the 83-kDa ClC-5 protein in these tissues. Indirect immunofluorescence studies showed that ClC-5 was mainly concentrated in the cytoplasm above the nuclei of enterocytes and colon cells. ClC-5 partially colocalized with the transcytosed polymeric immunoglobulin receptor but was not detectable together with the brush-border-anchored sucrase isomaltase. A subfractionation of vesicles obtained by differential centrifugation showed that ClC-5 is associated with the vacuolar 70-kDa H+-ATPase and the small GTPases rab4 and rab5a, two markers of early endosomes. Thus these results indicate that ClC-5 is present in the small intestine and colon of rats and suggest that it plays a role in the endocytotic pathways of intestinal cells

Ceramide mediated macroautophagy involves inhibition of protein kinase B and up-regulation of beclin 1

The sphingolipid ceramide is involved in the cellular stress response. Here we demonstrate that ceramide controls macroautophagy, a major lysosomal catabolic pathway. Exogenous C2-ceramide stimulates macroautophagy (proteolysis and accumulation of autophagic vacuoles) in the human colon cancer HT-29 cells by increasing the endogenous pool of long chain ceramides as demonstrated by the use of the ceramide synthase inhibitor fumonisin B1. Ceramide reverted the interleukin 13-dependent inhibition of macroautophagy by interfering with the activation of protein kinase B. In addition, C2-ceramide stimulated the expression of the autophagy gene product beclin 1. Ceramide is also the mediator of the tamoxifen-dependent accumulation of autophagic vacuoles in the human breast cancer MCF-7 cells. Monodansylcadaverine staining and electron microscopy showed that this accumulation was abrogated by myriocin, an inhibitor of de novo synthesis ceramide. The tamoxifen-dependent accumulation of vacuoles was mimicked by 1-phenyl-2-decanoylamino-3-morpholino-1-propanol, an inhibitor of glucosylceramide synthase. 1-Phenyl-2-decanoylamino-3-morpholino-1-propanol, tamoxifen, and C2-ceramide stimulated the expression of beclin 1, whereas myriocin antagonized the tamoxifen-dependent up-regulation. Tamoxifen and C2-ceramide interfere with the activation of protein kinase B, whereas myriocin relieved the inhibitory effect of tamoxifen. In conclusion, the control of macroautophagy by ceramide provides a novel function for this lipid mediator in a cell process with major biological outcomes