Magnetism and superconductivity in McM_{c}Ta2_{2}S2_{2}C (M = Fe, Co, Ni, and Cu)

Magnetic properties of $M_{c}$Ta$_{2}$S$_{2}$C ($M$ = Fe, Co, Ni, Cu) have been studied using SQUID DC and AC magnetic susceptibility. In these systems magnetic $M^{2+}$ ions are intercalated into van der Waals gaps between adjacent S layers of host superconductor Ta$_{2}$S$_{2}$C. Fe$_{0.33}$Ta$_{2}$S$_{2}$C is a quasi 2D $XY$-like antiferromagnet on the triangular lattice. It undergoes an antiferromagnetic phase transition at $T_{N}$ (= 117 K). The irreversible effect of magnetization occurs below $T_{N}$, reflecting the frustrated nature of the system. The AF phase coexists with two superconducting phases with the transition temperatures $T_{cu} = 8.8$ K and $T_{cl} = 4.6$ K. Co$_{0.33}$Ta$_{2}$S$_{2}$C is a quasi 2D Ising-like antiferromagnet on the triangular lattice. The antiferromagnetic phase below $T_{N} = 18.6$ K coexists with a superconducting phase below $T_{cu} = 9.1$ K. Both Ni$_{0.25}$Ta$_{2}$S$_{2}$C and Cu$_{0.60}$Ta$_{2}$S$_{2}$C are superconductors with $T_{cu}$ ($= 8.7$ K for Ni and 6.4 K for Cu) and $T_{cl}$ (= 4.6 K common to $M_{c}$Ta$_{2}$S$_{2}$C). Very small effective magnetic moments suggest that Ni$^{2+}$ and Cu$^{2+}$ spins are partially delocalized.Comment: 15 pages, 17 figures, and 3 table

Aging dynamics in reentrant ferromagnet: Cu0.2_{0.2}Co0.8_{0.8}Cl2_{2}-FeCl3_{3} graphite bi-intercalation compound

Aging dynamics of a reentrant ferromagnet Cu$_{0.2}$Co$_{0.8}$Cl$_{2}$-FeCl$_{3}$ graphite bi-intercalation compound has been studied using AC and DC magnetic susceptibility. This compound undergoes successive transitions at the transition temperatures $T_{c}$ ($= 9.7$ K) and $T_{RSG}$ ($= 3.5$ K). The relaxation rate $S(t)$ exhibits a characteristic peak at $t_{cr}$ close to a wait time $t_{w}$ below $T_{c}$, indicating that the aging phenomena occur in both the reentrant spin glass (RSG) phase below $T_{RSG}$ and the ferromagnetic (FM) phase between $T_{RSG}$ and $T_{c}$. The relaxation rate $S(t)$ ($=\text{d}\chi_{ZFC}(t)/\text{d}\ln t$) in the FM phase exhibits two peaks around $t_{w}$ and a time much shorter than $t_{w}$ under the positive $T$-shift aging, indicating a partial rejuvenation of domains. The aging state in the FM phase is fragile against a weak magnetic-field perturbation. The time ($t$) dependence of $\chi_{ZFC}(t)$ around $t \approx t_{cr}$ is well approximated by a stretched exponential relaxation: $\chi_{ZFC}(t) \approx \exp[-(t/\tau)^{1-n}]$. The exponent $n$ depends on $t_{w}$, $T$, and $H$. The relaxation time $\tau$ ($\approx t_{cr}$) exhibits a local maximum around 5 K, reflecting a chaotic nature of the FM phase. It drastically increases with decreasing temperature below $T_{RSG}$.Comment: 16 pages,16 figures, submitted to Physical Review

Nonlinear magnetic susceptibility and aging phenomena in reentrant ferromagnet: Cu0.2_{0.2}Co0.8_{0.8}Cl2_{2}-FeCl3_{3} graphite bi-intercalation compound

Linear and nonlinear dynamic properties of a reentrant ferromagnet Cu$_{0.2}$Co$_{0.8}$Cl$_{2}$-FeCl$_{3}$ graphite bi-intercalation compound are studied using AC and DC magnetic susceptibility. This compound undergoes successive phase transitions at the transition temperatures $T_{h}$ (= 16 K), $T_{c}$ (= 9.7 K), and $T_{RSG}$ (= 3.5 K). The static and dynamic behaviors of the reentrant spin glass phase below $T_{RSG}$ are characterized by those of normal spin glass phase with critical exponent $\beta$ = 0.57 $\pm$ 0.10, a dynamic critical exponent $x$ = 8.5 $\pm$ 1.8, and an exponent $p$ (= 1.55 $\pm$ 0.13) for the de Almeida -Thouless line. A prominent nonlinear susceptibility is observed between $T_{RSG}$ and $T_{c}$ and around $T_{h}$, suggesting a chaotic nature of the ferromagnetic phase ($T_{RSG} \leq T \leq T_{c}$) and the helical spin ordered phase ($T_{c} \leq T \leq T_{h}$). The aging phenomena are observed both in the RSG and FM phases, with the same qualitative features as in normal spin glasses. The aging of zero-field cooled magnetization indicates a drastic change of relaxation mechanism below and above $T_{RSG}$. The time dependence of the absorption $\chi^{\prime \prime}$ is described by a power law form ($\approx t^{-b^{\prime \prime}}$) in the ferromagnetic phase, where $b^{\prime \prime} \approx 0.074 \pm 0.016$ at $f$ = 0.05 Hz and $T$ = 7 K. No $\omega t$-scaling law for $\chi^{\prime \prime}$ [$\approx (\omega t)^{-b^{\prime \prime}}$] is observed.Comment: 14 pages, 16 figures, and 2 table

Dynamic scaling and aging phenomena in short-range Ising spin glass: Cu0.5_{0.5}Co0.5_{0.5}Cl2_{2}-FeCl3_{3} graphite bi-intercalation compound

Static and dynamic behavior of short-range Ising-spin glass Cu$_{0.5}$Co$_{0.5}$Cl$_{2}$-FeCl$_{3}$ graphite bi-intercalation compounds (GBIC) has been studied with SQUID DC and AC magnetic susceptibility. The $T$ dependence of the zero-field relaxation time $\tau$ above a spin-freezing temperature $T_{g}$ (= 3.92 $\pm$ 0.11 K) is well described by critical slowing down. The absorption $\chi^{\prime\prime}$ below $T_{g}$ decreases with increasing angular frequency $\omega$, which is in contrast to the case of 3D Ising spin glass. The dynamic freezing temperature $T_{f}(H,\omega)$ at which d$M_{FC}(T,H)/$d$H=\chi^{\prime}(T,H=0,\omega)$, is determined as a function of frequency (0.01 Hz $\leq \omega/2\pi \leq$ 1 kHz) and magnetic field (0 $\leq H \leq$ 5 kOe). The dynamic scaling analysis of the relaxation time $\tau(T,H)$ defined as $\tau = 1/\omega$ at $T = T_{f}(H,\omega)$ suggests the absence of SG phase in the presence of $H$ (at least above 100 Oe). Dynamic scaling analysis of $\chi^{\prime \prime}(T, \omega)$ and $\tau(T,H)$ near $T_{g}$ leads to the critical exponents ($\beta$ = 0.36 $\pm$ 0.03, $\gamma$ = 3.5 $\pm$ 0.4, $\nu$ = 1.4 $\pm$ 0.2, $z$ = 6.6 $\pm$ 1.2, $\psi$ = 0.24 $\pm$ 0.02, and $\theta$ = 0.13 $\pm$ 0.02). The aging phenomenon is studied through the absorption $\chi^{\prime \prime}(\omega, t)$ below $T_{g}$. It obeys a $(\omega t)^{-b^{\prime \prime}}$ power-law decay with an exponent $b^{\prime \prime}\approx 0.15 - 0.2$. The rejuvenation effect is also observed under sufficiently large (temperature and magnetic-field) perturbations.Comment: 14 pages, 19 figures; to be published in Phys. Rev. B (September 1, 2003

Gene content evolution in the arthropods

Arthropods comprise the largest and most diverse phylum on Earth and play vital roles in nearly every ecosystem. Their diversity stems in part from variations on a conserved body plan, resulting from and recorded in adaptive changes in the genome. Dissection of the genomic record of sequence change enables broad questions regarding genome evolution to be addressed, even across hyper-diverse taxa within arthropods. Using 76 whole genome sequences representing 21 orders spanning more than 500 million years of arthropod evolution, we document changes in gene and protein domain content and provide temporal and phylogenetic context for interpreting these innovations. We identify many novel gene families that arose early in the evolution of arthropods and during the diversification of insects into modern orders. We reveal unexpected variation in patterns of DNA methylation across arthropods and examples of gene family and protein domain evolution coincident with the appearance of notable phenotypic and physiological adaptations such as flight, metamorphosis, sociality, and chemoperception. These analyses demonstrate how large-scale comparative genomics can provide broad new insights into the genotype to phenotype map and generate testable hypotheses about the evolution of animal diversity

Helicobacter pylori infection and gastroduodenal diseases in Vietnam: a cross-sectional, hospital-based study

<p>Abstract</p> <p>Background</p> <p>The rate of <it>H. pylori </it>infection in Vietnam is reportedly high, but the spectrum of <it>H. pylori</it>-associated gastroduodenal diseases has not been systematically investigated. Moreover, despite the similarities of ethnicity and diet, the age-standardized incidence rate of gastric cancer in the northern city of Hanoi is higher than that in the southern city of Ho Chi Minh, but the reason for this phenomenon is unknown. The virulence of Vietnamese <it>H. pylori </it>has also not been investigated in detail.</p> <p>Methods</p> <p>Individuals undergoing esophagogastroduodenoscopy were randomly recruited. <it>H. pylori </it>infection status was determined based on the combined results of culture, histology, immunohistochemistry, rapid urine test and serum ELISA. Peptic ulcer (PU) and gastroesophageal reflux disease was diagnosed by endoscopy, and chronic gastritis was determined histologically. <it>H. pylori </it>virulence factors were investigated by PCR and sequencing.</p> <p>Results</p> <p>Among the examined patients, 65.6% were infected with <it>H. pylori</it>. The prevalence of infection was significantly higher in those over 40 years of age than in those aged ≤40. Chronic gastritis was present in all <it>H. pylori</it>-infected individuals, 83.1% of whom had active gastritis, and 85.3% and 14.7% had atrophy and intestinal metaplasia, respectively. PU was present in 21% of infected patients, whereas its incidence was very low in non-infected individuals. The prevalence of PU was significantly higher in Hanoi than in Ho Chi Minh. The prevalence of <it>vacA m1</it>, which has been identified as an independent risk factor for PU in Vietnam, was significantly higher among <it>H. pylori </it>isolates from Hanoi than among those from Ho Chi Minh.</p> <p>Conclusions</p> <p><it>H. pylori </it>infection is common in Vietnam and is strongly associated with PU, active gastritis, atrophy and intestinal metaplasia. <it>vacA m1 </it>is associated with an increased risk for PU and might contribute to the difference in the prevalence of PU and gastric cancer between Hanoi and Ho Chi Minh.</p

Genomic Profiling of Submucosal-Invasive Gastric Cancer by Array-Based Comparative Genomic Hybridization

Genomic copy number aberrations (CNAs) in gastric cancer have already been extensively characterized by array comparative genomic hybridization (array CGH) analysis. However, involvement of genomic CNAs in the process of submucosal invasion and lymph node metastasis in early gastric cancer is still poorly understood. In this study, to address this issue, we collected a total of 59 tumor samples from 27 patients with submucosal-invasive gastric cancers (SMGC), analyzed their genomic profiles by array CGH, and compared them between paired samples of mucosal (MU) and submucosal (SM) invasion (23 pairs), and SM invasion and lymph node (LN) metastasis (9 pairs). Initially, we hypothesized that acquisition of specific CNA(s) is important for these processes. However, we observed no significant difference in the number of genomic CNAs between paired MU and SM, and between paired SM and LN. Furthermore, we were unable to find any CNAs specifically associated with SM invasion or LN metastasis. Among the 23 cases analyzed, 15 had some similar pattern of genomic profiling between SM and MU. Interestingly, 13 of the 15 cases also showed some differences in genomic profiles. These results suggest that the majority of SMGCs are composed of heterogeneous subpopulations derived from the same clonal origin. Comparison of genomic CNAs between SMGCs with and without LN metastasis revealed that gain of 11q13, 11q14, 11q22, 14q32 and amplification of 17q21 were more frequent in metastatic SMGCs, suggesting that these CNAs are related to LN metastasis of early gastric cancer. In conclusion, our data suggest that generation of genetically distinct subclones, rather than acquisition of specific CNA at MU, is integral to the process of submucosal invasion, and that subclones that acquire gain of 11q13, 11q14, 11q22, 14q32 or amplification of 17q21 are likely to become metastatic

Molecular Evolutionary Analysis of the Influenza A(H1N1)pdm, May–September, 2009: Temporal and Spatial Spreading Profile of the Viruses in Japan

BACKGROUND: In March 2009, pandemic influenza A(H1N1) (A(H1N1)pdm) emerged in Mexico and the United States. In Japan, since the first outbreak of A(H1N1)pdm in Osaka and Hyogo Prefectures occurred in the middle of May 2009, the virus had spread over 16 of 47 prefectures as of June 4, 2009. METHODS/PRINCIPAL FINDINGS: We analyzed all-segment concatenated genome sequences of 75 isolates of A(H1N1)pdm viruses in Japan, and compared them with 163 full-genome sequences in the world. Two analyzing methods, distance-based and Bayesian coalescent MCMC inferences were adopted to elucidate an evolutionary relationship of the viruses in the world and Japan. Regardless of the method, the viruses in the world were classified into four distinct clusters with a few exceptions. Cluster 1 was originated earlier than cluster 2, while cluster 2 was more widely spread around the world. The other two clusters (clusters 1.2 and 1.3) were suggested to be distinct reassortants with different types of segment assortments. The viruses in Japan seemed to be a multiple origin, which were derived from approximately 28 transported cases. Twelve cases were associated with monophyletic groups consisting of Japanese viruses, which were referred to as micro-clade. While most of the micro-clades belonged to the cluster 2, the clade of the first cases of infection in Japan originated from cluster 1.2. Micro-clades of Osaka/Kobe and the Fukuoka cases, both of which were school-wide outbreaks, were eradicated. Time of most recent common ancestor (tMRCA) for each micro-clade demonstrated that some distinct viruses were transmitted in Japan between late May and early June, 2009, and appeared to spread nation-wide throughout summer. CONCLUSIONS: Our results suggest that many viruses were transmitted from abroad in late May 2009 irrespective of preventive actions against the pandemic influenza, and that the influenza A(H1N1)pdm had become a pandemic stage in June 2009 in Japan

Downregulation of SAV1 plays a role in pathogenesis of high-grade clear cell renal cell carcinoma

<p>Abstract</p> <p>Background</p> <p>Clinical outcome of patients with high-grade ccRCC (clear cell renal cell carcinoma) remains still poor despite recent advances in treatment strategies. Molecular mechanism of pathogenesis in developing high-grade ccRCC must be clarified. In the present study, we found that SAV1 was significantly downregulated with copy number loss in high-grade ccRCCs. Therefore, we investigated the SAV1 function on cell proliferation and apoptosis in vitro. Furthermore, we attempted to clarify the downstream signaling which is regulated by SAV1.</p> <p>Methods</p> <p>We performed array CGH and gene expression analysis of 8 RCC cell lines (786-O, 769-P, KMRC-1, KMRC-2, KMRC-3, KMRC-20, TUHR4TKB, and Caki-2), and expression level of mRNA was confirmed by quantitative RT-PCR (qRT-PCR) analysis. We next re-expressed SAV1 in 786-O cells, and analyzed its colony-forming activity. Then, we transfected siRNAs of SAV1 into the kidney epithelial cell line HK2 and renal proximal tubule epithelial cells (RPTECs), and analyzed their proliferation and apoptosis. Furthermore, the activity of YAP1, which is a downstream molecule of SAV1, was evaluated by western blot analysis, reporter assay and immunohistochemical analysis.</p> <p>Results</p> <p>We found that SAV1, a component of the Hippo pathway, is frequently downregulated in high-grade ccRCC. SAV1 is located on chromosome 14q22.1, where copy number loss had been observed in 7 of 12 high-grade ccRCCs in our previous study, suggesting that gene copy number loss is responsible for the downregulation of SAV1. Colony-forming activity by 786-O cells, which show homozygous loss of SAV1, was significantly reduced when SAV1 was re-introduced exogenously. Knockdown of SAV1 promoted proliferation of HK2 and RPTEC. Although the phosphorylation level of YAP1 was low in 786-O cells, it was elevated in SAV1-transduced 786-O cells. Furthermore, the transcriptional activity of the YAP1 and TEAD3 complex was inhibited in SAV1-transduced 786-O cells. Immunohistochemistry frequently demonstrated nuclear localization of YAP1 in ccRCC cases with SAV1 downregulation, and it was preferentially detected in high-grade ccRCC.</p> <p>Conclusions</p> <p>Taken together, downregulation of SAV1 and the consequent YAP1 activation are involved in the pathogenesis of high-grade ccRCC. It is an attractive hypothesis that Hippo signaling could be candidates for new therapeutic target.</p

Association of Transcription Factor Gene LMX1B with Autism

Multiple lines of evidence suggest a serotoninergic dysfunction in autism. The role of LMX1B in the development and maintenance of serotoninergic neurons is well known. In order to examine the role, if any, of LMX1B with autism pathophysiology, a trio-based SNP association study using 252 family samples from the AGRE was performed. Using pair-wise tagging method, 24 SNPs were selected from the HapMap data, based on their location and minor allele frequency. Two SNPs (rs10732392 and rs12336217) showed moderate association with autism with p values 0.018 and 0.022 respectively in transmission disequilibrium test. The haplotype AGCGTG also showed significant association (p = 0.008). Further, LMX1B mRNA expressions were studied in the postmortem brain tissues of autism subjects and healthy controls samples. LMX1B transcripts was found to be significantly lower in the anterior cingulate gyrus region of autism patients compared with controls (p = 0.049). Our study suggests a possible role of LMX1B in the pathophysiology of autism. Based on previous reports, it is likely to be mediated through a seretoninergic mechanism. This is the first report on the association of LMX1B with autism, though it should be viewed with some caution considering the modest associations we report