Suzaku Observation of HCG 62: Temperature, Abundance, and Extended Hard X-ray Emission Profiles

We present results of 120 ks observation of a compact group of galaxies HCG~62 ($z=0.0145$) with Suzaku XIS and HXD-PIN\@. The XIS spectra for four annular regions were fitted with two temperature {\it vapec} model with variable abundance, combined with the foreground Galactic component. The Galactic component was constrained to have a common surface brightness among the four annuli, and two temperature {\it apec} model was preferred to single temperature model. We confirmed the multi-temperature nature of the intra-group medium reported with Chandra and XMM-Newton, with a doughnut-like high temperature ring at radii 3.3--6.5$'$ in a hardness image. We found Mg, Si, S, and Fe abundances to be fairly robust. We examined the possible ``high-abundance arc'' at $\sim 2'$ southwest from the center, however Suzaku data did not confirm it. We suspect that it is a misidentification of an excess hot component in this region as the Fe line. Careful background study showed no positive detection of the extended hard X-rays previously reported with ASCA, in 5--12 keV with XIS and 12--40 keV with HXD-PIN, although our upper limit did not exclude the ASCA result. There is an indication that the X-ray intensity in $r<3.3'$ region is $70\pm 19$% higher than the nominal CXB level (5--12 keV), and Chandra and Suzaku data suggest that most of this excess could be due to concentration of hard X-ray sources with an average photon index of $\Gamma=1.38\pm 0.06$. Cumulative mass of O, Fe and Mg in the group gas and the metal mass-to-light ratio were derived and compared with those in other groups. Possible role of AGN or galaxy mergers in this group is also discussed.Comment: 29 pages with 9 figures, accepted for publication in PASJ Vol 60, second Suzaku special issu

Safety and Efficacy of FIT039 for Verruca Vulgaris: A Placebo-Controlled, Phase I/II Randomized Controlled Trial

TRIAL DESIGN: Human papillomavirus infection causes verruca vulgaris. CDK9 inhibitor FIT039 inhibits DNA virus proliferation in animal models. We conducted a multicenter, single-blind, placebo-controlled, randomized phase I/II clinical trial evaluating the safety and efficacy of FIT039 against verruca vulgaris. METHODS: Target lesions were treated with liquid nitrogen once, and a FIT039 patch or placebo patch was applied for 14 days. The primary endpoint was lesion disappearance. The secondary endpoints were safety and changes in dimension, cross-sectional area, and the number of petechial lesions. RESULTS: A total of 24 participants were randomly allocated to the FIT039 (n = 13, median age, 54 years) and placebo (n = 11, median age, 62 years) groups. Verruca vulgaris did not disappear. FIT039 decreased the dimension to 76% of the initial value on day 29, followed by an increase to 98% on day 57. Placebo showed a monotonic increase to 107% on day 57. Changes in the cross-sectional area and petechiae number were comparable between the groups. CONCLUSIONS: No drug-related adverse reactions occurred. FIT039 efficacy was not determined in this study

CNVs in Three Psychiatric Disorders

BACKGROUND: We aimed to determine the similarities and differences in the roles of genic and regulatory copy number variations (CNVs) in bipolar disorder (BD), schizophrenia (SCZ), and autism spectrum disorder (ASD). METHODS: Based on high-resolution CNV data from 8708 Japanese samples, we performed to our knowledge the largest cross-disorder analysis of genic and regulatory CNVs in BD, SCZ, and ASD. RESULTS: In genic CNVs, we found an increased burden of smaller (500 kb) exonic CNVs in SCZ/ASD. Pathogenic CNVs linked to neurodevelopmental disorders were significantly associated with the risk for each disorder, but BD and SCZ/ASD differed in terms of the effect size (smaller in BD) and subtype distribution of CNVs linked to neurodevelopmental disorders. We identified 3 synaptic genes (DLG2, PCDH15, and ASTN2) as risk factors for BD. Whereas gene set analysis showed that BD-associated pathways were restricted to chromatin biology, SCZ and ASD involved more extensive and similar pathways. Nevertheless, a correlation analysis of gene set results indicated weak but significant pathway similarities between BD and SCZ or ASD (r = 0.25–0.31). In SCZ and ASD, but not BD, CNVs were significantly enriched in enhancers and promoters in brain tissue. CONCLUSIONS: BD and SCZ/ASD differ in terms of CNV burden, characteristics of CNVs linked to neurodevelopmental disorders, and regulatory CNVs. On the other hand, they have shared molecular mechanisms, including chromatin biology. The BD risk genes identified here could provide insight into the pathogenesis of BD

Synthesis and Characterization of the Germathioacid Chloride Coordinated by an N-Heterocyclic Carbene §

Carboxylic acid chlorides are useful substrates in organic chemistry. Many germanium analogues of carboxylic acid chloride have been synthesized so far. Nevertheless, all of the reported germathioacid chlorides use bidentate nitrogen ligands and contain germanium-nitrogen bonds. Our group synthesized germathioacid chloride, Ge(S)Cl{C6H3-2,6-Tip2}(Im-i-Pr2Me2), using N-heterocyclic carbene (Im-i-Pr2Me2). As a result of density functional theory (DFT) calculation, it was found that electrons are localized on sulfur, and the germanium-sulfur bond is a single bond with a slight double bond property

The HEDGEHOG-GLI1 pathway is important for fibroproliferative properties in keloids and as a candidate therapeutic target

Abstract Keloids are benign fibroproliferative skin tumors caused by aberrant wound healing that can negatively impact patient quality of life. The lack of animal models has limited research on pathogenesis or developing effective treatments, and the etiology of keloids remains unknown. Here, we found that the characteristics of stem-like cells from keloid lesions and the surrounding dermis differ from those of normal skin. Furthermore, the HEDGEHOG (HH) signal and its downstream transcription factor GLI1 were upregulated in keloid patient–derived stem-like cells. Inhibition of the HH-GLI1 pathway reduced the expression of genes involved in keloids and fibrosis-inducing cytokines, including osteopontin. Moreover, the HH signal inhibitor vismodegib reduced keloid reconstituted tumor size and keloid-related gene expression in nude mice and the collagen bundle and expression of cytokines characteristic for keloids in ex vivo culture of keloid tissues. These results implicate the HH-GLI1 pathway in keloid pathogenesis and suggest therapeutic targets of keloids