Relation between space-time inversion and particle-antiparticle symmetry and the microscopic essence of special relativity

After analyzing the implication of investigations on the C, P and T transformations since 1956, we propose that there is a basic symmetry in particle physics. The combined space-time inversion is equivalent to particle-antiparticle transformation, denoted by ${\cal PT=C}$. It is shown that the relativistic quantum mechanics and quantum field theory do contain this invariance explicitly or implicitly. In particular, (a) the appearance of negative energy or negative probability density in single particle theory -- corresponding to the fact of existence of antiparticle, (b) spin- statistics connection, (c) CPT theorem, (d) the Feynman propagator are linked together via this symmetry. Furthermore, we try to derive the main results of special relativity, especially, (e) the mass-energy relation, (f) the Lorentz transformation by this one ``relativistic'' postulate and some ``nonrelativistic'' knowledge.Comment: 29 pages, Latex, 1 figur

Mean Response Models of Repeated Measurements in Presence of Varying Effectiveness Onset

Repeated measurements are often collected over time to evaluate treatment efficacy in clinical trials. Most of the statistical models of the repeated measurements have been focusing on their mean response as function of time. These models usually assume that the treatment has persistent effect of constant additivity or multiplicity on the mean response functions throughout the observation period of time. In reality, however, such assumption may be confounded by the potential existence of the so-called effectiveness action onset, although they are often unobserved or difficult to obtain. Instead of including nonparametric time-varying coefficients in the mean response models, we propose and study some semiparametric mean response models to accommodate such effectiveness times. Our methodologies will be demonstrated by a real randomised clinical trial data

Semiparametric Regression Analysis of Mean Residual Life with Censored Survival Data

As a function of time t, mean residual life is the remaining life expectancy of a subject given survival up to t. The proportional mean residual life model, proposed by Oakes & Dasu (1990), provides an alternative to the Cox proportional hazards model to study the association between survival times and covariates. In the presence of censoring, we develop semiparametric inference procedures for the regression coefficients of the Oakes-Dasu model using martingale theory for counting processes. We also present simulation studies and an application to the Veterans\u27 Administration lung cancer data

Spin transfer in a ferromagnet-quantum dot and tunnel barrier coupled Aharonov-Bohm ring system with Rashba spin-orbit interactions

The spin transfer effect in ferromagnet-quantum dot (insulator)-ferromagnet Aharonov-Bohm (AB) ring system with Rashba spin-orbit (SO) interactions is investigated by means of Keldysh nonequilibrium Green function method. It is found that both the magnitude and direction of the spin transfer torque (STT) acting on the right ferromagnet electrode can be effectively controlled by changing the magnetic flux threading the AB ring or the gate voltage on the quantum dot. The STT can be greatly augmented by matching a proper magnetic flux and an SO interaction at a cost of low electrical current. The STT, electrical current, and spin current are uncovered to oscillate with the magnetic flux. The present results are expected to be useful for information storage in nanospintronics.Comment: 17pages, 7figure

Estimating a Treatment Effect with Repeated Measurements Accounting for Varying Effectiveness Duration

To assess treatment efficacy in clinical trials, certain clinical outcomes are repeatedly measured for same subject over time. They can be regarded as function of time. The difference in their mean functions between the treatment arms usually characterises a treatment effect. Due to the potential existence of subject-specific treatment effectiveness lag and saturation times, erosion of treatment effect in the difference may occur during the observation period of time. Instead of using ad hoc parametric or purely nonparametric time-varying coefficients in statistical modeling, we first propose to model the treatment effectiveness durations, which are the varying time intervals between the lag and saturation times. Then some mean response models are used to include such treatment effectiveness durations. Our methodologies are demonstrated by simulations and an application to the dataset of a landmark HIV/AIDS clinical trial of short-course nevirapine against mother-to-child HIV vertical transmission during labour and delivery

Deletion of the V2 vasopressin receptor gene in two Chinese patients with nephrogenic diabetes insipidus

BACKGROUND: Congenital nephrogenic diabetes insipidus (NDI) is a rare X-linked inherited disorder characterized by the excretion of large volumes of diluted urine and caused by mutations in arginine vasopressin receptor 2 (AVPR2) gene. To investigate the mutation of AVPR2 gene in a Chinese family with congenital NDI, we screened AVPR2 gene in two NDI patients and eight family members by PCR amplification and direct sequencing. RESULTS: Five specific fragments, covering entire coding sequence and their flanking intronic sequences of AVPR2 gene, were not observed in both patients, while those fragments were all detected in the control subjects. Several different fragments around the AVPR2 locus were amplified step by step. It was revealed that a genomic fragment of 5,995-bp, which contained the entire AVPR2 gene and the last exon (exon 22) of the C1 gene, was deleted and a 3-bp (GAG) was inserted. Examination of the other family members showed that the mothers and the grandmother were carriers for this deletion. CONCLUSION: Our findings suggest that the two patients in a Chinese family suffering from congenital NDI had a 5,995-bp deletion and 3-bp (GAG) insertion at Xq28. The deletion contained the entire AVPR2 gene and exon 22 of the C1 gene