Dynamic Scaling of Magnetic Flux Noise Near the KTB Transition in Overdamped Josephson Junction Arrays

We have used a dc Superconducting QUantum Interference Device to measure the magnetic flux noise generated by the equilibrium vortex density fluctuations associated with the Kosterlitz-Thouless-Berezinskii (KTB) transition in an overdamped Josephson junction array. At temperatures slightly above the KTB transition temperature, the noise is white for $f<f_\xi$ and scales as $1/f$ for $f>f_\xi$. Here $f_\xi\propto\xi^{-z}$, where $\xi$ is the correlation length and $z$ is the dynamic exponent. Moreover, when all frequencies are scaled by $f_\xi$, data for different temperatures and frequencies collapse on to a single curve. In addition, we have extracted the dynamic exponent $z$ and found $z=1.98\pm0.03$.Comment: 5 pages, LaTeX (REVTeX) format, requires epsfig and amstex style files. 3 figures included. Tentatively scheduled for publication in Physical Review Letters, 18 March, 199

Critical Exponents of the Fully Frustrated 2-D Xy Model

We present a detailed study of the critical properties of the 2-D XY model with maximal frustration in a square lattice. We use extensive Monte Carlo simulations to study the thermodynamics of the spin and chiral degrees of freedom, concentrating on their correlation functions. The gauge invariant spin-spin correlation functions are calculated close to the critical point for lattice sizes up to $240\times 240$; the chiral correlation functions are studied on lattices up to $96\times 96$. We find that the critical exponents of the spin phase transition are $\nu=0.3069$, and $\eta=0.1915$, which are to be compared with the unfrustrated XY model exponents $\nu=1/2$ and $\eta=0.25$. We also find that the critical exponents of the chiral transition are $\nu_{\chi}=0.875$, $2\beta=0.1936$, $2\gamma= 1.82$, and $2\gamma\>\prime=1.025$, which are different from the expected 2-D Ising critical exponents. The spin-phase transition occurs at $T_{U(1)}=0.446$ which is about 7\% above the estimated chiral critical temperature $T_{Z_{2}}= 0.4206$. However, because of the size of the statistical errors, it is difficult to decide with certainty whether the transitions occur at the same or at slightly different temperatures. Finally, the jump in the helicity modulus in the fully frustrated system is found to be about 23\% below the unfrustrated universal value. The most important consequence of these results is that the fully frustrated XY model appears to be in a novel universality class. Recent successful comparisons of some of these results with experimental data are also briefly discussed. (TO APPEAR IN PRB)Comment: 47 pages (PHYZZX

Severe Exercise and Exercise Training Exert Opposite Effects on Human Neutrophil Apoptosis via Altering the Redox Status

Neutrophil spontaneous apoptosis, a process crucial for immune regulation, is mainly controlled by alterations in reactive oxygen species (ROS) and mitochondria integrity. Exercise has been proposed to be a physiological way to modulate immunity; while acute severe exercise (ASE) usually impedes immunity, chronic moderate exercise (CME) improves it. This study aimed to investigate whether and how ASE and CME oppositely regulate human neutrophil apoptosis. Thirteen sedentary young males underwent an initial ASE and were subsequently divided into exercise and control groups. The exercise group (n = 8) underwent 2 months of CME followed by 2 months of detraining. Additional ASE paradigms were performed at the end of each month. Neutrophils were isolated from blood specimens drawn at rest and immediately after each ASE for assaying neutrophil spontaneous apoptosis (annexin-V binding on the outer surface) along with redox-related parameters and mitochondria-related parameters. Our results showed that i) the initial ASE immediately increased the oxidative stress (cytosolic ROS and glutathione oxidation), and sequentially accelerated the reduction of mitochondrial membrane potential, the surface binding of annexin-V, and the generation of mitochondrial ROS; ii) CME upregulated glutathione level, retarded spontaneous apoptosis and delayed mitochondria deterioration; iii) most effects of CME were unchanged after detraining; and iv) CME blocked ASE effects and this capability remained intact even after detraining. Furthermore, the ASE effects on neutrophil spontaneous apoptosis were mimicked by adding exogenous H2O2, but not by suppressing mitochondrial membrane potential. In conclusion, while ASE induced an oxidative state and resulted in acceleration of human neutrophil apoptosis, CME delayed neutrophil apoptosis by maintaining a reduced state for long periods of time even after detraining

Chromosomal location of human genes encoding major heat-shock protein HSP70

The HSP70 family of heat-shock proteins constitutes the major proteins synthesized in response to elevated temperatures and other forms of stress. In eukaryotes members of the HSP70 family also include a protein similar if not identical to bovine brain uncoating ATPase and glucose-regulated proteins. An intriguing relation has been established between expression of heat-shock proteins and transformation in mammalian cells. Elevated levels of HSP70 are found in some transformed cell lines, and viral and cellular gene products that are capable of transforming cells in vitro can also stimulate transcription of HSP70 genes. To determine the organization of this complex multigene family in the human genome, we used complementary approaches: Southern analysis and protein gels of Chinese hamster-human somatic cell hybrids, and in situ hybridization to human chromosomes. We demonstrate that functional genes encoding HSP70 proteins map to human chromosomes 6, 14, 21, and at least one other chromosome .Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45535/1/11188_2005_Article_BF01534692.pd