Inherent Mach-Zehnder interference with "which-way" detection for single particle scattering in one dimension

We study the coherent transport of single photon in a one-dimensional coupled-resonator-array, "non-locally" coupled to a two-level system. Since its inherent structure is a Mach-Zehnder interferometer, we explain the destructive interference phenomenon of the transmission spectrums according to the effect of which-way detection. The quantum realization of the present model is a nano-electromechanical resonator arrays with two nearest resonators coupled to a single spin via their attached magnetic tips. Its classical simulation is a waveguide of coupled defected cavity array with double couplings to a side defected cavity.Comment: 5 papges, 4 figure

Mechanisms of Hypoxic Regulation of Plasminogen Activator Inhibitor-1 Gene Expression in Keloid Fibroblasts

Keloids are an excessive accumulation of extracellular matrix. Although numerous studies have shown elevated plasminogen activator inhibitor-1 (PAI-1) levels in keloid fibroblasts compared with those of normal skin. Their specific mechanisms involved in the differential expression of PAI-1 in these cell types. In this study, the upregulation of PAI-1 expression is demonstrated in keloid tissues and their derived dermal fibroblasts, attesting to the persistence, if any, of fundamental differences between in vivo and in vitro paradigms. We further examined the mechanisms involved in hypoxia-induced regulation of PAI-1 gene in dermal fibroblast derived from keloid lesions and associated clinically normal peripheral skins from the same patient. Primary cultures were exposed to an environmental hypoxia or desferroxamine. We found that the hypoxia-induced elevation of PAI-1 gene appears to be regulated at both transcriptional and post-transcriptional levels in keloid fibroblasts. Furthermore, our results showed a consistent elevation of HIF-1α protein level in keloid tissues compared with their normal peripheral skin controls, implying a potential role as a biomarker for local skin hypoxia. Treatment with antisense oligonucleotides against hypoxia-inducible factor 1α (HIF-1α) led to the downregulation of steady-state levels of PAI-1 mRNA under both normoxic and hypoxic conditions. Conceivably, our results suggest that HIF-1α may be a novel therapeutic target to modulate the scar fibrosis process

Mechanisms of Hypoxic Regulation of Plasminogen Activator Inhibitor-1 Gene Expression in Keloid Fibroblasts

Keloids are an excessive accumulation of extracellular matrix. Although numerous studies have shown elevated plasminogen activator inhibitor-1 (PAI-1) levels in keloid fibroblasts compared with those of normal skin. Their specific mechanisms involved in the differential expression of PAI-1 in these cell types. In this study, the upregulation of PAI-1 expression is demonstrated in keloid tissues and their derived dermal fibroblasts, attesting to the persistence, if any, of fundamental differences between in vivo and in vitro paradigms. We further examined the mechanisms involved in hypoxia-induced regulation of PAI-1 gene in dermal fibroblast derived from keloid lesions and associated clinically normal peripheral skins from the same patient. Primary cultures were exposed to an environmental hypoxia or desferroxamine. We found that the hypoxia-induced elevation of PAI-1 gene appears to be regulated at both transcriptional and post-transcriptional levels in keloid fibroblasts. Furthermore, our results showed a consistent elevation of HIF-1α protein level in keloid tissues compared with their normal peripheral skin controls, implying a potential role as a biomarker for local skin hypoxia. Treatment with antisense oligonucleotides against hypoxia-inducible factor 1α (HIF-1α) led to the downregulation of steady-state levels of PAI-1 mRNA under both normoxic and hypoxic conditions. Conceivably, our results suggest that HIF-1α may be a novel therapeutic target to modulate the scar fibrosis process

Intensified Antituberculosis Therapy in Adults with Tuberculous Meningitis

BACKGROUND Tuberculous meningitis is often lethal. Early antituberculosis treatment and adjunctive treatment with glucocorticoids improve survival, but nearly one third of patients with the condition still die. We hypothesized that intensified antituberculosis treatment would enhance the killing of intracerebral Mycobacterium tuberculosis organisms and decrease the rate of death among patients. METHODS We performed a randomized, double-blind, placebo-controlled trial involving human immunodeficiency virus (HIV)-infected adults and HIV-uninfected adults with a clinical diagnosis of tuberculous meningitis who were admitted to one of two Vietnamese hospitals. We compared a standard, 9-month antituberculosis regimen (which included 10 mg of rifampin per kilogram of body weight per day) with an intensified regimen that included higher-dose rifampin (15 mg per kilogram per day) and levofloxacin (20 mg per kilogram per day) for the first 8 weeks of treatment. The primary outcome was death by 9 months after randomization. RESULTS A total of 817 patients (349 of whom were HIV-infected) were enrolled; 409 were randomly assigned to receive the standard regimen, and 408 were assigned to receive intensified treatment. During the 9 months of follow-up, 113 patients in the intensified-treatment group and 114 patients in the standard-treatment group died (hazard ratio, 0.94; 95% confidence interval, 0.73 to 1.22; P=0.66). There was no evidence of a significant differential effect of intensified treatment in the overall population or in any of the subgroups, with the possible exception of patients infected with isoniazid-resistant M. tuberculosis. There were also no significant differences in secondary outcomes between the treatment groups. The overall number of adverse events leading to treatment interruption did not differ significantly between the treatment groups (64 events in the standard-treatment group and 95 events in the intensified-treatment group, P=0.08). CONCLUSIONS Intensified antituberculosis treatment was not associated with a higher rate of survival among patients with tuberculous meningitis than standard treatment. (Funded by the Wellcome Trust and the Li Ka Shing Foundation; Current Controlled Trials number, ISRCTN61649292.)

Effectiveness of cervical pessary compared to cervical cerclage with or without vaginal progesterone for the prevention of preterm birth in women with twin pregnancies and a short cervix : Study protocol for a two-by-two factorial randomised clinical trial

Peer reviewedPublisher PD

Formation of ionospheric irregularities over Southeast Asia during the 2015 St. Patrickˈs Day storm

We investigate the geospace response to the 2015 St. Patrickˈs Day storm leveraging on instruments spread over Southeast Asia (SEA), covering a wide longitudinal sector of the low-latitude ionosphere. A regional characterization of the storm is provided, identifying the peculiarities of ionospheric irregularity formation. The novelties of this work are the characterization in a broad longitudinal range and the methodology relying on the integration of data acquired by Global Navigation Satellite System (GNSS) receivers, magnetometers, ionosondes, and Swarm satellites. This work is a legacy of the project EquatoRial Ionosphere Characterization in Asia (ERICA). ERICA aimed to capture the features of both crests of the equatorial ionospheric anomaly (EIA) and trough (EIT) by means of a dedicated measurement campaign. The campaign lasted from March to October 2015 and was able to observe the ionospheric variability causing effects on radio systems, GNSS in particular. The multiinstrumental and multiparametric observations of the region enabled an in-depth investigation of the response to the largest geomagnetic storm of the current solar cycle in a region scarcely reported in literature. Our work discusses the comparison between northern and southern crests of the EIA in the SEA region. The observations recorded positive and negative ionospheric storms, spread F conditions, scintillation enhancement and inhibition, and total electron content variability. The ancillary information on the local magnetic field highlights the variety of ionospheric perturbations during the different storm phases. The combined use of ionospheric bottomside, topside, and integrated information points out how the storm affects the F layer altitude and the consequent enhancement/suppression of scintillations.Published12211–122331A. Geomagnetismo e Paleomagnetismo2A. Fisica dell'alta atmosfera1IT. Reti di monitoraggio e Osservazioni5IT. Osservazioni satellitariJCR Journalope

Effectiveness and safety of in vitro maturation of oocytes versus in vitro fertilisation in women with high antral follicle count : Study protocol for a randomised controlled trial

This work was supported by Ferring grant number 000323 and sponsored by My Duc Hospital.Peer reviewedPublisher PD

Genetical genomics: spotlight on QTL hotspots

No abstract available

Tnni3k Modifies Disease Progression in Murine Models of Cardiomyopathy

The Calsequestrin (Csq) transgenic mouse model of cardiomyopathy exhibits wide variation in phenotypic progression dependent on genetic background. Seven heart failure modifier (Hrtfm) loci modify disease progression and outcome. Here we report Tnni3k (cardiac Troponin I-interacting kinase) as the gene underlying Hrtfm2. Strains with the more susceptible phenotype exhibit high transcript levels while less susceptible strains show dramatically reduced transcript levels. This decrease is caused by an intronic SNP in low-transcript strains that activates a cryptic splice site leading to a frameshifted transcript, followed by nonsense-mediated decay of message and an absence of detectable protein. A transgenic animal overexpressing human TNNI3K alone exhibits no cardiac phenotype. However, TNNI3K/Csq double transgenics display severely impaired systolic function and reduced survival, indicating that TNNI3K expression modifies disease progression. TNNI3K expression also accelerates disease progression in a pressure-overload model of heart failure. These combined data demonstrate that Tnni3k plays a critical role in the modulation of different forms of heart disease, and this protein may provide a novel target for therapeutic intervention