Timed Consistent Network Updates

Network updates such as policy and routing changes occur frequently in Software Defined Networks (SDN). Updates should be performed consistently, preventing temporary disruptions, and should require as little overhead as possible. Scalability is increasingly becoming an essential requirement in SDN. In this paper we propose to use time-triggered network updates to achieve consistent updates. Our proposed solution requires lower overhead than existing update approaches, without compromising the consistency during the update. We demonstrate that accurate time enables far more scalable consistent updates in SDN than previously available. In addition, it provides the SDN programmer with fine-grained control over the tradeoff between consistency and scalability.Comment: This technical report is an extended version of the paper "Timed Consistent Network Updates", which was accepted to the ACM SIGCOMM Symposium on SDN Research (SOSR) '15, Santa Clara, CA, US, June 201

An Optimal Self-Stabilizing Firing Squad

Consider a fully connected network where up to $t$ processes may crash, and all processes start in an arbitrary memory state. The self-stabilizing firing squad problem consists of eventually guaranteeing simultaneous response to an external input. This is modeled by requiring that the non-crashed processes "fire" simultaneously if some correct process received an external "GO" input, and that they only fire as a response to some process receiving such an input. This paper presents FireAlg, the first self-stabilizing firing squad algorithm. The FireAlg algorithm is optimal in two respects: (a) Once the algorithm is in a safe state, it fires in response to a GO input as fast as any other algorithm does, and (b) Starting from an arbitrary state, it converges to a safe state as fast as any other algorithm does.Comment: Shorter version to appear in SSS0

Mycobacterium tuberculosis and the host response

Mycobacterium tuberculosis remains a leading cause of morbidity and mortality worldwide. Advances reported at a recent international meeting highlight insights and controversies in the genetics of M. tuberculosis and the infected host, the nature of protective immune responses, adaptation of the bacillus to host-imposed stresses, animal models, and new techniques

What’s so bad about scientism?

In their attempt to defend philosophy from accusations of uselessness made by prominent scientists, such as Stephen Hawking, some philosophers respond with the charge of ‘scientism.’ This charge makes endorsing a scientistic stance, a mistake by definition. For this reason, it begs the question against these critics of philosophy, or anyone who is inclined to endorse a scientistic stance, and turns the scientism debate into a verbal dispute. In this paper, I propose a different definition of scientism, and thus a new way of looking at the scientism debate. Those philosophers who seek to defend philosophy against accusations of uselessness would do philosophy a much better service, I submit, if they were to engage with the definition of scientism put forth in this paper, rather than simply make it analytic that scientism is a mistake

Effects of aleglitazar, a balanced dual peroxisome proliferator-activated receptor α/γ agonist on glycemic and lipid parameters in a primate model of the metabolic syndrome

<p>Abstract</p> <p>Background</p> <p>Glycemic control and management of dyslipidemia to reduce cardiovascular risk are major therapeutic goals in individuals with type 2 diabetes mellitus (T2DM). This study was performed to evaluate the effects of aleglitazar, a balanced dual peroxisome proliferator-activated receptor α/γ (PPARα/γ) agonist, on both lipid and glycemic parameters in obese, hypertriglyceridemic, insulin-resistant rhesus monkeys.</p> <p>Methods</p> <p>A 135-day efficacy study was performed in six rhesus monkeys. After a 28-day baseline assessment (vehicle only), monkeys received oral aleglitazar 0.03 mg/kg per day for 42 days, followed by a 63-day washout period. Plasma levels of markers of glycemic and lipid regulation were measured at baseline, at the end of the dosing period, and at the end of the washout period.</p> <p>Results</p> <p>Compared with baseline values, aleglitazar 0.03 mg/kg per day reduced triglyceride levels by an average of 89% (328 to 36 mg/dL; P = 0.0035 when normalized for baseline levels) and increased high-density lipoprotein cholesterol levels by 125% (46 to 102 mg/dL; P = 0.0007). Furthermore, aleglitazar reduced low-density lipoprotein cholesterol levels (41%) and increased levels of apolipoprotein A-I (17%) and A-II (17%). Aleglitazar also improved insulin sensitivity by 60% (P = 0.001). Mean body weight was reduced by 5.9% from baseline values with aleglitazar at this dose (P = 0.043).</p> <p>Conclusions</p> <p>Aleglitazar, a dual PPARα/γ agonist, has beneficial effects on both lipid and glucose parameters and may have a therapeutic role in modifying cardiovascular risk factors and improving glycemic control in patients with T2DM.</p

Joule spectroscopy of hybrid superconductor–semiconductor nanodevices

Hybrid superconductor-semiconductor devices offer highly tunable platforms, potentially suitable for quantum technology applications, that have been intensively studied in the past decade. Here we establish that measurements of the superconductor-to-normal transition originating from Joule heating provide a powerful spectroscopical tool to characterize such hybrid devices. Concretely, we apply this technique to junctions in full-shell Al-InAs nanowires in the Little-Parks regime and obtain detailed information of each lead independently and in a single measurement, including differences in the superconducting coherence lengths of the leads, inhomogeneous covering of the epitaxial shell, and the inverse superconducting proximity effect; all-in-all constituting a unique fingerprint of each device with applications in the interpretation of low-bias data, the optimization of device geometries, and the uncovering of disorder in these systems. Besides the practical uses, our work also underscores the importance of heating in hybrid devices, an effect that is often overlookedWe acknowledge funding by EU through the European Research Council (ERC) Starting Grant agreement 716559 (TOPOQDot), the FET-Open contract AndQC, by the Danish National Research Foundation, Inno vation Fund Denmark, the Carlsberg Foundation, and by the Spanish AEI through Grant No. PID2020-117671GB-I00 and through the “María de Maeztu” Programme for Units of Excellence in R&D (CEX2018- 000805-M) and the ”Ramón y Cajal” programme grant RYC 2015-1797

Use of H19 Gene Regulatory Sequences in DNA-Based Therapy for Pancreatic Cancer

Pancreatic cancer is the eighth most common cause of death from cancer in the world, for which palliative treatments are not effective and frequently accompanied by severe side effects. We propose a DNA-based therapy for pancreatic cancer using a nonviral vector, expressing the diphtheria toxin A chain under the control of the H19 gene regulatory sequences. The H19 gene is an oncofetal RNA expressed during embryo development and in several types of cancer. We tested the expression of H19 gene in patients, and found that 65% of human pancreatic tumors analyzed showed moderated to strong expression of the gene. In vitro experiments showed that the vector was effective in reducing Luciferase protein activity on pancreatic carcinoma cell lines. In vivo experiment results revealed tumor growth arrest in different animal models for pancreatic cancer. Differences in tumor size between control and treated groups reached a 75% in the heterotopic model (P = .037) and 50% in the orthotopic model (P = .007). In addition, no visible metastases were found in the treated group of the orthotopic model. These results indicate that the treatment with the vector DTA-H19 might be a viable new therapeutic option for patients with unresectable pancreatic cancer

Continuous photodetection model: quantum jump engineering and hints for experimental verification

We examine some aspects of the continuous photodetection model for photocounting processes in cavities. First, we work out a microscopic model that describes the field-detector interaction and deduce a general expression for the Quantum Jump Superoperator (QJS), that shapes the detector's post-action on the field upon a detection. We show that in particular cases our model recovers the QJSs previously proposed ad hoc in the literature and point out that by adjusting the detector parameters one can engineer QJSs. Then we set up schemes for experimental verification of the model. By taking into account the ubiquitous non-idealities, we show that by measuring the lower photocounts moments and the mean waiting time one can check which QJS better describes the photocounting phenomenon.Comment: 12 pages, 7 figures. Contribution to the conference Quantum Optics III, Pucon - Chile, November 27-30, 200

The Effect of Cone Opsin Mutations on Retinal Structure and the Integrity of the Photoreceptor Mosaic

Purpose. To evaluate retinal structure and photoreceptor mosaic integrity in subjects with OPN1LW and OPN1MW mutations. Methods. Eleven subjects were recruited, eight of whom have been previously described. Cone and rod density was measured using images of the photoreceptor mosaic obtained from an adaptive optics scanning light ophthalmoscope (AOSLO). Total retinal thickness, inner retinal thickness, and outer nuclear layer plus Henle fiber layer (ONL+HFL) thickness were measured using cross-sectional spectral-domain optical coherence tomography (SD-OCT) images. Molecular genetic analyses were performed to characterize the OPN1LW/OPN1MW gene array. Results. While disruptions in retinal lamination and cone mosaic structure were observed in all subjects, genotype-specific differences were also observed. For example, subjects with “L/M interchange” mutations resulting from intermixing of ancestral OPN1LW and OPN1MW genes had significant residual cone structure in the parafovea (∼25% of normal), despite widespread retinal disruption that included a large foveal lesion and thinning of the parafoveal inner retina. These subjects also reported a later-onset, progressive loss of visual function. In contrast, subjects with the C203R missense mutation presented with congenital blue cone monochromacy, with retinal lamination defects being restricted to the ONL+HFL and the degree of residual cone structure (8% of normal) being consistent with that expected for the S-cone submosaic. Conclusions. The photoreceptor phenotype associated with OPN1LW and OPN1MW mutations is highly variable. These findings have implications for the potential restoration of visual function in subjects with opsin mutations. Our study highlights the importance of high-resolution phenotyping to characterize cellular structure in inherited retinal disease; such information will be critical for selecting patients most likely to respond to therapeutic intervention and for establishing a baseline for evaluating treatment efficacy