Magnetization steps in a diluted Heisenberg antiferromagnetic chain: Theory and experiments on TMMC:Cd

A theory for the equilibrium low-temperature magnetization M of a diluted Heisenberg antiferromagnetic chain is presented. The magnetization curve, M versus B, is calculated using the exact contributions of finite chains with 1 to 5 spins, and the "rise and ramp approximation" for longer chains. Some non-equilibrium effects that occur in a rapidly changing B, are also considered. Specific non-equilibrium models based on earlier treatments of the phonon bottleneck, and of spin flips associated with cross relaxation and with level crossings, are discussed. Magnetization data on powders of TMMC diluted with cadmium [i.e., (CH_3)_4NMn_xCd_(1-x)Cl_3, with 0.16<=x<=0.50 were measured at 0.55 K in 18 T superconducting magnets. The field B_1 at the first MST from pairs is used to determine the NN exchange constant, J, which changes from -5.9 K to -6.5 K as x increases from 0.16 to 0.50. The magnetization curves obtained in the superconducting magnets are compared with simulations based on the equilibrium theory. Data for the differential susceptibility, dM/dB, were taken in pulsed magnetic fields (7.4 ms duration) up to 50 T, with the powder samples in a 1.5 K liquid-helium bath. Non-equilibrium effects, which became more severe as x decreased, were observed. The non-equilibrium effects are tentatively interpreted using the "Inadequate Heat Flow Scenario," or to cross-relaxation, and crossings of energy levels, including those of excited states.Comment: 16 pages, 14 figure

Critical Properties of Condensation of Field-Induced Triplet Quasiparticles

A review on the field-induced magnetic ordering is given, together with some results of a quantum Monte Carlo simulation focused on the critical behevior near the quantum critical point.Comment: Proceedings of SPQS, Sendai, 200

Thyrotropin-releasing hormone (TRH) promotes wound re-epithelialisation in frog and human skin

There remains a critical need for new therapeutics that promote wound healing in patients suffering from chronic skin wounds. This is, in part, due to a shortage of simple, physiologically and clinically relevant test systems for investigating candidate agents. The skin of amphibians possesses a remarkable regenerative capacity, which remains insufficiently explored for clinical purposes. Combining comparative biology with a translational medicine approach, we report the development and application of a simple ex vivo frog (Xenopus tropicalis) skin organ culture system that permits exploration of the effects of amphibian skin-derived agents on re-epithelialisation in both frog and human skin. Using this amphibian model, we identify thyrotropin-releasing hormone (TRH) as a novel stimulant of epidermal regeneration. Moving to a complementary human ex vivo wounded skin assay, we demonstrate that the effects of TRH are conserved across the amphibian-mammalian divide: TRH stimulates wound closure and formation of neo-epidermis in organ-cultured human skin, accompanied by increased keratinocyte proliferation and wound healing-associated differentiation (cytokeratin 6 expression). Thus, TRH represents a novel, clinically relevant neuroendocrine wound repair promoter that deserves further exploration. These complementary frog and human skin ex vivo assays encourage a comparative biology approach in future wound healing research so as to facilitate the rapid identification and preclinical testing of novel, evolutionarily conserved, and clinically relevant wound healing promoters

Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets