Note on the Relativistic Thermodynamics of Moving Bodies

We employ a novel thermodynamical argument to show that, at the macroscopic level,there is no intrinsic law of temperature transformation under Lorentz boosts. This result extends the corresponding microstatistical one of earlier works to the purely macroscopic regime and signifies that the concept of temperature as an objective entity is restricted to the description of bodies in their rest frames. The argument on which this result is based is centred on the thermal transactions between a body that moves with uniform velocity relative to a certain inertial frame and a thermometer, designed to measure its temperature, that is held at rest in that frame.Comment: To be published in J. Phys. A. A few minor corrections have been made to the earlier version of this articl

On the Question of Temperature Transformations under Lorentz and Galilei Boosts

We provide a quantum statistical thermodynamical solution of the long standing problem of temperature transformations of uniformly moving bodies. Our treatment of this question is based on the well established quantum statistical result that the thermal equilibrium conditions demanded by both the Zeroth and Second Laws of Thermodynamics are precisely those of Kubo, Martin and Schwinger (KMS). We prove that, in both the special relativistic and nonrelativistic settings, a state of a body cannot satisfy these conditions for different inertial frames with non-zero relative velocity. Hence a body that serves as a thermal reservoir, in the sense of the Zeroth Law, in an inertial rest frame cannot do so in a laboratory frame relative to which it moves with non-zero uniform velocity. Consequently, there is no law of temperature transformation under either Lorentz or Galilei boosts, and so the concept of temperature stemming from the Zeroth Law is restricted to states of bodies in their rest frames.Comment: A few minor corrections have been made. The article will be published in J. Phys.

Statistical Thermodynamics of Moving Bodies

We resolve the long standing question of temperature dependence of uniformly moving bodies by means of a quantum statistical treatment centred on the zeroth law of thermodynamics. The key to our treatment is the result, established by Kossakowski et al, that a macroscopic body behaves as a thermal reservoir with well-defined temperature, in the sense of the zeroth law, if and only if its state satisfies the Kubo-Martin-Schwinger (KMS) condition. In order to relate this result to the relativistic thermodynamics of moving bodies, we employ the Tomita-Takesaki modular theory to prove that a state cannot satisfy the KMS conditions with respect to two different inertial frames whose relative velocity is non-zero. This implies that the concept of temperature stemming from the zeroth law is restricted to states of bodies in their rest frames and thus that there is no law of temperature transformations under Lorentz boosts. The corresponding results for nonrelativistic Galilean systems have also been established.Comment: Based on an invited lecture at the 40'th Symposium on Mathematical Physics, held at Torun, Poland, June 25-28, 2008. To be published in "Reports on Mathematical Physics

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)