The FCC's Network Neutrality Ruling in the Comcast Case: Towards a Consensus with Europe?

In August 2008, the FCC found that Comcast's restrictions on peer-to-peer upload transmissions were unreasonably discriminatory, arbitrarily targeted a particular application, and deprived consumers of their rights to run Internet applications and use services of their choice. The Comcast ruling represents a significant change in the FCC's direction: given the FCC's past decisions that broadband Internet access services do not fall within the "common carrier" category, it is notable that the agency has now imposed nondiscrimination requirements on these services. This Article shows that the rationales articulated in the FCC's Comcast order, stressing both (i) concerns about protecting competition and (ii) concerns about protecting consumers from disruption of their ability to communicate freely and privately, are rooted in centuries of Anglo-American law defining he obligations of "common carriers." The FCC appears to be moving away from its traditional emphasis on the competition policy concerns, which justify asymmetrical regulation of dominant providers for the sake of enabling competition, and toward an emphasis on the consumer protection issues, which justify symmetrical regulation of all service providers regardless whether they have market power. These developments in the U.S. echo the discussion now going on in Europe in the context of the package of proposals on a new common regulatory framework for telecommunications, released by the European Commission on Nov. 13, 2007, and which is now being debated by the European Parliament and Council. On both sides of the Atlantic, a trend is emerging to permit network discrimination only if the discrimination is narrowly tailored to achieve legitimate objectives.network neutrality, discrimination, common carrier, network management, Comcast, European Directives.

Guardian Knight or Hands Off: The European Response to Network Neutrality. Legal considerations on the electronic communications reform

Network neutrality refers to a policy principle regarding access for online content and service providers to broadband infrastructures. It implies a general and ex ante obligation of non-discrimination for network operators when granting access to providers of online services, with the aim of excluding practices such as blocking access to non-affiliated content, degrading the quality of transmission, imposing unreasonable restrictions or prioritising affiliated content. Whether such obligation should be "cast in the Stone Tables" of the law was first fiercely debated in the United States, and the issue is now gaining increased attention in other parts of the world, including the European Union, where the regulatory framework for electronic communications is currently under review. This article examines whether existing rules already provide the relevant authorities with the necessary tools to take action against broadband providers illegitimately discriminating or blocking content of those who are not prepared to pay a "toll" for the use of higher speed networks or better quality services. It focuses in particular on the EU regulatory framework for electronic communications networks and services, including the reform proposals published by the European Commission on November 13th (type should be like 24th below) 2007 and the resolution adopted by the European Parliament on 24th September 2008.network neutrality, regulation, electronic communications, reform proposals.

Evolution of Multidrug Resistance during Staphylococcus aureus Infection Involves Mutation of the Essential Two Component Regulator WalKR

Antimicrobial resistance in Staphylococcus aureus is a major public health threat, compounded by emergence of strains with resistance to vancomycin and daptomycin, both last line antimicrobials. Here we have performed high throughput DNA sequencing and comparative genomics for five clinical pairs of vancomycin-susceptible (VSSA) and vancomycin-intermediate ST239 S. aureus (VISA); each pair isolated before and after vancomycin treatment failure. These comparisons revealed a frequent pattern of mutation among the VISA strains within the essential walKR two-component regulatory locus involved in control of cell wall metabolism. We then conducted bi-directional allelic exchange experiments in our clinical VSSA and VISA strains and showed that single nucleotide substitutions within either walK or walR lead to co-resistance to vancomycin and daptomycin, and caused the typical cell wall thickening observed in resistant clinical isolates. Ion Torrent genome sequencing confirmed no additional regulatory mutations had been introduced into either the walR or walK VISA mutants during the allelic exchange process. However, two potential compensatory mutations were detected within putative transport genes for the walK mutant. The minimal genetic changes in either walK or walR also attenuated virulence, reduced biofilm formation, and led to consistent transcriptional changes that suggest an important role for this regulator in control of central metabolism. This study highlights the dramatic impacts of single mutations that arise during persistent S. aureus infections and demonstrates the role played by walKR to increase drug resistance, control metabolism and alter the virulence potential of this pathogen

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

Throwing Out the Baby with the Bathwater: Reform in the System for Compensating Obstetric Accidents

Lawsuits for medical malpractice are supposed to serve two purposes: compensation of injured patients and deterrence of negligent conduct by doctors and hospitals. However, those goals are not being served in the area of obstetric medicine. Malpractice liability insurance premiums are increasing rapidly for obstetric care providers, and as a result, delivery and perinatal care have become more expensive and less available. At the same time, compensation is distributed inequitably. The liability crisis is more acute in obstetrics than in any other medical specialty because the cost of compensating birth injury sufferers, who are disabled for their lifetimes, is very high and has escalated rapidly

In Vitro Pharmacodynamics of Vancomycin and Cefazolin Alone and in Combination against Methicillin-Resistant Staphylococcus aureus

Previous studies employing time-kill methods have observed synergistic effects against methicillin-resistant Staphylococcus aureus (MRSA) when a β-lactam is combined with vancomycin. However, these time-kill studies have neglected the importance of human-simulated exposures. We evaluated the effect of human simulated exposures of vancomycin at 1 g every 8 h (q8h) in combination with cefazolin at 1 g q8h against various MRSA isolates. Four clinical isolates (two MRSA isolates [vancomycin MICs, 0.5 and 2.0 μg/ml], a heterogeneous vancomycin-intermediate S. aureus [hVISA] isolate [MIC, 2.0 μg/ml], and a vancomycin-intermediate S. aureus [VISA] isolate [MIC, 8.0 μg/ml]) were evaluated in an in vitro pharmacodynamic model with a starting inoculum of 106 or 108 CFU/ml. Bacterial density was measured over 48 to 72 h. Time-kill curves were constructed, and the area under the bacterial killing and regrowth curve (AUBC) was calculated. During 106 CFU/ml studies, combination therapy achieved greater log10 CFU/ml changes than vancomycin alone at 12 h (−4.31 ± 0.58 versus −2.80 ± 0.59, P < 0.001), but not at 48 h. Combination therapy significantly reduced the AUBC from 0 to 48 h (122 ± 14) compared with vancomycin alone (148 ± 22, P = 0.017). Similar results were observed during 108 CFU/ml studies, where combination therapy achieved greater log10 CFU/ml changes at 12 h than vancomycin alone (−4.00 ± 0.20 versus −1.10 ± 0.04, P < 0.001) and significantly reduced the AUBC (275 ± 30 versus 429 ± 37, P < 0.001) after 72 h of incubation. In this study, the combination of vancomycin and cefazolin at human-simulated exposures improved the rate of kill against these MRSA isolates and resulted in greater overall antibacterial effect, but no differences in bacterial density were observed by the end of the experiments