Physical Electronics

Contains reports on two research projects

Anomalous decay of a prepared state due to non-Ohmic coupling to the continuum

We study the decay of a prepared state $E_0$ into a continuum {E_k} in the case of non-Ohmic models. This means that the coupling is $|V_{k,0}| \propto |E_k-E_0|^{s-1}$ with $s \ne 1$. We find that irrespective of model details there is a universal generalized Wigner time $t_0$ that characterizes the evolution of the survival probability $P_0(t)$. The generic decay behavior which is implied by rate equation phenomenology is a slowing down stretched exponential, reflecting the gradual resolution of the bandprofile. But depending on non-universal features of the model a power-law decay might take over: it is only for an Ohmic coupling to the continuum that we get a robust exponential decay that is insensitive to the nature of the intra-continuum couplings. The analysis highlights the co-existence of perturbative and non-perturbative features in the dynamics. It turns out that there are special circumstances in which $t_0$ is reflected in the spreading process and not only in the survival probability, contrary to the naive linear response theory expectation.Comment: 13 pages, 11 figure

Physical Electronics

Contains reports on four research projects

Physical Electronics

Contains reports on three research projects

Physical Electronics

Contains research objectives and reports on four research projects

Physical Electronics

Contains reports on three research projects

Physical Electronics

Contains research objectives and reports on two research projects

Quantum decay into a non-flat continuum

We study the decay of a prepared state into non-flat continuum. We find that the survival probability $P(t)$ might exhibit either stretched-exponential or power-law decay, depending on non-universal features of the model. Still there is a universal characteristic time $t_0$ that does not depend on the functional form. It is only for a flat continuum that we get a robust exponential decay that is insensitive to the nature of the intra-continuum couplings. The analysis highlights the co-existence of perturbative and non-perturbative features in the local density of states, and the non-linear dependence of $1/t_0$ on the strength of the coupling.Comment: 10 pages, 4 figure

The IGSF1 deficiency syndrome may present with normal free T4 levels, severe obesity, or premature testicular growth

Our objective was to further expand the spectrum of clinical characteristics of the IGSF1 deficiency syndrome in affected males. These characteristic include almost universal congenital central hypothyroidism (CeH) with disharmonious pubertal development (normally timed testicular growth, but delayed rise of serum testosterone), macroorchidism, increased body mass index (BMI), and decreased attentional control. In addition, a subset of patients show prolactin deficiency, transient partial growth hormone deficiency in childhood and increased growth hormone secretion in adulthood. We present a family in which the proband was diagnosed with CeH and low serum prolactin. Severe weight gain started at two years old, with a BMI of 42.3 at 13.9 years. Testicular enlargement (5-6 mL, 3.8-4.3 standard deviation score) started aged three years. A pathogenic variant was found in the IGSF1 gene: c.3411_3412del, p.(Tyr1137*). His brother was referred for short stature at age 13 years and was diagnosed with CeH, normal serum prolactin and IGF-1, and disharmonious puberty. In four male relatives (the proband's brother and three cousins) with the variant (one adult), free thyroxine (fT4) was below the lower limit of the reference range in two, and just above this limit in the other two. Three were overweight or obese, adolescents had disharmonious pubertal development and the adult had profound macroorchidism. In conclusion, male hemizygous carriers of a pathogenic IGSF1 variant can present with fT4 concentration above the lower limit of the reference range while severe early onset obesity or premature testicular growth are part of the phenotypic spectrum.Genetics of disease, diagnosis and treatmen