RKR_K and $K^+\rightarrow\pi^+\nu\bar{\nu} with NA62 at CERN SPS

Recent results a future prospects of the NA62 experiment at CERN SPS are presented. The NA62 experiment performed the most precise measurement of the ratio $R_K$ of the $K^+\rightarrow e^\pm\nu$ and K^+\rightarrow \mu^\pm\nu$decay rates using the full data set collected in 2007. The result is in agreement with the Standard Model expectation. The ultra-rare decay$K^+\rightarrow\pi^+\nu\bar{\nu}$is an excellent processes to make tests of new physics at the highest scale complementary to the LHC thanks to their theoretically cleanness. The NA62 experiment at CERN SPS aims to collect of the order of 100$K^+\rightarrow\pi^+\nu\bar{\nu}$ events in two years of data taking, keeping the background at the level of 10%.Comment: Proceedings of CKM 2012, the 7th International Workshop on the CKM Unitarity Triangle, University of Cincinnati, USA, 28 September - 2 October 201

New physics limits from kaon decays

Searches for lepton flavour violation and lepton number violation in kaon decays by the NA62 and NA48/2 experiments at CERN are presented. A new measurement of the ratio of charged kaon leptonic decay rates $R_K=\Gamma(K_{e2})/\Gamma(K_{\mu2})$ to sub-percent relative precision is discussed. An improved upper limit on the lepton number violating $K^\pm\rightarrow\pi^\mp\mu^\pm\mu^\pm$ decay rate is also reported. The future 10% precision measurement of the branching ratio of the ultra-rare kaon decay $K^+\rightarrow\pi^+\nu\bar{\nu}$ with the NA62 experiment is finally reviewed

Alterations in carnitine–acylcarnitine translocase activity and in phospholipid composition in heart mitochondria from hypothyroid rats

AbstractChanges in mitochondrial fatty acid metabolism may underlie the decline in cardiac function in the hypothyroid animals. The effect of hypothyroidism on fatty acid oxidation, carnitine–acylcarnitine translocase activity and lipid composition in rat heart mitochondria has been examined. Rates of mitochondrial fatty acid oxidation as well as carnitine-carnitine and carnitine–palmitoylcarnitine exchange reactions were all depressed in heart mitochondria isolated from hypothyroid rats. Kinetic analysis of the carnitine–carnitine exchange reaction showed that the hypothyroid state affects the Vmax of this process, while having no effect on the Km value. Heart mitochondrial inner membrane lipid composition was significantly altered in hypothyroid rats. Cardiolipin, particularly, was found to decrease (by around 36%). Alterations in fatty acid pattern of mitochondrial inner membrane preparations from hypothyroid rats were also found. The effects of the hypothyroid state on fatty acids oxidation, carnitine translocase activity and phospholipid composition were completely reversed by following treatment of hypothyroid rats with thyroid hormone. A lower cardiolipin content in the mitochondrial inner membrane offers a plausible mechanism to explain the decline in the translocase activity in hypothyroidism

Stimulation of carnitine acylcarnitine translocase activity in heart mitochondria from hyperthyroid rats

AbstractThe effect of hyperthyroidism on fatty acid oxidation and on carnitine-acylcarnitine translocase activity in rat heart mitochondria has been studied. The rates of palmitoylcarnitine supported respiration as well as the carnitine-palmitoylcarnitine exchange reaction were both stimulated (approx. 36%) in heart mitochondria from hyperthyroid rats. Kinetic analysis of the carnitine-carnitine exchange reaction showed that thyroid hormone affects the Vmax of this process, while having no effect on the Km values. The level of cardiolipin was significantly higher (approx. 40%) in heart mitoplasts from hyperthyroid rats than from the control rats. It can be concluded that thyroid hormones produce a stimulation of heart mitochondrial carnitine translocase activity and that the basis of this effect is likely an increase in the cardiolipin content

Ca2+-induced reactive oxygen species production promotes cytochrome c release from rat liver mitochondria via mitochondrial permeability transition (MPT)-dependent and MPT-independent mechanisms: role of cardiolipin.

Release of cytochrome c from mitochondria is considered a critical, early event in the induction of an apoptosis cascade that ultimately leads to programmed cell death. Mitochondrial Ca(2+) loading is a trigger for the release of cytochrome c, although the molecular mechanism underlying this effect is not fully clarified. This study tested the hypothesis that distinct Ca(2+) thresholds may induce cytochrome c release from rat liver mitochondria by membrane permeability transition (MPT)-dependent and independent mechanisms. The involvement of reactive oxygen species (ROS) and cardiolipin in the Ca(2+)-induced cytochrome c release was also investigated. Cytochrome c was quantitated by a new, very sensitive, and rapid reverse-phase high performance liquid chromatography method with a detection limit of 0.1 pmol/sample. We found that a low extramitochondrial Ca(2+) level (2 microM) promoted the release of approximately 13% of the total alamethicin releasable pool of cytochrome c from mitochondria. This release was not depending of MPT; it was mediated by Ca(2+)-induced ROS production and cardiolipin peroxidation and appears to involve the voltage-dependent anion channel. High extramitochondrial Ca(2+) level (20 microM) promoted approximately 45% of the total releasable pool of cytochrome c. This process was MPT-dependent and was also mediated by ROS and cardiolipin. It is suggested that distinct Ca(2+) levels may determine the mode and the amount of cytochrome c release from rat liver mitochondria. The data may help to clarify the molecular mechanism underlying the Ca(2+)-induced release of cytochrome c from rat liver mitochondria and the role played by ROS and cardiolipin in this process

The guilty brain: the utility of neuroimaging and neurostimulation studies in forensic field

Several studies have aimed to address the natural inability of humankind to detect deception and accurately discriminate lying from truth in the legal context. To date, it has been well established that telling a lie is a complex mental activity. During deception, many functions of higher cognition are involved: the decision to lie, withholding the truth, fabricating the lie, monitoring whether the receiver believes the lie, and, if necessary, adjusting the fabricated story and maintaining a consistent lie. In the previous 15 years, increasing interest in the neuroscience of deception has resulted in new possibilities to investigate and interfere with the ability to lie directly from the brain. Cognitive psychology, as well as neuroimaging and neurostimulation studies, are increasing the possibility that neuroscience will be useful for lie detection. This paper discusses the scientific validity of the literature on neuroimaging and neurostimulation regarding lie detection to understand whether scientific findings in this field have a role in the forensic setting. We considered how lie detection technology may contribute to addressing the detection of deception in the courtroom and discussed the conditions and limits in which these techniques reliably distinguish whether an individual is lying

Image-Based Visual-Impedance Control of a Dual-Arm Aerial Manipulator

Three new image-based visual-impedance control laws are proposed in this paper allowing physical interaction of a dual-arm unmanned aerial manipulator equipped with a camera and a force/torque sensor. Namely, two first-order impedance behaviours are designed based on the transpose and the inverse of the system Jacobian matrix, respectively, while a second-order impedance behaviour is carried out as well. Visual information is employed both to coordinate the camera motion in an eye- in-hand configuration with the assigned task executed by the other robot arm, and to define the elastic wrench component of the proposed hybrid impedance equations directly in the image plane

Recent results from kaon physics

The $\pi\nu\nu$ is one of the theoretically cleanest meson decay where to look for indirect effects of new physics complementary to LHC searches. The NA62 experiment at CERN SPS is designed to measure the branching ratio of the $K^+\rightarrow\pi^+\nu\bar{\nu}$ decay with 10\% precision. NA62 took data in 2015 and 2016 reaching the Standard Model sensitivity. The KOTO experiment in Japan is investigating the decay $K_L\rightarrow\pi^0\nu\bar{\nu}$ reaching a higher background suppression. Both experiments are reviewed, and recent results and prospects are summarised