Bridging the Mid-Infrared-to-Telecom Gap with Silicon Nanophotonic Spectral Translation

Expanding far beyond traditional applications in optical interconnects at telecommunications wavelengths, the silicon nanophotonic integrated circuit platform has recently proven its merits for working with mid-infrared (mid-IR) optical signals in the 2-8 {\mu}m range. Mid-IR integrated optical systems are capable of addressing applications including industrial process and environmental monitoring, threat detection, medical diagnostics, and free-space communication. Rapid progress has led to the demonstration of various silicon components designed for the on-chip processing of mid-IR signals, including waveguides, vertical grating couplers, microcavities, and electrooptic modulators. Even so, a notable obstacle to the continued advancement of chip-scale systems is imposed by the narrow-bandgap semiconductors, such as InSb and HgCdTe, traditionally used to convert mid-IR photons to electrical currents. The cryogenic or multi-stage thermo-electric cooling required to suppress dark current noise, exponentially dependent upon the ratio Eg/kT, can limit the development of small, low-power, and low-cost integrated optical systems for the mid-IR. However, if the mid-IR optical signal could be spectrally translated to shorter wavelengths, for example within the near-infrared telecom band, photodetectors using wider bandgap semiconductors such as InGaAs or Ge could be used to eliminate prohibitive cooling requirements. Moreover, telecom band detectors typically perform with higher detectivity and faster response times when compared with their mid-IR counterparts. Here we address these challenges with a silicon-integrated approach to spectral translation, by employing efficient four-wave mixing (FWM) and large optical parametric gain in silicon nanophotonic wires

Effect of Qigong on hypertension: a randomised controlled study

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Molecular cloning of differentially expressed genes in human epithelial ovarian cancer

A DNA-fingerprinting approach has been adapted to detect differentially expressed genes in human ovarian carcinoma. This method is based on the use of arbitrary primers to generate fingerprints from total RNA isolated from normal ovarian epithelial cells and ovarian carcinoma cells by polymerase chain reaction (PCR). Using this method, we cloned two cDNA fragments (DOC-1 and DOC-2) which were present in normal ovarian surface epithelial cells but consistently absent in all of the ovarian cancer cell lines from the differential display. In addition, we also identified a cDNA fragment (LF4.0) which is overexpressed in most of the tumor cell lines and tumor tissues in comparison to the normal ovarian surface epithelial cells. The differential expression of the genes in the tumor cell lines as well as in the tumor tissues was also confirmed by Northern analysis. The clone DOC-2, which is a 800-bp cDNA fragment, has one open reading frame suggesting that the gene may be translated. Assuming that this frame is the sense strand, we generated both sense and antisense riboprobe for in situ mRNA hybridization. Only the antisense DOC-2 riboprobe revealed a hybridization signal which was restricted to the human surface ovarian epithelium. The potential functional roles of these genes is now under investigation.link_to_subscribed_fulltex

Anti-retroviral therapy reverses HIV-associated abnormalities in lymphocyte apoptosis

The objective of this study was to assess the role of anti-retroviral therapy (ART) on the susceptibility of peripheral blood lymphocytes (PBL) from HIV-1-infected individuals to activation-induced apoptosis and in comparison with changes in CD4 lymphocyte counts. Eleven symptomatic HIV+ patients were studied. Ex vivo apoptosis was measured in phytohaemagglutinin (PHA)-stimulated PBL and CD4 subsets by flow cytometry, at baseline and after 1 month (4–6 weeks) and 2/3 months of ART. Six patients had extended studies of the effects of therapy to a maximum of 21 months. Lymphocyte apoptosis was significantly elevated in HIV+ patients at baseline (median 22% compared with 7.5% in HIV− risk-matched controls; P < 0.05). This decreased to control levels on ART (7.4% at 4–6 weeks, P < 0.01, and 6.2% at 8–12 weeks, P < 0.05, compared with baseline). Similar changes occurred in the CD4+ subpopulation. The decrease in apoptosis was maintained for several months, but the effect was rapidly lost if ART was discontinued. CD4 counts showed a reciprocal relationship to changes in apoptosis. The association of changes in apoptosis with those in CD4 counts suggests a link between programmed cell death and lymphocyte depletion. Apoptosis reduced in some individuals without any reduction in viral load, suggesting apoptosis may be influenced by factors in addition to the overall extent of HIV replication