Energy Spectrum of Two-Dimensional Acoustic Turbulence.

We report an exact unique constant-flux power-law analytical solution of the wave kinetic equation for the turbulent energy spectrum, E(k)=C_{1}sqrt[ϵac_{s}]/k, of acoustic waves in 2D with almost linear dispersion law, ω_{k}=c_{s}k[1+(ak)^{2}], ak≪1. Here, ϵ is the energy flux over scales, and C_{1} is the universal constant which was found analytically. Our theory describes, for example, acoustic turbulence in 2D Bose-Einstein condensates. The corresponding 3D counterpart of turbulent acoustic spectrum was found over half a century ago, however, due to the singularity in 2D, no solution has been obtained until now. We show the spectrum E(k) is realizable in direct numerical simulations of forced-dissipated Gross-Pitaevskii equation in the presence of strong condensate.

An epidemic model for an evolving pathogen with strain-dependent immunity.

Between pandemics, the influenza virus exhibits periods of incremental evolution via a process known as antigenic drift. This process gives rise to a sequence of strains of the pathogen that are continuously replaced by newer strains, preventing a build up of immunity in the host population. In this paper, a parsimonious epidemic model is defined that attempts to capture the dynamics of evolving strains within a host population. The 'evolving strains' epidemic model has many properties that lie in-between the Susceptible-Infected-Susceptible and the Susceptible-Infected-Removed epidemic models, due to the fact that individuals can only be infected by each strain once, but remain susceptible to reinfection by newly emerged strains. Coupling results are used to identify key properties, such as the time to extinction. A range of reproduction numbers are explored to characterise the model, including a novel quasi-stationary reproduction number that can be used to describe the re-emergence of the pathogen into a population with 'average' levels of strain immunity, analogous to the beginning of the winter peak in influenza. Finally the quasi-stationary distribution of the evolving strains model is explored via simulation.

Amniocytes can serve a dual function as a source of iPS cells and feeder layers.

Clinical barriers to stem-cell therapy include the need for efficient derivation of histocompatible stem cells and the zoonotic risk inherent to human stem-cell xenoculture on mouse feeder cells. We describe a system for efficiently deriving induced pluripotent stem (iPS) cells from human and mouse amniocytes, and for maintaining the pluripotency of these iPS cells on mitotically inactivated feeder layers prepared from the same amniocytes. Both cellular components of this system are thus autologous to a single donor. Moreover, the use of human feeder cells reduces the risk of zoonosis. Generation of iPS cells using retroviral vectors from short- or long-term cultured human and mouse amniocytes using four factors, or two factors in mouse, occurs in 5-7 days with 0.5% efficiency. This efficiency is greater than that reported for mouse and human fibroblasts using similar viral infection approaches, and does not appear to result from selective reprogramming of Oct4(+) or c-Kit(+) amniocyte subpopulations. Derivation of amniocyte-derived iPS (AdiPS) cell colonies, which express pluripotency markers and exhibit appropriate microarray expression and DNA methylation properties, was facilitated by live immunostaining. AdiPS cells also generate embryoid bodies in vitro and teratomas in vivo. Furthermore, mouse and human amniocytes can serve as feeder layers for iPS cells and for mouse and human embryonic stem (ES) cells. Thus, human amniocytes provide an efficient source of autologous iPS cells and, as feeder cells, can also maintain iPS and ES cell pluripotency without the safety concerns associated with xenoculture.

Prevalence of metabolic syndrome and related characteristics in obese adolescents with and without polycystic ovary syndrome.

CONTEXT: Adults with polycystic ovary syndrome (PCOS) may be at increased risk for metabolic syndrome (MBS) and related cardiovascular disease. It is not clear whether PCOS diagnosed in adolescence increases the risk of MBS in this age group. OBJECTIVE: The aim was to compare the prevalence and related characteristics of MBS in obese adolescents with and without PCOS. DESIGN: We conducted a cross-sectional study of overweight and obese PCOS adolescents and BMI matched controls. PATIENTS AND PARTICIPANTS: A total of 74 subjects, 43 with PCOS and 31 controls, participated in the study. INTERVENTIONS: Each subject underwent a physical examination and laboratory evaluation for a diagnosis of MBS. Regional fat distribution was determined by computerized tomography scan in the PCOS adolescents. MAIN OUTCOME MEASURES: We measured the prevalence of MBS and its components in adolescent subjects and controls. RESULTS: The PCOS group had larger ovarian volume and higher measures of total testosterone and free androgen index than controls, but there were no differences in waist circumference, fasting glucose, blood pressure, or lipids. PCOS adolescents demonstrated more glucose abnormalities and higher plasminogen activator inhibitor-1. By pediatric criteria, 53% of the PCOS and 55% of the control adolescents had MBS. By adult criteria, 26% of PCOS and 29% of controls met diagnostic criteria for MBS. CONCLUSIONS: Obese adolescent women have a high prevalence of MBS, and PCOS does not add additional risk for MBS. There appears to be an association between MBS and visceral adiposity. PCOS is associated with increased incidence of glucose intolerance and increased plasminogen activator inhibitor-1. Our results reinforce the importance of obesity counseling in adolescents to recognize the possible risk of future cardiovascular disease in these young women.