A crystallographic phase transition within the magnetically ordered state of Ce_2Fe_17

X-ray diffraction experiments were performed on polycrystalline and single-crystal specimens of Ce$_{2}$Fe$_{17}$ at temperatures between 10 K and 300 K. Below $T_{\mathrm{t}}$ = 118$\pm$2 K, additional weak superstructure reflections were observed in the antiferromagnetically ordered state. The superstructure can be described by a doubling of the chemical unit cell along the $\mathbf{c}$ direction in hexagonal notation with the same space group $R \bar{3} m$ as the room-temperature structure. The additional antiferromagnetic satellite reflections observed in earlier neutron diffraction experiments can be conclusively related to the appearance of this superstructure.Comment: 8 pages, figures, submitted for publication in Phys. Rev.

Magnetic properties of the frustrated AFM spinel ZnCr_2O_4 and the spin-glass Zn_{1-x}Cd_xCr_2O_4 (x=0.05,0.10)

The $T$-dependence (2- 400 K) of the electron paramagnetic resonance (EPR), magnetic susceptibility, $\chi (T)$, and specific heat, $C_{v}(T)$, of the $normal$ antiferromagnetic (AFM) spinel ZnCr$_{2}$O$_{4}$ and the spin-glass (SG) Zn$_{1-x}$Cd$_{x}$Cr$_{2}$O$_{4}$ ($x=0.05,0.10$) is reported. These systems behave as a strongly frustrated AFM and SG with $$ $\approx T_{G}\approx 12$ K and -400 K $\gtrsim \Theta_{CW}\gtrsim -500$ K. At high-$T$ the EPR intensity follows the $\chi (T)$ and the $g$-value is $T$-independent. The linewidth broadens as the temperature is lowered, suggesting the existence of short range AFM correlations in the paramagnetic phase. For ZnCr$_{2}$O$_{4}$ the EPR intensity and $\chi (T)$ decreases below 90 K and 50 K, respectively. These results are discussed in terms of nearest-neighbor Cr$^{3+}$ (S $=3/2$%) spin-coupled pairs with an exchange coupling of $| J/k| \approx$ 50 K. The appearance of small resonance modes for $T\lesssim 17$ K, the observation of a sharp drop in $\chi (T)$ and a strong peak in $C_{v}(T)$ at $T_{N}=12$ K confirms, as previously reported, the existence of long range AFM correlations in the low-$T$ phase. A comparison with recent neutron diffraction experiments that found a near dispersionless excitation at 4.5 meV for $T\lesssim T_{N}$ and a continuous gapless spectrum for $T\gtrsim T_{N}$, is also given.Comment: 17 pages, 8 figures, 1 Table. Submitted to Physical Review

Identification of Ischemic Regions in a Rat Model of Stroke

Investigations following stroke first of all require information about the spatio-temporal dimension of the ischemic core as well as of perilesional and remote affected tissue. Here we systematically evaluated regions differently impaired by focal ischemia.Wistar rats underwent a transient 30 or 120 min suture-occlusion of the middle cerebral artery (MCAO) followed by various reperfusion times (2 h, 1 d, 7 d, 30 d) or a permanent MCAO (1 d survival). Brains were characterized by TTC, thionine, and immunohistochemistry using MAP2, HSP72, and HSP27. TTC staining reliably identifies the infarct core at 1 d of reperfusion after 30 min MCAO and at all investigated times following 120 min and permanent MCAO. Nissl histology denotes the infarct core from 2 h up to 30 d after transient as well as permanent MCAO. Absent and attenuated MAP2 staining clearly identifies the infarct core and perilesional affected regions at all investigated times, respectively. HSP72 denotes perilesional areas in a limited post-ischemic time (1 d). HSP27 detects perilesional and remote impaired tissue from post-ischemic day 1 on. Furthermore a simultaneous expression of HSP72 and HSP27 in perilesional neurons was revealed.TTC and Nissl staining can be applied to designate the infarct core. MAP2, HSP72, and HSP27 are excellent markers not only to identify perilesional and remote areas but also to discriminate affected neuronal and glial populations. Moreover markers vary in their confinement to different reperfusion times. The extent and consistency of infarcts increase with prolonged occlusion of the MCA. Therefore interindividual infarct dimension should be precisely assessed by the combined use of different markers as described in this study

Expression of the 60 kDa and 71 kDa heat shock proteins and presence of antibodies against the 71 kDa heat shock protein in pediatric patients with immune thrombocytopenic purpura

BACKGROUND: Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by platelet destruction resulting from autoantibodies against platelet proteins, particularly platelet glycoprotein IIb/IIIa. Heat shock proteins (Hsp) have been shown to be major antigenic determinants in some autoimmune diseases. Antibodies to Hsps have also been reported to be associated with a number of pathological states. METHODS: Using western blot, we measured the levels of the 60 kDa heat shock protein (Hsp60) and of the inducible 71 kDa member of the Hsp70 family (Hsp71) in lymphocytes and the presence of antibodies against these hsps in plasma of 29 pediatric patients with ITP before the treatment and in 6 other patients before and after treatment. RESULTS: Interestingly only one out of 29 patients showed detectable Hsp60 in lymphocytes while this heat shock protein was detected in the 30 control children. Hsp71 levels were slightly lower in lymphocytes of patients with ITP than in controls (1567.8 ± 753.2 via 1763.2 ± 641.8 integrated optical density (IOD) units). There was a small increase of Hsp71 after recovery from ITP. The titers of plasma antibodies against Hsp60 and Hsp71 were also examined. Antibodies against Hsp71 were more common in ITP patients (15/29) than in control children (5/30). The titer of anti-Hsp71 was also higher in children patients with ITP. The prevalence of ITP children with antibodies against Hsp71 (51.7%) was as high as those with antibodies against platelet membrane glycoproteins (58.3%). CONCLUSIONS: In summary, pediatric patients with ITP showed no detectable expression of Hsp60 in lymphocytes and a high prevalence of antibody against Hsp71 in plasma. These changes add to our understanding of the pathogenesis of ITP and may be important for the diagnosis, prognosis and treatment of ITP

Glial Hsp70 Protects K+ Homeostasis in the Drosophila Brain during Repetitive Anoxic Depolarization

Neural tissue is particularly vulnerable to metabolic stress and loss of ion homeostasis. Repetitive stress generally leads to more permanent dysfunction but the mechanisms underlying this progression are poorly understood. We investigated the effects of energetic compromise in Drosophila by targeting the Na+/K+-ATPase. Acute ouabain treatment of intact flies resulted in subsequent repetitive comas that led to death and were associated with transient loss of K+ homeostasis in the brain. Heat shock pre-conditioned flies were resistant to ouabain treatment. To control the timing of repeated loss of ion homeostasis we subjected flies to repetitive anoxia while recording extracellular [K+] in the brain. We show that targeted expression of the chaperone protein Hsp70 in glial cells delays a permanent loss of ion homeostasis associated with repetitive anoxic stress and suggest that this is a useful model for investigating molecular mechanisms of neuroprotection

Function of SSA Subfamily of Hsp70 Within and Across Species Varies Widely in Complementing Saccharomyces cerevisiae Cell Growth and Prion Propagation

BACKGROUND:The cytosol of most eukaryotic cells contains multiple highly conserved Hsp70 orthologs that differ mainly by their spatio-temporal expression patterns. Hsp70s play essential roles in protein folding, transport or degradation, and are major players of cellular quality control processes. However, while several reports suggest that specialized functions of Hsp70 orthologs were selected through evolution, few studies addressed systematically this issue. METHODOLOGY/PRINCIPAL FINDINGS:We compared the ability of Ssa1p-Ssa4p from Saccharomyces cerevisiae and Ssa5p-Ssa8p from the evolutionary distant yeast Yarrowia lipolytica to perform Hsp70-dependent tasks when expressed as the sole Hsp70 for S. cerevisiae in vivo. We show that Hsp70 isoforms (i) supported yeast viability yet with markedly different growth rates, (ii) influenced the propagation and stability of the [PSI(+)] and [URE3] prions, but iii) did not significantly affect the proteasomal degradation rate of CFTR. Additionally, we show that individual Hsp70 orthologs did not induce the formation of different prion strains, but rather influenced the aggregation properties of Sup35 in vivo. Finally, we show that [URE3] curing by the overexpression of Ydj1p is Hsp70-isoform dependent. CONCLUSION/SIGNIFICANCE:Despite very high homology and overlapping functions, the different Hsp70 orthologs have evolved to possess distinct activities that are required to cope with different types of substrates or stress situations. Yeast prions provide a very sensitive model to uncover this functional specialization and to explore the intricate network of chaperone/co-chaperone/substrates interactions

Gene Expression Profiling of Two Distinct Neuronal Populations in the Rodent Spinal Cord

BACKGROUND: In the field of neuroscience microarray gene expression profiles on anatomically defined brain structures are being used increasingly to study both normal brain functions as well as pathological states. Fluorescent tracing techniques in brain tissue that identifies distinct neuronal populations can in combination with global gene expression profiling potentially increase the resolution and specificity of such studies to shed new light on neuronal functions at the cellular level. METHODOLOGY/PRINCIPAL FINDINGS: We examine the microarray gene expression profiles of two distinct neuronal populations in the spinal cord of the neonatal rat, the principal motor neurons and specific interneurons involved in motor control. The gene expression profiles of the respective cell populations were obtained from amplified mRNA originating from 50-250 fluorescently identified and laser microdissected cells. In the data analysis we combine a new microarray normalization procedure with a conglomerate measure of significant differential gene expression. Using our methodology we find 32 genes to be more expressed in the interneurons compared to the motor neurons that all except one have not previously been associated with this neuronal population. As a validation of our method we find 17 genes to be more expressed in the motor neurons than in the interneurons and of these only one had not previously been described in this population. CONCLUSIONS/SIGNIFICANCE: We provide an optimized experimental protocol that allows isolation of gene transcripts from fluorescent retrogradely labeled cell populations in fresh tissue, which can be used to generate amplified aRNA for microarray hybridization from as few as 50 laser microdissected cells. Using this optimized experimental protocol in combination with our microarray analysis methodology we find 49 differentially expressed genes between the motor neurons and the interneurons that reflect the functional differences between these two cell populations in generating and transmitting the motor output in the rodent spinal cord

Establishment of endosymbiosis: the case of cnidarians and <i>Symbiodinium</i>

The symbiosis between cnidarians and Symbiodinium algae (dinoflagellates) is the keystone responsible for the formation of the huge and important structures that are coral reefs. Today many environmental and/or anthropogenic threats compromise this tight relationship and lead to more frequent events of drastic loss of Symbiodinium pigments and eventually of algae themselves from cnidarians, better known as cnidarian bleaching. While the mechanisms underlying the collapse of the algae–coral symbiosis are progressively getting unraveled, the understanding of the mechanisms involved in the de novo infection of bleached cnidarians by Symbiodinium remains elusive. In this review, we describe the various steps needed to establish a stable symbiotic relationship between Symbiodinium and cnidarians. We review the mechanisms implicated in host–symbiont recognition and in symbiosome formation and persistence, with a special emphasis on the role played by lectins and Rab proteins. A better understanding of these molecular mechanisms may contribute to the development of strategies to promote post-bleaching recovery of corals