Tests of Relativity using a cryogenic optical resonator.

A 190-day comparison of the optical frequencies defined by an optical cavity and a molecular electronic transition is analyzed for the velocity independence of the speed of light (Kennedy-Thorndike test) and the universality of the gravitational redshift. The modulation of the laboratory velocity and the gravitational potential were provided by Earth's orbital motion around the Sun. We find a velocity-dependence coefficient of ͑1.9 6 2.1͒ 3 10 25 , 3 times lower compared to the best previous test. Alternatively, the data confirm the gravitational redshift for an electronic transition at the 4% level. Prospects for significant improvements of the tests are discussed. DOI: 10.1103/PhysRevLett.88.010401 PACS numbers: 03.30. +p, 07.60. -j Special relativity (SR) is one of the fundamental theories of nature. The prominent role of the theory as a basis of our physical view of nature has motivated experimenters to test its foundations and predictions with ever increasing accuracy. Added motivation for tests is provided by the theoretical efforts to unify the forces of nature. For example, approaches towards a quantum theory of gravity have been put forward that lead to modified Maxwell equations which are not necessarily Lorentz covariant The relationship between gravity and the other forces of nature can also be probed by measuring the gravitational frequency shift ("redshift") of clocks based on these forces. The principle of local position invariance (LPI) Thanks to worldwide developments in frequency metrology and ultrastable oscillators, especially in the optical domain, the opportunity has arisen to improve the knowledge of SR and LPI by several orders of magnitude. Here we report on a first step in this direction, based on a laboratory experiment. We remark that space experiments have also been proposed Test of special relativity.-According to the kinematical analysis of Robertson [6] as well as Mansouri and Sexl A violation of the constancy of the speed of light implies a dependence of c͑v͒ on the magnitude y of the laboratory velocity relative to a hypothetical preferred frame of reference S, and on the angle u between the propagation direction of the light and the direction of v. The natural candidate for S is the cosmic microwave background. From isotropy in the preferred frame S, it follows that c͑v͒ is an even function of y. According to common test theories where c 0 is the constant speed of light in the preferred frame S. A and B vanish if SR is valid. In the test theory framework of The laboratory velocity y͑t͒ has contributions from the motion of the Sun through S with a constant velocity y s 377 km͞s, Earth's orbital motion around the Sun (orbital velocity y e 30 km͞s), and Earth's daily rotation (velocity y d ഠ 330 m͞s at the latitude of Konstanz), y͑t͒ y s 1 y e sin͓V y ͑t 2 t 0 ͔͒ cosF E Here F A ഠ 8 ± is the angle between the equatorial plane and the velocity of the sun. F E 6 ± is the declination between the plane of Earth's orbit and the velocity of the Sun [9], 2p͞V y 1 yr, 2p͞V d 1 sidereal day. t 0 and t d are determined by the phase and start date of the measurement, respectively. 010401-1 0031-9007͞02͞ 88(1)͞010401(4)$15.0

J. Exp. Med.

The cross talk between host and pathogen starts with recognition of bacterial signatures through pattern recognition receptors (PRRs), which mobilize downstream signaling cascades. We investigated the role of the cytosolic adaptor caspase recruitment domain family, member 9 (CARD9) in tuberculosis. This adaptor was critical for full activation of innate immunity by converging signals downstream of multiple PRRs. Card9(-/-) mice succumbed early after aerosol infection, with higher mycobacterial burden, pyogranulomatous pneumonia, accelerated granulocyte recruitment, and higher abundance of proinflammatory cytokines and granulocyte colony-stimulating factor (G-CSF) in serum and lung. Neutralization of G-CSF and neutrophil depletion significantly prolonged survival, indicating that an exacerbated systemic inflammatory disease triggered lethality of Card9(-/-) mice. CARD9 deficiency had no apparent effect on T cell responses, but a marked impact on the hematopoietic compartment. Card9(-/-) ranulocytes failed to produce IL-10 after Mycobaterium tuberculosis infection, suggesting that an absent antiinflammatory feedback loop accounted for granulocyte-dominated pathology, uncontrolled bacterial replication, and, ultimately, death of infected Card9(-/-) mice. Our data provide evidence that deregulated innate responses trigger excessive lung inflammation and demonstrate a pivotal role of CARD9 signaling in autonomous innate host defense against tuberculosis

Increasing abdominal pressure with and without PEEP: effects on intra-peritoneal, intra-organ and intra-vascular pressures

Intra-organ and intra-vascular pressures can be used to estimate intra-abdominal pressure. The aim of this prospective, interventional study was to assess the effect of PEEP on the accuracy of pressure estimation at different measurement sites in a model of increased abdominal pressure

Increasing abdominal pressure with and without PEEP: effects on intra-peritoneal, intra-organ and intra-vascular pressures

Intra-organ and intra-vascular pressures can be used to estimate intra-abdominal pressure. The aim of this prospective, interventional study was to assess the effect of PEEP on the accuracy of pressure estimation at different measurement sites in a model of increased abdominal pressure

Activation of the NLRP3 inflammasome by Mycobacterium tuberculosis is uncoupled from susceptibility to active tuberculosis.

As a hallmark of tuberculosis (TB), Mycobacterium tuberculosis (MTB) induces granulomatous lung lesions and systemic inflammatory responses during active disease. Molecular regulation of inflammation is associated with inflammasome assembly. We determined the extent to which MTB triggers inflammasome activation and how this impacts on the severity of TB in a mouse model. MTB stimulated release of mature IL-1β in macrophages while attenuated M. bovis BCG failed to do so. Tubercle bacilli specifically activated the NLRP3 inflammasome and this propensity was strictly controlled by the virulence-associated RD1 locus of MTB. However, Nlrp3-deficient mice controlled pulmonary TB, a feature correlated with NLRP3-independent production of IL-1β in infected lungs. Our studies demonstrate that MTB activates the NLRP3 inflammasome in macrophages in an ESX-1-dependent manner. However, during TB, MTB promotes NLRP3- and caspase-1-independent IL-1β release in myeloid cells recruited to lung parenchyma and thus overcomes NLRP3 deficiency in vivo in experimental models